Volume 95

WORLD HEALTH ORGANIZATION
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER
IARC Monographs on the Evaluation of

Carcinogenic Risks to Humans
VOLUME 95
Household Use of Solid Fuels and
High-temperature Frying
LYON, FRANCE
2010
WORLD HEALTH ORGANIZATION

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER
IARC Monographs on the Evaluation of

Carcinogenic Risks to Humans
VOLUME 95
Household Use of Solid Fuels and

High-temperature Frying
This publication represents the views and expert opinions

of an IARC Working Group on the
Evaluation of Carcinogenic Risks to Humans,
which met in Lyon,
1017 October 2006
2010
IARC MONOGRAPHS
In 1969, the International Agency for Research on Cancer (IARC) initiated a programme on the evaluation of the
carcinogenic risk of chemicals to humans involving the production of critically evaluated monographs on individual
chemicals. The programme was subsequently expanded to include evaluations of carcinogenic risks associated with
exposures to complex mixtures, lifestyle factors and biological and physical agents, as well as those in specific
occupations. The objective of the programme is to elaborate and publish in the form of monographs critical reviews of
data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations; to
evaluate these data in terms of human risk with the help of international working groups of experts in chemical
carcinogenesis and related fields; and to indicate where additional research efforts are needed. The lists of IARC
evaluations are regularly updated and are available on the Internet at http://monographs.iarc.fr/.
This programme has been supported since 1982 by Cooperative Agreement U01 CA33193 with the United
States National Cancer Institute, Department of Health and Human Services. Additional support has been provided
since 1986 by the Health, Safety and Hygiene at Work Unit of the European Commission Directorate-General for
Employment, Social Affairs and Equal Opportunities, and since 1992 by the United States National Institute of
Environmental Health Sciences, Department of Health and Human Services. The contents of this volume are solely
the responsibility of the Working Group and do not necessarily represent the official views of the U.S. National
Cancer Institute, the U.S. National Institute of Environmental Health Sciences, the U.S. Department of Health and
Human Services, or the European Commission Directorate-General for Employment, Social Affairs and Equal
Opportunities.
Published by the International Agency for Research on Cancer,
150 cours Albert Thomas, 69372 Lyon Cedex 08, France
International Agency for Research on Cancer, 2010

Distributed by WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland
(tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]).
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The designations employed and the presentation of the material in this publication do not imply the expression of
any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of
any country, territory, city, or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.
The mention of specific companies or of certain manufacturers products does not imply that they are endorsed
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Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
The IARC Monographs Working Group alone is responsible for the views expressed in this publication.
IARC Library Cataloguing in Publication Data
Household use of solid fuels and high-temperature frying / IARC Working Group
on the Evaluation of Carcinogenic Risks to Humans (2006: Lyon, France)
(IARC monographs on the evaluation of carcinogenic risks to humans; v. 95)
1. Air Pollution, Indoor analysis 2. Carcinogens 3. Cookery 4. Energy-Generating Resources
5. Fossil Fuels toxicity 6. Neoplasms etiology
I. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans II. Series
ISBN 978 92 832 1295 9
ISSN 1017-1606
(NLM Classification: W1)

PRINTED IN FRANCE
Photograph of woman with child cooking over an open fire in Guatemala, courtesy of Nigel Bruce
CONTENTS
NOTE TO THE READER .................................................................................................... 1
LIST OF PARTICIPANTS ................................................................................................... 3
PREAMBLE........................................................................................................................... 7
A. GENERAL PRINCIPLES AND PROCEDURES ......................................................... 9
1. Background ................................................................................................................ 9
2. Objective and scope................................................................................................. 10
3. Selection of agents for review................................................................................. 12
4. Data for the Monographs ........................................................................................ 12
5. Meeting participants ................................................................................................ 13
6. Working procedures................................................................................................. 14
B. SCIENTIFIC REVIEW AND EVALUATION............................................................ 15
1. Exposure data ........................................................................................................... 16
2. Studies of cancer in humans.................................................................................... 18
3. Studies of cancer in experimental animals ............................................................. 22
4. Mechanistic and other relevant data ....................................................................... 26
5. Summary .................................................................................................................. 30
6. Evaluation and rationale .......................................................................................... 31
References ............................................................................................................................. 36
GENERAL REMARKS ...................................................................................................... 39
THE MONOGRAPHS......................................................................................................... 41
Household use of solid fuels .............................................................................................. 43
1. Exposure Data .......................................................................................................... 45
1.1 Description and determinants of use of household fuels.............................. 45
1.2 Constituents of emissions ............................................................................... 56
1.3 Use and exposure ............................................................................................ 70
1.4 Interventions and policies to reduce exposure ............................................ 126
1.5 References ..................................................................................................... 131
vi
IARC MONOGRAPHS VOLUME 95
2. Studies of Cancer in Humans................................................................................ 144

2.1 Coal ................................................................................................................ 144
2.2 Biomass fuel (wood, dung, kang use other than with coal) ....................... 175
2.3 Mixed coal/biomass (coal and/or wood/dung/kang use)............................ 201
2.4 Proxies for indoor air pollution .................................................................... 209
2.5 References ..................................................................................................... 220
3. Studies of Cancer in Experimental Animals ........................................................ 225
3.1 Coal smoke and soots from household combustion of coal....................... 225
3.2 Wood smoke.................................................................................................. 230
3.3 References ..................................................................................................... 234
4. Mechanistic and Other Relevant Data.................................................................. 236
4.1 Toxicokinetics ............................................................................................... 236
4.2 Mechanisms of carcinogenesis..................................................................... 244
4.3 Genetic susceptibility.................................................................................... 272
4.4 Mechanistic considerations .......................................................................... 282
4.5 References ..................................................................................................... 283
5. Summary of Data Reported................................................................................... 299
5.1 Exposure data ................................................................................................ 299
5.2 Human carcinogenicity data......................................................................... 301
5.3 Animal carcinogenicity data......................................................................... 303
5.4 Mechanistic and other relevant data ............................................................ 304
6. Evaluation and Rationale....................................................................................... 307
6.1 Combustion of coal ....................................................................................... 307
6.2 Combustion of biomass ................................................................................ 307
High-temperature frying................................................................................................. 309
1. Exposure Data ........................................................................................................ 311
1.1 Definition....................................................................................................... 311
1.2 Constituents of cooking fumes..................................................................... 311
1.3 Effect of different parameters of cooking on emissions............................. 318
1.4 Human exposure ........................................................................................... 326
1.5 References ..................................................................................................... 333
2. Studies of Cancer in Humans................................................................................ 337
2.1 Introduction ................................................................................................... 337
2.2 Casecontrol studies .................................................................................... 342
2.3 Meta-analysis................................................................................................. 371
2.4 References ..................................................................................................... 372
CONTENTS
vii
3. Studies of Cancer in Experimental Animals ........................................................ 374

3.1 Cooking oil fumes......................................................................................... 374
3.2 References ..................................................................................................... 374
4. Mechanistic and Other Relevant Data.................................................................. 376
4.1 Toxicokinetics ............................................................................................... 376
4.2 Mechanisms of carcinogenesis..................................................................... 376
4.3 Genetic susceptibility.................................................................................... 385
4.4 Mechanistic considerations .......................................................................... 385
4.5 References ..................................................................................................... 385
5. Summary of Data Reported................................................................................... 389
5.1 Exposure data ................................................................................................ 389
5.2 Human carcinogenicity data......................................................................... 389
5.3 Animal carcinogenicity data......................................................................... 390
5.4 Mechanistic and other relevant data ............................................................ 390
6. Evaluation and Rationale....................................................................................... 392
LIST OF ABBREVIATIONS ........................................................................................... 395
CUMULATIVE INDEX TO THE MONOGRAPHS SERIES....................................... 397
NOTE TO THE READER

The term carcinogenic risk in the IARC Monographs series is taken to mean that an
agent is capable of causing cancer under some circumstances. The Monographs evaluate
cancer hazards, despite the historical presence of the word risks in the title.
Inclusion of an agent in the Monographs does not imply that it is a carcinogen, only
that the published data have been examined. Equally, the fact that an agent has not yet
been evaluated in a Monograph does not mean that it is not carcinogenic.
The evaluations of carcinogenic risk are made by international working groups of
independent scientists and are qualitative in nature. No recommendation is given for
regulation or legislation.
Anyone who is aware of published data that may alter the evaluation of the carcinogenic risk of an agent to humans is encouraged to make this information available to the
Section of IARC Monographs, International Agency for Research on Cancer, 150 cours
Albert Thomas, 69372 Lyon Cedex 08, France, in order that the agent may be considered
for re-evaluation by a future Working Group.
Although every effort is made to prepare the monographs as accurately as possible,
mistakes may occur. Readers are requested to communicate any errors to the Section of
IARC Monographs, so that corrections can be reported in future volumes.
IARC MONOGRAPHS ON THE EVALUATION OF

CARCINOGENIC RISKS TO HUMANS
VOLUME 95
HOUSEHOLD USE OF SOLID FUELS AND
HIGH-TEMPERATURE FRYING
Lyon, 1017 October 2006

LIST OF PARTICIPANTS
Working Group Members1,2
Kalpana Balakrishnan, Department of Environmental Health Engineering, Sri
Ramachandra Medical College and Research Institute, No. 1, Ramachandra Nagar,
Porur, Chennai 600116, India
Douglas Barnes, Energy Sector Management Assistance Program (ESMAP), Energy and
Water Department, The World Bank Group, 1818 H Street NW, MSN H4-403,
Washington DC 20433, USA (not present for evaluations)
James A. Bond, Chemico-Biological Interactions, Santa Fe, NM 87506-7782, USA
Nigel Bruce, Division of Public Health, University of Liverpool, Whelan Building,
Quadrangle, GB-Liverpool L69 3GB, United Kingdom
Robert S. Chapman, College of Public Health, Chulalongkorn University, Institute
Building 3, 10th Floor, Soi Chulalongkorn 62, Phyathai Road, Patumwan, Bangkok
10330, Thailand (unable to attend)
Guosheng Chen, Human Toxicology and Air Standards Section, Standards Development
Branch, Ministry of the Environment, 40 St. Clair Avenue West, 7th Floor, Toronto,
Ontario M4V 1M2, Canada
Working Group Members and Invited Specialists serve in their individual capacities as scientists and not as
representatives of their government or any organization with which they are affiliated. Affiliations are
provided for identification purposes only.
2
Each participant was asked to disclose pertinent research, employment, and financial interests. Current
financial interests and research and employment interests during the past 3 years or anticipated in the future are
identified here. Minor pertinent interests are not listed and include stock valued at no more than US$10 000
overall, grants that provide no more than 5% of the research budget of the experts organization and that do not
support the experts research or position, and consulting or speaking on matters not before a court or
government agency that does not exceed 2% of total professional time or compensation. All grants that support
the experts research or position and all consulting or speaking on matters before a court or government agency
are listed as significant pertinent interests.
David M. DeMarini, Environmental Carcinogenesis Division (B-143-06), U.S.

Environmental Protection Agency, Research Triangle Park, NC 27711, USA
(Subgroup Chair, Mechanistic and Other Relevant Data)
Yu-Tang Gao, Department of Epidemiology, Shanghai Cancer Institute, Shanghai
Jiaotong University, 2200/25 Xie Tu Road, Shanghai 200032, China
Qing Lan, Occupational & Environmental Epidemiology Branch, Division of Cancer
Epidemiology & Genetics, National Cancer Institute, 6120 Executive Blvd. EPS
Room 8109, Rockville, MD 20852, USA
Joellen Lewtas, Department Environmental and Occupational Health Sciences, School of
Public Health & Community Medicine, University of Washington, 4225 Roosevelt
Way, Suite 100, Rm 2331, Box 354695, Seattle, WA 98195-4695, USA (Subgroup
Chair, Cancer in Experimental Animals)
Matthew D. Reed3, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE,
Albuquerque, NM 87108-5127, USA
Isabelle Romieu, Center of Public Health Research, National Institute of Public Health,
Av. Universidad No 655, Col. Santa Maria Ahuacatitln, Cuernavaca, Morelos
62508, Mexico
Jonathan Sinton, Office of Non-Member Countries, International Energy Agency, 9, rue
de la Fdration, F-75739 Paris cedex 15, France (not present for evaluations)
Kirk R. Smith, Environmental Health Sciences, University Hall, University of California,
Berkeley, CA 94720-7360, USA (Meeting Chair)
Lance Wallace, National Exposure Research Laboratory, U.S. Environmental Protection
Agency (retired), Research Triangle Park, NC 27711, USA (Subgroup Chair,
Exposure Data)
Paul A. White, Mutagenesis Section, Safe Environments Program, Healthy Environments
& Consumer Safety Branch, Health Canada, Tunney's Pasture 0803A, Ottawa,
Ontario K1A 0K9, Canada
Anna H. Wu, Department of Preventive Medicine, Norris Comprehensive Cancer Center,
University of Southern California, 1441 Eastlake Avenue, MC 9175, Los Angeles,
CA 90089, USA (Subgroup Chair, Cancer in Humans; not present for evaluations)
Ignatius Tak-sun Yu, Professor, Department of Community & Family Medicine, The
Chinese University of Hong Kong, 4/F School of Public Health, Prince of Wales
Hospital, Shatin, N.T., Hong Kong SAR, China
Junfeng (Jim) Zhang, School of Public Health, University of Medicine and Dentistry of
New Jersey (UMDNJ) and Environmental and Occupational Health Sciences
Institute (EOHSI), Rutgers University, 683 Hoes Lane West, Piscataway, NJ 08854,
USA
Before 2005, Dr Reeds employer received funding from the Hearth, Patio & Barbecue Association, which
represents and promotes the interests of the hearth producers industry in North America.
PARTICIPANTS
Invited Specialist
Mitali Sen, Department of Sociology, University of Maryland, 2112 Art-Sociology
Building, College Park, MD 20742-1315, USA
Observers
None
IARC Secretariat
Robert Baan (Rapporteur, Mechanistic and Other Relevant Data)
Julien Berthiller
Vincent James Cogliano (Head of Programme)
Anne Cust
Frank de Vocht
Lars Egevad
Fatiha El Ghissassi (Co-rapporteur, Mechanistic and Other Relevant Data)
Yann Grosse (Rapporteur, Cancer in Experimental Animals)
Otto Hnninen, WHO European Centre for Environment and Health, Bonn
Farhad Islami
Jane Mitchell (Editor)
Nikolai Napalkov
Eva Rehfuess, WHO Public Health and Environment, Geneva
Beate Ritz
Amir Sapkota
Batrice Secretan (Rapporteur, Exposure Data)
Kurt Straif (Responsible Officer; Rapporteur, Cancer in Humans)
Eric van Dyck
Administrative assistance
Sandrine Egraz
Michel Javin
Brigitte Kajo
Martine Lzre
Helene Lorenzen-Augros
Post-meeting assistance
Lamia Benbrahim-Tallaa
Crystal Freeman
Neela Guha
Production team
Laurent Galichet
Anne-Sophie Hameau
Sylvia Moutinho
Dorothy Russell
PREAMBLE
IARC MONOGRAPHS ON THE EVALUATION OF

CARCINOGENIC RISKS TO HUMANS
PREAMBLE
The Preamble to the IARC Monographs describes the objective and scope of
the programme, the scientific principles and procedures used in developing a
Monograph, the types of evidence considered and the scientific criteria that guide
the evaluations. The Preamble should be consulted when reading a Monograph or
list of evaluations.
A. GENERAL PRINCIPLES AND PROCEDURES

1. Background
Soon after IARC was established in 1965, it received frequent requests for advice on
the carcinogenic risk of chemicals, including requests for lists of known and suspected
human carcinogens. It was clear that it would not be a simple task to summarize adequately the complexity of the information that was available, and IARC began to consider
means of obtaining international expert opinion on this topic. In 1970, the IARC Advisory
Committee on Environmental Carcinogenesis recommended ...that a compendium on
carcinogenic chemicals be prepared by experts. The biological activity and evaluation of
practical importance to public health should be referenced and documented. The IARC
Governing Council adopted a resolution concerning the role of IARC in providing
government authorities with expert, independent, scientific opinion on environmental
carcinogenesis. As one means to that end, the Governing Council recommended that
IARC should prepare monographs on the evaluation of carcinogenic risk of chemicals to
man, which became the initial title of the series.
In the succeeding years, the scope of the programme broadened as Monographs were
developed for groups of related chemicals, complex mixtures, occupational exposures,
physical and biological agents and lifestyle factors. In 1988, the phrase of chemicals was
dropped from the title, which assumed its present form, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans.
Through the Monographs programme, IARC seeks to identify the causes of human
cancer. This is the first step in cancer prevention, which is needed as much today as when
9
10
IARC was established. The global burden of cancer is high and continues to increase: the
annual number of new cases was estimated at 10.1 million in 2000 and is expected to
reach 15 million by 2020 (Stewart & Kleihues, 2003). With current trends in demographics and exposure, the cancer burden has been shifting from high-resource countries
to low- and medium-resource countries. As a result of Monographs evaluations, national
health agencies have been able, on scientific grounds, to take measures to reduce human
exposure to carcinogens in the workplace and in the environment.
The criteria established in 1971 to evaluate carcinogenic risks to humans were
adopted by the Working Groups whose deliberations resulted in the first 16 volumes of
the Monographs series. Those criteria were subsequently updated by further ad-hoc
Advisory Groups (IARC, 1977, 1978, 1979, 1982, 1983, 1987, 1988, 1991; Vainio et al.,
1992; IARC, 2005, 2006).
The Preamble is primarily a statement of scientific principles, rather than a specification of working procedures. The procedures through which a Working Group implements
these principles are not specified in detail. They usually involve operations that have been
established as being effective during previous Monograph meetings but remain, predominantly, the prerogative of each individual Working Group.
2. Objective and scope
The objective of the programme is to prepare, with the help of international Working
Groups of experts, and to publish in the form of Monographs, critical reviews and evaluations of evidence on the carcinogenicity of a wide range of human exposures. The
Monographs represent the first step in carcinogen risk assessment, which involves examination of all relevant information in order to assess the strength of the available evidence
that an agent could alter the age-specific incidence of cancer in humans. The Monographs
may also indicate where additional research efforts are needed, specifically when data
immediately relevant to an evaluation are not available.
In this Preamble, the term agent refers to any entity or circumstance that is subject to
evaluation in a Monograph. As the scope of the programme has broadened, categories of
agents now include specific chemicals, groups of related chemicals, complex mixtures,
occupational or environmental exposures, cultural or behavioural practices, biological
organisms and physical agents. This list of categories may expand as causation of, and
susceptibility to, malignant disease become more fully understood.
A cancer hazard is an agent that is capable of causing cancer under some circumstances, while a cancer risk is an estimate of the carcinogenic effects expected from
exposure to a cancer hazard. The Monographs are an exercise in evaluating cancer
hazards, despite the historical presence of the word risks in the title. The distinction
between hazard and risk is important, and the Monographs identify cancer hazards even
when risks are very low at current exposure levels, because new uses or unforeseen exposures could engender risks that are significantly higher.
PREAMBLE
11
In the Monographs, an agent is termed carcinogenic if it is capable of increasing the

incidence of malignant neoplasms, reducing their latency, or increasing their severity or
multiplicity. The induction of benign neoplasms may in some circumstances (see Part B,
Section 3a) contribute to the judgement that the agent is carcinogenic. The terms neoplasm and tumour are used interchangeably.
The Preamble continues the previous usage of the phrase strength of evidence as a
matter of historical continuity, although it should be understood that Monographs
evaluations consider studies that support a finding of a cancer hazard as well as studies
that do not.
Some epidemiological and experimental studies indicate that different agents may act
at different stages in the carcinogenic process, and several different mechanisms may be
involved. The aim of the Monographs has been, from their inception, to evaluate evidence
of carcinogenicity at any stage in the carcinogenesis process, independently of the underlying mechanisms. Information on mechanisms may, however, be used in making the
overall evaluation (IARC, 1991; Vainio et al., 1992; IARC, 2005, 2006; see also Part B,
Sections 4 and 6). As mechanisms of carcinogenesis are elucidated, IARC convenes
international scientific conferences to determine whether a broad-based consensus has
emerged on how specific mechanistic data can be used in an evaluation of human carcinogenicity. The results of such conferences are reported in IARC Scientific Publications,
which, as long as they still reflect the current state of scientific knowledge, may guide
subsequent Working Groups.
Although the Monographs have emphasized hazard identification, important issues
may also involve doseresponse assessment. In many cases, the same epidemiological
and experimental studies used to evaluate a cancer hazard can also be used to estimate a
doseresponse relationship. A Monograph may undertake to estimate doseresponse
relationships within the range of the available epidemiological data, or it may compare the
doseresponse information from experimental and epidemiological studies. In some
cases, a subsequent publication may be prepared by a separate Working Group with
expertise in quantitative doseresponse assessment.
The Monographs are used by national and international authorities to make risk
assessments, formulate decisions concerning preventive measures, provide effective
cancer control programmes and decide among alternative options for public health
decisions. The evaluations of IARC Working Groups are scientific, qualitative judgements on the evidence for or against carcinogenicity provided by the available data. These
evaluations represent only one part of the body of information on which public health
decisions may be based. Public health options vary from one situation to another and from
country to country and relate to many factors, including different socioeconomic and
national priorities. Therefore, no recommendation is given with regard to regulation or
legislation, which are the responsibility of individual governments or other international
organizations.
12
3. Selection of agents for review

Agents are selected for review on the basis of two main criteria: (a) there is evidence
of human exposure and (b) there is some evidence or suspicion of carcinogenicity. Mixed
exposures may occur in occupational and environmental settings and as a result of
individual and cultural habits (such as tobacco smoking and dietary practices). Chemical
analogues and compounds with biological or physical characteristics similar to those of
suspected carcinogens may also be considered, even in the absence of data on a possible
carcinogenic effect in humans or experimental animals.
The scientific literature is surveyed for published data relevant to an assessment of
carcinogenicity. Ad-hoc Advisory Groups convened by IARC in 1984, 1989, 1991, 1993,
1998 and 2003 made recommendations as to which agents should be evaluated in the
Monographs series. Recent recommendations are available on the Monographs programme website (http://monographs.iarc.fr). IARC may schedule other agents for review
as it becomes aware of new scientific information or as national health agencies identify
an urgent public health need related to cancer.
As significant new data become available on an agent for which a Monograph exists,
a re-evaluation may be made at a subsequent meeting, and a new Monograph published.
In some cases it may be appropriate to review only the data published since a prior
evaluation. This can be useful for updating a database, reviewing new data to resolve a
previously open question or identifying new tumour sites associated with a carcinogenic
agent. Major changes in an evaluation (e.g. a new classification in Group 1 or a determination that a mechanism does not operate in humans, see Part B, Section 6) are more
appropriately addressed by a full review.
4. Data for the Monographs
Each Monograph reviews all pertinent epidemiological studies and cancer bioassays
in experimental animals. Those judged inadequate or irrelevant to the evaluation may be
cited but not summarized. If a group of similar studies is not reviewed, the reasons are
indicated.
Mechanistic and other relevant data are also reviewed. A Monograph does not necessarily cite all the mechanistic literature concerning the agent being evaluated (see Part B,
Section 4). Only those data considered by the Working Group to be relevant to making
the evaluation are included.
With regard to epidemiological studies, cancer bioassays, and mechanistic and other
relevant data, only reports that have been published or accepted for publication in the
openly available scientific literature are reviewed. The same publication requirement
applies to studies originating from IARC, including meta-analyses or pooled analyses
commissioned by IARC in advance of a meeting (see Part B, Section 2c). Data from
government agency reports that are publicly available are also considered. Exceptionally,
PREAMBLE
13
doctoral theses and other material that are in their final form and publicly available may
be reviewed.
Exposure data and other information on an agent under consideration are also reviewed. In the sections on chemical and physical properties, on analysis, on production
and use and on occurrence, published and unpublished sources of information may be
considered.
Inclusion of a study does not imply acceptance of the adequacy of the study design or
of the analysis and interpretation of the results, and limitations are clearly outlined in
square brackets at the end of each study description (see Part B). The reasons for not
giving further consideration to an individual study also are indicated in the square
brackets.
5. Meeting participants
Five categories of participant can be present at Monograph meetings.
(a) The Working Group is responsible for the critical reviews and evaluations that
are developed during the meeting. The tasks of Working Group Members are: (i) to
ascertain that all appropriate data have been collected; (ii) to select the data relevant for
the evaluation on the basis of scientific merit; (iii) to prepare accurate summaries of the
data to enable the reader to follow the reasoning of the Working Group; (iv) to evaluate
the results of epidemiological and experimental studies on cancer; (v) to evaluate data
relevant to the understanding of mechanisms of carcinogenesis; and (vi) to make an
overall evaluation of the carcinogenicity of the exposure to humans. Working Group
Members generally have published significant research related to the carcinogenicity of
the agents being reviewed, and IARC uses literature searches to identify most experts.
Working Group Members are selected on the basis of (a) knowledge and experience and
(b) absence of real or apparent conflicts of interests. Consideration is also given to
demographic diversity and balance of scientific findings and views.
(b) Invited Specialists are experts who also have critical knowledge and experience
but have a real or apparent conflict of interests. These experts are invited when necessary
to assist in the Working Group by contributing their unique knowledge and experience
during subgroup and plenary discussions. They may also contribute text on noninfluential issues in the section on exposure, such as a general description of data on
production and use (see Part B, Section 1). Invited Specialists do not serve as meeting
chair or subgroup chair, draft text that pertains to the description or interpretation of
cancer data, or participate in the evaluations.
(c) Representatives of national and international health agencies often attend
meetings because their agencies sponsor the programme or are interested in the subject of
a meeting. Representatives do not serve as meeting chair or subgroup chair, draft any part
of a Monograph, or participate in the evaluations.
(d) Observers with relevant scientific credentials may be admitted to a meeting by
IARC in limited numbers. Attention will be given to achieving a balance of Observers
14
from constituencies with differing perspectives. They are invited to observe the meeting
and should not attempt to influence it. Observers do not serve as meeting chair or subgroup chair, draft any part of a Monograph, or participate in the evaluations. At the meeting, the meeting chair and subgroup chairs may grant Observers an opportunity to speak,
generally after they have observed a discussion. Observers agree to respect the Guidelines
for Observers at IARC Monographs meetings (available at http://monographs.iarc.fr).
(e) The IARC Secretariat consists of scientists who are designated by IARC and who
have relevant expertise. They serve as rapporteurs and participate in all discussions. When
requested by the meeting chair or subgroup chair, they may also draft text or prepare
tables and analyses.
Before an invitation is extended, each potential participant, including the IARC Secretariat, completes the WHO Declaration of Interests to report financial interests, employment and consulting, and individual and institutional research support related to the
subject of the meeting. IARC assesses these interests to determine whether there is a
conflict that warrants some limitation on participation. The declarations are updated and
reviewed again at the opening of the meeting. Interests related to the subject of the
meeting are disclosed to the meeting participants and in the published volume (Cogliano
et al., 2004).
The names and principal affiliations of participants are available on the Monographs
programme website (http://monographs.iarc.fr) approximately two months before each
meeting. It is not acceptable for Observers or third parties to contact other participants
before a meeting or to lobby them at any time. Meeting participants are asked to report all
such contacts to IARC (Cogliano et al., 2005).
All participants are listed, with their principal affiliations, at the beginning of each
volume. Each participant who is a Member of a Working Group serves as an individual
scientist and not as a representative of any organization, government or industry.
6. Working procedures
A separate Working Group is responsible for developing each volume of Monographs. A volume contains one or more Monographs, which can cover either a single
agent or several related agents. Approximately one year in advance of the meeting of a
Working Group, the agents to be reviewed are announced on the Monographs programme
website (http://monographs.iarc.fr) and participants are selected by IARC staff in consultation with other experts. Subsequently, relevant biological and epidemiological data are
collected by IARC from recognized sources of information on carcinogenesis, including
data storage and retrieval systems such as PubMed. Meeting participants who are asked to
prepare preliminary working papers for specific sections are expected to supplement the
IARC literature searches with their own searches.
For most chemicals and some complex mixtures, the major collection of data and the
preparation of working papers for the sections on chemical and physical properties, on
analysis, on production and use, and on occurrence are carried out under a separate
PREAMBLE
15
contract funded by the US National Cancer Institute. Industrial associations, labour unions
and other knowledgeable organizations may be asked to provide input to the sections on
production and use, although this involvement is not required as a general rule.
Information on production and trade is obtained from governmental, trade and market
research publications and, in some cases, by direct contact with industries. Separate
production data on some agents may not be available for a variety of reasons (e.g. not
collected or made public in all producing countries, production is small). Information on
uses may be obtained from published sources but is often complemented by direct contact
with manufacturers. Efforts are made to supplement this information with data from other
national and international sources.
Six months before the meeting, the material obtained is sent to meeting participants to
prepare preliminary working papers. The working papers are compiled by IARC staff and
sent, prior to the meeting, to Working Group Members and Invited Specialists for review.
The Working Group meets at IARC for seven to eight days to discuss and finalize the
texts and to formulate the evaluations. The objectives of the meeting are peer review and
consensus. During the first few days, four subgroups (covering exposure data, cancer in
humans, cancer in experimental animals, and mechanistic and other relevant data) review
the working papers, develop a joint subgroup draft and write summaries. Care is taken to
ensure that each study summary is written or reviewed by someone not associated with
the study being considered. During the last few days, the Working Group meets in plenary session to review the subgroup drafts and develop the evaluations. As a result, the
entire volume is the joint product of the Working Group, and there are no individually
authored sections.
IARC Working Groups strive to achieve a consensus evaluation. Consensus reflects
broad agreement among Working Group Members, but not necessarily unanimity. The
chair may elect to poll Working Group Members to determine the diversity of scientific
opinion on issues where consensus is not readily apparent.
After the meeting, the master copy is verified by consulting the original literature,
edited and prepared for publication. The aim is to publish the volume within six months
of the Working Group meeting. A summary of the outcome is available on the Monographs programme website soon after the meeting.
B. SCIENTIFIC REVIEW AND EVALUATION

The available studies are summarized by the Working Group, with particular regard
to the qualitative aspects discussed below. In general, numerical findings are indicated as
they appear in the original report; units are converted when necessary for easier comparison. The Working Group may conduct additional analyses of the published data and
use them in their assessment of the evidence; the results of such supplementary analyses
are given in square brackets. When an important aspect of a study that directly impinges
16
on its interpretation should be brought to the attention of the reader, a Working Group
comment is given in square brackets.
The scope of the IARC Monographs programme has expanded beyond chemicals to
include complex mixtures, occupational exposures, physical and biological agents, lifestyle factors and other potentially carcinogenic exposures. Over time, the structure of a
Monograph has evolved to include the following sections:
1. Exposure data
2. Studies of cancer in humans
3. Studies of cancer in experimental animals
4. Mechanistic and other relevant data
5. Summary
6. Evaluation and rationale
In addition, a section of General Remarks at the front of the volume discusses the
reasons the agents were scheduled for evaluation and some key issues the Working Group
encountered during the meeting.
This part of the Preamble discusses the types of evidence considered and summarized
in each section of a Monograph, followed by the scientific criteria that guide the evaluations.
1. Exposure data
Each Monograph includes general information on the agent: this information may
vary substantially between agents and must be adapted accordingly. Also included is
information on production and use (when appropriate), methods of analysis and detection,
occurrence, and sources and routes of human occupational and environmental exposures.
Depending on the agent, regulations and guidelines for use may be presented.
(a)
General information on the agent
For chemical agents, sections on chemical and physical data are included: the
Chemical Abstracts Service Registry Number, the latest primary name and the IUPAC
systematic name are recorded; other synonyms are given, but the list is not necessarily
comprehensive. Information on chemical and physical properties that are relevant to
identification, occurrence and biological activity is included. A description of technical
products of chemicals includes trade names, relevant specifications and available information on composition and impurities. Some of the trade names given may be those of
mixtures in which the agent being evaluated is only one of the ingredients.
For biological agents, taxonomy, structure and biology are described, and the degree
of variability is indicated. Mode of replication, life cycle, target cells, persistence, latency,
host response and clinical disease other than cancer are also presented.
For physical agents that are forms of radiation, energy and range of the radiation are
included. For foreign bodies, fibres and respirable particles, size range and relative dimensions are indicated.
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For agents such as mixtures, drugs or lifestyle factors, a description of the agent,
including its composition, is given.
Whenever appropriate, other information, such as historical perspectives or the
description of an industry or habit, may be included.
(b)
Analysis and detection
An overview of methods of analysis and detection of the agent is presented, including

their sensitivity, specificity and reproducibility. Methods widely used for regulatory
purposes are emphasized. Methods for monitoring human exposure are also given. No
critical evaluation or recommendation of any method is meant or implied.
(c)
Production and use
The dates of first synthesis and of first commercial production of a chemical, mixture
or other agent are provided when available; for agents that do not occur naturally, this
information may allow a reasonable estimate to be made of the date before which no
human exposure to the agent could have occurred. The dates of first reported occurrence
of an exposure are also provided when available. In addition, methods of synthesis used in
past and present commercial production and different methods of production, which may
give rise to different impurities, are described.
The countries where companies report production of the agent, and the number of
companies in each country, are identified. Available data on production, international
trade and uses are obtained for representative regions. It should not, however, be inferred
that those areas or nations are necessarily the sole or major sources or users of the agent.
Some identified uses may not be current or major applications, and the coverage is not
necessarily comprehensive. In the case of drugs, mention of their therapeutic uses does
not necessarily represent current practice nor does it imply judgement as to their
therapeutic efficacy.
(d)
Occurrence and exposure
Information on the occurrence of an agent in the environment is obtained from data

derived from the monitoring and surveillance of levels in occupational environments, air,
water, soil, plants, foods and animal and human tissues. When available, data on the
generation, persistence and bioaccumulation of the agent are also included. Such data may
be available from national databases.
Data that indicate the extent of past and present human exposure, the sources of
exposure, the people most likely to be exposed and the factors that contribute to the
exposure are reported. Information is presented on the range of human exposure, including occupational and environmental exposures. This includes relevant findings from
both developed and developing countries. Some of these data are not distributed widely
and may be available from government reports and other sources. In the case of mixtures,
industries, occupations or processes, information is given about all agents known to be
18
present. For processes, industries and occupations, a historical description is also given,
noting variations in chemical composition, physical properties and levels of occupational
exposure with date and place. For biological agents, the epidemiology of infection is
described.
(e)
Regulations and guidelines
Statements concerning regulations and guidelines (e.g. occupational exposure limits,

maximal levels permitted in foods and water, pesticide registrations) are included, but
they may not reflect the most recent situation, since such limits are continuously reviewed
and modified. The absence of information on regulatory status for a country should not be
taken to imply that that country does not have regulations with regard to the exposure. For
biological agents, legislation and control, including vaccination and therapy, are described.
2. Studies of cancer in humans
This section includes all pertinent epidemiological studies (see Part A, Section 4).
Studies of biomarkers are included when they are relevant to an evaluation of carcinogenicity to humans.
(a)
Types of study considered
Several types of epidemiological study contribute to the assessment of carcinogenicity

in humans cohort studies, casecontrol studies, correlation (or ecological) studies and
intervention studies. Rarely, results from randomized trials may be available. Case reports
and case series of cancer in humans may also be reviewed.
Cohort and casecontrol studies relate individual exposures under study to the
occurrence of cancer in individuals and provide an estimate of effect (such as relative
risk) as the main measure of association. Intervention studies may provide strong
evidence for making causal inferences, as exemplified by cessation of smoking and the
subsequent decrease in risk for lung cancer.
In correlation studies, the units of investigation are usually whole populations (e.g. in
particular geographical areas or at particular times), and cancer frequency is related to a
summary measure of the exposure of the population to the agent under study. In correlation studies, individual exposure is not documented, which renders this kind of study
more prone to confounding. In some circumstances, however, correlation studies may be
more informative than analytical study designs (see, for example, the Monograph on
arsenic in drinking-water; IARC, 2004).
In some instances, case reports and case series have provided important information
about the carcinogenicity of an agent. These types of study generally arise from a suspicion, based on clinical experience, that the concurrence of two events that is, a
particular exposure and occurrence of a cancer has happened rather more frequently
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than would be expected by chance. Case reports and case series usually lack complete
ascertainment of cases in any population, definition or enumeration of the population at
risk and estimation of the expected number of cases in the absence of exposure.
The uncertainties that surround the interpretation of case reports, case series and
correlation studies make them inadequate, except in rare instances, to form the sole basis
for inferring a causal relationship. When taken together with casecontrol and cohort
studies, however, these types of study may add materially to the judgement that a causal
relationship exists.
Epidemiological studies of benign neoplasms, presumed preneoplastic lesions and
other end-points thought to be relevant to cancer are also reviewed. They may, in some
instances, strengthen inferences drawn from studies of cancer itself.
(b)
Quality of studies considered
It is necessary to take into account the possible roles of bias, confounding and chance
in the interpretation of epidemiological studies. Bias is the effect of factors in study design
or execution that lead erroneously to a stronger or weaker association than in fact exists
between an agent and disease. Confounding is a form of bias that occurs when the
relationship with disease is made to appear stronger or weaker than it truly is as a result of
an association between the apparent causal factor and another factor that is associated
with either an increase or decrease in the incidence of the disease. The role of chance is
related to biological variability and the influence of sample size on the precision of estimates of effect.
In evaluating the extent to which these factors have been minimized in an individual
study, consideration is given to a number of aspects of design and analysis as described in
the report of the study. For example, when suspicion of carcinogenicity arises largely
from a single small study, careful consideration is given when interpreting subsequent
studies that included these data in an enlarged population. Most of these considerations
apply equally to casecontrol, cohort and correlation studies. Lack of clarity of any of
these aspects in the reporting of a study can decrease its credibility and the weight given
to it in the final evaluation of the exposure.
Firstly, the study population, disease (or diseases) and exposure should have been
well defined by the authors. Cases of disease in the study population should have been
identified in a way that was independent of the exposure of interest, and exposure should
have been assessed in a way that was not related to disease status.
Secondly, the authors should have taken into account in the study design and
analysis other variables that can influence the risk of disease and may have been
related to the exposure of interest. Potential confounding by such variables should have
been dealt with either in the design of the study, such as by matching, or in the analysis,
by statistical adjustment. In cohort studies, comparisons with local rates of disease may or
may not be more appropriate than those with national rates. Internal comparisons of
frequency of disease among individuals at different levels of exposure are also desirable
20
in cohort studies, since they minimize the potential for confounding related to the difference in risk factors between an external reference group and the study population.
Thirdly, the authors should have reported the basic data on which the conclusions are
founded, even if sophisticated statistical analyses were employed. At the very least, they
should have given the numbers of exposed and unexposed cases and controls in a case
control study and the numbers of cases observed and expected in a cohort study. Further
tabulations by time since exposure began and other temporal factors are also important. In
a cohort study, data on all cancer sites and all causes of death should have been given, to
reveal the possibility of reporting bias. In a casecontrol study, the effects of investigated
factors other than the exposure of interest should have been reported.
Finally, the statistical methods used to obtain estimates of relative risk, absolute rates
of cancer, confidence intervals and significance tests, and to adjust for confounding
should have been clearly stated by the authors. These methods have been reviewed for
casecontrol studies (Breslow & Day, 1980) and for cohort studies (Breslow & Day,
1987).
(c)
Meta-analyses and pooled analyses
Independent epidemiological studies of the same agent may lead to results that are
difficult to interpret. Combined analyses of data from multiple studies are a means of
resolving this ambiguity, and well-conducted analyses can be considered. There are two
types of combined analysis. The first involves combining summary statistics such as
relative risks from individual studies (meta-analysis) and the second involves a pooled
analysis of the raw data from the individual studies (pooled analysis) (Greenland, 1998).
The advantages of combined analyses are increased precision due to increased sample
size and the opportunity to explore potential confounders, interactions and modifying
effects that may explain heterogeneity among studies in more detail. A disadvantage of
combined analyses is the possible lack of compatibility of data from various studies due
to differences in subject recruitment, procedures of data collection, methods of measurement and effects of unmeasured co-variates that may differ among studies. Despite these
limitations, well-conducted combined analyses may provide a firmer basis than individual
studies for drawing conclusions about the potential carcinogenicity of agents.
IARC may commission a meta-analysis or pooled analysis that is pertinent to a
particular Monograph (see Part A, Section 4). Additionally, as a means of gaining insight
from the results of multiple individual studies, ad-hoc calculations that combine data from
different studies may be conducted by the Working Group during the course of a Monograph meeting. The results of such original calculations, which would be specified in the
text by presentation in square brackets, might involve updates of previously conducted
analyses that incorporate the results of more recent studies or de-novo analyses.
Irrespective of the source of data for the meta-analyses and pooled analyses, it is important that the same criteria for data quality be applied as those that would be applied to
individual studies and to ensure also that sources of heterogeneity between studies be
taken into account.
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(d)
21
Temporal effects
Detailed analyses of both relative and absolute risks in relation to temporal variables,
such as age at first exposure, time since first exposure, duration of exposure, cumulative
exposure, peak exposure (when appropriate) and time since cessation of exposure, are
reviewed and summarized when available. Analyses of temporal relationships may be
useful in making causal inferences. In addition, such analyses may suggest whether a
carcinogen acts early or late in the process of carcinogenesis, although, at best, they allow
only indirect inferences about mechanisms of carcinogenesis.
(e)
Use of biomarkers in epidemiological studies
Biomarkers indicate molecular, cellular or other biological changes and are increasingly used in epidemiological studies for various purposes (IARC, 1991; Vainio et al.,
1992; Toniolo et al., 1997; Vineis et al., 1999; Buffler et al., 2004). These may include
evidence of exposure, of early effects, of cellular, tissue or organism responses, of individual susceptibility or host responses, and inference of a mechanism (see Part B, Section
4b). This is a rapidly evolving field that encompasses developments in genomics, epigenomics and other emerging technologies.
Molecular epidemiological data that identify associations between genetic polymorphisms and interindividual differences in susceptibility to the agent(s) being evaluated
may contribute to the identification of carcinogenic hazards to humans. If the polymorphism has been demonstrated experimentally to modify the functional activity of the
gene product in a manner that is consistent with increased susceptibility, these data may
be useful in making causal inferences. Similarly, molecular epidemiological studies that
measure cell functions, enzymes or metabolites that are thought to be the basis of
susceptibility may provide evidence that reinforces biological plausibility. It should be
noted, however, that when data on genetic susceptibility originate from multiple comparisons that arise from subgroup analyses, this can generate false-positive results and
inconsistencies across studies, and such data therefore require careful evaluation. If the
known phenotype of a genetic polymorphism can explain the carcinogenic mechanism of
the agent being evaluated, data on this phenotype may be useful in making causal inferences.
(f)
Criteria for causality
After the quality of individual epidemiological studies of cancer has been summarized
and assessed, a judgement is made concerning the strength of evidence that the agent in
question is carcinogenic to humans. In making its judgement, the Working Group considers several criteria for causality (Hill, 1965). A strong association (e.g. a large relative
risk) is more likely to indicate causality than a weak association, although it is recognized
that estimates of effect of small magnitude do not imply lack of causality and may be
important if the disease or exposure is common. Associations that are replicated in several
studies of the same design or that use different epidemiological approaches or under
22
different circumstances of exposure are more likely to represent a causal relationship than
isolated observations from single studies. If there are inconsistent results among investigations, possible reasons are sought (such as differences in exposure), and results of studies
that are judged to be of high quality are given more weight than those of studies that are
judged to be methodologically less sound.
If the risk increases with the exposure, this is considered to be a strong indication of
causality, although the absence of a graded response is not necessarily evidence against a
causal relationship. The demonstration of a decline in risk after cessation of or reduction
in exposure in individuals or in whole populations also supports a causal interpretation of
the findings.
A number of scenarios may increase confidence in a causal relationship. On the one
hand, an agent may be specific in causing tumours at one site or of one morphological
type. On the other, carcinogenicity may be evident through the causation of multiple
tumour types. Temporality, precision of estimates of effect, biological plausibility and coherence of the overall database are considered. Data on biomarkers may be employed in
an assessment of the biological plausibility of epidemiological observations.
Although rarely available, results from randomized trials that show different rates of
cancer among exposed and unexposed individuals provide particularly strong evidence
for causality.
When several epidemiological studies show little or no indication of an association
between an exposure and cancer, a judgement may be made that, in the aggregate, they
show evidence of lack of carcinogenicity. Such a judgement requires firstly that the
studies meet, to a sufficient degree, the standards of design and analysis described above.
Specifically, the possibility that bias, confounding or misclassification of exposure or outcome could explain the observed results should be considered and excluded with
reasonable certainty. In addition, all studies that are judged to be methodologically sound
should (a) be consistent with an estimate of effect of unity for any observed level of
exposure, (b) when considered together, provide a pooled estimate of relative risk that is
at or near to unity, and (c) have a narrow confidence interval, due to sufficient population
size. Moreover, no individual study nor the pooled results of all the studies should show
any consistent tendency that the relative risk of cancer increases with increasing level of
exposure. It is important to note that evidence of lack of carcinogenicity obtained from
several epidemiological studies can apply only to the type(s) of cancer studied, to the dose
levels reported, and to the intervals between first exposure and disease onset observed in
these studies. Experience with human cancer indicates that the period from first exposure
to the development of clinical cancer is sometimes longer than 20 years; latent periods
substantially shorter than 30 years cannot provide evidence for lack of carcinogenicity.
3. Studies of cancer in experimental animals
All known human carcinogens that have been studied adequately for carcinogenicity
in experimental animals have produced positive results in one or more animal species
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(Wilbourn et al., 1986; Tomatis et al., 1989). For several agents (e.g. aflatoxins, diethylstilbestrol, solar radiation, vinyl chloride), carcinogenicity in experimental animals was
established or highly suspected before epidemiological studies confirmed their carcinogenicity in humans (Vainio et al., 1995). Although this association cannot establish that
all agents that cause cancer in experimental animals also cause cancer in humans, it is
biologically plausible that agents for which there is sufficient evidence of carcinogenicity
in experimental animals (see Part B, Section 6b) also present a carcinogenic hazard to
humans. Accordingly, in the absence of additional scientific information, these agents are
considered to pose a carcinogenic hazard to humans. Examples of additional scientific
information are data that demonstrate that a given agent causes cancer in animals through
a species-specific mechanism that does not operate in humans or data that demonstrate
that the mechanism in experimental animals also operates in humans (see Part B, Section
6).
Consideration is given to all available long-term studies of cancer in experimental
animals with the agent under review (see Part A, Section 4). In all experimental settings,
the nature and extent of impurities or contaminants present in the agent being evaluated
are given when available. Animal species, strain (including genetic background where
applicable), sex, numbers per group, age at start of treatment, route of exposure, dose
levels, duration of exposure, survival and information on tumours (incidence, latency,
severity or multiplicity of neoplasms or preneoplastic lesions) are reported. Those studies
in experimental animals that are judged to be irrelevant to the evaluation or judged to be
inadequate (e.g. too short a duration, too few animals, poor survival; see below) may be
omitted. Guidelines for conducting long-term carcinogenicity experiments have been
published (e.g. OECD, 2002).
Other studies considered may include: experiments in which the agent was administered in the presence of factors that modify carcinogenic effects (e.g. initiationpromotion
studies, co-carcinogenicity studies and studies in genetically modified animals); studies in
which the end-point was not cancer but a defined precancerous lesion; experiments on the
carcinogenicity of known metabolites and derivatives; and studies of cancer in nonlaboratory animals (e.g. livestock and companion animals) exposed to the agent.
For studies of mixtures, consideration is given to the possibility that changes in the
physicochemical properties of the individual substances may occur during collection,
storage, extraction, concentration and delivery. Another consideration is that chemical and
toxicological interactions of components in a mixture may alter doseresponse relationships. The relevance to human exposure of the test mixture administered in the animal
experiment is also assessed. This may involve consideration of the following aspects of
the mixture tested: (i) physical and chemical characteristics, (ii) identified constituents
that may indicate the presence of a class of substances and (iii) the results of genetic
toxicity and related tests.
The relevance of results obtained with an agent that is analogous (e.g. similar in
structure or of a similar virus genus) to that being evaluated is also considered. Such
results may provide biological and mechanistic information that is relevant to the
24
understanding of the process of carcinogenesis in humans and may strengthen the biological plausibility that the agent being evaluated is carcinogenic to humans (see Part B,
Section 2f).
(a)
Qualitative aspects
An assessment of carcinogenicity involves several considerations of qualitative importance, including (i) the experimental conditions under which the test was performed,
including route, schedule and duration of exposure, species, strain (including genetic
background where applicable), sex, age and duration of follow-up; (ii) the consistency of
the results, for example, across species and target organ(s); (iii) the spectrum of neoplastic
response, from preneoplastic lesions and benign tumours to malignant neoplasms; and
(iv) the possible role of modifying factors.
Considerations of importance in the interpretation and evaluation of a particular study
include: (i) how clearly the agent was defined and, in the case of mixtures, how
adequately the sample characterization was reported; (ii) whether the dose was monitored
adequately, particularly in inhalation experiments; (iii) whether the doses, duration of
treatment and route of exposure were appropriate; (iv) whether the survival of treated
animals was similar to that of controls; (v) whether there were adequate numbers of
animals per group; (vi) whether both male and female animals were used; (vii) whether
animals were allocated randomly to groups; (viii) whether the duration of observation was
adequate; and (ix) whether the data were reported and analysed adequately.
When benign tumours (a) occur together with and originate from the same cell type as
malignant tumours in an organ or tissue in a particular study and (b) appear to represent a
stage in the progression to malignancy, they are usually combined in the assessment of
tumour incidence (Huff et al., 1989). The occurrence of lesions presumed to be preneoplastic may in certain instances aid in assessing the biological plausibility of any
neoplastic response observed. If an agent induces only benign neoplasms that appear to be
end-points that do not readily undergo transition to malignancy, the agent should nevertheless be suspected of being carcinogenic and requires further investigation.
(b)
Quantitative aspects
The probability that tumours will occur may depend on the species, sex, strain,
genetic background and age of the animal, and on the dose, route, timing and duration of
the exposure. Evidence of an increased incidence of neoplasms with increasing levels of
exposure strengthens the inference of a causal association between the exposure and the
development of neoplasms.
The form of the doseresponse relationship can vary widely, depending on the
particular agent under study and the target organ. Mechanisms such as induction of DNA
damage or inhibition of repair, altered cell division and cell death rates and changes in
intercellular communication are important determinants of doseresponse relationships
for some carcinogens. Since many chemicals require metabolic activation before being
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converted to their reactive intermediates, both metabolic and toxicokinetic aspects are
important in determining the doseresponse pattern. Saturation of steps such as
absorption, activation, inactivation and elimination may produce non-linearity in the
doseresponse relationship (Hoel et al., 1983; Gart et al., 1986), as could saturation of
processes such as DNA repair. The doseresponse relationship can also be affected by
differences in survival among the treatment groups.
(c)
Statistical analyses
Factors considered include the adequacy of the information given for each treatment
group: (i) number of animals studied and number examined histologically, (ii) number of
animals with a given tumour type and (iii) length of survival. The statistical methods used
should be clearly stated and should be the generally accepted techniques refined for this
purpose (Peto et al., 1980; Gart et al., 1986; Portier & Bailer, 1989; Bieler & Williams,
1993). The choice of the most appropriate statistical method requires consideration of
whether or not there are differences in survival among the treatment groups; for example,
reduced survival because of non-tumour-related mortality can preclude the occurrence of
tumours later in life. When detailed information on survival is not available, comparisons
of the proportions of tumour-bearing animals among the effective number of animals
(alive at the time the first tumour was discovered) can be useful when significant differences in survival occur before tumours appear. The lethality of the tumour also requires
consideration: for rapidly fatal tumours, the time of death provides an indication of the
time of tumour onset and can be assessed using life-table methods; non-fatal or incidental
tumours that do not affect survival can be assessed using methods such as the MantelHaenzel test for changes in tumour prevalence. Because tumour lethality is often difficult
to determine, methods such as the Poly-K test that do not require such information can
also be used. When results are available on the number and size of tumours seen in
experimental animals (e.g. papillomas on mouse skin, liver tumours observed through
nuclear magnetic resonance tomography), other more complicated statistical procedures
may be needed (Sherman et al., 1994; Dunson et al., 2003).
Formal statistical methods have been developed to incorporate historical control data
into the analysis of data from a given experiment. These methods assign an appropriate
weight to historical and concurrent controls on the basis of the extent of between-study
and within-study variability: less weight is given to historical controls when they show a
high degree of variability, and greater weight when they show little variability. It is
generally not appropriate to discount a tumour response that is significantly increased
compared with concurrent controls by arguing that it falls within the range of historical
controls, particularly when historical controls show high between-study variability and
are, thus, of little relevance to the current experiment. In analysing results for uncommon
tumours, however, the analysis may be improved by considering historical control data,
particularly when between-study variability is low. Historical controls should be selected
to resemble the concurrent controls as closely as possible with respect to species, gender
and strain, as well as other factors such as basal diet and general laboratory environment,
26
which may affect tumour-response rates in control animals (Haseman et al., 1984; Fung et
al., 1996; Greim et al., 2003).
Although meta-analyses and combined analyses are conducted less frequently for
animal experiments than for epidemiological studies due to differences in animal strains,
they can be useful aids in interpreting animal data when the experimental protocols are
sufficiently similar.
4. Mechanistic and other relevant data
Mechanistic and other relevant data may provide evidence of carcinogenicity and also
help in assessing the relevance and importance of findings of cancer in animals and in
humans. The nature of the mechanistic and other relevant data depends on the biological
activity of the agent being considered. The Working Group considers representative
studies to give a concise description of the relevant data and issues that they consider to
be important; thus, not every available study is cited. Relevant topics may include toxicokinetics, mechanisms of carcinogenesis, susceptible individuals, populations and lifestages, other relevant data and other adverse effects. When data on biomarkers are informative about the mechanisms of carcinogenesis, they are included in this section.
These topics are not mutually exclusive; thus, the same studies may be discussed in
more than one subsection. For example, a mutation in a gene that codes for an enzyme
that metabolizes the agent under study could be discussed in the subsections on toxicokinetics, mechanisms and individual susceptibility if it also exists as an inherited polymorphism.
(a)
Toxicokinetic data
Toxicokinetics refers to the absorption, distribution, metabolism and elimination of

agents in humans, experimental animals and, where relevant, cellular systems. Examples
of kinetic factors that may affect doseresponse relationships include uptake, deposition,
biopersistence and half-life in tissues, protein binding, metabolic activation and detoxification. Studies that indicate the metabolic fate of the agent in humans and in experimental animals are summarized briefly, and comparisons of data from humans and
animals are made when possible. Comparative information on the relationship between
exposure and the dose that reaches the target site may be important for the extrapolation
of hazards between species and in clarifying the role of in-vitro findings.
(b)
Data on mechanisms of carcinogenesis
To provide focus, the Working Group attempts to identify the possible mechanisms
by which the agent may increase the risk of cancer. For each possible mechanism, a
representative selection of key data from humans and experimental systems is summarized. Attention is given to gaps in the data and to data that suggests that more than one
mechanism may be operating. The relevance of the mechanism to humans is discussed, in
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particular, when mechanistic data are derived from experimental model systems. Changes
in the affected organs, tissues or cells can be divided into three non-exclusive levels as
described below.
(i)
Changes in physiology
Physiological changes refer to exposure-related modifications to the physiology
and/or response of cells, tissues and organs. Examples of potentially adverse
physiological changes include mitogenesis, compensatory cell division, escape from
apoptosis and/or senescence, presence of inflammation, hyperplasia, metaplasia
and/or preneoplasia, angiogenesis, alterations in cellular adhesion, changes in
steroidal hormones and changes in immune surveillance.
(ii) Functional changes at the cellular level
Functional changes refer to exposure-related alterations in the signalling
pathways used by cells to manage critical processes that are related to increased risk
for cancer. Examples of functional changes include modified activities of enzymes
involved in the metabolism of xenobiotics, alterations in the expression of key genes
that regulate DNA repair, alterations in cyclin-dependent kinases that govern cell
cycle progression, changes in the patterns of post-translational modifications of
proteins, changes in regulatory factors that alter apoptotic rates, changes in the
secretion of factors related to the stimulation of DNA replication and transcription
and changes in gapjunction-mediated intercellular communication.
(iii) Changes at the molecular level
Molecular changes refer to exposure-related changes in key cellular structures at
the molecular level, including, in particular, genotoxicity. Examples of molecular
changes include formation of DNA adducts and DNA strand breaks, mutations in
genes, chromosomal aberrations, aneuploidy and changes in DNA methylation
patterns. Greater emphasis is given to irreversible effects.
The use of mechanistic data in the identification of a carcinogenic hazard is specific to
the mechanism being addressed and is not readily described for every possible level and
mechanism discussed above.
Genotoxicity data are discussed here to illustrate the key issues involved in the evaluation of mechanistic data.
Tests for genetic and related effects are described in view of the relevance of
gene mutation and chromosomal aberration/aneuploidy to carcinogenesis (Vainio
et al., 1992; McGregor et al., 1999). The adequacy of the reporting of sample
characterization is considered and, when necessary, commented upon; with
regard to complex mixtures, such comments are similar to those described for
animal carcinogenicity tests. The available data are interpreted critically according to the end-points detected, which may include DNA damage, gene mutation,
sister chromatid exchange, micronucleus formation, chromosomal aberrations and
28
aneuploidy. The concentrations employed are given, and mention is made of

whether the use of an exogenous metabolic system in vitro affected the test result.
These data are listed in tabular form by phylogenetic classification.
Positive results in tests using prokaryotes, lower eukaryotes, insects, plants
and cultured mammalian cells suggest that genetic and related effects could occur
in mammals. Results from such tests may also give information on the types of
genetic effect produced and on the involvement of metabolic activation. Some
end-points described are clearly genetic in nature (e.g. gene mutations), while
others are associated with genetic effects (e.g. unscheduled DNA synthesis). Invitro tests for tumour promotion, cell transformation and gapjunction intercellular communication may be sensitive to changes that are not necessarily the
result of genetic alterations but that may have specific relevance to the process of
carcinogenesis. Critical appraisals of these tests have been published (Montesano
et al., 1986; McGregor et al., 1999).
Genetic or other activity manifest in humans and experimental mammals is
regarded to be of greater relevance than that in other organisms. The demonstration that an agent can induce gene and chromosomal mutations in mammals in
vivo indicates that it may have carcinogenic activity. Negative results in tests for
mutagenicity in selected tissues from animals treated in vivo provide less weight,
partly because they do not exclude the possibility of an effect in tissues other than
those examined. Moreover, negative results in short-term tests with genetic endpoints cannot be considered to provide evidence that rules out the carcinogenicity
of agents that act through other mechanisms (e.g. receptor-mediated effects,
cellular toxicity with regenerative cell division, peroxisome proliferation) (Vainio
et al., 1992). Factors that may give misleading results in short-term tests have
been discussed in detail elsewhere (Montesano et al., 1986; McGregor et al.,
1999).
When there is evidence that an agent acts by a specific mechanism that does not
involve genotoxicity (e.g. hormonal dysregulation, immune suppression, and formation of
calculi and other deposits that cause chronic irritation), that evidence is presented and
reviewed critically in the context of rigorous criteria for the operation of that mechanism
in carcinogenesis (e.g. Capen et al., 1999).
For biological agents such as viruses, bacteria and parasites, other data relevant to
carcinogenicity may include descriptions of the pathology of infection, integration and
expression of viruses, and genetic alterations seen in human tumours. Other observations
that might comprise cellular and tissue responses to infection, immune response and the
presence of tumour markers are also considered.
For physical agents that are forms of radiation, other data relevant to carcinogenicity
may include descriptions of damaging effects at the physiological, cellular and molecular
level, as for chemical agents, and descriptions of how these effects occur. Physical
agents may also be considered to comprise foreign bodies, such as surgical implants of
various kinds, and poorly soluble fibres, dusts and particles of various sizes, the patho-
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29
genic effects of which are a result of their physical presence in tissues or body cavities.
Other relevant data for such materials may include characterization of cellular, tissue and
physiological reactions to these materials and descriptions of pathological conditions
other than neoplasia with which they may be associated.
(c)
Other data relevant to mechanisms
A description is provided of any structureactivity relationships that may be relevant

to an evaluation of the carcinogenicity of an agent, the toxicological implications of the
physical and chemical properties, and any other data relevant to the evaluation that are not
included elsewhere.
High-output data, such as those derived from gene expression microarrays, and highthroughput data, such as those that result from testing hundreds of agents for a single endpoint, pose a unique problem for the use of mechanistic data in the evaluation of a carcinogenic hazard. In the case of high-output data, there is the possibility to overinterpret
changes in individual end-points (e.g. changes in expression in one gene) without considering the consistency of that finding in the broader context of the other end-points (e.g.
other genes with linked transcriptional control). High-output data can be used in assessing
mechanisms, but all end-points measured in a single experiment need to be considered in
the proper context. For high-throughput data, where the number of observations far
exceeds the number of end-points measured, their utility for identifying common mechanisms across multiple agents is enhanced. These data can be used to identify mechanisms
that not only seem plausible, but also have a consistent pattern of carcinogenic response
across entire classes of related compounds.
(d)
Susceptibility data
Individuals, populations and life-stages may have greater or lesser susceptibility to an

agent, based on toxicokinetics, mechanisms of carcinogenesis and other factors. Examples
of host and genetic factors that affect individual susceptibility include sex, genetic polymorphisms of genes involved in the metabolism of the agent under evaluation, differences
in metabolic capacity due to life-stage or the presence of disease, differences in DNA repair capacity, competition for or alteration of metabolic capacity by medications or other
chemical exposures, pre-existing hormonal imbalance that is exacerbated by a chemical
exposure, a suppressed immune system, periods of higher-than-usual tissue growth or
regeneration and genetic polymorphisms that lead to differences in behaviour (e.g.
addiction). Such data can substantially increase the strength of the evidence from
epidemiological data and enhance the linkage of in-vivo and in-vitro laboratory studies to
humans.
(e)
Data on other adverse effects
Data on acute, subchronic and chronic adverse effects relevant to the cancer evaluation are summarized. Adverse effects that confirm distribution and biological effects at
30
the sites of tumour development, or alterations in physiology that could lead to tumour
development, are emphasized. Effects on reproduction, embryonic and fetal survival and
development are summarized briefly. The adequacy of epidemiological studies of reproductive outcome and genetic and related effects in humans is judged by the same criteria
as those applied to epidemiological studies of cancer, but fewer details are given.
5. Summary
This section is a summary of data presented in the preceding sections. Summaries can
be found on the Monographs programme website (http://monographs.iarc.fr).
(a)
Exposure data
Data are summarized, as appropriate, on the basis of elements such as production,

use, occurrence and exposure levels in the workplace and environment and measurements
in human tissues and body fluids. Quantitative data and time trends are given to compare
exposures in different occupations and environmental settings. Exposure to biological
agents is described in terms of transmission, prevalence and persistence of infection.
(b)
Cancer in humans
Results of epidemiological studies pertinent to an assessment of human carcinogenicity are summarized. When relevant, case reports and correlation studies are also
summarized. The target organ(s) or tissue(s) in which an increase in cancer was observed
is identified. Doseresponse and other quantitative data may be summarized when
available.
(c)
Cancer in experimental animals
Data relevant to an evaluation of carcinogenicity in animals are summarized. For each

animal species, study design and route of administration, it is stated whether an increased
incidence, reduced latency, or increased severity or multiplicity of neoplasms or preneoplastic lesions were observed, and the tumour sites are indicated. If the agent produced
tumours after prenatal exposure or in single-dose experiments, this is also mentioned.
Negative findings, inverse relationships, doseresponse and other quantitative data are
also summarized.
(d)
Mechanistic and other relevant data
Data relevant to the toxicokinetics (absorption, distribution, metabolism, elimination)

and the possible mechanism(s) of carcinogenesis (e.g. genetic toxicity, epigenetic effects)
are summarized. In addition, information on susceptible individuals, populations and lifestages is summarized. This section also reports on other toxic effects, including reproductive and developmental effects, as well as additional relevant data that are considered
to be important.
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31
6. Evaluation and rationale

Evaluations of the strength of the evidence for carcinogenicity arising from human
and experimental animal data are made, using standard terms. The strength of the mechanistic evidence is also characterized.
It is recognized that the criteria for these evaluations, described below, cannot
encompass all of the factors that may be relevant to an evaluation of carcinogenicity. In
considering all of the relevant scientific data, the Working Group may assign the agent to
a higher or lower category than a strict interpretation of these criteria would indicate.
These categories refer only to the strength of the evidence that an exposure is
carcinogenic and not to the extent of its carcinogenic activity (potency). A classification
may change as new information becomes available.
An evaluation of the degree of evidence is limited to the materials tested, as defined
physically, chemically or biologically. When the agents evaluated are considered by the
Working Group to be sufficiently closely related, they may be grouped together for the
purpose of a single evaluation of the degree of evidence.
(a)
Carcinogenicity in humans
The evidence relevant to carcinogenicity from studies in humans is classified into one
of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal
relationship has been established between exposure to the agent and human cancer.
That is, a positive relationship has been observed between the exposure and cancer in
studies in which chance, bias and confounding could be ruled out with reasonable
confidence. A statement that there is sufficient evidence is followed by a separate
sentence that identifies the target organ(s) or tissue(s) where an increased risk of
cancer was observed in humans. Identification of a specific target organ or tissue does
not preclude the possibility that the agent may cause cancer at other sites.
Limited evidence of carcinogenicity: A positive association has been observed between
exposure to the agent and cancer for which a causal interpretation is considered by the
Working Group to be credible, but chance, bias or confounding could not be ruled out
with reasonable confidence.
Inadequate evidence of carcinogenicity: The available studies are of insufficient quality,
consistency or statistical power to permit a conclusion regarding the presence or
absence of a causal association between exposure and cancer, or no data on cancer in
humans are available.
Evidence suggesting lack of carcinogenicity: There are several adequate studies covering
the full range of levels of exposure that humans are known to encounter, which are
mutually consistent in not showing a positive association between exposure to the
agent and any studied cancer at any observed level of exposure. The results from
32
these studies alone or combined should have narrow confidence intervals with an
upper limit close to the null value (e.g. a relative risk of 1.0). Bias and confounding
should be ruled out with reasonable confidence, and the studies should have an
adequate length of follow-up. A conclusion of evidence suggesting lack of carcinogenicity is inevitably limited to the cancer sites, conditions and levels of exposure,
and length of observation covered by the available studies. In addition, the possibility
of a very small risk at the levels of exposure studied can never be excluded.
In some instances, the above categories may be used to classify the degree of evidence related to carcinogenicity in specific organs or tissues.
When the available epidemiological studies pertain to a mixture, process, occupation
or industry, the Working Group seeks to identify the specific agent considered most likely
to be responsible for any excess risk. The evaluation is focused as narrowly as the available data on exposure and other aspects permit.
(b)
Carcinogenicity in experimental animals
Carcinogenicity in experimental animals can be evaluated using conventional bioassays, bioassays that employ genetically modified animals, and other in-vivo bioassays
that focus on one or more of the critical stages of carcinogenesis. In the absence of data
from conventional long-term bioassays or from assays with neoplasia as the end-point,
consistently positive results in several models that address several stages in the multistage
process of carcinogenesis should be considered in evaluating the degree of evidence of
carcinogenicity in experimental animals.
The evidence relevant to carcinogenicity in experimental animals is classified into one
of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal
relationship has been established between the agent and an increased incidence of
malignant neoplasms or of an appropriate combination of benign and malignant
neoplasms in (a) two or more species of animals or (b) two or more independent
studies in one species carried out at different times or in different laboratories or
under different protocols. An increased incidence of tumours in both sexes of a single
species in a well-conducted study, ideally conducted under Good Laboratory
Practices, can also provide sufficient evidence.
A single study in one species and sex might be considered to provide sufficient
evidence of carcinogenicity when malignant neoplasms occur to an unusual degree
with regard to incidence, site, type of tumour or age at onset, or when there are strong
findings of tumours at multiple sites.
Limited evidence of carcinogenicity: The data suggest a carcinogenic effect but are
limited for making a definitive evaluation because, e.g. (a) the evidence of carcinogenicity is restricted to a single experiment; (b) there are unresolved questions regarding the adequacy of the design, conduct or interpretation of the studies; (c) the agent
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increases the incidence only of benign neoplasms or lesions of uncertain neoplastic

potential; or (d) the evidence of carcinogenicity is restricted to studies that demonstrate only promoting activity in a narrow range of tissues or organs.
Inadequate evidence of carcinogenicity: The studies cannot be interpreted as showing
either the presence or absence of a carcinogenic effect because of major qualitative or
quantitative limitations, or no data on cancer in experimental animals are available.
Evidence suggesting lack of carcinogenicity: Adequate studies involving at least two
species are available which show that, within the limits of the tests used, the agent is
not carcinogenic. A conclusion of evidence suggesting lack of carcinogenicity is
inevitably limited to the species, tumour sites, age at exposure, and conditions and
levels of exposure studied.
(c)
Mechanistic and other evidence judged to be relevant to an evaluation of carcinogenicity and of sufficient importance to affect the overall evaluation is highlighted. This
may include data on preneoplastic lesions, tumour pathology, genetic and related effects,
structureactivity relationships, metabolism and toxicokinetics, physicochemical parameters and analogous biological agents.
The strength of the evidence that any carcinogenic effect observed is due to a
particular mechanism is evaluated, using terms such as weak, moderate or strong.
The Working Group then assesses whether that particular mechanism is likely to be
operative in humans. The strongest indications that a particular mechanism operates in
humans derive from data on humans or biological specimens obtained from exposed
humans. The data may be considered to be especially relevant if they show that the agent
in question has caused changes in exposed humans that are on the causal pathway to
carcinogenesis. Such data may, however, never become available, because it is at least
conceivable that certain compounds may be kept from human use solely on the basis of
evidence of their toxicity and/or carcinogenicity in experimental systems.
The conclusion that a mechanism operates in experimental animals is strengthened by
findings of consistent results in different experimental systems, by the demonstration of
biological plausibility and by coherence of the overall database. Strong support can be
obtained from studies that challenge the hypothesized mechanism experimentally, by
demonstrating that the suppression of key mechanistic processes leads to the suppression
of tumour development. The Working Group considers whether multiple mechanisms
might contribute to tumour development, whether different mechanisms might operate in
different dose ranges, whether separate mechanisms might operate in humans and experimental animals and whether a unique mechanism might operate in a susceptible group.
The possible contribution of alternative mechanisms must be considered before concluding that tumours observed in experimental animals are not relevant to humans. An
uneven level of experimental support for different mechanisms may reflect that disproportionate resources have been focused on investigating a favoured mechanism.
34
For complex exposures, including occupational and industrial exposures, the chemical composition and the potential contribution of carcinogens known to be present are
considered by the Working Group in its overall evaluation of human carcinogenicity. The
Working Group also determines the extent to which the materials tested in experimental
systems are related to those to which humans are exposed.
(d)
Overall evaluation
Finally, the body of evidence is considered as a whole, in order to reach an overall

evaluation of the carcinogenicity of the agent to humans.
An evaluation may be made for a group of agents that have been evaluated by the
Working Group. In addition, when supporting data indicate that other related agents, for
which there is no direct evidence of their capacity to induce cancer in humans or in
animals, may also be carcinogenic, a statement describing the rationale for this conclusion
is added to the evaluation narrative; an additional evaluation may be made for this broader
group of agents if the strength of the evidence warrants it.
The agent is described according to the wording of one of the following categories,
and the designated group is given. The categorization of an agent is a matter of scientific
judgement that reflects the strength of the evidence derived from studies in humans and in
experimental animals and from mechanistic and other relevant data.
Group 1:
The agent is carcinogenic to humans.
This category is used when there is sufficient evidence of carcinogenicity in
humans. Exceptionally, an agent may be placed in this category when evidence of
carcinogenicity in humans is less than sufficient but there is sufficient evidence of
carcinogenicity in experimental animals and strong evidence in exposed humans that
the agent acts through a relevant mechanism of carcinogenicity.
Group 2.
This category includes agents for which, at one extreme, the degree of evidence
of carcinogenicity in humans is almost sufficient, as well as those for which, at the
other extreme, there are no human data but for which there is evidence of carcinogenicity in experimental animals. Agents are assigned to either Group 2A (probably
carcinogenic to humans) or Group 2B (possibly carcinogenic to humans) on the basis
of epidemiological and experimental evidence of carcinogenicity and mechanistic and
other relevant data. The terms probably carcinogenic and possibly carcinogenic have
no quantitative significance and are used simply as descriptors of different levels of
evidence of human carcinogenicity, with probably carcinogenic signifying a higher
level of evidence than possibly carcinogenic.
Group 2A:
The agent is probably carcinogenic to humans.
This category is used when there is limited evidence of carcinogenicity in humans
and sufficient evidence of carcinogenicity in experimental animals. In some cases, an
agent may be classified in this category when there is inadequate evidence of carcino-
PREAMBLE
35
genicity in humans and sufficient evidence of carcinogenicity in experimental animals

and strong evidence that the carcinogenesis is mediated by a mechanism that also
operates in humans. Exceptionally, an agent may be classified in this category solely
on the basis of limited evidence of carcinogenicity in humans. An agent may be
assigned to this category if it clearly belongs, based on mechanistic considerations, to
a class of agents for which one or more members have been classified in Group 1 or
Group 2A.
Group 2B:
The agent is possibly carcinogenic to humans.
This category is used for agents for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental
animals. In some instances, an agent for which there is inadequate evidence of
carcinogenicity in humans and less than sufficient evidence of carcinogenicity in
experimental animals together with supporting evidence from mechanistic and other
relevant data may be placed in this group. An agent may be classified in this category
solely on the basis of strong evidence from mechanistic and other relevant data.
Group 3:
The agent is not classifiable as to its carcinogenicity to humans.
This category is used most commonly for agents for which the evidence of
carcinogenicity is inadequate in humans and inadequate or limited in experimental
animals.
Exceptionally, agents for which the evidence of carcinogenicity is inadequate in
humans but sufficient in experimental animals may be placed in this category when
there is strong evidence that the mechanism of carcinogenicity in experimental
animals does not operate in humans.
Agents that do not fall into any other group are also placed in this category.
An evaluation in Group 3 is not a determination of non-carcinogenicity or overall
safety. It often means that further research is needed, especially when exposures are
widespread or the cancer data are consistent with differing interpretations.
Group 4:
The agent is probably not carcinogenic to humans.
This category is used for agents for which there is evidence suggesting lack of
carcinogenicity in humans and in experimental animals. In some instances, agents for
which there is inadequate evidence of carcinogenicity in humans but evidence
suggesting lack of carcinogenicity in experimental animals, consistently and strongly
supported by a broad range of mechanistic and other relevant data, may be classified
in this group.
(e)
Rationale
The reasoning that the Working Group used to reach its evaluation is presented and
discussed. This section integrates the major findings from studies of cancer in humans,
36
studies of cancer in experimental animals, and mechanistic and other relevant data. It includes concise statements of the principal line(s) of argument that emerged, the conclusions of the Working Group on the strength of the evidence for each group of studies,
citations to indicate which studies were pivotal to these conclusions, and an explanation
of the reasoning of the Working Group in weighing data and making evaluations. When
there are significant differences of scientific interpretation among Working Group Members, a brief summary of the alternative interpretations is provided, together with their
scientific rationale and an indication of the relative degree of support for each alternative.
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GENERAL REMARKS
This ninety-fifth volume of IARC Monographs considers household use of solid fuels
for heating and cooking, a practice that can generate substantial quantities of indoor air
pollution. The World Health Report 2002 identified indoor smoke from solid fuels as one
of the top ten risks in terms of the global burden of disease (WHO, 2002). This health
burden occurs almost exclusively in low-to-medium-resource countries, as solid fuels
(e.g. wood, other biomass, and coal) are typically used only when other fuels are not
available or not affordable.
An Advisory Group on priorities for future evaluations had recommended that IARC
review indoor air pollution with high priority (IARC, 2003). This was reaffirmed and
refined by a subsequent Advisory Group convened to plan a series of Monographs on air
pollution. The first two volumes of this series, Volume 92 on polycyclic aromatic
hydrocarbons and Volume 93 on low-solubility low-toxicity particles, evaluated these two
major components of emissions from household use of solid fuels, and this volume builds
on those reviews.
Some epidemiological studies of household solid-fuel use also reported data on
cooking methods as a potentially confounding factor. Because many of these studies were
conducted in countries where common cooking practices include stir-frying, deep-frying,
and pan-frying, the results provide a basis for evaluating the potential carcinogenic hazard
of high-temperature frying. Accordingly, this volume includes a second Monograph on
the subject. High-temperature frying occurs in a wide range of populations living in low-,
medium-, and high-resource countries.
Emissions from household use of solid fuels are complex mixtures containing
thousands of chemical compounds at varying concentrations, and these may be admixed
and adsorbed to particulate matter of widely varying dimensions. Accordingly, careful
consideration must be given in using the available studies to make inferences about risks
in other exposure circumstances. For example, do the results on household use of coal
apply only to the specific sources of coal that were studied, or does other information
make it reasonable to apply these results to other types of coal or even to other types of
fuel? In making these determinations, it is necessary to consider the degree of similarity
of the varying emissions mixtures, with respect both to composition and to biological
activity. The Working Group spent much time discussing how narrowly or broadly to
interpret the available studies. In doing this, data on the composition and the genetic
toxicity of various mixtures were important in different ways.
39
40
The adverse health effects caused by household practices considered in this volume
may be attributable primarily to products of incomplete combustion. In addition, the
emissions from these solid-fuel stoves contain many chemical components known or
likely to cause cancer in humans. Some of these are known to cause cancer outside the
respiratory tract (e.g., benzene is causally associated with an increased risk of leukaemia).
As the available epidemiological studies on household use of solid fuels did not examine
these other cancers, the full burden of disease is not yet known and merits further
investigation.
It is curious that although the most commonly used solid fuels are wood and other
biomass, few epidemiological studies and cancer bioassays have investigated their
potential cancer risks. The utility of further research is magnified by the high
concentrations of emissions that can occur and by data showing that wood smoke is
mutagenic in exposed humans.
A summary of the findings of this volume appears in The Lancet Oncology (Straif et
al., 2006).
References
IARC (2003) Report of an Ad-Hoc IARC Monographs Advisory Group on Priorities for Future
Evaluations. Lyon, International Agency for Research on Cancer, Internal Report No. 03/001
[available at http://monographs.iarc.fr/ENG/Publications/internrep/03-001.pdf]
Straif K, Baan R, Grosse Y et al. (2006) Carcinogenicity of household solid fuel combustion and of
high-temperature frying. Lancet Oncol 7: 977978. PM:17348122
WHO (2002) The World Health Report 2002: Reducing Risks, Promoting Healthy Life, Geneva,
World Health Organization [available at http://www.who.int/whr/2002/en/]
THE MONOGRAPHS
HOUSEHOLD USE OF SOLID FUELS
1. Exposure Data
1.1
Description and determinants of use of household fuels
1.1.1
Introduction
All over the developing world, meals are cooked and homes are treated with homemade traditional stoves or open fires. These stoves are fired with either biomass fuels,
such as wood, branches, twigs or dung, or coal. When these are not available, agricultural
residues or even leaves and grass are used. The smoke emitted from such stoves is made
up of particles and gaseous chemicals. It is estimated that as many as 70% of households
in developing countries use fuels such as wood, dung and crop residues for cooking
(International Energy Agency, 2002; WHO, 2006). The seemingly free availability of
biomass fuels from nature makes them the primary fuel source for household purposes.
The problems related to the use of biomass as an energy source have been an issue of
concern for more than three decades. The traditional stoves commonly used for burning
biomass energy have long been found to be highly inefficient and to emit copious
quantities of smoke due to the incomplete combustion of fuels. This inefficiency has also
had consequences on the environment, since intense collection of fuelwood has resulted
in deforestation in highly populated areas. The use of such fuels has also adversely
affected health. In addition, the cost involved in terms of human energy and time required
to collect and process such fuel has serious implications for productivity and gender
equity.
Attempts to convert households from these fuels to modern fuels or from traditional
stoves to more efficient and cleaner burning stoves through reform of the energy sector or
indigenous innovative technology have been very effective in some countries, but dismal
or non-existent in others. This section provides a description of the various fuels and some
background on their energy content and the efficiency of their use. Thereafter, the current
trends and the known determinants that explain the widespread use of biomass fuels and
coal are reviewed. Since indoor air pollution from the use of biomass and coal in the
45
46
domestic sector is largely a phenomenon of the developing world, emphasis is mainly on

these countries.
1.1.2
Description of household fuels

(a)
Types of solid fuel
A wide variety of fuels are used in households in developing countries for cooking
and heating. Solid fuels refer to both biomass fuels and coal. The most common fuel used
for cooking and heating is wood, followed by other solid biomass fuels, such as charcoal,
dung, agricultural residues and sometimes even leaves and grass. These fuels are often
collected from the local environment in rural areas and are purchased through markets in
urban areas.
In some rural areas, farmers who own or manage livestock have the option of using a
digester to turn dung and agricultural waste into biogas, which is a fuel that can be used
for both heating and/or lighting. Electricity is not commonly used in developing countries
for cooking, but is often used for other purposes, such as lighting and powering
appliances. In China and some coal-producing regions in India and South Africa, coal is
used as a cooking and heating fuel, sometimes in combination with other biomass fuels.
Raw coal may be used in many forms from lumps to briquettes to fine powders. Coal may
be processed as simply as forming coal balls or cakes by hand followed by sun-drying, or
may undergo a sophisticated procedure, such as being blended into a uniform mixture
with binders to reduce sulfur and particulate emissions and formed into briquettes
designed to burn efficiently and cleanly in special stoves.
Modern fuels include liquefied petroleum gas (LPG), kerosene and electricity.
(b)
Energy density and efficiency of fuels
Fuels differ in their energy densities and efficiency (Table 1.1). Modern fuels such as
LPG have the highest energy content per kilogram of fuel at approximately 45 MJ/kg. In
contrast, crop residues and dung have energy densities of about 14 MJ/kg of fuel. The
efficiency of a fuel is measured by the amount of energy used for cooking compared with
that which escapes from the stove without actually heating the food. The efficiency of
cooking with LPG is estimated to be approximately 60% compared with only 12% for
agricultural residues burnt in traditional stoves. This is one of the reasons that commercial
fuels such as LPG are considered to be superior to crop residue and dung (see below).
Coal is a highly variable fuel, and ranges from anthracite with a high heating value
anthracite through various forms of bituminous coal to lignite and peat. Each of these
types of coal can contain different levels of moisture, non-combustible inorganic material
(ash), sulfur and sometimes significant levels of other impurities, such as arsenic, fluorine,
lead and mercury.
All fuels are burned in various types of device to provide the heat necessary for
cooking. The device can be relatively efficient or inefficient and be associated with high
or low levels of pollution. As indicated in Table 1.1, conversion efficiencies for kerosene
47
stoves range from 35% for wick stoves to 55% for pressure stoves; those for fuelwood
stoves range from 15% for traditional stoves to 25% for improved stoves. Improved
stoves have the potential to reduce indoor air pollution levels, to burn wood or other
biomass more efficiently and sometimes to reduce average cooking times.
Table 1.1. Typical efficiencies at the final consumption stage of cooking
Fuel source
Energy content
(MJ/kg)
Typical
conversion
efficiencya (%)
Useful energy
at final
consumption
stage of
cooking
(MJ/kg)
27.3
Approximate
quantity of fuel
necessary to
provide 5 GJ of
useful energy
for cooking
(kg)
Liquefied petroleum gas
45.5
60
Natural gas
38 [MJ/m3]
60
180
Kerosene (pressure)
43.0
55
23.6
Kerosene (wick)
43.0
35
15.1
Biogas (60% methane)
22.8 [MJ/m3]
60
Charcoal (efficient stoves)
30.0
30
9.0
Charcoal (traditional stoves)
30.0
20
6.0
830
Bituminous coal
22.5
25
5.6
880
Fuelwood (efficient stoves), 15%

moisture
16.0
25
4.0
1250
Fuelwood (traditional stoves), 15%

moisture
16.0
15
2.4
2000
Crop residue (straw, leaves, grass), 5%

moisture
13.5
12
1.6
3000
Dung, 15% moisture
14.5
12
1.7
2900
219 [m3]
210
330
365 [m3]
550
From Sullivan & Barnes (2006)

a
The typical conversion efficiency for charcoal, fuelwood and kerosene is based on their respective stove types.
1.1.3
Use of solid fuels worldwide
Biomass is often the primary source of household energy in developing countries. Just
over three billion people use biomass fuels for cooking and heating in developing
countries and approximately 800 million people, mostly in China, use coal. As indicated
in Figure 1.1, these statistics have been relatively stable over the last 1520 years and are
expected to continue into the future (WHO, 2006). Thus, it is anticipated that the use of
solid fuels and especially biomass fuels will persist for many years to come.
Significant regional variations occur as well as differences between urban and rural
areas. The findings that have been collected from national surveys conducted by the
48
Demographic and Health Surveys (DHS), the World Banks Livings Standards
Measurement Study (LSMS) and other similar studies are presented in Table 1.2. The
estimates in Figure 1.2 are averages of main fuel use across the set of countries found in
Table 1.2.
Figure 1.1. Population using solid fuels (millions) in 1990, 2003 (mid-point) and 2015
8 000
Non-solid fuel users
7 000
Solid fuel users

million 6 000
people
5 000
4 000
3 000
2 000
1 000
0
1990
2003
2015
Adapted from WHO (2006) (Figure 14: Trends in solid fuel use)
Data for 2015 are based on:
a business-as-usual scenario that applies the observed annual increase in the number of people with
access to cleaner fuels from 1990 to 2003 to the period 200315;
the voluntary Millennium Development Goal target proposed by the UN Millennium Project to halve
the number of people without access to modern cooking fuels between 1990 and 2015.
Table 1.2. Household use of main cooking fuels in selected developing countries,
national household surveys 19962003
Countries
AFRICA
Benin
Burundi
Cameroon
Eritrea
Ethiopia
Ghana
Kenya
Madagascar
% Solid fuelsa
% Modern fuelsa
Rural
Urban
National
98.7
99.9
98.2
97.4
99.9
99.4
94.7
98.8
87.5
98.1
62.2
30.4
72.9
88.0
33.8
96.2
94.6
99.8
82.8
79.7
95.4
95.8
81.8
98.2
Rural
1.3
0.2
1.8
2.6
0.1
0.6
5.1
1.1
Datab
Urban
National
Source
Year
12.5
1.9
37.8
69.6
27.1
12.0
66.1
3.7
5.4
0.2
17.3
20.3
4.6
4.2
18.1
1.7
DHS
EP
ECAM
DHS
DHS
CWIQ
CWIQ
EP
2001
1998
2001
1995
2000
1997
1997
1999
49
Table 1.2. (contd)

Countries
AFRICA (contd)
Malawi
Mali
Niger
Nigeria (eight states)
Rwanda
Uganda
Zambia
Zimbabwe
% Solid fuelsa
% Modern fuelsa
Rural
Urban
National
99.6
99.8
98.4
94.2
99.9
98.7
98.1
93.6
83.0
98.4
94.8
57.4
98.1
85.0
62.4
4.7
97.4
97.9
97.8
85.7
99.8
96.8
85.9
59.7
80.4
38.3
7.1
2.7
Rural
Datab
Urban
National
Source
Year
0.4
0.2
1.6
5.9
0.1
1.3
1.9
6.4
17.0
1.6
5.2
42.6
1.9
15.0
37.6
95.3
2.6
0.4
2.2
14.0
0.2
3.2
14.1
40.3
DHS
DHS
EPCES
CWIQ
DHS
DHS
DHS
DHS
2000
2001
1995
2002
2000
2001
2001
1999
34.4
9.3
19.6
61.7
92.9
97.3
65.6
90.7
DHS
PNAD
1998
1999
LATIN AMERICA
Bolivia
Brazil
Chile
Colombia
Costa Rica
El Salvador
Mexico
Paraguay
Uruguay
Haiti
Nicaragua
48.2
23.9
71.7
3.4
3.6
17.6
19.5
11.8
37.9
51.8
76.1
28.3
96.6
96.4
82.4
80.5
88.2
62.1
ENH
EHPM
EHPM
2000
2000
2000
71.3
1.8
99.6
93.3
22.0
0.4
91.0
46.1
43.3
1.1
96.4
64.4
28.7
98.2
0.4
6.8
78.0
99.6
9.0
53.9
56.7
98.9
3.6
35.6
EPH
ECH
DHS
LSMS
2000
2000
2000
2001
ASIA
India
Nepal
Pakistan
Cambodia
Indonesia
Papua New Guinea
Yemen, Republic of
90.2
95.6
95
98.7
83.2
98.2
53.1
29.2
39.9
28
82.0
20.4
34.4
3.0
73.7
89.7
76
96.3
72.2
89.6
41.6
8.5
4.4
5
1.3
16.8
1.7
46.9
66.3
60.1
72
18.0
79.6
65.5
97.0
24.3
10.3
24
3.7
27.8
10.3
58.4
NSS
DHS
HHS
DHS
Ag. Cens.
HHS
HBS
2000
2001
2001
2000
2003
1996
1998
Ag.Cens., Agricultural Census; CWIQ, Core Welfare Indicators Questionnaire; DHS, Demographic and Health
Survey; ECAM, Enqute Camerounaise Auprs des Mnages; ECH, Encuesta Continua de Hogares; EHPM,
Encuesta de Hogares de Propositos Multiples; ENH, Encuesta Nacional de Hogares; EP, Enqute Prioritaire;
EPCES, Enqute Permanente de Conjoncture conomique et Sociale; EPH, Encuesta Permanente de Hogares;
HBS; Household Budget Survey; HHS, Household Survey; LSMS, Living Standards Measurement Study; NSS,
National Sample Survey; PNAD, Presquisa Nacional por Amostra de Domicilios
No national survey for China, but other estimates suggest that 50% of urban households have access to LPG.
a
Most households mix solid and modern fuels.
b
Surveys involve average of main fuel used.
In Africa, use of biomass is common in both urban and rural areas (Table 1.2;
Figure 1.2), and 89% of households in the countries surveyed depend on some type of
50
solid fuel, which includes both biomass and charcoal. In rural areas of Africa, virtually all
households use biomass fuels.
Figure 1.2. Percentage use of solid fuel reported as main household cooking
energy in national surveys, 19962003
% Using solid fuel
100.0
Africa
90.0
Asia
80.0
Latin America
70.0
60.0
50.0
40.0
30.0
20.0
10.0
0.0
Rural
Urban
From World Bank (2003)

The figures are based on averages from the countries in Table 1.2.
In Asia, rural areas remain dependent on biomass energy, but many urban areas are
increasingly switching to modern fuels (Figure 1.2). Overall, 74% of households in Asia
report use of solid fuels, mostly in the form of biomass. However, in countries such as
India and China, there are signs of significant change. In a case study in Hyderabad, India
(World Bank, 1999; Barnes et al., 2005), most urban people in this large metropolitan
area had switched to either kerosene or LPG for cooking in the 1990s (Figure 1.3). Recent
national figures in India indicate that only about 2030% of the urban population uses
biomass energy, which is a significant change from 25 years ago. While rural areas are
still dominated by biomass or other solid fuels, rising urban incomes and policies to
facilitate the heterogeneity of modern fuel use in urban areas, including a significant
conversion to kerosene and LPG in Asia, have been the main contributory factors to this
trend.
The lack of regular national household energy surveys makes it impossible to
quantify with confidence the state of household fuel use, but a variety of evidence can be
used to establish estimates with some degree of confidence. For example, in China, the
overall picture of household fuel use comes from the National Bureau of Statistics, which
prepares national and provincial balances of commercial energy, excluding biofuels (e.g.
National Bureau of Statistics, 2006), and the Ministry of Agriculture, which collects and
occasionally publishes estimates of biofuel use by province (e.g. EBCREY, 1999).
Published data do, however, show that more than 51% of urban households have access
51
Figure 1.3. Changes in choice of household cooking fuel in Hyderabad from

1982 to 1994
100%
% Households using fuels
LPG only
80%
LPG only
Kerosene and
LPG
60%
40%
20%
Kerosene
and LPG
Kerosene
only
Wood and
kerosene
Wood only
Kerosene
only
Wood and kerosene
0%
1982
1994
From Barnes et al. (2005)

LPG, liquefied petroleum gas
to gas fuels (National Bureau of Statistics, 2005). While access to gas in rural areas is
growing, fewer than 10% of rural households use gas fuels as their main cooking fuel
(Sinton et al., 2004a). All but about 1% of households have at least nominal access to
electricity. Despite the rapidly growing availability of electricity and gas, coal and
especially biomass remain the overwhelming energy sources for households nationwide
(Figure 1.4).
In Latin America, although some extremely poor countries such as Haiti have fuel use
patterns that are similar to those seen in Africa, many other countries are switching to
modern cooking fuels such as kerosene and LPG (Table 1.2). With the exception of a few
countries, less than 10% of the populations in most urban areas in Latin America use
biomass energy for cooking (Table 1.2), and the use of modern fuels is also growing in
rural areas. For instance, in rural Costa Rica, the use of biomass energy has declined to
less than one-quarter of its population, the majority of which has switched to modern
fuels.
The transition from biomass fuels to modern fuels has been associated with
improvement in economic prosperity and development (Figure 1.5). At very low levels of
income or development, households depend on biomass fuels such as agricultural waste,
dung or firewood. As incomes rise or the country becomes more developed, households
52
Figure 1.4. Total residential primary energy use in China
Total residential energy use (1018J)
10
8
Biomass
6
Coal
Electricity
Gas fuels
2
0
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
From International Energy Agency (2006a,b)
Figure 1.5. Transition from use of biomass fuels to use of modern fuels
Increasing use of cleaner, more efficient and more

convenient fuels for cooking
Very low
income
Low income
Middle income
High income
Electricity
Natural gas
Gas, liquefied petroleum gas
Ethanol, methanol
Non-solid
fuels
Kerosene
Solid fuels
Coal
Charcoal
Wood
Crop waste, dung
Increasing prosperity and development
From WHO (2006) (Figure 2: The energy ladder: household energy and development inextricably
linked)
Note: Ethanol and methanol are rarely, if ever, used.
Dash: estimate
53
begin to convert to non-solid fuels such as kerosene, LPG or electricity. At middle income
levels, households typically use both solid and non-solid fuels.
All over the developing world, significant variations in the use of biomass energy and
coal are observed. Both rural and urban populations are switching to modern fuels.
However, it is known that very poor countries generally can not afford to use modern
fuels, and the richest of countries have already adopted them due to their convenience and
cleanliness (see Section 1.4 on intervention and policies).
1.1.4
Determinants of choice of fuel and energy use
Most studies have found that three factors determine the choice of fuel (Leach, 1987;
Leach & Mearns, 1988; Boberg, 1993; Barnes et al., 2005). The first is access to both
modern fuels and to local biomass; the second involves affordability, as determined by
household income, since modern fuels must be purchased on the market; the third is the
policy options available, such as prices, subsidies and taxes, to reduce dependence on
biomass.
(a)
Availability and access to biomass and modern energy
The evolution of energy markets in developing countries is irregular. For modern

fuels, the institutions that serve both urban and rural markets can be diverse: in some
countries, government-run agencies control the flow of kerosene and LPG; in others,
there is one dominant supplier that has a virtual monopoly; and in some others, a
significant degree of competition exists among a limited number of private companies. In
contrast, the supply of biomass is generally characterized by self production or collection
of the fuel, local sales, or a market chain that spreads out from urban to rural areas. There
is growing evidence that, if households have access to a variety of fuels, a greater
acceptance of modern fuels occurs not only in urban (Barnes et al., 2005) but also often in
some rural areas.
The type of biomass used in an area largely depends on what is available in the local
environment. In Africa, wood is more readily available than in most other parts of the
developing world. Most people rely on firewood in rural areas and both firewood and
charcoal in urban areas to cook their meals. The use of wood, branches and, increasingly,
brush is widespread in Asia and Africa. Dung cakes or balls are used more commonly in
Asia and Latin America.
As wood becomes scarce due to deforestation, the use of agricultural residues as a
source of energy increases. Crop residues are a very poor source of energy for cooking. In
countries in Africa, charcoal is widely available and is thus used to almost the same extent
as wood fuels. In China, coal is commonly used to cook and heat. In Bangladesh, a very
densely populated country, the amount of local wood available to people is decreasing. A
recent survey in Bangladesh (World Bank, 2006) indicated that people who live in areas
where access to firewood from the local environment is minimal are turning towards
54
tree leaves, crop residue and dung (Table 1.3). In this situation, people are actually
moving
Table 1.3. Consumption of energy in domestic activities: all divisions (per
household/year: average over all households) in Bangladesh (2005)
Type of energy
All use
Biomass
Firewood (kg)
Tree leaves (kg)
Crop residue (kg)
Dung cake/stick (kg)
Saw dust (kg)
Non-biomass
Candle (piece)
Kerosene (litre)
Natural gas (Tk.)
LPG/LNG (litre)
Grid electricity (kWh)
Solar PV (kWh)
Storage cell (kWh)
Dry cell battery (piece)
Heating
1186
502
708
524
8
16
29
10
0.05
144
0.53
0.55
15
Cooking
Parboiling rice
Other
1065
471
539
504
8
29
30
164
16
0.02
93
0.9
2.7
4.2
0.02
1.8
10
0.05
0.25
0.07
4.00
From Asaduzzaman & Latif (2005)
down the energy ladder to lower and more polluting fuels. In Bangladesh, very little LPG
is available in rural areas. In urban areas, the development of modern cities has resulted in
a gradual decline in the use of biomass energy.
As seen in Table 1.4, when the population of a city reaches about 1 million, the use of
biomass energy declines sharply, since access to local biomass energy becomes difficult.
However, energy policies also play a role in the choice of household fuel. Thus, access to
both biomass and modern fuels is an extremely important element in the choice of
household fuel.
Table 1.4. Size and energy use in 45 cities in Bangladesh, 198088
City type
Town
Population
(in thousands)
Monthly
income (US $
per capita)
Fuel (%)
Firewood
Charcoal
Kerosene
LPG
Electricity
64
33
38
52
40
33
46
Small city
102
41
25
36
37
60
78
Middle city
526
35
47
53
64
23
69
Large city
3718
55
28
61
37
95
From World Bank (1988, 1989, 1990a,b,c,d, 1991a,b, 1992, 1993, 1996a, 1999) (hereinafter ESMAP Household
Energy Surveys)
(b)
55
Income and affordability
Poverty is inextricably linked to the use of biomass. Most homes in developing

countries use biomass energy, but there is a growing transition to modern fuels as well as
a trend in the opposite direction. Modern fuels cost moneywhen households can afford
to move up the energy ladder and access to modern fuels is not an issue, the transition is
almost inevitable.
Affordability is only an issue if there is adequate access to modern fuels, which is
often dictated by whether a household lives in an urban or a rural area. In many
developing countries, an interesting pattern can be seen between income and fuel use. In
the urban areas of India, Nepal, Guatemala and Nicaragua, for instance, the type of fuels
used is dependent upon household income: solid fuels are more common among the
poorer households and modern fuels are used by the rich. In some large urban areas, even
the poor use kerosene and, in some instances, LPG for cooking. In contrast, in the rural
areas of these countries, income has less influence on the type of fuel used. Across
households of all income classes, solid fuels are common (World Bank, 2003).
In rural areas, affordability largely contributes to the widespread use of biomass
energy. Households in rural areas are generally poor and biomass is often available to
them from the local environment. The price of using biomass energy is simply the labour
required in collecting it (World Bank, 1996a,b; WHO, 2006).
The amount of money spent by the poor on the small quantities of energy that they
use is a very important portion of their overall household expenditure. The poor spend
less on energy than the more wealthy households, but the percentage of income that they
spend on energy is typically much greater. The urban poor spend between 10 and 20% of
their income on energy, whereas the wealthy spend less than 5%.
In addition, the cost of energy services for the poor is also higher than that for the rich
because cooking with fuelwood and lighting with kerosene are inefficient compared with
cooking and lighting with modern fuels. Moreover, the poor often buy fuelwood and
charcoal in small amounts, and the higher transaction costs of buying in small quantities
inflate the price. Once the comparative efficiencies and transaction costs have been taken
into consideration, the delivered energy for cooking often is more expensive for poorer
people than for wealthy households.
Poorer people generally use biomass energy except under unusual circumstances. One
study based on evidence from 45 cities has classified general points at which people
switch from biomass to modern fuels (Barnes et al., 2005). Based on income figures
given in 1980 US dollars, the study indicated that people start switching from wood at
surprisingly low incomesbetween US $12 and US $30 per person per month. However,
where wood is inexpensive and readily available, people may continue its use at incomes
of up to US $100 per person per month. The use of modern fuels, including electricity and
LPG, generally intensifies at incomes of about US $4050 per person per month. This
suggests that definitive income cut-offs for fuel substitution can not be identified
precisely, only very broadly. The reason for this is the variation in access, pricing and
56
government policies. In addition, the study found that modern fuel consumption was
higher than that anticipated among poorer households. This can reflect both the
attractiveness of modern fuels and particular subsidy policies for some fuels; for example,
subsidies for kerosene in Indonesia, coal in China and LPG in some countries.
1.1.5
Conclusion
The negative impact of biomass energy on the daily lives of populations (especially
women and children) in the poorest parts of the developing world cannot be
underestimated. Furthermore, evidence would strongly suggest that the persistent and
widespread use of biomass energy largely depends on the factors of access, affordability
and pricing policies.
1.2
Constituents of emissions
Wood consists primarily of two polymers: cellulose (5070% by weight) and lignin
(approximately 30% by weight) (Simoneit et al., 1999). Other biomass fuels (e.g. grasses,
wheat stubble) also contain these polymers, although their relative proportions differ. In
addition, small amounts of low-molecular-weight organic compounds (e.g. resins, waxes,
sugars) and inorganic salts are present in wood. During combustion, pyrolysis occurs and
the polymers break apart to produce a variety of smaller molecules. Even when they are
intrinsically free of contaminants, biomass fuels and coals are difficult to burn in small
simple combustion devices such as household cooking and heating stoves without
substantial emissions of pollutants, principally due to the difficulty of completely premixing the fuel and air during burning, which is easily done with liquid and gaseous fuels.
Consequently, a substantial fraction of the fuel carbon is converted to products of
incomplete combustion, i.e. compounds other than the ultimate product of complete
combustion, carbon dioxide. For example, typical household coal and biomass stoves in
China and India divert between more than 10% and up to ~30% of their fuel carbon into
products of incomplete combustion (Smith et al., 2000; Zhang et al., 2000). Emissions of
products of incomplete combustion from coal and biomass overlap largely depending on
fuel species and stove types.
An individual product of incomplete combustion can be present in the gas phase,
particle phase or both phases, depending on its volatility. Hence, products of incomplete
combustion released from the combustion of biomass are a complex mixture of
particulate and gaseous chemical species, including carbon monoxide, nitrogen dioxide
and particulate matter (PM). Products of incomplete combustion also include a large
number of hydrocarbons that are precursor components of photochemical smog and
comprise ozone, aldehydes and particles (Tsai et al., 2003). Compared with biomass,
many coals contain more intrinsic contaminants from their mineral deposits, such as
sulfur, arsenic, silica, fluorine, lead and/or mercury. During combustion, these
contaminants are not destroyed but are released into the air in their original or oxidized
57
form. Therefore, coal combustion tends to emit other pollutants in addition to products of
incomplete combustion. In households that use sulfur-rich coals, for example, sulfur
dioxide is present at elevated levels. Since the temperature of coal combustion is normally
substantially higher than that of biomass combustion, higher emissions of oxides of
nitrogen were measured for household coal combustion than for biomass combustion
(Zhang et al., 2000).
Depending on the measurement and analytical methods used, the chemical
constituents of biomass and coal smoke have been reported in different studies in the form
of individual chemical compounds (e.g. carbon monoxide, benzene, formaldehyde),
groups of compounds (e.g. total non-methane hydrocarbon, total organic carbon),
elements (e.g. carbon, arsenic) or ions (e.g. fluoride, sulfate). The smoke constituents
identified to date are summarized in Tables 1.51.7, by class of compound, element and
ion, respectively. It should be noted that many of the wood smoke species reported in
Table 1.5 were isolated from measurements of US appliances (e.g. woodstoves,
fireplaces) and open-field combustion (e.g. wild fire, prescribed forest fire), because few
studies have been conducted to characterize detailed chemical speciation for biomass
stoves in developing countries. Compounds that are present in emissions from the
combustion of wood or coal and have been evaluated by the IARC are listed in Table 1.8.
One study has reported emission factors of some 60 hydrocarbons and ~17 aldehydes and
ketones from ~28 commonly used fuel/stove combinations in China and emission factors
of hydrocarbons from 28 fuel/stove combinations commonly used in India in the early
1990s (Smith et al., 2000; Zhang et al., 2000). In contrast, several hundred individual
compounds have been detected in smoke samples of residential wood combustion,
wildfire and prescribed burns (Rogge et al., 1998; McDonald et al., 2000; Oros &
Simoneit, 2001; Schauer et al., 2001; Fine et al., 2002). Although less well characterized,
many of the same chemicals were reported in smoke emissions from other types of
biomass, including grasses, rice straw, sugar cane and ferns (Simoneit et al., 1993, 1999;
Rinehart et al., 2002). Selected chemicals that are associated with carcinogenicity are
discussed below.
Table 1.5. Constituents of biomass smoke and coal smoke, by chemical class
Compound
Inorganic
compounds
Wood smoke
Coal smoke
Species
References
Species
Carbon monoxide
McDonald et al.
(2006)
Carbon monoxide
Sulfur dioxide
Nitric oxide
Ammonia
Sulfur dioxide
Nitric oxide
References
58
Table 1.5. (contd)

Compound
Coal smoke
Wood smoke
Species
References
Species
References
Alkanes
C1C7
Rogge et al. (1998);

McDonald et al.
(2000); Schauer et al.
(2001); Fine et al.
(2002); McDonald et
al. (2006)
C2C10
Yan et al. (2002);

Tsai et al. (2003)
Alkenes
C2C7 (including 1,3butadiene)

McDonald et al.
(2000); Fine et al.
(2002); McDonald et
al. (2006)
C2C10 (including 1,3- Yan et al. (2002);

butadiene)
Tsai et al. (2003)
Aromatics
Benzene
Xylene
Toluene
Styrene
PAHs and
substituted
PAHs
Acenaphthene
Anthracene
Benz[a]anthracene
Benzo[b+j+k]fluorene
Benzo[ghi]perylene
Benzo[a]pyrene
Benzo[e]pyrene
Biphenyl
acenaphthylene
Chrysene
Coronene
1,7-Dimethylphenanthrene
Fluoranthene
Fluorene
Indeno[123-cd]pyrene
1-Menaphthalene
2-Menaphthalene
1-Methylphenanthrene
Naphthalene
Phenanthrene
Pyrene
Retene
Hydrocarbons
Tsai et al. (2003)

McDonald et al.
(2006)
Chuang et al. (1992);
McDonald et al.
(2000); Oros &
Simoneit (2001);
Schauer et al. (2001);
Fine et al. (2002);
McDonald et al.
(2006)
Benzene
Xylene
Toluene
Styrene
Tsai et al. (2003)
Acenaphthene
Acenaphthylene
Acephenanthrylene
Anthracene
Benz[a]anthracene
Benzanthrone
Benzo[b]chrysene
Benzo[a]coronene
Benzo[b]fluoranthene
Benzo[k]fluoranthene
Benzo[b+j+k]fluorene
Benzo[a]fluorine
Benzo[b]naphtha[2,ld]thiophene
Benzo[pqr]naphtha[8,
1,2-bcd]perylene
Benzo[ghi]perylene
Benzo[a]pyrene
Benzo[e]pyrene
Chrysene
Coronene
Cyclopenta[def]chrysene-4-one
Chuang et al. (1992);

Wornat et al. (2001);
Ross et al. (2002);
Yan et al. (2002);
Chen et al. (2004,
2005); Lee et al.
(2005)
59
Table 1.5. (contd)

Compound
Coal smoke
Wood smoke
Species
References
PAHs (contd)
Species
References
Cyclopent[hi]acephenanthrylene
Cyclopenta[cd]benzo[ghi]perylene
Cyclopenta[bc]coronene
Cyclopenta[cd]fluoranthrene
Cyclopenta[cd]pyrene
Dibenz[a,c]anthracene
Dibenz[a,h]anthracene
Dibenz[a,j]anthracene
Dibenzo[b,k]fluoranthene
Dibenzo[a,e]pyrene
Dibenzo[e,l]pyrene
Dicyclopenta[cd,mn]pyrene
Dicyclopenta[cd,jk]pyrene
Fluoranthene,
Fluorene
Indeno[123-cd]pyrene
Naphtho[1,2-b]fluoranthene
Naphtho[2,1-a]pyrene
4-Oxa-benzo[cd]pyrene-3,5-dione
Phenanthrene
Picene
Pyrene
Triphenylene
Tribenzo[e,ghi,k]perylene
Total nonmethane
hydrocarbon
McDonald et al.
(2001); McDonald et
al. (2006)
Unresolved
complex
mixture
Oros & Simoneit

(2001); Fine et al.
(2002)
Tsai et al. (2003)
60
Table 1.5. (contd)

Compound
Coal smoke
Wood smoke
Species
References
Species
References
Formaldehyde
Acetaldehyde
Acetone
Acrolein
Propionaldehyde
Crotonaldehyde
2-Butanone
Isobutyraldehyde
Butyraldehyde
Benzaldehyde
Isovaleraldehyde
Valeraldehyde
ortho-Tolualdehyde
meta,paraTolualdehyde
Hexaldehyde
2,4-Dimethylbenzaldehyde
Miller et al. (1994);

Zhang & Smith
(1999)
Oxygenated organics
Alkanols
Methanol (+ methyl
formate)
Ethanol (+ acn +
acrolein)
McDonald et al. (2000);

Oros & Simoneit
(2001); Fine et al.
(2002); McDonald et al.
(2006)
Carboxylic
acids
Heptanoic acid
Octanoic acid
Nonanoic acid
Decanoic acid
Undecanoic acid
Dodecanoic acid
Tridecanoic acid

Oros & Simoneit
(2001); Fine et al.
(2006)
Aldehydes and
ketones
Formaldehyde
Acetaldehyde
Proponal
Butanal
Pentanal
Octanal
Nonanal (+
undecene)
Glyoxal
Acetone (+
propanal)
3-Buten-2-one
Butanone
3-Methyl-3-buten2-one

Fine et al. (2002);
McDonald et al. (2006)
Alkyl esters
Nonyl dodecanoate
Decyl dodecanoate
Undecyl
dodecanoate
Dodecadienyl
dodecanoate
Tridecyl
dodecanoate
Oros & Simoneit (2001)
Methoxylated
phenolic
compounds

Fine et al. (2002);
McDonald et al. (2006)
61
Table 1.5. (contd)

Compound
Coal smoke
Wood smoke
Species
References
Species
References
Other organic compounds

Other
substituted
aromatic
compounds
n-9-Octadecenoic
acid
n-9,12Octadecadienoic
acid
PCDDs
PCDFs
PCBs

Oros & Simoneit
(2001); Fine et al.
(2002); Gullett et al.
(2006)
Sugar
derivatives
1,4:3,6-DianhydroR-D-Glucopyranose
Galactosan
Mannosan
Levoglucosan
Monomethylinosito
Oros & Simoneit

(2001); Fine et al.
(2006)
Coumarins and Coumarin

flavonoids
tetramethoxyisoflavone
Fine et al. (2002)
Phytosteroids

Fine et al. (2002)
Stigmasterol
-Sitosterol
Stigmastan-3-ol
Stigmastan-3-one
Resin acids and Pimaric acid

terpenoids
Isopimaric acid
Abietic acid
Levopimaric acid
Neoabietic acid

Oros & Simoneit
(2001); Fine et al.
(2002)
Unresolved
compounds

Fine et al. (2002)
PAH, polycyclic aromatic hydrocarbon; PCB, polychlorinated biphenyl; PCDD, polychlorinated dibenzo-paradioxin; PCDF, polychlorinated dibenzofuran
Table 1.6. Elemental constituents of wood smoke and coal smoke

Wood smoke (particle phase)
Coal smoke (particle phase)
Element
Element
Reference
Reference
Carbon, including
McDonald et al. Carbon, including
Watson et al.
elemental carbon and (2000); Watson et elemental carbon and (2001) ; Ge et al.
organic carbon
al. (2001); Hays organic carbon
(2004)
et al. (2002)
62
Table 1.6. (contd)

Element
Reference
Element
Metals
Na, Mg, Al, K, Ca,

Ti, V, Cr, Mn, Fe,
Co, Ni, Cu, Zn, Ga,
As, Se, Br, Rb, Sr,
Yt, Zr, Mo, Pd, Ag,
In, Sn, Sb, Ba, La,
Au, Hg, Tl, Pb
Kleeman et al.
Na, Mg, Al, K, Ca,
(1999); Watson et Ti, V, Cr, Mn, Fe,
al. (2001)
Co, Ni, Cu, Zn, Ga,
As, Se, Br, Rb, Sr,
Yt, Zr, Mo, Pd, Ag,
In, Sn, Sb, Ba, La,
Au, Hg, Tl, Pb
Kauppinen &
Pakkanen (1990);
Watson et al.
(2001) ; Ross et
al. (2002); Ge et
al. (2004)
Non-metals
S, P, Si, Cl, Br
Watson et al.
(2001); Kleeman
et al. (1999)
Watson et al.
(2001); Ge et al.
(2004)
1.2.1
S, P, Si, Cl, Br
Reference
Particles as a whole versus particle components
Particles emitted from biomass and coal combustion are fine and ultrafine in size
(<1 m in diameter) (Kleeman et al., 1999; Hays et al., 2002). Fresh coal or biomass
smoke contains a large number of ultrafine particles, <1 m in diameter, which condense
rapidly as they cool and age. The smoke may contain some larger particles resulting from
suspension of ash and solid fuel debris. Because combustion-generated particles and
ash/debris particles have different chemical compositions and because particle size
determines how deep the particles can travel within and beyond the respiratory tract,
ascertaining size distribution plays an important role in the assessment of health impacts
(see Section 4). For this reason, there has been a switch in recent studies to the
measurement of inhalable (<10 m, referred to as PM10) or respirable (<2.5 m, referred
to as PM2.5) particles rather than of total suspended particles (TSP) as in earlier studies.
A large number of chemical species are contained in combustion particles and many
chemical species are not stable (Rogge et al., 1998). Although it is impractical to cover a
large number of individual compounds in a single study, a component of a specific
physicochemical property may be targeted. For example, total carbon content of particles
is a measure of the carbonaceous aerosol. Total carbon may be further segregated into
elemental carbon and organic carbon. Although approximately 520% of wood smoke
particulate mass consists of elemental carbon, the composition of the organic carbon
fraction varies considerably with the specific fuel being burned and with the combustion
conditions. Elemental carbon has a characteristic carbon core onto which many metals
and organic compounds can be readily absorbed or adsorbed.
Earlier studies also focused on different solvent extracts of particles (soot) emitted
from biomass or coal combustion. For example, in Xuan Wei County, China, particles
released from smoky coal combustion contained the highest amount of organic
compounds extractable with dichloromethane, followed by particles released from wood
63
combustion and then by those released from anthracite (smokeless) coal combustion
(Mumford et al., 1987). Some combustion emission particles carry stabilized free
radicals. Very limited data have shown that free radicals of the semi-quinone type are
present in wood smoke particles as well as diesel smoke and cigarette smoke, but not in
coal smoke which may contain or carry free radicals of graphite carbon type (Tian, 2005).
Analytical techniques such as ion chromatography can measure chemicals in the
extracts of combustion particles in their dissociated form (ions). Commonly identified
ions are shown in Table 1.7. These are the most abundant ions in smoke particles.
Table 1.7. Ionic constituents of wood smoke and coal smoke
Ion
Anions
Species
References
Species
References
SO42-
Watson et al. (2001); Hays et al. (2002);

Kleeman et al. (1999)
SO42-
Watson et al. (2001)
Cl
NO3Cations
NH4+
K+
Ca2+
Cl
NO3Watson et al. (2001); Hays et al. (2002);

Kleeman et al. (1999)
NH4+
Watson et al. (2001)
K+
Hays et al. (2002)
Table 1.8. IARC evaluationsa of compounds present in emissions from the

combustion of wood or coal
Agent
Polynuclear aromatic
hydrocarbons
Benz[a]anthracene
Benzo[a]pyrene
Chrysene
Indeno[1,2,3-cd]pyrene
Naphthalene
IARC Monographs evaluation of

carcinogenicity
Monographs volume,
year
In animals
In humans
IARC
Group
Sufficient
Sufficient
Sufficient
Sufficient
Sufficient
Sufficient
Sufficient
Sufficient
Sufficient
Inadequate
Inadequate
Inadequate
Inadequate
Inadequate
Inadequate
Inadequate
Inadequate
Inadequate
2B
2B
2B
1
2A
2B
2A
2B
2B
92, 2010
92, 2010
92, 2010
92, 2010
92, 2010
92, 2010
92, 2010
92, 2010
82, 2002
64
Table 1.8. (contd)

Agent
IARC Monographs evaluation of

carcinogenicity
Monographs volume,
year
In animals
In humans
IARC
Group
Volatile organic compounds

Acetaldehyde
Benzene
1,3-Butadiene
Formaldehyde
Styrene
Sufficient
Sufficient
Sufficient
Sufficient
Limited
Inadequate
Sufficient
Limited
Sufficient
Inadequate
2B
1
2A
1
2B
S7, 1987; 71, 1999

29, 1982; S7, 1987
S7, 1987; 71, 1999
88, 2006
82, 2002
Metals and metal compounds

Arsenic
Nickel
Sufficient
Sufficient
Sufficient
Sufficient
1
1
84, 2004
S7, 1987; 49, 1990
Only those agents classified as Group 1, 2A or 2B are listed here.
1.2.2
Polycyclic aromatic hydrocarbons (PAHs) and substituted PAHs
Polycyclic aromatic hydrocarbons (PAHs) are formed during incomplete combustion

of all carbon-based fuels and organic materials, including biomass and coal. At typical
ambient temperature, lower-molecular-weight PAHs (with 24 aromatic rings) are present
predominantly in the gas phase while higher-molecular-weight PAHs are present
predominantly in the particle phase. Because PAHs of higher cancer potency are
predominantly present in the particle phase (IARC, 2010), combustion particles have
often been subjected to compositional analysis for PAHs and PAH derivatives. A detailed
analysis of PAHs in the dichloromethane extracts of soot deposits from coal-burning
stoves in several homes of Hunan Province, China, identified 32 individual PAHs ranging
in size from three to eight fused aromatic rings. The PAHs found in the soot deposits
included 20 benzenoid PAHs, six fluoranthene benzologues, one cyclopenta-fused PAH,
one indene benzologue, three oxygenated PAHs and one sulfur-containing aromatic (see
Table 1.5) (Wornat et al., 2001). Carcinogenic PAHs, methylated PAHs and nitrogencontaining heterocyclic aromatic compounds were detected in large abundance in the
particles emitted from smoky coal combustion, as typically found in numerous
households in Xuan Wei County,1 Yunnan Province, China (Mumford et al., 1987;
Chuang et al., 1992; Granville et al., 2003; Keohavong et al., 2003). In the aromatic
fraction, coal combustion particles appeared to contain higher concentrations and more
species of methylated PAHs than wood combustion particles (Chuang et al., 1992).
1
Xuan Wei County is a site where decade-long studies have been conducted to examine lung
cancer and household coal combustion.
65
However, profiles of specific PAHs and their abundance vary largely depending on the
fuel types and combustion conditions. Between biomass smoke or coal smoke, it is
difficult to discern which has the higher PAH content (Tian, 2005).
1.2.3
Hydrocarbons and partially oxidized organic compounds
Hydrocarbons identified to date include: in wood smokealkanes with 17 carbons,

and alkenes with 27 carbons (including 1,3-butadiene); in coal smokealkanes with 1
10 carbons and alkenes with 210 carbons (including 1,3-butadiene); in both wood and
coal smokearomatic compounds (e.g. benzene, xylenes, toluene, styrene) (see Table
1.5). Partially oxidized organic compounds identified in wood and/or coal smoke include
alkanols, aldehydes and ketones (carbonyls), carboxylic acids, alkyl esters and
methoxylated phenolic compounds. In addition, partially oxidized aromatic compounds
and substituted aromatic compounds (e.g. aromatic organic acids, polychlorinated
dibenzodioxins, polychlorinated dibenzofurans, polychlorinated biphenyls), sugar
derivatives, coumarins and flavonoids, resin acids and terpenoids have been identified in
wood smoke (see Table 1.5). Both biomass smoke and coal smoke contain gas-phase
carcinogens (e.g. benzene, 1,3-butadiene, formaldehyde) in addition to particle-phase
PAHs that have carcinogenic potential. A detailed analysis of organic wood smoke
aerosol found nearly 200 distinct organic compounds, many of which are derivatives of
wood polymers and resins (see Table 1.5; Rogge et al., 1998).
1.2.4
Metals and other toxic substances
Some carcinogenic substances in coal were found to be released into the air during the
combustion of lignites used in Shenyang City of northern China and smoky coals used in
Xuan Wei County, China. It was reported that lignites from a local Shenyang coal field
had very high concentrations of nickel (75 ppm) and chromium (79 ppm) (Ren et al.,
1999, 2004) when compared with the levels reported elsewhere in the world (0.550 ppm
for nickel and 0.560 ppm for chromium) (Swaine, 1990). Microfibrous quartz has been
found in some smoky coals from Xuan Wei County and the resulting coal smoke but not
in wood smoke (Tian, 2005). Particles emitted from burning coals contaminated with
toxic elements (e.g. fluorine, arsenic, mercury) in Guizhou Province of China and other
areas have been reported to contain high levels of the corresponding elements (Gu et al.,
1990; Yan, 1990; Shraim et al., 2003). As shown in Table 1.6, metal and non-metal
elements have also been found in wood smoke particles, which reflects the intake of these
elements from the soil by trees.
1.2.5
Emission factors of some carcinogens
The emission factor of a particular chemical species can be measured as the mass of
the species emitted per unit mass of fuel combusted or the mass of the species emitted per
unit energy produced or delivered through combustion. A very small number of studies
66
have been conducted to date to quantify emission factors of common pollutants for
household stoves used in developing countries.
The available data for selected human carcinogens or probable carcinogens (benzene,
1,3-butadiene, formaldehyde and benzo[a]pyrene) are summarized in Table 1.9. The sum
of PAHs, when 14 individual PAHs were measured, is also shown in Table 1.9. The
cited studies measured PAHs most commonly reported in the literature: acenaphthene,
acenaphthylene, anthracene, benz[a]anthracene, benzo[b]fluoranthene, benzo[a]pyrene, benzo[ghi]perylene, benzo[k]fluoranthene, chrysene, dibenz[ah]anthracene,
fluoranthene, fluorene, indeno[1,2,3-cd]pyrene, naphthalene, phenanthrene and pyrene.
Table 1.9. Emission factors of carcinogenic compounds in the smoke of solid fuel
combustion in household stoves (and fireplaces)
Compound
Fuel type
Emission
Location (fuel Emission
source)
factora (mg/kg factora
fuel)
(mg/MJ)
Wood (1 type)
China
Reference
Benzene
264629
159161b
Tsai et al. (2003)
Wood (hardwood) USA
1190
McDonald et al.
(2000)
Fireplace wood
(2 types)
USA
225312
McDonald et al.
(2000)
Coal (4 types)
China
2.711050
0.9390b
Tsai et al. (2003)
Wood (1 type)
China
0.81.0
0.20.6b
Tsai et al. (2003)
1,3-Butadiene
Wood (hardwood) USA
197
McDonald et al.
(2000)
Fireplace wood
(2 types)
USA
6395
McDonald et al.
(2000)
Coal (4 types)
China
ND21.3
ND7.9b
Tsai et al. (2003)
Wood (1 type)
China
ND
ND
Tsai et al. (2003)
Styrene
Wood (hardwood) USA
117
McDonald et al.
(2000)
Fireplace wood
(2 types)
USA
3540
McDonald et al.
(2000)
Coal (4 types)
China
ND
ND
Tsai et al. (2003)
67
Table 1.9. (contd)

Compound
Fuel type

Emission
source)
fuel)
(mg/MJ)
Reference
Formaldehyde
Wood (2 types)
China
42261
18100b
Zhang & Smith

(1999)
Wood (hardwood) USA
246
McDonald et al.
(2000)
Fireplace wood
(2 types)
USA
113 178
McDonald et al.
(2000)
Coal (3 types)
China
251
0.912b
Zhang & Smith

(1999)
Wood (2 types)
China
41371
17145b
Zhang & Smith

(1999)
Acetaldehyde
Wood (hardwood) USA
361
McDonald et al.
(2000)
Fireplace wood
(2 types)
USA
301450
McDonald et al.
(2000)
Coal (3 types)
China
0.881
0.320b
Zhang & Smith

(1999)
Naphthalene
Wood (Petocarpus Thailand
indicus)
Wood (hardwood) USA
3.96
28
Fireplace wood
USA
(2 types)
Wood (eucalyptus Thailand
chip)
Charcoal
Thailand
2155
Coal briquettes
44.5
Viet Nam
39.1
7.48
Kim Oanh et al.

(2002)
McDonald et al.
(2000)
McDonald et al.
(2000)
Kim Oanh et al.
(1999)
Kim Oanh et al.
(1999)
Kim Oanh et al.
(1999)
Benzo[a]pyrene
indicus)
0.41
Kim et al. (2002)

chip)
0.69
Kim Oanh et al.

(1999)
68
Table 1.9. (contd)

Compound
Fuel type

Emission
source)
fuel)
(mg/MJ)
Benzo[a]pyrene (contd)
Wood (hardwood) USA
0.20
Reference
McDonald et al.
(2000)
Gullett et al.
(2003)
McDonald et al.
(2000)
Gullett et al.
(2003)
Gachanja &
Worsforld (1993)
Kim Oanh et al.
(1999)
Kim et al. (2002)
Wood (oak)
USA
0.56
Fireplace wood
(2 types)
Fireplace wood
(3 types)
Charcoal (two
types)
Charcoal
USA
0.150.34
USA
0.310.58
Kenya
0.010.12
Thailand
0.17
Sawdust briquettes Thailand
0.53
Coal briquettes
0.30
Kim Oanh et al.

(1999)
0.56
McDonald et al.
(2000)
Kim et al. (2002)
Viet Nam
Benz[a]anthracene
Wood (hardwood) USA
indicus)
chip)
Wood (oak)
USA
Fireplace wood
(3 types)
Fireplace wood
(2 types)
Charcoal
0.62
0.82
0.73
USA
0.340.79
USA
0.310.45
Thailand
0.06
1.04
Coal briquettes
0.11
Viet Nam
Kim Oanh et al.

(1999)
Gullett et al.
(2003)
Gullett et al.
(2003)
McDonald et al.
(2000)
Kim Oanh et al.
(1999)
Kim et al. (2002)
Kim Oanh et al.
(1999)
69
Table 1.9. (contd)

Compound
Fuel type
Wood (oak)
Wood (Petocarpus
indicus)
Wood (eucalyptus
chip)
Fireplace wood
(3 types)
Charcoal

Emission
source)
fuel)
(mg/MJ)
Reference
USA
0.04
Thailand
0.15
Gullett et al.
(2003)
Kim et al. (2002)
Thailand
0.6
USA
0.030.08
Thailand
ND
0.24
Coal briquettes
ND
Viet Nam
Sum of PAHs (14 individual PAHs)

indicus)
chip)
Wood (hardwood) USA
Kim Oanh et al.

(1999)
Gullett et al.
(2003)
Kim Oanh et al.
(1999)
Kim et al. (2002)
Kim Oanh et al.
(1999)
66
0.97c
Kim et al. (2002)
110
5.6c
Kim Oanh et al.

(1999)
McDonald et al.
(2000)
Gullett et al.
(2003)
McDonald et al.
(2000)
Gullett et al.
(2003)
Kim Oanh et al.
(1999)
Kim et al. (2002)
75
Wood (oak)
USA
147
Fireplace wood
(2 types)
Fireplace wood
(3 types)
Charcoal
USA
80167
USA
31144
Thailand
24.7
0.8c
260
6.3c
Coal briquettes
102
4.4b
Viet Nam
Kim Oanh et al.

(1999)
ND, not detected (below method detection limit); PAH, polycyclic aromatic hydrocarbon
a
The values are ranges of the means reported in individual studies
b
Denotes milligrams per megajoule of energy delivered to the pot
c
Denotes milligrams per megajoule of energy generated through combustion
70
Fuelwood combustion in two different Chinese cooking stoves generated 264 and
629 mg benzene for every kilogram of wood burned. Burning four types of household
coal fuels (honeycomb coal briquette, coal briquette, coal powder and water-washed coal
powder) in three different coal stoves generated a very wide range of benzene emissions
(2.711050 mg/kg fuel) (Tsai et al., 2003). When the wood emission factors of benzene
have been translated into indoor concentrations for a typical village kitchen, benzene
concentrations are expressed in parts per million (Zhang & Smith, 1996). As was the case
for benzene, 1,3-butadiene emission factors had a wider range for coal combustion (see
Table 1.9). However, wood combustion produced a higher formaldehyde emission factor
than that obtained with coal combustion. Using the formaldehyde emission factors, Zhang
and Smith (1999) predicted that a wood stove could produce sub-part-per-million and
part-per-million peak formaldehyde concentrations in a typical village kitchen, depending
on kitchen size and ventilation rate. Emission factors of benzo[a]pyrene for wood stoves
appeared to be consistent across studies conducted in different countries, depending on
fuel species (see Table 1.9). Interestingly, benzo[a]pyrene emission factors for fireplaces
appeared to be similar to those for wood stoves and to depend on the wood species used.
The benzo[a]pyrene emission factor for sawdust briquette was within the range of wood
stove emission factors. In contrast, benzo[a]pyrene emission factors for coal and charcoal
appeared to be lower. PAHs combined had the highest emission factor for sawdust
briquette and the lowest for charcoal. Wood fuels/stoves (including fireplaces) and coal
briquettes had overlaps in emission factor ranges for the PAHs combined. These emission
factor patterns (wood versus coal) were, in general, consistent with indoor air
concentration patterns measured in households that used coal and wood stoves (see
Section 1.3).
1.3
Use and exposure
1.3.1
General considerations on exposure to solid fuels

(a)
Determinants of exposure to indoor air pollution
Exposure to indoor air pollution resulting from the combustion of solid fuels is
influenced by multiple factors. Individual exposure may be most directly influenced by
the interaction of these factors with the source and the surrounding environment.
However, many factors can contribute to this interaction indirectly. For example, the type
of fuel and room dimensions may directly determine personal exposures but income,
climatic conditions, cooking habits and family size may indirectly influence the type of
fuel/stove (source) or the dimensions of the living space (surroundings). Determinants of
exposure could therefore be described by classifying them broadly into proximal (or
microenvironmental) determinants that are directly in the exposure pathway and distal
(or macroenvironmental) determinants that contribute to differences in exposure through
their effects on the systems that each of the proximal determinants may represent. Among
the studies conducted in developing countries, there is a great deal of similarity in the
71
types of determinant that have been found to affect exposures. Hence, this section gives a
general description of these determinants, while their specific contributions to population
exposures may be found in individual studies described in Sections 1.3.21.3.5. A
schematic illustration depicting the causal pathway and its interlinkage with some major
classes of determinants is shown in Figure 1.6.
Figure 1.6. A schematic illustration of possible determinants of exposure to indoor air
pollution related indoor cooking and heating with solid fuels. The outer circle represents
distal determinants while the inner circle represents proximal determinants.
Food
habits
Cooking
habits
Fuel
quantity/
cooking
duration
Climatic
variables
Gender
issues
Exposure
Time
activity
profiles
Housing
-rooms
-layout
-family size
Stove
ventilation
Emissions
Home
ventilation
Kitchen
location
Education
Fuel type
Stove type
Income
Drawn by the Working Group
Energy
market
structures
Cultural
factors
Access to
clean fuel
72
(i)
Macroenvironmental (distal) determinants
Socioeconomic (and demographic) determinants
These determinants operate largely through their influence on choice of fuel (one of
the biggest contributors to indoor emissions and exposures, as described in Section 1.1).
Income and education can also be expected to affect family size and type of housing that
in turn affect fuel quantities or the number of rooms and/or location of the kitchen. Access
to cleaner fuels may also be independently influenced by the prevalent national and
regional energy market structures, which in turn would be linked to the gross domestic
product of individual countries. Countries with a low gross domestic product per capita
may experience greater gender inequities in terms of income, education, access to health
care, social position and sociocultural preferences, all of which could potentially influence
the exposures of vulnerable groups, such as women and children.
Geographic determinants
Although exposures result from indoor sources, external ecological variables can have
a significant effect on the intensity and duration of pollution. Extreme temperature
differentials between seasons, rainfall, altitude and even meteorological factors such as
wind speed, wind direction and relative humidity, for example, could determine whether
solid fuels are used for both cooking and heating and also affect aerosol dispersion and/or
deposition. Patterns of vegetation (e.g. tropical rain forest versus scrub) could contribute
to household decisions to seek alternative energy sources. Conditions of temperature
and/or altitude that favour low dispersion (as may be commonly encountered in hilly/cold
areas) may also favour higher ambient levels of pollution (resulting from indoor sources)
which in turn contribute to increased exposure of the population.
(ii) Microenvironmental determinants
While the socioeconomic variables usually influence exposures indirectly through
their effect on choice of fuel, several determinants directly influence spatial and temporal
patterns of exposure within the household. Use and maintenance of improved stoves,
household layout (including the location of kitchen), household ventilation, timeactivity
profiles of individual household members and behavioural practices (such as location of
children while cooking) have been shown to influence pollution levels and individual
exposures to them. Cultural habits may influence cooking practices which in turn may
affect duration of cooking or the quantity of fuel used. While the available literature does
not allow a detailed attribution of exposures to each of these variables, they can be
expected to make varying contributions and must be considered when creating local or
regional profiles of the exposure situation.
(b)
Methods used to assess exposures
Exposures to indoor air pollutants that result from the combustion of solid fuels occur
in the homes of millions of people on a daily basis. Multiple determinants affect these
exposures directly or indirectly. While it would be impossible to create exposure profiles
73
by routine sampling of thousands of households, systematic assessments that use a

combination of qualitative and quantitative methods have been necessary to identify the
extent, levels and nature of exposures as well as to understand the relative contributions of
specific determinants. An exposure pyramid that illustrates commonly applied approaches
used in studies in developing countries is shown in Figure 1.7. As can be seen in the
figure in general, as the geographic scale decreases, specificity increases, the availability
of pre-existing or routinely collected data decreases and the cost of original data collection
increases.
Figure 1.7. A schematic illustration of exposure assessment methods (tiers) used in
studies in developing countries (adapted from Mehta & Smith, 2002; Balakrishnan et al.,
2004)
1 Regional/national fuel use

2 Sub-national household fuel use
Geographic scale
3 Household fuel use, housing characteristics
4 Household indoor air concentrations
5 Individual exposure
6 Biomarkers
Categorical/qualitative data
Continuous data
At the top of the pyramid are secondary data sources (tier No. 1). Some qualitative
data on exposures, e.g. by primary fuel type, are routinely collected in national surveys
such as the census and serve as readily available low-cost exposure indicators, but they
often lack precision for estimating exposures at the household level. The influence of
multiple household-level variables such as the type of fuel, type and location of kitchen
and type of stove on actual household level concentrations/exposures is poorly understood
in such assessments. However, this information has been very useful in estimating the
proportions of people at risk for these exposures across multiple regions of the world and
74
also in tracking changes in the prevalence of some key determinants such as fuel and
stove use in response to policy measures. More accurate (but more expensive) ways to
measure exposures are actual household sample surveys of fuel use (tier No. 2). Indeed,
this measure has been often used as the indicator of exposure in many epidemiological
studies. Even better (but yet more expensive) methods include surveys not only of fuel
use, but also of household characteristics such as type of construction material, stove type,
number of rooms and windows and room ventilation (tier No. 3). The next stage, which is
higher still in cost but more accurate, involves air pollution studies that use stationary air
sampling devices set in one or more locations of the household over various lengths of
time (tier No. 4). Some studies have been conducted in which people actually wore
devices to measure their (personal) exposures to pollution, or in which exposures were
reconstructed using concentration data and detailed timeactivitylocation records of
individual household members (tier No. 5). Biological fluid or tissue biomarkers (tier No.
6) have not been applied in field settings, although some laboratory exposure chamber
studies have been carried out. Finally, some methods that use a combination of qualitative
information on a large number of households together with quantitative and qualitative
information on a smaller subset of households have allowed the construction of models
that predict levels of household exposure on the basis of qualitative information on
selected determinants.
Using methods that collect primary data, a great deal of variation has been observed
across studies that estimated either area concentrations or personal exposures (tiers 4 and
5). The choice of sampling locations, the time and duration of sampling,
methods/instrumentation used for air sampling and exposure reconstruction coupled with
a great deal of interhousehold variability in distribution of determinants such as fuel
quantity, room dimensions, ventilation and stove type even within small geographical
clusters make it difficult to compare quantitative estimates across studies directly. Of
particular importance is the contribution of intense exposures over very short-term periods
(i.e cooking periods) within a very small area (usually the kitchen) that often selectively
target individual family members (usually women and young children). Figure 1.8 shows
a typical distribution of pollutant levels over the course of a day within a single household
and illustrates the importance of some of the factors mentioned above for exposures and
measurements. The broad range in measurement results described in the following
sections thus represents the variation that arises from differences in both exposure and
sampling or study methodologies.
1.3.2
China
China had a population of nearly 1.3 billion in 2004 (National Bureau of Statistics,
2005). Approximately 757 million lived in rural households, most of whom were
dependent on solid fuels for the bulk of their energy needs. Many urban residents also still
rely on substantial amounts of coal; relatively few use biomass for occasional tasks.
Although household coal is now officially discouraged or banned in all Chinese cities,
75
there is still significant but declining use in many, i.e. 510% of households, and a much
larger proportion of usage in past decades. Thus, despite rapid urbanization and spread of
the use of gas and electricity for cooking and heating, the majority of Chinas population
depends mainly on solid fuels for household energy and is frequently exposed to the
products of their combustion. A broad spectrum of information is available on population
numbers that use different fuels under various conditions and their resulting pollutant
levels (see for instance Impact Carbon (formerly CEIHD) at http://impactcarbon.org/).
This information is not complete nor are all sources concordant with each other, but
sufficient data exist to enable estimation of ranges of population exposures to a variety of
pollutants.
Figure 1.8. Typical variations in PM10 level observed during the course of the day relative to
daily means
From Mehta & Smith (2002)
(a)
Use and determinants of use of solid fuels
(i)
Types and amounts of fuel
The energy yearbooks published by the National Bureau of Statistics (Table 1.10)
include some data from the Ministry of Agriculture on household use of biofuels (crop
wastes, wood and biogas) by province, but the estimates of fossil fuel consumption in the
National Bureau of Statistics national and provincial balances (which estimate both
urban and rural household energy use) differ substantially from those in the relatively rare
publications from the Ministry of Agriculture that report the use of fossil fuels in rural
households (Table 1.11). National Bureau of Statistics sources report the level of fossil
fuel use for rural households to be only about 40% of that cited by the Ministry of
Agriculture, possibly due to differences in allocating fuel use to agricultural and
household purposes. While the levels of biofuel use are necessarily the same in both sources,
76
Table 1.10. Household energy use in China, 2004

Original measurements
Category
Raw coal
Washed coal
Briquettes
Coke
Coal gas
Gasoline
Kerosene
Diesel
LPG
Natural gas
Delivered heat
Electricity
Crop wastes
Wood
Biogas
Total
Population
Household size
Unit
Urban
Mt
Mt
Mt
Mt
Bcm
Mt
Mt
Mt
Mt
Bcm
PJ
TWh
Mt
Mt
Bcm
17.33
3.43
5.39
0.55
13.70
2.24
0.02
0.84
11.27
6.69
413.95
148.33
Millions
Persons
542.83
2.98
Rural
45.65
5.55
4.36
0.51
0.11
0.63
0.25
0.30
2.24
0.03
98.10
339.86
210.92
5.59
Conversion into PJ
Urban
Rural
409
53
96
16
155
96
1
36
566
261
414
534
1077
86
78
14
1
27
11
13
113
1
353
4273
3530
117
9694
2636
757.05
4.08
From National Bureau of Statistics (2005, 2006)

Mt, million tonnes; Bcm, billion cubic metres; LPG, liquefied petroleum gas; PJ, petajoules; TWh,
terawatthours
N.B. Biofuel use published in National Bureau of Statistics (2006) is attributed to the Ministry of
Agriculture. Data in the same categories as in this table are available from the same sources for
nearly all of Chinas provinces and provincial-level municipalities.
Table 1.11. Rural household energy use in China, 1998

Category
Units
Coal
LPG
163.45
1.95
Oil products
Electricity
4.51
74.54
Crop wastes
Wood
286.24
147.13
Biogas
Total
1.67
Conversion in PJ
Mt
Mt
Mt
TWh
Mt
Mt
Bcm
3421
98
189
269
3599
2462
35
10 074
From EBCREY (1999)

Mt, million tonnes; Bcm, billion cubic metres; LPG, liquefied petroleum
gas; PJ, petajoules; TWh, terawatt-hours
77
the difference between estimates of coal use mean that average dependence on biofuels
could be approximately between 60% and 80%. Wood accounts for about two-fifths of
biofuel use, and crop wastes make up the remainder; biogas use is still very small by
comparison. Depending on the data source, coal use in rural households is either of the
same order as that of crop wastes, or only a quarter as large.
Nevertheless, available data sources agree on at least one point: overall, rural
households in China depend on solid fuels for about 95% of their energy needs. The
corresponding proportion for urban households has fallen, and in 2004 was reported to be
22%. This percentage represented nearly 27 million tonnes of coal use. The assessment of
the contribution of coal type in different areas of China has been complicated by the fact
that the generic terms smoky coal and smokeless coal are widely applied in both rural
and urban China. Generally, it appears that smoky coal is bituminous or sub-bituminous
and smokeless coal is anthracite (For distinctions, see the glossary at
http://www.eia.doe.gov/kids/energyfacts/sources/non-renewable/coal.html). The more
smoky varieties have higher volatile contents, which makes them easier to ignite, but
more difficult to burn cleanly in small combustion devices. Furthermore, household coal
is frequently mixed with an earth or clay binder and produced as honeycomb coal, i.e. in
a cylindrical form of standard dimensions with vertical holes that facilitate lighting and
combustion. Briquetting is also common. Such mixing has been associated with reduced
indoor air pollution emissions, but no systematic testing across the many varieties under
household conditions has been done. In addition to the honeycomb form, such mixed
forms are variously known as coal cakes and coal balls. The same term probably has
different meanings in different places. For example, the term coal cakes is used both in
rural Xuan Wei and urban Shanghai, although the specific composition of the coal cakes
inevitably differs between the two locations and even within each location.
Gas fuels have become more widely available in many areas, and families spend
relatively large amounts on their purchase. Government-sponsored projects at the
household and village level have brought biogas into many homes, and some biomass
gasification projects exist, but these serve a relatively small proportion of the rural
population. Only the wealthiest families can afford to use LPG more than occasionally,
and household digesters rarely produce enough to satisfy a familys entire cooking needs;
thus, total use of gas fuels remains small.
Ad hoc household energy survey reports provide useful points of comparison in an
attempt to establish the broader picture. Tables 1.121.15 present some of the information
available on energy use at the household level. Survey methods, samples and locations
differ among studies; therefore, comparisons of results need to be carried out with care.
The information from the National Bureau of Statistics suggests that the average rural
household energy use in 2004 was 52 GJ/householdyear, or about 13 GJ/personyear.
The range of figures in household surveys is spread widely around this average, as do
provincial averages derived from statistical publications. Surveys of over
3200 households in six provinces in different regions conducted between 1987 and 1991
found annual household energy use ranging from about 7 to 24 GJ/personyear, compared
78
Table 1.12. Per-capita energy use in rural households in Liangshui County, Jiangsu Province, and Guichi
County, Anhui Province (China), 2003
Location
End use
Energy source (MJ/year)

Wood
Lighting
Cooking
Animal feed
Guichi
County,
Anhui
(n=340)
Kerosene
LPG
0.3
Animal feed
3904
65%
260
177
123
11
0.3
571
10%
169
345
46
561
9%
27
12
43
1%
1107
1731
431
0.3
18%
29%
7%
0.005%
27%
3791
1384
45
67
197
Other
Share
109
363
Water heating
Total
16%
1258
55
1%
Lighting
Cooking
940
735
1647
53
937
Electricity
1387
Other
Share
Coal
Water heating
Total
Biogas
Share
269
1046
17%
1059
1059
16%
13
5457
80%
112
2%
199
3%
2
3836
56%
1650
24%
From Wang et al. (2006)

Electricity is converted from the value of fuel inputs to power generation.
6017
2
271
4%
1072
16%
6829
0.03%
Liangshui
County,
Jiangsu
(n=356)
Straw
Total
79
with the average rural household energy use in 1990 of 11 GJ/personyear (Wang &
Feng, 1996; Sinton et al., 2004b).
Wang and Feng (1997a,b, 2001) and Wang et al. (1999, 2002) have reported a large
series of rural energy surveys in eastern China. In a detailed 2003 survey of nearly
700 rural homes in Anhui and Jiangsu in villages where rates of biogas use are very high
(24% and 29%, respectively), Wang et al. (2006) showed that the level of use of
commercial energy remains low (Table 1.12). Including biogas, biofuels accounted for
7580% of average household energy. Observed energy use per capita in these villages
which enjoy the mild climate of the central seaboard provinces was about half the national
average for rural households. Unlike most surveys, this study also provided a breakdown
by end-use which showed that, in these households where no space heating was recorded,
cooking tasks far outweighed all others, even when families used large amounts of fuel
for the preparation of pig feed. Households without biogas digesters used about 70%
more energymainly solid fuelsthan those with biogas digesters, which provides a
basis for estimating the change in exposure resulting from adding gas to the household
fuel mix. Notably, LPG use in households with biogas remained significant. An earlier
study in Liangshui showed a similar result (Wang & Li, 2005).
In a 200304 winter survey of rural areas near Xian, in the northern province of
Shaanxi, Tonooka et al. (2006) found that most of the households used a wide variety of
fuels, but most relied mainly on biomass for cooking and heating (Table 1.13). Only 28%
of the survey sample, located in a small village, depended mainly on coal. The use of
LPG there was also widespread, but was mainly limited to the wealthiest families.
Table 1.13. Stoves and fuels used in rural households near Xi'an, Shaanxi, winter 200304
Main stoves and fuels
Crop residues-kang-traditional
Crop residues-traditional stove
Crop residues-kang-improved
Crop residues-improved stove
Twigs-kang
Twigs-traditional stove
Twigs-kang-improved
Twigs-improved stove
Coal
LPG
Electricity/unknown
Total
From Tonooka et al. (2006)
A kang is a heated brick bed.
Cooking
Space heating
No. of
households
Share
No. of
households
Share
110
9
18
4
2
5
5
0
35
30
0
218
50%
4%
8%
2%
1%
2%
2%
0%
16%
14%
0%
100%
105
5
17
0
4
4
7
0
72
0
4
218
48%
2%
8%
0%
2%
2%
3%
0%
33%
0%
2%
100%
80
A 2002 survey of nearly 35 000 households in Shaanxi, Zhejiang and Hubeia 10%
subsample of which was monitored for indoor air quality (Sinton et al., 2004a,c)
documented the highly diverse fuel and stove use patterns that are typical throughout the
country (Tables 1.14 and 1.15). For instance, in the database of households where indoor
air quality was measured, 28 different fuel combinations were used in kitchens in winter
and 34 different fuel combinations were used in summer (Sinton et al. 2004c). In the
larger sample of the study, the survey results were generally in line with those arising
from national statistics. In some areas, availability of LPG had made improved solid-fuel
stoves obsolete, and some households had advanced from traditional solid-fuel stoves
directly to LPG. In most cases, however, households used both gas and solid fuels for
cooking. Most households in Shaanxi reported that they heated with coal in winter. In
Zhejiang and Hubei, where nearly half of the surveyed households did not heat at all in
winter, a surprisingly large fraction cooked with charcoalwhich is illegal to produce
and sell in many areas.
Table 1.14. Main cooking and heating fuels, rural households in Zhejiang,
Hubei and Shaanxi, China, 2002
Fuel
Zhejiang
Main cooking fuel (number of households)

Wood
807
Crop residues
300
Coal
3
LPG
109
Electricity
11
Biogas
Charcoal
Missing
6
Total
Hubei
65.3%
24.3%
0.2%
8.8%
0.9%
0.5%
1236
Main heating fuel (number of households)

Wood
231
Crop residues
5
Coal
19
Charcoal
347
Electricity
59
LPG and kerosene
5
No space heating/missing
570
Total
1236
490
220
318
69
8
6
1
3
Shaanxi
43.9%
19.7%
28.5%
6.2%
0.7%
0.5%
0.1%
0.3%
1115
18.7%
0.4%
1.5%
28.1%
4.8%
0.4%
46.1%
222
8
66
324
2
2
491
1115
75
276
686
25
7.0%
25.9%
64.4%
2.3%
1
1
1
0.1%
0.1%
0.1%
1065
19.9%
0.7%
5.9%
29.1%
0.2%
0.2%
44.0%
49
205
750
1
24
36
1065
4.6%
19.2%
70.4%
0.1%
2.3%
0.0%
3.4%
From Sinton et al. (2004a)

Wood includes logs, twigs and other woody biomass. Crop residues include other non-woody
biomass and dung.
81
Table 1.15. Types of stove in rural households in Zhejiang, Hubei and

Shaanxi, 2002
Stove type
Flue
Zhejiang
Hubei
No. with
stove type
Fraction of No. with

sample
stove type
Shaanxi
Fraction of No. with
sample
stove type
Fraction of
sample
Traditional
biomass
Yes
235
18.9%
60
5.4%
166
15.6%
No
0.5%
50
4.5%
0.1%
Improved
biomass
Yes
684
55.0%
829
74.3%
212
19.9%
No
0.6%
35
3.1%
0.6%
Coal
Yes
0.2%
141
12.6%
538
50.6%
No
145
11.7%
671
60.2%
275
25.8%
LPG
No
723
58.1%
258
23.1%
173
16.3%
Biogas
No
0.2%
34
3.0%
Open Fire
No
121
10.9%
Other
Yes
90
8.5%
85
8.0%
No
0.3%
0.8%
From Sinton et al. (2004c)

Many households own more than one type of stove, so the numbers of stove types reported are
larger than the household samples (n=3746). Many households also have more than one stove of the
same type. In Shaanxi, other stoves probably include some type of coal stove.
(ii) Stove types, efficiencies and tasks (cooking and heating)

Programmes to promote improved stoves have long been introduced in China (Smith
et al., 1993; Sinton et al., 2004c). As the survey results in Sinton et al. (2004c) described,
the complex fuel situation mirrors diverse patterns of stove ownership. Most households
surveyed, typically had one or more coal and one or more biomass stoves, and commonly
had a gas (LPG or biogas) stove as well. Households with improved biomass stoves
commonly had portable coal stoves without flues. Nearly 12% of the households reported
having four or more stoves. In the overall survey sample, 95% of the biomass stoves had
flues (and 77% were classified as improved); only 38% of the coal stoves were
equipped with flues, although most coal stoves are of relatively recent vintage, often burn
briquettes and often incorporate convenient and energy-efficient features such as water
boilers and small steam/oven chambers.
More than half of the households surveyed used biomass stoves for their main
cooking, and about half as many used coal stoves. Many more households had LPG
82
stoves than used them for their main cooking; many use the stoves only occasionally
because of the cost of LPG and the ready availability of biofuels in many seasons.
Although coal and biomass were commonly used for heating, many households in the
sample (especially in Hubei) also used charcoal for heating. It is sometimes difficult to
distinguish cooking from heating because cookstoves may be started earlier in the day and
left to burn longer in the evening to provide some space heating. Moreover, air pollution
and fuel-use surveys in China show a complicated situation in which several fuels and
stoves are often in use in different parts of the house in different seasons. In addition to
cookstoves and space-heating stoves, for example, the use of kangs, which are bed
platforms heated from underneath by coal or biomass combustion, is common in different
configurations: connected to a cookstove, with a special kang combustion chamber fueled
from outside, or arranged such that a portable coal stove used during the day for heating
and/or cooking is moved under the platform at night. In either case, kangs are connected
to chimneys, but smoke can nevertheless leak into the bedroom. Most surveyed
households71% in Zhejiang, 80% in Hubei and 81% in Shaanxipossessed an
improved stove of some type. These proportions differed somewhat from the official
figures of the Ministry of Agriculture on the wider adoption of improved stoves, but the
latter are still indicative of the current predominance of improved stoves. Many small
portable coal stoves still do not have chimneys, but are often ignited outside so that their
smokiest stage of combustion does not occur indoors. There is also no assurance that the
coal types in use today are the same as those used many decades ago in any particular
area.
Improvements to biomass stoves have tended to focus on combustion efficiency and
the venting of emissions outdoors. However, improved stoves can have higher emissions
of pollutants per unit of delivered energy (Zhang et al., 2000). Improved coal stoves in
China have been shown to increase exposure to pollutants dramatically since many are
unvented (Sinton et al., 2004c).
(iii) Regional and socioeconomic variation
Region is highly correlated with socioeconomic status; per-capita income in eastern
coastal provinces is typically two to three times higher than that in central and western
provinces, for both rural and urban areas (National Bureau of Statistics, 2005). Provincial
and national statistical data show that different patterns of fuel use are associated with
different socioeconomic and geographical conditions (see Section 1.1). In wealthier
provinces, use of electricity and LPG is highest. Where coal resources are richest
generally in the northcoal use is highest. In regions where coal is less readily available
and incomes are low, biomass use is highest. In examining Ministry of Agriculture data
for rural energy use by province, Wang and Feng (2005) found that, while electricity use
was correlated with income, the fraction of total per-capita energy use from biomass was
not correlated with income. The use of biofuels was higher in the Anhui households that
had incomes more than double those of the Jiangsu households (Wang et al., 2006).
83
Recent survey results also showed patterns that suggest that solid fuel use does not
necessarily decline with rising income, although the use of improved energy forms is
positively correlated with income (Sinton et al., 2004c). In all three provinces, ownership
of improved stoves was associated with lower incomes and, in Hubei and Shaanxi, they
were significantly associated with lower levels of education. Fuels followed a similar
pattern; the use of commercial fuels (coal, LPG and electricity) was generally associated
with higher incomes.
(iv) Variations between rural and urban locations
No statistics have been published on biofuel use in urban areas, although a brief
assessment of large coastal cities showed that a certain amount of biofuel continues to be
used. Relatively large amounts of charcoal are used for cooking and winter heating in
some areas according to anecdotal evidence. In terms of the total proportion of urban
household energy use, however, the use of charcoal is probably small.
While studies generally reflect the fact that wealthier rural households use more gas
and electricity than others and usually only the poorest burn solid fuels in pit stoves, there
is a widespread lack of correlation between socioeconomic status and type of solid fuel
used and type of stove (traditional or improved) used in rural areas. Tonooka et al. (2006)
found this in Shaanxi, as did Sinton et al. (2004a,c). Wang and Feng (2003) found that,
despite higher rates of LPG and electricity use, rural households in wealthy areas still
depended on biomass for 50% or more of their energy, and sometimes up to 80%, i.e. to
the same extent as households in poorer areas.
(b)
Pollutant levels and exposures
Since the 1980s, many studies of indoor air quality in China have been published. The
focus in the 1980s and early 1990s was on combustion-related pollutants (Sinton et al.,
1995). Table 1.16 shows the range of values for particulates (TSP and PM10),
benzo[a]pyrene, sulfur dioxide, nitrogen oxide and carbon monoxide. For households that
use solid fuels, average levels were often in excess ofsometimes several times over
levels set for ambient air quality standards.
In recent years, some attention has returned to combustion products as a result of
projects with international participation. Some of these recent studies and a few from the
early 1990s are summarized in Saksena et al. (2003).
The measured range of levels of particulates is quite wide; means start in the tens of
micrograms per cubic metre, but more typically reach into the hundreds of micrograms
per cubic metre, or even well into the thousands, as shown in Table 1.17a sample of the
many monitoring studies carried out. Most monitoring has focused on TSP, although
PM10 is much more common now, and a few studies have examined PM4 and smaller
fractions. Studies of PM10 levels in kitchens during meal preparation indicate that cooks
are exposed daily to levels of 600 g/m3 or even three times that much. A recent study
examined winter levels of PM4 in households in Guizhou and Shaanxi, in areas where
84
coal is contaminated with fluorine, and found that average levels in kitchen and living
areas were from about 200 g/m3 to 2000 g/m3 (He et al., 2005).
Table 1.16. Indoor air pollution in Chinese residences: ranges of pollutant
levels in research articles (198294) (arithmetic means)
Pollutant
Fuel
Urban
(mg/m3)
Rural
(mg/m3)
Standardsa
(Class II, mg/m3)
TSP
Coal
Gas
Biomass
0.212.8
0.150.51
0.0120
0.19
0.172.6
Daily average
Max. at any time
0.3
1
PM10
Coal
Gas
Biomass
0.162.7
0.140.45
0.1226
0.8322
Daily average
Max. at any time
0.15
0.5
CO
Coal
Gas
Biomass
0.5897
0.2236
0.7087
2.4
0.516
Daily average
Max. at any time
SO2
Coal
Gas
Biomass
0.015.8
0.011.3
0.0123
0.020.07
0.019.1
Annual average
Daily average
Max. at any time
0.06
0.15
0.5
NOx
Coal
Gas
Biomass
0.011.8
0.010.88
0.011.7
0.030.05
0.01.32
Daily average
Max. at any time
0.1
0.15
BaP
(ng/m3)
Coal
Gas
Biomass
0.3190
4.793
5.319 000
3.73100
4
10
From Sinton et al. (1995)

BaP, benzo[a]pyrene; CO, carbon monoxide; Max., maximum; NOx, nitrogen oxide; PM, particulate
matter; SO2, sulfur dioxide; TSP, total suspended particles
a
Class II air quality standards are intended to protect human health and apply to residential areas.
Particulate levels are typically lower in summer, sometimes by an order of magnitude,

but this is not the case universally. While differences in indoor pollutant levels between
similar households that use solid fuels and gas fuels are clear, the differences between
solid fuels are not always evident. Studies in Inner Mongolia and Gansu have shown that
dung fuels lead to both higher and lower levels of PM10 than coal in similar households
(Jin et al., 2005). Furthermore, as can be seen in Figure 1.9, coal use in rural areas can
apparently be cleaner than use of biomass. This alone could account for the large
difference in the range of concentrations found between urban and rural households that
Table 1.17. Selected studies with quantitative measurements of particulates in indoor air pollution related to the use of solid
fuel in China
Reference
Household
location
No. of households
Season
Fuel
Stove type
Particulate
type
Meana
(g/m3)
CV
Range
Sampling
location
Sampling Method
duration
Short-term (e.g. cooking)

Baodong,
Sichuan
Province
Raw coal
Pengshui,
Sichuan
Province
Qinjiang,
Sichuan
Province
Zigui,
Sichuan
Province
Rural
Rural
Wushan,
Sichuan
Province
Gao et al.
(1993)
Changsha,
Hunan
Province
Rural
710
0.311.26 Kitchen
Briquette
930
0.482.39
Anthracite
970
0.432.04
Anthracite
1120
0.112.23
5
3
Raw coal
Anthracite
1810
1260
0.614.55
0.223.29
5
4
Summer
Coal
Wood
No flue
PM10
PM10
640
1060
550 (SD)
1050 (SD)
Kitchen
Cooking
Zhao & Long

(1991)
Cooking
(23 day
avg)
85
86
Table 1.17 (contd)

Reference
Household
location
No. of households
Smith et al.
(1994)
Beijing
Urban
58
Season
Fuel
Stove type
Coal
Improved
Particulate
type
PM10
CV
1900
0.6
120
399
Range
Sampling
location
Sampling Method
duration
Meal
Cyclone
Longer-term
Zhang (1988)
Gansu
Province
Rural
4
4
Chang & Zhi

(1990)
Inner
Mongolia
Rural
15
Winter
Cow dung
Coal
TSP
3020
3765
Dung
TSP
PM10
TSP
PM10
TSP
PM10
TSP
PM10
1939
1674
1061
830
1743
500
1559
393
Summer
6
Winter
Coal
Summer
Qin et al.
(1991)
Chengde,
Hebei
Province
Urban
15
Winter
Summer
Coal
Traditional TSP
TSP
665
63
Shenyang,
Liaoning
Province
Urban
15
Winter
Summer
Coal
Traditional TSP
TSP
651
125
Shanghai
Urban
15
Winter
Summer
Coal
Traditional TSP
TSP
384
411
Wuhan
Urban
15
Winter
Summer
Coal
Traditional TSP
TSP
291
112
25583623
18765117
3-day
avg
Daily
average
Breathing 24 h
zone
Cyclone
Meana
(g/m3)
Table 1.17 (contd)

CV
Traditional TSP
41
Coal
Traditional TSP
Coal
Traditional TSP
Household
location
No. of households
Season
Fuel
Stove type
Xu & Wang
(1993)
Haidian,
Beijing
Urban
31
Summer
Coal
Dongcheng,
Beijing
Urban
Summer
Shijingshan,
Beijing
Urban
10
Summer
Venners et al. Anqing,

(2001)
Anhui
Province
Rural
165
Lan et al.
(2002)
Rural
15
Xuanwei,
Yunnan
Province
Summer
Wood
Coal
Particulate
type
PM10
traditional
(n=2);
improved
(n=13)
PM10
Range
Sampling
location
Sampling Method
duration
139
Bedroom
8h
90
110
Bedroom
8h
152
137
Bedroom
8h
248
2080
Data are arithmetic means.

avg, average; CV, coefficient of variation; PM, particulate matter; SD, standard deviation; TSP, total suspended particulates
Kitchen
and
bedroom
1.2 m
Gravimetric
Gravimetric
24 h/day, Gravi5 conse- metric
cutive
days
Meana
(g/m3)
Reference
87
88
Figure 1.9. Concentrations of pollutants measured in households that use solid fuel, China

From Sinton et al. (2004b)
The central line of each box plot indicates the sample median. The tops and bottoms of the boxes represent 75th percentiles, and the top and bottom
horizontal lines represent the 95th percentiles.
B(a)P, benzo[a]pyrene; PM, particulate matter
89
use solid fuels. The former are exposed to much lower levels of PM10, but the levels are
still significantly higher in general than recognized ambient and/or indoor standards.
The impact on indoor air quality of improved stoves is similarly dependent on
particular circumstances. For instance, improved stoves do not always have lower
emissions factors (Zhang & Smith, 1999). Confounding factors such as differences in fuel
combinations, shifting patterns of tasks and fuel use over time and use of multiple stoves
may all influence exposure levels. The three-province survey (Sinton et al., 2004a) found
that, taking smoking into account, in summer when stove use was dominantly for
cooking, households that used coal experienced higher particulate (PM4) levels than those
that used biomass combinations, and traditional stoves emitted higher particulate levels
than improved stoves (Table 1.18). Such differences disappeared during the winter
heating season, however, when many households used unvented stoves; tobacco smoke
was a confounding factor throughout. Even in summer and in households with no
smokers, average PM4 levels were in the range of 180450 g/m3.
The same study (Sinton et al., 2004a) found that, in some cases, kitchens were not the
sites with the highest average particulate levels. Those households that used coal or a
combination of coal and biomass, unlike those that used biomass or a combination of
biomass and gas, had higher particulate levels in living rooms than in kitchens. In living
rooms, heating, smoking and perhaps other factors can result in levels over time that are
higher than those in kitchens, despite the peaks associated with cooking. Among all the
fuel combinations, average winter levels ranged from just under 100 to over 300 g/m3.
A recent survey of indoor air in households that used coal and biomass fuels in four
provinces (Jin et al., 2005) showed that a variety of stove and fuel combinations in
different seasons leads to average PM4 levels in the hundreds of micrograms per cubic
metre (Table 1.19). Differences between rooms with and without stoves were small.
A large number of studies that monitored benzo[a]pyrene were restricted to
households in Xuan Wei County, Yunnan Province, but many others have reported assays
performed elsewhere (Table 1.19). Measured indoor levels of benzo[a]pyrene were in a
range spanning four orders of magnitude, from single digits (1.16 ng/m3) to over
10 000 ng/m3 in some of the studies in Xuan Wei County, in which bituminous coal led to
much higher indoor levels than anthracite. In studies performed in other parts of the
country, household averages rarely exceeded 40 ng/m3. The relative preponderance in the
literature of the Xuan Wei County studies may account in part for the difference observed
in a comparison of the results of monitoring studies in urban and rural households that
used solid fuels (Figure 1.9).
The combustion of wood fuels (using traditional stoves) emits levels of
benzo[a]pyrene that fall within the range found in households that use coal (in improved
stoves), and, in fact, have an upper range that far exceeds that found in the studies of coal.
In the households in Xuan Wei County that used wood fuels (using traditional stoves),
levels were often much higher than those in households that used coal (in improved
stoves) in other parts of the country, which highlights the role played by stove type.
90
Table 1.18. Indoor air pollution levels in rural households in Hubei and Shaanxi, summer 2002
Room
Fuel
Smoking
Living room
Wood twigs, agricultural

residues, coal
Yes
No
Yes
No
Coal products
Yes
No
Kruskal Wallis test
HOBO CO
(mean ppm)
CO Dosimeter
tube (ppm)
15
316
8
235
130
341
58
222
79
301
51
284
0.36
5
1
2
0
13
17
4
1
15
11
8
17
0.09
5
38
2
23
14
130
6
20
16
85
8
73
0.00
Agricultural residues, coal
N
Mean
N
Mean
N
Mean
N
Mean
N
Mean
N
Mean
Asymp. Sig.
PM4
(/m3)
Table 1.18 (contd)

Fuel
Smoking
Kitchen
Wood twigs, agricultural

residues, coal
Yes
No
Agricultural residues, coal
Yes
No
Coal products
Yes
No
Kruskal Wallis test
N
Mean
N
Mean
N
Mean
N
Mean
N
Mean
N
Mean
Asymp. sig.
From Sinton et al. (2004a)

Asymp. sig., asymptote significance; co, carbon monoxide; N, number; PM, particulate matter
N.B. Most households that use agricultural residues and wood also used some coal.
PM4
(/m3)
HOBO CO
(mean ppm)
CO Dosimeter
tube (ppm)
15
478
8
191
37
418
16
188
29
263
15
451
0.29
4
4
1
0
5
11
1
3
3
8
2
35
0.06
5
38
2
23
6
147
2
25
4
125
2
125
0.00
Room
91
92
Table 1.19. Concentrations of PM4 in rural households in four provinces in

China, 2003
Province
Primary
cooking
fuel
Primary
heating
fuel
Indoor location
Gansu
Biomass
Biomass Kitchen
with
some
Living/bedroom
coal
March
December
March
December
96
33
96
33
518
661
351
457
364671
467855
205500
280634
Inner
Mongolia
Biomass
Coal
Single room (pt 1)
and
Single room (pt 2)
biomass
December
61
61
718
719
538898
480958
Guizhou
Coal
Coal
March
December
March
December
96
32
96
32
352
301
315
202
224480
178425
186443
159245
March
December
March
December
March
December
100
36
25
29
98
24
187
223
215
329
186
361
143230
164282
136293
261397
132241
266355
Kitchen
Living/bedroom
Shaanxi
Biomass
and coal
Coal
Kitchen
Living room
Bedroom
Month
No. of
Mean
observations (g/m3)
95% CI
From Jin et al. (2005)

CI, confidence interval
Some timeallocation (timeactivity) survey data have been published but they do not
provide information regarding indoor environments (e.g. Ohtsuka et al., 1998; Jiang et al.,
2006). A few studies of exposures to pollution and health impacts include the gathering of
timeallocation information (Table 1.20). Pan et al. (2001), for instance, monitored
indoor air quality in several locations from rural residents in Anqing, Anhui Province, and
found that exposure to PM10 was dominated by the time spent indoors where levels were
up to twice as high as those outdoors (Table 1.21).
1.3.3
South Asia
South Asia has nearly 1.5 billion inhabitants, who account for approximately a quarter
of the worlds population. Since nearly 70% of the population of this region lives in rural
areas (WHO, 2005a) and approximately 74% relies on solid fuels for household energy
requirements (Rehfuess et al., 2006), the region accounts for a major fraction of global
exposure to indoor air pollution from smoke that is attributable to combustion of solid
fuels. Recent estimates of disease burdens calculated by WHO indicate that nearly 4% of
the disease burden in the region may be attributable to consequent exposures, and women
and children under the age of 5 years bear the largest share of this burden (WHO, 2002,
Table 1.20. Selected studies with quantitative measurements of benzo[a]pyrene in indoor air pollution related to the use of
solid fuel in China
Reference
Household
location
No. of
households
Fuel
Stove type
1977
Bituminous
coal
Anthracite
Kang
Kang
Meana
(ng/m3)
CV
Range
Sampling
location
Sampling
duration
Method
453.2
18.35992.4
Meal
Fluorescence
preparation spectrometry
69.1
17.7191.7
Living
room
Living
room
Short-term (e.g. cooking)

Yunnan
Province
Health
Station
(1984)
Xuanwei,
Yunnan
Province
Rural
Yang et al.
(1988)
Xuanwei,
Yunnan
Province
Rural
6
6
1
1
Wood
Bituminous
coal
1
1
1
67.5
399.1
2h
Fluorescence
spectrometry
295.5
8.5
25.5
Anthracite
Longer-term
Guo & Tang
(1985)
Mumford et
al. (1987)
Nanning,
Guangxi
Province
Xuanwei,
Yunnan
Province
Urban
Autumn
Coal
briquette
1.2
2
3
Rural
8
4
4
1
Kitchen
2-day
averages
1.5 m
12 h
Season
4.1
1.4
Autumn
Autumn
Coal
Wood
Bituminous
coal
Anthracite
Improved
13.4
3100
14 700
421
GC/MS
0.323
0.204
600
93
94
Table 1.20 (contd)

Reference
Household
location
Wang et al.
(1989)
Harbin,
Urban 13
Heilongjiang
4
Province
4
Winter
Coal
34.0
43.1
23.4
Du & Ou
(1990)
Guangzhou,
Guangdong
Province
Urban 20
4-season
average
Coal
13
He et al.
(1991)
Xuanwei,
Yunnan
Province
Rural
Coal/wood/
Traditional
smokeless
coal different
composition
%
76.1
Xian et al.
(1992)
Xuanwei,
Yunnan
Province
Rural
Guo et al.
(1994)
Taiyuan,
Shanxi
Province
Urban
Zhejiang
Province
Urban
Wood
Bituminous
coal
8
Briquette
7.9
Briquette
10.9
Briquette
7.3
Coal
Improved
Winter
25
110
Summer
10
CV
Range
Sampling
location
Sampling
duration
Method
10.659.8
26.751.1
10.639.9
Bedroom
3-day
averages
Fluorescence
spectrophoto
metry
12 h/day
for 3
consecutive days
Fluorescence
spectrophoto
metry
24 h TWA
Personal
monitoring
0.754
6.375
69180
Apartment 3-day
bedroom averages
Apartment
kitchen
Singlestorey
dwelling
217
1.5 m
12 h
HPLC
Fuel
27
Stove type
Meana
(ng/m3)
Season
Liu et al.
(2001)
No. of
households
Table 1.20 (contd)

Household
location
Lan et al.
(2002)
Xuanwei,
Yunnan
Province
No. of
households
Rural
15
Season
Fuel
Stove type
Meana
(ng/m3)
Coal
Traditional
(2);
improved
(13)
1660
CV
Range
Sampling
location
Sampling
duration
Method
1.2 m
24 h for
5 consecutive days
HPLC
CV, coefficient of variation; GC/MS, gas chromatography/mass spectrometry; HPLC, high-pressure liquid chromatography; L, living room; TWA, time-weighted
average
a
Data are arithmetic means
Reference
95
96
Table 1.21. Indoor air pollution in levels, time budgets and exposures in rural
residences, Anqing, Anhui, China
Indoor pollutant levels (geometric meansSD)
Location
Sample size
PM10 (g/m3)
SO2 (g/m3)
CO (mg/m3)
Kitchen
373
51827
12.436
2.09.9
Bedroom
504
3409
10.918
1.66.0
Living room
366
2879
11.019
1.64.5
55
27010
10.818
2.04.5
Outdoor (among crops)
Time allocation (arithmetic meansSD)

Location
Male (n=245)
Female (n=222)
Kitchen
1.362.15
3.782.48
Bedroom
9.594.09
10.563.59
Living room
2.442.51
2.692.16
Outdoor (among crops)
0.842.66
0.621.49
Other
8.876.12
5.076.06
Personal average daily exposures

Pollutant
Sex
Sample size
Geometric
meansSD
PM10 (g/m3)
Male
Female
201
175
556535
659646
SO2 (g/m3)
Male
Female
194
170
2367
2570
CO (mg/m3)
Male
Female
193
169
2.251.6
2.52.4
From Pan et al. (2001)

CO, carbon monoxide; PM, particulate matter; SD, standard deviation; SO2, sulfur dioxide
2005b). Nearly all countries in the region are classified as belonging to medium or low
human development categories (UNDP, 2001) and the profile of several determinants of
indoor air pollution that result from cooking and heating is similar within countries of the
region.
Given the heterogeneous, decentralized nature of exposures across multiple
geographical zones and the limitations of financial and technical capacity, few large-scale
quantitative assessments have been possible in this region. Exposure assessments have
involved multiple levels of accuracy and resolution and representative exposures are
therefore difficult to describe. Nevertheless, an attempt has been made to describe the
levels of indoor air pollution in relation to specific determinants that operate at the
97
household (microenvironmental), socioeconomic and geographical (macroenvironmental)

levels.
(a)
Exposure data
Since they are currently outside the regulatory purview in most countries of the
region, methods for the measurement of indoor air pollution have followed considerations
of research as opposed to uniform protocols in adherence to national or international
standards. Field logistics, contributions from multiple determinants and resource
limitations have further contributed to additional challenges in making such
measurements. Exposure assessments/estimations have thus been made on different
scales with various levels of accuracy and resolution, in large part by individual research
groups. As described earlier (Figure 1.9), the methods used in the region have ranged
from fuel surveys to quantitative assessments of one or more pollutants under multiple
exposure configurations. A few studies have also developed models to estimate exposure
potentials. Accordingly, the results of exposure studies in the region are described below,
by broadly classifying them as qualitative or quantitative assessments.
(i)
Qualitative studies of exposure
Methods that rely on categorical qualitative variables collected from large populations
can be expected to be less accurate and representative than those based on direct
measurements of household or individual levels. However, as described below, every
single quantitative measurement in this region unequivocally points to overwhelming
pollution loads in homes that use solid fuel, which are often an order of magnitude higher
than those in homes that do not use such fuels and several fold higher than commonly
available exposure guidelines for specific pollutants. This has allowed reported solid fuel
use to be used quite reliably as a proxy for exposure in many epidemiological studies.
Furthermore, the inclusion of information on the use of fuel in routinely administered
population-based surveys, including national census surveys in many countries of this
region, has allowed the generation of regional, national and sub-national estimates for
percentages of total population at risk of such exposures to indoor air pollution. Exposure
estimates recently generated by WHO (2002) for the purposes of assessing attributable
(region-specific/global) disease burdens are an example of such an exercise. Results from
selected recent studies that provided estimates of country levels are summarized in Table
1.22.
Information on several determinants (described in the previous section) other than the
use of fuel has been collected in some national and many regional surveys. Many of these
determinants are not independently associated with exposures to indoor air pollution and
their contributions may be significant, but remain secondary to the type of fuel used.
Many of these have, however, been found to be useful for extrapolation in models in
which either data on fuel use have not been available (e.g. using data on income,
education, energy market structures) or for further stratification of exposures on the basis
98
Table 1.22. Studies that reported percentages of solid fuel use in countries of South Asia as an indicator of the
fraction of the population exposed
References
India
Pakistan Thailand
Nepal
Sri
Lanka
Bangladesh Malaysia
Viet Nam Indonesia
81
76
72
97
89
96
29
98
63
Rehfuess et al. (2006)b
74
72
72
80
67
88
<5
70
72
Smith (2000)
81
460 million people (~52% of the 1991 population) were estimated to be at risk of full exposure and nearly
252 million (~30% of the 1991 population) at risk of partial exposure in India
Wickramsinghe (2005)d
Choudhari & Pfaff (2003);
SCEA report (2006)e
68
83
67
15 million people (~83% of total and nearly 100% of the rural

population in 1991) relied on solid fuels in Sri Lanka.
86% of rural and 32% of urban households used solid fuels with a weighted average of 67% in
Pakistan. The latter reference cites an 80% overall prevalence of solid fuel use based on routine
data from a subset of 4800 households.
Global household fuel use database compiled using data from the national census, US Bureau of Census and UN Statistics Division wherever
available and modelled (shown in bold) using demographic variables for other countries (as described in Mehta & Smith, 2002, Smith et al., 2004)
using 1991 as the base year for census data.
b
Global household fuel use database compiled using data from Demographic Health Survey (DHS, 2004), The World Health Survey (WHS, 2005)
and The World Bank Living Standards Measurements Study (LSMS, World Bank 2006), wherever available and modelled using demographic
variables, for other countries (as described in Mehta & Smith, 2002; Smith et al., 2004).
c
Indian National Census data (1991) and data from The National Family Health Survey (1992), a population weighted national sample survey, was
used to the extract information on household fuel use and related demographic variables.
d
Data cited in a report compiled from the Food and Agricultural Organization (FAO) initiatives on Community Forestry and Regional Wood
Energy Development Programme; no additional details are available.
e
Data from Pakistan National Census Survey (1998) and The Pakistan Integrated Household Survey (PIHS, 1991) a national survey implemented
jointly by the Federal Bureau of Statistics, Government of Pakistan and World Bank (as a part of the World Bank LSMS survey) was used to
extract data on fuel use and related demographic variables. Census estimates were considerably lower than PIHS estimates.
Mehta & Smith (2002);

Desai et al. (2004); Smith
et al. (2004)a
Korea
99
of other quantitative studies (e.g. using data on stove type, ventilation, kitchen location,
age, gender). Results from a selection of such studies are provided in Table 1.23.
Table 1.23. Studies that reported household survey/modelled data for potential
exposures related to the use of solid fuel in South Asia
Country
Description of study results
Reference
Bangladesh
Quantitative measurement (of PM10) results and

Dasgupta et al. (2004a,b)
determinant information from a stratified sample of
236 homes were extrapolated using regression models
to predict air pollution levels in six regions within
Bangladesh. Predicted levels in poorest, least educated
households were found to be twice as high as those in
the richest and most educated with significant
geographical variations reflecting differences in
distribution of fuel use and house construction
materials. Exposures for young children and poorly
educated women were found to be fourfold higher
than those for men in higher income households with
educated women (range of 24-h average levels
measured, ~133638 g/m3 PM10)
India
Systematic laboratory measurements of particulates

Smith et al. (2000)
and greenhouse gas emissions from 26 fuel/stove
combinations used in conjunction with a rural fuel use
database and information on stove use from the
relevant Government Ministry to generate state-level
information on biofuel use, stove use, extent of
improved stoves and emissions from solid fuel use.
The emissions inventory shows major contributions to
greenhouse gas and health-damaging pollutants from
biomass-burning stoves. (Although several
determinants intervene between emission and
exposure, total emissions are largely driven by fuel
type similar to concentrations and exposures across
states making secondary data on total emissions a
useful proxy for population exposure).
India
Quantitative measurement (of respirable particulate

matter) results from a stratified sample of
420 households and determinant information from
1032 households identified fuel type, kitchen
configuration, ventilation, age and gender to be the
most important determinants of exposures in three
districts of the southern state of Andhra Pradesh.
Evaluation of the national improved stove programme
across six states found little evidence of sustained use
and maintenance following distribution. Reported
stove use currently remains a poor proxy for potential
exposure reductions (range of 24-h average levels
measured, ~73732 g/m3 PM4).
World Bank (2002a,

2004a)
100
Table 1.23. (contd)

Country
Description of study results
Reference
India
Quantitative data from ESMAP study above used to

generate district level concentration and exposure
profiles based on distribution of fuel use, kitchen
configuration, age and sex distribution for the state of
Andhra Pradesh. District level distributions largely
driven by differences in fuel use. Differences were
relatively modest compared with the high average
exposures estimated for each district (range of
modelled 24-h weighted average estimates for the
district, ~350450 g/m3 PM4).
Balakrishnan et al. (2004)
India
Information on quantities of biofuel used compiled

Habib et al. (2004)
from food consumption statistics and specific energy
requirements for food cooking for all major states and
regions of India. Total biofuel consumption was
estimated (with significantly lower uncertainties than
that previously estimated using energy surveys) at
379 Tg/year with a national average biofuel mix of
74:16:10 for fuel-wood, dung and crop residues
respectively. North and eastern regions of the country
show higher biofuel consumption together with high
per-capita food consumption and higher prevalence of
dung and crop residue use. (Since consumption is
linked to emissions and emissions to exposures, this
represents a new measure to judge exposure potential
related to cooking with biomass).
Sri Lanka
Questionnaire survey of 1720 households from three

villages in Sri Lanka used to prepare a profile of
gender and poverty dimensions of energy access.
Approximately 96% of surveyed households used
biomass with 42% using some form of improved
stoves and 67% of all stoves having chimneys. About
79% had attached kitchens and ~20% had kitchens
well separated from the main house.
Wickramsinghe (2005)
(ii) Quantitative studies of exposure

While domestic combustion of solid fuel generates a mixture of pollutants, because of
limited technical feasibilities and difficult field logistics, most studies in the region have
restricted themselves to cross-sectional measurements of single pollutants (most often PM
and/or carbon monoxide). However, a few large-scale studies (that mostly measured
fractions of PM) carried out in India, Nepal and Bangladesh across multiple exposure
configurations have provided considerable understanding of spatial, temporal and other
determinants of population exposure related to solid fuel use in the region. A few have
101
also assessed levels of other gaseous pollutants including sulfur dioxide, nitrogen dioxide
and select air toxics including PAHs and formaldehyde. Limited evidence is currently
available to indicate (i) whether PM and carbon monoxide are representative indicator
pollutants, (ii) whether the two are themselves consistently correlated under a wide range
of exposure circumstances and (iii) how levels and proportions of other toxic constituents
may vary with alternative distributions of determinants (most importantly with fuel type).
The following sections describe selected studies conducted within the region that
measured levels of indoor air pollution to illustrate the scale and extent of exposures
associated with the use of solid fuels for cooking and heating indoors. Several smaller
studies have also been conducted, and, while an exhaustive listing of all studies conducted
could not be compiled, Table 1.24 lists the major studies available in the published
literature as well as in reports of projects available in the public domain. The global
database of indoor air pollution studies maintained by the Department of Environmental
Health Sciences, University of California Berkeley, USA (Saksena et al., 2003; WHO,
2005a), the bibliography of indoor air pollution studies maintained by The Energy
Research Institute, New Delhi, India, and independent articles retrieved through internet
search engines served as the basis for this compilation.
(iii) Measurement studies in India
Quantitative measurement studies have been conducted in India since the early 1980s.
Many of the earlier studies only measured TSP matter during short cooking periods. One
of the earliest large-scale studies of exposure assessment was conducted in the households
of Garhwal, Himalayas (Saksena et al., 1992), and involved nearly 122 households in
three villages across three seasons. Daily integrated exposure to TSP matter and carbon
monoxide was assessed by personal and stationary sampling of air in six
microenvironments. Concentrations of pollutants measured at the time of cooking were
found to be very high (5.6 mg/m3 and 21 ppm for TSP matter and carbon monoxide,
respectively) but comparable with those measured in the Indian plains. The mean
concentration in the kitchen while cooking often exceeded the concentration in other
microenvironments, including the living rooms, and outdoors by an order of magnitude or
more. Combining area measurements with individual timeactivity records, the daily
exposure of adult women to TSP matter and carbon monoxide was estimated to be
37 mgh/m3 and 110 gh/m3, respectively.
More recently, two large-scale exposure assessment exercises for respirable
particulates have been completed in India in the southern states of Tamil Nadu and
Andhra Pradesh, respectively. In Tamil Nadu (Balakrishnan et al., 2002), a total of
436 rural households across four districts were monitored for respirable particulates
(median aerodynamic diameter, 4 m). Concentrations were determined during several
cooking and non-cooking sessions in households and 24-h exposures were calculated on
the basis of these concentrations in conjunction with timeactivity records of household
members. Concentrations of respirable particulate matter ranged from 500 to 2000 g/m3
during cooking in households that used biomass (geometric mean [GM], 10431346 g/m3)
102
Table 1.24. Major studies with quantitative measurement results for indoor air pollution related to the use of solid fuel in
South Asia
Reference,
location
Fuel
Stove type
Pollutant
Locationa
Sampling
durationb
Method
Range of levels
reported (g/m3)c
5 urban homes
Wood
Traditional
TSP
PAH
(BaP)
Kitchen (1.5 m)
0.25 h (C)
Gravimetric
TLC
7203
1270 (ng/m3)
4 urban homes
Dung
Traditional
TSP
PAH
(BaP)
Kitchen (1.5 m)
0.25 h (C)
Gravimetric
TLC
15 966
8248 (ng/m3)
3 urban homes
Charcoal
Traditional
TSP
PAH
(BaP)
Kitchen (1.5 m)
0.25 h (C)
Gravimetric
TLC
26 147
4207 (ng/m3)
Wood
Traditional
TSP
BaP
Kitchen
(breathing zone)
Meal
duration
Gravimetric
TLC
6400
4100 (ng/m3)
Improved
TSP
BaP
Gravimetric
TLC
4600
2400 (ng/m3)
No. of
households
Season
Short-term exposure (<8 h)
Smith et al.
(1983), India
28 rural homes
Winter
8 rural homes
Davidson
et al. (1986),
Nepal
18 rural homes
Winter
Wood
Traditional
TSP
PM10
Kitchen
Kitchen
12 h (C)
12 h (C)
Gravimetric
Gravimetric
880 (GM)
4700 (GM)
Reid et al.
(1986), Nepal
60 rural homes
Autumn
Wood
Traditional
Improved
TSP
TSP
Personal
exposures
12 h (C)
12 h (C)
Gravimetric
Gravimetric
17503170
8701370
Pandey et al.
(1990), Nepal
cited in GDB
20 rural homes
at 1500 m
Summer
Wood/crop
residue
Traditional
PM2.5
Personal
exposures
1 h (C)
Gravimetric
8200
Improved
PM2.5
Personal
exposures
1 h (C)
Gravimetric
3000
Aggarwal
et al. (1982),
India
cited in GDB
Table 1.24 (contd)

Reference,
location
No. of
households
Season
Saksena et al.
(1992), India
12 rural
Winter/
homes/6 micro- summer
environments
Fuel
Stove type
Pollutant
Locationa
Sampling
durationb
Method
Range of levels
reported (g/m3)c
Wood
Traditional
TSP
CO
Personal
exposures
Meal
duration
Gravimetric
TLC
Electrochemical
sensors
5600
21
Dung/wood/
charcoal
Traditional
TSP
BaP
Kitchen
(breathing zone)
Meal
duration
Gravimetric
TLC/HPLC
11903470
38410 (ng/m3)
Smith et al.
(1994), India
61 urban
homes
Wood/crop
residue
Traditional
PM10
Personal
exposures
Meal
duration
Gravimetric
9001100
Smith et al.
(1994),
Bangkok
17 urban
homes
Charcoal
PM10
Personal
exposures
Meal
duration
Gravimetric
550
TERI (1995),
India
cited in GDB
20 homes with
1820 measurements in
each home
Wood
Traditional
PM5
Kitchen
(breathing zone)
Meal
duration
Gravimetric
8501460
Mandal et al.
(1996), India
cited in GDB
12 urban
homes
Wood
Traditional
TSP
Kitchen
(breathing zone)
4 h (C)
Gravimetric
646
Ellegard
(1997), Viet
Nam
cited in GDB
35 urban
homes
Wood
PM10
Kitchen
(breathing zone)
Meal
duration
Gravimetric
770
Raiyani et al. 20 urban

(1993a), India homes in each
fuel category
103
104
Table 1.24 (contd)

Fuel
Stove type
Pollutant
Locationa
Sampling
durationb
Method
Range of levels
reported (g/m3)c
436 rural
Summer
homes from
4 districts
stratified across
four kitchen
types
Wood/wood
chips/crop
residues
Traditional
PM4
Personal
exposures
Living
12 h (C)
Gravimetric
13071535 (GM)
(wood fuel)
Saksena et al.
(2003)
40 urban
homes
Wood
Traditional
PM5
Kitchen
(breathing zone)
Meal
duration
Gravimetric
1200
Bhargava
et al. (2004),
India
10 rural homes
Wood
Dung
Traditional
BaP
Kitchen (1.5 m)
(C)
1h
HPLC
7001700 ng/m3
9801860 ng/m3
Wood
Traditional
TSP
Kitchen
24 h
Gravimetric
8420
Wood
Traditional
TSP
Kitchen
8h
Gravimetric
6400
Improved
TSP
Kitchen
8h
Gravimetric
4600
Traditional
PM4
Personal
exposures
24 h
Gravimetric
172226
Reference,
location
No. of
households
Balakrishnan
et al. (2002),
India
Season
8471327
(wood fuel)
Long-term exposure (824 h)

Hessen et al.
(1996), Nepal
34 rural homes
Yadav et al.
(1996), Nepal
cited in GDB
39 rural homes
at 2500 m
Balakrishnan
et al. (2002),
India
Summer
436 rural
homes from
4 districts
stratified across
four kitchen
types
Winter
Wood/wood
chips/crop
residues
Summer/
winter
24 h (C)
Table 1.24 (contd)

Stove type
Pollutant
Locationa
Sampling
durationb
Method
Range of levels
reported (g/m3)c
412 rural
Summer
homes from
3 districts
stratified across
four kitchen
types
Wood/dung/
crop residues
Traditional
PM4
Personal
exposures
Kitchen
Living
2224 h
Gravimetric and
direct read out
431467
236 rural
homes
Wood, dung,
crop residues
Personal
exposures
Kitchen/living
2224 h
No. of
households
Balakrishnan
et al. (2004),
India
Dasgupta
et al.
(2004a,b),
Bangladesh
Season
Summer
Traditional
PM10
297666
215357
Gravimetric and
direct read out
196264
601165
BaP, benzo[a]pyrene; CO, carbon monoxide; GM, geometric mean; HPLC, high-pressure liquid chromatography; PAH, polycyclic aromatic hydrocarbons; PM2.5,
particulate matter <2.5 m; PM4, particulate matter of 4 m; PM5, particulate matter of 5 m; PM10, particulate matter <10 m; TLC, thin-layer chromatography;
TSP, total suspended particulate matter
a
Personal exposures usually refer to exposures of cooks.
b
C denotes sampling during cooking. Meal duration refers to the sampling duration that covers the cooking period and typically ranges from 1 to 2 h.
c
Most studies report arithmetic means unless otherwise specified. Distributions of levels have been found to be skewed in many studies but few report geometric
means.
Fuel
Reference,
location
105
106
and average 24-h exposures ranged from 9021 g/m3 for those not involved in cooking
to 231109 g/m3 for those who cooked; 24-h exposures were around 8239 g/m3 in
households that used clean fuels (with similar exposures across household subgroups).
The study in Andhra Pradesh (World Bank, 2002b; Balakrishnan et al., 2004)
quantified daily average concentrations of respirable particulates (median aerodynamic
diameter, 4 m) in 412 rural homes from three of its districts and recorded timeactivity
data from 1400 household members. Mean 24-h average concentrations ranged from
73 to 732 g/m3 (GM, 61470 g/m3) in households that used gas versus solid fuel,
respectively. Concentrations were significantly correlated with fuel/kitchen type and
quantity of fuel. Mean 24-h average exposures ranged from 80 g/m3 to 573 g/m3
among users of solid fuel. Mean 24-h average exposures were the highest for women
cooks (GM, 317 g/m3) and were significantly different from those for men (GM,
170 g/m3) and children (GM, 184 g/m3). Among women, exposures were highest
between the ages of 15 and 40 years (most likely to be involved in cooking or helping to
cook), while among men, exposures were highest between the ages of 65 and 80 years
(most likely to be indoors). The exposures were also characterized by dramatic temporal
differences between cooking and non-cooking periods. Large peaks in concentrations
during cooking accounted for most of the exposure potentials. Fuel type, type and
location of the kitchen and the time spent near the kitchen while cooking were thus the
most important determinants of exposure across these households in southern India
among the other parameters examined that included stove type, cooking duration and
smoke from neighbourhood cooking.
A few measurements of particulate size fractions have also been made in households
that use biomass and coal (Aggarwal et al., 1982; Raiyani et al., 1993a). In these studies,
which were carried out in households of peri-urban Gujarat (in western India) and
measured TSPs (using a cascade impactor) during cooking, the proportion of particles less
than 9 m in aerodynamic diameter was estimated to be 96% (dung), 86% (wood) and
92% (coal). Dung use also gave the highest proportion of particles less than 2 m in
aerodynamic diameter (80%), followed by coal (70%) and wood (47%).
Finally, a few studies have measured emissions, area concentrations and size
distributions of volatile and semi-volatile particle-bound PAHs released during solid fuel
combustion. Personal exposure concentrations of benzo[a]pyrene measured over 1530min average sampling periods (in 15 urban households in western India) during wood and
dung-cake combustion ranged from 1.30 to 9.30 g/m3 (Aggarwal et al., 1982). In
another study in northern India (Bhargava et al., 2004), personal exposure and area
measurements for PAHs were made during the cooking period in 20 households over two
seasons. Concentrations of total PAHs in the respirable particulate fraction ranged from
4.5 to 33.5 g/m3. Personal exposure concentrations for cooks who used biofuels were
significantly higher than corresponding area concentrations. Personal exposure
concentrations during cooking were nearly an order of magnitude higher than those
during other periods. Both concentrations were also higher in winter than in summer.
107
Area concentrations of 16 particulate PAHs measured over a cooking period of 45

60 min (five for each category of fuel; in households from a peri-urban cluster in western
India) were 2.01, 3.46 and 3.56 g/m3, respectively, from wood, wood/dung-cake and
dung-cake combustion (Raiyani et al., 1993b). Particulate PAH size distributions
measured in these same indoor environments showed that houses that used cattle dung,
wood and coal had 96%, 80% and 76% of the PAH mass, respectively, contained in
particulates of ~ <2 m aerodynamic diameter (Raiyani et al., 1993a). There was a
predominance of benzo[a]pyrene (20%) and dibenz[a,h]anthracene (25%) and of
chrysene (10%) and benzo[a]pyrene (13%), respectively, in particles from wood and
dung-cake combustion. Laboratory emission studies for PAHs (Venkataraman et al.,
2002) that used wood, dung cakes and biofuel briquettes in traditional and improved
stoves have shown that dung-cake and briquette fuels are significantly more polluting
than wood in terms of total emissions. The PAH profiles showed a predominance of
fluoranthene, pyrene and benz[a]anthracene from all biofuels. The PAH size distributions
from all stovefuel systems were unimodal with mass median aerodynamic diameters in
the 0.401.01 m range for both semivolatile and nonvolatile PAHs.
(iv) Measurement studies in Nepal
While most studies within the region have been conducted in India and give a
reasonably representative picture of pollution levels experienced in the area, a few studies
conducted in Nepal illustrate the exposure situation in cold, hilly regions where solid fuels
are used for cooking as well as heating. Ecological and climatic conditions play a central
role in fuel choices and quantities, with associated implications for exposure. Earlier
studies conducted in the 1980s (Davidson et al., 1986) reported stove use for cooking and
heating in Nepali households to average 11.6 h per day, with additional use of a fireplace
or nearly all-day operation of stoves for heating in many instances (in comparison, the
average duration of stove use in the region without heating needs is estimated at 2.9 h per
day). Correspondingly, fuel quantities used and time spent for fuel collection were higher
(8.2 kg per day at high elevations and 2.8 kg per day in the lower elevations for 7.7 h per
day, compared with an average of 1.9 kg per day for 0.5 h per day in Indian households at
lower elevations during the same period). Levels of TSPs were in the range of 3
42 mg/m3, with respirable suspended particles in the range 114 mg/m3 in the houses
sampled. Concentrations of potassium and methyl chloride (indicators for biomass
sources) in outdoor air indicated significant contributions from indoor sources to outdoor
air pollution in the area as well.
More recently, results from measurements of TSP matter, PM2.5 and carbon monoxide
have been reported (Reid et al., 1986; Pandey et al., 1990) in homes that used solid fuels
in traditional and improved stoves. Use of improved stoves resulted in a two- to threefold
reduction in cooking period concentrations of total TSP matter, PM2.5 and carbon
monoxide. Values for TSP matter in traditional stoves ranged from 1750 to 3170 g/m3
compared with 870 to 1370 g/m3 for improved stoves; mean values for PM2.5 were
8200 g/m3 compared with 3000 g/m3 for improved stoves; and mean values for carbon
108
monoxide ranged from 64 to 310 g/m3 compared with 41 to 80 g/m3 for improved
stoves. This finding is similar to that reported in other regions with improved stoves (e.g.
in Guatemala, Kenya), where, despite being substantially lowered, the concentrations
remain considerably higher than levels in households that used gaseous fuels as well as
common health-based guideline values.
(v) Measurements in Bangladesh
Until recently, few measurement results had been reported from Bangladesh. A recent
study conducted by the World Bank (Dasgupta et al., 2004a,b) now provides a substantial
amount of information on the levels and distribution of pollutants across a very large
number of exposure configurations. Using methods similar in nature to recent large-scale
assessments in southern India, a stratified sample of 236 households was monitored using
direct read-out and traditional gravimetric methods for particulates for periods of 2224 h.
Households were stratified on the basis of fuel, kitchen location and housing materials.
Across households, 24-h average PM10 concentrations varied from 84 to 1165 g/m3 for
firewood, 60 to 755 g/m3 for dung and 72 to 727 g/m3 for jute. Many houses reported
fairly low levels during parts of the night and afternoon, when indoor readings resembled
ambient readings. However, differences in cooking practices, structural arrangements and
ventilation made a significant impact on overall concentrations. While most houses that
used biomass reported high PM10 levels, a few were similar to households that used
cleaner fuels such as LPG or natural gas, which suggests that ventilation is an important
factor in reducing pollution levels. Improved stove use was found to be minimal which is
similar to the situation found in the Indian studies. Exposure reconstructions using time
activity records in conjunction with area measurements confirmed observations from
other studies of the region. Women in all age groups and children under the age of 5 years
of both sexes in homes that used biomass faced the highest exposures compared with men
in the working age group (24-h exposure concentrations of PM10 for women ranged from
209 to 264 g/m3 and for children from 156 to 209 g/m3 compared with 118 g/m3 for
men in the age group of 2060 years). Time spent outdoors was a major contributor to
reduced exposures, as reflected by much lower exposures for adult men who spend a
considerable fraction of the day outdoors. The study developed regression models that
used the measurement results in conjunction with survey information on household level
determinants and socioeconomic variables to create a basis for extrapolation to six regions
within the country. Significant geographical differences were found, based: directlyon
differential distribution of determinants including fuel choice, household ventilation and
materials used for construction; and indirectlyon income, education and demographic
variables through their effects on choice of fuel and prevalent household conditions.
(b)
Conclusions and recommendations for further research
Exposure to indoor air pollutants associated with the combustion of solid fuels for
cooking and heating is extensive in South Asia. Multiple determinants affect individual
109
exposures but it is clear that all users of solid fuel experience very high air pollution
leading to exposure to a mixture of pollutants for extended periods during their lifetime.
Exposures are widespread and prevalent in half to three-quarters of the population in
most countries of the region. Although evidence of extreme exposures has been available
in the published literature for the last three decades, only recently have countries in the
region undertaken efforts to collect information systematically on the extent of solid fuel
use and estimated exposures. Despite limitations of being outside regulatory purviews and
hence not being within a framework for consistent and routine data collection, the region
has a robust series of research studies to document evidence of exposures. While
quantitative assessments have been performed in many countries, a great majority focused
on a few pollutants (such as PM and carbon monoxide) and showed limited evidence of
their correlation to other toxic emissions; it would therefore be important for future
research studies to undertake measurements of multiple pollutants. Additional
measurements of carcinogenic compounds in biomass smoke are especially needed as
very little is currently available in the region. Models that validate the choice of indicator
pollutants and monitoring schemes that adequately describe the temporal and spatial
variations are also urgently needed. Since most countries in the region have not yet
developed specific standards, such models would facilitate guidance on what, when,
where and how to monitor issues that duly take into account the technical and financial
feasibilities of individual countries.
Women and children probably bear the largest burden of health risks from these
exposures. Poverty, income and education are likely to aggravate further exposure
potentials for vulnerable groups. Within the context of the Millennium Development
Goals, it would be pertinent and almost necessary to identify and include indoor air
pollution issues as an integral part of addressing the health problems of women and
children in all countries. Indeed, if the region is to progress towards achieving even
moderate human development indices within the next decades, indoor air pollution will
probably be an important category of environmental risk factors in need of solutions.
1.3.4
Latin America
(a)
Use of fuels
In Latin America, biomass fuels are mostly used in rural areas. Nearly 25% of the
population of Latin America lives in rural areas where biomass fuels are most frequently
used for cooking and heating. This rural population represents nearly 127 million people
who are potentially exposed to biomass-related air pollution (Cordeu & Cerda, 2000). The
percentage of the rural population varies from country to country and can be as high as
60%, for example in Guatemala. In Mexico, nearly 25 million people use biomass,
particularly wood, as a primary source of energy for daily cooking. This number will
probably remain similar or increase in the near future, since most rural families do not
have the possibility of using a fuel that would be higher in the energy ladder such as gas
or electricity. A study conducted in Central America that included Guatemala, Honduras
110
and El Salvador concluded that 95% of the rural households used wood burning as a
source of energy for cooking (Organizacin Latinoamerica de Energa, 2000). Using data
from local estimates, surveys and some demographic and development indicators, Smith
et al. (2004) built a model to predict the national use of solid fuels. For Latin America,
those estimates were 24.6% (18.830.8%) for Mexico and Brazil and 52.9% (42.6
63.2%) for Ecuador.
In general, there is an inverse correlation between the size of the locality and the use
of biomass; the smaller and most disperse communities are those that use biomass fuel
most extensively (Riojas, 2003). In rural communities in Mexico, it has been estimated
that the mean quantity of wood used per person per day is approximately 3 kg. For a
typical family, consumption per year is equivalent to 4 tonnes of wood (Riojas, 2003).
(b)
Exposure data
Several factors affect the concentration of pollutants within the household during the
burning of open fires, in particular the volume and ventilation of the room, and the
intensity of the fire. Climatic conditions are major determinants of exposure and are
particularly important in some Latin American countries (e.g. Bolivia, Ecuador or Peru)
where a large proportion of the rural population lives at high altitude. In addition, the type
of cooking will also have an impact on exposure. Data from Mexico show that women
can spend nearly 67 h per day close to biomass open-fire cooking (Brauer et al., 1996).
Most of the studies that measured pollutant concentrations were conducted in rural
settings and attempted to characterize the distribution of levels in the kitchen. Cooking
times for meals varied from study to study and ranged from 30 min to 3 h. However, time
spent close to a burning fire can reach up to 12 h. The highest exposure occurs among
women and their young children; however, other members of the households are also
exposed because, in many cases, the kitchen is not a separate room or meals are eaten
near the stove (Naeher et al., 2005).
(i)
Qualitative data
In a study conducted in Guatemala, PM10 levels close to 1000 g/m3 or higher were
observed in homes that used open fires and those of carbon monoxide were about 5
10 ppm and reached 2550 ppm during use of the fire (Boy et al., 2002).
(ii) Quantitative studies
Table 1.25 presents results from studies conducted in Latin America, mostly in
Guatemala and Mexico, on pollutant concentrations in households that use biomass fuel.
Studies in Guatemala
Several studies have compared different types of indoor cookstove conditions to
determine the potential impact of intervention. Naeher et al. (2000a,b) determined
particulate and carbon monoxide concentrations in highland Guatemala and compared
different cookstove conditions: background (no stove use), traditional open stove,
improved stove (plancha) and bottled gas (LPG) stove. Measurements were taken for
Table 1.25. Concentrations of pollutants in selected studies on the use of biomass fuel conducted in Latin America
No. of
Season
households
Fuel
Stove type
Naeher et al.
(2000a), indoor
air, western
highland of
Guatemala,
Quetzaltenango,
25002800 m
Wood
Fall
Rainy
season
Pollutant
Area
Average
time
Method
Open fire
Average
Plancha
CO
LPG/open fire
Kitchen
22 h
Drager CO
Open fire
Average
PM2.5
Plancha
LPG/open fire
Kitchen
Gravimetry
(SKC Universal
Flow sample
pump)
527.9
96.5
56.8
Open fire
Average
Plancha
PM10
LPG/open fire
Kitchen
Gravimetry
717.1
186.3
210.2
Open fire
Average
Plancha
CO
LPG/open fire
Personal
monitoring
mother
Open fire
Average
Plancha
PM2.5
LPG/open fire
Personal
monitoring
mother
Gravimetry
Open fire
Average
Plancha
CO
LPG/open fire
Personal
monitoring child
Drager CO
passive difusion
Average
PM2.5
Personal
monitoring child
Gravimetry
1012 h
Drager CO
passive difusion
Range of levels
reported (g/m3
for PM, mg/m3
[ppm] for gases)
5.9 ppm
1.3 ppm
1.3 ppm
6.7
2.4
1.5
481.2
257.2
135.6
Reference,
location
2.7
1.9
2.0
279.1
169.7
148.5
111
112
Table 1.25 (contd)

No. of
Season
households
Albalak et al.
(2001), western
highland of
Guatemala, La
Victoria rural
community in
San Juan
Ostuncalco,
20002300 m
30
Dry season Wood

Part of rainy
season
Naeher et al.
(2001), western
highland of
Guatemala,
Quetzaltenango,
25002800 ma
15 open
fire
25
improved
stove
Summer
(rainy
season)
Wood
Dry winter
season
50% open fire

30% chimney
stoves (plancha)
20%
combination
gas/open fires
Wood,
agricultural
residues
Bruce et al.
29
(2004),
Guatemala,
western highland,
La Victoria
Fuel
Stove type
Pollutant
Area
Average
time
Method
Range of levels
reported (g/m3
for PM, mg/m3
[ppm] for gases)
Open fire
PM3.5
Plancha
LPG/open fire
Kitchen
24 h
average
(women
spent 5
h/day )
SKC Aircheck
samplers
Gravimetry
1560 (GM)
280 (GM)
850 (GM)
Open fire
Plancha
CO
Kitchen
24 h
Stain tube
4.022.7
0.07.1
Open fire
Plancha
PM2.5
Kitchen
24-h
Gravimetric
3242198
33409
CO
Open fire
Plancha
Open fire (11) PM3.5
Plancha (5)
Gas/other (8)
Kitchen
24-h
Gas diffusion
tubes
Gravimetry
12.4 (10.214.5)
3.09 (1.874.30)
1019 (SD, 547)
351 (SD, 333)
579 (SD, 205)
Reference,
location
Table 1.25 (contd)

No. of
Season
households
Fuel
Stove type
Pollutant
Area
Average
time
Method
Brauer et al.
(1996), Mexico,
San Jose Solis,
2450 m
22 homes
Biomass (corn
stalks and
husks)
Wood and LPG
Open fire
Average
PM2.5
Kitchen
Biomass
Biomass+LPG
LPG
Biomass
Biomass+LPG
LPG
9h
Gravimetry
Kitchen
Cooking area
Stove
Open fire
Children area
Stove
Open fire
16 h
AprilMay
Dry season
LPG
Riojas-Rodriguez 38
et al. (2001),
Mexico
Dry season
Wood
PM10
Ceta stove and Average

open fire
PM10
Rainy
season
Regalado et al.
(2006), Mexico
n=778
samples
554.7 (SD,492.9)
203.6 (SD, 180.6)
69.4 (SD, 54.2)
767.9 (SD, 540.5)
311.2 (SD, 247.8)
225.5 (SD, 260.8)
Gravimetry
230
265
233
202
Cooking area
Stove
Open fire
Children area
Stove
Open fire
Biomass
cooking fuel
Wood stove
12% with
chimney
PM10
PM2.5
Kitchen while
cooking
Range of levels
reported (g/m3
for PM, mg/m3
[ppm] for gases)
206
287
Reference,
location
158
305
1 h during
cooking
Nephelometer
113
690 average
1390 peak
490 average
1040 peak
114
Table 1.25 (contd)

Reference,
location
No. of
Season
households
Winter Nov
to January
Hamada et al.
(1991), Brazil,
rural southern
Brazil, 930 m
28 wood
stoves
Winter
Caceres et al.
(2001), Chile,
urban Santiago
24
Stove type
Pollutant
Area
Average
time
Method
Range of levels
reported (g/m3
for PM, mg/m3
[ppm] for gases)
Wood
Open stove
PM2.5
Near stove
In kitchen
On patio
Near stove
In kitchen
On patio
48 h
Gravimetric
693 (2461338)
658 (671448)
94 (36236)
246 (63614)
255 (59864)
92 (51295)
DBA
BaP
SPM
NO2
Kitchen
24 h
HPLC/spectrofluorometer
Gravimetry
Kitchen
Personal
24 h
9.79 [ng/m3]
36.2 [ng/m3]
108 g/m3
14.6 [ppb]
9.0 [ppb]
PM10
CO
SO2
Kitchen
24 h
Gravimetric
250
42
192 ppb
Patsari
(improved
stove)
Winter
Wood
Coal
Firewood
Closed stove
with flues
PM10
CO
SO2
Real-time
portable monitor
489
57
295 ppb
Zuk et al. (2007), 53

Mexico, rural
Michocan,
2600 m
Fuel
Table 1.25 (contd)

No. of
Season
households
Fuel
Stove type
Pollutant
Area
Average
time
Method
Albalak et al.
(1999), Bolivia,
Altiplano,
4100 m
24
n=621
samples
Biomass fuel
Open fire
PM10
Kitchen
Indoor cooking
Outdoor cooking
Home
Indoor cooking
Outdoor cooking
6 h during
cooking
period in
the
morning
Gravimetry
January to
October
Range of levels
reported (g/m3
for PM, mg/m3
[ppm] for gases)
1830 (SD, 2990)

430 (SD, 140)
280 (SD, 330)
840 (SD, 400)
This study also reports results presented in Naeher et al. (2000a).

BaP, benzo[a]pyrene; CO, carbon monoxide; DBA, dibenzanthracene; GM, geometric mean; HPLC, high-pressure liquid chromatography; LPG, liquid petroleum
gas; NO2, nitrogen dioxide; PM, particulate matter; SD, standard deviation; SO2, sulfur dioxide; SPM, suspended particulate matter
Reference,
location
115
116
22 hour during the rainy season in nine houses. Background kitchen PM2.5 levels were
56 g/m3; levels were 528 g/m3 for open fires, 97 g/m3 for planchas and 57 g/m3 for
gas stoves. Similar trends were observed for personal exposures of mothers and children.
However, the authors mentioned that improved stoves (planchas) deteriorate over time
and that maintenance is important to control indoor pollutant levels. In a similar study, the
same authors collected samples from 15 homes that used open fires and 25 homes that
had improved stoves and reported concentrations similar to those of the first study
(Naeher et al., 2001). In another study conducted in the western highlands of Guatemala,
24-h PM3.5 concentrations were monitored over 8 months for three fuel/cookstove
combinations (10 in each category): a traditional open-fire cookstove, an improved
cookstove called plancha mejorada and LPG stove/open-fire combination for which
mean levels were reported to be 1560 g/m3, 280 g/m3 and 850 g/m3, respectively
(Albalak et al., 2001). Similar orders of magnitude of PM3.5 levels were observed in the
study of Bruce et al. (2004).
Studies in Mexico
A follow-up study in two rural communities of the state of Chiapas, Mexico,
compared families who used an improved stove for cooking with those who used
traditional open fires. Measurements (16-h) of PM10 showed that the concentration of
particles was significantly lower in the kitchen area (158 g/m3 versus 233 g/m3) during
the rainy season compared with the dry season (Riojas-Rodrguez et al., 2001). Two
studies conducted in Mexico evaluated the impact of the use of biomass on the respiratory
health of women. In a casecontrol study, 127 cases with chronic bronchitis or chronic
airway obstruction and 280 controls were recruited at the National Institute of Respiratory
Disease in Mexico (Prez-Padilla et al., 1996). Cases reported a mean of 3 h of cooking
with a wood stove per day and a range from none to 12 h. The mean duration of cooking
with a wood stove was 28 years and ranged from none to 71 years. It was calculated that
the hyear value of exposure (years of exposure multiplied by the average number of
hours of exposure per day) was 80 (mean) and values ranged from 0 to 552 hyears. No
objective measurement of particle levels was carried out; however, measurements taken
in rural Mexico showed average levels of PM2.5 of 555 g/m3 (range, 301492 g/m3)
when biomass was burned in open fires (Brauer et al., 1996). Using an integrated
nephelometer during 1 h of cooking time, levels of exposure to PM2.5 measured in homes
with stoves with (and without) a chimney averaged 490 (SD, 610) g/m3 with a peak of
1040 (SD, 1010) g/m3 (Regalado et al., 2006).
As part of a large health intervention study, Zuk et al. (2007) evaluated the impact of
improved wood burning stoves on indoor air pollution in 52 homes in the rural town of
Michoacan, Mexico, and monitored levels before and after the improved wood-burning
stoves were received. Mean PM2.5 concentrations (48-h) in homes that burned wood in
open fires were 693 g/m3 near the stove and 658 g/m3 in the kitchen away from the
stove. Paired measurements taken before and after installation of the patsari (improved
117
stove) indicated a median 71% reduction in PM2.5 concentrations near the stove and a
58% reduction in the kitchen concentration.
Studies in other Latin American countries
In a study conducted in a rural community of southern Brazil during the winter,
concentrations of PAHs and suspended particulate matter were assessed in homes that
used wood and gas stoves. Higher levels of PAHs and suspended particulate matter were
observed in homes that used wood stoves (Hamada et al., 1991).
Indoor air pollution was also measured in 24 houses in an area of low socioeconomic
status in Santiago, Chile. The highest concentrations of PM10, carbon monoxide and
sulfur dioxide were measured during the time of heating with higher levels observed for
firewood burning than coal. Coal, firewood and cigarette smoke were all sources of
carcinogenic PAHs (Cceres et al., 2001).
In a study conducted in a rural village of the Bolivian altiplano located at 4100 m
above sea level, PM10 levels were measured in a total of 621 samples. In homes in which
cooking was carried out indoors, the mean PM10 concentration in kitchens was
1830 g/m3 and ranged from 580 to 15 040 g/m3 over a 6-h cooking period. Daily
exposure for women involved in indoor cooking was 11 280 gh/m3 during the working
season (harvesting and planting season) and 15 120 gh/m3 during the non-work season
(Albalak et al., 1999).
(iii) Intervention studies
Several intervention studies have shown the impact of improved stoves or installation
of hoods or chimneys on exposure levels. Studies conducted in Guatemala showed that,
compared with open fires alone, the LPG/open fire combination showed a 45% reduction
in PM3.5 (p<0.07) while the plancha mejorada showed a 85% reduction in PM3.5
concentration compared with open fires (p<0.0001). Season did not affect pollutant
concentration and the reduction of PM3.5 was maintained throughout the 8 months of the
study (Albalak et al., 2001). Bruce et al. (2004) reported an almost 65% reduction in
indoor PM3.5 levels with improved stoves. Similarly, a study conducted in Mexico
showed that improved stoves could provide a median 71% reduction in PM2.5
concentration near the stove and a 58% reduction in the kitchen (Zuk et al., 2007).
1.3.5
Africa (Table 1.26)

(a)
Indoor air and personal exposure data
The percentage of households that use solid fuel in African has been estimated to be
approximately 73% (6878%) in Saharan Africa and 86% (8189%) in sub-Saharan
Africa (Smith et al., 2004). Studies from Africa have mainly been carried out in Kenya,
The Gambia and South Africa. Daily measurements of PM10 usually exceeded
1500 g/m3 (Saksena & Smith, 2003). Recent data from Zimbabwe showed that women
spend on average 5 h per day in the kitchen area and that the levels of PM10 were in the
118
Table 1.26. Concentrations of pollutants in selected studies on the use of biomass fuel conducted in Africa
No. of
households
Season
Fuel
Stove type
Pollutant
Area
Average
time
Method
Range of levels
reported (g/m3 for
PM, mg/m3 [ppm] for
gases)
Cleary &
Blackburn
(1968), New
Guinea
Not
reported
Wood
Not reported
Smoke
density,
aldehydes,
CO
Native huts,
new Guinea
highlands
Different
times for
each hut
described
Brass filter
holder, hand
pumps
666 (average)
21.3 ppm (average)

150 ppm (peak)
CO
WHO/UNEP
(1988), The
Gambia
Dry and
rainy
seasons
Wood
Boleij et al.
36 randomly
(1989), Kenya selected from
250 in area
Rainy
season
(April,
May)
Mostly wood
sometimes
biomass fuels
(agricultural
waste)
Traditional 3- Respirable
particles
stone open
NO2
fire within
house (58%),
or in separate
kitchen (42%)
Collings et al. 40
(1990),
Zimbabwe
Spring
Wood,
paraffin, gas,
electricity
Mostly open
fires in
thatched huts.
24-h SPM
PM
1.08 ppm (average)

3.8 ppm (peak)
14 h
2000 (GM) dry

2100 (GM) rainy
Rural area of
Maragua,
Kenya;
kitchens
7 h/day
(fire
burning)
Measurements 24 h
average
Pump (Dupont 1400 (mean)

P2500) and
PAS-6 filter
180 (mean)
holder with
glass fibre
filters
Kitchen
2h
Casella
3131 TT
personal
sampler with
Whatman 42
filter paper.
EEL
Densitometer
No. 19
546 and 1998
Reference,
location
Table 1.26 (contd)

Reference,
location
No. of
households
Season
Ellegard &
Egneus
(1993),
Lusaka,
Zambia
Stove type
Biomass,
tobacco,
outdoor
pollution
268
housewives
Gachanja &
9
Worsfold
(1993), Kenya
Not
reported
Pollutant
Area
Median TSP
Average
time
Method
12.1 h
Range of levels
reported (g/m3 for
PM, mg/m3 [ppm] for
gases)
310 (school day)
298 (holiday)
Wood,
charcoal,
electricity
Wood
Charcoal
Electricity
Mean
respirable
particles
<7.1 m
Personal
sample
2.5 h
cooking
time; 4-5 h
monitoring
time
Air pumps
890
(Gil-Air) with 380
cyclone,
240
Millipore
SCWP 03700
filter, Drager
colorimetric
diffusion tubes
Biomass fuels,
wood,
charcoal, dung,
crop residues
Compared
2 charcoal
burning stoves
traditional
3-stone and
ceramic-lined
Total PAH
Chrysene,
benzo[a]anthracene,
benzo[a]pyrene,
benzo[ghi]perylene, 3methylcholanthrene
Kenya
highlands;
kitchens
24 h
Glass
microfibre
filter and
XAD-2 resin
cartridge
2.6 (max.)
1540 [ng/m3] (range)
Terblanche et
al. (1992),
South Africa
Fuel
119
120
Table 1.26 (contd)

No. of
households
Season
Fuel
Stove type
Pollutant
Area
Average
time
Method
Range of levels
reported (g/m3 for
PM, mg/m3 [ppm] for
gases)
Ellegard
(1994),
Zambia
Not reported
March
Wood,
charcoal,
electricity
Wood
Charcoal
Electricity
Charcoal
producer
Mean TSP
(respirable
suspended
particulates)
Kamaila,
Chisamba,
Zambia
4.7 h
4.8 h
4.5 h
2.3 h
Air pumps
(Gil-Air SC)
fitted with
filter &
cyclone
890
380
240
1400
Campbell
(1997), The
Gambia
18 (6 in each
of 3 villages)
Over
Biomass fuels
12 months, (wood, dung,
dry and wet crop residues)
season
Not reported
TSP
Benzo[ghi]perylene
Pyrene
Benzo[a]anthracene
(particulates,
NO2, PAH)
2 Mandika
villages, 1
Fula hamlet;
kitchens
24 h
Boleij et al.
(1988a,b)
2000 (mean)
246 [g/g] (AM)
Not
reported
Wood
Charcoal
Electricity
LPG
Kerosene
Coal
Mean
respirable
particulates
10 suburban
bairros around
Maputo;
cooking place
varied.
2.84 h per
day;
monitoring
period
equal to
actual
cooking
time (av
1.5h)
Ellegard
(1997),
Maputo
1000
Mainly wood
and charcoal;
less common:
electricity,
LPG, kerosene,
coal
160 [g/g] (AM)

147 [g/g] (AM)
Air pumps
(Gil-Air SC)
with cyclone.
Diffusion tube
(Drager
6733191)
1200
540
380
200
760
940
Reference,
location
Table 1.26 (contd)

No. of
households
Season
Fuel
Bailie et al.
(1999)
75
Winter
Ezzati et al.
55
(2000), Kenya
Sanyal &
Madunaa
(2000), South
Africa
115
Stove type
Pollutant
Area
Average
time
Method
Paraffin and
Not reported
electricity most
common; gas
and wood less
common
TSP
Poor urban
environment
Includes
peak fuel
use
periods
Electrochemic 7.15432
al Exotox
continuous daily
Model 75
monitoring
continous
monitors, GilAir model
224-XR pumps
Wood, dung,
charcoal
Wood
Charcoal
Average
daily PM10
14 h/day,
>200 days
Personal data
RAM
nephelometer
27954898
3 times:
June-Sept,
Oct-Dec,
Mar-May
Wood, dung,
coal
Very low
income
Low income
Middle
income
CO
6h
(morning
and
afternoon)
EXOTOX
Model
75 continuous
gas monitors
180
Residential
area of
Victoria East;
cooking and
living areas
Range of levels
reported (g/m3 for
PM, mg/m3 [ppm] for
gases)
118
67
Reference,
location
121
122
Table 1.26 (contd)

No. of
households
Season
ITDG (2002),
West Kenya
and Kajiado
50
2 rounds Wood,
wet and dry residues,
season
biomass,
kerosene
2 rounds
wet and dry
season
50
Fuel
Stove type
Pollutant
Area
Average
time
Method
Range of levels
reported (g/m3 for
PM, mg/m3 [ppm] for
gases)
Before
intervention
PM and CO
West Kenya
Kajiado
3.8
2.5
Air sampler,
stain tubes
1713 (PM), 10.1 (CO)

5526 (PM), 74.7 (CO)
After
intervention
PM and CO
West Kenya
Kajiado
3.14
1.52
Air sampler,
stain tubes
628.9 (PM), 4.7 (CO)

3522.4 (PM),
51.4 (CO)
Wood
Charcoal
Electricity
Mean CO
8.5
13
2.1
Mishra et al.
(2004),
Zimbabwe
150
15 August Wood, dung,

Unvented
30 Nov
charcoal,
cook stoves
electricity,
LPG, kerosene
CO
PM10
Zimbabwe,
10 provinces;
kitchen
Rllin et al.
(2004), South
Africa
105
Summer
PM
South African 24 h
rural villages,
North-West
Province;
kitchen and
on-person
Wood, paraffin With/without

(kerosene),
chimney
electricity
5h
3001000 (range)
10004000 (range)
Pumps with
cyclones,
Drager passive
diffusion tubes
Unelectrified areas:
median, 107;
electrified areas:
median, 37.5
CO, carbon monoxide; GM, geometric mean; LPG, liquid petroleum gas; NO2, nitrogen dioxide; PAH, polycyclic aromatic hydrocarbons; PM, particulate matter;
SO2, sulfur dioxide; SPM, suspended particulate matter; TSP, total suspended particulates
Reference,
location
123
range of 10004000 g/m3 and those of carbon monoxide were in the range of 3001000
ppm (Mishra et al., 2004).
A study conducted in The Gambia, where combustion of biofuels is predominantly
related to cooking fires, reported a mean level of suspended particulate matter (24-h
average) of 2000 g/m3 with a range of 6753444 g/m3. High concentrations of PAHs
were also seen, with a mean level of benzo[a]pyrene of 102 ng/m3 that ranged from 69 to
351 ng/m3 and a mean level of dibenzo[a,h]anthracene of 149 ng/m3 that ranged from 101
to 513 ng/m3 (Campbell, 1997). Data from Kenya also reported high particulate levels
during home cooking on three traditional stone open fires (using mostly wood). Fires
were burning for almost 7 h per day. Average levels of suspended particulate (24-h) were
approximately 1400 g/m3 (SD, 1000). PAHs were also measured; average levels of
benzo[a]pyrene on filters were 60 g/m3 (SD, 50) and those of dibenz[a,h]anthracene
were 100 g/m3 (SD, 90) (Boleij et al., 1989).
Indoor concentrations of 12 PAHs were measured in Burundi in 16 rural houses that
used traditional wood stoves. In addition, 32 residents of these homes provided data on
urinary excretion of 1-hydroxypyrene. Mean airborne concentrations of four volatile
PAHs (naphthalene, fluorene, phenanthrene and acenaphthene) exceeded 1 g/m3 and
that of benzo[a]pyrene was 0.07 g/m3. Naphthalene was the main PAH contaminant.
Mean urinary 1-hydroxypyrene excretion of residents of traditional houses was
1.50 mol/mol creatinine (range, 0.2615.62 mol/mol), a value that was 30 times higher
than that of people who lived in the capital city of Burundi (Viau et al., 2000).
In a study conducted in Kenya, personal exposure from biomass burning in a rural
population was determined using data on type of activity, emission concentrations, time
spent in different microenvironments and proximity to the fire during the burning period.
Because exposure to biomass burning varies from day to day (depending on the moisture
content or density of the fuel, the type of food cooked, the choice of stove and fuel) and
from season to season (different activity pattern, ventilation of the home), a detailed
exposure measurement was made over several days (200 days) and seasons. Exposure
was higher for women than men, but was similar in children of either sex under 5 years of
age. The highest exposure was observed in women aged 1549 years and reached
4.9 mg/m3 per day (Ezzati & Kammen, 2001).
In a study conducted in Zambia, personal exposure to respirable particles (<7.1 m)
was measured in housewives exposed to different types of fuel during cooking time.
Women exposed to emissions from wood burning had the highest level (890 g/m3)
compared with those who used charcoal (380 g/m3) or electricity (240 g/m3) (Ellegard
& Egneus, 1993).
(b)
Impact of intervention studies
Using data from a study conducted in Kenya, Ezzati and Kammen (2002) estimated
that various energy- or behaviour-based interventions can result in a 3595% reduction in
exposure to PM10. It is clear that acceptance of the intervention is a crucial component for
124
its success and that, in each case, social, economic and environmental components need
to be considered.
1.3.6
Exposure in developed countries
The previous sections have dealt with exposure from solid fuel combustion in
developing countries; this section provides comparable figures on exposure from solid
fuel combustion in developed countries. The two main sources of exposure to particles
from biomass burning are wildfires and residential wood burning.
[Exposures due to agricultural burning also exist in developed countries but are
localized in both space and time and do not affect a significant portion of the population.
For example, in the early 1990s, agricultural burning in California contributed about
3.5 million tonnes per year to atmospheric particles, but that corresponded to only 1% of
all emissions (Jenkins et al., 1992). As an indication of the maximum PM concentrations
that might be achieved, agricultural burning in Brazil is now carried out on a huge
industrial scale, but is limited to 2 weeks per year; a 1-week monitoring programme
during the burning season showed PM3.5 levels of 191 g/m3, but this would correspond to
a contribution to annual average concentrations of only 8 g/m3 (Reinhardt et al., 2001).
Exposures elsewhere would in general be much smaller and therefore are not discussed
further here.]
Wildfires are not dealt with here as they relate to outdoor exposure.
(a)
Indoor air pollution
A study on a Navajo reservation in Arizona showed higher levels of respirable

particles in homes that used wood for heating or cooking than in homes that used
electricity or gas (Robin et al., 1996).
(b)
Residential wood burning
All of the following studies relate to ambient (outdoor) air pollution due to wood
burning for heating or to recreational use of fireplaces.
Source apportionment studies indicate that wood smoke is a major source of ambient
PM during the winter months in several parts of the USA and Canada, particularly the
western areas (Table 1.27). For example, 42% of the PM10 during winter months in San
Jose, CA, was attributed to wood burning (Fairley, 1990). Chemical mass balance
receptor-modelling of fine particles in Fresno and Bakersfield (CA) during wintertime
identified both hardwood and softwood as sources of PM and organic compounds
(Schauer & Cass, 2000), which were probably due to residential wood burning.
Outdoor PM levels in Seattle (WA) are also heavily influenced by residential
woodstoves. Data from 3 years of sampling in Seattle were analysed for sources using
positive matrix factorization (Maykut et al., 2003). The analysis found that vegetative
burning contributed 34% to the total sources of PM in Seattle over 3 years.
125
Table 1.27. Wood smoke in developed countries: a sample of studies

Location
Indoor/personal
Seattle personal
Seattle indoor
Fort Defiance, AZ
Wood smoke concentration
Reference
35% of total PM2.5 mass

Larson et al. (2004)
Indoor PM10 dominated by woodstove Robin et al. (1996)
smoke
Outdoor
Santa Clara Co., CA
Seattle
Atascadero, CA
Atlanta
Vermont
Christchurch, New
Zealand
42% of chemical mass balance

Levoglucosan
1018% of PM2.5
90% of PM2.5 in winter
Fairley (1990)
Manchester-Neesvig et al. (2003)
Polissar et al. (2001)
Polissar et al. (2001)
McGowan et al. (2002)
PM, particulate matter
Another study used a large data set from a 2-year exposure assessment and health
effects panel study in Seattle during September 2000May 2001. Data on indoor, outdoor,
personal and fixed-site PM monitoring were available (Larson et al., 2004). Five sources
contributed to indoor and outdoor samples: vegetative burning, mobile emissions,
secondary sulfate, a chlorine source and a crustal-derived source. Vegetative burning
contributed the largest fraction of PM mass in all the samples (49%, 62% and 35% in
indoor, outdoor and personal mass, respectively).
The distribution of particle-phase organic compounds was measured in communities
that had children who participated in the Southern California Children's Health Study
(Manchester-Neesvig et al., 2003). Concentrations of levoglucosan, an efficient tracer for
wood smoke aerosol, were seen in all 12 communities in the study. The average
concentration increased in the winter, as would be expected for wood smoke emissions.
The concentrations of levoglucosan were highest at the Atascadero site, which is about
15 miles inland. Earlier, these investigators identified two additional sugar anhydride
tracers of wood smoke (galactosan and mannosan) in a study of urban sites in the San
Joaquin Valley, CA (Nolte et al., 2001).
In Canada, where the winters are cold and the forests are abundant, wood smoke is a
major source of particle emissions.
Christchurch, New Zealand, is another city that is impacted by wood smoke. It is
estimated that more than 90% of wintertime ambient PM comes from heating stoves and
open fires burning wood (McGowan et al., 2002). Frequent periods of air stagnation
compound the problem by trapping PM near the ground and local meteorologists estimate
that the relatively even mixing results in fairly homogeneous population exposure to PM.
126
Emissions inventories in Launceston, Australia, indicated that household wood

burning accounted for 85% of annual PM10 emissions in 2000 (Jordan & Seen, 2005).
Source apportionment studies in Denmark showed that household wood burning was
responsible for 47% of national PM2.5 emissions in 2002 (Naeher et al., 2007). In addition,
household wood burning increased by about 50% during the 1990s, compared with only a
7% increase for total energy use.
Earlier studies of the contribution of wood smoke to ambient PM were summarized
by Larson and Koenig (1994). Eighteen studies in 40 locations in the Pacific Northwest
(Alaska, Washington, Oregon, Idaho, Montana) were included. The ranges of
concentrations for PM2.5 and PM10 were 1268 g/m3 and 7205 g/m3, respectively. The
interquartile range for the fractional contributions of wood smoke to these concentrations
was about 2070% with a median value of 54%.
1.4
Interventions and policies to reduce exposure

(a)
Encouragement of the adoption of efficient biomass stoves
One major solution that could provide a bridge between biomass energy and the
switch to commercial fuels but is unfortunately overlooked is the improvement of stoves
that burn biomass. This is generally less expensive for households that are dependent on
biomass and these stoves are often designed with chimneys to vent smoke out of the
home. It is generally accepted that improved biomass stoves reduce smoke in households
that use them, but the reduction is not as significant as that for households that switch
completely to LPG.
International programmes for improved stoves can provide some insights into both
the successes and problems that are involved in the promotion of efficient biomass stoves
(Sinton et al., 2004a,c; Barnes et al., 2007). In addition, energy efficiency and
increasingly improved health are recognized to be important selling points for improved
stoves.
During the last 3040 years, diverse programmes have been initiated on household
energy, from small-scale initiatives led by non-governmental organizations and
communities to very ambitious national programmes, the largest of which has seen the
installation of some 200 million improved stoves in rural China. Although few have been
subjected to rigorous evaluation, the Indian national programme of improved cookstoves
(Table 1.28), the Chinese national improved stoves programme (Table 1.29) (Smith et al.,
1993; Sinton et al., 2004a) and the promotion of LPG (UNDP, 2004) have been assessed.
Several smaller initiatives have also been reported: for example, the ceramic and metal
stoves in East Africa which have proved popular and provided local employment
(Njenga, 2001) and improved stove interventions in Guatemala (UNDP/ESMAP, 2003).
Current projects also include the evaluation of several household energy programmes in
India, Mexico and Guatemala, which seek to promote effective and sustainable markets
for improved biomass stoves.
127
Table 1.28. Key features and lessons from the Indian national stove programme
The Indian National Programme of Improved Cookstoves was established in 1983 with goals common
to many initiatives such as:
conserving fuel,
reducing smoke emissions in the cooking area and improving health conditions,
reducing deforestation,
limiting the drudgery of women and children and reducing cooking time, and
improving employment opportunities for the rural poor.

While the Ministry of Non-Conventional Energy Sources was responsible for planning, setting targets
and approving stove designs, state-level agencies relayed this information to local government agencies
or non-governmental organizations. A Technical Backup Unit in each state trained rural women or
unemployed youths to become self-employed workers to construct and install the stoves.
Between 1983 and 2000, the Programme distributed more than 33 million improved chulhas, but
despite extensive government promotion efforts, improved chulhas now account for less than 7% of all
stoves. Among those that have been adopted, poor quality and lack of maintenance have resulted in a
lifespan of 2 years at most and typically much less. Evaluation of the Programme identified four main
problems:
Most states placed inadequate emphasis on commercialization, now seen as crucial for
effective and sustainable uptake.
Overall, there was insufficient interaction with users, self-employed workers and nongovernmental organizations, so that designs did not meet the needs of households, and there
was very poor uptake of user training.
Quality control for installation and maintenance of the stove and its appropriate use was
lacking.
High levels of subsidy (about 50% of the stove cost) were found to reduce household
motivation to use and maintain the stove.
The more successfully managed areas of the Programme focused resources on technical assistance,
research and development, marketing and dissemination of information. Recently, the government of
India decentralized the programme and transferred all responsibility for implementation to the state
level. Since 2000, the Programme promotes only durable cement stoves with chimneys that have a
minimum lifespan of 5 years. The introduction of these stoves will make adhesion to technical
specifications and quality control much easier.
Table 1.29. Household impacts of China's National Improved Stove Programme

In 2002, an independent multidisciplinary evaluation was undertaken by a team of US and Chinese
researchers to evaluate (i) implementation methods used to promote improved stoves, (ii)
commercial stove production and marketing organizations that were created, and (iii) household
impacts of the programmes, including health, stove performance, socioeconomic factors and
monitoring of indoor air quality. The first two objectives were assessed through a facility survey of
108 institutions at all levels. The third objective was assessed through a survey of nearly 4000
households in three provinces: Zheijang, Hubei and Shaanxi. Key findings were:
The household survey revealed highly diverse fuel usage patterns: 28 and 34 different fuel
combinations were used in kitchens in winter and summer, respectively. Most households
owned at least one or more coal and one or more biomass stoves; 77% of the biomass stoves
but only 38% of the coal stoves were classified as improved. On average, improved stoves had
a mean efficiency of 14%, which is well below the Programme target of between 20% and
30%, but above the mean efficiency of 9% for traditional stoves.
128
Table 1.29. (contd)

With respect to air quality (measured by PM4, the thoracic fraction of particulate matter and
carbon dioxide, coal stoves showed significantly higher concentrations than biomass stoves
during the summer but not during the winter. Among households that used biomass fuels (but
not among those that used combinations of fuels that included coal or LPG), improved stoves
showed significantly lower PM4 and carbon dioxide concentrations than traditional stoves.
In both children and adults, coal use was associated with higher levels of exposure as measured
by carbon dioxide in exhaled breath, and improved biomass stoves had lower levels. Reported
childhood asthma and adult respiratory disease were negatively associated with use of
improved stoves and good stove maintenance. These results should, however, be treated as
indicative due to the limited sample size.
Overall, several important conclusions emerge with relevance to future improved stove
programmes:
A wide range of combinations of different fuel and stove types may limit the impact of an
improved stoves programme.
Given the importance of space heating, providing an improved biomass stove for cooking may
not be a sufficient strategy to reduce indoor air pollution. There is a need to promote improved
coal stoves among rural Chinese households.
Even among households that used improved stoves, PM4 and carbon dioxide levels were higher
than Chinese national indoor air standards, implying that a large fraction of Chinas rural
population is still chronically exposed to pollution levels substantially above those determined
by the Chinese government to harm human health.
Implementation of the Chinese national programme differed substantially from that in

India, and offers an interesting comparison. Although the rural populations concerned are
poor, they have greater effective purchasing power than those in many developing
countries, which allowed the development of a programme in which the majority of
consumers purchased the stoves at almost full price (Smith et al., 1993). Among the key
features of the Chinese programme that are reported to have contributed to its success are
decentralization of administration, a commercialization strategy that provided subsidies
for the development of rural energy enterprises and quality control through the central
production of critical components, such as parts of the combustion chamber, and
engaging local technical institutions to modify national stove designs to meet local needs.
National-level stove competitions generated contests among counties for contracts, to
ensure local interest and allow the best-placed counties to proceed first; financial
payments were only provided to counties after completion of an independent review of
their achievements. No large flow of funds came from central government (in contrast, for
example, with India, Table 1.30) and the major financial contributions were provided by
local governments. As a result, delays and other problems associated with transferring
large amounts of money were avoided. The Chinese programme succeeded in shifting
norms: most biomass stoves now available on the market have flues and other technical
features that classify them as improved.
129
Table 1.30. Characteristics of the national programme on improved chulhas in India

compared with international experience
International practices in stove
dissemination
Practices of the national programme on improved

chulhas
Focus on need-based users
Targeted approach, stress on number of villages to be

covered rather than households; demand for stoves not
taken into consideration
Minimal subsidy for the stove from

government or donors
Subsidy on stove accounted for the largest share (50%)

of government support. Users in periurban areas were
willing to pay greater amounts subject to guarantee on
stove quality.
Maximum support for research and

development, production and distribution
of stoves, credit, capacity building and
public awareness
Programme funded technical back-up units, but

inadequate support given for research and development,
with no such support extended to non-governmental
organizations. Support for capacity and awareness
generation not adequate
Close interaction among the designers,

producers and users of stoves
Adequate interaction between producer and user, but

interaction negligible between designer, and producer
and user
Dependence on centralized production of

stove and stove parts to enable availability
to larger number of people due to lower
cost of supply
For fixed stoves, there was no scope for centralized

production as these are built at users homes. Mass
production of stove parts (chimney, cowl) undertaken
by private manufacturer. No mass production of the
firebox.
Onus on producers and designers to meet

needs of consumers
Consumer needs met by self-employed workers/nongovernmental organizations through changes in stove

design with low inputs from designers.
Long-term funding
Long-term target-based funding by government routed

through nodal agencies and disbursed through nongovernmental organizations for implementation.
The lessons from international programmes have been compared with a programme
in India that was recently cancelled due to poor performance. The most successful
international programmes target subsidies for the commercialization of the stoves rather
than providing the user with extensive subsidies. The idea is to stimulate entrepreneurs to
build the stoves and to create a real market for them. The role of subsidies in Indias
programme is mixed. In the successful programmes, subsidies have encouraged possible
stove owners to purchase them. However, once purchased, there are no follow-up
subsidies for spare parts or maintenance. Subsidies can be used to support the
development of the technical back-up units, quality control facilities for testing stoves,
monitoring surveys to discern stove functionality and the opinions of users on the stoves,
and training or education regarding subjects such as stove design, indoor air pollution and
130
energy efficiency. However, this should be done in a way that integrates the design,
construction and convenience of the stoves for users.
The best international programmes have developed stove programmes in the regions
that have the greatest needs to conserve energy, such as those that have significant
biomass shortages and emerging markets in the sale of fuelwood. The lack of availability
of components and component parts appears to be a weakness in most of the programmes.
Both producers and users complained about their availability and quality.
(b)
Importance of electrification and other fuels
Electrification has an important role in development (International Energy Agency,

2002). There is some evidence from South Africa that communities with grid access
experience lower pollutant exposure (Rllin et al., 2004). Electricity is not expected to
bring about large reductions in exposure to indoor air pollution in most low-income
countries, however, since most poor households can only afford to use it for lighting and
entertainment appliances but not for the much more energy-intensive and polluting
requirements of cooking and space heating. The International Energy Agency (2002) has
recently carried out a detailed review of electrification, including the issues involved in
supply and cost recovery among poor (and especially rural) communities.
Experience in the promotion of LPG has also been reported, for example from the
Indian Deepam Scheme (UNDP/ESMAP, 2002; World Bank, 2004b), and from the LPG
rural energy challenge (UNDP, 2004). This latter initiative, developed by UNDP and the
World LPG Association in 2002, promotes the development of new, viable markets for
LPG in developing countries. Key elements include the development of partnerships in
countries, enabling regulatory environments which facilitate LPG business development
and product delivery, taking steps that reduce barriers to adoption: for example, the
introduction of smaller (more affordable) gas bottles, and greater government and
consumer awareness of costs and benefits. McDade (2004) has recently identified several
key lessons that emerged from experience with the promotion of LPG markets.
(c)
Key lessons
Too often, intervention technologies have been developed without adequate reference
to users needs, and as a result have been poorly used and maintained, or abandoned.
Consequently, it is important to involve users, particularly women, in assessing needs and
developing suitable interventions. Sustainable uptake should also be promoted through
greater availability of a choice of appropriately priced interventions in local markets.
A wide variety of interventions are already available, and new technologies and
approaches are emerging. However, the greatest challenge is in securing widespread
uptake of effective interventions among those most at risk (in effect, the rural and urban
poor), in ways that are sustainable. Enabling policy across sectors, and at different levels
in societies, is required.
131
Although levels of indoor air pollution associated with biomass and other solid fuel
use can be reduced substantially, particularly by stoves with flues, experience shows that
exposure levels are not reduced as much due to the fact that emissions remain high and
people are exposed in the vicinity of their homes and from neighbours homes. Biomass
stoves using secondary combustion may offer advantages due to much reduced emissions.
Cleaner fuels, in particular LPG and natural gas, offer the largest reductions in indoor
air pollution and exposure, but cost and practical issuesin particular whether these fuels
meet the needs of poor householdsmay result in lesser reductions being achieved in
practice. Electricity is important for development, but is unlikely to contribute to
substantial reductions in exposure to indoor air pollution as it is rarely used for cooking
(and space heating where needed) in poor communities due to the high cost of supply
infrastructure and use. Finally, behavioural changes can complement technical
interventions, but appear to have limited potential alone.
1.5
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144
2. Studies of Cancer in Humans

The studies described below focus predominantly on the risk of lung cancer following
exposure to fumes from cooking and heating with fuels. The studies are organized by fuel
type (coal, biomass, mixed coal/biomass) and region (inside China, outside China).
2.1
Coal
2.1.1
Lung cancer
(a) Casecontrol studies in China (organized from North to South) (see
Table 2.1)
The text below summarizes the individual studies from China that assess indoor air
pollution resulting from the burning of coal for cooking or heating. Selected results are
highlighted in the text below but more detailed information can be found in Table 2.1.
(i)
Northern China
Xu et al. (1989) conducted a casecontrol study in Shenyang that included 1249 lung
cancer cases (729 men, 520 women) and 1345 population-based controls (788 men,
557 women); 86% of male and 55% of female cases and 70% of male and 35% of female
controls were tobacco smokers. Pathological or cytological confirmation was obtained for
85.1% and 75.0% of lung cancers in men and women, respectively; 31% of these were
adenocarcinoma of the lung. The risk for lung cancer was generally positively associated
with exposure metrics reflecting coal use for heating, and, to a more limited degree, with
coal use for cooking. After adjustment for age, education and active smoking, lung cancer
risk increased in a doseresponse fashion with increasing duration of using coal-heated
burning kangs (beds heated by stoves). Risk also increased with increasing duration of
use of a coal stove with pipes to other rooms. Risk was higher when cooking took place in
the bedroom or entry corridor to the bedroom than in a separate kitchen or elsewhere in
the house. In men, the adjusted odds ratios were 1.0, 1.2 and 2.1 in relation to cooking in
the bedroom for 0, 129 and 30 years, respectively (p for trend <0.05); the
corresponding adjusted odds ratios in women were 1.0, 1.5 and 1.8 (p for trend <0.05).
[This study overlaps with Sun et al. (1991).]
Wu-Williams et al. (1990) conducted a casecontrol study of 965 female lung cancer
cases in northern China (445 in Harbin, 520 in Shenyang) and 959 female controls (404 in
Harbin, 555 in Shenyang); 417 cases and 602 controls were nonsmokers. Seventy-four
per cent (714) of the lung cancers were histologically/cytologically confirmed, of which
44% were adenocarcinoma. Cases and controls were compared with respect to indoor
coal use (largely use of coal-heated kangs, cooking practices) and other risk factors. In
multivariable logistic regression models, risk for lung cancer was generally positively and
Table 2.1. Casecontrol studies of lung cancer and use of coal in China
Reference,
Characteristics of
study location, cases and controls
study period
Exposure
assessment
Exposure categories No. of

exposed
cases
In-person
interview using
a structured
questionnaire;
developed
continuous
index of indoor
exposure to
coal smoke
from heating
and cooking
Coal stove with

pipes to other
rooms
Men
119
>20
Women
119
>20
Cooking place in
bedroom
Men
129
>30
Women
129
>30
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
Northern China
1249 cases (729 men,
520 women) in
Shenyang aged 30
69 yrs; cell type
histologically
confirmed in 83% of
men and 73% of
women
1345 populationbased controls (788
men, 557 women)
selected by
3-stage procedure
from urban
Shenyang;
frequency-matched
on gender and age
119
48
1.1 (p>0.05)
2.3 (p<0.05)
81
35
1.4 (p>0.05)
1.5 (p>0.05)
75
84
1.2 (p>0.05)
2.1 (p<0.05)
34
51
1.5 (p>0.05)
1.8 (p<0.05)
Age, education, Population

tobacco smoking overlapped with the
study by WuWilliams et al.
(1990)
Xu et al.
(1989),
Shenyang,
198587
145
146
Table 2.1 (contd)

Reference,
Characteristics of
study period
965 incident female
cases from local
registries; age
<70 yrs;
cytologically verified
959 control women
selected by
multistage random
sampling from
general populations
of Shenyang and
Harbin; frequencymatched by 5year age group

exposed
cases
In-person
interview using
structured
questionnaire
Duration of heating
device use (yrs)
versus no exposure
Coal stoves
2140
>41
Non-coal stove
120
2120
>31
Heated walls/floors
120
>21
Coal heaters
120
>21
Central heat
120
>21
Odds ratiosa
(95% CI)
511
253
1.2 (1.01.6)
1.3 (1.01.7)
367
259
118
0.8 (0.61.1)
0.7 (0.50.9)
0.8 (0.51.1)
127
243
1.5 (1.12.1)
1.4 (1.11.9)
258
173
1.2 (1.01.6)
1.1 (0.81.4)
258
173
1.0 (0.81.3)
0.8 (0.61.0)
Adjustment for
potential
confounders
Comments
Age, education,
smoking, study
area
Experiencing eye
irritation during
cooking (sometimes
or frequently) due to
exposure to burning
coal significantly
increased the risk for
lung cancer;
population
overlapped with the
study by Xu et al.
(1989)
Wu-Williams
et al. (1990),
Shenyang and
Harbin,
198587
Exposure
assessment
Table 2.1 (contd)

Characteristics of
Reference,
study period
Sun et al.
(1991),
Harbin,
198587
120 nonsmoking
women; 3069 yrs
old; lived in Harbin
>10 yrs; 100%
pathologically
confirmed
120 randomly
selected community
controls matched on
gender, 5-year age
group and
nonsmoking status

exposed
cases
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Using smoky (soft)

coal
Time-trend effect
Using brazier
(presumably
unvented)
NG
2.26 (1.533.33)
NG
p<0.001
1.36 (1.011.83)
Overlaps with Xu et
Pneumonia,
al. (1989)
pulmonary
emphysema,
smoky (soft) coal,
tuberculosis, nonsmoky coal
(possibly
anthracite),
smoking,
bronchitis, family
cancer history,
open fire basin,
heating by open
fire basin before
16 yrs old
In-person
Coal stove in
interview using bedroom
a questionnaire
119 yrs
20 yrs *
Coal heating
124 yrs
2534 yrs
Exposure to coal
dust 10 yrs
Not specified
NG
NG
4.46 (1.6112.33)
18.75 (3.9429.32)
NG
NG
NG
5.81 (1.6720.22)
4.70 (1.2817.18)
2.66 (1.096.52)
Comments
Fried and deep fried

cooking >5 times per
month significantly
lung cancer
* Article erroneously
reports 30
418 women in whom Questionnaire

266 (63.6%)
histologically or
cytologically
confirmed
398 community
controls: women
randomly selected
from Harbin
(sampling method not
specified)
Dai et al.
(1996),
Harbin,
199293
Exposure
assessment
147
148
Table 2.1 (contd)

Reference,
Characteristics of
study period
135 incident
nonsmoking female
cases from
18 hospitals; aged
3569 yrs;
54.5% ADC, 16.4%
SCC, 20.4% smallor oat-cell
135 nonsmoking
controls matched by
gender and age;
randomly chosen
from urban areas of
Shenyang
Zhou et al.
(2000),
Shenyang
City, Liaoning
Province,
199195
72 female incident
cases of
adenocarcinoma; aged
3569 yrs; from 18
major hospitals
72 women randomly
selected from the
Shenyang general
population; agematched (5 yrs) to
Liaoning lung cancer
cases in 198889

exposed
cases
In-person
Bivariate analysis
interview using
Cooking fume
a structured
exposure
questionnaire
Coal smoke
exposure during
cooking
Multivariate analysis
Cooking fume
exposure
Coal smoke
exposure during
cooking
In-person
Coal burning
interview using
standardized
questionnaire
Odds ratiosa
(95% CI)
NG
3.79 (2.296.27)
NG
2.37 (1.443.91)
NG
4.02 (2.386.78)
NG
Not statistically significant [NG]
NG
0.97 (0.641.48)
Adjustment for
potential
confounders
Comments
Not specified
Modelled results
may have been
conservative; coal
use not associated
with lung cancer, but
100/135 cases and
107/135 controls
used coal; no
association of kang
use for heating and
lung cancer
Not specified
Both cases and

controls had high
level of exposure to
coal smoke
Wang et al.
(1996),
Shenyang
City, Liaoning
Province,
199294
Exposure
assessment
Table 2.1 (contd)

Adjustment for
potential
confounders
Comments
220
1.41 (1.091.82)
95
148
108
1.04 (0.771.39)
1.00 (0.761.34)
1.44 (1.022.04)
0.04
Gender, age,
prefecture,
television and
cattle ownership
(for
socioeconomic
status), tobacco
use
Indoor levels of
PM10, PAH and
gaseous pollutants
were measured in 25
homes that burned
coal and biomass.
No significant
differences in
pollutant levels or
ventilation rates
were observed.
62
207
1.69 (1.152.47)
1.60 (1.222.10)
0.013
58
1.03 (0.661.63)
51
59
26
1.48 (0.942.32)
1.18 (0.751.88)
0.93 (0.521.67)
0.53
62
207
2.83 (1.605.00)
1.33 (0.832.14)
0.63
Exposure
assessment

exposed
cases
Kleinerman et
al. (2002),
2 prefectures
(Pingliang and
Qingyang) of
Gansu
Province,
199498
Interview using
structured
questionnaire
ascertained 30year history of
main cooking
and heating
fuels and
annual average
coal use
Men
Main fuel coal
versus biomass
Amount of coal
used, tertile versus 0
1
2
3
p for trend
Percentage of time
using coal versus 0
0.756
>56
p for trend
Women
Main fuel coal
versus biomass
Amount of coal
used, tertile versus 0
1
2
3
p for trend
Percentage of time
using coal versus 0
0.756
>56
p for trend
846 patients (626

men, 220 women)
diagnosed by an
expert review panel
of physicians; aged
3570 yrs
1740 randomly
selected controls
from the 1968 and
1990 population
census lists of the 2
prefectures;
frequency-matched
on gender, age and
prefecture
Odds ratiosa
(95% CI)
Characteristics of
Reference,
study period
149
150
Table 2.1 (contd)

Characteristics of
Reference,
study period
Exposure
assessment

exposed
cases
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
Age, length of
menstrual cycle,
age at
menopause,
family history of
lung cancer and
chronic
bronchitis
Methods unclear: all

study subjects were
former smokers but
amount of past
smoking was not
specified nor was it
considered as a
potential confounder
in the analysis.
Xuan Wei County, Yunnan
Lan et al.
(2000),
199596
Interview using
standardized,
field-tested
questionnaire
that queried
fuel type,
history of
smoky
139 age-matched ( 2 (bituminous)
yrs) female
coal use,
population controls
specifically
from Laibin
coal mine
Smoky coal from

Laibin Mine
Use versus no use
Tons/year used
versus 0
<3
3
p for trend
Period started use
versus never
After age 20
Before age 20
Lifelong
p for trend
122 incident cases;

100% confirmed by
different methods
Smoky coal use

without ventilation
130 tonnes vs
130 tonnes
139 nonsmoking
women (55
confirmed by
pathology or
cytology, 84 by Xrays and clinical
history)
122 population
controls taken
randomly from the
list of household
registrations;
individually matched
by sex, age, village
and type of fuel
currently used for
cooking and heating
In-person
interviews
using a
standardized
questionnaire
74
7.53 (3.3117.17)
23
51
8.24 (2.3329.17)
7.53 (3.0318.72)
<0.001
12
10
57
1.84 (0.566.05)
5.10 (0.9726.81)
9.89 (3.9524.75)
<0.001
71
2.4 (1.34.4)
Total smoky coal

use without
ventilation, packyrs, COPD and
family history of
lung cancer
Lan et al.
(1993),
198890
Table 2.1 (contd)

Characteristics of
Reference,
study period
Exposure
assessment

exposed
cases
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
1.59 (1.012.07)
Unclear
The primary goal

was to assess diet. [It
is unclear what the
reference group was,
but it was possibly
biomass.]
3.72 (0.8815.71)
Unclear
Results are presented

for SCC. Fuel types
within solid fuel
category were not
specified. [Statistical
tests were reported
as one-sided, but
implications are not
clear.]
Central China, excluding Xuan Wei

135 pre-invasive
lung cancer patients
at three provincial
hospitals
Shen et al.
(1996),
Nanjing,
198693
263 cases (83 SCC, Standardized

180 ADC) who were questionnaire
Nanjing residents for
20 yrs
In-person
Indoor coal burning NG
interview using
a questionnaire
135 healthy subjects

without respiratory
illness from the same
hospitals; matched on
gender and age
263 population
controls who were
Nanjing residents;
matched 1:1 for
gender, age, ethnicity
and street address
Coal heating stove
Huang et al.
(1992),
Chengdu,
Sichuan,
199091
151
152
Table 2.1 (contd)

Reference,
Characteristics of
study period
70 never-smoking
women diagnosed
with primary lung
ADC; all were
20 yrs

exposed
cases
Coal stove for

In-person
interview using heating
a standardized
questionnaire
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
1.78 (0.794.02)
Unclear
The main purpose of

the study was to
assess lung cancer
risk associated with
passive smoking.
This study may
overlap with Shen et
al. (1996).
0.92 (0.631.35)
Age, education,
income, vitamin
C intake,
respondent
status, exposure
to environmental
tobacco smoke,
occupation,
family history of
lung cancer
70 healthy
community controls,
matched 1:1 for
gender, age,
neighbourhood and
occupation
Zhong et al.
(1999),
Shanghai,
19921994
504 never-smoking
female incident
cases; 3569 yrs old;
identified from the
Shanghai Cancer
Registry
601 never-smoking
women; frequencymatched on age
distribution of female
lung cancer cases
during 198789;
randomly selected
from the Shanghai
Residential Registry
In-person
Coal and gas vs.
interview using coal only
a structured
questionnaire
96
Shen et al.
(1998),
Nanjing,
1993
Exposure
assessment
Table 2.1 (contd)

Reference,
Characteristics of
study period
Exposure
assessment

exposed
cases
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
0.32 (p=0.15)
Unclear
The reference
category is unclear
for ever coal use.
Southern China (Guangzhou and Hong Kong)

200 female lung
cancer patients; mean
age 61.8 yrs; 44%
never smokers; 90%
histologically
confirmed (28%
SCC, 18.5% smallcell, 34.5% ADC)
200 female
community controls,
matched on age (5
yrs), residential
district and housing
type; mean age 60.6
yrs; 69% never
smokers
Interviews with Ever used coal for

semi-structured cooking
questionnaire,
using a life
history
approach;
assessed use
and duration of
using coal,
biomass fuels,
kerosene, LPG
and gas
Koo et al.
(1983),
Hong Kong,
198183
153
154
Table 2.1 (contd)

Reference,
Characteristics of
study period
Liu et al.
(1993),
Guangzhou,
198384

exposed
cases
In-person
Coal use for
interview using cooking
structured
Men
questionnaire
Women
on smoking
habits, cooking
fuel use and
other variables
200
81
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Not having a
separate kitchen,
poor air circulation,
small size of
ventilation openings
in living area and
kitchen and smaller
room height
lung cancer.
1.0 (reference)
1.0 (reference)
316 hospital controls

matched on gender,
age, residential
district and date of
diagnosis; respiratory
and coronary heart
disease excluded
Du et al.
(1996),
Guangzhou,
2 casecontrol
studies with
cases who died
in 1985
849 deceased lung

cancer patients (566
men, 283 women);
smokers and nonsmokers
849 subjects who
died of causes
unrelated to lung
cancer, matched on
gender, age and
residence
Standard
Exposure to coal
questionnaire
fumes
administered to
Men
next of kin of
Women
lung cancer
patient
None
NG
NG
0.90 (p>0.05)
2.21 (1.164.21)
Comments
Mantel-Haenszel
analysis tested for
effects of coal
smoke; data
collection methods
not specified; results
on 120 nonsmokers
were presented but
the exposure was
unclear.
316 incident cases

(224 men, 92
women);
55% diagnosed by Xray/clinical history,
13% by
bronchoscopy, 32%
by cytology or
histology
Exposure
assessment
Table 2.1 (contd)

Exposure
assessment

exposed
cases
Lei et al.
(1996),
Guangzhou,
1986
In person
interviews with
next of kin
using a
standardized
questionnaire
Exposure to coal
smoke (versus
infrequent)
Regular
Men
Women
Living conditions
index (versus good)
Men
Fair
126
Poor
288
Women
Fair
64
Poor
111
792 cases deceased

from primary lung
cancer (563 men, 229
women) identified
from 1986 death
certificates
792 controls (563
men, 229 women)
matched on street of
residence, year of
death, gender and
age; no history of
respiratory diseases
or tumours
Luo et al.
(1996),
Fuzhou
102 cases (78 men,

Indoor air pollution NG
In-person
24 women); 57 ADC, interview using due to coal burning
39 SCC
a standardized
SCC
NG
questionnaire
ADC
NG
306 community
controls matched on
gender, age and
ethnicity
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
None
91.9% of families
used coal in the last
20 yrs (46.2% used
wood
simultaneously).
There was an
increased risk for
lung cancer in
women with a
fair/poor living
condition index
which may indirectly
point to coal smoke
exposure or cooking
practices as risk
factors.
Living condition
index = living area
per person/room
ventilation
[1.08 (0.851.39)]
[0.90 (0.571.42)]
1.17 (0.891.54)
0.99 (0.971.01)
2.56 (1.394.70)
1.89 (1.25 2.85)
7.6 (3.715.7)
14.1 [11.816.4]
6.0 [4.97.1]
Characteristics of
Reference,
study period
Personal and
passive smoking,
deep inhalation
of smoke,
income, history
of chronic
bronchitis
155
156
Table 2.1 (contd)

Characteristics of
Reference,
study period
Exposure
assessment

exposed
cases
Odds ratiosa
(95% CI)
Adjustment for
potential
confounders
Comments
Taiwan, Province of China

In-person
Coal for cooking
interview using ADC
a structured
vs.hospital
questionnaire
controls
on the use of
vs.
coal and other
neighbourhood
fuels for
controls
262 hospital controls cooking
SCC/small-cell
(ophthalmology)
vs.hospital
matched on gender,
controls
age (5 yrs),
vs.
interview date and
neighbourhood
insurance status;
controls
262 neighbourhood
SCC/small-cell
controls matched on
vs.hospital
gender, age and
controls
residence location
vs.
neighbourhood
controls
131 lung cancer

patients (72 ADC,
30 SCC, 29 smallcell); 100%
histopathologically
confirmed
7
1.44 (0.444.69)
Matching factors
0.56 (0.201.54)
Matching factors
3.73 (1.2711.02)
Matching factors
10.00 (2.1945.61)
Matching factors
4.41 (1.2016.20)
Unclear
24.34 (2.97199.49)
Unclear
10
10
A higher percentage
of proxy interviews
were conducted for
cases (21%) than
controls from the
neighbourhood
(17%) or hospitals
(12%)
[matching on
location of residence
may have influenced
effect estimates for
fuel type due to
overmatching.]
Ger et al.
(1993),
Taipei,
199091
Table 2.1 (contd)

Reference,
Characteristics of
study period
105 nonsmoking
female lung cancer
patients
105 (presumably
nonsmoking) women
from same hospital's
ophthalmic service or
coming to hospital
for routine check-up;
matched on age
( 2 yrs) and
interview date

exposed
cases
In-person
By age of exposure
interview using Coal vs. gas or none
a structured
<20 yrs
questionnaire
2040 yrs
>40 yrs
Odds ratiosa
(95% CI)
0.5 (0.21.6)
1.1 (0.43.0)
1.1 (0.18.0)
Adjustment for
potential
confounders
Comments
Socioeconomic [Selection of cases

status, education, and controls from
residential area
same hospital may
have caused
overmatching on
exposures. The nearsignificant positive
association of lung
cancer risk with
wood/charcoal use is
unusual, conceivably
related to the
matching strategy.]
Further adjusting for
other covariates (not
specified) did not
affect the statistical
significance nor
magnitude of effects.
Risk for lung cancer
was significantly
increased if the
kitchen did not have
a fume extractor.
Ko et al.
(1997)
Kaohsiung,
199293
Exposure
assessment
157
158
Table 2.1 (contd)

Exposure
assessment
Le et al.
(2001),
Kaohsiung,
199399
In-person
Women
interview using
Coal vs. gas or none
a structured
SCC or small-cell
questionnaire
carcinoma
Coal or anthracite
ADC
Coal or anthracite
527 histologically
confirmed cases (236
men, 291 women);
1883 yrs old; 28.2%
SCC and small-cell
carcinoma and 47.7%
ADC
805 controls from
same hospital without
tobacco-related
illness; matched on
gender and age ( 2
yrs)

exposed
cases
Odds ratiosa
(95% CI)
14
1.2 (0.53.0)
49
2.1 (1.23.7)
Adjustment for
potential
confounders
Comments
Smoking,
residential area
(urban, suburban,
rural), education,
socioeconomic
status
Only 7% of men
reported cooking for
the family and thus
data were not shown.
In women, stirfrying, frying and
deep-frying fumes
emitted were
statistically
significantly
associated with risk
for ADC but not
SCC or small-cell
carcinoma. Longterm residence near
industrial district
was associated with
lung cancer risk,
especially in women.
Risk for lung cancer
was significantly
increased if the
kitchen did not have
a fume extractor.
ADC, adenocarcinoma; COPD, chronic obstructive pulmonary disease; LPG, liquid petroleum gas; NG, not given; PAH, polycyclic aromatic hydrocarbons; PM10,
particulate matter 10 m; SCC, squamous-cell carcinoma; yrs, years
a
p-value reported if confidence interval was not specified
Characteristics of
Reference,
study period
159
statistically significantly associated with duration of use of the following: kangs

(especially directly-heated ones), coal stoves or floor/wall heating by pipes from the
cooking stove.
[The Working Group noted that female lung cancer cases and controls included in the
study by Xu et al. (1989) were also included in the study by Wu-Williams et al. (1990).
Assessment of cooking practices was relatively limited in these two studies. It was also
noted that both studies were large and well-conducted, but assessment of coal-related
exposure may have been hampered by lack of exposure contrasts, i.e. coal exposures were
mainly compared with exposure to biomass fuels possibly leading to an underestimation
of the effect. This comment also applies to Wang et al. (1996) and Zhou et al. (2000).]
Dai et al. (1996) conducted a study of 120 nonsmoking women with adenocarcinoma
of the lung and an equal number of nonsmoking population controls; all were long-term
residents of Harbin. After adjustment, risk for adenocarcinoma was positively and
significantly associated with several metrics of domestic coal use, including having a coal
stove in the bedroom, having coal heating and long-term residential exposure to coal
dust. [The Working Group noted that confidence intervals in this report were wide,
reflecting the relatively small number of subjects.]
In Shenyang, Wang et al. (1996) compared the experiences of 135 female lifetime
nonsmokers diagnosed with primary lung cancer with those of an equal number of
nonsmoking population control women. Of the lung cancers included, 57.2% were
diagnosed pathologically or cytologically, 54.5% of which were adenocarcinoma. In
bivariate analysis, but not multivariable analysis, exposure to coal smoke during cooking
was positively and significantly associated with lung cancer risk. Other metrics of coal
use were not associated with risk. [The Working Group noted that this study was small
and the exposure was limited to dichotomized (no/yes) assessment. The specific variables
included in the multivariable analysis were not described. The validity of a diagnosis of
adenocarcinoma is questionable because the authors stated that determining the
histological cell type was based on relevant medical records, chest X-rays, CT films, and
cytological and histological slides.]
Two studies in the Kaohsiung area, Taiwan, were reported by Ko et al. (1997) and Le
et al. (2001) (described in detail in the monograph on high-temperature frying).
Compared with those who did not cook or cooked with gas, the odds ratio for lung cancer
was near unity for those who cooked with coal (odds ratio, 1.1; 95% confidence interval
[CI], 0.43.6) (Ko et al., 1997).
In a subsequent report (Le et al., 2001), the relationship between cooking fuel and risk
for lung cancer was examined separately by lung cancer cell type. In the analysis which
included 82 squamous-cell and small-cell lung cancers and 129 controls, the odds ratio
was 1.2 for use of coal and/or anthracite (95% CI, 0.53.0) when compared with women
who did not cook or used gas for cooking. In contrast, the risk for adenocarcinoma of the
lung (158 cases, 262 controls) increased in relation to use of coal (odds ratio, 2.1; 95% CI,
1.23.7). Tobacco smoking, residential area, education and social class were adjusted for
160
in the analysis. [The Working Group noted that information on duration of wood and coal
use was not reported in these two studies.]
Zhou et al. (2000) published another report using a subset of women from Wang et
al. (1996) in Shenyang. Specifically, 72 women (52 nonsmokers) who had been
diagnosed with adenocarcinoma of the lung between 1991 and 1995 were compared with
an equal number of control women (49 of whom were nonsmokers). There was no
association between coal burning and risk for lung cancer. [The Working Group noted
that most of the lung cancer cases and controls included in the analysis by Zhou et al.
(2000) were already in the report by Wang et al. (1996). Unadjusted odds ratios were
reported. This study was small and the confidence intervals were very wide.]
Kleinerman et al. (2002) conducted a casecontrol study of lung cancer in relation to
household use of coal and biomass fuel in two rural prefectures of Gansu Province,
China; about 25% of subjects used coal and most coal users reported using bituminous
coal. Of the patients, 846 were deemed to have lung cancer by an expert review panel,
and 1740 controls were frequency-matched to patients on gender, age and prefecture of
residence. Multivariable logistic regression analyses were conducted separately for men
and women. In men, the risk for lung cancer was associated positively and significantly
with use of coal (versus use of biomass), the amount of coal used and the percentage of
time that coal was most frequently used as fuel in the past 30 years. None of these metrics
for coal versus biomass exposure were significantly associated with the risk for lung
cancer in women.
(ii) Xuan Wei County, Yunnan Province
Rural Xuan Wei County, Yunnan Province, is impacted by indoor air pollution due to
traditionally used fuel types: smoky coal (bituminous coal), smokeless coal
(anthracite) and wood. The great majority of residents were farmers, and residential
stability was very high. There have been few stationary or mobile sources of outdoor air
pollution.
Liu et al. (1991) and He et al. (1991) reported a casecontrol study in Xuan Wei that
included 110 incident cases of lung cancer (56 men, 54 women) identified in regional
hospitals/clinics in 198586, and 426 population controls (224 men, 202 women). Cases
and controls were matched on gender, age, occupation (all were farmers) and village of
residence. [Matching on village of residence overmatched on type of indoor fuel and type
of home.] Smoky coal was used at least four times more often than wood in this
population. While duration and frequency of cooking food were significantly associated
with risk for lung cancer in an exposureresponse manner after adjustment for other risk
factors, this precluded assessment of risk for lung cancer in relation to specific fuel types.
[Although the analyses were duplicated in both studies, the Working Group noted
discrepancies in the results. The instability of the risk estimates is demonstrated with the
different choice of category cut-points in both studies. The Working Group also noted that
inferences from these two studies are limited by the relatively small sample size and the
uncertainty of the significance of the reference group.]
161
Another casecontrol study conducted among female farmers in Xuan Wei (Lan et
al., 1993) was based on 139 incident female lung cancers that were diagnosed between
1988 and 1990 and 139 age-matched controls. Of the lung cancer cases, 55 (39.6%) were
diagnosed cytologically/ pathologically. All cases and controls were current nonsmokers
but all were former smokers. Use of smoky coal from the Laibin mine was significantly
associated with risk for lung cancer by frequency and duration of use. [Although all
participants were former smokers, the amount of past smoking was not specified nor was
it considered as a potential confounder in the analysis.]
Lan et al. (2000) carried out a population-based casecontrol study of 122 cases and
122 controls. This study was designed to evaluate the relationship between genetic
susceptibility and lung cancer. Controls were individually matched to cases by sex, age,
village and type of fuel currently used for cooking and heating. Compared with subjects
whose cumulative smoky coal use was less than 130 tonnes, subjects who used more than
130 tonnes of smoky coal had a 2.4-fold increased risk for lung cancer (95% CI, 1.34.4;
71 exposed cases; adjusted for total smoky coal use without ventilation, packyears of
smoking, chronic obstructive pulmonary disease and family history of lung cancer). [The
Working Group noted that even with matching on fuel type, the study observed a
cumulative effect of smoky coal.]
(iii) Central China excluding Xuan Wei
In Chengdu, Sichuan Province, Huang et al. (1992) performed a casecontrol study of
135 pre-invasive lung cancer patients drawn from three provincial hospitals and
135 healthy controls individually matched to cases on gender and age. Controls were
enlisted from persons coming to the same three hospitals for routine health check-ups and
matched on residential area. The primary goal of this study was to assess dietary risk
factors for lung cancer. Burning coal indoors was associated with a statistically
significantly higher risk for lung cancer than not burning coal indoors (Odds ratio, 1.59;
95% CI, 1.012.07). [It is unclear what the exposure of the reference group was, but it
may have been biomass.]
Shen et al. (1998) conducted a casecontrol study in women in Nanjing that included
70 never-smoking lung cancer patients and 70 healthy community controls, matched 1:1
with cases on gender, age, neighbourhood and occupation. Subjects appear to have been a
subset of those in Shen et al. (1996). Use of solid fuel (versus non-solid fuel) and of coal
stoves was assessed, together with cooking-related metrics and other covariates. Use of a
coal stove for heating was marginally significantly associated with lung cancer risk (odds
ratio, 1.78; 95% CI, 0.794.02, p=0.08). [The Working Group noted several limitations in
this study. The report lacked details regarding the study design (e.g. response rate),
characteristics of the study population (e.g. gender distribution, active smoking history)
and covariates included in the statistical models.]
Zhong et al. (1999) conducted a casecontrol study in Shanghai that included a total
of 649 women who had been diagnosed with incident lung cancer during 199294 and
675 population controls. Subjects who had smoked at least one cigarette a day for at least
162
6 months (145 cases, 74 controls) were excluded from the analyses. Thus, results were
based on 504 cases and 601 controls who were lifetime nonsmokers. Seventy-seven per
cent of the lung cancers were diagnosed histologically or cytologically and 76.5%
(n=296) of these were adenocarcinoma. The analysis explored cooking-related
associations in more detail than those related to fuel. In multivariable logistic regression
models, coal and gas use versus coal only was not associated with risk for lung cancer
(odds ratio, 0.92; 95% CI, 0.631.35) but kitchen smokiness during cooking was
positively and significantly associated with risk for lung cancer in a doseresponse
manner. [The Working Group noted that the contrast was between coal and gas versus
coal only and therefore does not address the risk associated with exposure to coal.]
(iv) Southern China
Koo et al. (1983) reported a casecontrol study in Hong Kong Special Administrative
Region that included 200 women hospitalized with lung cancer and 200 community
controls matched on gender, age (5 years), residential district and type of housing. Data
were obtained by in-person interview using a semi-structured questionnaire and taking a
life-history approach. The investigators assessed use and duration of use of biomass fuels,
coal, kerosene, LPG and gas. Only 12 of 400 subjects (3%) used coal as cooking fuel
this proportion was 1.5% in cases and 4.5% in controls. The few subjects who had ever
used coal had used it only when they had lived in mainland China but discontinued its use
when they moved to Hong Kong Special Administrative Region. Unadjusted relative
risks were calculated for matched and unmatched data. Use of coal was inversely and
non-significantly associated with the risk for lung cancer (odds ratio, 0.32; p=0.15). [The
Working Group noted that, in view of the few subjects using coal (three cases, nine
controls), this study probably did not allow a very informative test of lung cancer risk in
relation to coal use.]
Liu et al. (1993) conducted a casecontrol study in Guangzhou during 19831984
that included 316 incident lung cancer cases (224 men, 92 women) and 316 hospital
controls individually matched by gender, age (2 years), residential district and date of
diagnosis. Controls were not chosen from the Tumor Hospital or Chest Hospital and those
with respiratory and coronary heart disease were further excluded. Analyses using
multivariable conditional logistic regression models adjusted for education, occupation,
occupational exposure, history of tuberculosis, chronic bronchitis, family history of
cancer, smoking, living area and passive smoke (in women only) were stratified by
gender. Use of coal for cooking was the reference category (odds ratio, 1.0) for examining
the risk for lung cancer associated with other cooking fuels (gas, wood); 89% (200/224)
of men and 88% (81/92) of women had ever used coal for cooking.
Du et al. (1996) reported another casecontrol study in Ghangzhou. Cases were
849 deceased lung cancer patients (566 men, 283 women) who died in 1985 and controls
were persons who died of causes unrelated to lung cancer, matched with cases on gender,
age (2 years) and residence. A standardized questionnaire was used to interview next of
kin of the lung cancer patients [and presumably the controls]. Lung cancer risk in women
163
was positively and significantly associated with smoking and exposure to coal fumes.
Risk in men was significantly associated only with smoking.
Luo et al. (1996) reported a casecontrol study in Fuzhou that included 102 lung
cancer cases (78 men, 24 women) and 306 community controls, matched with cases on
gender, age and ethnicity. Data were analysed using conditional logistic regression, and
separate analyses were conducted for squamous-cell carcinoma and adenocarcinoma. The
presence of smoke in the living room during cooking with coal was positively and
statistically significantly associated with risk for lung cancer (odds ratio, 7.6; 95% CI,
3.715.7 for all lung cancers; odds ratio, 14.1 [95% CI, 11.816.4]; p=0.026 for
squamous-cell carcinoma; odds ratio, 6.0 [95% CI, 4.97.1]; p=0.002 for
adenocarcinoma). [The Working Group noted that smoking was significantly associated
with the risk for squamous-cell carcinoma, but only moderately for adenocarcinoma (not
statistically significant).]
(v) Taiwan
Ger et al. (1993) conducted a casecontrol study in Taipei that included 131 primary
lung cancers (92 men, 39 women) identified between 1990 and 1991. All were
histologically confirmed (59 squamous-cell/small-cell carcinoma, 72 adenocarcinoma).
Two control groups were interviewed: 262 hospital controls were matched to cases on
sex, date of birth (5 years), date of interview and insurance status whereas
262 neighbourhood controls were matched to cases on age, sex and residence of the case
at the time of diagnosis. When lung cancer cases were compared with neighbourhood
controls, use of coal for cooking was unrelated to risk for adenocarcinoma (odds ratio,
0.56; 95% CI, 0.201.54; adjusted for matching factors; seven exposed cases), but was
strongly associated with risk for squamous-cell/small-cell carcinoma (odds ratio, 10.00;
95% CI, 2.1945.61; adjusted for matching factors; 10 exposed cases). In multivariable
analysis, use of coal as a cooking fuel remained a significant risk factor for squamouscell/small-cell carcinomas. The magnitude of effect was smaller but also statistically
significant when cases were compared with hospital controls. [The Working Group noted
that this study included few female nonsmoking lung cancer patients: 48 cases compared
with 229 controls (111 hospital controls, 118 neighbourhood controls) were nonsmokers.
It is not clear whether the results for coal burning related to usual, past or current
practices. The prevalence of coal burning differed substantially between the
neighbourhood controls who were matched to the adenocarcinoma (14.6%) or the
squamous-cell lung cancer cases (1.7%). The corresponding figures for the hospital
controls selected for adenocarcinoma and squamous-cell lung cancer patients were 7.6%
and 5.1%, respectively. Thus, the significantly increased risk for squamous-cell/small-cell
cancers associated with coal burning may be related to differences among the control
subjects. Furthermore, the Working Group also noted that a higher percentage of proxy
interviews was conducted for cases (21%) than controls from the neighbourhood (17%)
or hospitals (12%), and that matching on location of residence may have influenced effect
estimates for fuel type due to overmatching.]
164
The study by Le et al. (2001) included lung cancer patients who had been diagnosed
between 1993 and 1999. Women diagnosed with squamous-cell or small-cell carcinoma
(n=84) or adenocarcinoma of the lung (n=162) and corresponding controls (n=407) were
included in the analysis. Women with other lung cancer cell types (n=45 cases) were
excluded. Risk for lung cancer was associated with type of cooking fuel: women who
used coal or anthracite as a cooking fuel versus those who used gas or no fuel had a
significantly increased risk for adenocarcinoma (odds ratio, 2.1; 95% CI, 1.23.7;
49 exposed cases) but not for squamous- or small-cell carcinoma (odds ratio, 1.2; 95% CI,
0.53.0; 14 exposed cases).
A third study by this research group (Ko et al., 2000) addressed lung cancer and
cooking in some detail, but did not specifically address fuel or fuel smoke. This study is
described in the monograph on high-temperature frying.
(b)
Casecontrol studies outside China (see Table 2.2)
Wu et al. (1985) conducted a casecontrol study among white women in Los Angeles
County, CA, USA. One hundred and forty-nine cases of adenocarcinoma and 71 cases of
squamous-cell carcinoma of the lung identified from population-based tumour registry
and a group of age-matched neighbourhood controls were interviewed by telephone. No
information on the number of years that coal was used was available. Exposure to burning
coal (used for heating or cooking) during the majority of childhood and teenage years
increased the risk for lung cancer: the odds ratio for adenocarcinoma was 2.3 (95% CI,
1.05.5) and that for squamous-cell carcinoma was 1.9 (95% CI, 0.56.5) after adjusting
for tobacco smoking. An increased risk for lung adenocarcinoma was seen when stratified
by smoking status (odds ratio for nonsmokers, 3.2; 95% CI, 0.911.8; odds ratio for
former smokers, 4.3; 95% CI, 1.017.8; odds ratio for current smokers, 9.5; 95% CI, 2.1
41.9). Multivariable logistic regression that adjusted for personal smoking, childhood
pneumonia and -carotene intake produced similar results.
Sharpe et al. (1989) conducted a casecontrol study of renal-cell carcinoma in
Montreal, Canada. One hundred and sixty-four histologically confirmed cases of renalcell carcinoma, diagnosed between 1982 and 1987 in four hospitals in the Montreal area,
who responded to a mailed questionnaire were included in this analysis. One hundred and
sixty-one controls without urinary tract tumours who were identified from urology files
and who were matched to cases on sex, date of birth and urologist were also included in
the analysis. Those who had been exposed indoors to burning coal had a non-statistically
significantly increased risk for lung cancer compared with subjects who were not
exposed. For those who lived in a house where coal was used as a fuel but did not handle
it, the odds ratio was 1.07 (95% CI, 0.581.96; 53 exposed cases). The odds ratio for
subjects who had handled coal only domestically was 1.41 (95% CI, 0.762.62;
56 exposed cases). [The covariates included in the multivariable logistic regression
models were not specified. Four hundred and three cases were identified but only 168 cases
Table 2.2. Casecontrol studies of lung cancer and use of coal outside China
Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Wu et al.
(1985),
Los Angeles,
USA,
198182
220 white women

diagnosed with lung
cancer (149 ADC,
71 SCC) were
identified from the
tumour registry
Telephone
interview
using a
structured
questionnaire
Use of coal for

heating/cooking in majority
of childhood and teenage
yrs
SCC
ADC
Nonsmoker and
unexposed to coal
Nonsmoker
Former smoker
Smoker
220 healthy white

women matched by
age (5 yrs) and
neighbourhood
Malats et al.
(2000),
Brazil,
France,
Germany,
Italy, Poland,
Romania,
Russia,
Sweden,
[period not
specified]
122 nonsmoking
cases (17 men, 105
women) diagnosed
with histologically
or cytologically
confirmed lung
cancer
In-person
interview
using a
standard
questionnaire
Indoor pollution from

coal (>17 yrs)
No. of
exposed
cases
Odds ratios (95%

CI)
NG
NG
NG
1.9 (0.56.5)
2.3 (1.05.5)
1.0 (reference)
NG
NG
NG
3.2 (0.911.8)
4.3 (1.017.8)
9.5 (2.141.9)
NG
0.4 (0.11.1)
Adjustment for
potential
confounders
Comments
Tobacco smoking
The results did not

change after adjusting for
personal smoking,
childhood pneumonia
and -carotene.
Age, gender, centre
Study period not

specified
Reference,
study
location,
study period
121 nonsmoking
controls (34 men, 87
women) identified
from the Swedish
population registry
or the same hospitals
as cases (admitted
for non-tobacco
related diseases)
165
166
Table 2.2 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Gupta et al.
(2001),
Chandigarh,
India,
199597
265 histologically
confirmed lung
cancer paitents
(235 men,
30 women)
In-person
interview
using a
questionnaire
Yrs of exposure to coal vs

none
For cooking
Men
145 yrs
>45 yrs
Women
145 yrs
>45 yrs
For heating
Men
145 yrs
>45 yrs
Women
145 yrs
>45 yrs

(435 men,
90 women) matched
by age and sex
No. of
exposed
cases
Odds ratios (95%

CI)
Adjustment for
potential
confounders
Age, smoking,
education,
cumulative tobacco
consumption
14
23
0.72 (0.361.46)
0.88 (0.491.57)
2
6
0.63 (0.113.63)
1.52 (0.336.98)
14
42
1.06 (0.512.17)
1.20 (0.751.91)
2
5
0.96 (0.156.26)
1.12 (0.264.84)
Comments
Reference,
study
location,
study period
Table 2.2 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
No. of
exposed
cases
Odds ratios (95%

CI)
Adjustment for
potential
confounders
Comments
Lissowska et
al. (2005),
Central and
Eastern
Europe and
United
Kingdom,
1998-2002
2861 cases (2205

men, 656 women)
from 15 hospitals
In-person
interview
using a
structured
questionnaire
Ever used coal only for

cooking
Ever used coal only for
heating
872
1.13 (0.941.38)
772
1.08 (0.891.31)
Age, sex, education,

tobacco pack-yrs,
centre
Coal was the most

common type of fuel
used for heating (50%) or
cooking. (44%); controls
were hospital-based
except in Warsaw,
Poland and Liverpool,
United Kingdom, where
they were populationbased. The authors could
not rule out that the
associations were due to
some mixed (wood and
coal) exposures, because
subjects provided their
principal fuel (if they
used mainly coal but
some wood, they would
have indicated coal).
3118 hospital and

population-based
controls (2305 men,
813 women)
matched by age, sex
and area; persons
with cancer or
tobacco-related
diseases were
excluded
Reference,
study
location,
study period
ADC, adenocarcinoma; CI, confidence interval; NG, not given; SCC, squamous-cell carcinoma; yrs, years
167
168
and matched controls agreed by telephone to receive a mailed questionnaire. Of those

who received a mailed questionnaire, 164 cases and 161 controls responded.]
Malats et al. (2000) conducted a multicentre casecontrol study in eight countries
(Brazil, France, Germany, Italy, Poland, Romania, the Russian Federation, Sweden) that
primarily investigated the interaction between glutathione S-transferase (GST) M1 and T1
genotypes and environmental risk factors in 122 lung cancer cases (14% male) and
121 controls (58 population-based, 63 hospital-based). All cases were confirmed by
histology or cytology. Information on exposure was obtained through personal interview
using a standardized questionnaire. Indoor air pollution from the use of wood or coal for
cooking or heating was dichotomized according to the median number of years of
exposure to both sources of combustion among controls. Using coal for more than
17 years (versus less than 17 years) was not associated with an increased risk for lung
cancer (odds ratio, 0.4; 95% CI, 0.11.1). [The Working Group noted that there could be
possible confounding by smoking because nonsmokers were defined as occasional
smokers (up to 400 cigarettes in a lifetime) and never smokers. The Working Group also
noted the heterogeneous background of the study subjects and the fact that controls were
not matched by age and sex may present difficulties in the interpretation of the results.
Furthermore, the crude exposure indices used (i.e. <20 years of fuel use) did not enable a
good assessment of the exposureresponse relationship.]
Two hundred and sixty-five histologically confirmed, incident cases of lung cancer
(235 men, 30 women) who were seen at the Department of Pulmonary Medicine,
Chandigarh, India, and 525 age- and sex-matched controls (435 men, 90 women) who
were selected among visitors and attendants of the patients were recruited in a case
control study conducted between January 1995 and June 1997 (Gupta et al., 2001).
Trained interviewers collected information on demographic factors, lifetime tobacco
smoking history, detailed occupational history and residence. Exposure to indoor air
pollution was assessed on the basis of the type of fuel used for cooking or heating and the
number of years spent in that household. Unconditional logistic regression models
stratified by gender were adjusted for age, cumulative tobacco consumption and
education. The odds ratio for exposure to indoor air pollution as measured by 45 or more
years of exposure to coal for heating was 1.20 (95% CI, 0.751.91; 42 exposed cases) for
men and 1.12 (95% CI, 0.264.84; 5 exposed cases) for women. The odds ratio for the
use of coal for cooking for 45 or more years was 0.88 (95% CI, 0.491.57; 23 exposed
cases) for men and 1.52 (95% CI, 0.336.98; six exposed cases) for women.
Lissowska et al. (2005) conducted a multicentre casecontrol study during 1998
2002 in six eastern and central European countries (Czech Republic, Hungary, Poland,
Romania, the Russian Federation and Slovakia) and the United Kingdom to examine the
association between burning coal and unprocessed biomass and the incidence of lung
cancer in men and women. Cases included 2861 histologically or cytologically confirmed
incident lung cancer patients (2205 men, 656 women) who were identified through the
main hospitals in the 15 participating centres. A total of 3118 (2305 men, 813 women)
hospital-based (13 centres) and population-based controls (two centres), who were
169
frequency-matched to cases by geographic area, 5-year age group and gender, were
studied. A common structured questionnaire was used to collect information on risk
factors for lung cancer such as active and passive tobacco smoking, occupational history,
lifetime residential history and fuel use at every residence of at least 1 year. The study
examined risk patterns in relation to modern non-solid fuels (gas, kerosene and electricity)
versus traditional solid fuels (coal and biomass, mainly wood) used for cooking and
heating after adjusting for centre, age, gender, education and tobacco packyears. The
odds ratios for exposure to coal were 1.13 (95% CI, 0.941.38; 872 exposed cases) for
cooking and 1.08 (95% CI, 0.891.31; 772 exposed cases) for heating. [The Working
Group noted many strengths in this large multicentre casecontrol study which used a
common, standardized study protocol and questionnaire and collected information on
lifetime fuel use and relevant covariates from in-person interviews with the study
participants. The response rate was high in both cases and controls (>90%). Although the
analysis was very thorough, exposureresponse analyses by type of solid fuels (separately
for coal and wood) were not provided.]
(c)
Cohort studies (see Table 2.3)
Lan et al. (2002) followed a cohort of 21 232 farmers (11 168 men, 10 064 women)
in China retrospectively from 1976 to 1992. The farmers were born between 1917 and
1951 into homes in which smoky coal and unvented stoves were used; however,
17 184 of these subjects (80.9%) later changed permanently to the use of vented stoves
with chimneys. (The Chinese Government offered a small subsidy for the purchase of
stoves with chimneys in 1976). Nearly all subjects were born in Xuan Wei (about 1% of
men and 13% of women were born outside the immediate study area). In multivariable
Cox proportional hazard models stratified by gender, in which stove improvement,
duration of cooking (for women only) and duration of smoking (for men only; only 0.9%
of women had ever smoked) were treated as time-dependent covariates, stove
improvement was associated with a statistically significant reduction in the incidence rate
of lung cancer (hazard ratio for men, 0.59; 95% CI, 0.490.71; hazard ratio for women,
0.54; 95% CI, 0.440.65). In both men and women, duration of cooking food was also
positively and significantly associated with an increased risk for lung cancer, as was the
daily average number of hours spent indoors through to the age of 20 years. [The
Working Group noted that although fewer men than women cooked food, the
significantly protective effect of stove improvement was of similar magnitude in both
genders, which suggests that the protective effect of stove improvement related largely to
the reduction of cooking fuel smoke.]
(d)
Ecological studies
Rural Xuan Wei County, Yunnan Province, China, is impacted by indoor air pollution
due to traditionally used fuel types: smoky coal (bituminous coal), smokeless coal
(anthracite) and wood. The great majority of residents were farmers, and residential stability
170
Table 2.3. Cohort studies of use of coal and cancer in China

Cohort
description
Exposure
assessment
Exposure categories
Lan et al.
(2002)
Xuan Wei,
Yunnan,
197692
21 232 farmers,
born 191751
into homes with
unvented smoky
coal stoves;
11 168 men,
10 068 women;
total 313 579
personyrs; all
subjects were
lifelong smoky
coal users.
Did or did not

install chimneys
on previously
unvented stoves,
as ascertained by
structured
questionnaire.
In 15 homes,
indoor PM10 and
benzo[a]pyrene
levels were
compared during
coal burning with
chimneys blocked
and open.
Men and women with and

without chimney
installation (stove
improvement)
Before chimney
installation
After installation
After chimney
installation
versus before
Men
Women
Cooking duration (yrs)
vs 20 yrs
Men
>20
Women
2029
3039
40
Born outside study area
Men
Women
No of
exposed
cases/deaths
Relative risk (95%

CI)
Adjustment for
potential
confounders
Comments
Age-adjusted lung
cancer incidence per
100 000 personyrs
554
All subjects: lung

cancer in spouse
and first-degree
relatives, house
and family size,
COPD and
tuberculosis
history, time
indoors in early
life, annual coal
consumption,
birthplace,
education, birth
cohort, cooking
history; men only:
smoking,
occupation
Analysed with
Cox models, time
axis = age, timedependent
covariates for
stove
improvement,
smoking and
cooking; mean
indoor levels of
PM10 and
benzo[a]pyrene
(g/m3) in 15
homes: chimney
blocked, 2080
and 1.66;
chimney open,
710 and 0.25
383
NG
NG
0.59 (0.490.71)
0.54 (0.440.65)
1.42 (1.051.93)
NG
NG
NG
NG
NG
NG
1.38 (0.872.20)
1.79 (1.092.93)
3.08 (1.805.26)
0.34 (0.111.05)
0.49 (0.350.67)
Reference,
study location,
study period
Table 2.3 (contd)

Cohort
description
Exposure
assessment
Exposure categories
Wu et al.
(2004),
Chia-Yi city,
Taiwan,
19992000
Subjects for the

nested case
control study
were selected
from 32 466
women who
underwent Pap
smear screening
in Chai-Yi City;
19 yrs of age.
In-person
interview using
structured
questionnaire
Fuel used for cooking

vs. gas
While 2040 yrs of age
Coal and gas
Coal
While >40 yrs of age
Coal/coal and gas
No of
exposed
cases/deaths
Relative risk (95%

CI)
3
21
0.65 (0.143.05)
2.09 (0.865.10)
1.53 (0.1714.19)
Adjustment for
potential
confounders
Comments
Age, educational
levels, cigarette
smoking, number
of prior Pap
smears, age at first
intercourse, work
as a professional
chef
100 women with

biopsy
confirmed
lesions CIN2
who completed a
questionnaire.
197 population
controls were
randomly
selected from
women who
lived in the same
area as cases and
had negative Pap
smear results.
Reference,
study location,
study period
CI, confidence interval; CIN, cervical intraepithelial neoplasia; COPD, chronic obstructive pulmonary disease; Pap, Papanicolaou; PM10, particulate matter 10 m; yrs,
years
171
172
was very high. There have been few stationary or mobile sources of outdoor air pollution.
In a 1982 survey of all households in 11 of 20 Xuan Wei communes, the proportion of
households that used smoky coal before 1958 was highly correlated with communespecific mortality from lung cancer from 1973 to 1975 (r=0.82; p=0.002; Mumford et al.,
1987; Chapman et al., 1988). Also during 197375, average annual lung cancer mortality
was 34.7 per 100 000 in 14 communes that had smoky coal mines and 4.1 per 100 000 in
six communes that did not [p=0.015] (Mumford et al., 1987).
Tao et al. (1991), in an ecological study from Shanghai, China, showed that men in a
group that used coal indoors had 1.44 times higher mortality from lung cancer than a
group that used coal-gas indoors and 30.4% of total lung cancer deaths in the former
group could possibly be attributed to coal use indoors. The authors noted that this was a
preliminary exploration.
(e) Aggregate analyses of studies of indoor air pollution and lung cancer
in China
Gao (1996) reviewed risk factors for lung cancer in nonsmoking Chinese women
using evidence from published casecontrol and cohort studies. The major conclusions
were as follows: (i) the proportion of lung cancer cases that cannot be attributed to
smoking varies by region in China; (ii) coal burning in poorly ventilated houses may
contribute to 1020% of the reported lung cancer cases; (iii) the volatile emissions
generated by heating rapeseed and soya bean oil may contribute to an increased risk for
lung cancer, especially among Chinese women who heat these oils to high temperatures
during cooking; (iv) there is a consistent positive association between personal history of
non-malignant lung disease and risk for lung cancer; this may be especially important in
view of the heavy burden of such respiratory diseases in China; (v) infrequent
consumption of fresh vegetables and fruit, especially those rich in carotene and vitamin C,
increases the risk for lung cancer; (vi) although occupational factors increase the risk for
lung cancer in highly industrialized cities, their contribution to the population-attributable
risk for lung cancer is relatively small; (vii) observed effects of environmental tobacco
smoke on lung cancer are ambiguous and inconsistent in casecontrol studies; (viii)
outdoor air pollution is not unequivocally associated with lung cancer risk, as observed
among a cohort of nonsmokers in Shanghai; and (ix) the menstrual histories of women
warrant further study as a potential risk factor for lung cancer.
Zhao et al. (2006) conducted a meta-analysis of casecontrol studies in China that
evaluated aggregate associations of lung cancer with indoor air pollution from coal
consumption for heating and cooking, exposure to coal dust, exposure to cooking oil
fumes and exposure to environmental tobacco smoke. Although the authors could not rule
out the possibility of publication bias, they concluded that their meta-analysis confirmed
the association of indoor air pollution with lung cancer in the Chinese population. Using a
random-effects model, coal consumption through heating and cooking was associated
with an increased risk for lung cancer (odds ratio for both sexes; 2.66; 95% CI, 1.395.07;
odds ratio for women only, 1.83; 95% CI, 0.625.41). [The Working Group noted that
173
this analysis, together with previous publications, indicates joint contributions of coal
smoke and cooking smoke to indoor air pollution but does not quantify their relative
contributions. It is unclear whether exposure to coal dust represents an occupational
exposure or serves as a proxy measure for coal smoke.]
2.1.2
Cancer of the salivary glands
All residents of urban Shanghai aged 2075 years who were newly diagnosed with
cancer of the salivary glands (International Classification of Diseases [ICD]-9, 142)
during the period from 1 January 1988 to 28 February 1990 were eligible to participate in
a casecontrol study (Zheng et al., 1996). A total of 44 eligible cases (19 men, 25 women)
were identified from the Shanghai population-based cancer registry during the period in
question. Of all identified cases, 41 (93.2%) were interviewed and three other cases could
not be located or were too ill to be interviewed. Adenocarcinoma and adenoid cystic
carcinoma were the two major cancers diagnosed and accounted for 46.3% and 24.4% of
total cases, respectively. Controls were randomly selected from the general population of
urban Shanghai by use of a frequency-matching method in accordance with the sexage
distribution of cases of all head and neck cancers reported to the Shanghai cancer registry
during 198586. A total of 462 controls were selected, among whom 414 (89.6%) were
interviewed. Information on demographic factors, tobacco and alcohol consumption,
dietary habits, lifetime job history, occupational and household exposures and previous
disease history was collected from each study subject. After adjusting for gender, age and
income, the odds ratio was 1.6 for the use of coal for cooking (95% CI, 0.55.6;
38 exposed cases). [The Working Group noted that the sample size was relatively small.]
2.1.3
Cancer of the oesophagus
A nested casecontrol study within a cohort of workers of an ironsteel complex was

carried out in Anshan, China, to evaluate the relationship of oesophageal cancer with
occupational exposure to silica and other dusts, taking lifestyle exposure factors into
consideration (Pan et al., 1999). A total of 141 men who were confirmed as having died
from oesophageal cancer during 198088 were selected as cases. Two male controls were
randomly selected and matched on age (within 5-year age groups) for each case from the
death registry file of the company over the same period. The first control group consisted
of workers who had died of diseases other than cancer or respiratory or digestive diseases
(non-cancer controls) and the second control group consisted of workers who had died of
cancers other than of the stomach or respiratory system (cancer controls). The number of
cases whose relatives could be interviewed was 125 (88.7%). Each of the two groups of
controls consisted of the same number of subjects (125) as the cases. Either the wife or a
first-degree relative was interviewed for 95.2% of cases and 96.0% of controls.
Information was obtained for smoking, drinking, diet, method of cooking and heating in
the household and lifetime occupational history. A job-exposure matrix was applied to
174
lifetime job histories and dust exposures were categorized into no exposure, refractory
silica dust, other silica dust, iron dust, founding dust, coal dust, wood dust, welding dust
and other dusts. The results were presented for both controls combined since the results of
the analysis using two control groups were very similar. In a univariate analysis,
occupational exposure to silica dust, other silica dust and any dust, domestic exposure
to coal heating, cooking with coal, heavy smoking, alcohol drinking and consumption of
salted vegetables were shown to be risk factors. Central heating, cooking with gas and
consumption of fish, meat, eggs and fruit were found to be protective factors. In
multivariate analysis, the odds ratio was 2.01 for cooking with coal (95% CI, 1.093.70).
Exposure to silica dust for 25 years and more and cooking with coal for 20 years and
more gave the highest risk: the odds ratio for the former was 8.87 (95% CI, 1.6747.08)
and that for the latter was 2.48 (95% CI, 1.294.78). [The Working Group noted that the
findings were among long-term male steelworkers and not the general population, thus
making extrapolations to other groups difficult. Comparison of deceased cases with
deceased controls and the use of information obtained from relatives, not from subjects
themselves, are the weakness of the study.]
2.1.4
Cancer of the nasal cavity, paranasal sinuses and middle ear
Cases of cancer of the nasal cavity, paranasal sinuses and middle ear (ICD-9, 160),
aged 2075 years, who had been newly diagnosed during the period from 1 January 1988
to 28 February 1990 were eligible to participate in a casecontrol study (Zheng et al.,
1992). A total of 63 cases were identified from the Shanghai population-based cancer
registry during the study period. Of these, 60 cases (39 men and 21 women) were
interviewed and three cases (4.8%) could not be located; 51 cases (85%) were
pathologically diagnosed. Controls were randomly selected from the general population
of the Shanghai urban area by use of frequency-matching in accordance with the sexage
distribution of incident cases of oral, pharyngeal, laryngeal and nasal cancers reported to
the Shanghai cancer registry in 198586. A total of 462 controls were identified and 414
(89.6%) were interviewed. Information on demographic factors, tobacco and alcohol
consumption, dietary habits, occupational and household exposures and previous disease
history was collected. Unconditional logistic regression was used to adjust for
confounders and to calculate adjusted odds ratios. After adjusting for age, the odds ratio
for coal used as cooking fuel was 1.1 (95% CI, 0.52.6; 53 exposed cases).
2.1.5
Cancer of the cervix (see Table 2.3)
Wu et al. (2004) conducted a nested casecontrol study of 100 women with cervical
cancer and 197 population controls selected from a cohort of 32 466 women who
underwent Papanicolaou (Pap) smear screening in Chai-Yi City, Taiwan, China. Use of
coal compared to gas was positively, although not significantly, associated with the risk
for cervical cancer (odds ratio, 2.09; 95% CI, 0.865.10; 21 exposed cases).
2.1.6
175
Cancer of the kidney (renal-cell carcinoma) (see Table 2.4)
Sharpe et al. (1989) conducted a hospital based casecontrol study in Montreal,

Canada, that included 164 cases of renal-cell carcinoma (62% men) identified
retrospectively from medical records and 161 age- and sex-matched controls who
attended the same urologists; all were given mailed questionnaire with telephone followup. Cases were survivors and had less advanced disease. Occupational exposure to
burning coal showed a doseresponse relationship with renal- cell carcinoma by duration
in months (p<0.05) Intensity of exposure, assessed by combining domestic and
occupational exposures in a hierarchical ordinal manner, also showed a doseresponse
trend (p<0.025). Multivariable analysis adjusting for sex and age (smoking was not a
statistically significant confounder and was removed from final model) showed that
handling coal in a setting where it was being burned between the ages of 10 and 24 years
was a risk factor. [Results on the duration of occupational exposure or the intensity of
exposure (combining domestic and occupational) were not reported. In general, the results
were not presented in a clear or understandable manner.]
2.2
Biomass fuel (wood, dung, kang use other than with coal)
2.2.1
Cancer of the lung (see Table 2.5)
Koo et al. (1983) (described in detail in Section 2.1.1) reported a casecontrol study
in Hong Kong Special Administrative Region, China. Use of wood/grass did not have any
appreciable effect on the risk for lung cancer (odds ratio, 0.74; p=0.50).
Sobue (1990) conducted a hospital-based casecontrol study of lung cancer in Osaka,
Japan, that included 144 nonsmoking female lung cancer patients and 731 nonsmoking
female controls. Newly admitted patients were asked to complete a questionnaire that
asked about tobacco smoking habits, exposure to environmental tobacco smoke and other
sources of indoor air pollution (i.e. use of straw or wood for cooking, use of heating
appliances fueled with kerosene, gas, coal and charcoal and wood stoves without
chimneys, and use of charcoal footwarmers). The odds ratio for lung cancer in
nonsmoking Japanese women who used wood or straw compared with those who did not
at age 30 years was 1.77 (95% CI, 1.082.91; 32 exposed cases; adjusted for age,
exposure to passive smoke in adulthood and mother smoked during childhood). Current
and previous (at ages 15 and 30 years) use of charcoal footwarmers for sleeping was not
associated with risk. [The Working Group noted that the exposure variables were not well
defined and were limited to dichotomized categorization. The reference category was not
clearly defined and may have included the use of coal.]
In the study of Wu-Williams et al. (1990) (described in detail in Section 2.1.1)
duration of use of non-coal, generally biomass-fueled stoves was not associated with risk,
and there was no discernible association of risk with central heating (in which the heating
fuel source was outside the home).
176
Table 2.4. Casecontrol study of renal cancer and coal use

Characteristics of
cases and controls
Exposure
assessment
Organ
site
(ICD
code)
Exposure categories
No. of
exposed
cases
Odds ratios (95%

CI)
Adjustment
for potential
confounders
Comments
Sharpe et
al. (1989),
Montreal,
Canada,
198287
164 histologically
confirmed cases
diagnosed in 4
hospitals
Mailed
questionnaire
with
telephone
follow-up
Renal
(ICD-8,
189.0)
Lived in a house with

coal used as a fuel but did
not handle coal
53
1.07 (0.581.96)
Not clear
Domestic coal handling

only
56
1.41 (0.762.62)
Occupational handing
with or without domestic
handling
14
2.42 (0.817.46)
Concurrent occupational
and domestic handling
Subjects who mined

or delivered coal
were excluded.
Occupationally
exposed cases
included janitors,
foundry workers,
locomotive engineers,
cooks, prisoners of
war doing forced
labour, sailors and
those involved in
heating buildings.
161 controls
without urinary
tract tumors
identified from
urologist files;
matched by age,
sex, urologist
CI, confidence interval; ICD, International Classification of Diseases
8.45 (0.42168.68)
Reference,
study
location,
study
period
Table 2.5. Casecontrol studies of lung cancer and use of biomass fuel
Characteristics of cases
and controls
Exposure
assessment
Exposure categories
Koo et al.
(1983),
Hong Kong,
China,
198183
200 female lung cancer

patients; mean age
61.8 yrs; 44% never
smokers; 90%
histologically
confirmed (28% SCC,
18.5% small-cell,
34.5% ADC)
Interviews with
semi-structured
questionnaire, using
a life history
approach, assessed
use and duration of
using coal, biomass
fuels, kerosene,
LPG and gas
Ever fuel use

Wood/grass
Charcoal
In-person interview
using a structured
questionnaire;
developed
continuous index of
indoor exposure to
coal smoke from
heating and cooking
No use (referent)
Burning kang (yrs)
Men
119
>20
Women
119
>20
No. of
exposed
cases
Odds ratios
(95% CI)
179
32
0.74 (p=0.50)
0.96 (p=1.00)
Adjustment for
potential
confounders
Comments
Unclear
The reference category is

unclear for ever fuel use.
Age, education,
smoking
Population overlapped
with the study by WuWilliams et al. (1990)
200 female community

controls, matched on
age (5 yrs), residential
district and housing
type; mean age 60.6
yrs; 69% never smokers
Xu et al.
(1989),
Shenyang,
China,
198587

520 women) in
Shenyang aged 3069
yrs; cell type
histologically
confirmed in 83% of
men and 73% of
women.
1.7 (p<0.05)
2.1 (p<0.05)
40
65
1.3 (p>0.05)
2.3 (p<0.05)
177
1345 population-based
controls (788 men,
557 women), selected
by 3-stage procedure
from urban Shenyang;
frequency-matched on
gender and age
91
82
Reference,
study
location,
study period
178
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
No. of
exposed
cases
Odds ratios
(95% CI)
Adjustment for
potential
confounders
Comments
Sobue
(1990),
Osaka,
Japan,
198688
144 nonsmoking
women enrolled from
multiple hospitals; 40
79 yrs old; 100%
microscopically
confirmed (78% ADC,
8% SCC, 5% small-cell
carcinoma; 5% largecell carcinoma; 4%
other)
Self-administered
questionnaire
Used straw or wood

for cooking at age 30
32
1.77 (1.082.91)
Age at
admission, other
household
members smoked
in adulthood,
mother smoked
in childhood
5% used wood for

heating; no increased risk
for use of charcoal
footwarmers or fuel in
heating stoves; no
significantly increased
risks seen for exposure to
straw, wood or charcoal
at age 15; controls
(cancers of the breast,
stomach or other sites;
benign neoplasms;
circulatory, respiratory,
infectious or digestive
diseases) were younger
with higher education;
excluding breast cancer
controls (46%) did not
change results
731 unmatched
nonsmoking women
without lung cancer
enrolled from multiple
hospitals; 4079 yrs old
Reference,
study
location,
study period
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
WuWilliams et
al. (1990),
Shenyang
and Harbin,
northern
China,
198587
965 incident female

cases from local
registries; age <70 yrs;
cytologically verified
In-person interview
using structured
questionnaire
Kang (yrs)
139
4049
50
Burning kangs (yrs)
120
>21
Liu et al.
(1993),
Guangzhou,
China,
198384
959 women selected by

multistage random
sampling from general
populations of
Shenyang and Harbin
frequency-matched by
5-year age group
316 incident cases
(224 men, 92 women);
55% diagnosed by Xray/clinical history,
13% by bronchoscopy,
32% by cytology or
histology
matched on gender, age,
residential district and
date of diagnosis;
respiratory and
coronary heart disease
excluded
In-person interview
using structured
questionnaire on
smoking habits,
cooking fuel use
and other variables
Wood used for

cooking fuel vs. coal
Men
Women
No. of
exposed
cases
Odds ratios
(95% CI)
384
135
415
1.4 (0.82.4)
1.1 (0.62.8)
1.6 (0.92.8)
106
173
1.2 (0.91.7)
1.5 (1.12.0)
8
3
0.57 (0.113.0)
0.67 (0.0411.7)
Adjustment for
potential
confounders
Comments
Age, education,
smoking, study
area
Deep frying at least once

a month significantly
lung cancer.
Education,
occupation,
occupational
exposure, history
of tuberculosis,
chronic
bronchitis,
family history of
cancer, smoking,
living area,
passive smoking
Reference,
study
location,
study period
179
180
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
Shen et al.
(1996),
Nanjing,
China,
198693
263 cases (83 SCC, 180

ADC) who were
20 yrs
Standardized
questionnaire
SCC
Solid fuel vs. nonsolid fuel
263 population controls

who were Nanjing
residents; matched 1:1
for gender, age,
ethnicity and street
address
No. of
exposed
cases
Odds ratios
(95% CI)
4.97 (0.8030.88)
Adjustment for
potential
confounders
Comments
Unclear
Fuel types within solid

fuel category were not
specified. Statistical
tests were reported as
one-sided, but
implications are not
clear.
Reference,
study
location,
study period
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
Ko et al.
(1997),
Kaohsiung,
Taiwan,
Province of
China,
199293
105 nonsmoking female

lung cancer patients
In-person interview
using a structured
questionnaire
By age of exposure
Cooking fuel vs. gas
or none
Wood or charcoal
<20 yrs
2040 yrs
>40 yrs
105 (presumably
nonsmoking) women
from same hospital
ophthalmic service or
coming to hospital for
routine check-up;
matched on age (2 yrs)
and interview date
No. of
exposed
cases
56
53
4
Odds ratios
(95% CI)
2.5 (1.35.1)
2.5 (1.15.7)
1.0 (0.23.9)
Adjustment for
potential
confounders
Comments
Socioeconomic
status, education,
residential area
[Selection of cases and

controls from same
hospital may have caused
overmatching on
exposures. The nearsignificant positive
association of lung
cancer risk with
wood/charcoal use is
unusual, conceivably
related to the matching
strategy.] Further
adjusting for other
covariates [not specified]
did not affect the
statistical significance or
magnitude of effects.
Risk for lung cancer was
significantly increased if
the kitchen did not have a
fume extractor.
Reference,
study
location,
study period
181
182
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
No. of
exposed
cases
Odds ratios
(95% CI)
Adjustment for
potential
confounders
Comments
Malats et al.
(2000)
Brazil,
France,
Germany,
Italy,
Poland,
Romania,
Russia,
Sweden,
[period not
specified]
122 nonsmoking cases

(17 men, 105 women)
diagnosed with
histologically or
cytologically confirmed
lung cancer
In-person interview
using a standard
questionnaire
Indoor pollution from

wood (>20 yrs) vs. no
use
NG
2.5 (1.06.2)
Age, gender,
centre
Not adjusted for smoking

history although there
was a difference in
smoking history between
cases and controls.
121 nonsmoking
controls (34 men, 87
women) identified from
the Swedish population
registry or the same
hospitals as cases
(admitted for nontobacco related
diseases)
Reference,
study
location,
study period
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
Gupta et al.
(2001),
Chandigarh,
India,
199597
265 histologically
confirmed lung cancer
paitents (235 men,
30 women)
In-person interview
using a
questionnaire
Yrs of exposure to
wood
For cooking
Men
145
>45
Women
145
>45
For heating
Men
145
>45
Women
145
>45

(435 men, 90 women)
matched by age and sex
No. of
exposed
cases
Odds ratios
(95% CI)
51
105
0.94 (0.581.54)
0.87 (0.581.30)
6
12
0.74 (0.202.65)
1.11 (0.343.60)
4
67
2.62 (0.4714.5)
0.97 (0.651.43)
0
13
NG
2.78 (0.977.98)
Adjustment for
potential
confounders
Comments
Age, education,
smoking, sex
The selection of controls

may have resulted in
overadjustment.
Reference,
study
location,
study period
183
184
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
Lee et al.
(2001),
Kaohsiung,
Taiwan,
Province of
China,
199399
527 histologically
confirmed cases (236
men, 291 women), 18
83 yrs old; cases SCC
and small-cell
carcinoma (28.2%) and
ADC (47.7%)
In person interview
using a structured
questionnaire
Women
Wood or charcoal vs.
gas or none
SCC or small-cell
carcinoma
ADC
805 controls from same

hospital without
tobacco-related illness;
matched on gender, age
(2 yrs)
No. of
exposed
cases
Odds ratios
(95% CI)
22
3.1 (1.09.2)
40
3.0 (1.46.4)
Adjustment for
potential
confounders
Comments
Smoking,
residential area
(urban, suburban,
rural), education,
socioeconomic
status
Only 7% of men reported

cooking for the family
and thus data were not
shown. In women, stir
frying, frying and deep
frying after fumes
emitted were statistically
significantly associated
with risk for ADC but
not SCC or small-cell
carcinoma. Long-term
residence near industrial
district was associated
with lung cancer risk,
especially in women.
Risk for lung cancer was
significantly increased if
the kitchen did not have a
fume extractor.
Reference,
study
location,
study period
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
HernndezGarduo et
al. (2004),
Mexico
City,
Mexico,
19861994
113 histologically
confirmed never
smoking women
identified from medical
records at the National
Institute for Respiratory
Disease (INER); 44
yrs of age
Medical records
Yrs of cooking with

wood vs. none
120
2150
>50
273 nonsmoking
women, 44 yrs of age;
identified by medical
records, hospitalized at
INER (99 pulmonary
tuberculosis, 110
interstitial lung disease,
64 miscellaneous
pulmonary conditions)
during the same time
period as cases
No. of
exposed
cases
15
15
47
Odds ratios
(95% CI)
0.6 (0.31.2)
0.6 (0.31.3)
1.9 (1.13.5)
Adjustment for
potential
confounders
Comments
Age, education,
environmental
tobacco smoke,
socioeconomic
status
Use of patient records

may lead to error.
Difficult to interpret as
different control groups
used. Although diseases
in which wood smoke
could be a risk factor
were excluded (i.e.
COPD, cancer or
asthma), use of controls
with respiratory diseases
may underestimate the
relative risk because
these diseases may also
be indirectly related to
exposure to wood smoke.
Confounding by the use
of coal is not a concern
in this study since coal is
not used in Mexico.
Reference,
study
location,
study period
185
186
Table 2.5 (contd)

and controls
Exposure
assessment
Exposure categories
Lissowska
et al.
(2005),
Central and
eastern
Europe and
United
Kingdom,
19982002
2861 cases (2205 men,

656 women) from 15
hospitals
In-person interview
using a structured
questionnaire
Ever used wood only

For cooking
For heating
3118 hospital and

population-based
controls (2305 men,
813 women) matched
by age, sex and area;
persons with cancer or
tobacco-related diseases
were excluded
No. of
exposed
cases
Odds ratios
(95% CI)
1065
1105
1.23 (1.001.52)
1.31 (1.061.61)
Adjustment for
potential
confounders
Comments
Age, sex,
education,
tobacco, centrre
Coal was the most

common type of fuel
used for heating (50%)or
cooking.(44%); Controls
were hospital based
except in Warsaw,
Poland and Liverpool,
United Kingdom where
they were populationbased; Authors could not
rule out that the
associations were due to
some mixed (wood and
coal) exposures, because
subjects provided their
principal fuel (if they
used mainly coal but
some wood, they would
have indicated coal).
[Although the analysis
was very thorough, dose
response analyses by
type of solid fuels
(separately for coal and
wood) were not
provided.]
ADC, adenocarcinoma; CI, confidence interval; COPD, chronic obstructive pulmonary disease; LPG, Liquid petroleum gas; SCC, squamous cell carcinoma; yrs, years
Reference,
study
location,
study period
187
In a hospital-based casecontrol study conducted in Guangzhou, China, Liu et al.

(1993) studied the risk for lung cancer associated with the use of different cooking fuels
(described in Section 2.1.1). Analyses using multivariable conditional logistic regression
models adjusted for education, occupation, occupational exposure, history of tuberculosis,
chronic bronchitis, family history of cancer, smoking, living area and passive smoke (in
women only) were stratified by gender. Compared with use of coal for cooking, use of
wood was inversely associated (although not statistically significant) with the risk for lung
cancer in both men (odds ratio, 0.57; 95% CI, 0.113.0; eight exposed cases) and women
(odds ratio: 0.67; 95% CI, 0.0411.7; three exposed cases).
Two hospital-based casecontrol studies were conducted in Kaohsiung, a heavily
industrialized city in Taiwan, China (Ko et al., 1997; Le et al., 2001). The first study
included 117 female lung cancer cases identified between 1992 and 1993 who were
compared with 117 female hospital controls admitted for a health check-up (n=55) or for
eye diseases (n=62) (Ko et al., 1997). Information on histological type was not provided.
Active smokers (11 cases, three controls) were excluded so that the analysis was based on
105 casecontrol pairs who were nonsmokers. Use of wood or charcoal before the age of
40, as opposed to other fuels including coal, was associated with an increased risk for
lung cancer, after adjusting for socioeconomic status, education and residential area.
The casecontrol study by Le et al. (2001) included women diagnosed with
squamous-cell or small-cell carcinoma (n=84) or adenocarcinoma of the lung (n=162) and
corresponding controls (n=407) (described in detail in Section 2.1.1). Risk for lung cancer
was associated with type of cooking fuel: women who used wood or charcoal as a
cooking fuel compared with those who cooked with gas or did not cook showed a 3.1fold (95% CI, 1.09.2; 22 exposed cases) increased risk for squamous-cell and small-cell
cancer and a 3.0-fold (95% CI, 1.46.4; 40 exposed cases) increased risk for
adenocarcinoma. Risk was also significantly higher for those who cooked in a kitchen
without a fume extractor: the odds ratio was 3.0 (95% CI, 1.37.1; 31 exposed cases) for
squamous-/small-cell cancer and 3.9 (95% CI, 2.36.6; 74 exposed cases) for
adenocarcinoma. Only 7% of men reported cooking for the family and thus these data
were not reported.
In a hospital-based casecontrol study among nonsmokers (including occasional
smokers of up to 400 cigarettes in a lifetime), Malats et al. (2000) (described in detail in
Section 2.1.1) presented an overall odds ratio for lung cancer for >20 years of use of
wood of 2.5 (95% CI, 1.06.2). [The Working Group noted that there could be possible
confounding by smoking because nonsmokers were defined as never smokers and
occasional smokers (up to 400 cigarettes in a lifetime). The Working Group also noted the
heterogeneous background of the study subjects and the fact that controls were not
matched by age and sex may present difficulties in the interpretation of the results.
Furthermore, the crude exposure indices used (i.e. <20 years of fuel use) did not enable a
good assessment of the exposureresponse relationship.]
In a casecontrol study of lung cancer in Chandigarh, India, Gupta et al. (2001)
(described in detail in Section 2.1.1) reported that the odds ratio for the use of wood for
188
heating for 45 or more years was 0.97 (95% CI, 0.651.43; 67 exposed cases) for men
and 2.78 (95% CI, 0.977.98; 13 exposed cases) for women. The odds ratio for the use of
wood for cooking for 45 or more years was 0.87 (95% CI, 0.581.30; 105 exposed cases)
for men and 1.11 (95% CI, 0.343.60; 12 exposed cases) for women. [The Working
Group noted that the selection of controls may have resulted in overadjustment.]
In a study conducted in Mexico, Hernndez-Garduo et al. (2004) determined the
association between long-term exposure to wood smoke from cooking and lung cancer in
nonsmoking Mexican women. Cases and controls, aged 44 years or more, were identified
through a review of patient records (discharged between 1986 and 1994) at the Instituto
Nacional de Enfermedades Respiratorias, a specialized hospital for respiratory diseases in
Mexico City. All cases (n=113) were nonsmoking women with a histological
confirmation of lung adenocarcinoma. Controls (n=273) were hospitalized at the same
institute during the same period of time for pulmonary tuberculosis (n=99), interstitial
lung disease (n=110) and other miscellaneous pulmonary conditions (n=64), of which 55
were pneumonia. Information on environmental exposures including wood smoke (ever
used wood for cooking in their household, years of exposure) was obtained by personal
interview at admission and abstracted from medical records for this study. Potential cases
and controls with no information on cooking fuel exposure or socioeconomic status were
excluded [numbers not given]. Of the patients, 75% were currently living in Mexico City
or in the state of Mexico while the remainder lived in other states of Mexico. Cases were
slightly older and more likely to come from rural areas and had lower socioeconomic
status than controls, although the difference was not significant. The majority of women
reported some use of wood for cooking during their lifetime (68.1% of cases; control
groups: 67.7% with tuberculosis, 67.0% with interstitial lung disease, 62.5% with
miscellaneous pulmonary conditions and 66.1% of the combined control group). For
those who had ever used wood for cooking, the duration of exposure to wood smoke was
significantly higher in the cases (median, 56 years) than in each of the control groups
(median for the combined controls, 38 years). The percentage of women exposed for 1
20 and 2050 years to wood smoke was higher in the control groups; however, the
percentage of exposure over 50 years was higher in the cases. In a multivariate analysis
adjusting for age, exposure to environmental tobacco smoke, education and
socioeconomic status, the odds ratio for lung cancer for more than 50 years of exposure to
wood smoke was 1.9 (95% CI, 1.13.5) compared with all control groups combined. This
risk was higher when compared with the control group of miscellaneous pulmonary
conditions (odds ratio, 2.6; 95% CI, 1.06.3). However, for the duration of exposure of 1
20 and 2150 years, the odds ratios were less than 1 and not statistically significant. [The
Working Group noted that the use of controls whose disease might be related to wood
exposure could underestimate the relative risk but may also reduce interviewer bias. No
information was provided on the cases and controls that were excluded due to lack of
information on exposure to wood smoke. Since coal is not used in Mexico, confounding
by the use of coal is not a concern in this study. The doseresponse results are difficult to
interpret with the use of multiple control groups.]
189
In a multicentre casecontrol study of lung cancer, Lissowska et al. (2005) (described

in detail in Section 2.1.1) reported odds ratios for principal exposure to wood for cooking
(odds ratio, 1.23; 95% CI, 1.001.52; 1065 exposed cases) and heating (odds ratio, 1.31;
95% CI, 1.061.61; 1105 exposed cases) after adjusting for centre, age, gender, education
and tobacco packyears. [The Working Group noted many strengths in this large
multicentre casecontrol study which used a common, standardized study protocol and
questionnaire and collected information on lifetime fuel use and relevant covariates from
in-person interviews with the study participants. The response rate was high in both cases
and controls (>90%). Although the analysis was very thorough, doseresponse analyses
by type of solid fuels (separately for coal and wood) were not provided.]
2.2.2
Cancers of the oral cavity, pharynx and larynx (see Table 2.6)
Two partially overlapping hospital-based casecontrol studies conducted in Brazil

(So Paulo, Curitiba and Loiania) examined the risk for cancers of the larynx, pharynx
(excluding nasopharynx) and mouth (excluding salivary glands) in relation to the use of
wood stoves for cooking and/or heating (Franco et al., 1989; Pintos et al., 1998). Franco
et al. (1989) compared 232 oral cancer cases with 464 non-cancer control patients
matched by age, sex, study site and trimester of admission and reported an odds ratio for
ever/never use of wood stove adjusted for alcohol and tobacco use of 2.5 (95% CI, 1.6
3.9; 134 exposed cases). Pintos et al. (1998) identified 784 incident cases of cancer of the
larynx, pharynx and mouth and 1568 controls from hospital inpatients (patients with
cancer or mental disorders were excluded), matched to cases on age, sex, study site and
trimester of hospital admission. Ever/never use of wood stoves, adjusted for tobacco and
alcohol consumption, was associated with an increased risk for cancer at all sites (odds
ratios: for all sites, 2.39; 95% CI, 1.883.05; mouth, 2.34; 95% CI, 1.673.29; pharynx,
2.78; 95% CI, 1.704.53; larynx, 2.37; 95% CI, 1.404.02). Presenting results of wood
stove exposure by levels of tobacco and alcohol consumption resulted in statistically
significant odds ratios above 2.0. [The increased risk seen in the groups that consumed the
least alcohol and tobacco suggested that residual confounding was unlikely.] Stratifying
by gender and subsite while also adjusting for race, income, rural residence and schooling
resulted in statistically significant odds ratios above 2.0 for men while the point estimates
varied considerably with wide confidence intervals for women because the data for
women were sparse (adjusted odds ratio for laryngeal cancer: in men 2.03; 95% CI, 1.12
3.67; in women, 16.24; 95% CI, 2.6699.1). [The Working Group noted that exposure
assessment was crude; use of wood stoves for cooking or heating was ascertained only via
a single yes/no question. No attempt was made to determine duration of use and the
reference group was not described.]
190
Table 2.6. Casecontrol studies of cancer of the upper aerodigestive tract

Reference,
study
and controls
location,
study period
Exposure
assessment
Organ site
(ICD code)
Exposure
categories
No. of
exposed
cases
Odds ratios
(95% CI)
Adjustment
for potential
confounders
Comments
Smoking,
alcohol
Interviewers were blinded

to etiological hypotheses
being tested. There is
probably considerable
overlap of the two oral
cancer case groups with
Pintos et al. (1998).
Biomass
232 incident cases from 3
Brazilian hospitals; 100%
histopathologically
confirmed; 87% men
Tongue, gum, Use of woodstove

mouth floor,
for cooking and
oral cavity
heating
(141, 143145)
134
2.5 (1.63.9)
464 hospital-based
controls excluding
neoplastic diseases and
mental disorders;
matched by age, sex,
study site and trimester of
admission
Tongue
Other oral
cavity
NG
NG
6.5 (2.815.0)
1.4 (0.82.4)
Franco et al.
(1989),
Brazil,
198688
Table 2.6 (contd)

Reference,
study
and controls
location,
study period
784 cases (salivary glands
and nasopharynx
excluded) with SCC from
3 Brazilian hospitals;
100% histopathologically
confirmed; 87% men.
1568 hospital-based
controls excluding
neoplastic diseases and
mental disorders;
matched by age, sex,
study site and trimester of
admission
Exposure
categories
No. of
exposed
cases
Odds ratios
(95% CI)
Adjustment
for potential
confounders
Comments
In-person
interview
using
questionnaire
UADT
Use of woodstove
for cooking or
heating
397
2.39 (1.883.05)
NG
2.34 (1.673.29)
NG
2.78 (1.704.53)
Tobacco,
alcohol,
matching
factors (by
conditional
logistic
regression)
NG
2.37 (1.404.02)
Presenting results of
wood stove exposure by
levels of tobacco and
alcohol consumption
resulted in statistically
significant odds ratios
above 2.0. The increased
risk seen in the groups
that consumed the least
alcohol and tobacco
suggested that residual
confounding was
improbable. Stratifying by
gender and UADT subsite
while also adjusting for
race, income, rural
residence and schooling
resulted in statistically
significant odds ratios
above 2.0 for men while
the point estimates varied
considerably with wide
confidence intervals for
women. Exposure
assessment was crude:
only yes/no use of wood
stoves for cooking or
heating was ascertained
and duration was not
recorded. The reference
group was not described.
Mouth
(140145)
Pharynx
(146149)
Larynx
(161)
191
Organ site
(ICD code)
Pintos et al.
(1998),
Brazil,
198789
Exposure
assessment
192
Table 2.6 (contd)

Exposure
assessment
Organ site
(ICD code)
Exposure
categories
Dandara et
al. (2006),
South
Africa,
19972003
In-person
interview
using a
questionnaire
Oesophagus
Use of wood and

charcoal for
cooking and
heating in the last
20 yrs compared
with electricity
Blacks
Mixed ancestry
245 patients admitted for

dysphagia with
histologically confirmed
SCC; 59% men
288 healthy, agematched, population
based controls recruited
from the same
geographical area as
cases; 57% men
No. of
exposed
cases
63
28
Odds ratios
(95% CI)
Adjustment
for potential
confounders
Comments
Alcohol,
tobacco
Difference in risk by
ethnicity not explained
Tobacco,
alcohol
consumption
Percentage use of separate

fuels provided but no
statistical tests; fossil
fuels were considered to
be coal, briquettes, coke,
peat, gas and oil.
15.2 (8.228.2)
1.2 (0.62.3)
Mixed coal/biomass
Dietz et al.
(1995),
Heidelberg,
Germany,
198992
Patients with cancers of

the larynx (n=164), oral
cavity (n=100), and
oropharynx and
hypopharynx (n=105)
4 controls selected from
medical clinics and
general outpatient
departments matched to
cases (656 for larynx, 400
for oral cavity, 420
oropharynx and
hypopharynx) by age,
sex, size of residence
Interview
Larynx
Pharynx
Oral cavity
NG
>40 yrs use of
single stove heating NG
NG
units with fossil
fuels vs. 020 yrs
use
2.0 (1.103.46
3.3 (1.437.55)
2.4 (1.264.4)
Larynx
Pharynx
Oral cavity
>40 yrs use of

single stoves with
fossil fuels for
cooking vs. 020
yrs use
NG
NG
NG
1.4 (0.762.41)
2.5 (1.036.30)
1.6 (0.902.97)
ADC, adenocarcinoma; NG, not given; SCC, squamous cell carcinoma; UADT, upper aerodigestive tract; yrs, years
Reference,
study
and controls
location,
study period
2.2.3
193
Cancer of the salivary glands
In a casecontrol study of cancer of the salivary glands, Zheng et al. (1996)

(described in detail in Section 2.1.2), the odds ratio was 1.6 for use of wood/straw for
cooking (95% CI, 0.64.4; six exposed cases) after adjusting for gender, age and income.
2.2.4
Cancer of the nasopharynx (see Table 2.7)
The earliest publication on cancer and indoor pollution from biomass fuel focused on
nasopharyngeal cancer using an ecological comparison of rates by elevation in rural
Kenya (Clifford, 1972). A small (eight-household) indoor air pollution survey during
evening cooking was undertaken to indicate that concentrations of total PM, total organic
matter, benzo[a]pyrene and benz[a]anthracene from wood burning varied by elevation,
presumably because of lower ventilation and more fuel use due to the need for more space
heating at higher elevations. The incidence of nasopharyngeal cancer varied by region.
Shanmugaratnam et al. (1978) conducted a casecontrol study of nasopharyngeal
carcinoma (NPC) among persons of Chinese origin who were permanent residents of
Singapore. A total of 379 histologically confirmed NPC patients (266 men, 113 women)
were recruited from the Ear, Nose and Throat (ENT) Department of Singapore General
Hospital. Two control groups were enrolled: 595 (311 men, 284 women) ENT patients
without NPC and 1044 (738 men, 306 women) other hospital controls. Trained
interviewers conducted in-person interviews between March 1966 and August 1968 using
a standardized questionnaire that included the main type of fuel used over a period of
more than 10 years. Charcoal use was not significantly associated with the risk for NPC
(odds ratio, <1.0; p>0.05) using either control group as a comparison. Firewood use was
significantly associated with NPC compared with ENT controls (odds ratio, 1.71; p<0.01)
but not when compared with other hospital controls (odds ratio, 0.87; p>0.05). [The
Working Group noted that a greater proportion of the ENT controls may have used gas
instead of firewood since this group had a higher socioeconomic status.]
In a casecontrol study (Zheng et al., 1992) of cancer of the nasal cavity, paranasal
sinuses and middle ear (ICD-9, 160) (described in detail in Section 2.1.4) after adjusting
for age, ever-use of wood or straw as cooking fuels was associated with a significantly
increased risk for nasal cancer (ICD-9, 160) (odds ratio, 3.3; 95% CI, 1.76.7). In
multivariate analysis after adjusting for related variables such as age, intake of
oranges/tangerines, consumption of salted fish/meat/vegetables, ever exposure to
wood/silica/petroleum products and ever diagnosed with chronic nasal diseases, ever use
of wood/straw as cooking fuels was associated with a risk for nasal cancer and yielded an
odds ratio of 3.3 (95% CI, 1.57.3). Consistent associations in both men and women were
found for use of wood/straw as cooking fuels (odds ratio for men, 2.2; 95% CI, 0.95.4;
odds ratio for women, 8.5; 95% CI, 2.331.8). [The Working Group noted that the sample
size was relatively small. The variable use of wood/straw as cooking fuels was only classified
194
Table 2.7 Casecontrol studies of nasopharyngeal cancer

Reference, study
location and period
Characteristics of
cases and controls
Exposure
assessment
Exposure categories
379 (266 men,

113 women)
Chinese patients
from ENT
department of
Singapore
General hospital;
age 10>70 yrs,
histologically
confirmed
Trained
intervieweradministered
standardized
questionnaire
in the local
dialect of
interviewees
Main type of fuel

used over the past 10
yrs
Charcoal
ENT controls
Other controls
Firewood
ENT controls
Other controls
No. of
exposed
cases
Odds Ratio (95%

CI)
Adjustment for
potential confounders
Comments
Age, sex, interviewer
Greater
proportion of the
ENT controls
may have used
gas instead of
firewood since
this group had
higher
socioeconomic
status;
participants were
all permanent
residents of
Singapore
Biomass
Two sets of
Chinese controls:
595 (311 men,
284 women) ENT
patients without
NPC; 1044 (738
men, 306 women)
other hospital
controls
NG
NG
0.69 (p>0.05)
0.75 (p>0.05)
NG
NG
1.71 (p<0.01)
0.87 (p>0.05)
Shanmugaratnam et
al. (1978),
Singapore,
196668
Table 2.7 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Hubert et al. (1993);

Zheng et al. (1994),
Guangxi, China,
January 1986
unspecified
88 cases of
histologically
confirmed
undifferentiated
NPC enrolled
from regional
cancer institutes
(29 in Wuzhou,
59 in Zangwu);
73% men; 15.9%
aged 30, 32.9%
between 31 and
40; 34.2%
between 41 and
50 and 17% older
than 50
Intervieweradministered
standardized
questionnaire
Wood fuel use vs.

none in the year
before diagnosis
Yes
Yes
176 population
controls matched
on age (4 year),
sex and
neighbourhood;
interviewed the
same week as the
case
No. of
exposed
cases
80
80
Odds Ratio (95%

CI)
6.4 (p=0.003)
5.4 (1.519.8)
Adjustment for
Socioeconomic score
Socioeconomic score,
consumption of
herbal tea in year
before diagnosis and
consumption of salted
fish in porridge
before the age of 2
yrs
Matching variables
adjusted for in
conditional logistic
regression analyses
Comments
Socioeconomic
score based on
type of housing
in childhood,
presence of
windows in
house and
monthly income
the year before
diagnosis; this
study completely
overlaps with
Hubert et al.
(1993)
Reference, study
location and period
195
196
Table 2.7 (contd)

Exposure categories
Characteristics of
cases and controls
Exposure
assessment
Chelleng et al. (2000)

Nagaland, India,
199697
47 histologically
confirmed cases
who were
permanent
residents of
Nagaland; 72%
men
Soot in house
In-person
Wood vs. gas for
interview
using standard cooking fuel
questionnaire
No. of
exposed
cases
Odds Ratio (95% CI)
Adjustment for
Comments
20
42
1.4 (0.63.3)
1.6 (0.46.6)
Yes but unclear
This study was

not well powered;
significant
association with
smoked meat:
11.5 (3.438.5)
94 neighbourhood
controls; matched
by age, sex and
ethnicity
Mixed coal/biomass
Cai & Ye (1996),
Fujian, China,
1991
115 primary NPC

patients, pathology
confirmed and lived
in Fujian more than
10 yrs; 86 men
230 (115 nontumour, 115
tumour) controls,
who lived in Fujian
more than 10 yrs;
matched on age,
gender, diagnosis
date
In-person
interview
using a
questionnaire
Use of coal or
firewood/straw as fuels
Non-tumour control in
1978,
6.52 (1.9022.32)
Tumour control in
1968, 3.14 (1.188.36)
Tumour and nontumour control in
1968, 3.35 (1.368.27)
Coal and
firewood/straw
were not reported
separately. In
1978 and 1968
means fuel use
under conditions
in different eras.
Reference, study
location and period
197
into two groups (never, ever) which resulted in a lack of information on doseresponse
relationship.]
Eighty-eight incident cases of NPC diagnosed after 1 January 1 1986 in Zanhwu and
Wuzhou, an area in China that is endemic for NPC, were enrolled in a casecontrol study
(Hubert et al., 1993; Zheng et al., 1994). One hundred and seventy-six controls were
selected in the immediate neighbourhood, matched on sex, age (4 years) and place of
residence. The controls were interviewed within the same week as the patients and under
the same conditions. Information was collected on past and present conditions including
educational level, marital status, place of birth, residential history, personal or family
income, housing, types of fuel used, kitchen and toilet equipment and sleeping conditions,
as well as diet (including methods of preparation and preservation). A sociodemographic
score was established to describe living conditions according to three variables: monthly
income, lack of house windows during the preceding year and type of housing in
childhood. Odds ratios and 95% CIs were calculated using conditional logistic regression.
Use of wood as fuel in the year before diagnosis was positively associated with the risk
for NPC after adjusting for sociodemographic score (odds ratio, 6.4; p=0.003; 80 exposed
cases) and after additional adjustment for consumption of herbal tea in year before
diagnosis and consumption of salted fish in porridge before the age of 2 years (odds ratio,
5.4; 95% CI, 1.519.8; 80 exposed cases). Exposure to wood as a fuel in early childhood
was not significantly associated with NPC. The risk for NPC from the use of wood fire
was also studied in conjunction with other environmental factors that may affect the level
of exposure. [The Working Group noted that exposure to wood fuel was assessed crudely,
in that it was classified as a dichotomous variable, and no information on a doseresponse
relationship was presented. The Working Group noted that almost all subjects were
exposed to wood combustion in early childhood and therefore current use may be a
better surrogate for cumulative exposure.]
A casecontrol study was designed in Nagaland, India, to evaluate the determinants
of nasopharyngeal cancer (Chelleng et al., 2000). The study included 47 histologically
confirmed cases recruited at the Bhobaneswar Boruah Cancer Institute between 1996 and
1997 and 94 neighbourhood controls matched on age, sex and ethnicity. Information on
risk factors including dietary, environmental and sociodemographic factors was obtained
from an in-person interview using a standard questionnaire. Of the cases, 72.3% were
men and a large majority (68.1%) were over 40 years of age at the time of diagnosis.
Questions on biomass exposure included presence of soot in the house, cooking fuel used,
location of the kitchen, and type of house and the number of windows. None of these
variables was significantly associated with the risk for nasopharyngeal cancer. In the
multivariate logistic regression that accounted for tobacco smoking and socioeconomic
status among other factors, the presence of soot in the house gave an odds ratio of 1.4
(95% CI, 0.63.3; 20 exposed cases) and use of wood for cooking (versus gas) gave an
odds ratio of 1.6 (95% CI, 0.46.6; 42 exposed cases). [The Working Group noted that
the consumption of smoked meat and a previous history of nasal drop use were
significantly related to cancer. The Working Group further noted that this study had a
198
poor characterization of exposure to wood burning (dichotomous wood versus gas) and
no specification on current or past exposure. In addition, the power was low due to the
small number of cases.]
2.2.5
Cancer of the oesophagus and its precursors
Chronic oesophagitis is considered to be a precusor condition for oesophageal cancer.

A study was carried out to collect information on the prevalence of chronic oesophagitis
at early ages in a high-risk area for oesophageal cancer and to identify risk factors
associated with the prevalence of this disease (Chang-Claude et al., 1990). Study subjects
were young adults aged 1525 years from all households where cases of oesophageal
cancer had been diagnosed after 1981 until October 1987 and twice the number of
randomly selected households where no oesophageal cancer was diagnosed (with neither
a diagnosis nor a family history of oesophageal cancer or dysplasia). A total of 227 and
660 young adults from these two types of household were eligible for inclusion in the
study. In May 1988, 545 (62%) subjects participated in the study. They were interviewed
and information was collected on dietary habits in the early 1970s and in the past 5 years,
methods of food preparation, types of oil used, alcohol consumption, tobacco smoking,
use of coal and other fuels, cooking fumes, ventilation, family history of oesophageal
cancer, occupation and dental hygiene. A physical examination with collection of a 10-ml
blood sample and early morning urine was conducted for each subject. Endoscopic
examination of the oesophagus and stomach was also performed. Variables identified in
univariate analysis were then evaluated in multivariate logistic regression models. A total
of 538 subjects (354 men, 184 women) underwent an oesophagoscopy with biopsy. Of
these, 166 came from cancer households and 372 from non-cancer households. Since the
distributions of variables of interest among subjects with very mild oesophagitis were
similar to those with a normal oesophagus, very mild oesophagitis was classified as
normal in the analysis of risk factors for chronic oesophagitis. In univariate analysis (the
household was controlled for as a confounder), in addition to other significant risk factors,
cottonseed oil used for cooking most frequently (odds ratio for men, 2.3; 95% CI, 1.2
4.5; odds ratio for women, 1.6; 95% CI, 0.55.9), use of wood as fuel in the early 1970s
(odds ratio for men, 2.5; 95% CI, 1.25.2; odds ratio for women, 2.6; 95% CI, 0.79.2)
and use of wood as fuel in the past 5 years (odds ratio for men, 1.4; 95% CI, 0.37.0; odds
ratio for women, 9.9; 95% CI, 2.343.2) were statistically significant variables for the risk
for chronic oesophagitis in this rural area. In multivariate analysis, there was no
statistically significant association of these variables, adjusted for other risk factors
including age and sex (adjusted odds ratio for use of wood as fuel in the past 5 years,
1.72; p=0.19). The authors stated that the unexpected finding of an association of the use
of wood as fuel with disease occurrence could be a chance association, since the
relationship virtually disappeared in multivariate analysis. [The Working Group noted
that the participation rate (62%) in this study was relatively low, and selection bias might
exist.]
199
A study was conducted to determine whether functional polymorphisms in xenobiotic

metabolizing genes could affect the risk for oesophageal cancer in different population
groups (Dandara et al., 2006, in Table 2.6). A total of 245 patients with histologically
confirmed squamous-cell carcincinoma and admitted for dysphagia were recruited from a
hospital in Cape Town, South Africa. A total of 288 age-matched, healthy population
controls were recruited from the same geographical location as the patients; 145 cases and
194 controls were black and 100 cases and 94 controls were of mixed ancestry. As part of
the questionnaire, information on cooking and heating fuels used during the past 20 years
was recorded and smokers were classified as individuals who had smoked at least one
cigarette per day for at least 1 year. Subjects were also classified as alcohol consumers if
they consumed alcohol regularly (at least once at week). Among black subjects, the
burning of wood or charcoal for cooking and heating (compared with electricity) was
significantly associated with an increased risk for oesophageal cancer (odds ratio, 15.2;
95% CI, 8.1528.2; p=0.001; 63 exposed cases), as were smoking pipes and consumption
of home brewed beer. In the subjects of mixed ancestry, wood or charcoal use was not
associated with oesophageal cancer (odds ratio, 1.19; 95% CI, 0.602.34; p=0.62;
28 exposed cases); however, alcohol consumption and tobacco smoking were strong risk
factors for oesophageal cancer. [The Working Group noted that the exposure variable
used was dichotomous and that no doseresponse information was available. There was
concern for residual confounding because the risk estimates were adjusted for overall
consumption of alcohol and tobacco (not associated in the data set with oesophageal
cancer in blacks) but not for pipe smoking or home brewed beer consumption (which
were strong risk factors oesophageal cancer in the black population).]
2.2.6
Cancer of the cervix (see Table 2.8)
A casecontrol study was conducted in Honduras to determine whether exposure to

wood smoke increases the risk for invasive cervical cancer (Velema et al., 2002). One
hundred and twenty-five women aged 2064 years who had different grades of cervical
intraepithelial neoplasia (CIN) (44 CIN I, 36 CIN II, 45 CIN III) were recruited from a
screening programme. Each case was matched by age, clinic and calendar time to two
controls (241 controls in total) without cervical abnormalities. All women were from low
socioeconomic backgrounds. Cervical scrapes were tested for the presence of human
papilloma virus (HPV) and HPV genotyping was performed. An interview was conducted
in the clinic for case and control women to determine whether they had ever cooked with
wood and, if so, the duration of use and the number of years since stopping use of wood
for cooking. Exposure to wood during childhood was also determined. HPV DNA was
detected in 48% of women with CIN I, 67% with CIN II and 89% with CIN III. Exposure
to wood smoke for 35 or more years increased the risk for CIN III (odds ratio, 4.89; 95%
CI, 0.5147.1; p=0.017; nine exposed cases) compared with women with no exposure.
Restriction of the analysis to women who reported exposure yielded a positive association
with development of CIN III for women exposed for more than 35 years versus those
200
Table 2.8. Casecontrol study of cervical cancer

Characteristics of cases and
controls
Exposure
assessment
Exposure
categories
Velema et
al.
(2002),
Tegucigalpa
City,
Honduras,
199395
125 women with CIN (44

CIN I, 36 CIN II, 45 CIN
III) from 14 hospitals; aged
2064 yrs
In-person
interview
In CIN III
women, yrs of
exposure to
wood smoke
vs. none
114
1524
2534
35+
241 women without

cervical abnormalities from
the same screening clinic as
cases; matched by age,
clinic, calendar time
No. of
exposed
cases
11
8
8
9
Odds ratio
(95% CI)
0.36 (0.111.18)
0.35 (0.091.39)
1.34 (0.209.18)
4.89 (0.5147.1)
CI, confidence interval; CIN, cervical intraepithelial neoplasia; HPV, human papillomas virus; yrs, years
Adjustment for
potential
confounders
Comments
Adjusted for
matching factors
by conditional
logistic
regression
When stratified by HPV

status (positive, negative),
the authors concluded that
there was a significant
doseresponse effect
among HPV- positive
patients; however, the
Working Group thought
the analytical approach was
questionable.
Reference,
study
location,
study period
201
exposed for 114 years (odds ratio, 9.5; 95% CI, 1.1677.4; p=0.017; nine exposed
cases). There was no significant association with CIN I or II. [The Working Group noted
that this significant association was observed only when unexposed women were
excluded from the analysis and unstable point estimates resulted after stratification by
CIN stages and duration of exposure.] Among HPV-positive women, more than 35 years
of exposure to wood smoke increased the risk for CIN compared with 114 years of
exposure to wood smoke (odds ratio, 5.69; 95% CI, 1.0032.70). [The Working Group
also noted that these results are difficult to interpret because women who reported not
having used wood in the kitchen had a risk higher than those with low or intermediate
exposure and the analytical approach was questionable.]
2.3
Mixed coal/biomass (coal and/or wood/dung/kang use)
2.3.1
Chen et al. (1990) conducted a casecontrol study in Taipei, Taiwan, China that
included 323 serial lung cancer cases from four teaching hospitals (133 epidermoid, 47
small-cell and 134 adenocarcinomas) and 617 healthy controls who were ophthalmic
patients in the study hospitals that were frequency-matched to cases on hospital, gender
and age. Logistic regression models adjusted for sex and age showed no significant effect
of burning coal or wood compared to other fuels (charcoal, gas) and electricity.
Mzileni et al. (1999) conducted a hospital-based casecontrol study that included
288 men and 60 women who had been diagnosed with incident lung cancer between 1993
and 1995 in the main tertiary referral hospital in the northern Province of South Africa.
Controls were 183 men and 197 women who had been diagnosed with other incident
cancers (predominantly of the prostate, liver and breast, colorectal and haematological
cancers) in the same hospital as cases during the same study period. Cases and controls
were interviewed regarding their tobacco smoking habits, residence, main occupation and
fuel use (wood and coal) at home. The risk for lung cancer was increased in relation to the
use of wood or coal in the house in men (odds ratio, 1.9; 95% CI, 0.93.3; 260 exposed
cases) and women (odds ratio, 1.4; 95% CI, 0.63.2; 51 exposed cases) after adjusting for
smoking, dusty occupation and residential exposure to asbestos. The positive association
between the risk for lung cancer and the use of wood or coal in the house was statistically
significant in men and women combined (adjusted odds ratio, 2.0; 95% CI, 1.13.6).
Active tobacco smoking and living in asbestos-polluted areas were also significantly
associated with risk for lung cancer in men and women combined after adjusting for age,
sex, dust and use of wood for fuel. [The Working Group noted that results were presented
for wood and coal use combined and as a dichotomous variable (no/yes). The
independent effects of coal and wood could not be examined because the information on
these two types of fuel were not presented separately. Because of the strong significantly
positive associations between risk for lung cancer, smoking and residence in asbestos-
202
Table 2.9. Casecontrol studies of lung cancer and use of mixed coal/biomass fuel
Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Chen et al.
(1990),
Taipei, Taiwan,
Province of
China
[period not
specified]
323 serial cases from

4 teaching hospitals in
Taipei, all
pathologically
confirmed: 133
epidermoid, 47 smallcell and 134 ADC
In-person
interview
using a
structured
questionnaire
Burning coal or wood

versus other fuels
(charcoal, gas) and
electricity
Epidermoid
Small-cell
ADC
In-person
interview
Wood or coal use at

home
Men
Women
No. of
exposed
cases
Odds ratio
(95% CI)
Adjustment for
potential
confounders
Comments
Age, sex
NG
NG
NG
0.85 (p>0.05)
1.08 (p>0.05)
1.02 (p>0.05)
311
2.0 (1.13.6)
260
51
1.9 (0.93.3)
1.4 (0.63.2)
617 ophthalmic
patients from study
hospitals; frequencymatched on hospital,
gender, age
Mzileni et al.
(1999),
northern
Province,
South Africa,
199395
348 cases (288 men,

60 women) enrolled
from a referral
hospital
380 patients (183
men, 197 women)
with cancers not
thought to be related
to smoking
Smoking, dusty
job, household
asbestos
Coal and wood were not

reported separately. The
northern Province is one
of the poorest provinces
in South Africa and also
an important source for
exposure to asbestos.
Reference,
study location,
study period
Table 2.9 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
No. of
exposed
cases
Odds ratio
(95% CI)
Adjustment for
potential
confounders
Comments
Behera &
Balamugesh
(2005),
Chandigarh,
India,
199902
67 women enrolled
from a lung cancer
clinic; 75%
nonsmokers; 100%
confirmed by
histology or cytology
Questionnaire
Biomass use for cooking

compared with LPG
users
In nonsmokers
NG
3.6 (1.112.0)
Smoking,
environmental
tobacco smoke
NG
5.3 (1.716.7)
Exposure and duration

were not clearly defined;
biomass fuel was
considered as coal, wood,
cow dung cake,
agricultural waste,
although about 95% of
the Indian rural
population still relies
primarily on biomass
fuels (dung, crop residues
and wood); no age
adjustment; selection of
controls with respiratory
diseases could
underestimate the relative
risk.
46 women with noncancer respiratory

disease; 93%
nonsmokers
Reference,
study location,
study period
203
204
Table 2.9 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Pisani et al.
(2006),
Lampang
Province,
Thailand,
199395
211 cases (66% men)

enrolled from the
provincial hospital;
confirmed by
histology or cytology
In-person
interview
using a
standard
questionnaire
Cumulative index of
years of exposure to
domestic fumes
<9
914
1520
>21
In nonsmokers
<15
>15
Age and sex matched

population (n=202)
and hospital controls
(n=211; also matched
to cases by
residence); tobaccorelated diseases
excluded
No. of
exposed
cases
Odds ratio
(95% CI)
51
67
43
50
1.0
1.3 (0.72.2)
0.8 (0.41.4)
0.8 (0.51.5)
11
5
1.0
0.4 (0.12.0)
Adjustment for
potential
confounders
Comments
Age, sex,
cumulative
cigarettes smoked
Both coal and wood

exposure contributed to
domestic fumes and were
not assessed separately.
Tests for trend were not
presented. No trend
versus index level.
Index = years cooking
with coal/wood indoors
+0.5 of the time spent
cooking outdoors
Reference,
study location,
study period
Table 2.9 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Ramanakumar,
et al. (2007),
Montreal,
Canada,
19962001
1205 cases from 18

hospitals (61% male);
100% histologically
confirmed; 37%
proxy respondents
In-person
interview
using a
structured
questionnaire
Women only
Wood or coal stove for
heating the living space
vs. no exposure
Any exposure
Age <20 yrs
Age 20 yrs
Smoking status
Medium/heavy
None/light
Respondent type
Self
Proxy
Wood or gas stove for
cooking vs. no exposure
Any exposure
Age <20 yrs
Age >20 yrs
Smoking status
Medium/heavy
None/light
Respondent type
Self
Proxy
Exposed for
Heating only
Cooking only
Heating and
cooking
1541 population
controls; matched by
age, sex; 8% proxy
respondents
No. of
exposed
cases
Odds ratio
(95% CI)
289
239
185
2.0 (1.42.8)
2.0 (1.42.9)
2.4 (1.53.7)
219
70
2.1 (1.43.3)
1.7 (1.02.9)
192
97
2.0 (1.42.9)
1.2 (0.34.3)
358
315
176
1.6 (1.12.3)
1.7 (1.22.6)
1.3 (1.12.0)
264
94
2.0 (1.23.2)
1.3 (0.72.3)
247
111
1.8 (1.22.7)
0.3 (0.11.5)
32
102
253
1.8 (1.03.2)
1.2 (0.71.9)
2.5 (1.53.6)
Adjustment for
potential
confounders
Comments
Age, ethnic
groups, family
income, smoking,
place of birth,
surrogate or not,
education,
occupational
hazard
No significantly
increased risks were
observed in men. Most
cases were ever smokers.
Coal, wood and gas
exposures were not
defined separately. Risks
were the most increased
for small-cell carcinoma
(in women) and
squamous-cell carcinoma
(men and women)
Reference,
study location,
study period
ADC, adenocarcinoma; CI, confidence interval; LPG, liquefied petroleum gas; NG, not given; yrs, years
205
206
polluted areas, it is difficult to rule out the role potential confounding effects of these
exposures in the association between wood/coal use and lung cancer.]
Two studies in the Kaohsiung area, Taiwan, were reported by Ko et al. (1997) and Le
et al. (2001) (described in detail in the monograph on high-temperature frying). Risk
patterns associated with cooking fuels were reported. The first report included 106
nonsmoking lung cancer cases and an equal number of hospital controls (Ko et al., 1997).
Compared with women who did not cook or cooked with gas at age 20 years or younger,
those who cooked with coal experienced no increased risk for lung cancer (odds ratio, 0.5;
95% CI, 0.21.6) whereas those who cooked with wood and/or charcoal had more than a
twofold increased risk (odds ratio, 2.5; 95% CI, 1.35.1). Results were similar when they
examined cooking practices between the ages of 2040 years. Compared with those who
did not cook or cooked with gas, the risk for lung cancer was increased among those who
cooked with wood/charcoal (odds ratio, 2.5; 95% CI, 1.15.7). Few subjects cooked with
wood or coal after 40 years of age and thus meaningful analyses could not be conducted.
In a subsequent report (Le et al., 2001) (described in detail in Section 2.1.1), the
relationship between cooking fuel and risk for lung cancer was examined separately by
lung cancer cell type. The use of wood was associated with a threefold increased risk for
lung cancer (odds ratio, 3.1; 95% CI, 1.09.2) compared with women who did not cook
or used gas for cooking. In contrast, the risk for adenocarcinoma of the lung (158 cases,
262 controls) increased in relation to the use of wood (odds ratio, 3.0; 95% CI, 1.46.4).
Tobacco smoking, residential area, education and social class were adjusted for in the
analysis. [The Working Group noted that information on duration of wood and coal use
was not reported in these two studies.]
Sixty-seven women who had histologically or cytologically confirmed lung cancer
seen at the Department of Pulmonary Medicine, Chandigarh, India, and 46 controls with
non-malignant respiratory disease were recruited in a casecontrol study between January
1999 and December 2002 (Behera & Balamugesh, 2005). A questionnaire was used to
collect information on demographic factors, lifetime exposure to smoking, detailed
occupational history, residence and exposure to indoor air pollution due to burning of
organic fuels. [The Working Group noted that organic fuels were not clearly defined but
probably included coal, wood, cow dung cake and agricultural waste.] Unconditional
logistic regression models were used for analyses. Among the lung cancer cases, 50
(74.6%) were nonsmokers among whom adenocarcinoma was the predominant histology
(50%). In women who smoked, squamous- and small-cell carcinoma were the most
common histological types. When adjusted for active and passive smoking [not stated if
adjusted for age] and compared with the use LPG as the reference category, the odds ratio
for use of biomass fuel was 3.6 (95% CI, 1.112.0). Among nonsmokers, the
corresponding odds ratio was 5.3 (95% CI, 1.716.7). [These results were presented in a
table and in the text and it was unclear if the analyses were stratified or unstratified
univariate. The Working Group also noted that the selection of controls with respiratory
diseases could underestimate the relative risk.]
207
Pisani et al. (2006) carried out a casecontrol study of lung cancer with 211 hospital
cases (66% men; including smokers and nonsmokers), 202 population controls and
211 hospital controls without tobacco-related diseases matched by age and sex (and also
residence for the hospital controls). This study primarily investigated the interactions
between smoking and genetic polymorphisms in northern rural Thailand. Information was
obtained through in-person interviews. The exposure index of solid fuel use was
calculated by combining years of cooking with coal/wood indoors (weight=1) and
outdoors (weight=0.5). The majority of cases (99%) were microscopically verified; 45%
were squamous-cell carcinomas and 21% were adenocarcinomas. Only 7% of men and
33% of women in the overall study group were never smokers. No significant effects or
trends were found for the cumulative index of exposure to domestic fumes for the whole
group after adjusting for age and sex (and also cumulative smoking in smokers). [The
Working Group noted that the coal and wood exposures were not separated and therefore
made the study results uninformative for either type of fuel. The use of fuel for cooking
and heating was also not separated.]
Ramanakumar et al. (2007) conducted a hospital-based casecontrol study in
Montreal, Canada, which was originally designed to examine occupational risk factors.
This analysis included 1205 (739 men, 466 women) histologically confirmed lung cancer
patients who were diagnosed between 1996 and 1997 at the 18 largest hospitals in the
study area. A total of 1541 (925 men, 616 women) population controls were selected from
electoral lists and were interviewed. Structured interviews were conducted to collect
information on smoking history, occupational history, sources of traditional heating
(defined as wood or coal stove in living space) and cooking (defined as a wood or gas
stove) and other risk factors. To assess exposure to traditional cooking sources, subjects
were asked if they had ever lived full-time in a house/apartment where the cooking was
carried out on a gas or wood stove. Similarly, to assess exposure to traditional heating
sources, subjects were asked if they had ever lived in a house/apartment that was mainly
heated by a stove or fireplace located in the living quarters. No significant associations
with exposure to traditional heating or cooking were found for men, with most of the odds
ratios below 1.0. For women, however, most of the odds ratios associated with traditional
heating or cooking were above 1.0 and were statistically significant. In women, elevated
risks associated with traditional heating were found in subjects who were older
(60 years) at the age of onset, self-respondent, and in smokers. An increased risk for
lung cancer was also observed in women classified as nonsmokers and light smokers.
[The Working Group noted that the assessment of traditional cooking combined
cooking with gas and wood whereas the assessment of traditional heating may have
included exposure to wood/coal. In addition, there was incomplete specification of fuel
use; for example, no mention was made of the use of electricity for cooking or oil and
electricity for heating which further complicated the interpretation of this study.]
208
2.3.2
Cancer of the oral cavity, pharynx and larynx (see Table 2.6)
Three concurrent casecontrol studies were conducted in Heidelberg, Germany, to

examine the association between fossil fuel stoves and the risk for laryngeal, pharyngeal
and oral cavity cancer (Dietz et al., 1995; Maier & Tisch, 1997). A total of 164, 100 and
105 cases of laryngeal, oral cavity and pharyngeal cancer, respectively, were ascertained
between 1989 and 1992 from all patients seeking treatment at the Otorhinolaryngology
Department within 3 years from first diagnosis. Almost all cases were current or former
smokers. Controls were recruited from the same medical centre and general outpatient
department at the University of Heidelberg from among non-cancer patients and matched
to cases on sex, age and size of the place of residence. Fossil fuel emissions from stoves
and cooking and the type of burning materials used (coal, briquette, coke, peat, gas and
oil) were ascertained. Use of fossil fuel stoves or cookers were associated with all three
types of cancer: adjusting for tobacco and alcohol use, the odds ratio for >40 versus 0
20 years was 2.0 for fossil fuel heating (95% CI, 1.103.46) and 1.4 for cooking (95% CI,
0.762.41) for laryngeal cancer, 3.3 for fossil fuel heating (95% CI, 1.437.55) and
2.5 for cooking (95% CI, 1.036.30) for pharyngeal cancer and 2.4 for fossil fuel heating
(95% CI, 1.264.40) and 1.6 for cooking (95% CI, 0.902.97) for oral cavity cancer. [The
Working Group noted that no doseresponse trend with duration of use and no
association for the 2040-year exposure category for any of the cancer sites were
observed; also, the specific type of fuel responsible for the increase in risk at the highest
duration of stove use could not be determined.]
2.3.3
Cancer of the nasopharynx (see Table 2.7)
A casecontrol study of 115 cases of NPC (86 men, 29 women) newly diagnosed
pathologically in the hospitals of Fujian Province during the period from March to May
1991, who had lived in Fujian at least for 10 years, was conducted (Cai & Ye, 1996).
Controls (115 cancer controls and 115 non-cancer controls) were randomly selected from
the patients and matched on sex, age (within 5-year age group) and date of hospitalization
(same month) to the cases. The controls had also lived in Fujian at least for 10 years. The
cancer controls were patients with cancers other than of the respiratory system, while the
non-cancer controls were patients without cancer or respiratory diseases. Information in
1968 and 1978 on demographic factors, residential, dietary and occupational history,
smoking and alcohol drinking, family history of cancer and chronic diseases of ear, nose,
pharynx and larynx was collected. In multivariate analysis using non-cancer controls, the
odds ratio for use of straw as domestic fuel was 6.52 in 1978 (95% CI, 1.9022.32). Use
of coal and firewood/straw in 1968 was positively associated with NPC for cancer
controls (odds ratio, 3.14; 95% CI, 1.188.36) and for the combined control groups (odds
ratio, 3.35; 95% CI, 1.368.26). [The Working Group noted that the odds ratio for straw
was estimated using coal fuel as a reference group. Consumption of salted fish was only
assessed in 1978, but not in childhood, and because both salted fish consumption and
209
straw use may be associated with socioeconomic status, the odds ratio for straw may be
confounded.]
A hospital-based casecontrol study of NPC (Huang et al., 2002) was carried out in
Guangxi to search for risk factors of NPC other than Epstein-Barr virus (EBV) infection;
175 cases of NPC (132 men, 43 women) pathologically diagnosed and treated at First
Hospital and Cancer Hospital affiliated to Guangxi Medical University during the period
from March 2000 to May 2001 were involved in the study. The cases had lived in
Guangxi for at least 10 years and had originated from Guangxi. A total of 350 controls
(264 men, 86 women) were selected from patients without cancer or respiratory diseases
treated at the same hospital and same period, and matched on sex, age (4 years),
occupation, at least 10 years of living in Guangxi and same place of origin as the cases.
Information on demographic factors, occupational history, residential environment, life
and dietary habits, previous diseases, family history of NPC and psychological factors
was collected by use of a structured questionnaire. Use of coal or firewood as fuel was
associated with a significantly increased risk for NPC (odds ratio, 3.68; 95% CI, 2.15
6.29).
2.4
Proxies for indoor air pollution
2.4.1
The studies that are included in this section of mixed exposures did not examine
specific exposures such as type of cooking oil or frequency of high-temperature cooking
but rather examined measures related to general cooking practices (e.g. age started or
years of cooking) or ventilation.
The first study that included data on cooking practices and lung cancer was a hospitalbased casecontrol study conducted in Singapore (MacLennan et al., 1977) which
included 233 lung cancer cases (147 men, 39 Cantonese women, 47 non-Cantonese
women) and 300 hospital control subjects (134 men, 80 Cantonese women, 86 nonCantonese women) who were identified from three main hospitals. In total, 46 lung
cancer cases (20%) and 124 controls (41%) were nonsmokers. Thirty-six per cent
(84/233) of the lung cancer cases were histologically confirmed. The risk for lung cancer
in relation to domestic cooking was 1.55 [95% CI, 0.753.22] in men, 1.74 [95% CI,
0.674.47] in Cantonese-speaking women and 0.40 [95% CI, 0.210.92] in nonCantonese-speaking women. [The Working Group noted that no adjustment for active
smoking or use of gas/kerosene was made in the analysis. No description of the questions
asked on cooking was given: the frequency, duration and intensity of cooking were not
included.]
In a casecontrol study in Shenyang, China, Xu et al. (1989) (described in Section
2.1.1) developed a continuous index of average long-term indoor air pollution intensity,
based on duration of living at each residence, presence of coal heating, cooking fuel and
location of cooking place (e.g. separate or not). This index was positively associated with
210
Table 2.10. Case-control studies of lung cancer and proxies of indoor air pollution
Characteristics of
cases and controls
Exposure
assessment
Exposure categories
MacLennan
et al. (1977),
Singapore,
197274
233 cases (147 men,

86 women) from 3
hospitals; 36% confirmed histologically;
80% smokers
In-person interview
Ever cooked
Men
Cantonese
Women
Non-Cantonese
women
No. of
exposed
cases
Odds ratio (95%

CI)a
80
21
32
27
1.01 (p>0.05)
1.55 [0.753.22]
1.74 [0.674.47]
0.40 [0.210.92]
300 (134 men, 166

women) controls who
did not have smoking-related disease;
matched on sex, age,
dialect; 59% smokers
Xu et al.
(1989),
Shenyang,
China,
198587

520 women) in
Shenyang aged 3069
yrs; cell type
histologically
confirmed in 83% of
men and 73% of
women
1345 populationbased controls (788
men, 557 women),
selected by 3-stage
procedure from urban
Shenyang; frequencymatched on gender,
age
In-person interview
using a structured
questionnaire;
continuous index of
indoor exposure to
coal smoke from
heating and
cooking
Indoor air index

versus <1
Men
1.01.4
1.51.9
>2.0
Women
1.01.4
1.51.9
>2.0
Perceived indoor
smokiness during
heating versus none
Men
Somewhat smoky
Smoky
Women
Somewhat smoky
Smoky
258
168
94
1.1 (0.81.4)
1.2 (0.91.6)
1.6 (1.12.3)
183
110
56
1.2 (0.91.6)
1.3 (0.91.9)
1.5 (1.02.4)
249
198
1.2 (1.01.5)
1.3 (1.01.7)
146
116
1.2 (0.91.6)
2.0 (1.42.8)
Adjustment for
potential
confounders
Comments (covariates
considered)
None
Exposure index not well

defined; gas/kerosene use
was not a risk factor.
The Working Group
calculated the confidence
intervals assuming an
unmatched analysis. It
was not clear how the
authors calculated the
odds ratio for the ever
cooked category.
The indoor air index
ranged from 0 to 3, with
values below 1 indicating
potential for relatively low
lifetime exposure to
indoor air pollution from
burning coal. [This study
overlaps with Sun et al.
(1991)]
Reference,
study
location,
study period
Table 2.10 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
He et al.
(1991); Liu et
al. (1991),
Xuan Wei,
China,
198586
110 diagnosed lung

cancer patients (56
men, 54 women)
In-person interview
using a structured,
field-tested
questionnaire
Men
Often cooks food
Women
Age started cooking
versus >15 yrs
1115
10
p for trend
Yrs of cooking
versus 30
3144
45
p for trend
45 yrs using
unventilated fire pit
(versus <45 yrs)
Men
Women
426 controls (224

men, 202 women);
matched on gender,
age (+2 yrs)
occupation (all
farmers), village of
residence; 1
5 controls per case
(mean, 3.87)
No. of
exposed
cases
Odds ratio (95% CI)a
12
3.36 (1.278.88)
30
11
2.37 (1.095.15)
1.25 (0.453.49)
>0.05
28
19
9.18 (1.7647.49)
14.70 (1.61134.03)
>0.05
34
33
1.78 (0.466.93)
0.73 (0.202.60)
Adjustment
for potential
confounders
considered)
Unclear
Although the analyses

were duplicated in both
studies, the Working
Group noted discrepancies
in the results. The
instability of the risk
estimates is demonstrated
with the different choice
of category cut-points in
both studies. Matching by
village provided matching
on indoor fuel type and
home type, allowing more
incisive analysis of other
factors such as smoking
and duration and
frequency of cooking
food.
Male and female subjects
burned more smoky coal
(range; 4.04.2 tonnes/yr
than wood (range; 0.81.0
tonnes/yr)
Reference,
study
location,
study period
211
212
Table 2.10 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Liu et al.
(1991)
Xuan Wei,
China
198586
110 cases (56 men, 54

women); 17%
histologically
confirmed; 52 men
and 0 women smoked
In-person interview
Men
Often cooked food
No
Yes
Women
Age started to cook
>15 yrs
1115 yrs
10 yrs
p for trend
Yrs of cooking
30
3144
45
p for trend
426 controls (224

men, 202 women);
matched by age ( 2
yrs), sex, village of
residence; 205 men, 1
woman smoked
No. of
exposed
cases
Odds ratio (95%

CI)a
44
12
1.0
3.36 (1.278.88)
13
30
11
1.0
2.37 (1.095.15)
1.25 (0.453.49)
>0.05
7
28
19
1.0
5.18 (1.7647.49)
14.70 (1.61134.0)
>0.05
Adjustment for
potential
confounders
considered)
Smoking index
(yrsamount of
smoking)
Conditional logistic
regression was used to
adjust for matching
factors.
Unspecified
Reference,
study
location,
study period
Table 2.10 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Koo & Ho
(1996),
Hong Kong,
198183
200 female lung

cancer patients, mean
age 61.8 yrs; 44%
never smokers; 90%
histologically
confirmed (28% SCC,
18.5% small-cell,
34.5% ADC)
Interviews with
semi-structured
questionnaire, using
a life history
approach; assessed
use and duration of
using biomass
fuels, coal,
kerosene, LPG and
gas.
Yrs of cooking
among never
smokers
025
2640
41
p for trend
Standardized
questionnaire
Cooking fumes
SCC
ADC
200 female
community controls;
matched on age (+5
yrs), residential
district, housing type;
mean age 60.6 yrs;
69% never smokers
Shen et al.
(1996),
Nanjing,
China
198693
263 cases (83 SCC,

180 ADC) who were
20 yrs
263 population
controls who were
Nanjing residents;
matched 1:1 for
gender, age, ethnicity,
street address
No. of
exposed
cases
Odds ratio (95%

CI)a
NG
NG
NG
1.00
0.38 (0.170.88)
0.37 (0.140.96)
<0.001
NG
NG
3.81 (1.0613.73)
2.99 (1.685.34)
Adjustment for
potential
confounders
considered)
Age, number of
live births,
education
Risk associated with

cooking fumes was
evaluated.
Unclear
Fuel types within solid

fuel category were not
specified. Statistical tests
were reported as onesided, but implications are
not clear.
Reference,
study
location,
study period
213
214
Table 2.10 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Shen et al.
(1998),
Nanjing,
China,
1993
70 never-smoking
women diagnosed
with primary lung
ADC; all were
20 yrs
In-person interview
using a
standardized
questionnaire
Cooking fumes
In-person interview
using a structured
questionnaire
Not cooking in
separate kitchen
Cooking hot with
visible fumes
Kitchen smokiness
during cooking
Somewhat
Considerable
Eye irritation during
cooking
Rarely
Sometimes
Frequently
No. of
exposed
cases
Odds ratio (95%

CI)a
Adjustment for
potential
confounders
considered)
2.45 (1.065.66)
Unclear
The main purpose of the

study was to assess lung
cancer risk associated
with passive smoking.
This study may overlap
with Shen et al. (1996).
248
1.28 (0.981.68)
165
1.64 (1.242.17)
241
86
1.67 (1.252.21)
2.38 (1.583.57)
49
74
43
1.49 (0.912.43)
1.75 (1.162.62)
1.68 (1.022.78)
Age, education,
income, vitamin
C intake,
respondent
status, exposure
to
environmental
tobacco smoke,
occupation,
family history of
lung cancer
70 healthy
community controls;
matched 1:1 for
gender, age,
neighbourhood,
occupation
Zhong et al.
(1999),
Shanghai,
China,
199294
504 never-smoking
female incident cases,
3569 yrs old,
identified from the
Shanghai Cancer
Registry
601 never-smoking
women; frequencymatched on age
distribution of female
lung cancer cases
during 198789;
randomly selected
from the Shanghai
Residential Registry
Reference,
study
location,
study period
Table 2.10 (contd)

Characteristics of
cases and controls
Exposure
assessment
Exposure categories
Zhou et al.
(2000),
Shenyang
City,
Liaoning
Province,
China,
199195
72 female incident
cases of adenocarcinoma, aged 35
69 yrs, from 18 major
hospitals
In-person interview
using standardized
questionnaire
Kitchen location
versus separate
kitchen
In living room
In bedroom
Eye irritation from
smoke versus none
Infrequent
Sometimes
Frequent
p for trend
Smokiness during
cooking versus none
Slight
Medium
Heavy
p for trend
72 women randomly
selected from the
Shenyang general
population, agematched (5 yrs) to
Liaoning lung cancer
cases in 198889
No. of
exposed
cases
Odds ratio (95%

CI)a
63
3
1.40 (0.414.88)
1.00 (0.118.93)
35
22
3
1.33 (0.533.35)
7.33 (1.9229.76)
1.67 (0.2212.93)
0.006
15
35
3
0.73 (0.281.90)
2.71 (1.096.80)
1.32 (0.189.50)
0.027
Adjustment for
potential
confounders
considered)
Not specified
Fuel type not specified for

exposure to cooking
fumes
ADC, adenocarcinoma; CI, confidence interval; LPG, liquefied petroleum gas; NG, not given; SCC, squamous-cell carcinoma; yrs, years
a
p-value is specified if no confidence interval is indicated
Reference,
study
location,
study period
215
216
lung cancer risk in a doseresponse fashion in both men and women. [This study overlaps
with Sun et al. (1991).]
One study in Xuan Wei County, China (Liu et al., 1991), was based on 110 incident
lung cases (56 men, 54 women) identified in regional hospitals and clinics between 1985
and 1986 and 426 population controls (224 men, 202 women) matched on age, sex,
occupation and village of residence. Almost all of the men (52 cases, 205 controls) but
few of the women (no cases, one control) were smokers. Only 17% of the lung cancers
were pathologically or cytologically confirmed. Men who reported that they often cooked
food had a significantly increased risk for lung cancer (odds ratio, 3.36; 95% CI, 1.27
8.88; 12 exposed cases) after adjusting for smoking and other unspecified covariates.
Women who started cooking at a young age showed an increased risk but there was no
significant trend of increasing risk with decreasing age when starting to cook. Compared
with women who started cooking at age 15 years or older, the adjusted odds ratio for lung
cancer was 2.37 (95% CI, 1.095.15; 30 exposed cases) for starting cooking at age 11
15 years and 1.25 (95% CI, 0.453.49; 11 exposed cases) for starting cooking at age
10 years or younger (p for trend >0.05). However, the risk increased with increasing years
of cooking (adjusted odds ratios, 1.00, 9.18 and 14.70 for 30, 3144 and 45 years of
cooking, respectively; p for trend >0.05), but the confidence intervals were very wide.
[The Working Group noted that this small study had only indirect measures of cooking
practices, based on age when started cooking and duration of cooking. The study was
limited because only 83% of the lung cancers were diagnosed clinically or radiologically.
Potential confounding was not adequately addressed in the statistical analysis.]
Liu et al. (1993) presented the results of a hospital-based casecontrol study of indoor
air pollution and lung cancer in Guangzhou, China (described in detail in Section 2.1.1).
After the in-person interview, the interviewer measured the size of the windows and doors
that opened onto the outside of the building, thereby providing an estimation of
ventilation capacity. If the subject had lived in his or her present home for less than
20 years, the interviewer asked similar questions regarding the preceding residences and
their ventilation conditions. Data on up to three residences were collected. Not having a
separate kitchen and poor air circulation were significantly associated with the risk for
lung cancer in men and women. There was a significant doseresponse relationship (p for
trend <0.05) and a significant inverse association with risk for lung cancer seen with size
of ventilation openings in the kitchen and living area and room height. Increased risks for
lung cancer were found for men (adjusted odds ratio, 2.4; 95% CI, 1.44.2) and women
(adjusted odds ratio, 5.9; 95% CI, 2.116.0) who lived in homes that did not have a
separate kitchen. Similarly, living in a house with poor air circulation was associated with
an increased risk in men (adjusted odds ratio, 2.1; 95% CI, 1.23.6) and women (adjusted
odds ratio, 3.6; 95% CI, 1.49.3). In contrast, significant trends of decreasing risk were
observed in association with better ventilation, based on variables that measured size of
ventilation openings in living areas and in kitchens (see Table 2.10). However, no
differences were observed between cases and controls in the number of meals they
cooked per day or the presence of chimneys in their homes. [The Working Group noted
217
that this study did not include direct measures of cooking fumes/practices. However, this
was one of the few studies that attempted to obtain a more objective measure of
ventilation. As part of the study, the interviewers measured the size of the windows and
doors that opened onto the outside of the building in each participants home. In addition,
information on ventilation in up to three previous residences was obtained. A limitation is
that a high percentage of the lung cancers were not cytologically/histologically
confirmed].
Du et al. (1996) also reported a casecontrol study in which cases were
120 nonsmokers drawn from 849 decedent cases. In conditional logistic regression
models, risk for lung cancer in women was significantly associated with increasing indoor
air pollution and decreasing kitchen size. These factors were not associated with risk in
men. [The Working Group noted that these studies are limited by use of proxy
respondents and overall exposure assessment.]
Lei et al. (1996) conducted a casecontrol study in Guangzhou, China, among
792 cases who had died from primary lung cancer (563 men, 229 women), identified
from 1986 death certificates, and 792 controls matched on gender, age, street of residence
and year of death. Controls had no history of respiratory diseases or tumours. Women
with a fair or poor living conditions index (living area per person/room ventilation) had a
significantly increased risk for lung cancer while this association was much weaker and
only of borderline statistical significance in men.
Koo and Ho (1996) examined the role of cooking fumes and lung cancer risk in a
casecontrol study that included 200 female lung cancer cases and 200 neighbourhood
controls. Histology was determined in 90.5% of the cases of which 34% were
adenocarcinoma. Forty-four per cent of cases (88/200) and 68.5% of controls (137/200)
were never smokers (Koo et al., 1983). A significant inverse association was observed
between the duration of cooking and risk for lung cancer among never smokers. After
adjusting for age, number of live births and education, the risk for lung cancer declined
with increasing years of cooking; the adjusted odds ratios were 1.0, 0.38 (95% CI, 0.17
0.88) and 0.37 (95% CI, 0.140.96) for 025, 2640 and 41 years of cooking (p for
trend <0.001). [The Working Group noted that this study only presented results on
indirect measures of cooking and that results in smokers were not reported. From an
earlier report by Koo et al. (1983), kerosene was the main fuel that was used and thus
confounding by coal use is unlikely to be a main issue in this analysis.]
In Shen et al. (1996, 1998) (described in detail in Section 2.1.1), multivariable
analysis showed that exposure to fumes or pollution from cooking was significantly
associated with risk for lung cancer (odds ratio, 2.45; 95% CI, 1.065.66; p=0.02). [The
Working Group noted several limitations in this study. The report lacked details regarding
the study design (e.g. response rate), characteristics of the study population (e.g. gender
distribution, active smoking history) and covariates included in the statistical models.]
In two hospital-based casecontrol studies conducted in Kaohsiung, a heavily
industrialized city in Taiwan (China) (Ko et al., 1997; Le et al., 2001) (in detail in Section
218
2.1.1), the use of a fume extractor in the kitchen was also significantly associated with a
reduced risk for lung cancer.
Zhou et al. (2000) (described in detail in Section 2.1.1) showed that, compared with
women who had a separate kitchen for cooking, the risk for lung cancer was not increased
for cooking in the living room (crude odds ratio, 1.40; 95% CI, 0.414.88) or bedroom
(crude odds ratio, 1.00, 95% CI, 0.118.93). However, in multivariable regression
analysis, frequent eye irritation from smoke had an independent impact on risk.
Compared with women who reported no eye irritation from smoke, those who reported
slight, medium and heavy eye irritation had elevated risks; the respective adjusted odds
ratios were 1.58, 11.45 and 3.41 (p for trend=0.002). [The Working Group noted that
most of the lung cancer cases and controls included in the analysis by Zhou et al. (2000)
were already in the report by Wang et al. (1996). Unadjusted odds ratios were reported.
This study was small and the confidence intervals were very wide.]
In the casecontrol study of lung cancer by Le et al. (2001) (described in detail in
Section 2.1.1), risk was significantly higher for those who cooked in a kitchen without a
fume extractor: the odds ratio was 3.0 (95% CI, 1.37.1; 31 exposed cases) for squamous/small-cell cancer and 3.9 (95% CI, 2.36.6; 74 exposed cases) for adenocarcinoma. Only
7% of men reported cooking for the family and thus these data were not reported.
2.4.2
Cancer of the nasopharynx
A hospital-based casecontrol study of NPC was conducted in Minan Prefecture,

Fujian Province, China (Ye et al., 1995), on 135 cases of NPC that were pathologically
diagnosed and treated at Second Hospital affiliated to Fujian Medical University in
Quanzhou. Controls were patients of surgical and osteological departments of the same
hospital without cancer or respiratory diseases, were matched on sex, age (within 5-year
group) and date of hospitalization and had lived in Minan Prefecture for at least for
10 years with the same place of origin. Information on demographic factors, residence,
family cancer history, dietary history, smoking, alcohol drinking, tea drinking,
occupational history and chronic diseases of the ear, nose, pharynx and larynx was
collected. In a multivariable conditional logistic regression analysis, smokiness during
cooking was associated with an elevated risk for NPC with an odds ratio of 2.30
(P=0.012). The other significant factors associated with risk were intake of green melon
(protective factor), index of passive smoking during adulthood, consumption of salted
preserved vegetables and cooking (risk factors).
In a casecontrol study (Hubert et al., 1993; Zheng et al., 1994) (described in detail in
Section 2.2.4), absence of windows, poor ventilation, cooking outside the house in a
shack and the presence of a fireplace in the kitchen during childhood significantly
increased the excess of risk for NPC associated with using wood as a fuel.
Two hospital-based casecontrol studies on NPC that used a similar study design and
questionnaire were conducted in Guangzhou and Heilungjiang Province (Huang et al.,
1997). A total of 104 cases of NPC who were pathologically diagnosed at each of two
219
hospitals (cancer hospitals affiliated to Sun Yat-Sen Medical University in Guangzhou

and Harbin Medical University in Harbin) during the period from 1 October 1992 to
1 March 1994 and who had lived in Guangzhou or Heilungjiang for more than 80% of
their life were involved in the study. The cases were recruited sequentially in accordance
with the order of entrance to each hospital until 104 cases had been obtained. One control
per case was matched on sex, age (5 years) and some place of origin as the case and was
selected from residents without cancer in the next residential community to the cases.
Information on demographic factors, residence, occupation, dietary history, previous
diseases and family cancer history was collected from cases and controls by use of a
unified questionnaire. In multivariate analysis, cooking inside the house and use of a stove
without a chimney were two significant variables associated with the risk for NPC.
Taking the odds ratio for cooking inside the house for 35 or less than 35 years as 1.0, the
odds ratio for more than 35 years was 1.96 (95% CI, 1.233.71). Taking the odds ratio for
use of a stove without a chimney for 10 or less than 10 years as 1.0, the odds ratio for
more than 10 years was 2.69 (95% CI, 1.544.68). In Harbin, in comparison with the use
of coal or wood, the use of gas as fuel decreased the risk for NPC, with an odds ratio of
0.93 (95% CI, 0.900.97; p=0.027). [The Working Group noted the discrepancy between
the relatively small number of subjects and the narrow confidence intervals.]
Sihui City, Guangdong Province, is one of the endemic areas of NPC in China with
an incidence rate of about 20/105. A casecontrol study on NPC was conducted that
included 57 cases who were alive and pathologically diagnosed in Sihui City between
January 1998 and June 1999 (Cao et al., 2000). The control group consisted of spouses
and relatives of spouses of these 57 cases. In multivariate analysis, family cancer history,
connection of the bedroom with the kitchen during childhood and tobacco smoking were
significant risk factors for NPC. The odds ratio for separation of the bedroom from the
kitchen was 0.48 (95% CI, 0.300.78).
2.4.3
Cancer of the cervix
A nested casecontrol study to investigate the association of exposure to cooking oil

fumes with the risk for cervical neoplasm was carried out between October 1999 and
December 2000 on 32 466 women aged over 19 years who underwent Pap smear
screening in Chi-Yi City of Taiwan, China (Wu et al., 2004). Among 420 women newly
diagnosed as having CIN lesions CIN1, 349 were followed-up by biopsy. Among the
349 subjects with biopsy follow-up, 116 women had lesions CIN2 confirmed by biopsy.
These 116 women were eligible as cases for the study. The controls were randomly
selected from women whose Pap smear results were negative in the first screening of the
study period. The casecontrol ratio was 1:2 with matches for age (2 years), residence
and the time that the Pap smear was performed (within 6 months of the cases). The
findings of previous Pap smears taken before this study were found to be normal in both
cases and controls. The subjects were interviewed in their homes between October 2000
and March 2001. Information on demographical characteristics, education, smoking,
220
exposure to environmental tobacco smoke, exposure to X-ray examinations or hair dye,

occupation (especially professional chef), sexual and reproductive history and times of
prior cervical smears, as well as cooking and kitchen ventilation status, was collected. A
multivariable logistic regression model was used to assess the association between case
control status and different cooking and ventilation conditions, after adjusting for age,
education, smoking, age at first intercourse, number of prior Pap smears and profession as
a chef. Of the 116 cases with CIN2, 16 women who had no questionnaire information
were excluded from the study. Among the 100 cases with a completed questionnaire, 39,
12, 46 and three cases had CIN2, CIN3, carcinoma in situ and invasive cancer,
respectively. The results of the age at which one started cooking, years of cooking and
hours spent on cooking were insignificant. Subjects who cooked in a kitchen without a
fume extractor at 2040 years of age had a 2.29-fold higher risk (95% CI, 1.084.87) for
developing CIN than those who used a fume extractor, after adjusting for corresponding
factors. The odds ratio was 3.16 (95% CI, 1.198.43) for women who cooked in kitchens
without fume extractors at >40 years of age. The use of coal as cooking fuel had a higher
risk for CIN than that of gas for the women in the group who cooked at 2040 years of
age (adjusted odds ratio, 2.09; 95% CI, 0.865.10) and at >40 years of age (adjusted odds
ratio, 1.53; 95% CI, 0.1714.19), but the difference in risk was insignificant. Among the
women over 40 years of age, those who did not have kitchen fume extractors at home at
both 2040 years and >40 years of age had a 3.46-fold greater risk of developing CIN
than those who did have fume extractors during the same two periods, after adjusting for
corresponding factors. The odds ratio for having a fume extractor only during one period
but not the other was 2.05 (95% CI, 0.864.86). It was also found that women who had
been professional cooks had a 3.97-fold greater risk (95% CI, 1.0215.41) than those who
had not. [The Working Group noted that the results were not stratified by or adjusted for
HPV.]
2.5
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3.
225
Studies of Cancer in Experimental Animals
A series of animal and human studies of cancer were begun in China in the 1980s due
to the generally high concentrations of air pollution from burning coal for fuel. Coal was
widely used in China; in fact, in Xuan Wei County, Yunnan Province, mortality from
lung cancer is among the highest in China and could not be accounted for by tobacco or
occupational exposures. The emissions from smoky coal that were collected indoors in
homes where it was used for cooking and heating without chimney ventilation contained
a large proportion of submicron particles with a high concentration of PAHs. These
studies evaluated the carcinogenicity of emissions from several types of coal (e.g. smoky
coal and smokeless coal), wood smoke and, in several studies, particles from different
cities in China were compared (e.g. Xuan Wei, Beijing and Tai Yuan) (Mumford et al.,
1987).
3.1
Coal smoke and soots from household combustion of coal
3.1.1
Whole-body and inhalation exposure

(a)
Mouse
Two studies of whole-body exposure to coal soot that were reported in the 1930s
were reviewed by a previous IARC Working Group that was convened to evaluate soots
(IARC, 1985). These included an early study that used soot from a coal furnace as
bedding in the cages that housed 3-month-old Buffalo strain mice. The exposure was
maintained by shaking the cages two to three times per day. Eight lung adenocarcinomas
were reported in the 100 exposed mice and one in controls (Seeling & Benignus, 1936).
[At that time, the Working Group noted the unusually high mortality in controls and lack
of reporting on skin tumours.] The second study used an inhalation chamber to expose
mice, 3 months of age [strain unknown] for 1 year to a moderate cloud of soot, once an
hour, for 6 h on 5 days per week. No increase in the incidence of lung tumours was found
at the end of 2 years and no skin tumours were found (Campbell, 1939). [At that time, the
Working Group noted the short duration of treatment.]
Groups of 113160 male and 5058 female randomly bred Kunming mice, weighing
~21 g, [age unspecified] were exposed to indoor air pollution or control air for 15 months.
The two exposure rooms had a round shallow pit dug in the centre and bituminous coal
was incompletely burned to simulate the normal indoor air conditions under which human
exposures occur in Xuan Wei County, China. The control room air moved freely between
indoors and outdoors and no coal was burned where the control mice were housed.
Pollutants were monitored several times a day and included TSP (0.91 mg/m3 for the
controls and 14.38 mg/m3 for coal smoke), sulfuric acid fume and carbon monoxide. The
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concentrations of benzo[a]pyrene were: control group, 1.47 g/10 m3; and coal smoke,
506.44 g/10 m3. The total incidence of lung cancer was 17% of 171 mice in the control
group (adenocarcinomas only) and 89.5% of 210 mice in the coal smoke-exposed group.
The coal smoke-treated group also had the highest incidence of all three types of lung
cancer identified including squamous-cell carcinomas (11.4%), adenosquamous
carcinomas (21.4%) and adenocarcinomas (56.6%). The total incidence of pulmonary
tumours (including adenomas) in the coal smoke-exposed group was 196/210 (93.3%)
(Liang et al., 1988).
Groups of 30 male and 30 female Kunming mice, 40 days of age and weighing
131 g, were exposed by inhalation for 2 years to coal smoke from burning 60, 105 and
160 g coal per day to simulate the normal indoor air conditions under which human
exposures occur in Harbin City, Hei Long Jang Province, China. Controls had no
exposure to smoke [no exposure metric was used to provide exposure concentration]. The
incidence of lung tumours (all adenocarcinomas) was 3.6% in the control group, 9.4% at
the lowest (60 g) dose, 12.8% at the mid (105 g) dose and 24.3% at the high (160 g) dose.
The cancer incidence in the two highest doses was significantly higher than that in the
control group (p<0.05) (Lin et al., 1995).
(b)
Rat
Groups of 5562 male and 5163 female randomly bred Wistar rats, weighing
~105 g, [age unspecified] were exposed to indoor air pollution or control air for
19 months. The two exposure rooms had a round shallow pit dug in the centre and
bituminous coal and wood were incompletely burned to simulate the normal indoor air
conditions under which human exposures occur in Xuan Wei County, China. The control
room air moved freely between indoors and outdoors and no coal was burned where the
control rats were housed. Pollutants were monitored several times a day and included TSP
(0.91 mg/m3 for the controls and 14.38 mg/m3 for coal smoke), sulfuric acid fume and
carbon monoxide. The concentrations of benzo[a]pyrene were: controls, 1.47 g/10 m3;
and coal smoke-exposed, 506.44 g/10 m3. The total incidence of lung cancer was 0.9%
of 110 rats in the control group and 67.2% of 125 rats in the coal smoke-exposed group.
All cancers in the coal smoke-exposed group were squamous-cell carcinomas. No
squamous-cell carcinomas were observed in control animals. The only adenocarcinoma
occurred in the control group and none was observed in the coal smoke-exposed rats. The
total incidence of pulmonary tumours (including adenomas) was 84/125 (67%) in the coal
smoke-exposed group and 1/110 (0.9%) in the control group (Liang et al., 1988).
3.1.2
Intratracheal administration
(a)
Mouse
Coal-fume extracts were generated from collections of coal smoke from an area of
high cancer incidence in Xuan Wei County, China. Soot was extracted with an aqueous
solution of Tween-80 and 0.1 mL vehicle solution. Vehicle solution containing
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12.5 mg/mL soot was instilled intratracheally into 43 and 72 male Kunming mice,
respectively, once every 10 days for an average period of 100 days; the animals were then
held until 18 months, at which time they were killed. Overall lung tumour incidence
(adenomas and adenocarcinomas combined) was 25.6 and 52.8% in the vehicle and soot
instilled mice, respectively. The incidence of lung adenocarcinomas was 16.3 and 40.3%
(p<0.01) in the vehicle and treated groups, respectively (Yi et al., 1984).
(b)
Rat
One intratracheal instillation study in rats (Vsame, 1979) was reviewed by an

IARC Working Group that was convened to evaluate coal soot (IARC, 1985). [The
Working Group noted that the experimental details were unclear and felt that the study
did not contribute to the evaluation of coal soot in experimental animals.]
3.1.3
Dermal application
(a)
Mouse
Carcinogenicity studies of coal-derived soot extracts and fractions, and also of shale
oil-derived soot, woodsoot, fuel-oil soot extracts, applied to mouse skin were reported
between 1922 and 1979 and were reviewed by an IARC Working Group that was
convened to evaluate soots (IARC, 1985). The studies on dermal application that were
reviewed included studies of mice treated with various types of coal-derived soot extracts
and fractions. The sources of these soots included bituminous coal-derived household
soot, domestic chimney coal-derived soot, oil-derived soots and solid shale oil-derived
soot. It was concluded that coal-soot extracts applied to the skin of mice produced skin
tumours in three studies (Passey, 1922; Passey & Carter-Braine, 1925; Campbell, 1939).
Studies of shale oil-derived soot applied to mouse skin also produced skin tumours in
mice (Bogovski, 1961; Vsame, 1963, 1979). The wood-derived and fuel oil-derived
soot extracts were inadequately tested by skin application (Sulman & Sulman, 1946;
Mittler & Nicholson, 1957).
Indoor coal smoke particles (<10 m) were collected from Xuan Wei County, China,
for a study of tumour initiationpromotion. Groups of 40 female Kunming mice [age
unspecified] received skin applications of 1, 5, 10 or 20 mg acetone extracts of each
smoke type. Control groups included a group that received 50 mg benzo[a]pyrene in
0.2 mL and groups treated with the tumour promoter 12-O-tetradecanoylphorbol-13acetate (TPA) or acetone. One week after initiation, the animals in the treatment group
and TPA group received twice-weekly skin applications of 2 g TPA (dissolved in
0.2 mL acetone) for 26 weeks and were then held for an additional 6 weeks of
observation. A doseresponse in skin tumour incidence was observed in the coal smoketreated group at weeks 20, 26 and 32, respectively. At week 26, the skin tumour incidence
was 2560% in the coal smoke-treated groups, 50% in the benzo[a]pyrene-treated group,
10% in the TPA-treated group and 0% in the acetone control group. The tumour
incidence in the coal smoke-treated groups and benzo[a]pyrene-treated group were
228
significantly higher than those in TPA-treated group and control group (p<0.01). The first
tumour was observed during weeks 912 in coal smoke-treated groups and at week 11 in
the benzo[a]pyrene-treated group. The higher dose of the coal smoke extract resulted in a
shorter time to the incidence of the first tumour. The largest number of tumours (11 skin
tumours/mouse) was observed in the group treated with 10 mg coal-smoke extract (Liang
& Wang, 1987).
Indoor air particles (<10 m) were collected during cooking periods in Xuan Wei
homes without chimneys and in different communes that had access to one of the
following fuels: smoky coal, smokeless coal and wood (pine). The smoky coal was lowsulfur (0.9%) coal with high heating value (27.1 MJ/kg) and 20% ash content
(comparable with US medium-volatile bituminous coal). The smokeless coal was a lowgrade coal with 14.5 MJ/kg heating value, 1.9% sulfur and 49% ash. The PAH content
per milligram of organic matter was high for both the smoky coal and smokeless coal
compared with the wood; however, the concentrations of PAH per microgram per cubic
metre were at least 10-fold higher in the homes that used smoky coal compared with those
that used smokeless coal and wood. Groups of 40 female SENCAR mice, 79 weeks of
age, received dermal applications of 0, 1, 2, 5, 10 or 20 mg dichloromethane extracts of
coal particles, benzo[a]pyrene (positive control) or solvent alone (control). One week
after tumour initiation with the particle extracts, 2 g TPA in 0.2 mL acetone were
applied twice weekly to each mouse for 26 weeks and, beginning at 6 weeks, animals
were scored for skin papillomas weekly until the study was terminated. The survival rate
was over 95% and all three samples showed a dose-related response in both incidence and
multiplicity of the papillomas. The tumour-initiating activity of the extracts at 1 mg was
2.7 papillomas/mouse for the smoky-coal extracts and 1.3 papillomas/mouse for the
smokeless-coal extracts (Mumford et al., 1990).
In the same study, groups of 40 female SENCAR mice, 79 weeks of age, received
dermal applications of 1 mg/mouse dichloromethane extracts of smoky coal from Xuan
Wei County twice a week for 52 weeks and were then held for an additional 25 weeks.
Smokeless coal was not tested. The negative and positive control groups were treated
with acetone (0.2 mL/mouse) and benzo[a]pyrene (50 g/mouse) twice a week,
respectively. A high percentage (88%) of the mice treated with smoky-coal extract
developed carcinomas (1.1 carcinoma/tumour-bearing mouse on average) at the end of
the study at 77 weeks. No carcinomas were observed in the acetone-treated controls
(Mumford et al., 1990).
3.1.4
Subcutaneous injection
(a)
Mouse
A group of 30 hybrid F1 (C57BlCBA) male mice, 1.52 months of age, received

five subcutaneous injections of 3.5 mL olive oil containing coal extracts collected from
individual houses that were heated by brown coal [type of coal and burning conditions not
specified] over an 8-week period (total amount of benzo[a]pyrene, 0.2 mg/animal).
229
Vehicle (olive oil) and positive (0.2 mg benzo[a]pyrene) control groups were included in
the experiment. The experiment was terminated after 55 weeks. Tumours appeared in
benzo[a]pyrene-treated mice at 15 weeks with almost 80% mortality by week 39. In the
coal soot-treated animals, five (17%) mice developed subcutaneous tumours [tumour type
not specified] at approximately the same time. No tumours or mortality occurred in
control mice (Khesina et al., 1977).
Groups of 3857 male Kunming mice [age unspecified], weighing 1826 g, received
weekly 0.1-mL subcutaneous injections of 0, 500 or 1000 mg cyclohexane extracts of
coal soot collected from Xuan Wei County or 2 mg benzo[a]pyrene dissolved in Tween
80 and saline solution into the back of the neck week for 10 weeks. The experiment was
terminated after 10 months. The total incidence of lung cancer (squamous-cell carcinoma,
adenosquamous carcinoma and adenocarcinoma) was: 1/38 (2.6%) control, 44/57
(77.2%) low-dose, 36/56 (64.3%) high-dose and 6/38 (15.8%) benzo[a]pyrene-treated
animals. The total incidence of lung cancer in the soot extract-treated groups was
significantly higher than that in control or benzo[a]pyrene-treated groups. The incidence
of squamous-cell carcinoma was 8/57 (14.0%) and 12/56 (21.4%) in low- and high-dose
animals, respectively. The incidence of adenosquamous carcinoma was 10/57 (17.5%)
and 6/56 (10.7%) in low- and high-dose animals, respectively. Lung squamous-cell
carcinoma and adenosquamous carcinoma were not observed in the control or
benzo[a]pyrene-treated group. The incidence of adenocarcinoma was 26/57 (45.6%) lowdose animals, 18/56 (32.1%) high-dose animals, 6/38 (15.8%) benzo[a]pyrene-treated
animals and 1/38 (2.6%) controls, and that of fibrosarcoma was 1/57 (1.7%) and 4/38
(10.5%) in low-dose and benzo[a]pyrene-treated animals, respectively. In addition, the
incidence of adenoma was 5/38 (13.2%) control, 2/57 (3.5%) low-dose, 5/56 (8.9%) highdose and 3/38 (7.9%) benzo[a]pyrene-treated animals. At the injection site, the incidence
of tumours in situ was 5/57 (8.8%) dermal squamous-cell carcinomas, 1/57 (1.8%)
fibrosarcoma and 2/57 (3.5%) adenomas in the low-dose group; and 2/56 (3.6%) dermal
squamous-cell carcinomas, 1/56 (1.8%) fibrosarcoma and 0/57 adenomas in the high-dose
group. No dermal squamous-cell carcinoma was found in the benzo[a]pyrene-treated
group, while the incidence of fibrosarcoma was 32/38 (84.2%). No tumour was found in
other tissues except for a few thymus tumours (Liang et al., 1983).
Groups of about 60 male Kunming mice (weighing 1822 g) [age unspecified]
received weekly 0.1-mL subcutaneous injections of extracts of coal soot collected from
Xuan Wei County dissolved in Tween 80 and saline solution in the back of the neck for
10 weeks (total doses, 119 mg (0.15 g benzo[a]pyrene) and 400 mg (0.52 g
benzo[a]pyrene)). Sixty control animals were injected with Tween 80/saline only. The
experiment was terminated at 311 days. The total incidence of lung cancer was 52/58
(89.5%) [p<0.001] and 39/59 (66.1%) [p<0.001] in low- and high-dose animals,
respectively. The incidence of squamous-cell carcinoma was: 1/58 (1.7%) and 8/59
(13.6%) in low- and high-dose animals, respectively; that of adenosquamous carcinoma
was: 3/58 (5.2%) and 7/59 (11.9%) in low- and high-dose animals, respectively; and that
of adenocarcinomas was: 48/58 (82.8%) and 24/59 (40.7%) in low- and high-dose
230
animals, respectively. One fibrosarcoma of the lung was also found in a low-dose animal.
Control animals developed 6/60 (10%) lung cancers which were all adenocarcinomas.
Some adenomas were also found in all groups (Liang et al., 1984).
3.1.5
Veterinary epidemiology
(a)
Dog
A casecontrol study of the influence of environmental exposures on sinonasal

cancers was conducted in pet dogs. All cases of canine intranasal or sinus cancer
(diagnosed between 1989 and 1993) in the histopathology database at the University of
Pennsylvania School of Veterinary Medicine were included. The controls (unmatched)
included other non-respiratory related cancers (e.g. stomach, bowel and liver) from the
same database and diagnosed during the same 5-year period. The study included 129 dogs
with sinonasal cancers and 176 controls. Indoor use of coal was a strong risk factor with a
significant adjusted odds ratio of 4.24 (95% CI, 1.3016.52). Exposure to environmental
tobacco smoke was not significant (odds ratio, 0.70, 95% CI, 0.411.19) (Bukowski et al.,
1998).
3.2
Wood smoke
3.2.1

(a)
Mouse
Groups of 58 male and 59 female Kunming and 60 male Beijing mice (Kunming
strain), weighing ~21 g, [age unspecified] were exposed for 12 h per day for 15 months to
incompletely combusted wood smoke [burn rates not specified] generated from a fire pit
located in the centre of a room [size unspecified] to mimic that of peasants in the Xuan
Wei County of southwestern China. Similar numbers and strains of mice were exposed to
ambient air in a similar open-air room. As measured by PM, exposures to wood smoke
averaged 14.99 mg/m3 over the course of the study (control, 0.91 mg/m3). The concentrations of benzo[a]pyrene were: control, 1.47 g/10 m3; and wood smoke-treated,
43.1 g/10 m3. At the end of the exposure period, lung tumour incidence was calculated
and tumours were classified. The overall incidence of lung tumours in mice (combined
sexes and strains) was 45.8% (81/177) in exposed groups and 17.0% (29/171) in the
control groups. Female Kunming mice had the highest tumour incidence in both the
exposed and control groups (49.3% and 26.9%, respectively), followed by male Kunming
mice (37.9% of exposed and 13.2% of controls) and male Beijing mice (30% of exposed
and 10% of controls). Tumours were generally classified as adenocarcinoma. The
induction time of tumours in all mice was similar to that of controls (Liang et al., 1988).
Groups of 20 male and 20 female Strain A/J mice, ~6 weeks of age, were exposed by
whole-body inhalation to clean air (control) or to 30, 100, 300 and 1000 g/m3 whole
hardwood-smoke emissions (as measured by PM) for 6 h per day on 7 days per week for
231
6 months. The hardwood smoke was generated from an uncertified wood stove (Pineridge
Model 27000) that burnt wood of mixed oak species (from Missouri, USA). The fire was
started (i.e. initiation of animal exposures) with unprinted/unbleached newspaper
(newspaper end-rolls) and split hardwood kindling (the same wood type was used for the
entire test). Daily exposures included three burn phases: kindling (~1520 min with
newspaper and kindling wood), a high burn rate (~90 min with ~46 kg wood) and a low
burn rate (remainder of exposure period with an additional ~46 kg wood) that were
controlled by the air intake damper. The sliding damper position ranged from open
(maximum air intake) during the kindling and high-burn phases to an aperture of
approximately 0.36.5 cm during the low-burn cycle. Transition through each phase of
the burn cycle was indicated by ~75% of the fuel mass being burned. The atmosphere was
extensively characterized for over 1000 individual physical and chemical species
(McDonald et al., 2006). Mice were held for 6 months after exposures, at which time they
were killed and tumours were classified and enumerated under gross examination. No
exposure-related mortality was observed. No significant difference in lung tumorigenesis
measured as either the percentage of mice with tumours or the number of tumours per
tumour-bearing mouse was observed between exposed groups and controls, and no
evidence of a progressive exposure-related trend was observed. The percentage of mice
(both sexes combined) that had tumours ranged from 47 to 58%; the mean number of
tumours per mouse ranged from 0.67 to 0.75; and the mean number of tumours per
tumour-bearing mouse ranged from 1.24 to 1.43 among all exposure groups and controls.
Representative lung tumours from both control and exposed mice were characterized
histologically as bronchioalveolar adenomas (Reed et al., 2006).
(b)
Rat
Groups of 55 male and 55 female Wistar rats (weighing ~105 g) [age unspecified]
were exposed for 12 h per day for 19 months to incompletely combusted wood smoke
[burn rates not specified] generated from a fire pit located in the centre of a room [size
unspecified] to mimic that of peasants in the Xuan Wei County of southwestern China.
Similar numbers of rats were exposed to ambient air in a similar open-air room. As
measured by PM, exposures to wood smoke averaged 14.99 mg/m3 over the course of the
study (controls, 0.91 mg/m3). The concentrations of benzo[a]pyrene were: control,
1.47 g/10 m3; and wood smoke-treated, 43.1 g/10 m3. At the end of the exposure
period, lung tumours were enumerated (incidence) and classified. Only one (0.9%)
pulmonary cancer was reported in control rats and none in rats exposed to wood smoke
(Liang et al., 1988).
3.2.2
Subcutaneous injection
(a)
Mouse
A group of 30 hybrid F1 (C57BlCBA) male mice, 1.52 months of age, received

five subcutaneous injections of 2.5 mL olive oil containing soot extracts collected from a
232
wood-fired wood-working atelier [type of wood and burn conditions not specified] over
an 8-week period (total amount of benzo[a]pyrene, 0.2 mg/animal). Vehicle (olive oil)
and positive (0.2 mg benzo[a]pyrene) control groups were included in the experiment.
The experiment was terminated after 55 weeks. Tumours appeared in benzo[a]pyrenetreated mice at 15 weeks with almost 80% mortality by week 39. In the wood-soot treated
animals, five (17%) mice developed subcutaneous tumours [tumour type not specified]
approximately at the same time. No tumours or mortality occurred in 30 control mice
(Khesina et al., 1977).
Two groups of about 60 Kunming male mice (weighing 1822 g) [age unspecified]
received weekly 0.1-mL subcutaneous injections of extracts of wood smoke collected
from Xuan Wei County dissolved in Tween 80 and saline solution in the back of the neck
for 10 weeks (total dose, 148 mg (0.074 g benzo[a]pyrene) and 296 mg (0.15 g
benzo[a]pyrene)). Sixty control animals were injected with Tween 80/saline only. The
experiment was terminated at 311 days. The total incidence of lung cancer was 6/60
(10%) controls, 31/60 (51.7%) [p<0.001] low-dose animals and 36/58 (62.1%) [p<0.001]
high-dose animals. All lung cancers were adenocarcinomas. Some adenomas were also
found in all groups (Liang et al., 1984).
3.2.3
Subcutaneous implantation
(a)
Rat
Groups of 18 female and 18 male rats, weighing 120 and ~150 g respectively, [strain
and age unspecified] received subcutaneous implants of fragments (520 mg) of wood
(eucalyptus) soot, from the smoking chamber of a sausage factory, near the right axilla
and in the scrotal sac, respectively. No tumour was found in male rats after 2.5 years of
observation. Three female rats developed sarcomas at the site of implantation with latent
periods of 12, 17 and 24 months, respectively. No tumour was observed in 18 male and
18 female untreated controls observed during the same interval (Sulman & Sulman 1946).
[The Working Group noted that survival data were not provided.]
3.2.4
Dermal application
(a)
Mouse
A group of 10 adult female mice [strain and age unspecified] received daily dermal
applications on the neck skin of an ethanol extract of wood (eucalyptus) soot from the
smoking chamber of a sausage factory for 2 years. No skin tumour was observed. Two
mice developed para-urinary bladder sarcomas after 5 and 12 months, respectively, and
one mouse developed a bladder carcinoma 21 months after the beginning of the
experiment. No tumour was reported in 20 control mice after 2 years of observation
(Sulman & Sulman, 1946). [The Working Group noted the small group size and the
inadequate reporting of the treatment of the control group.]
233
In a tumour initiationpromotion study, eight groups of 40 female Kunming mice

(average weight, 28.7 g) [age unspecified] received a dermal application of 1, 5, 10 or
20 mg/kg extracts of inhalable particles (<10 m) of indoor wood smoke collected from
Xuan Wei County. The study also included a positive-control group that received an
application of 50 mg/kg benzo[a]pyrene, and control groups that received applications of
TPA or the solvent acetone. One week after initiation, the animals in the extract-treated
group and TPA-treated group received twice weekly applications of 2 g TPA dissolved
in 0.2 mL acetone for 26 weeks and were then held for an additional 6 weeks of
observation. A clear doseresponse in skin tumour incidence was observed in the wood
smoke-treated group at weeks 20, 26 and 32, respectively. At week 26, the tumour
incidence was 12.541% for wood smoke-treated groups, 50% for the benzo[a]pyrenetreated group, 10% for the TPA-treated group and 0% for acetone control group. The skin
tumour incidence in the wood smoke-treated and benzo[a]pyrene-treated groups was
significantly higher than that in TPA-treated and control groups (p<0.01). The first
tumour was observed at weeks 1013 in the wood smoke-treated group and at week 11 in
the benzo[a]pyrene-treated group. Moreover, the time to first tumour incidence was
decreased with increasing dose of the smoke extract. The results indicated that wood
smoke was carcinogenic through tumour initiation (Liang & Wang, 1987).
In a tumour initiation study, groups of 40 female SENCAR mice, 79 weeks of age,
received two dermal applications of 1, 2, 5, 10 and 20 mg/kg body weight (bw) woodsmoke extract in 0.2 mL acetone over a 15-day period. PM (<10 m) from the
combustion of pine was collected from homes during cooking periods in the Rhu Shui
commune, Xuan Wei County, by high-volume sampling onto glassfibre filters.
Dichloromethane extracts obtained form Soxhelet extraction of filter samples were
evaporated under nitrogen and transferred to acetone. One week after initiation, mice
received twice-weekly applications of 2 g TPA for 26 weeks. In a complete
carcinogenesis study, groups of 40 female SENCAR mice, 79 weeks of age, received
twice weekly skin applications of 1 mg/kg bw extract for 52 weeks and were held for an
additional 25 weeks. All mice were observed daily and skin papillomas were scored on a
weekly basis. Dose-related responses to initiation by wood-smoke extract were observed
and tumour incidence levelled at 23 weeks of treatment. Incidence was ~40, 45, 70, 80
and 90% for each respective dose level versus ~10% in control animals. Tumour
multiplicity ranged from 0.4 to 1.0 tumours per mouse with doses of 1, 2 and 5 mg/kg to
2.0 and 2.8 tumours per mouse with doses of 10 and 20 mg/kg, respectively.
Approximately 0.2 tumours per mouse were observed in control animals. In the complete
carcinogenesis study, only two mice (5%) treated with the wood-smoke sample
developed carcinomas versus no animals [not significant] in an acetone-control group and
100% of mice treated with benzo[a]pyrene as a positive control (Mumford et al., 1990).
A series of tumour initiationpromotion studies in female SENCAR mice using the
same protocol described by Mumford et al. (1990) was summarized in Lewtas (1993).
One study was reported on the tumour-initiating potency of extracts of particle emissions
of a mixture of softwoods (e.g. pine) and a mixture of hardwoods (e.g. oak) burned in a
234
wood stove, using the same doses (1, 2, 5, 10 and 20 mg) of extracts (dichloromethane
extracts administered in 0.2 mL acetone after removal of dichloromethane). The extracts
of wood-stove particle emissions from softwoods were more tumorigenic
(0.046 papillomas/mouse/mg;
40
mice)
than
the
hardwood
mixtures
(0.0087 papillomas/mouse/mg; 40 mice). In another study, two ambient air samples of
particle extracts were collected in Boise, Idaho (USA), and apportioned into wood-smoke
and mobile source contributions to the organic mass (Lewtas, 1993; Cupitt et al., 1994).
One of these composite ambient air samples with 78% wood smoke (and 11% mobile
sources and 11% residual unidentified mass) was positive in the tumour initiation
promotion protocol in female SENCAR mice using the same doses (1, 2, 5, 10 and
20 mg) applied dermally. The tumour-initiation potency was 0.095 papillomas/mouse/mg
(40 mice) (Lewtas, 1993; Cupitt et al., 1994).
3.2.5
Veterinary epidemiology
Dog
A casecontrol study investigated the utility of using canine sinonasal cancers as an
indicator of risk for human cancer from residential exposures. Primary cases of sinonasal
cancers that occurred between 1989 and 1993 were obtained from the histopathology
database at the University of Pennsylvania and were included and compared with a set of
unmatched controls. Data on exposures, confounders and behaviour were obtained by
questionnaire and telephone from veterinarians and owners. A total of 129 cases were
compared with 176 controls. Overall exposure to wood fires within a residence was
weakly associated with the risk for cancer (odds ratio, 1.58 [95% CI, 0.813.09]) even
with more than 220 cumulative occurrences of exposure to wood fire (Bukowski et al.,
1998).
3.3
References
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Academy of Science Estonian SSR, pp. 245250.
Bukowski JA, Wartenberg D, Goldschmidt M (1998). Environmental causes for sinonasal cancers
in pet dogs, and their usefulness as sentinels of indoor cancer risk. J Toxicol Environ Health A,
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Campbell JA (1939). Carcinogenic agents present in the atmosphere and incidence of primary
tumours in mice. Br J Exp Pathol, 20:122132.
Cupitt LT, Glen WG, Lewtas J (1994). Exposure and risk from ambient particle-bound pollution in
an airshed dominated by residential wood combustion and mobile sources. Environ Health
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IARC (1985). Polynuclear aromatic compounds, Part 4, Bitumens, coal-tars and derived products,
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Khesina AIa, Gaevaia TIa, Linnik AB (1977). [Polycyclic aromatic hydrocarbon content and
carcinogenic activity of soot extracts from the heating systems]. Gig Sanit, 8:107109.
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Lewtas J (1993). Complex mixtures of air pollutants: characterizing the cancer risk of polycyclic
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Liang CK, Quan NY, Cao SR et al. (1988). Natural inhalation exposure to coal smoke and wood
smoke induces lung cancer in mice and rats. Biomed Environ Sci, 1:4250. PMID:3268107
Liang C-K, Wang W (1987). [Kunming mouse skin tumor-initiating activity of extracts of
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PMID:3452506
Lin C, Dai X, Sun X (1995). [Expression of oncogene and anti-oncogene in mouse lung cancer
induced by coal-burning smoke.] Zhonghua Zhong Liu Za Zhi, 17:432434. PMID:8697995
smoke inhalation exposure atmospheres. J Aerosp Sci Technol, 40:573584
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Mittler S, Nicholson S (1957). Carcinogenicity of atmospheric pollutants. Ind Med Surg, 26:135
138. PMID:13405573
Mumford JL, Helmes CT, Lee XM et al. (1990). Mouse skin tumorigenicity studies of indoor coal
and wood combustion emissions from homes of residents in Xuan Wei, China with high lung
cancer mortality. Carcinogenesis, 11:397403 doi:10.1093/carcin/11.3.397. PMID:2311182
Passey RD (1922). Experimental soot cancer. Br Med J, ii:11121113.
Passey RD, Carter-Braine J (1925). Experimental soot cancer. J Pathol Bacteriol, 28:133144
doi:10.1002/path.1700280202.
Reed MD, Campen MJ, Gigliotti AP et al. (2006). Health effects of subchronic exposure to
environmental
levels
of
hardwood
smoke.
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Seeling MG, Benignus EL (1936). Coal smoke soot and tumors of the lung and mice. Am J
Cancer, 28:96111.
Sulman E, Sulman F (1946). The carcinogenicity of wood soot from chimney of a smoked sausage
factory. Cancer Res, 6:360367.
Vsame AI (1963). On the blastomogenic action of the estonian shale oil soot and the soot of
liquid fuel obtained from the processing of shale oil. Acta Unio Int Contra Cancrum, 19:739
741. PMID:14050654
Vsame AI (1979). Carcinogenicity studies of Estonian oil shale soots. Environ Health Perspect,
30:173176 doi:10.2307/3429120. PMID:446448
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of Yiwei coal fume extracts.] Wei Shen Yan Jin, 13:2125.
236
4. Mechanistic and Other Relevant Data

4.1
Toxicokinetics
4.1.1
General considerations
The toxicokinetics of inhaled compounds is defined by exposure, absorption of the

material and its local metabolites, the tissueplasma concentrationtime curve, distribution
within the body, and overall metabolism and excretion. Under controlled conditions of
animal studies and human clinical trials, total exposures and estimated doses of individual
compounds or simple mixtures of aerosols, gases and PM can readily be defined.
However, methods for defining the toxicokinetic and toxicodynamic properties of
mixtures at this time are ill equipped to deal with exposures to atmospheres that contain
thousands of individual components at varying concentrations. In general, attempts have
been made to model and define empirically the disposition of only very simple mixtures.
For example, the most complex of toxicokinetic data and models generated have been
with refined gasoline and seven to eight primary chemical components (Dennison et al.,
2003, 2004). The caveat to these studies is that, unlike the variety of chemical
components that are contained within combustion-derived materials, many liquid- and
vapour-phase gasoline components have similar structure and generally similar pathways
of absorption, metabolism, distribution and excretion.
The definition of the toxicokinetics of anthropogenic indoor air pollutants such as
those from wood smoke and coal combustion emissions are complicated by two main
factors: (a) the diversity and concentration of components and (b) the phase distribution
of components.
(a)
Diversity and concentration of components
Combustion emissions are composed of hundreds to thousands of individual

components that can overlap in many cases yet be discrete in others, depending on the
material burned (coal versus wood versus dung), its subtype (species of wood, type of
coal), its application (open fire, stove, pit, cooking, heating) and the burn rate (hot
fire/smoldering fire). The sheer number of components, many in very small quantities,
makes an empirical definition of the toxicokinetics of individual compounds or classes of
compounds extremely challenging. In addition, up to 85% of the PM within some
complex mixtures remains ill-defined which makes assessments of these species
impossible (McDonald et al., 2006).
PAHs in hardwood-smoke emissions may be used to highlight this issue. Combined
PAHs (58 individual compounds) from the vapour-phase semivolatile organic compounds
of diluted whole hardwood smoke generated from a wood stove operated over a threephase burn cycle and delivered to an animal exposure chamber system totalled ~11 g/m3
237
on average. In the same atmosphere, particle-phase PAH mass totalled only 465 ng/m3 (of
~1000 g/m3 total PM mass). This value was minuscule compared with the 85% of the
PM mass that remained unidentified in these experiments. Overall, total PAHs equaled
only ~0.06% of the total mass of material within the exposure atmosphere (total mass,
~20.4 mg/m3) (McDonald et al., 2006; Reed et al., 2006). The impact of these hundreds
of other organic, inorganic and elemental species probably plays a profound role in the
toxicokinetics of PAHs (see also Section 4.1.2).
(b)
Phase distribution of components
Combustion emissions are composed of gaseous, semivolatile and particulate physical

phases. Each phase has independent physical and chemical characteristics that determine
the relative dose of the chemical components contained therein to the lung. As described
in Section 4.1.2, aerodynamic physical traits determine the deposition of PM, but the
chemical make-up and physical state (liquid or carbonaceous) may determine the dose
distribution and toxicokinetics subsequent to deposition. At the opposite end of the
spectrum, simple diffusion generally dictates gaseous transport and effective dose of gasphase components. Gas-phase furans for example, present in relatively small quantities in
wood smoke and other combustion emissions (McDonald et al., 2006), have been
evaluated as reasonably anticipated to be human carcinogens (National Toxicology
Program, 1999) or possibly carcinogenic to humans (IARC, 1995).
Semivolatile organic compounds that undergo a phase transition among the gaseous
and PM phases of combustion mixtures complicate the situation. A definition of dose
(gas/diffusion/particle/deposition) and ultimately the toxicokinetics of such compounds
remains challenging. PAHs were present in the PM and gas phases within the example of
a hardwood-smoke atmosphere noted above. The PM contribution of PAHs was minor
(0.05%) compared with the remainder of the PAH mass contained in the gaseous phase
(McDonald et al., 2006). In this case, the overall dose and toxicokinetics of PAHs were
probably influenced heavily by the gaseous components and the inherent diffusive
processes that determine the overall final disposition and kinetics.
The physical solid/liquid state of PM may also play a role in this process. In the
hardwood smoke generated above, the PM phase was mostly liquid in origin, while in
other atmospheres such as diesel emissions, coal emissions and wood smoke generated
under higher burn conditions, PM may be more carbonaceous/elemental in nature (e.g.
coal ash) (Liang et al., 1988; McCrillis & Burnet, 1990; Tesfaigzi et al., 2002; Reed et al.,
2004). In the latter case, particle clearance and the leach rate of associated chemicals
would play a more important role in the toxicokinetics of specific chemical species. With
particles that form in the liquid state, dissolution of chemicals within the liquid droplet
into airway lining fluid and the hydrophobicity or hydrophilicity of the individual
chemical or chemical class determine the toxicokinetics.
238
(c)
Other parameters of toxicokinetics
The concentration of combustion-derived chemical components deposited in the lung

combined with time and clearance parameters define overall exposure (area under the
curve [AUC]). As mentioned above, the daily exposure to individual chemicals or classes
of compounds of interest can be minimal. Chemical methods developed for tissue
analyses are generally specific to an individual chemical or class, are not trivial to develop
and validate and in many cases lack the sensitivity required to measure trace amounts of
compounds within the biological milieu. When one combines the limitations of assay
methodology with the limited quantities of many components deposited within the lung, a
definition of the collective or individual AUC of the multiple components with
combustion-derived material remains a challenge.
Transport and excretion of lung-deposited components of mixtures to and from other
compartments, organs or cell types may be of less relative importance for lung cancer
than some other pollutant-associated disease types (e.g. cardiovascular disease). Because
the lung is the affected organ, it is unlikely (although unproven) that transport, metabolic
activation or sequestration at distant sites around the body lead to a sustained or transient
re-exposure of lung tissue to chemical species associated with the mixture. It is unclear
how processes such as these might lead to initiation or promotion events that are relevant
to lung carcinogenesis. Assuming this is the case, any processes associated with exposure
to the mixture and subsequent carcinogenic events would be expected to take place in the
local environment of the lung.
The lung is fully capable of metabolizing multiple chemical species. It is difficult to
imagine how the plethora of chemical compounds within combustion mixtures might
affect the metabolic processes. However, it is important to note that elimination of
metabolites of gas-phase or PM-phase components from the lung is probably processed
through pathways similar to those described for the parent compounds.
4.1.2
PAHs and inhalable particles
As indicated above, combustion products associated with most chemical mixtures,

including those evaluated in this monograph, typically comprise many chemical classes,
such as PAHs and aromatic amines. Although the Working Group recognized that
toxicokinetic information is available for many of these chemical classes, the evidence for
the role of PAHs in some of the combustion emissions evaluated in this monograph has
been well documented. In addition, the particulate fraction in these emissions also
contributes to the development of adverse respiratory effects. Therefore, the toxicokinetics of PAHs and of inhalable particles are discussed below.
A detailed overview of the toxicokinetics of selected PAHs is available in a previous
volume of IARC Monographs (IARC, 2010a); some of this information is summarized
here. Although some data on this topic have been determined in humans, including
analyses of urinary PAH metabolites and PAHDNA adducts in lymphocytes, most of the
239
available data on the toxicokinetics of PAHs derive from studies of PAHs in experimental
animals, much of which involve studies of a single PAH, benzo[a]pyrene.
The biological properties of PAHs, as they pertain to combustion sources, are
influenced by four main factors: phase distribution (vapour pressure, adsorption onto
surfaces of solid carrier particles), absorption into liquid carriers, lipid/aqueous partition
coefficient in tissues, and limits of solubility in the lipid and aqueous phases of tissues.
(a) Absorption through the respiratory tract, gastrointestinal tract and
skin
The phase distribution of PAHs is dependent on their vapour pressure, which
decreases with increasing molecular weight: two-ringed compounds are largely in the gas
phase, whereas five-ringed compounds are mostly in the solid phase (generally adsorbed
on airborne particles at room temperature) (IARC, 2010a).
Exposure comes from virtually all media: air, soil, water and food. PAHs are
generally transported by diffusion across lipid/lipoprotein membranes, which facilitates
their absorption by the respiratory tract, gastrointestinal tract and skin. PAHs that have
two or three rings are absorbed more rapidly and extensively than those that have five or
six rings (IARC, 2010a).
The rate and extent of absorption by the respiratory tract of PAHs from particles that
contain them are generally dependent on particle size, i.e. aerodynamic diameter, which
influences regional deposition in the respiratory tract and the rate of release of PAHs from
the particle. Highly lipophilic PAHs that are released from particles deposited in the
conducting and bronchial airways are largely retained for several hours and absorbed
slowly by a diffusion-limited process. In contrast, PAHs that are released from particles in
alveolar airways are generally absorbed within minutes (Gerde & Scott, 2001; IARC,
2010a). The metabolism of PAHs in the epithelium probably accelerates transport of
lipophilic PAHs into the circulation. However, the low mobility of the highly lipophilic
PAHs in tissues complicates the toxicokinetics of PAHs. Thus, the delayed equilibration
between blood and tissue needs to be taken into account. The relatively longer retention of
PAHs released in the conducting airways (compared with the air-exchange region) may
allow substantial metabolism within this region of deposition (IARC, 2010a).
PAHs can be absorbed by the gastrointestinal tract via diffusion across cellular
membranes based on the lipophilicity of the PAH and via the normal absorption of dietary
lipids (ONeill et al., 1991). Results from animal studies indicate that absorption is rapid,
that fractional absorption of lower-molecular-weight PAHs may be more complete than
that of higher-molecular-weight PAHs and that the presence of other materials, such as
bile salts or components of the diet, can influence the rate or extent of absorption of PAHs
from the intestine (IARC, 2010a).
Dermal absorption of PAHs in humans has been confirmed by the detection of
elevated levels of PAH metabolites in the urine after exposure to complex PAH mixtures.
Studies in animals indicate that dermal absorption of PAHs can be rapid and extensive
(IARC, 2010a).
240
(b)
Distribution
In rats, adsorbed PAHs are distributed widely to most organs and tissues. PAHs tend
to accumulate in fatty tissues, which can serve as storage sites from which they may be
released. The gastrointestinal tract can contain high levels of PAHs and their metabolites
after exposure by any route due to mucociliary clearance from the respiratory tract and
hepatobiliary excretion of metabolites (IARC, 2010a). For example, in rats exposed to
benzo[a]pyrene aerosols, this PAH is eliminated rapidly from the lung, and higher levels
are found in the stomach and small intestine than in any other tissue, although significant
amounts are detected in the liver and kidneys. Similar results have been obtained in rats
exposed by inhalation to benzo[a]pyrene absorbed onto ultrafine particles. Thus, PAHs
are generally cleared rapidly from the site of initial deposition in the respiratory tract and
are then distributed to a significant extent in the gastrointestinal tract, liver and kidney
(IARC, 2010a).
Transporter proteins may play a role in the biological activity of PAHs. For example,
ATP binding cassette (ABC) transporters transport specific molecules across lipid
membranes, including hydrophobic compounds (Schinkel & Jonker, 2003). Among these
ABC transporters, multidrug resistance 1 P-glycoprotein transports mainly nonmetabolized compounds and multidrug resistance protein-1 and -2 transport conjugates of
xenobiotic compounds (Haimeur et al., 2004). In addition, some ABC transporters are
polymorphic (Sakaeda et al., 2004).
(c)
Metabolism
PAHs are metabolized rapidly to more soluble metabolites (quinones, epoxides,

phenols, dihydrodiols, phenol dihydrodiols, dihydrodiol epoxides and tetrols) through a
series of enzymatic reactions (IARC, 2010a; see also Section 4.2.1). PAH oxidation by
cytochrome P450 (CYP) mono-oxygenase is complex and involves a one electron
abstraction rebound mechanism as well as a one-electron radical cation mechanism
(Cavalieri & Rogan, 2002; Mulder et al., 2003). CYP1A1, CYP1A2 and members of the
CYP1B, CYP2B, CYP2C and CYP3A families of enzyme can catalyse the initial
oxidation of benzo[a]pyrene and other PAHs to varying extents (WHO, 1998; Xue &
Warshawsky, 2005). PAHs can induce CYP enzymes and, thus, can influence the balance
of phase I and phase II enzymes that may be associated with a decreased or increased
tumorigenic response (WHO, 1998).
Epoxides may rearrange spontaneously to phenols, be hydrated via epoxide hydrolase
catalysis to dihydrodiols or be conjugated with glutathione (GSH), either spontaneously
or via glutathione-S-transferase (GST) catalysis (WHO, 1998; IARC, 2010a). Cavalieri et
al. (1988) proposed that CYP isoforms convert PAHs to hydroxyl-PAHs and then to
quinones, which then can be converted to hydroquinone derivatives by quinone reductase
or else conjugated with GSH, sulfate or glucuronic acid (WHO, 1998; IARC, 2010a).
Dihydrodiol derivatives can be oxidized further by CYPs to form phenol dihydrodiols
or dihydrodiol epoxides. Dihydrodiol epoxides may also be formed from dihydrodiols by
241
reaction with peroxyl radicals generated from the oxidative biosynthesis of prostaglandins
from fatty acids via prostaglandin H synthase (IARC, 2010a).
Dihydrodiol epoxides may be conjugated with GSH or bind covalently to
macromolecules, such as DNA, resulting in DNA damage that might be processed into a
mutation (IARC, 2010a). Dihydrodiols may also be metabolized to ortho-quinones by
aldo-keto reductases (AKR) 1C11C4 and AKR1A1. The resulting ortho-quinone
derivatives may produce reactive oxygen species, via redox cycling with the reduced form
of nicotinamide adenine dinucleotide phosphate (NADPH) and copper (Penning et al.,
1999). PAH ortho-quinones, are also ligands for the aryl hydrocarbon receptor (AhR),
which may play a role in the mutagenicity and carcinogenicity of PAHs (Burczynski &
Penning, 2000). The stereochemistry of dihydrodiol epoxide derivatives also plays a
critical role in the mutagenicity and carcinogenicity of the resulting PAH metabolite
(WHO, 1998).
In addition to the phase I enzymes such as the CYPs, AKRs and epoxide hydrolase,
phase II enzymes, such as GSTs, uridine diphosphate-N-acetylglucosamine transferase
and sulfotransferases also play a role in the metabolism of PAHs. Many of these phase I
and phase II enzymes are polymorphic in humans, and this genetic variability can modify
the activity of the enzymes. Studies in humans indicate that genetic variants of these
enzymes modify cancer risk due to exposure to PAHs, adding an additional level of
complexity to assessments of health risks involving PAHs (IARC, 1999).
(d)
Elimination
Animal studies show that PAH metabolites can form conjugates with sulfate, GSH or
glucuronic acid. PAHs are eliminated from the body principally as conjugated metabolites
in the faeces via biliary excretion and in the urine. If not conjugated, these metabolites
may bind covalently with macromolecules, such as DNA, to form DNA adducts (WHO,
1998; IARC, 2010a).
4.1.3
Insoluble particles
In this section, the toxicokinetics, including deposition, clearance and retention, of

insoluble particles are discussed for both humans and laboratory animals.
(a) Particle deposition, clearance and retention in the human respiratory
tract
The deposition of a particle within a region of the respiratory tract depends on the
particle characteristics and the physical factors that influence the transport of particles in
the airways (e.g. air velocity and airway structure). The primary mechanisms for
deposition of particles in the respiratory tract are sedimentation, impaction and diffusion.
Deposition by sedimentation and impaction depends on the aerodynamic diameter of the
particle, while deposition by diffusion depends on its thermodynamic diameter (ICRP,
1994).
242
Following inhalation, particles may either deposit in the extrathoracic,

tracheobronchial or pulmonary airways or remain in the air stream and be eliminated
through exhalation. The deposition of particles in the respiratory tract depends primarily
on the size of the inhaled particle, the route of breathing (i.e. through the nose and/or
mouth) and the breathing pattern (e.g. volume and frequency). Particles near 0.3 m in
diameter have minimal mobility in air, i.e. they are large enough that their diffusive
mobility is minimal but are small enough that their sedimentation and impaction are also
minimal. As a consequence, particles in this size range also have minimal deposition in
the lung. In general, the deposition fraction for humans for most particle sizes less than 3
4 m (aerodynamic diameter) is greater for the alveolar region than for the tracheobronchial airways. The deposition fraction decreases in the alveolar region for particles
above 34 m and below 0.01 m due to their removal in the extrathoracic (particularly
during nasal breathing) and tracheobronchial airways (NCRP, 1997; Maynard &
Kuempel, 2005).
Several terms have been adopted to refer to the characterization of airborne particles
and their deposition in the respiratory tract. The term respirable refers to particles that
are capable of penetrating into the alveolar or gas-exchange region of the lungs
(2.5 m). Particle size fractions include ultrafine or nanoparticle (<0.1 m diameter of
primary particle), fine (0.12.5 m) and coarse (>2.510 m). The term thoracic refers
to particles that are capable of depositing in the tracheobronchial region (10 m) (ISO,
1995).
Particles are frequently aggregates of smaller primary particles. The aerodynamic and
thermodynamic properties of these aggregates (rather than the primary particles) affect
their behaviour in the air and their probability of deposition in the respiratory tract. Once
deposited, properties such as the size and surface area of both the aggregate and primary
particle can potentially affect the kinetics of clearance (ICRP, 1994; Oberdrster, 1996).
Few experimental studies are available in humans on the kinetics of clearance and
retention of inhaled particles in the respiratory tract. Retention is determined by the
balance between the rate of deposition and the rate of clearance. Particles that deposit in
the tracheobronchial region are cleared by mucociliary clearance, which is relatively rapid
(retention half-times of approximately 2448 h) (Oberdrster, 1988; ICRP, 1994),
although some fraction of the particles that deposit in the airways is cleared more slowly
than expected (Stahlhofen et al., 1995). For particles that deposit in the alveolar region,
the primary mechanism of clearance is phagocytosis by alveolar macrophages followed
by migration of the macrophages to the terminal bronchioles and subsequent mucociliary
clearance; the particles are eventually swallowed or expectorated (Oberdrster, 1988;
ICRP, 1994). Particles that deposit in the alveolar region are associated with a slow
clearance phase (retention half-times from months to years in humans) (Bailey et al.,
1985; Freedman & Robinson, 1988; ICRP, 1994). Translocation of particles to the
interstitial region (interstitium) further increases the retention time of particles in the lungs
(Oberdrster, 1988; Freedman & Robinson, 1988; ICRP, 1994). Some fractions of
particles that deposit in the alveolar region may also be translocated to the lung-associated
243
lymph nodes. Translocation may occur by transepithelial migration of alveolar

macrophages following phagocytosis of the particle or by translocation of free particles to
the interstitium, where they may be phagocytosed by interstitial macrophages.
Inflammation may alter mucociliary clearance, phagocytosis by alveolar macrophages
and the uptake and transport of particles to and through the respiratory epithelium
(Oberdrster, 1988; ICRP, 1994).
The deposition and clearance of particles vary among individuals for a number of
reasons, including age, gender, tobacco smoking status and health status. Pre-existing
lung diseases or conditions such as asthma or chronic obstructive pulmonary disease can
influence the efficiency and pattern of deposition within the respiratory tract. Deposition
also depends on the level of activity and breathing patterns. Deposition and retention
determine the initial and retained dose of particles in each region and may therefore
influence the risk for developing diseases specific to those respiratory tract regions
(Oberdrster, 1988; ICRP, 1994).
(b) Particle deposition, clearance and retention in the rodent respiratory
tract
As in humans and other species, the deposition of particles in the rodent respiratory
tract depends on the aerodynamic characteristics of the particles, the airflow properties
and the airway structure. The rat is the most frequently used animal in experimental
studies of inhaled particles. Significant differences in the respiratory physiology of rats
and humans must be considered when assessing hazards for humans based on studies in
rats (Miller, 2000). Rats are obligatory nose breathers. In contrast, humans breathe
through both the nose and mouth, with the proportion varying among individuals and with
activity level (the proportion of mouth breathing generally increases with exertion). Rats
have more extensive airways in the nasal region, and particle deposition in this region is
greater for rats than humans. The size of particles that are inhalable (capable of entering
respiratory tract) differs in rats and humans (Mnache et al., 1995; Miller, 2000). The
airway branching system is symmetric (bi- or tripodal) in humans and asymmetric
(monopodal) in rats. The type of branching system influences the site of deposition
(airway impaction tends to be greater in the human tracheobronchial region). Rats do not
have respiratory bronchioles, while humans do. All of these factors influence the kinetics
of particle deposition in the respiratory tract and thus potential differences between rats
and humans (Mnache et al., 1996; Miller, 2000).
Once insoluble particles are deposited, their removal or retention is based on
mechanisms of biological clearance. In rats, like humans, particles in the tracheobronchial
region are cleared by the mucociliary pathway and by alveolar macrophages in the
alveolar region. Particles that enter the interstitium may also enter the lymph and blood
circulation. Although the mechanisms are similar, the rates at which they occur may differ
between rats and humans. While tracheobronchial clearance is relatively rapid in both rats
and humans (half-times of the order of hours or days), the normal alveolar clearance rate
in rats is approximately 10 times faster than that in humans (Snipes, 1989).
244
Studies in rodents (primarily rats) have shown that, depending on the concentrations
and durations of exposure, the long-term retention of particles can be greater than that
predicted from studies that used lower concentrations or shorter durations. This increase
in particle retention has been attributed to the overloading or impairment of alveolar
macrophage-mediated clearance (Morrow, 1988, 1992; ILSI Risk Science Institute
Workshop Participants, 2000). The mechanisms of particle overload, the lung responses
to overload and the implications for carcinogenic hazard are discussed in Section 4.2.
4.2
Mechanisms of carcinogenesis
4.2.1
Polycyclic aromatic hydrocarbons (PAHs)
Ample evidence (summarized in IARC, 2004, 2010a) supports a role for PAHs in
lung cancer due to exposure to indoor emissions from smoky coal or from cigarette
smoking. A general genotoxic mechanism has emerged in which PAHs such as
benzo[a]pyrene are metabolized to electrophilic forms that adduct to DNA. If these
adducts are not repaired, then misreplication converts them to GT transversion
mutations in the TP53 gene in the lung. An overrepresentation of GT transversions has
been found on the non-transcribed strand, of DNA, which is consistent with the lack of
transcription-coupled DNA repair on that strand and results in mutations. A preference for
GT transversions in the methylated CpG dinucleotides in human lung tumours also has
been found, in agreement with in-vitro studies that show the same dinucleotide as a target
of benzo[a]pyrene diol epoxide. Accumulation of additional mutations in key genes
within stem cells, together with epigenetic and/or non-genetic changes, such as disruption
of cellcell communication, apoptosis and cell-cycle regulation, can result in tumour
formation (IARC, 2010a).
Based on several lines of evidence (IARC, 2010a), PAHs may be activated via two
main pathways: (i) mono-oxygenation to yield diol epoxides and (ii) one-electron
oxidation to form radical cations. The two reactive intermediates, diol epoxides and
radical cations, can bind to DNA to form adducts, with the potential to be processed into
mutations, resulting presumably in tumour formation. Some PAHs are activated
exclusively to diol epoxides, such as 5-methylchrysene, and benzo[c]phenanthrene,
whereas several other PAHs, such as benzo[a]pyrene, dibenzo[a,l]pyrene, 7,12-dimethylbenz[a]anthracene (DMBA) and 3-methylcholanthrene, are activated by formation of diol
epoxides and radical cations.
Adenine and guanine are the two DNA bases most susceptible to the nucleophilic
attack of PAHs. The adducted nucleotides can be processed into mutations by two general
mechanisms: (i) error-prone DNA repair and (ii) erroneous replication through any
unrepaired lesions. Apurinic sites generated by depurinating DNA adducts appear to be
mutated by error-prone repair (Chakravarti et al., 2000, 2001), whereas the repair of
stable DNA adducts is largely error-free (Choi et al., 1996). However, replication through
unrepaired adducted bases can sometimes cause mutations (Moriya et al., 1996). In
245
conclusion, the induction of specific mutations by PAHs is determined by mechanisms

that determine (i) adduct formation at specific DNA sequences and (ii) the incorporation
of mispaired bases (either by error-prone repair or by erroneous replication) at lesions in
specific DNA sequence contexts.
(a)
Bay- and fjord-region PAH diol epoxides
The bay-region theory of PAH metabolism emphasizes that angular benzo ring
fusions on PAHs create a topological indentation on the polycyclic ring structure, which
is called the bay region. For example, the bay region of benzo[a]pyrene encompasses four
carbons (carbons 10, 10a, 10b and 11) and three carboncarbon bonds. Metabolism by
CYPs at the C7C8 aromatic double bond creates an arene oxide (i.e. benzo[a]pyrene7,8-oxide) that disrupts the aromatic nucleus by saturating that carboncarbon bond. The
arene oxide is hydrated by epoxide hydrolase to form a dihydrodiol (diol), which is
further epoxidized by CYPs at the C9C10 double bond to give the bay-region diol
epoxide, benzo[a]pyrene-7,8-diol-9,10-oxide. This diol epoxide possesses an inherent
activity to undergo carbonoxygen bond scission or ring opening to form a carbocation
(or carbonium, i.e. a positively charged carbon atom) on carbon 10. Carbocations are
highly reactive species that react with nucleophiles such as DNA and proteins to form
covalent adducts. The more reactive the carbocation, the greater is the tumorigenic
activity of the PAH (Jerina et al., 1976).
PAHs such as dibenzo[a,l]pyrene contain a fjord region, which encompasses five
carbons and four carboncarbon bonds. In some cases, the steric interactions between
atoms within the fjord region forces the PAH ring system out of planarity (Katz et al.,
1998). Some PAH fjord-region diol epoxides are non-planar and these non-planar PAH
diol epoxides possess high reactivities (Lewis-Bevan et al., 1995). The formation and
degradation of stereochemically specific diol epoxides are dependent on species, strain,
sex, organ, tissue, type of CYPs and phase II enzymes (IARC, 2010a).
One of the original tenets of the mechanism for bay-region or fjord-region diol
epoxides is that, as the PAH is metabolically activated in sequence through the diol to the
diol epoxide, this process creates intermediates that generally possess greater biological
activities than their precursors. This is true for some (Wislocki et al., 1979) but not all
PAHs (Buening et al., 1979).
Bay-region and fjord-region diol epoxides possess many biological activities, and one
of the most important of these is their ability to form stable covalent adducts with DNA.
The nature of these adducts is influenced by the absolute configuration, molecular
conformation and stereochemistry of the diol epoxide, the specific purine or pyrimidine
base that is adducted, the site of adduction within the base and the sequence of the DNA
that is adducted (Jerina et al., 1986). When diol epoxides react with DNA, each can form
both cis and trans adducts, to give a total of 16 possible DNA adducts. These DNA
adducts can then either be repaired, or they can be misrepaired or not repaired at all, in
which case translesion DNA synthesis can result in mutationi.e. a change in DNA
246
sequence (Rodriguez & Loechler, 1995; Frank et al, 2002). PAH diol epoxideDNA
adducts are generally repaired by nucleotide excision repair (Geacintov et al., 2002).
Bay- and fjord-region diol epoxides of PAHs induce DNA damage and mutations in a
wide variety of biological organisms and systems, and they induce mutations in critical
genes associated with chemical carcinogenesis, such as proto-oncogenes (e.g. ras;
Prahalad et al., 1997; Chakravarti et al., 1998) and tumour-suppressor genes (e.g. p53;
Ruggeri et al., 1993; Rmet et al., 1995). In general, DNA adducts induced by PAHs at
deoxyguanosine result in mutations in the ras gene at codons 12 or 13, whereas adducts
formed by PAHs at deoxyadenosine result in mutations in the ras gene at codon 61.
Adducts induced by PAHs at both purine bases result in both types of mutations (Ross &
Nesnow, 1999). Diol epoxideDNA adducts of PAHs also have been found in
populations exposed to complex mixtures containing PAHs, such as foundry workers,
coke-oven workers, cigarette smokers, chimney sweeps and people exposed to emissions
from smoky coal (IARC, 2010a). In addition to their genotoxic effects, some bay- or
fjord-region diol epoxides can induce apoptosis and cell-cycle arrest (Chramostov et al.,
2004).
(b)
Radical cations
Removal of one electron from the system (the system of six delocalized electrons)
by CYPs or peroxidases generates a radical cation in which the positive charge is
localized mainly at an unsubstituted carbon atom or adjacent to a methyl group.
Nucleophilic attack at the position of highest charge density in the first case produces an
intermediate radical that is then further oxidized to an arenium ion to complete the
substitution reaction. When the charge is localized adjacent to the methyl group, the latter
becomes electrophilic and can react with a nucleophile (Cavalieri & Rogan, 1985, 1992).
The notion that radical cations play an important role in the metabolic activation of
some PAHs derives from certain features that are common to several carcinogenic PAHs.
These characteristics are (i) a relatively low ionization potential, which allows the
removal of one electron and the formation of a relatively stable radical cation, (ii) a
charge localization in the radical cation that renders this intermediate specifically and
efficiently reactive toward nucleophile and (iii) an optimal geometric configuration that
allows the formation of appropriate intercalating radical cation complexes with DNA and
favours the formation of covalent adducts with DNA (IARC, 2010a).
(c) Formation of ortho-quinones and generation of reactive oxygen
species
PAHs with a terminal benzo-ring in a bay region can be metabolically activated or
form arene oxides, which can then be hydrated by epoxide hydratase to form non-K
region R,R-trans-dihydrodiols (Shimada et al., 1996; IARC, 2010a). These transdihydrodiols can undergo further mono-oxygenation by CYPs to form predominantly
247
bay-region anti-diol epoxides. The formation of trans-dihydrodiols represents a branch

point in PAH metabolism (IARC, 2010a).
Non-K region trans-dihydrodiols also undergo NADP-dependent dehydrogenation
that is catalysed by monomeric cytosolic oxidoreductases of the AKR superfamily to
yield ketols, which rearrange spontaneously to yield catechols. The catechols are
extremely air-sensitive and undergo two sequential one-electron auto-oxidation events to
yield the corresponding reactive and redox-active PAH ortho-quinones (Smithgall et al.,
1988; IARC, 2010a). An intermediate in this auto-oxidation is the corresponding orthosemiquinone anion radical. Each one-electron oxidation event (either catechol to orthosemiquinone anion radical or ortho-semiquinone anion radical to ortho-quinone) yields
reactive oxygen species (superoxide anion, hydrogen peroxide and hydroxyl radical)
(Penning et al., 1996, 1999; IARC, 2010a).
The resulting PAH ortho-quinone is a highly reactive Michael acceptor and can
undergo 1,4- or 1,6- Michael addition reactions with cellular nucleophiles to yield
conjugates (Sridhar et al., 2001; IARC, 2010a) or with macromolecules to yield adducts
(Balu et al., 2004; IARC, 2010a). PAH ortho-quinones also can be reduced back to the
catechol, either non-enzymatically by the addition of 2H+ + 2e- by cellular reducing
equivalents (e.g. NADPH) or in two sequential one-electron steps catalysed by
NADPH:CYP reductases (Flowers-Geary et al., 1993, 1995). Once re-formed, the
catechol can undergo further auto-oxidation to create a futile redox cycle in which each
round of auto-oxidation forms reactive oxygen species, generating a reactive oxygen
species amplification system. Generation of reactive oxygen species continues until the
reducing equivalent is exhausted, which leads to oxidative stress and a pro-oxidant state.
The PAH ortho-quinones and the reactive oxygen species that they generate have the
capacity to form either mutagenic lesions in DNA or to act as electrophilic and prooxidant signals that may have consequences on cell growth (promotion). In this manner,
the pathway may contribute to the complete carcinogenicity of the parent PAH. In
humans, five AKR isoforms catalyse the oxidation of non-K region trans-dihydrodiols to
ortho-quinones (Palackal et al., 2002a,b; IARC, 2010a).
Much remains to be understood regarding the possible role of the PAH ortho-quinone
pathway and reactive oxygen species in carcinogenesis: (i) only a few relevant PAHs
have been examined for their metabolism via this pathway; (ii) human AKRs, other than
AKR1A1 and AKR1C1AKR1C4, may be involved in the activation of PAH transdihydrodiols; (iii) there is little information regarding the competing roles of CYP- versus
AKR-mediated activation of PAHs; (iv) covalent DNA adducts or oxidative lesions
produced by PAHs through the AKR pathway have yet to be detected; (v) the
mutagenicity of PAH ortho-quinones in mammalian cells has not been completely
demonstrated; (vi) the transforming potential of the PAH ortho-quinones has not yet been
determined; and (vii) the tumorigenicity of PAH ortho-quinones as initiators, promoters
or both has not been examined systematically (IARC, 2010a).
248
(d)
Cyclopenta-ring oxidation
The mechanism of cyclopenta-ring oxidation involves the formation of the arene

oxide at a highly electron-rich isolated double bond that is located at a five-membered
ring within a PAH. The cyclopenta ring is an external five-membered carbocyclic ring
that is situated on a carbocyclic hexameric fused-ring system. In general, cyclopenta-ring
derivatives of PAHs are more mutagenic (Kohan et al., 1985) and more carcinogenic
(Nesnow et al., 1998) than their unsubstituted counterparts. CYPs (e.g. 1A1, 1A2, 3A4)
metabolize cyclopenta-fused PAHs at the cyclopenta ring double bond to give
cyclopenta-ring oxides and diols (IARC, 2010a). The cyclopenta-ring oxides are reactive
intermediates that form DNA adducts (Hsu et al., 1999), that result in mutations and cell
transformation (Bartczak et al., 1987; Nesnow et al., 1991). They are hydrated by epoxide
hydrolase to diols, and some are conjugated to sulfate esters, which are also highly
reactive intermediates (Surh et al., 1993).
(e)
Meso-region biomethylation and benzylic oxidation
The role of the mechanisms of meso-region biomethylation and benzylic oxidation in

the carcinogenesis of PAHs is based on the formation of methylated PAHs from
unsubstituted PAHs and the subsequent metabolic activation of the methyl group to
electrophilic forms. The meso region of PAHs (also known at the L-region) has been
reported to be a region of high reactivity either in an aromatic nucleus or on a side chain
(Flesher et al., 2002, 2004). Accordingly, the chemical and biochemical pathways of the
activation of both unsubstituted and meso-substituted PAHs are essentially the same
because unsubstituted PAHs are converted to generally more carcinogenic meso-methylsubstituted PAHs in the process of metabolic activation (IARC, 2010a).
The first step in a series of three transformation reactions is the aralkylation
(methylation) of unsubstituted PAHs at a meso centre of high reactivity. This conversion
is mediated by the methyl donor, S-adenosyl methionine. The second step is the
hydroxylation of a meso-region methyl group by CYPs, and a chemical one-electron
oxidation process has also been proposed. The third step is the formation of a reactive
ester (e.g. sulfuric acid ester) catalysed by 3-phosphoadenosine-5-phosphosulfate
sulfotransferase (PAPS SULT). Sulfoxymethyl esters generate a highly reactive benzylic
carbonium ion and react with DNA to form DNA adducts; some of the latter are
mutagenic (Flesher et al., 2004; Ravi Kumar et al., 2005; IARC, 2010a).
(f)
Receptor-mediated mechanism
Several of the biological effects of PAHs, such as enzyme induction,

immunosuppression, teratogenicity and carcinogenicity, may be mediated by activating
the arylhydrocarbon receptor (AhR). This receptor is widely distributed and has been
detected in most cells and tissues. There is also evidence that AhR signals through a
variety of pathways and with other nuclear receptors to enable cell type- and tissuespecific control of gene expression (IARC, 2010a).
249
Responses of AhR signalling involve a variety of cellular responses. AhR induces

phase I and II enzymes; additional responses include lipid peroxidation and production of
arachidonic acid-reactive metabolites, decreased levels of serum thyroxine and vitamin A,
persistent activation of thyroid hormone receptor and communication with steroid
hormone receptors. Responses to altered AhR signalling may, therefore, be designated as
adaptive or toxic and/or as perturbations of endogenous pathways (IARC, 2010a).
(g)
Immunological and haematological mechanisms
A significant number of studies have demonstrated that PAHs are immunosuppressive in animal models and also in human leukocytes exposed in vitro. In animals,
the concentrations of PAHs that are required to produce immunosuppression are generally
quite high compared with those that produce cancer. There are limited human
epidemiological data that show that PAHs are immunosuppressive following
environmental exposures (IARC, 2010a).
The biological and toxicological actions of PAHs on the immune and haematopoietic
systems represent a complicated interplay between the ability of a specific PAH to bind to
endogenous AhR and induce CYPs in central and peripheral organs, which results in the
formation of oxidative and electrophilic metabolites and the removal of reactive
molecules via secondary metabolic processes. Thus, the toxicity of PAHs to the immune
system is dependent upon the exposure of cells and tissues to circulating parent
compounds and metabolites, their ability to activate AhR and their propensity to form
bioactive versus detoxified metabolites. The dose and route of exposure to PAHs are
important determinants of immunotoxicity in animals and humans. In general, the total
cumulative dose of exposure to PAHs correlates with immunoxicity in mice. It should be
noted that PAHs have been observed to produce biphasic doseresponse curves in which
low doses stimulate immune responses and high doses produce inhibition (Burchiel &
Luster, 2001; Booker & White, 2005; IARC, 2010a).
The overall effects of PAHs on the immune and haematopoietic systems result from
activation of both genotoxic and epigenetic pathways. Because of the heterogeneity of
lymphoid and myeloid cell populations and the complex interplay between different types
of cells and secreted products, the mechanisms of action of PAHs have been difficult to
assess. Many PAHs clearly exert effects on the developing as well as the mature immune
system, and some correlation exists between the carcinogenicity of PAHs and their ability
to produce immunosuppression (IARC, 2010a).
As reported previously, the AhR plays a critical role in the activation of immunotoxic
PAHs such as benzo[a]pyrene, via diol epoxide mechanisms, which lead to DNA
interactions that cause genotoxicity and suppress immunity by P53-dependent pathways.
Benzo[a]pyrene diol epoxide may also affect protein targets and modulate lymphocyte
signalling pathways via epigenetic mechanisms. Certain oxidative PAHs may be formed
via CYP-dependent and -independent (peroxidase) pathways. Redox-cycling PAHquinones may exert oxidative stress in lymphoid cells. Human exposures to PAHs are
usually in the form of complex mixtures, and it is difficult to attribute the relative
250
contributions of individual PAHs to the overall immunotoxic effects. Although there is

some evidence that environmental exposures to PAHs may produce immunotoxicity,
further epidemiological studies are needed (IARC, 2010a).
(h)
Phototoxicity
Early studies indicated that ultraviolet (UV) radiation could enhance the
carcinogenicity of PAHs on mouse skin (Santamaria et al., 1966), and two pathways can
result in phototoxicity. The first is dynamic phototoxicity or damage to cells during
photo-transformation of chemical species. This includes excited-state energy transfer to
biological macromolecules resulting in electron transfer that may convert both the PAH
and the biological molecule into free radicals, and the production of short-lived reactive
intermediates such as reactive oxygen species (Yu, 2002). The second is the formation of
toxic photoproducts during photolysis. They consist of some relatively light-stable
compounds that may be toxic both in the presence or absence of metabolic or lightinduced activation (Sinha & Chignell, 1983).
Upon absorption of light energy, PAHs are excited to upper energy states (singlet or
triplet) that undergo electron or energy transfer to molecular oxygen, solvents or
biological molecules in the cell to generate reactive species. These reactive species or
intermediates damage cellular constituents such as the cell membrane, nucleic acids or
proteins. Thus PAHs are activated by light irradiation to cause cellular damage and exert
toxicity, including carcinogenicity. This activation pathway is usually similar to the
enzymatic activation pathway in that it converts relatively inert PAHs to reactive species
(IARC, 2010a).
DNA damage resulting from the interaction of light with a PAH includes PAHDNA
adducts, single- and double-strand DNA breaks, DNADNA and DNAprotein crosslinks, depurination/depyrimidiation and the formation of the oxidative product
8-hydroxyguanine (IARC, 2010a). Yan et al. (2004) showed that 11 of 16 PAHs were
photomutagenic in the Ames mutagenicity assay, and a close association was observed
between the photomutagenicity and reported carcinogenicity.
Phototoxicity, including photomutagenicity, is closely related to the photochemical
reactions that generate reactive PAH intermediates and reactive oxygen species during
photolysis (Yu, 2002). Certain PAHs with extended aromatic ring systems can absorb
light in the UVA (320400 nm) and visible (> 400 nm) region. Usually, PAHs with three
or four aromatic rings can absorb UVA light and those with five or more aromatic rings
as well as the hydroxyl-, amino- and nitro-substituted PAHs with three or four aromatic
rings can absorb visible light (Dabestani & Ivanov, 1999).
(i)
Non-genetic effects
PAHs, such as benzo[a]pyrene, can increase cell proliferation (Tannheimer et al.,

1998) and can cause an influx of extracellular Ca2+ into the cell (perhaps by perturbing the
physical organization of phosphatidylcholine membranes) (Jimnez et al., 2002). This
251
may be important for the activation of protein kinase C pathways, which are associated
with tumour promotion (Tannheimer et al., 1999). PAH quinones may also increase the
epidermal growth factor receptor pathway, the serine-threonine kinase Akt and the
extracellular signal-regulated kinase activity (Burdick et al., 2003). Benzo[a]pyrene can
induce P53 accumulation and a partial S-phase arrest (Plskov et al., 2005).
Benzo[a]pyrene diol epoxide increases the level of Cdc25B (which regulates cell-cycle
progression and genetic stability), mRNA and protein levels in terminal squamous
differentiated human bronchial epithelial cells and lung cancer cells but not in
undifferentiated bronchial cells (Oguri et al., 2003).
Benzo[a]pyrene also has been shown to induce apoptosis in murine and human cells
(Chen et al., 2003; Raychoudhury & Kubinski, 2003; Ko et al., 2004). There are many
ways by which compounds can induce apoptosis, and PAHs may affect different
pathways in different cell types.
Gap-junctional communication is important in cell proliferation, differentiation and
apoptosis, and it has been suggested to be important for the promotion of carcinogenesis.
Of 35 PAHs tested for inhibition of gap-junctional communication in rat liver epithelial
cells, 12, including benzo[a]pyrene, were found to be strong but transient inhibitors
(Blha et al., 2002).
4.2.2
Particles
This section addresses the mechanisms of carcinogenesis of particles and is based on

an extensive database for poorly soluble, respirable particles of low toxicity that can be
found in a previous volume of the Monographs (IARC, 2010b). The extent to which these
mechanisms are fully relevant for particles generated from combustion is not known.
(a)
Lung overload
The concept of overload is central to the relevance of using rodent studies for the
evaluation of human health hazards from inhaled particles. Overload is a biological
mechanism that involves the dose-dependent impairment of alveolar macrophagemediated clearance of respirable particles. In the alveolar region of the respiratory tract,
the primary mechanism for particle clearance is phagocytosis by alveolar macrophages
with subsequent removal of particle-containing macrophages by mucociliary clearance.
High particle burdens in the lungs can result in overload because alveolar macrophagemediated clearance is overwhelmed, which results in a decreased rate of clearance and an
increased retention of particles. Overloading of lung clearance has been observed in rats,
mice and hamsters exposed to different insoluble respirable particles (e.g. carbon black,
titanium dioxide, talc, toner and diesel exhaust particulates) (Strom et al., 1989; Muhle et
al., 1990; Bellmann et al., 1991; National Toxicology Program, 1993; Warheit et al.,
1997; Bermudez et al., 2002, 2004; Elder et al., 2005) and asbestos fibres (Davis et al.,
1978; Bolton et al., 1983).
252
(i)
Mechanisms that underlie lung overload
Experimentally, overloading of lung clearance has been inferred from the observation
of a greater lung burden of particles or fibres than that expected on the basis of results
from lower concentrations or shorter durations of exposure (Davis et al., 1978). A steadystate lung burden should be achieved when the rate of deposition equals the rate of
clearance, and overloading represents a deficit in that clearance. Impaired clearance
attributed to overloading has been expressed as a reduction in the clearance rate
coefficient (Muhle et al., 1990; Bellmann et al., 1991) or an increase in the amount of
particles retained in the lungs following exposure (Strom et al., 1989; Bermudez et al.,
2002, 2004; Elder et al., 2005). Increased translocation of particles to the lung-associated
lymph nodes has also been observed at doses at which overload occurs (Strom et al.,
1989; Bellmann et al., 1991).
Morrow (1988) hypothesized that overload was a consequence of macrophages that
become progressively immobilized and aggregated. When the dose of particles reaches a
critical particle volume, clearance by macrophages is suppressed and particles accumulate
in the lungs. Based on the lung burden of particle mass associated with increased retention
in rat lungs (approximately 1 mg/g of lung tissue for unit density particles) and data on the
volume and number of alveolar macrophages in rat lungs, it was hypothesized that
impairment of clearance would be initiated when the particle volume exceeded an average
of 6% of the macrophage volume, and clearance would be completely impaired when
particle volume exceeded an average of 60% of the macrophage volume. The upper
particle volume estimate (60%) was supported by Oberdrster et al. (1994), who
showed that clearance was no longer detectable 200 days after instillation of 10-m
diameter polystyrene particles in rat lungs. The overload mechanism pertains specifically
to poorly soluble respirable (<10 m) particles of low toxicity. Factors other than the
volumetric overload can lead to impaired alveolar clearance. For example, particles that
are toxic to macrophages (e.g. crystalline silica) can cause impaired clearance at doses
lower than those of low-toxicity particles (Bellmann et al., 1991). Ultrafine particles have
been recognized as differing from fine particles with regard to overloading. Morrow
(1992) noted that ultrafine particles impair clearance at lower mass or volume
concentrations than those expected for larger respirable particles. Oberdrster (1996)
confirmed this observation and showed that increased particle retention and inflammation
were related to particle surface area.
One mechanism for the impaired clearance of ultrafine particles may be their
ineffective phagocytosis (Churg et al., 1998; Renwick et al., 2001, 2004; Geiser et al.,
2005), which leaves the particles free in the alveolar region and more readily able to
translocate to the lung interstitium (Ferin et al., 1992, 1994). The surface properties of
particles may also influence phagocytosis. For example, Castranova (2000) found that
chronic inhalation exposure to 2 mg/m3 coal dust activated alveolar macrophages, while
the same exposure to diesel exhaust depressed phagocytic activity. Wolff et al. (1986)
noted that additional factors other than non-specific particle effects must be important
because the exposure level that resulted in overloading and lung tumours was higher for
253
some particles than others (e.g. 250 mg/m3 fine-sized titanium dioxide versus ~7 mg/m3
diesel exhaust).
(ii) Mechanisms that underlie lung response to overload
An increase in neutrophilic inflammation has been defined as the critical biological
response to lung overload (ILSI Risk Science Institute Workshop Participants, 2000). An
increase in polymorphonuclear leukocytes (granulocytes) in bronchioalveolar lavage
(BAL) fluid in rats has been associated with increased retention of particles in the lungs
(Tran et al., 1999). Mice also appear to be susceptible to overloading doses and adverse
pulmonary responses, but they regain normal clearance more readily when exposure
ceases. Hamsters clear particles much faster than rats or mice, experience overloading at
higher doses and recover more easily. Lung responses follow the clearance kinetics for
inhaled particlesrats show a more severe, sustained response to inhaled particles than
mice, while hamsters have only a temporary inflammatory response (Bermudez et al.,
2002, 2004; Elder et al., 2005). In rats, lung responses to overloading include increased
lung weight, chronic inflammation, fibrosis and lung cancer (Muhle et al., 1991).
The cascade of events that describes the biological process that starts from particle
deposition at critical target cells or tissues within the rat lung and results in tumours
includes: sustained inflammation, production of reactive oxygen species, depletion of
antioxidants and/or impairment of other defence mechanisms, cell proliferation and gene
mutations. These individual steps comprise an overall mode of action that can be used to
compare responses of rats with those of other species including humans (IARC, 2010b).
At a lung burden of particle mass at which overload is observed in rats (estimated to
begin at ~0.5 mg/g of lung tissue and to be fully developed at ~10 mg/g), a sustained and
widespread cellular inflammatory response occurs. The cell population is dominated by
activated and probably (under these conditions) persistent neutrophil granulocytes and
secretes a collection of mediators (pro- and anti-inflammatory cytokines, proteases,
cytotoxins, fibrogenic mediators and other growth factors) that act through the pulmonary
milieu on surrounding cells or tissues and surrounding structures (Castranova, 2000;
IARC, 2010b).
The degree of sustained inflammation experienced by rodents (most notably rats) at
high lung burdens is not observed in humans. However, humans may experience
sustained inflammation in certain disease states. One such human condition (which may
be particle-stimulated, e.g. by silica, or may be cryptogenic) is late-stage interstitial
pulmonary fibrosis. Patients who have interstitial pulmonary fibrosis and chronic
inflammation have been reported to experience a higher incidence of lung tumours
(Daniels & Jett, 2005). Rom (1991) found a statistically significant increase in the
percentage of neutrophil granulocytes in BAL fluid of workers with respiratory
impairment who had been exposed to asbestos, coal or silica (4.5% in cases versus 1.5%
in controls). Elevated levels (sevenfold increase over controls) of neutrophil granulocytes
have been observed in the BAL fluid of miners who had simple coal workers
254
pneumoconiosis (Vallyathan et al., 2000) and in patients with acute silicosis (a 10-fold
increase over controls) (Goodman et al., 1992; Lapp & Castranova, 1993).
The precise role of chronic inflammation in the development of cancer is uncertain,
but considerable evidence shows that chronic inflammation may have a multi-faceted role
in this process. Activated cells in the lung are known to release various reactive
intermediates, most notably those derived from oxygen. Sustained excess of oxidant
activity is known to deplete antioxidant defences gradually. Clear differences among
these defence mechanisms in the lungs exist between humans and rats, and evidence
shows that humans overall are relatively deficient in some of these mechanisms relative to
rats (Hatch et al., 1985). Reactive oxygen species within cells may damage DNA directly
and potentially induce mutations. Moreover, cell damage and promitotic stimuli initiated
by reactive oxygen species promote cell turnover and proliferation, both of which may
enhance the risk for DNA replication error and/or expand a mutated or transformed cell to
initiate the tumorigenic process (see Section 4.2.1).
(iii) Dosimetric correlation between lung particle burden and
response
Because particle overload is the critical determinant that underlies the adverse
biological response to inhaled particles, an understanding of the appropriate dosimetric
expression for overload is essential for hazard evaluation. A number of studies have
shown that, for particles of different sizes but with the same chemical composition, the
dose expressed as particle surface area is a better predictor of adverse pulmonary
inflammation than particle mass (Oberdrster et al., 1992; Tran et al., 1999; Bermudez et
al., 2002, 2004). Particle surface area is also related to pulmonary inflammation in mice
(Lison et al., 1997). Oberdrster and Yu (1990) and Driscoll et al. (1996) showed that
particle surface area is also a better predictor of lung tumours than particle mass in rats
exposed to various poorly soluble particles of fine or ultrafine size.
The particle characteristics and method used to estimate particle surface area may
influence the magnitude of the observed response. For example, carbon black that has a
high specific surface area (220 m2/g) was shown to cause a lower inflammatory response
than that expected based on the total particle surface area dose (Driscoll et al., 1996). This
could be due to less disaggregation of deposited carbon black into smaller units compared
with ultrafine titanium dioxide for instance (Oberdrster, 1996). It may also be due to a
more porous carbon black surface (carbon black has a higher internal surface than
titanium dioxide), which may increase the surface area measured by nitrogen absorption
but does not accurately measure the effective surface area in contact with the epithelial
cell surface (Tran et al., 1999).
(b)
Interspecies comparison of particle retention in the lung
Impairment of clearance leads to an increased retention of particles, which is the

hallmark of lung overload. Thus, an understanding of interspecies differences in the
mechanisms of particle retention can aid hazard evaluation and risk assessment.
255
Differences in the patterns of particle retention of coal dust or diesel exhaust were
observed in rats and monkeys; a higher volume percentage of coal dust was retained in
the alveolar lumen in rats and in the interstitium in monkeys that were exposed by
inhalation to 2 mg/m3 coal dust and/or diesel exhaust particulate for 2 years (Nikula et al.,
1997a,b). A greater proportion of particles were also retained in the interstitium in
humans compared with rats. In humans, as the duration of exposure and assumed
concentration of coal dust increased, the pattern of retention changed so that the
proportion of particles in the interstitium increased. In contrast, the pattern of retention in
rats did not vary with increasing concentrations of diesel exhaust particulate from 0.35 to
7.0 mg/m3 (Nikula et al., 2001).
One class of insoluble particlescarbon blackhas been identified in human lungs,
although no quantitative data are available on its retention in humans. However, based on
studies with other poorly soluble particulate materials, it can be assumed that the normal
retention half-times of particles such as carbon black in humans is longer than that
measured in rats and mice. For example, Bailey et al. (1985) found that the retention time
of inhaled monodisperse 1- and 4-m diameter fused aluminosilicate particles in humans
followed a two-component exponential function with phases having half-times of the
order of tens of days and several hundred days, respectively. At 350 days after inhalation,
retention of the remaining material averaged 4611% for the 1-m particles and 5511%
for the 4-m particles. In contrast, data in rats (Oberdrster, 1995) and mice (Kreyling,
1990) demonstrate retention half-times of ~70 days and ~55 days, respectively.
Heavy exposure to particles in occupational settings may lead to high particle burdens
in the human lung. By analogy to the rat, if the human lung burden exceeds ~0.51 mg/g
lung, it would be expected that the normal retention half-time may be prolonged. Indeed,
there is some evidence that workers in occupations that are associated with high particle
burden in the lungs (e.g. coal mining) show increased long-term retention of particles
(Stber et al., 1965; Freedman & Robinson, 1988). Retention half-times of the order of
years have been measured in a number of human studies that involved accidental
exposure to radionuclides (ICRP, 1994).
Little is known about overloading in non-rodent species including humans. Perhaps
the most often cited human data are in coal miners, which is one of the best studied
occupational cohorts regarding quantitative exposureresponse relationships (Attfield &
Kuempel, 2003). Coal miners have historically experienced high rates of occupational
lung diseases including increased morbidity and mortality from pneumoconiosis and
chronic obstructive lung diseases (National Institute for Occupational Safety and Health,
1995). Excess mortality from lung cancer has generally not been observed in coal miners
(National Institute for Occupational Safety and Health, 1995), although in a more recent
study of German coal miners, elevated lung cancer mortality was detected in miners who
had developed pneumoconiosis (standardized mortality ratio, 1.57), which was
independent of the effect of tobacco smoking (Morfeld et al., 2002).
Retained lung burdens have also been relatively high; an average of ~14 mg/g lung
has been observed historically in coal miners in the USA (Kuempel et al., 2001) and the
256
United Kingdom (Tran & Buchanan, 2000). This mean lung burden is comparable with
retained mass lung burdens in rats that had overload. Because an elevated incidence of
lung cancer has generally not been observed in coal miners, it has been suggested that the
rat may not be a good model to predict lung cancer in humans. However, although the
mean lung burden is relatively high in coal miners, it is actually lower than the mean lung
burdens associated with the excess incidence of lung tumours in rats. For example, in rats
chronically exposed to coal dust, mass lung burdens of 24 mg/g lung tissue were
associated with an 11% incidence of lung tumours (versus 0% in unexposed controls)
(Martin et al., 1977). In rats exposed to fine-sized titanium dioxide, lung burdens up to
~35 mg/g were not associated with lung tumours, and increased incidences of lung
tumours were observed only in rats with lung burdens greater than ~100 mg/g
(approximately 16% in male and female rats, excluding keratinizing cystic squamous-cell
carcinomas) (Lee et al., 1985a,b, 1986). In female rats that chronically inhaled talc for
two years, 9 mg talc/g lung tissue was not associated with an elevated incidence of lung
tumours (0/48, 0%), while an average retained burden of 29 mg/g lung was associated
with a 26% (13/50) incidence of alveolar/bronchiolar tumours (National Toxicology
Program, 1993).
Based on these chronic inhalation studies in rats exposed to various fine-sized, poorly
soluble particles of relatively low toxicity, lung tumours were not observed in rats that
had lung burdens similar to those of coal miners. Rats that developed lung tumours
following chronic inhalation of these particles had retained mean mass lung burdens that
were at least twice as high as those in coal miners. Thus, the observed lung tumour
response in rats and the absence of reported tumours in coal miners when both are
exposed chronically to fine-sized, poorly soluble particles such as coal dust are somewhat
consistent.
The surface area of particles may be a more appropriate dose metric for predicting
response; therefore, it is useful to evaluate rat and human responses to particle surface
area dose in addition to particle mass dose. In rat lungs, fine and ultrafine particles of
similar composition have shown consistent doseresponse relationships when dose is
expressed as particle surface area rather than as particle mass. The mean surface area dose
of coal dust in miners lungs from studies in the USA and United Kingdom can be
calculated as 0.1 m2 coal dust/g lung tissue (assuming 7.4 m2/g coal dust; Vallyathan et
al., 1988; Tran & Buchanan, 2000; Kuempel et al., 2001). In rats, the lowest observed
surface area doses associated with elevated incidences of lung tumours (excluding
keratinising cystic squamous-cell tumours) following chronic inhalation were: 0.18 m2
coal dust/g lung tissue in female rats, (assuming 7.4 m2/g coal dust), with an 11% tumour
incidence versus 0% in controls (Martin et al., 1977); 0.58 m2 carbon black/g lung tissue
for female rats, with a 7.5% tumour incidence versus 0% in controls (Nikula et al., 1995);
6.9 m2 carbon black/g lung tissue in female rats, with a 28% tumour incidence versus
0.46% in controls (Heinrich et al., 1995); 1.3 m2 ultrafine titanium dioxide/g lung tissue in
female rats, with a 19% tumour incidence versus 0.46% in controls (Heinrich et al.,
1995); 1.2 m2 fine titanium dioxide/g lung tissue, with a 16 or 17% tumour incidence in
257
male and female rats versus 2 or 0% in male and female controls, respectively (Lee et al.,
1985a); and 0.27 m2 talc/g lung tissue in female rats, with a 26% tumour incidence versus
2% in controls (National Toxicology Program, 1993). These comparisons show that the
retained particle surface area dose in coal miners was lowerby a factor of
approximately 270than that associated with elevated incidences of lung tumours in
rats exposed to either fine or ultrafine poorly soluble particles. Thus, using particle surface
area as the dose metric, excess lung cancer would not necessarily be expected to be
observed in coal miners given the relatively low particle surface area dose compared with
that associated with lung tumours in rats.
These comparisons illustrate the importance of using normalized doses to compare
responses across species. Furthermore, due to the faster clearance rate, rats do not attain
lung burdens comparable with those observed in humans who work in dusty jobs (e.g.
coal miners) unless they experience overloading of lung clearance.
(c) Relevance of mechanistic data for assessing carcinogenic hazard in
humans
To evaluate the appropriateness of the rat as an experimental model to assess the
carcinogenic hazard of poorly soluble particles in the lungs of humans, it is useful to
evaluate the scientific evidence that allows for comparisons among species regarding
exposure, doseresponse and mode of action. A conceptual framework is presented in
Figure 4.1.
(i)
Exposuredose
Inhaled particles may present a hazard when they deposit in sufficient quantities
(dose) and interact with cells/tissues at responsive target sites along the respiratory tract.
The relationship between particle exposure and inhaled dose is described by the kinetics
of particle deposition and clearance, and that retained at or within respiratory tract tissues
(Section 4.1.2). Inhaled and deposited particles clear from the normal lungs of healthy rats
at a faster rate than those from humans. However, at high lung burdens, normal clearance
from the rat lung can be impaired and overwhelmed, such that in time clearance
effectively ceases. This phenomenon (termed overload) is observed with particles that
are poorly soluble and are generally considered to be of low toxicity (Morrow, 1988).
Particle lung burdens observed in humans in some dusty jobs (e.g. coal miners) have
sometimes approximated the overload dose in rats. At sufficient concentrations and
durations of inhalation, rats may accumulate particles to a greater extent than the lung
burdens seen in most workers. For ultrafine particles, the attained mass doses associated
with impaired clearance in rodents approximate those that could occur in workers. For
any experimental model used for hazard assessment in humans or to evaluate dose
response relationships, it is widely appreciated that it is important to evaluate doses in
experimental animals that are comparable with those that may occur in humans.
258
Figure 4.1. Conceptual framework of carcinogenesis induced by poorly soluble

particles in rats
Inhalation of particles
Clearance of
particles
Deposition of
particles
Reactive oxygen
species
Mutations
Uptake of particles by
phagocytes and other
cells
Cytokines, growth
factors, proteases and
other mediators
Inflammation
Cell injury
Cell proliferation
Cancer
Fibrosis
The scheme represents the sequence of events and modes of action that are considered to be involved in the
formation of tumours that are observed in the lungs of rats after high exposure to poorly soluble particles (from
IARC, 2010b)
Lung clearance can be impaired in humans and experimental animals for many
reasons. In humans, toxic gases and particles have been shown to impair clearance by
affecting normal cilia function, mucus rheology and phagocytosis. Ultrafine particles may
be cleared less effectively due to impaired phagocytosis compared with larger particles
(Renwick et al., 2001, 2004; Geiser et al., 2005).
Much more is known about overload in rats than in humans. Overwhelmed or
impaired clearance in rats has been postulated as a pivotal factor in the development of
lung overload (Morrow, 1988). It is clear that the same factors that can interfere with
clearance in rats may contribute to mass dose accumulation in humans (e.g. the
cytotoxicity of the material and/or ineffective phagocytosis). Overload was originally
described in terms of mass- or volume-based dose. For fine and ultrafine carbon black and
titanium dioxide, surface area dose has been shown to be a better predictor of impaired
clearance (Oberdrster & Yu, 1990; Oberdrster et al., 1992; Oberdrster, 1996; Tran et
al., 1999).
Impaired clearance and overload are not unique to the rat, but can also occur in other
species although to different degrees. For example, overload has not been observed in
hamsters at concentrations at which it readily appears in rats and mice (Bermudez et al.,
259
2002, 2004; Elder et al., 2005). How human lung clearance would behave under similar
circumstances is unclear but, by analogy to coal workers, impairment of clearance does
occur with chronic exposure and often persists long after exposure ceases (Freedman &
Robinson, 1988).
Rats chronically exposed to sufficiently high concentrations of poorly soluble
particles experience a steady reduction in their alveolar clearance rates and an
accumulation of particles in the alveolar lumen and interstitium (Ferin et al., 1992, 1994;
Warheit et al., 1997; Bermudez et al., 2002, 2004). In rodents, ultrafine particles
translocate to the interstitium to a greater extent than fine particles (Ferin et al., 1992;
Oberdrster, 1996). In studies that compare the patterns of particle retention in the lungs
of rats, monkeys and humans exposed to coal dust and/or diesel exhaust, the largest
volume percentage of dust was observed in the alveolar lumen in rats and in the
interstitium of monkeys and humans (Nikula et al., 1997a,b, 2001); however, no data
were available to compare the actual retained doses in the specific lung regions of each
species. The biological significance of the interstitial/lumenal distribution in the
development of overload and the toxic sequelae is not clear, either within a given species
or among species.
(ii) Doseresponse and mode of action
With continued inhalation of high concentrations of particles, rats that achieve
overload may develop pulmonary fibrosis and both benign and malignant tumours (Lee et
al., 1985a,b, 1986; Warheit et al., 1997). Oberdrster (1996, 2002) has proposed that
high-dose effects observed in rats may be associated with two thresholds: (i) a pulmonary
dose that results in a reduced macrophage-mediated clearance leading to overload and (ii)
a higher dose associated with overload at which normal antioxidant defences within the
lung are overwhelmed and pulmonary tumours may be induced.
As discussed above, a cascade of events proposed to describe the biological process
that starts with some particle deposition at critical target cells or tissues within the rat lung
and results in rat lung tumours includes: sustained inflammation, production of reactive
oxygen species, depletion of antioxidants and/or impairment of other defence
mechanisms, cell proliferation and gene mutations. These individual steps comprise an
overall mode of action that can be used to compare rat responses with those of other
species including humans (see Figure 4.1).
At a particle mass lung burden at which overload is observed in the rat (estimated to
begin at ~0.5 mg/g lung and to be fully developed at ~10 mg/g lung; Muhle et al., 1990),
a sustained and widespread cellular inflammatory response occurs. The degree of
sustained inflammation experienced by rodents (most notably the rat) at high lung
burdens is not observed in humans, although humans may experience sustained
inflammation in certain disease states.
260
(iii) Interspecies extrapolation

Several studies have shown that rats, but not mice or hamsters, develop an excess
incidence of lung cancer at chronic overloading doses of inhaled poorly soluble
particles. A number of studies have discussed this phenomenon and the challenges it
poses for the extrapolation of chronic effects in rats to the human situation (Morrow,
1994; Levy, 1995; Oberdrster, 1995; Watson & Valberg, 1996; ILSI Risk Science
Institute Workshop Participants, 2000; Miller, 2000; Oberdrster, 2002; Hext et al.,
2005).
Uncertainty remains with regard to the identification in detail of the cascade of events
that lead to lung cancer in rats following inhalation of poorly soluble particles (i.e. talc,
carbon black, titanium dioxide). However, as shown in Figure 4.1, a number of important
steps can be identified that are supported by a substantial rodent database. An important
question that needs to be addressed is the extent to which the steps outlined in Figure 4.1
for rat lung cancer are also operative in other animal species including humans. The
majority of animal studies that have evaluated the effects of poorly soluble particles on
the respiratory tract have been conducted in rats. It is necessary to consider species
differences such as particle inhalability, breathing conditions, respiratory tract structure
and pulmonary defences when extrapolating toxicological findings from rodents to
humans (Brown et al., 2005).
All animals species that are routinely used in particle toxicology, as well as humans,
are susceptible to impairment of clearance of poorly soluble particles from the lungs.
Impaired clearance is probably one of the first steps necessary to initiate a sequence of
events that may lead to lung cancer in rats (see Figure 4.1). Importantly, however,
different animal species exhibit differences in particle-induced impairment of clearance,
which can result in different lung burdens (expressed as mass or surface area) following
exposures to the same particle concentrations.
Similarly, pulmonary inflammation has been reported as a consequence of exposures
to poorly soluble particles in both experimental animals and humans. The pathophysiology of particle-induced fibrosis in humans and fibrosis and lung cancer in rats
from lung overload involves chronic inflammation, hyperplasia and cell proliferation, and
altered collagen deposition and architecture.
Rats and mice, in contrast to hamsters, exhibit sustained inflammation associated with
particle lung burden, but lung tumours induced by poorly soluble particles have been
observed only in rats. It has been shown that the rat is uniquely susceptible to particleinduced lung cancer relative to the mouse and hamster. Although some of the steps
indicated in Figure 4.1 have been demonstrated in humans exposed to poorly-soluble
particles, it is not known to what extent humans are susceptible to particle-induced lung
cancers.
4.2.3
261
Genetic and related effects

(a)
Humans
(i)
Biomarkers of exposure (DNA adducts, cytogenetic effects and
mutagenic activity)
Biomarkers of exposure to mutagens

The presence of mutagenic PAH metabolites in urine, that of PAHDNA adducts and
the mutagenic activity of urine extracts or concentrates have been employed as biomarkers of human exposure to mutagenic substances in indoor air.
Significantly increased levels of urinary 1-hydroxypyrene were observed in Polish
children who were exposed to emissions from indoor heating and cooking with coalburning stoves in comparison with those exposed to emissions from other heating or
cooking facilities (Siwiska et al., 1999). Mumford et al. (1995) studied PAHs, hydroxyPAHs and methylated PAHs in urine samples from smoking men and nonsmoking
women in the Xuan Wei region of China who were exposed to unvented emissions from
smoky coal. Controls were nonsmoking men and women from Kunming (China) and
nonsmoking Chinese American women who used gas/electricity. The results indicated
that the concentrations of 9-hydroxybenzo[a]pyrene were significantly (p<0.05) higher in
Xuan Wei residents than in controls. The mean levels of methylated phenanthrene, pyrene
and benz[a]anthracene in the urine of Xuan Wei men and women were 5.8- and 9.8-fold
higher than those of the parent PAHs, respectively. The high urinary level of methylated
PAHs is consistent with the high concentrations of methylated PAHs measured in smoky
coal emissions.
Casale et al. (2001) used liquid chromatography/quadrupole ion-trap MS (LC/QMS)
to detect the presence of the depurinated benzo[a]pyrene-adducted DNA bases, 7(benzo[a]pyren-6-yl)guanine and 7-(benzo[a]pyren-6-yl)adenine, in urine samples from
three of seven women exposed to smoky coal emissions in the Xuan Wei region. These
adducts were not detected in 13 control subjects. Depurinating benzo[a]pyrene adducts
profile were correlated with the profile of GT transversions observed in the P53 gene
of human lung tumours.
A supportive occupational study by Kato et al. (2004) monitored urinary
mutagenicity and excretion of urinary metabolites (i.e. 2-naphthol and 1-pyrenol) in
Brazilian charcoal workers exposed to high levels of eucalyptus wood smoke. The results
showed markedly enhanced levels of urinary mutagenicity (odds ratio, 5.31; 95% CI,
1.8515.27) and metabolite excretion (odds ratio, 17.13; 95% CI, 6.9142.44) in the
highly exposed kiln tenders in comparison with unexposed tree cutters.
262
Cytogenetic effects (sister chromatid exchange, micronucleus formation and

chromosomal aberrations)
Cytogenetic effects such as sister chromatid exchange, micronuclei and chromosomal
aberrations have been documented in studies that examined the genotoxic effects of
human exposure to indoor combustion emissions.
Biomass combustion (including wood)
ztrk et al. (2002) investigated the frequency of sister chromatid exchange in
peripheral blood lymphocytes from 20 patients who experienced acute carbon monoxide
intoxication from exposure to indoor wood or coal combustion emissions. They found
significantly higher levels of sister chromatid exchange frequency (p=0.008) in the
exposed group (8.12.4 per metaphase) compared with 20 healthy controls (6.31.6 per
metaphase). Musthapa et al. (2004) investigated cytogenetic effects in 179 Indian women
exposed to cooking emissions generated using various biofuels, including cow dung, cow
dung/wood combinations, wood and kerosene. Because it was difficult to find suitable
controls with no exposure to cooking fuel smoke, users of LPG were used as a control
group because LPG generates comparatively low levels of smoke and respirable airborne
particulates. Micronucleus formation in human blood lymphocytes in women burning
cow dung (30.03.6 micronucleated cells/1000 binucleates), cow dung/wood (26.23.1)
or wood (22.94.0) was significantly higher (p<0.05) than that in LPG users (10.32.7).
Analyses of the frequency of chromosomal aberrations showed a similar trend (i.e. cow
dung [10.8%] > cow dung/wood [8.2%] > wood [7.0%] > LPG [3.1%]; p<0.05 versus
LPG users).
Coal combustion
Analyses of the peripheral blood lymphocytes of 184 villagers from Guizhou
province, China (Zhang et al. 2007), where arsenism linked to indoor exposure to coal
combustion emissions is endemic, showed significantly higher levels of sister chromatid
exchange, chromosomal aberrations and micronucleus formation compared with those of
53 villagers who did not use coal containing high levels of arsenic.
DNA adducts and DNAprotein cross-links
Coal combustion
Levels of DNA adducts have been employed as a sensitive biomarker of internal dose
and DNA damage in tissues from Xuan Wei women exposed to emissions from the
indoor combustion of smoky coal.
A study of DNA adduct levels and profile (by 32P-postlabelling) in placenta, blood
and lung cells of Xuan Wei residents exposed to unvented indoor emissions from smoky
coal failed to show significant increases in either placental or white blood cell DNA
adducts, compared with controls from Kunming who used electricity/gas. However,
levels of DNA adducts in lung BAL cells from coal smoke-exposed individuals (n=24)
were fourfold higher (25.5 adducts/108 bases) than in those from unexposed individuals
263
(5.9 adducts/108 bases; n=8) (Gallagher et al., 1993). Similarly, much higher levels of
PAHDNA adducts were found in brush cells from fibrobronchoscopies of 30 lung
cancer patients from Xuan Wei exposed to coal smoke compared with those of
10 controls from Kunming with no exposure to coal smoke. The authors suggest that the
relatively high levels of DNA adducts in lung cells indicates that the respiratory tract is
the target tissue for exposure to emissions from smoky coal (Xu et al., 1997). Moreover,
enzyme-linked immunosorbent assay (ELISA) measurements in placentas and peripheral
and cord white blood cells from Xuan Wei women exposed to emissions from smoky
coal showed higher levels of DNA adducts in placentas and peripheral white blood cells
in comparison with Beijing residents exposed to natural gas combustion emissions
(Mumford et al., 1993).
Sensitive analytical techniques such as LCQ/MS and capillary electrophoresis with
laser-induced fluorescence detection have also been applied to assess the levels of
benzo[a]pyrene-adducted DNA bases in urine samples from women in Xuan Wei
exposed to coal smoke. The results showed high levels of the benzo[a]pyrene-adducted
DNA base 7-(benzo[a]pyren-6-yl)guanine, which were about 20300-fold greater than
those of 7-(benzo[a]pyren-6-yl)adenine. The authors suggested that the presence of
benzo[a]pyrene-adducted DNA bases in urine could be a promising biomarker for
enhanced cancer risk linked to chronic indoor exposures to PAHs (Casale et al., 2001). In
addition, Zhang et al. (2000, 2007) reported that exposure to coal combustion emissions is
associated with increased levels of DNAprotein cross-links and unscheduled DNA
synthesis in peripheral blood lymphocytes. However, the authors concluded that the
observed DNA damage was probably due to exposure to arsenic in coal emissions.
Wood combustion
Reddy et al. (1990) reported that residential wood combustion in the USA did not
increase the level of aromatic DNA adducts (measured by 32P-postlabelling) in 12 DNA
samples of white blood cells or placentas from nonsmoking women, but tissue-specific
endogenous adducts were observed. [The Working Group noted that this lack of enhanced
DNA adduct levels in human blood cells may suggest that the exposure dose was low
and/or duration was short.] A similar Dutch study failed to show increased levels of
aromatic DNA adducts in white blood cells in five individuals from homes where
residential wood combustion occurred, despite the fact that indoor air monitoring showed
that wood combustion in an open fireplace increased the mutagenicity of indoor air
samples in the Salmonella TA98 strain, as well as the benzo[a]pyrene and pyrene
concentrations (Heussen et al., 1994). However, competitive fluorescence ELISA did
reveal enhanced levels of DNA adducts in 56% (9/16) of the placental samples from
Xuan Wei women who used wood as cooking fuel compared with 25% (4/16) of the
samples from Beijing women who used natural gas (Mumford et al., 1993).
264
(ii)
Mutations in TP53 and KRAS, and P53 protein accumulation
Mutation spectrum analyses

Coal combustion
DeMarini et al. (2001) investigated the spectrum of P53 and KRAS mutations in lung
tumours associated with smoky coal combustion among Xuan Wei residents. The results
clearly showed that GCTA transversions were the predominant mutation for both
KRAS (86%) and P53 (76%), which is consistent with the mutation spectrum induced by
exposures to PAHs. Moreover, Keohavong et al. (2003) compared the KRAS mutations in
lung carcinomas from 41 nonsmoking women and 61 smoking men exposed to smoky
coal in Xuan Wei and found that 67 and 86% of the KRAS mutations were GCTA
transversions, respectively. When analysed by Granville et al. (2003) using the
Salmonella mutagenicity assay, PAH-rich extracts of smoky coal combustion emissions
from Xuan Wei showed enhanced potency (more than threefold) in the base-pair mutation
strain TA100 in comparison with the frameshift mutation strain TA98. In addition, the
mutagenic activity in strain TA100 was enhanced (8.7-fold) in the presence of an Aroclor
1254-induced postmitochondrial supernatant from male rat liver. Furthermore,
investigations of the mutation spectra of smoky coal combustion emissions in strain
TA100 also showed that the mutations were primarily (7886%) GCTA transversions.
Because of the similarity between the mutation spectrum observed in lung tumours linked
epidemiologically with exposures to smoky coal emissions (i.e. GCTA transversions)
and that observed in strain TA100 following exposure to PAH-rich extracts of smoky coal
emissions, the authors suggested that the high concentration of PAHs in smoky coal
emissions plays a critical role in the induction of mutations and lung tumours.
In a later study of 15 Xuan Wei women who had lung cancer, Keohavong et al.
(2004) used a laser capture micro-dissection method to isolate epithelial cells from
sputum samples and to score P53 and KRAS mutations. The results confirmed P53 and/or
KRAS mutations in sputum cells from seven patients (five patients with KRAS mutation,
one with P53 mutation, one with KRAS and P53 mutations). This method proved to be
more sensitive than earlier, more conventional methods that detected mutations in only
two of the 15 samples. This sensitive method has also been applied by Keohavong et al.
(2005) to screen for P53 and KRAS mutations in sputum samples from 92 Xuan Wei
individuals with no evidence of lung cancer. Cells from 13 individuals (14.1%) showed
mutations in P53, cells from one individual showed a mutation in KRAS and one
individual showed mutations in both. Mutation spectrum analyses again showed that
GCTA transversions (71%) were the predominant type of mutation in the epithelial
cells collected. The high frequency of P53 mutations and, in particular, the high
proportion GCTA transversions in cells from sputum are consistent with exposure to
PAH-rich emissions from smoky coal. Moreover, the authors suggested that the
prevalence of P53 mutations in sputum cells might be a useful biomarker of risk for lung
cancer.
265
P53 protein accumulation

Coal and wood combustion
Using an immunofluorescent assay, accumulation of P53 protein was observed in
nine of 16 tumour cell samples obtained from the sputum of Xuan Wei lung cancer
patients (nine smoking men and seven nonsmoking women) who had a history of
exposure to emissions from smoky coal combustion. In contrast, none of the sputum
samples from 17 healthy Xuan Wei residents also exposed to smoky coal emissions
showed P53 accumulation (Feng et al., 1999). A population-based casecontrol study in
Xuan Wei County confirmed that more frequent use of smoky coal is associated with a
higher incidence of lung cancer. Moreover, the associations were stronger when the
analyses were restricted to female Xuan Wei residents (almost all of whom were
nonsmokers) who were exposed to high levels of smoky coal emissions and who showed
overexpression and accumulation of P53 protein in exfoliated tumour cells isolated from
sputum samples (Lan et al., 2001).
Other epidemiological studies showed elevated levels of several proteins, including
P53, RAS, NEU [HER2] and murine double minute 2 (MDM2), in cancer patients
exposed to emissions from wood or coal combustion. For example, Li et al. (1997) found
significantly higher serum concentrations of RAS, P53 and NEU proteins in 19 lung
cancer patients who were exposed to emissions from coal burning, relative to
19 unexposed cases without lung cancer. Delgado et al. (2005) studied lung cancer
associated with exposure to wood smoke and used western blot analyses to demonstrate a
significant increase in P53, phosphorylated-P53 and MDM2 proteins in plasma samples
from 24 lung cancer patients with a history of exposure to domestic wood smoke in
comparison with nine smokers who had chronic obstructive pulmonary disorder and nine
healthy control volunteers with no exposure to wood smoke. Hu et al. (2001) used
immunohistochemical techniques to show significantly elevated (p<0.01) levels of
mutated P53 protein in 18 skin carcinoma patients with arseniasis caused by coal burning
in comparison with 11 patients who presented precancerous lesions or 39 controls.
(b)
Experimental systems
(i)
In-vivo systems
Coal combustion
An inhalation study in Kunming mice (Lin et al., 1995) showed that all 13 lung
tumours induced by samples of coal smoke showed overexpression of p53, and nine of
the 13 tumours showed c-myc over-expression whereas no p53 or c-myc expression was
detected in control animals.
266
(ii)
In-vitro systems
Coal combustion
Several types of mammalian cell have been employed to assess the genotoxicity of
combustion emissions in the indoor environment. Qin et al. (1985) reported a
concentration-dependent increase in sister chromatid exchange frequency in Chinese
hamster ovary (CHO) cells exposed, in both the presence and absence of metabolic
activation, to organic extracts of respirable indoor particulates (<10 m) from homes
where coal or wood were burned. The results showed significant induction of sister
chromatid exchange but no significant difference in genotoxic potency between particles
from homes where coal or wood were burned (Qin et al., 1985). Significant
morphological transformation, including random or criss-cross orientations and dense
piling of cells, have been observed in diploid Syrian hamster embryo cells exposed to
extracts of coal smoke (Zhang et al., 1989). Yu et al. (1993) studied the indoor air particle
size distribution and size-associated mutagenic and carcinogenic activity of samples
collected in Xuan Wei homes that used smoky coal. Particles were divided into five
fractions (>7.0 m, 3.37.0 m, 2.0<3.3 m, 1.1<2 m and <1.1 m), and the finest
fraction accounted for 61% of the total mass and 73% of the total extractable organic
compounds. The finest particles (<1.1 m) had the greatest mutagenic potency in
Salmonella (3248 revertants/m3 with and 1085 revertants/m3 without metabolic activation,
which accounted for 62 and 77%, respectively, of the total mutagenic activity). Analyses
of CHO cells showed a dose-related increase in sister chromatid exchange frequency,
with similar responses observed for all size fractions. Nevertheless, the finest particles
yielded the highest frequency of sister chromatid exchange when expressed per cubic
metre of sampled air. The authors suggested that the mutagenic potency of particles in
coal smoke are inversely related to particle size.
Biomass combustion (including wood)
Hytnen et al. (1983) reported that the emissions from an airtight residential wood
stove induced a dose-related increase in sister chromatid exchange frequency in CHO
cells exposed both in the presence and absence of exogenous metabolic activation. The
response was highest without metabolic activation. Wood smoke samples generated under
air-starved conditions were an order of magnitude more potent than those generated under
standard conditions. Salomaa et al. (1985) investigated the genotoxicity of smoke
emissions collected from a residential wood stove and showed that organic extracts of
both the particle (i.e. collected on a filter) and vapour phases (i.e. adsorbed on to XAD-2
resin) significantly increased sister chromatid exchange frequency in CHO cells in a
concentration-related manner. A significant positive response was obtained in the absence
of exogenous metabolic activation, and the response increased in the presence of
exogenous metabolic activation. Chemical fractionation of the organic extracts
demonstrated that the most potent genotoxic activity was present in the non-polar, PAHcontaining fraction. Moreover, the authors noted that the potency of the extracts of wood
267
combustion emissions, in terms of their ability to induce sister chromatid exchange in

CHO cells, was comparable with that of cigarette-smoke condensate. A similar study by
Alfheim et al. (1984a) noted that organic extracts of both the particle and vapour phases
significantly increased the frequency of sister chromatid exchange in CHO cells. The
polar fraction, which would be expected to contain compounds such as aza-arenes and
aromatic ketones, and the non-polar fraction were the most active. The authors also noted
the same pattern of activity in the Syrian hamster embryo cell transformation assay.
Leonard et al. (2000) have shown that wood smoke is able to generate stable carboncentred radicals as well as reactive hydroxyl radicals in the presence of hydrogen
peroxide. These reactive species are known to induce cellular toxicity via lipid
peroxidation and DNA damage, and the authors also showed that these wood smoke
emissions induced DNA damage (as measured by the comet assay) and lipid peroxidation
in RAW 264.7 mouse macrophage cells.
Karlsson et al. (2006) showed induction of DNA damage (comet assay) in cultured
human lung carcinoma AS49 cells after exposure to wood combustion particles.
(iii) Salmonella reverse-mutation assay
Numerous studies have used the Salmonella reverse mutation assay to assess the
mutagenic activity of indoor air samples and/or source-specific samples of emissions
from the combustion of coal or biomass-derived fuels. Moreover, enhanced levels of
indoor air mutagenicity have been associated with an enhanced risk for lung cancer,
particularly in indoor environments contaminated by unvented coal combustion
emissions, such as in Xuan Wei County (Mumford et al., 1987a,b). Early studies, such as
that by Lioy et al. (1985), showed that, although the organic extracts of indoor air
particulates elicit a significant positive response in the Salmonella mutagenicity assay, the
exact source(s) of the mutagenic activity could not be identified. Subsequently, a wide
range of source-specific studies has confirmed the Salmonella mutagenic activity of
emissions from smoky coal combustion (e.g. Mumford et al., 1987a,b) and wood/biomass
combustion (e.g. Alfheim et al., 1984a; van Houdt et al., 1986, 1989; Bell et al., 1990;
Asita et al., 1991; Heussen et al., 1994), and highlighted that these sources are significant
contributors to the mutagenic activity of indoor air. Moreover, several studies have noted
a positive empirical relationship between the Salmonella mutagenic activity of indoor air
(in revertants/m3) and the concentration of airborne PM (Mumford et al., 1987b). This
relationship is logical because combustion emissions are composed of PM, and several
researchers (e.g. Maertens et al., 2004, 2008) have commented on the tendency for
mutagens in combustion emissions, such as PAHs, to adsorb onto particulate material and
solid surfaces (e.g. upholstery, carpets). Analyses of indoor areas contaminated with coal
combustion emissions have noted PM concentrations as high as 39 mg/m3 (Mumford et
al., 1987b). Much lower particle concentrations have been recorded in indoor
environments contaminated with emissions from wood combustion (Sexton et al., 1984).
Table 4.1 provides a summary of some studies that have used the Salmonella
mutagenicity assay to investigate the mutagenic activity of indoor air particulates from
268
biomass, coal and wood combustion. The data indicate that organic extracts of indoor air
particulate material collected from areas with no obvious source of combustion have
Salmonella mutagenic potency values in the range of 110 TA98 revertants/m3 (e.g.
Heussen et al., 1994; Nardini et al., 1994). Table 4.2 provides a summary of some studies
that investigated the mutagenic potency of organic extracts of source-specific particulate
emissions from wood/biomass and coal combustion.
The highest reported mutagenic potency values (5.9104 TA98 revertants/m3 and
3120 TA98 revertants/mg of particle with metabolic activation) correspond to indoor
environments contaminated with emissions from unvented smoky coal combustion
(Mumford et al., 1987a; Nakanishi et al., 1997). The enhanced mutagenic activity in the
presence of exogenous metabolic activation is consistent with the supposition that PAHs
from unvented smoky coal combustion are responsible for much of the mutagenic
activity. The most mutagenic sources, in terms of TA98 potency with metabolic
activation, also included emissions from wood combustion. The highest reported
mutagenic potency in the presence of exogenous metabolic activation was 1.1104 TA98
revertants/m3 and 4700 revertants/mg of particle (Mumford et al., 1987a; Ramdahl et al.,
1982).
[On average, smoky coal emissions are five times or 10 times more mutagenic than
those from wood in terms of activity per miligram of particle or activity per cubic metre
of air, respectively.]
Bioassay-directed fractionation studies have frequently been employed to determine
the identity and/or physicochemical properties of the putative mutagens in complex
extracts of indoor air PM and emissions from the combustion of selected solid fuels.
Numerous studies in the Xuan Wei region of China have revealed that PAHs and
alkylated PAHs are the major Salmonella mutagens in smoky coal emissions and smoky
coal-contaminated indoor air, which again suggests that these compounds probably play a
critical role in the enhanced frequency of lung cancer observed in Xuan Wei women
(Chuang et al., 1992a,b). However, substantial levels of direct-acting mutagenic activity
support the hypothesis that the mutagenic activity of smoky coal emissions cannot be
accounted for by PAHs alone. Bioassay-directed fractionation analyses of emissions from
wood combustion indicate that there are several sources of mutagenic activity. Several
studies have noted that a substantial, albeit variable, portion of the metabolically activated
mutagenic activity (approximately 1050%) can be attributed to PAHs, or PAHcontaining non-polar neutral fractions (Alfheim et al., 1984a,b; Kamens et al., 1985; Bell
et al., 1990). Variability in the fraction of metabolically activated mutagenic activity that
can be attributed to PAHs and PAH derivatives is consistent with studies that have noted
a relationship between wood types or burning conditions and the emission rate of
genotoxic PAHs (Zou et al., 2003). In addition, several studies have highlighted the
involvement of polar compounds in the determination of the level of direct-acting
mutagenic activity of extracts of wood combustion particulates. Kamens et al. (1985)
noted that chemical fractions containing compounds with the polarity of aromatic ketones
could explain 4% of the total direct-acting mutagenic activity of wood smoke emission
Table 4.1. Salmonella mutagenicity of organic extracts of indoor air particulate matter from biomass, coal and
wood combustion
Indoor activity
Source
Country
Particle
concentration
(g/m3)
Mutagenic potency
(revertants/m3)
Without
metabolic
activation
With
metabolic
activation
1601
ND
ND
ND
736
53
48
4
5
6
7
13
6
7
71
ND
1155
58 900
17 000
1300
667
100
150
16
12
13
12
21
14
23
96
11 000
Nardini et al. (1994)

Mumford et al. (1987a)
Alfheim & Ramdahl (1984)
Heussen et al. (1994)
van Houdt et al. (1986)
200
200
50
60

Charcoal
Smoky coal
Smoky coal
Smokeless coal
Wood
Wood
Wood
Wood
Wood
Wood
Wood
Wood
Wood
Wood
Wood
Wood
Italy
China
China
China
Italy
Norway
Norway
Netherlands
Netherlands
Netherlands
Netherlands
Netherlands
Netherlands
Netherlands
Netherlands
China
1300
24 400
9500
1100
2800
US
US
39.3
38.8
47.6
38.9
US
US
US
US
22 300
TA100
Open fireplace
Open fireplace
Wood
Wood
Norway
Norway
US
US
TA98
Coal combustion
Coal combustion
Coal combustion
Coal combustion
Wood combustion
Open fireplace
Open fireplace
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Reference
ND, no data; US, unspecified
269
Indoor activity
Dried cow dung

Coconut shell
Dried cow dung
Crop residue
Peat
Pine
Red oak
Wood
White mangrove
Red mangrove
Mahogany
Abura
Alstonia
Black afara
Ponderosa Pine
Willow
Hickory
Hickory (impinger)
Synthetic log
Pine
Oak
Birch
Spruce
Charcoal
Charcoal
Coke
Coal
Smoky coal
Country
USA, Hawaii
USA, Hawaii
India
India
US
US
US
Italy
Japan
Japan
Japan
Japan
Japan
Japan
USA
USA
USA
USA
USA
USA
USA
Norway
Norway
Norway
Italy
USA
China
China
Particle
concentration
(g/m3)
Mutagenic potency (revertants/mg)

Without
metabolic
activation
With metabolic
activation
~30
~30
~30
~30
~30
~30
~30
2800
US
US
US
US
US
US
US
US
US
US
US
US
US
US
US
US
1300
US
US
US
40
1560
280
40
250
480
90
254
ND
ND
ND
ND
ND
ND
140
67
100
160
670
290
150
4700
900
14
982
ND
635
1280
630
1580
1000
280
380
1200
810
215
150
300
100
140
250
140
380
1500
1100
56
240
1300
900
4700
1800
6
795
1200
1810
3120
Reference
Bell & Kamens (1990)

Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
Dasch (1982)
Dasch (1982)
Dasch (1982)
Dasch (1982)
Dasch (1982)
Lewtas (1982)
Lewtas (1982)
Ramdahl et al. (1982)
Lewtas (1982)
Yu et al. (1993)
Nakanishi et al. (1997)
TA98
Biomass combustion
Biomass combustion
Biomass combustion
Biomass combustion
Biomass combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Coal combustion
Coal combustion
Coal combustion
Coal combustion
Coal combustion
Source
270
Table 4.2. Salmonella mutagenicity of organic extracts of particulate emissions from biomass, coal and wood combustion
Table 4.2 (Contd)

Indoor activity
Source
Country
Particle
concentration
(g/m3)

Without
metabolic
activation
Reference
With metabolic
activation
Smoky coal
Smoky coal
Coalite
Smokeless coal
China
China
China
China
US
US
US
US
TA98NR
Wood combustion
Coal combustion
Wood
Charcoal
Italy
Italy
2800
1300
227
1024
ND
ND

YG1024
Coal combustion
Coal
China
US
6200
ND
Taga et al. (2005)
TA100
Biomass combustion
Biomass combustion
Biomass combustion
Biomass combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Wood combustion
Dried cow dung

Coconut shell
Dried cow dung
Crop residue
White mangrove
Red mangrove
Abura
Alstonia
Black Afara
Red oak
USA
USA
India
India
Japan
Japan
Japan
Japan
Japan
USA
~30
~30
~30
~30
US
US
US
US
US
~30
20
2610
630
120
ND
ND
240
ND
ND
210
240
240
120
150
390
410
210
270
150
830
910
420
300
560
250
900
310
310


Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
Asita et al. (1991)
TA98 (contd)
Coal combustion
Coal combustion
Coal combustion
Coal combustion
271
272
extracts. Bell et al. (1990) noted that the polar acidic fractions of organic wood-smoke
extracts (phenolic compounds) could account for 28% of the direct-acting mutagenic
activity. Alfheim et al. (1984a,b) noted that the direct-acting mutagenic activity of an
organic extract of particulate material collected from the combustion of a spruce/birch
mixture was predominantly contained in the most polar chemical fractions. The authors
suggested that the putative mutagens include aza-arenes (aromatic amines) and/or
nitroarenes, and the involvement of nitroarenes was confirmed by assays performed with
the nitroreductase-deficient strains of Salmonella which showed a clear mutagenicity
reduction.
4.3
Genetic susceptibility
4.3.1
Polymorphisms in carcinogen-metabolizing genes
Carcinogenic PAHs are formed during incomplete combustion of carbon-based fuels

such as coal, wood and biomass. Numerous phase I and phase II enzymes are involved in
the metabolic activation and detoxification of PAHs. Genetic variation in the enzymes
responsible for activating and detoxifying PAHs or other carcinogens present in these
environments may confer susceptibility to individuals exposed to coal, wood and biomass
smoke, as well as to cooking oil fumes, and could result in significant interindividual
differences in risk at the same level of exposure (Table 4.3).
Most studies of cancer and the above-mentioned exposures have focused on lung
cancer, whereas a few have studied cervical and oesophageal cancer. Of these, only a few
have evaluated genetic variants and performed a quantitative or semi-quantitative
exposure assessment. The main focus of genetic studies has been on analysis of variants
in phase I and phase II genes that play a key role in metabolizing PAHs, although other
chemicals can serve as substrates for these enzymes. Studies are included in this review if
indoor air pollution was shown previously to play an important role in the etiology of
cancer in the study population, if subgroups of the population were identified who were
exposed to indoor air pollution or if genetic risk factors were studied among nonsmokers
in a population thought to have potential exposure to indoor air pollution, even if
exposure assessment was not carried out in the reported study. Studies in which tobacco
smoke was thought to be the primary cause of lung cancer in the study population were
excluded if no analyses were presented among subgroups exposed to some measure of
indoor air pollution, or if no analyses were presented among nonsmokers with some
potential for exposure to indoor air pollution.
The association between CYP1A1 and GSTM1 polymorphisms and lung cancer was
evaluated in urban Shenyang, China, in a population-based casecontrol study of 200
female cases and 144 female age-matched controls (Yang et al., 2004). An excess
incidence of lung cancer had been found in this region previously and was linked to indoor
Table 4.3. Polymorphisms of genes involved in metabolism and exposure to indoor cooking and heating with
coal, wood and biomass in relation to risk for lung cancer
Gene
Mutation/allele
Country
No. of
cases/
controls
Odds ratio (95% CI)
Comments
Yang et al.
(2004)
CYP1A1
Exon 7
Ile462Val
China
200/144
S: Ile/Val vs Ile/Ile, 2.7 (1.74.3)

NS: Val/Val vs Ile/Ile, 1.7 (0.64.6)
GSTM1
Gene deletion
All cases and controls were

women, 55% of cases and
37% of controls were ever
smokers
S: Combination of
CYP1A1 variant
heterozygous or
homozygous carrier (Val)
and GSTM1 null
GSTM1
Gene deletion
GSTT1
Gene deletion
GSTM1
Gene deletion
GSTT1
Gene deletion
Lan et al.
(2000)
Malats et
al. (2000)
NS: GSTM1 null
Xuan Wei
County,
China
122/122
S: GSTM1 null, 2.3 (1.34.2)
S: Interaction between
smoky coal use and
GSTM1 null genotype
(p=0.05), study subjects
were farmers
Reference
NS: GSTT1 null

Brazil,
France,
Germany,
Italy, Poland,
Romania,
Russia and
Sweden
122/121
NS: GSTM1 null, 1.5 (0.92.7)
273
NS: GSTT1 null
All study subjects were

nonsmokers; 86% of cases
and 72% of controls were
women
274
Table 4.3 (contd)

Gene
Mutation/allele
Country
ChanYeung et
al. (2004)
GSTM1
Gene deletion
China, Hong
Kong SAR
GSTT1
Gene deletion
GSTM1
Gene deletion
GSTT1
GSTP1
Gene deletion
Wild-type Ile
NAT2
Rapid acetylator
Chen et al.
(2006)
No. of
cases/
controls
Odds ratio (95% CI)
Comments
NS: GSTM1 null
Study subjects were

potentially exposed to
indoor pollution due to
cooking and heating; 57%
of cases and 40% of
controls were smokers
S: GSTT1 null, 1.7 (1.12.6)

Hunan
Province,
China
97/197
S: GSTT1 null, 2.0 (1.23.2)
S: GSTT1 null, 2.1 (1.33.4)

NS: Variant GSTP1 Val vs wild-type
Ile
NS: rapid vs slow acetylators
All study subjects were

nonsmokers, with potential
indoor air pollution
exposure; no exposure
assessment performed
S: Any two or three at

risk genotype combination
of GSTM1 null, GSTT1
null, GSTP1 (Val); all four
at risk genotypes
combined (all three GSTs,
NAT2 rapid acetylator)
Reference
Table 4.3 (contd)

Gene
Mutation/allele
Country
No. of
cases/
controls
Odds ratio (95% CI)
Comments
Lan et al.
(2004)
AKR1C3
Gln5Gln
Xuan Wei
County,
China
119/113
NS: Gln5Gln vs His/His+His/Gln,

1.8 (1.03.5); S: female HSCU,
13.0 (2.2107.8); NS: male HSCU
Only 4 or 5 subjects in
some of the cells in
stratified analysis; test for
interaction with smoky
coal use was not
significant
MnSOD
Val/Ala or
Ala/Ala
NS: Val/Ala or Ala/Ala vs Val/Val
NQO1
Pro/Ser or
Ser/Ser
NS: Pro/Ser or Ser/Ser vs Pro/Pro
CYP1A1
Exon 7
Ile462Val or
*2C; MspI RFLP
or *2A
GSTM1
Gene deletion
Pisani et
al. (2006)
Thailand
211/211
NS: CYP1A1*2A and *2C
NS: GSTM1 null
93% cases and

81% controls were
smokers; no indoor air
pollution exposure
assessment
Reference
275
276
Table 4.3 (contd)

Gene
Mutation/allele
Country
No. of
cases/
controls
Odds ratio (95% CI)
Comments
Shen et al.
(2005a)
CBS
Ex12+41 CC,
IVS3-1489AA,
Ex8+33CT
Xuan Wei
County,
China
119/113
S: Ex12+41, TC vs TT, 4.3 (1.710.9),

CC vs TT, 2.0 (1.13.6);
NS: IVS3-1489AA or Ex8+33CT
S: Smoky coal use <130

tons, CC vs TT, 7.9 (2.1
29.2); only 5 controls
carried CC genotype for
subjects that used < 130
tonnes of smoky coal, test
for interaction was not
significant
MTHFR
Ala222Val,
Ala429Glu
SLC19A1
Ex4-254CC,
Ex7-233TT
S: Ala/Val vs Ala/Ala, 2.6 (1.44.8),

Ala/Val+Val/Val, 2.5 (1.44.4);
NS: Ala429Glu
S: Ex4-254, CC vs TT, 2.1 (1.04.5);
NS: Ex7-233TT
CI, confidence interval; HSCU, heavy smoky coal user; NS, not significant; S, significant
S: Coal use <130 tonnes,

TC vs TT, 4.6 (1.712.6),
CC vs TT, 3.3 (1.19.8);
test for interaction with
smoky coal use, p=0.03
Reference
277
coal use (Xu et al., 1991). Genotyping was performed via the Taqman assay, and the
CYP1A1 genotype was in Hardy-Weinberg equilibrium for controls. The frequencies of
CYP1A1 Val 462Val were 5.6% and 4.8% for cases and controls, respectively. There was
a significant increased risk for lung cancer for the variant CYP1A1 462Val genotypes
(odds ratio, 2.5; 95% CI, 1.64.0) compared with CYP1A1 Ile462Ile, when adjusted for
age, ever-smoking status, family history of cancer and eye irritation when cooking (an
indication of indoor air pollution). Stratification by smoking status yielded significant
results only among the nonsmokers (odds ratio, 3.7; 95% CI, 1.97.3), although a test of
multiplicative interaction was not significant (p=0.13). This study did not find any
association with the GSTM1 null genotype (58% in cases and 54% in controls) (odds
ratio, 1.2; 95% CI, 0.81.8) and risk for lung cancer or a significant interaction between
CYP1A1 Ile462Val and GSTM1 null genotypes. No interaction was demonstrated
between the indoor air pollution index and genotype.
The CYP1A1 and GSTM1 genotypes were also studied in a casecontrol study of
211 lung cancer cases and two sets of controls, one that was recruited from the resident
population (n=197) and a second group of patients who were admitted to the hospital for
diseases predominantly unrelated to tobacco smoking (n=211) in Lampang, Thailand
(Pisani et al., 2006). Controls were frequency-matched to cases by gender and age.
Genotyping was performed by polymerase chain reaction (PCR) methodology. The two
CYP1A1 single nucleotide polymorphisms rs1048943 (also called CYP1A1*2C or
CYP1A1-Ile462Val) and rs4646903 (also called CYP1A1*2A or CYP1A1 MspI) studied
were in Hardy-Weinberg equilibrium for controls. An index of exposure to domestic
fumes (total years spent using coal or wood) was derived from the type of fuel used (coal
or wood versus none, gas or electricity), indoor or outdoor cooking and the number of
years lived in the particular exposure environments. Exposure to domestic fumes was not
associated with an increased risk for lung cancer. This study found no association
between lung cancer and the CYP1A1*2C (odds ratio for variant homozygous, 0.8; 95%
CI, 0.31.7) or CYP1A1*2A (odds ratio for variant homozygous, 1.5; 95% CI, 0.82.7),
or the GSTM1 null (odds ratio, 0.8; 95% CI, 0.51.2) genotypes when adjusting for
gender, age and lifetime total tobacco smoke. No interaction was tested between exposure
to domestic fumes and genotypes.
A population-based casecontrol study in Xuan Wei, China, assessed the risk for lung
cancer caused by indoor coal combustion in relation to GSTM1 and GSTT1 genotypes
(Lan et al., 2000). Previous studies have shown an etiological link between lung cancer
mortality and domestic smoky coal use (Mumford et al., 1987a). Using a PCR-based
method, 122 cases and 122 controls, matched on age (2 years), gender, village and type
of fuel currently used for cooking and heating at home were genotyped. Genotyping
results were adjusted for total smoky coal use without ventilation, packyears of smoking,
chronic obstructive pulmonary disease and family history of lung cancer. The frequency
of the GSTM1 null genotype was 67% among cases and 51% among controls. Subjects
with the GSTM1 null genotype were 2.3 times more likely to have lung cancer than
subjects with a positive GSTM1 genotype (odds ratio, 2.3; 95% CI, 1.34.2). A potential
278
geneenvironment interaction between the GSTM1 null genotype and smoky coal was
evaluated. For all subjects, the risk for lung cancer increased 1.7 fold per 100 tonnes of
lifetime coal use (95% CI, 1.32.4). When stratified by GSTM1 genotype, risk was nonsignificantly increased by 1.2-fold per 100 tonnes (95% CI, 0.81.9) for GSTM1-positive
subjects and increased by 2.4-fold per 100 tonnes for those with the GSTM1 null genotype
(95% CI, 1.63.9) (test for multiplicative interaction, p=0.05). The GSTT1 null genotype
yielded non-significant results (odds ratio, 1.3; 95% CI, 0.72.3).
A casecontrol study of nonsmokers in eight countries (Brazil, France, Germany,
Italy, Poland, Romania, Russia and Sweden) evaluated the association between GSTM1
and GSTT1 and risk for lung cancer (Malats et al., 2000). Cases were histologically or
cytologically confirmed in the same hospitals where the majority of controls were
recruited among patients with non-tobacco-related diseases. The remaining controls were
from population registries from two countries (Germany and Sweden). Using a multiplex
PCR, genotypes for the 122 nonsmoking lung cancer cases and 121 nonsmoking controls
were determined. Among them, 86% of cases and 72% of controls were women.
Although subjects in this study population were suspected to have relatively low levels of
environmental exposures to indoor fuel combustion and cooking oil fumes, data were
analysed regarding exposure to indoor wood combustion. In general, more cases resided
in rural than in urban settings (p=0.004), were exposed to more indoor air pollution from
wood combustion (p=0.001), were exposed to more environmental tobacco smoke
(p=0.04) and were more likely to be occasional smokers [p=0.01] than the controls. The
frequency of the GSTM1 null genotype was 54% among cases and 44% among controls.
Subjects with the GSTM1 null genotype had a non-significant increased risk for lung
cancer (odds ratio, 1.5; 95% CI, 0.92.7) compared with GSTM1-positive subjects when
adjusted for gender, age and centre. The GSTT1 null genotype was not associated with
lung cancer (odds ratio, 0.6; 95% CI, 0.31.2). The effect of exposure to emissions from
wood combustion was also evaluated after stratification by GSTM1 and GSTT1
genotypes. Compared with subjects with less than 20 years of wood-smoke exposure,
subjects with more than 20 years of exposure had a higher risk for lung cancer among
those with the GSTM1 null genotype (odds ratio, 6.2; 95% CI, 1.525). In contrast, longterm exposure to emissions from wood combustion was associated with a lower risk
(odds ratio, 1.8; 95% CI, 0.57.1) among those with the GSTM1-positive genotype,
although the test for interaction was not significant. No geneenvironment interactions
were observed for the GSTT1 null genotype.
The effect of genetic variants of the GSTM1 and GSTT1 genotypes on modifying the
risk for lung cancer was also evaluated in a population-based casecontrol study in Hong
Kong of 229 consecutive incident cases and 197 healthy controls (Chan-Yeung et al.,
2004). Based on a previous study that evaluated the risk for lung cancer in Hong Kong,
the study subjects were suspected of having been exposed to cooking oil fumes without
an exposure assessment (Chan-Yeung et al., 2003). Genotyping was carried out using a
multiplex PCR methodology. Only the GSTT1 null genotype was associated with lung
cancer when adjusting for age, gender, education and tobacco smoking (odds ratio,
279
1.7; 95% CI, 1.12.6). The frequency of the GSTT1 null genotype was 62% among cases
and 52% among controls. Repeated analysis stratified by smoking status yielded only
significant results for nonsmokers (odds ratio, 2.2; 95% CI, 1.23.9). No associations
were found with the GSTM1 null genotype (odds ratio, 0.8; 95% CI, 0.61.3).
Another casecontrol study consisting of 97 nonsmoking lung cancer patients
(55 women and 42 men) and 197 healthy nonsmoking controls (101 women and 96 men)
from a screening survey in Hunan Province, China, evaluated the phase II metabolic
genotypes, GSTM1, GSTT1, GSTP1 and NAT2 (Chen et al., 2006). The study population
was believed to have indoor air exposure to cooking and heating fuels, as well as cooking
oil fumes; however, no exposure assessment was performed. Genotyping was carried out
by PCR, Hardy-Weinberg equilibrium results were not presented and only crude odds
ratios were provided. Both the GSTM1 null (odds ratio, 2.0; 95% CI, 1.23.2) and GSTT1
null (odds ratio, 2.1; 95% CI, 1.33.4) genotypes were associated with an increased risk
for lung cancer, whereas the GSTP1 Ile/Val genotype was not (odds ratio, 1.2; 95% CI,
0.72.1). The GSTM1 null genotype was found in 62% of cases and 45% of controls; the
GSTT1 null genotype was found in 61% of cases and 43% of controls. Combined effects
of the various genotypes were evaluated. Subjects who had any two of these three GST at
risk genotypes (odds ratio, 2.3; 95% CI, 1.14.9) or who had all three genotypes (odds
ratio, 4.7; 95% CI, 1.713.2) had an increased risk for lung cancer compared with
subjects who were positive for the GSTM1, GSTT1 and GSTP1 Ile/Ile genotypes. Only 14
cases and 10 controls possessed all three GST at risk genotypes. NAT2 genotypes were
not associated with risk for lung cancer. However, an increased risk for lung cancer was
seen in subjects who had the NAT2 rapid-acetylating genotype, were null for GSTM1 and
GSTT1 and were wild-type for GSTP1 (odds ratio, 5.5; 95% CI, 1.224.8) compared with
subjects who were positive for GSTM1 and GSTT1 and had GSTP Ile/Ile and NAT2 slowacetylating genotypes; however, these results are based on only 12 cases and six controls.
Polymorphisms in other genes, such as oxidative stress-related genes (AKR1C3,
NQO1 and MnSOD; Lan et al., 2004), one-carbon metabolism-related genes (BHMT,
CBS, FPGS, FTHFD, GGH, MTHFD2, MTHFR, MTHFS, MTRR, SHMT1, SLC19A and
TYMS; Shen et al., 2005a) and DNA repair-related genes (ERCC1, ERCC2/XPD,
ERCC4/XPF, ERCC5/XPG, RAD32B, XPC, OGG1, APEX1, LIG3, XRCC1, ADPRT and
NBS1; Shen et al., 2005b,c; Lan et al., 2004, 2005), have been studied for their
association with lung cancer. No firm conclusion can be drawn from these analyses due to
small sample sizes (Tables 4.3 and 4.4).
A limited number of studies have evaluated populations exposed to indoor air
pollution from the combustion of coal, wood, biomass or cooking oil fumes for
associations between polymorphisms in genes that are involved in xenobiotic metabolism
and risk for lung cancer. However, sample sizes were small for almost all studies, which
can result in both false-negative and false-positive findings. There is some evidence that
the GSTM1 null genotype was associated with increased risk for lung cancer in some
studies in which at least part of the study population was definitely or probably exposed to
280
Table 4.4. Polymorphisms of DNA repair genes and associations with exposure to indoor cooking and heating with
coal, wood and biomass in relation to risk for lung cancer
Gene
Mutation/allele
Country/
ethnicity
No. of cases/
controls
Odds ratio (95% CI)
Comments
Shen et al.
(2005b)
ERCC2
Ex23+61A>C
(Lys751Gln),
IVS19-70 C>T,
Ex6-10A>C
(Arg156Arg)
Ala249Val
Xuan Wei
County,
China
119/113
S: Ex23+61A>C, CC+AC vs AA, 0.4

(0.20.9), IVS19-70 C>T, CT+TT vs CC
0.4 (0.20.9); BS: Ex6-10A>C, CC vs
AA, 0.5 (0.21.0)
Haplotype analysis of ERCC2

genes yield similar results to
the single SNP analysis; no
gene-environment interaction
was found
RAD23B and XPC work
collectively to recognize DNA
damage. Subjects with both the
XPC 939Gln/Gln genotype and
either the RAD23B 249Ala/Val
or 249Val/Val genotype had a
6-fold increased risk for lung
cancer
RAD23B
Lan et al.
(2004)
XPC
Lys939Gln,
Ala499Val,
Ex16+315C>G
OGG1
Ser326Cys
S: Ala/Val+Val/Val vs Ala/Ala, 1.8

(1.03.1)
NS: all variant genotypes
Xuan Wei
County,
China
119/113
S: Ser/Cys vs Ser/Ser, 2.0 (1.13.6);

NS: Cys/Cys vs Ser/Ser, 1.9 (0.84.1)
S: Increased risk for lung

cancer for Ser/Cys women
who used more than 130
tonnes of smoky coal
compared with Cys/Cys
women who used less than 130
tonnes
Reference
Table 4.4 (contd)

Gene
Mutation/allele
Country/
ethnicity
No. of cases/
controls
Odds ratio (95% CI)
Comments
Shen et al.
(2005c)
XRCC1
Arg399Gln,
Arg280His,
Arg194Trp
Xuan Wei
County,
China
119/113
S: Arg/Gln vs Arg/Arg, 0.6 (0.31.0);

NS: Gln/Gln vs Arg/Arg
Effect of XRCC1 on lung

cancer was not modified by
age, gender or lifetime smoky
coal use.
Lan et al.
(2005)
NSB1
Exon 2
Leu34Leu
Xuan Wei
County,
China
119/113
S: AA vs. GG, 2.15 (0.95.1);

NS: GA vs GG, 1.4 (0.82.4)
No significant interaction
between smoky coal use and
genotypes. All women were
nonsmokers. Two SNPs highly
correlated
Exon 5
Gln185Glu
BS: Glu/Glu vs Gln/Gln, 2.5 (1.16.1);

NS: Gln/Glu vs Gln/Gln, 1.4 (0.82.5)
BS, borderline significant; CI, confidence interval; NS, not significant; S, significant; SNP, single nucleotide polymorphisms
Reference
281
282
indoor air pollution, particularly when exposure to PAHs was suspected to be a

contributing agent. However, results for polymorphisms in other genes are inconsistent or
have been analysed in only one study. Therefore, no firm conclusion can be made
regarding the effect of polymorphisms of genes other than GSTM1 on the risk for lung
cancer in these populations.
4.4
Mechanistic considerations
The most extensive exposure, animal and other experimental data for the combustion
emissions considered in this monograph have been generated for coal compared with
wood and other biomass fuel. Human, animal and other experimental data from coal
combustion emissions, and especially those from poorly ventilated homes using smoky
coal in Xuan Wei County, Yunnan Province, China, are consistent with the following
carcinogenic mechanism.
At least six major pathways must be disrupted by a mixture of genetic and epigenetic
changes for a normal cell to be transformed to a tumour cell (Hanahan & Weinberg,
2000). Molecular analyses show that exposure to smoky coal emissions disrupts many of
these pathways. For example, lung tumours from nonsmokers who had been exposed to
smoky coal emissions in poorly vented homes and whose lung tumours were linked
epidemiologically to such exposures had mutations in the KRAS gene, which affects cell
growth and signalling, and in the P53 gene, which effects cell growth and replication,
among other pathways.
Chemical analyses and bioassay-directed fractionation of smoky coal emissions have
identified PAHs as an important chemical class that accounts for much of the
mutagenicity and carcinogenicity of such emissions. The epidemiological link between
exposure to smoky coal emissions and an increased risk for lung cancer is strengthened
mechanistically by the fact that the mutation spectra of the P53 tumour-suppressor gene
and the KRAS oncogene in lung tumours from nonsmokers exposed to the emissions from
smoky coal reflect an exposure to PAHs and is distinct from the mutation spectra found in
these genes in lung tumours from cigarette smokers. Thus, the mutation spectra in lung
tumours from nonsmokers whose cancers are linked epidemiologically to exposure to
emissions from smoky coal reflect the primary DNA damage induced by the most
prominent class of mutagens/carcinogens in these emissions.
The available data support a multistep model of carcinogenesis in which components
of the emissions from smoky coal are the direct cause of the cellular changes that
accumulate to initiate the carcinogenic process. There are many varieties of coal, and
these may produce emissions with a range of carcinogenic potencies and chemical
compositions. Nevertheless, the carcinogenesis model described here may be generally
applicable to the risk for lung cancer associated with exposure to combustion emissions
from coal other than smoky coal.
Compared with smoky coal, less extensive molecular epidemiological evidence exists
for lung cancer risk and exposure to emissions from wood and other biomass fuel.
283
However, the available data suggest that the mechanism described above for emissions
from smoky coal may be plausible for the lung cancer risk associated with these other
emissions. In contrast to smoky coal, the indoor emissions from wood combustion
comprise relatively low levels of PAHs, and the mutagenicity of these emissions are due
to a combination of chemical classes, including PAHs and acidic/polar compounds such
as aza-arenes, aromatic ketones, nitroarenes and phenolic compounds. Molecular
evidence, including changes in P53 protein phosphorylation in lung cancer patients whose
cancers are associated with exposure to combustion emissions from wood, as well as
systemic genotoxicity among charcoal workers, is consistent with the mechanism
described above.
The relevance of mechanisms for particle-induced lung cancer to particles generated
from combustion of the agents evaluated in this monograph has not been thoroughly
investigated. For particle-induced lung cancer, the cascade of events that starts with
particle deposition at critical target cells and results in lung tumours includes sustained
inflammation, production of reactive oxygen species, depletion of antioxidants,
impairment of other defence mechanisms, cell proliferation and gene mutations. These
events are well documented in experimental animals but, for humans, information is
incomplete. However, some of these events have been observed in experimental animals,
humans exposed to the combustion products of coal and wood, or coal miners exposed to
coal dust.
Although the emissions described in this monograph have some similarities in
chemical composition and biological effects, they are also clearly distinctive. Thus,
carcinogenic mechanisms unique to each of the types of emission may also underlie the
general carcinogenic mechanisms described here.
4.5
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5. Summary of Data Reported
5.1
Exposure data
The use of solid matter as household fuel is widespread and affects approximately
half of the human population, almost exclusively in countries with low and medium
resources, and the use of biomass is much more frequent than that of coal in most parts of
the world. Exposure to emissions from the combustion of these fuels occurs as a result of
cooking or heating, usually in poorly ventilated spaces. Women and young children
especially may be exposed to extremely high levels of these emissions.
The factors that determine the use of solid fuels involve a combination of issues
related to economics, social status, convenience and physical availability. Income and
education play a major role in the selection of fuel; the households that use solid fuels
tend to have lower levels of education and income because biomass fuels are frequently
collected from the local environment, whereas liquid fuels must be purchased at a local
market or fuel retailer.
Access to both solid and liquid fuels also plays a major role in the selection of fuel for
household use. The ready availability of biomass from the local environment or
agricultural residues encourages its use as a cooking fuel, since cash expenditure is not
required. When liquid fuels are not available in local markets or significant initial costs
represent a barrier to their adoption, the probability that solid fuels will be used is greater.
Energy policies in specific countries that involve issues of access and energy prices,
taxes or subsidies also play a role in the selection of the type of fuel used. Taxes on liquid
fuels reduce the probability that people will use them for cooking, whereas subsidies
encourage their use. Additional factors that influence exposure to indoor air pollution
from solid fuels include the type and quality of the fuel, the type and condition of stoves,
the presence of a flue, the type of ventilation and housing, the task, the skill of the stove
operator and weather conditions, all of which play a role in determining the level of
pollutants. These factors vary by day, season and year, and generalization of the levels of
exposure that can occur from individual monitoring studies that are conducted under
widely differing conditions is difficult.
Typical household combustion of biomass and coal diverts 1030% of fuel carbon
into products of incomplete combustion. Total emissions of these products from coal and
biomass overlap, largely depending on the species of fuel and the type of stove.
Thousands of chemical species have been identified in the gas-phase and particle-phase of
products of incomplete combustion. The mixture contains fine and ultrafine particles and
a large number of semi-volatile and non-volatile organic compounds, including known
carcinogens such as benzene, formaldehyde and benzo[a]pyrene. On the basis of results
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from a limited number of studies that measured emission factors, combustion of the same
amount of coal and wood in household stoves generates relatively comparable amounts of
benzene and benzo[a]pyrene. However, combustion of wood appears to generate larger
amounts of formaldehyde and acetaldehyde than combustion of the same amount of coal.
Virtually all of the rural population of China (about 740 million) uses solid fuels, and
most rely on coal or a variety of biomass fuels for most of their energy needs. A
considerable portion of the urban population (560 million) uses coal, which is
increasingly in the form of briquettes. Improved biomass fuel stoves are very common, as
are unvented portable coal stoves. Typical average indoor exposure levels of particulate
matter <10 m in size range from several tens to several hundred micrograms per cubic
metre and those for benzo[a]pyrene range from low single digits to more than 40 ng/m3.
In some households, average exposure levels can be an order of magnitude higher. While
gas fuels and electricity are progressively replacing solid fuels, the latter remain prevalent,
even in wealthier rural households.
Exposure to indoor air pollutants that are associated with the combustion of solid
fuels for cooking and heating is extensive in South Asia. Exposures are widespread and
prevalent in half to three-quarters of the population in most countries of the region. In
Latin America, nearly 25% of the population live in rural areas where biomass fuels are
most frequently used for cooking and heating. In Africa, biomass fuel is used almost
exclusively in rural areas and is still widely used in most urban areas.
Although there is some variability in exposure levels as a result of a differential
distribution of determinants, levels of pollutants that range from several hundreds of
micrograms per cubic metre of particulate matter of varying size during the day to several
thousands of micrograms per cubic metre during cooking have consistently been reported
in many countries in these regions.
A variety of interventions are already available, and new technologies and approaches
are emerging. A small body of evidence shows that interventions can substantially reduce
exposure and the incidence of lung cancer (chimney stoves, switching to cleaner fuels)
and chronic obstructive pulmonary disease (chimney stoves). Levels of indoor air
pollutants associated with the use of biomass and other solid fuels can be substantially
reduced, particularly by stoves with flues, but experience shows that exposure levels
remain high and people are exposed in the vicinity of their homes and from neighbours
homes. Biomass stoves that use secondary combustion may offer advantages due to
greatly reduced emissions. Cleaner fuels, in particular liquefied petroleum gas and natural
gas, offer the largest reductions in exposure, but cost and practical issues may result in
lesser reductions being achieved in practice. Electricity is important for development, but
is unlikely to contribute to substantive reductions in exposure as it is rarely used for
cooking and heating in poor communities due to the high cost of supply, infrastructure
and use. Behavioural changes can complement technical interventions, but appear to have
limited potential alone.
5.2
Human carcinogenicity data
5.2.1
Lung cancer
(a)
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Combustion of coal
More than 20 casecontrol studies and one cohort intervention study reported on the
association between exposure to coal smoke and the risk for lung cancer. The majority of
them were conducted in China; in addition, a few studies were available from North
America and Europe. Several studies that used different epidemiological designs
originated from Xuan Wei County, China. Initially, an ecological study from this area
showed a strong correlation between communities that used several different types of
smoky coal and mortality from lung cancer. Two population-based casecontrol studies
reported a positive association between the use of smoky coal and an increased risk for
lung cancer. A statistically significant exposureresponse relationship between the
amount of smoky coal used and risk for lung cancer was observed in both of these studies.
In one of these, in which controls were matched to cases on village and fuel type, the
amount of smoky coal used was still significantly associated with risk for lung cancer in
an exposureresponse manner. A cohort study carried out in Xuan Wei County that
included more than 20 000 farmers who used smoky coal throughout their lifetimes and
approximately 1300 lung cancer cases showed that transition to the use of a stove with a
chimney was associated with a reduced risk for lung cancer in both men and women that
became evident 10 years and more after the intervention.
Two casecontrol studies from northern China that used general population controls
provided evidence for an association between exposure to indoor air pollution from coal
smoke and the risk for lung cancer. The first, a large, well-conducted study in Shenyang,
reported internally consistent, positive exposureresponse associations for different
metrics of exposure to coal smoke, including a cumulative index of indoor exposure to
coal smoke from heating and cooking, that were adjusted for tobacco smoking and
education. The second study, from Harbin, reported a strong exposureresponse
relationship among nonsmoking women for years of use of a coal stove in the bedroom
and risk for lung cancer after adjustment for several potential confounders.
One hospital-based casecontrol study from Taiwan, China, observed a statistically
significant twofold increase in risk for adenocarcinoma of the lung with use of coal or
anthracite as cooking fuel that was adjusted for smoking and socioeconomic status; no
exposureresponse results were provided. A population-based casecontrol study on lung
cancer among women in Los Angeles (CA, USA) reported a twofold increased risk for
adenocarcinoma of the lung with the use of coal for heating or cooking in childhood and
adolescence; results were adjusted for potential confounders, but exposureresponse
analyses were not provided.
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(b)
Combustion of biomass
To examine the role of biomass in the risk for lung cancer, the Working Group
considered that four studies that collected information on the use of this fuel type for
cooking and/or heating were the more informative, and that, among these, a casecontrol
study conducted in Taiwan, China, and a large well-conducted European multicentre
casecontrol study were the most informative. In the study in Taiwan, compared with
people who did not use wood, nonsmoking women who used wood for cooking showed a
significant twofold increased risk for lung cancer. In a subsequent expanded study, use of
wood was also associated with a significant threefold increased risk for squamouscell
carcinoma and adenocarcinoma of the lung. In the large European casecontrol study,
compared with men and women who never used coal and/or wood for cooking or heating,
a significant 2030% increased risk for lung cancer was found among those who cooked
or heated with wood but never with coal after adjustment for active tobacco smoking and
other potential confounders. However, neither the Taiwanese nor the European studies
provided information on duration of exposure to wood smoke and thus exposure
response relationships could not be examined.
The other two informative studies were in nonsmoking women, one in Japan and one
in Mexico, and found an increased risk for lung cancer in relation to exposure to smoke
from wood or wood and straw. No information on duration of exposure was available in
the Japanese study and the significantly increased risk was restricted to women who had
been exposed to wood smoke at the age of 30 years. In the Mexican study, an
approximate twofold increased risk was restricted to women who had used wood for
>50 years whereas the risks were not increased for those who had used wood for 120 or
2150 years. Thus, the accumulated evidence suggests that exposure to smoke from wood
that was used for heating and/or cooking may be associated with an increased risk for
lung cancer but information on the effect of duration and intensity of exposure was
lacking.
5.2.2
Aerodigestive tract cancers and combustion of coal or biomass
Several studies investigated the relationship between the use of coal or biomass and
the risk for nasopharyngeal carcinoma (the majority of which were conducted in Chinese
populations and one in India). One study of nasopharyngeal carcinoma among Chinese
reported a statistically significant fivefold increased risk associated with current use of
wood as fuel after adjustment for consumption of salted fish during weaning; however, no
information on an exposureresponse relationship was presented, except for some
assessment of ventilation conditions. In other studies of nasopharyngeal carcinoma,
assessment of exposure was also crude, the baseline comparison group was not clearly
specified or included people who used coal or fuels other than coal and wood and no
adjustment was made for consumption of salted fish.
A few studies by cancer site investigated the relationship of exposure to emissions
from the combustion of coal or biomass and other cancers of the aerodigestive tract,
303
including the oral cavity, pharynx, larynx, nasal cavities and oesophagus. These studies
were not very informative because they were very small, the baseline comparison group
was not clearly specified and mixed exposures were investigated or the exposure was
based on a dichotomized variable with no information on exposureresponse
relationships.
5.3
Animal carcinogenicity data
5.3.1
Coal
In one study, inhalation exposure to a high concentration of emissions generated from

coal burned under conditions similar to those of human exposure in Xuan Wei County,
China, increased the incidence of various types of malignant lung tumour (squamous-cell
carcinomas, adenosquamous carcinomas and adenocarcinomas) in male and female
Kunming mice and that of squamous-cell carcinomas in male and female Wistar rats. In
another study in Kunming mice exposed by inhalation to an unspecified concentration of
coal emissions from an unspecified source in Harbin City, China, the incidence of
adenocarcinoma was increased.
Intratracheal administration of extracts of coal-derived soot from Xuan Wei County
induced an increase in the incidence of lung adenocarcinomas. In two studies,
subcutaneously administered extracts of coal emissions from Xuan Wei County increased
the incidence of various types of malignant pulmonary tumours (squamous-cell
carcinomas, adenosquamous carcinomas and adenocarcinomas) in Kunming mice. These
extracts were used in a complete carcinogenesis study by dermal application and induced
an increase in the incidence of skin carcinomas in SENCAR mice. Extracts of coal
emissions from the same region increased the incidence of benign skin papillomas in two
tumour initiationpromotion studies by dermal application in Kunming and SENCAR
mice.
A veterinary epidemiological study of dogs also showed an association between
exposure to coal emissions and sinonasal cancer.
5.3.2
Wood smoke
In one study, inhalation exposure to a high concentration of emissions generated from

wood burned under conditions similar to those of human exposure in Xuan Wei County
increased the incidence of lung adenocarcinomas in male and female Kunming mice. The
same inhalation exposure failed to increase the incidence of lung tumours in either sex of
Wistar rats. Wood smoke generated from oak of mixed species that was burned in an
uncertified wood stove over a simulated cycle induced no increase in tumour formation in
Strain A mice exposed for 6 months and held for a 6-month period with no exposure.
Subcutaneously administered extracts of wood smoke from Xuan Wei County
increased the incidence of pulmonary adenocarcinomas in male Kunming mice. Extracts
304
of wood smoke from the same region increased the incidence of benign skin papillomas
in two tumour initiationpromotion studies by dermal application in female Kunming and
SENCAR mice. Similar regional extracts used in a complete carcinogenesis study by
dermal application induced a non-statistically significant increase in the incidence of skin
carcinomas in female SENCAR mice. Extracts of relevant particulate matter from wood
smoke generated from a wood stove in which hardwood and softwood were burned
increased the incidence of benign skin papillomas in tumour initiationpromotion studies
in female SENCAR mice following multiple topical applications to the skin.
5.4
Emissions from the combustion of organic materials, such as coal or wood, are
complex mixtures that contain numerous different gases, aerosols and chemical
compounds admixed with and/or adsorbed onto particulate matter.
The primary mechanisms for deposition of airborne particles in the respiratory tract
are sedimentation, impaction and diffusion. Deposition by sedimentation and impaction
depends on the aerodynamic diameter of the particle, whereas deposition by diffusion
depends on its thermodynamic diameter. Following inhalation, particles may either
deposit in the extrathoracic, tracheobronchial or pulmonary airways or remain in the air
stream and be eliminated upon exhalation. The deposition of particles in the respiratory
tract depends primarily on the size of the inhaled particle, the route of breathing (i.e.
through the nose and/or mouth) and the breathing pattern (e.g. volume and frequency).
Particles are frequently aggregates or agglomerates of smaller primary particles. The
aerodynamic and thermodynamic properties of these aggregates (rather than the primary
particles) affect their behaviour in the air and their probability of deposition in the
respiratory tract. Once deposited, properties such as the size and surface area of both the
aggregate and primary particle can potentially affect the kinetics of clearance.
The deposition and clearance of particles vary among individuals for a number of
reasons, including age, gender, tobacco smoking status and health status. Pre-existing
lung diseases or conditions such as asthma or chronic obstructive pulmonary disease can
influence the efficiency and pattern of deposition within the respiratory tract. Deposition
also depends on the level of activity and breathing patterns. Deposition and retention
determine the initial and retained dose of particles in each region and may, therefore,
influence the risk for developing diseases specific to those regions of the respiratory tract.
Studies in rodents (primarily rats) have shown that, depending on the concentrations
and durations of exposure, the long-term retention of particles in humans can be greater
than that predicted from rodent studies that used lower concentrations or shorter durations
of exposure.
A cascade of events proposed to describe the biological process that starts from some
particle deposition on critical target cells or tissues within the rat lung and results in rat
lung tumours includes sustained inflammation, production of reactive oxygen species,
depletion of antioxidants and/or impairment of other defence mechanisms, cell
305
proliferation and gene mutations. These individual steps comprise an overall mode of
action that can be used to compare responses of rats with those of other species, including
humans. Particle surface area is a better predictor of lung tumours than particle mass in
rats exposed to various poorly soluble particles of fine or ultrafine size.
Among other compounds, polycyclic aromatic hydrocarbons are important chemical
components of combustion emissions. These compounds are absorbed through the
respiratory tract, gastrointestinal tract and skin, and smaller molecules (two to three rings)
are absorbed more rapidly than larger ones. Active transport and passive diffusion are
both involved, and, once absorbed, polycyclic aromatic hydrocarbons are distributed
widely to most organs and tissues and tend to accumulate in fatty tissue. They are
metabolized rapidly to more soluble (and in some cases more reactive) metabolites, such
as epoxides, phenols, dihydrodiols, phenol dihydrodiols, dihydrodiol epoxides, quinones
and tetrols. At least three pathways of metabolism are involved: the cytochrome P450
pathway, the cytochrome P450/aldo-keto reductase (oxidative) pathway and a
cytochrome P450/peroxidase (radical cation) pathway. In addition to these phase I
metabolic pathways, polycyclic aromatic hydrocarbon metabolites may bind with
macromolecules, which can lead to toxic, mutagenic or carcinogenic effects, or they may
be eliminated in a conjugated form via phase II metabolism.
Polycyclic aromatic hydrocarbons may be metabolized to their bay- and fjord-region
diol epoxides or undergo cyclopenta-ring oxidation. These can be electrophilic and bind
to DNA and proteins, which results in genotoxic effectsprimarily through the formation
of DNA adducts. Polycyclic aromatic hydrocarbons also have non-genotoxic effects that
may include the interruption of gap-junctional communication and changes in gene
expression; radical cations, ortho-quinones and reactive oxygen species may also be
formed by their metabolism. They may also operate through receptor-mediated
mechanisms that involve the aryl hydrocarbon receptor. These compounds can have
immunological and haematological effects and can also be phototoxic.
Several studies evaluated populations who are exposed to indoor air pollution from
coal, wood or other biomass fumes for associations between polymorphisms in genes that
are involved in xenobiotic metabolism and risk for lung cancer. However, multiple
comparisons and generally small sample sizes could have resulted in both false-positive
and false-negative findings. Some evidence indicated that the GSTM1 null genotype was
associated with increased risk for lung cancer in studies in which at least part of the study
population was definitely or probably exposed to indoor air pollution, particularly when
exposure to polycyclic aromatic hydrocarbons was suspected to be a contributing agent.
However, results for polymorphisms in other genes are inconsistent or have been analysed
in only one study. Therefore, no firm conclusion can be made regarding the effect of
polymorphisms of genes other than GSTM1 on risk for lung cancer in these populations.
The available information on the mutagenicity and genotoxicity of smoky coal
emissions from Xuan Wei County includes a wide range of end-points that encompasses
mutations in KRAS and TP53 genes in lung tumours from nonsmokers who were exposed
to smoky coal emissions and whose tumours were linked epidemiologically to exposure
306
to the emissions. In addition, studies show that such an exposure results in the excretion
of several polycyclic aromatic hydrocarbon metabolites, and that exposed individuals
exhibit elevated levels of PAHDNA adducts and accumulation of TP53 protein. Two
studies also showed that emissions from other types of coal induced sister chromatid
exchange in exposed individuals.
The available information on the genotoxicity and mutagenicity of emissions from
wood combustion includes a number of human studies that showed the induction of
cytogenetic damage in exposed individuals, including micronuclei, sister chromatid
exchange and chromosomal aberrations. Also, exposed individuals had an elevated level
of DNA adducts, DNA damage and accumulation of TP53 protein. In cultured cells,
extracts of the emissions (mostly from wood) induced DNA strand breaks and sister
chromatid exchange.
In many experiments, extracts or condensates of emissions from coal and wood were
mutagenic in Salmonella. In strain TA98 in the presence of a metabolic activation system,
the potency in terms of revertants per milligram of particle can reach 3000 for smoky coal
and 4700 for wood. However, on average, smoky coal emissions were five times more
mutagenic than those from wood in terms of activity per milligram of particle. In contrast,
the mutagenic potencies of these emissions expressed as revertants per cubic metre of air
reached 60 000 for smoky coal and 11 000 for wood. On average, smoky coal emissions
were 10 times more mutagenic than those from wood. This larger range of potencies
reflects the range of the amount of organic compounds (together with the potency of the
organic compounds) emitted under the test conditions by the two combustion processes.
Bioassay-directed fractionation studies with Salmonella have identified that, for
smoky coal, most of the mutagenic activity is due to polycyclic aromatic hydrocarbons
and methylated polycyclic aromatic hydrocarbons. For wood, these compounds contribute
1050% of the activity and polar aromatic compounds (aromatic amines and ketones) and
nitropolycyclic aromatic hydrocarbons contribute to some of the remaining activity.
307
6. Evaluation and Rationale
6.1
Combustion of coal
There is sufficient evidence in humans for the carcinogenicity of household

combustion of coal. Household combustion of coal causes cancer of the lung.
There is sufficient evidence in experimental animals for the carcinogenicity of
emissions from combustion of coal.
There is sufficient evidence in experimental animals for the carcinogenicity of extracts
from coal-derived soot.
Overall evaluation
Indoor emissions from household combustion of coal are carcinogenic to humans
(Group 1).
6.2
Combustion of biomass
There is limited evidence in humans for the carcinogenicity of household combustion

of biomass fuel (primarily wood). Household combustion of biomass fuel (primarily
wood) causes cancer of the lung.
There is limited evidence in experimental animals for the carcinogenicity of emissions
from combustion of wood.
There is sufficient evidence in experimental animals for the carcinogenicity of woodsmoke extracts.
Overall evaluation
Indoor emissions from household combustion of biomass fuel (primarily wood) are
probably carcinogenic to humans (Group 2A).
In reaching this evaluation, the Working Group considered mechanistic and other
relevant data. These data include (i) the presence of polycyclic aromatic hydrocarbons
and other carcinogenic compounds in wood smoke, (ii) evidence of mutagenicity of wood
smoke and (iii) multiple studies that show cytogenetic damage in humans who are
exposed to wood smoke.
1. Exposure Data
1.1
Definition
Cooking fumes or cooking oil fumes is the term commonly used to describe the
visible emissions generated during cooking by frying with oil. However, these emissions
are not technically fumes. In occupational and environmental hygiene, fumes are
defined as submicron-sized solid particles (particulate matter) created by the cooling of
hot vapour. During cooking, such vapour is formed when the cooking oil is heated above
its boiling point. In addition to this ultrafine particulate matter, cooking, especially frying
and grilling, generates aerosol oil droplets, combustion products, organic gaseous
pollutants, and steam from the water contents of the food being cooked.
1.2
Constituents of cooking fumes
Cooking, in particular frying, generates substantial amounts of airborne particulate

matter (PM), which includes ultrafine particles (UFP) and fine PM (PM2.5), and is a major
contributor to their indoor levels. In addition, particles created during cooking have
organic substances adsorbed on their surface. These include polycyclic aromatic
hydrocarbons (PAHs) and heterocyclic amines. Certain gaseous pollutants such as
formaldehyde (IARC, 2006), acetaldehyde (IARC, 1999), acrylamide (IARC, 1994) and
acrolein (IARC, 1995) are also produced during cooking.
The concentrations of these constituents measured in cooking fumes in field and
controlled studies are presented below.
1.2.1
Ultrafine and fine particulate matter
The Particle Total Exposure Assessment Methodology (PTEAM) study was carried
out by the Research Triangle Institute and the Harvard University School of Public Health
in the USA in 198990 (Clayton et al., 1993). Particle concentrations were measured for a
probability-based sample of 178 nonsmokers who represented the non-institutionalized
population of Riverside, CA (~139 000 persons). Personal samples of PM10 were taken;
311
312
the indoor and outdoor samples included both PM10 and PM2.5. Cooking produced both
fine and coarse particles. Homes where cooking took place during monitoring (about
55%) had average PM10 concentrations ~20 g/m3 higher than those where no cooking
took place (zkaynak et al., 1996a,b). The proportion of PM2.5 and PM10 due to cooking
was 25% for both particle sizes (Figure 1.1). However, when considered as a fraction of
particles due to indoor sources alone, the proportion was 65% and 55%, respectively
(zkaynak et al., 1996b).
Figure 1.1 Fraction of PM2.5 due to cooking (top); fraction of PM10 due to cooking
(bottom).
Other
8%
Smoking
5%
Cooking
25%
Outdoor
62%
Other
16%
Smoking
4%
Outdoor
55%
Cooking
25%
313
A large-scale study of personal, indoor and outdoor exposures was undertaken for
more than 100 persons living in Seattle, WA, USA (Seattle Study; Liu et al., 2003).
Based on 195 cooking events, the average PM2.5 concentration due to cooking was
estimated to be 5.5 (standard error [SE], 2.3) g/m3 (Allen et al., 2004).
A study of personal, indoor and outdoor exposure to PM2.5 and associated elements
was carried out on 37 residents of the Research Triangle Park area in North Carolina,
USA (Research Triangle Park Study; Wallace et al., 2006a,b). Burned food added an
average of 1112 g/m3 to the indoor concentration (Wallace et al., 2006b). In continuous
measurements, the mean estimated PM2.5 personal exposures during more than 1000 h of
cooking were found to be 56 g/m3 higher than background (Wallace et al. 2006b). The
24-h average increase due to cooking was about 2.5 g/m3. A different analysis of the
results from this study concluded that cooking contributed 52% of personal exposure to
PM2.5 and more than 40% of the indoor concentration of PM2.5 (Zhao et al., 2006).
A long-term study of indoor and outdoor particle concentrations was carried out
between 1997 and 2001 in an occupied townhouse in Reston, VA, USA (Reston, VA
Townhouse Study). Cooking produced about an order of magnitude higher number of the
smallest UFP (1050 nm) and from 1.2- to 9.4-fold higher levels of the larger particles
compared with identical times when no cooking occurred (Table 1.1; Wallace et al.,
2004). The mean mass concentration increased at dinner (4-h averages) from 3.7 g/m3 to
11.8 g/m3 assuming a density of combustion particles of 1 g/cm3. About 70% of the
particles emitted during dinnertime were <0.05 m.
Table 1.1. Number and concentration of PM2.5 during dinnertime
cooking compared with no cooking
Size (m)
Dinnertime cooking
No cooking
Mean
SE
Mean
SE
6472
13363
7085
2226
277
76
5
1
165
342
221
77
10
3
0.086
0.016
465
1507
1701
807
128
16
1.3
0.15
10
22
29
11
1.4
0.15
0.015
0.0016
0.0002
0.01
0.04
0.10
0.12
0.05
0.0006
0.039
0.4
1.1
1.2
0.5
0.00001
0.0006
0.006
0.014
0.013
0.005
Numbera
0.0100.018
0.0180.05
0.050.1
0.10.2
0.20.3
0.30.5
0.51
12.5
Concentration (g/m3)
0.0100.018
0.0085
0.0180.05
0.3
0.050.1
1.4
0.10.2
2.9
0.20.3
2.6
0.30.5
2.4
314
Table 1.1. (contd)

Size (m)
Dinnertime cooking
No cooking
Mean
SE
Mean
SE
0.01
0.04
0.2
0.3
3.7
0.003
0.003
Concentration (g/m3) (contd)

0.51
12.5
Sum (PM2.5)
0.8
1.4
11.8
From Wallace et al. (2004)

PM, particulate matter; SE, standard error
a
No. of samples between 2400 and 12 800
In a more detailed analysis, 44 high-particle-production (frying, baking, deep-frying)

cooking episodes on a gas stove were assessed (Wallace et al., 2004). Most of the
particles were in the ultrafine range, but the largest volume was contributed by particles
between 0.1 m and 0.3 m in diameter. The total particle volume concentration created
by the 44 high-particle-production cooking events averaged a little more than 50
(m/cm)3, corresponding to an average concentration of about 50 g/m3, about an order of
magnitude higher than average values for all types of cooking combined.
The size distribution of ultrafine particles during cooking was studied by Wallace
(2006) and Ogulei et al. (2006). Stir-frying using one gas burner produced a peak of PM
~35 nm, whereas deep-frying using one gas burner followed by baking in the oven
produced a peak about twice as high and at a diameter of 64 nm (Figure 1.2).
Brauer et al. (2000) reported PM2.5 concentrations in the range of 24201 g/m3 in
residential kitchens during frying, with peak PM2.5 concentrations above 400 g/m3.
Kamens et al. (1991) estimated that 518% of an 8-h personal particle exposure could be
attributed to cooking one meal in one of three homes that they studied.
Abt et al. (2000) studied 17 selected cooking events in three homes that provided
mean peak volume concentrations of particles between 20 and 500 nm ranging between
29 and 57 (m/cm)3. Long et al. (2001) studied nine homes for 612 days each and found
mean peak volume concentrations for UFP (20100 nm) of 2.218.2 (m/cm)3. He et al.
(2004a) studied 15 homes for 48 h during cooking under good and poor ventilation
conditions and found a range of peak submicrometer number concentrations for cooking
events between 16 000 and 180 000 particles/cm3. Estimates of the emission rate ranged
between 0.24 1012 particles/min. Finally, 24 cooking events with high concentrations
and well-shaped decay curves, including concurrent air exchange rate measurements,
were analysed more accurately, taking into account losses due to deposition during the lag
time required to reach the peak, for their source strengths (Wallace et al., 2004). A value
of 31012 UFP/min was obtained.
315
Figure 1.2. Size distribution of ultrafine particles from cooking. n = number of 5-min
measurements. Error bars are standard errors. Stir-frying on one gas burner produced
a peak at 35 nm; deep-frying on one gas burner followed by baking in the oven
produced a peak at 64 nm that was twice as high.
1400
no indoor sources
(n = 214 000)
stir-fry on gas
burner (n = 629)
1200
deep-fry + oven
bake (n = 2107)
1000
cm -3
800
600
400
200
0
10
100
Diameter (nm)
1000
316
A study in Amsterdam and Helsinki found that cooking increased PM2.5

concentrations by 1.93.4 g/m3 (1424%) among two groups of 47 and 37 elderly
residents in the two cities, respectively (Brunekreef et al., 2005; the ULTRA Study).
Kleeman et al. (1999) used an industrial charbroiling facility to cook >100 hamburgers.
The particle mass consisted mainly of organic compounds, with a very small amount of
elemental carbon, and a large unknown component. Most of the particle mass came from
particles between 0.1 and 0.4 m in diameter.
Emission rates during cooking with commercial institutional-scale deep-fryers have
been reported (Schauer et al., 1998). Professional chefs prepared vegetables by stir-frying
in soya bean or canola oil and deep-frying potatoes in oil. Fine particle emission rates
were 21.51.2, 29.51.3 and 13.11.2 mg/kg for stir-frying vegetables in the two oils and
deep-frying potatoes, respectively. [Emissions during food preparation by a professional
chef using large commercial cookers may differ substantially from emissions in a
residence.]
In a recent study in a residential setting in Canada (Evans et al. 2008), real-time
measurements were taken during frying to estimate the time-integrated exposure to PM
associated with frying food. The production rates and concentrations of UFP and PM2.5
during and at the end of frying a variety of breakfast foods typical of the Canadian diet at
medium temperatures were assessed (Table 1.2).
Table 1.2. The production rates and concentrations of UFP and PM2.5 during
and at the end of frying of various types of foods
Production rate during frying
Concentration at the end

of frying
Food
Food temperature
(C)a
UFP
(particles/cm3 s)
PM2.5
(g/m3 s)
UFP
(particles/cm3)
PM2.5
(g/m3)
Bacon
Pancakes
Peppers and onions
Vegetable stir-fry
Vegetable mix
Fried egg
Fried rice
Breaded eggplant
Overall
314
297
336
280
249
271
274
280
45
25
78
31
59
60
6
88
44
0.092
0.17
0.12
ND
ND
ND
ND
1.1
0.13
2.2*104
2.5*104
2.0*104
2.0*104
4.5*104
2.5*104
1.0*104
8.0*104
38
55
60
ND
ND
ND
ND
1000
From Evans et al. (2008)

ND, not determined because no elevated PM2.5 concentration was observed; PM, particulate matter;
UFP, ultrafine particles
a
Refers to maximum temperature
1.2.2
317
Volatile organic compounds
A large proportion of the vapours generated during cooking is steam from the water
contents of the food or from the water used to cook the food. However, during frying
(with oil), fatty acid esters that are constituents of edible oils and fat can decompose and
produce volatile organic compounds, as well as semi-volatile compounds that can
condense to form particles. A wide variety of organic compounds have been identified in
cooking emissions, including alkanes, alkenes, alkanoic acids, carbonyls, PAHs and
aromatic amines. Felton (1995) reported that the main volatile compounds generated
during frying were aldehydes, alcohols, ketones, alkanes, phenols and acids. Of particular
concern in relation to carcinogenicity are PAHs, heterocyclic amines and aldehydes.
(a)
PAHs
Dubowsky et al. (1999) reported peak total particle-bound PAH concentrations in a

range from undetectable to 670 ng/m3 during cooking when measured with a Gossen PAS
monitor.
A study in Taiwan found several PAHs in the fumes of three cooking oils (safflower,
vegetable and corn oil) (Chiang et al., 1999a).
By contrast, Wallace (2000) did not measure increased concentrations of total PAHs
during cooking.
(b)
Aldehydes
Schauer et al. (1998) reported emissions of 20 100 g formaldehyde/g of food during

stir-frying of vegetables on an institutional-size cooker. They reported emissions of
12 400 g/g formaldehyde and 20 900 g/g acetaldehyde during deep-frying of potatoes.
(c)
Aromatic amines
One study found the aromatic amines 2-naphthylamine and 4-aminobiphenyl in the
fumes of three different cooking oils (sunflower oil, vegetable oil and refined lard)
(Chiang et al., 1999b).
(d)
Other volatile compounds
Rogge et al. (1991) measured the fine aerosol emission rates for single organic
compounds from charbroiling and frying hamburger meat. The compounds detected were
n-alkanes, n-alkanoic acids, n-alkenoic acids, dicarboxylic acids, n-alkanals and nalkenals, n-alkanones, alkanols and furans.
Ho et al. (2006) studied emissions of 13 carbonyl compounds in cooking exhaust
fumes from 15 restaurants in Hong Kong Special Administrative Region, China, and
developed a new method of analysis using Tenax coated with a hydrazine compound
followed by thermal desorption and mass spectrometry. This allowed them to separate
three similar compounds: acetone, acrolein and propanal. The most prevalent compounds
were formaldehyde (in all but four of the restaurants), acrolein, acetaldehyde and nonanal,
318
which accounted for 72% of all carbonyl emissions. Based on a small sample of
restaurants, the authors estimated total annual emissions for acrolein, formaldehyde and
acetaldehyde of 7.7, 6.6 and 3.0 tonnes per year from cooking compared with 1.8, 10 and
33 tonnes per year, respectively, from vehicles.
1.3
Effect of different parameters of cooking on emissions
The chemical composition of cooking emissions varies widely depending on the

cooking oils used, the temperature, the kind of food cooked, as well as the method and
style of cooking adopted.
1.3.1
Effect of the type of oil and temperature

(a)
Mixture of volatile components
Studies were undertaken to identify qualitatively the volatile components emitted

during the heating of cooking oils to 265275C (Li, et al. 1994; Pellizzari et al. 1995;
Shields et al. 1995; Chiang et al., 1999a; Wu et al. 1999). The oils tested were rapeseed,
canola, soya bean and peanut. The major constituents identified in the oil vapours were
saturated, unsaturated and oxygenated hydrocarbons. These studies detected a variety of
agents in emissions from heated cooking oils including 1,3-butadiene, benzene,
benzo[a]pyrene, dibenz[a,h]anthracene, acrolein, formaldehyde and acetaldehyde.
Emissions were highest for rapeseed oil and lowest for peanut oil. In one study, the
emission levels of 1,3-butadiene and benzene were approximately 22-fold and 12-fold
higher, respectively, for rapeseed oil than for peanut oil (Shields et al., 1995). Compared
with rapeseed oil heated to 275C, fourfold and 14-fold lower levels of 1,3-butadiene
were detected when the oils were heated to 240C and 185C, respectively.
(b)
PAHs and nitro-PAHs
In a study performed in a controlled environment (Air Resources Board of the State

of California Study; Fortmann et al., 2001), five untreated cooking oils were extracted
and analysed for PAHs (Table 1.3). All were found to contain some PAHs; olive oil and
peanut oil contained generally higher concentrations than rapeseed, corn or vegetable oils.
In a similar study, PAHs levels in samples of five raw cooking oils (canola, olive,
corn, soya bean and vegetable oil) were not increased compared with the blank (Kelly,
2001).
Fume samples from three different commercial cooking oils commonly used in
Taiwan, China (lard oil, soya bean oil and peanut oil), were collected and tested for
PAHs. All samples contained dibenz[a,h]anthracene and benz[a]anthracene; extracts of
fume samples from the latter two also contained benzo[a]pyrene (Chiang et al., 1997). In
a later study, fume samples from safflower, olive, coconut, mustard, vegetable and corn
oil were similarly tested (Chiang et al., 1999a). Extracts of fumes from safflower oil,
319
vegetable oil and corn oil contained benzo[a]pyrene, dibenz[a,h]anthracene, benzo[b]fluoranthene, and benz[a]anthracene. Concentrations are shown in Table 1.4.
Table 1.3. Concentrations (ng/g) of polycyclic aromatic hydrocarbons in
untreated cooking oils
Compound
Olive
Peanut
Rapeseed
Corn
Vegetable
Acenaphthylene
Acenaphthene
Phenanthrene
Anthracene
Fluoranthene
Pyrene
Benz[a]anthracene
Chrysene
Benzo[b+j+k]fluoranthene
Benzo[e]pyrene
Benzo[a]pyrene
Benzo[ghi]perylene
Fluorene
Perylene
Dibenzo[a,h+a,c]anthracene
Naphthalene
1-Methylnaphthalene
Biphenyl
2,6+2,7-Dimethyl naphthalene
2,3,5+i-Trimethyl naphthalene
ND
19.9
10.7
1.12
4.07
7.10
4.49
3.29
77.3
0.26
8.32
16.2
5.31
1.73
4.25
1.50
9.26
31.7
10.1
2.99
8.63
4.63
ND
ND
ND
2.60
1.28
10.2
13.6
14.7
72.8
19.4
24.5
30.3
26.6
ND
0.74
15.5
27.1
13.9
ND
0.12
ND
0.16
ND
ND
ND
1.12
0.71
1.79
6.51
ND
ND
ND
ND
2.67
18.7
0.21
3.56
ND
ND
15.5
ND
0.72
ND
0.63
ND
ND
ND
1.54
0.65
ND
ND
ND
4.68
2.70
11.0
2.03
3.20
0.28
3.59
1.90
0.59
13.3
ND
0.26
ND
ND
ND
ND
ND
0.56
1.64
ND
2.22
2.22
5.28
3.66
4.22
9.84
8.40
0.30
4.38
3.06
9.20
17.6
0.66
ND
ND
0.32
From Fortmann et al. (2001)

ND, not detected
Table 1.4. The polycyclic aromatic hydrocarbon contents (g/m3) of

fumes from various oils heated to 250
10C for 30 min
Carcinogens
Benzo[a]pyrene
Benz[a]anthracene
From Chiang et al. (1999a)
Cooking oil
Safflower
Vegetable
Corn
22.71.5
2.80.2
1.80.3
2.50.1
21.61.3
3.20.1
2.60.2
2.10.4
18.70.9
2.40.2
2.00.1
1.90.1
320
Wei See et al. (2006) studied three ethnic food stalls in a food court for levels of
PM2.5 and PAHs. PAHs varied from 38 to 141 to 609 ng/m3 at the Indian, Chinese and
Malay stalls, respectively. The trend was considered to be related to the cooking
temperature and amount of oil used (simmering, stir-frying and deep-frying). Frying
provided relatively more high-molecular-weight PAHs compared with simmering, which
produced relatively more low-molecular-weight PAHs.
In addition to PAHs, fumes from three different commercial cooking oils frequently
used in Chinese cooking (lard oil, soya bean oil and peanut oil) also contained nitro-PAHs
such as 1-nitropyrene and 1,3-dinitropyrene (Table 1.5) (Wu et al., 1998).
Table 1.5. Concentrations of PAHs and nitro-PAHs (g/m3)
in fumes from various oils heated to 250
10C for 30 min
Carcinogens
Type of cooking oil

Lard
Soya bean
Peanut
ND
2.30.2
2.00.3
21.10.8
2.10.5
2.40.4
19.60.5
1.50.2
1.90.1
1.10.1
0.90.1
2.90.3
3.40.2
1.50.1
0.40.1
PAHs
Benzo[a]pyrene
Benz[a]anthracene
Nitro-PAHs
1-Nitropyrene
1,3-Dinitropyrene
From Wu et al. (1998)
ND, not detected
Zhu and Wang (2003) studied 12 PAHs in the air of six domestic and four
commercial kitchens. Mean concentrations of benzo[a]pyrene were 624 ng/m3 in the
domestic kitchens and 150440 ng/m3 in the commercial kitchens. Cooking oils were
ranked lard>soya bean oil>rapeseed oil. Increases in cooking temperature produced
increased PAH concentrations.
Various samples of cooking oil fumes were analysed in an effort to study the
relationship between the high incidence of pulmonary adenocarcinoma in Chinese women
and cooking oil fumes in the kitchen (Li et al., 1994). The samples included oil fumes
from three commercial cooking oils. All samples contained benzo[a]pyrene and
dibenz[a,h]anthracene. The concentration of dibenz[a,h]anthracene in the fume samples
was 5.722.8 times higher than that of benzo[a]pyrene. Concentrations of benzo[a]pyrene
and dibenz[a,h]anthracene were, respectively, 0.463 and 5.736 g/g in refined vegetable
oil, 0.341 and 3.725 g/g in soya bean oil and 0.305 and 4.565 g/g in vegetable oil.
(c)
321
Heterocyclic amines
Hsu et al. (2006) studied the formation of heterocyclic amines in the fumes from
frying French fries in soya bean oil or lard. Lard was more susceptible to form these
compounds than soya bean oil heated alone (Hsu et al., 2006). Fumes from soya bean oil
heated alone were found to contain three heterocyclic amines, namely, 2-amino-3methylimidazo[4,5-f]quinoxaline (IQx), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and
1-methyl-9H-pyrido[4,3-b]indole (Harman), whereas two additional amines, 2-amino-3,4dimethylimidazo[4,5-f]quinoline (MeIQ) and 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole
(Trp-P-1), were generated with lard.
(d)
Aldehydes and other volatile organic compounds
Higher aldehydes [C>7] have been detected in emissions from pan-frying beefsteak
using four different types of oil (Table 1.6) (Sjaastad & Svendsen 2008). The aldehyde
trans,trans-2,4-decadienal (t,t-2,4-DDE) has been found and quantified in both frying oils
and fumes generated during frying. The quantity of t,t-2,4-DDE in fried potatoes was
considered to be dependent on the oil used, on the frying process and, to a lesser extent,
on oil deterioration. The degree of unsaturation of the frying oil was also considered to
promote the formation of t,t-2,4-DDE.
Table 1.6. Levelsa of total particles (mg/m3) and higher aldehydes (g/m3)
measured in the breathing zone of the cook during pan-frying of beefsteak
using different oils or margarine
Margarine
Rapeseed oil
Soya bean oil
Olive oil
Total particles
t,t-2,4-Decadienal
11.6 (0.7)
10.33 (2.52)
1.0 (0.3)
0.63 (1.32)
1.4 (0.7)
0.52 (0.80)
1.0 (1.1)
ND
2,4-Decadienal
t-2-Decenal
25.33 (4.51)
25.33 (9.70)
ND
3.60 (6.40)
ND
0.50 (1.20)
ND
0.50 (1.20)
s-2-Decenal
2-Undecenal
ND
20.67 (7.64)
0.82 (1.08)
3.81 (5.21)
2.20 (5.29)
2.02 (3.62)
3.67 (2.94)
3.33 (2.34)
Alkanals
Alkenals
426.00 (70.00)
55.70 (11.00)
107.00 (75.00)
1.80 (4.00)
128.00 (53.00)
4.00 (2.70)
121.00 (85.00)
0.90 (1.30)
From Sjaastad & Svendsen (2008)

ND, not detected; ; s, cis; t, trans
The results are given as arithmetic mean (standard deviation)
Emissions of low-molecular-weight aldehydes from deep-frying with extra virgin

olive oil, olive oil and canola oil (control) were investigated at two temperatures, 180 and
240C, for 15 and 7 h, respectively. Seven alkanals (C-2 to C-7 and C-9), eight 2-alkenals
(C-3 to C-10) and 2,4-heptadienal were found in the fumes of all three cooking oils. The
322
generation rates of these aldehydes were found to be dependent on heating temperature,

and showed significant increases with increases in temperature. The emissions of lowmolecular-weight aldehydes from both kinds of olive oil were very similar and were
lower than those observed from canola oil under similar conditions (Fullana et al.,
2004a,b).
The composition of the fumes was studied at different temperatures (190200, 230
240 and 270280C). A strong peak was observed within the wavelength range of 260
270 nm in each condensate sample. From gas chromatographymass spectrometry results,
it was tentatively deduced that there were some 2,4-dialkylenaldehydes and other
conjugated compounds in the condensates. Large amounts of hexanal and 2-heptenal
were present in the cooking oil fumes. The total aldehyde peak areas of the condensates
from four kinds of oil were around 3050% of the total peak area at 270280C (Zhu et
al., 2001).
Concentrations of ethylene oxide and acetaldehyde were assessed during the
simulated frying of soya bean oil without or with flavouring herbs and spices (garlic,
onion, ginger, basil) under nitrogen or air at 1atm (Lin et al., 2007). The tests were
performed at 130, 150, 180 and 200C.
The concentration of both ethylene oxide and acetaldehyde in the oil and vapour
phases increased with frying temperature within the range of 130 to 200C. Under air, the
amounts of ethylene oxide and acetaldehyde generated in either phase were several times
higher when compared with amounts generated under nitrogen. In the oil phase,
concentrations of ethylene oxide and acetaldehyde increased linearly from 7.6 ppm at
130C to 26.2 ppm at 200C, and from 6.0 ppm to 16.6 ppm, respectively. Similarly,
ethylene oxide concentrations in the vapour phase increased from 7 ppm to 85 ppm.
The impact of the combination of flavouring sources and soya bean oil was assessed.
Both ethylene oxide and acetaldehyde were distributed between the gas phase and the oil
phase after cooking each herb or spice at 150C for 5 minutes under either atmosphere. In
each scenario, the amounts of ethylene oxide and acetaldehyde produced were different
when compared with heating soya bean oil alone.
1.3.2
Effect of the type of food, type of cooking or mode of frying

(a)
Studies in a controlled environment
In an experimental study, airborne cooking by-products from frying beef

(hamburgers), pork (bacon strips) and soya bean-based food (tempeh burgers) were
collected, extracted and chemically analysed. 2-Amino-1-methyl-6-phenylimidazo[4,5b]pyridine (PhIP) was the most abundant heterocyclic amine, followed by 2-amino-3,8dimethylimidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-3,4,8-trimethylimidazo[4,5f]quinoxaline (DiMeIQx). No 2-amino-9H-pyrido[2,3-b]indole (AC) was detected in the
food samples fried at about 200C, although it was present in the collected airborne
products. The total amounts of heterocyclic amines in the smoke condensates were 3 ng/g
323
from fried bacon, 0.37 ng/g from fried beef and 0.177 ng/g from fried soya-based food
(Table 1.7) (Thibaud et al., 1995).
Table 1.7. Concentration of heterocyclic amines from frying meat and soyabased patties (ng/g of cooked samples)
Food sample
(average
temperature)
Beef patties (198C)
Beef patties (277C)
Bacon strip (208C)
Soya-based patties
(226C)
In the fried food sample
In the bead-trap smoke condensate
MeIQx
DiMeIQx
PhIP
AC
MeIQx
DiMeIQx
PhIP
AC
4.3
16
45
ND
1.3
4.5
12
ND
4.9
68
106
ND
ND
21
ND
ND
0.14
1.1
ND
ND
0.006
0.25
ND
ND
0.14
1.8
1.0
0.007
0.084
4.0
2.0
0.17
From Thibaud et al. (1995)

AC, 2-amino-9H-pyrido[2,3-b]indole; DiMeIQx, 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline;
ND, not detected (<0.1ng/g); PhIP, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine; MeIQx,
2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline
One study compared emissions of particles, nitrogen oxides, carbon monoxide, PAHs
and formaldehyde in an experimental chamber during seven different types of cooking
activity including pan-frying (Table 1.8; Kelly, 2001). Samples were integrated over
periods of 14 h. [Temperatures were measured but not reported.]. Except for the
hamburger cooked on gas, all tests showed an increase in total PAHs, with indoor levels
averaging about twice or more the outdoor concentrations. Since the outdoor
concentrations would be expected to be roughly half of those indoors in the absence of
indoor sources, the increase over normal indoor levels is by a factor of about 3. For seven
particle-bound PAHs that are considered to be probably carcinogenic, indoor:outdoor
ratios averaged from 11.5. Emissions of nitrogen dioxide were found only when the gas
stove was used, and were 10 mg/kg for pan-frying of hamburgers. Emissions of
formaldehyde remained below 10 ppb (see footnote in Table 1.8).
Another major controlled study of cooking emissions was sponsored by the Air
Resources Board of the State of California (Fortmann et al., 2001). PM2.5 and PM10
particles, carbon monoxide, nitrogen oxide, nitrogen dioxide, PAHs and aldehydes were
measured. Cooking activities included wok stir-frying of chicken and vegetables, deepfrying of French fries and pan-frying of bacon, tortillas or hamburgers. The cooking
activities were studied under standard conditions or worst-case scenarios. Wok stir-frying
was performed with 65 g peanut oil for 1 or 3 min at high temperatures, using chicken
and vegetables as food. The concentrations of PM2.5 particles emitted during the cooking
activities under different conditions are given in Table 1.9. Of the 13 PAHs targeted for
analysis, pyrene, benzo[e]pyrene, benzo[a]pyrene and benzo(b+j+k)phenanthrenes were
detected in more than 60% of the samples. Duplicate samples collected during the worstcase stir-fry test showed that the precision of the PAH sampling method was poor.
324
[Because of the short test, the mass of PAHs in the samples was low, and there was large
analytical uncertainty associated with the measurement.]
Table 1.8. Concentrationsa of PM2.5, PAHs and formaldehyde in a research
house during pan-frying
Type of stove
Food cooked
Gas
Hamburger
Steak
Electric
Hamburger
Steak
PM2.5 (g/m3)
Total PAHs (ng/m3) Seven PAHsb (ng/m3) Formaldehydec (ppb)
Stove Kitchen Indoor
Outdoor
Indoor
Outdoor
Indoor
115
2270
60
2670
294
833
288
189
0.93
3.70
1.76
1.93
3
48
252
542
160
457
425
610
251
431
3.59
2.56
1.68
3.24
<2
9
From Kelly (2001)

PAH, polycyclic aromatic hydrocarbon; PM, particulate matter
a
Average of three replicate runs
b
Benz[a]anthracene, chrysene, benzo[b+k]fluoranthene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene,
dibenzo[a,h]anthracene, benzo[ghi]perylene
c
Values were confounded by background emissions from building materials and by variations due to
purging air between tests.
(b)
Field studies
Samples of cooking oil fumes from three catering shops were analysed (Li et al.,
1994). All samples contained benzo[a]pyrene and dibenz[a,h]anthracene. PAH
concentrations at the three catering shops showed levels of benzo[a]pyrene of 41.8 ng/m3
at a Youtiao (deep-fried twisted dough sticks) shop, 22.8 ng/m3 at a Seqenma (candied
fritters) workshop and 4.9 ng/m3 at a kitchen of a restaurant; concentrations of
dibenz[a,h]anthracene were 338, 144 and 30.3 ng/m3, respectively.
Another study in China showed that the cooking method affected the concentration of
benzo[a]pyrene in kitchen air (Du et al., 1996). In the same kitchens, the level of
benzo[a]pyrene was elevated in indoor air from the baseline value of 0.41 g/100m3 to
0.65 g/100m3 when meat was boiled, and was further increased to 2.64 g/100m3 when
meat was stir-fried.
Li et al. (2003) measured PAHs emitted from the rooftop exhausts of four types of
restaurant in Taiwan, China. Although gaseous PAHs outweighed particle-bound PAHs
by about 4:1, when expressed in benzo[a]pyrene-equivalents, the ratio was reversed.
Chinese food contributed the majority of the level of benzo[a]pyrene-equivalents, while
western food contributed about seven times less and fast food and Japanese food
contributed negligible amounts. Compared with traffic in the city, restaurants contributed
somewhat less total PAHs but about 10 times the benzo[a]pyrene-equivalent amount.
Zhu and Wang (2003) studied 12 PAHs in the air of six domestic and four
commercial kitchens. Mean concentrations of benzo[a]pyrene were 624 ng/m3 in the
Table 1.9. PM2.5 concentrations under different cooking conditions in a research house
Type of cooking
Stir-frying
Food
Chicken and
vegetables
Bacon
Hamburger
Kitchen
79.6
85b
Replicate
88.3100
Worst cased
Vegetable oil
119124
95.3104
Standard
105
Standardd
d
Gas
Gas
Electric
Tortillas
Burner
Gas
Electric
Pan-frying
Food
Living room
Bedroom
Outdoors
241
191
185
418439
185
323
301
8.8
284398
295513
1289
392
850
294
798
303
8.1
8.1
289
214
1124
364
5.6
Standard
182
729
195
71.9
83.3
4.2
Replicate
186.9c
277
162
91.9
70.5
4.1
446
374
94.7
90.2
5.7
Standard
171.4
Standard
148156
105108
482
142
286
Worst case
143.6184.1
268337
484
711
771
8.8
Standard
72.873.7
272298
207
276
235
5.7
566
260
1269
1175
Gas
Standard
172
97
Electric
Standard
232.9c
ND
Gas
Cast iron pan
93.093.7
270304
Gas
Cast iron pan
95.3
ND
Gas
Pan lid
NR
253300
153
51.9
355
77.4
1173
4.2
5.7
7.73
8.64
1.5
8.6
8.8
3.6
5.8
6.4
325
From Fortmann et al. (2001)

ND, not detected; NR, not reported; PM, particulate matter
a
Peak temperature of the food during the test; average temperature for burner or oven during the test
b
Thermocouple proble location for this test was inconsistent with later tests that yielded variable flame temperatures, but other parameters indicate
similar cooking temperatures.
c
Temperature of cooking oil
d
Peanut oil
French fries
PM2.5 concentration (g/m3)
Conditions
Electric
Deep-frying
Temperature (C)a
Type of
stove
326
domestic kitchens and 150440 ng/m3 in the commercial kitchens. Cooking practices
produced PAHs in the rank order broiling>frying>>boiling.
The influence of frying conditions (deep-frying, pan-frying) was studied (Boskou et
al., 2006). In all cases tested, the highest concentration of trans,trans-2,4-decadienal was
detected during deep-frying.
Studies have shown that the total amount of organic compounds per milligram of
particulate organic matter is much higher in western-style fast food cooking than in
Chinese cooking; however, Chinese cooking has a much greater contribution of PAHs to
particulate organic matter (Table 1.10) (Zhao et al., 2007a,b).
Table 1.10. Concentrations of organic compounds from
western-style fast food and from Chinese cooking (ng/mg of
particulate organic matter)
Organic compounds
Western-style fast
food cookinga
Chinese cookingb
n-Alkanes
Polycyclic aromatic hydrocarbons
n-Alkanals
n-Alkanones
Lactones
Amides
Saturated fatty acids
Unsaturated fatty acids
Dicarboxylic acids
Monosaccharide anhydrides
Sterols
Other compounds
3 863
40
29 172
22 702
13 323
4 692
374 699
93 299
57 877
97
487
63
1 883
2 855
3 444
2 443
2 142
531
26 804
29 028
2 051
314
1 684
208
From Zhao et al. (2007a,b)

a
Average of six samples
b
Average of four different styles of Chinese cooking
1.4
Human exposure
Neither occupational nor non-occupational exposure to emissions from cooking has

been characterized systematically. Most of the available studies examined the nature and
amount of emissions produced during different types of cooking in different settings,
including the release of emissions from kitchens into the ambient environment. As the
substances measured varied widely among studies, it is difficult to summarize
quantitatively exposures in different settings. Furthermore, co-exposures were not
specifically mentioned. Results from various field studies, carried out primarily in SouthEast Asia, are summarized in Tables 1.11 and 1.12.
Only one recent study provided information on biological monitoring of exposure and
effect in the occupational setting (Table 1.11) (Pan et al., 2008).
Table 1.11. Occupational exposures to emissions from high-temperature frying

Setting
Study design/
samples
Exposure(s) measured
Main results
Vainiotalo &
Matveinen
(1993),
Finland
8 workplaces
(2 bakeries, a food
factory, 5 restaurant
kitchens)
Field
measurements,
sampling during
frying/grilling of
meat or fish or
during deepfrying
Fat aerosol
Highest concentrations (916 mg/m3) in kitchens using the

ordinary frying method; lower concentrations at other
workplaces (<0.013.2 mg/m3)
Range, 0.010.59 mg/m3
Highest concentrations in grill kitchens (0.24 and 0.75 mg/m3)
Highest concentrations in bakeries (0.67 and 1.5 mg/m3)
Mutagenic heterocyclic amines below detection limits
Low concentrations
Svendsen et
al. (2002),
Norway
4 hotels, 2
hamburger chain
restaurants, 10 la
carte restaurants
and 3 small local
restaurants, serving
mostly fried food
Personal
sampling in
kitchens
Fat aerosols
He et al.
(2004b),
Shen Zhen,
China
2 cooking styles of
Chinese cuisine:
Hunan cooking
and Cantonese
cooking
Sampling of
cooking fumes
during regular
operation
PM, organic compounds
Acrolein
Formaldehyde
Acetaldehyde
Heterocyclic amines
PAHs
Aldehydes
Highest concentration (6.6 mg/m3) in a small local restaurant;

arithmetic mean for all kitchens, 0.62 mg/m3
Highest level of the sum of the aldehydes, 186 g/m3;
arithmetic mean, 69 g/m3
More than half of the PM2.5 mass is due to organic

compounds, and over 90 species of organic compound were
identified and quantified, accounting for 26.1% of bulk
organic particle mass and 20.7% of PM2.5. Fatty acids, diacids
and steroids were the major organic compounds emitted from
both styles of cooking. Of the quantified organic mass, over
90% was fatty acids. The mass of organic species, and the
molecular distribution of n-alkanes and PAHs indicated the
dissimilarities between the two different cooking styles, but
generally the major parts of the organic particulate emissions
of the two restaurants were similar.
Reference,
location
327
328
Table 1.11. (contd)

Setting
Study design/
samples
Main results
He et al.
(2004b),
Beijing,
China
2 commercial
restaurants, 1 with
Chinese foods
cooked over gas
flame, 1 Uigur
style (mutton
charbroiled by
charcoal)
Sampling during
regular operation
PM2.5, organic
compounds including
series of alkanes, nalkanoic acids, nalkanals, alkan-2-ones
and PAHs
Mass concentrations of fine particles, alkanes, n-alkanoic

acids and PAHs in air emitted from the Uigur [Chinese
Islamic] style cooking were a hundred times higher than
ambient PM2.5 in Beijing.
Lee & Jeong

(2008),
South Korea
3 types of
restaurants: Korean
barbecue house,
Chinese restaurant,
Japanese restaurant
Personal
exposure
measurements in
the breathing
zone during
eating periods
PM [PM10, PM2.5 and

PM1.0]
Highest concentrations at Korean barbecue house, with

average concentrations of PM10, PM2.5 and PM1.0 of 169, 124,
and 63 g/m3, respectively; average exposure ratios for
PM1.0/PM10, PM2.5/PM10 and PM1.0/PM2.5 at the barbecue
house were 0.38, 0.73 and 0.52, respectively, which were
much higher than those at other restaurants. Second highest
PM2.5 and PM10 concentrations at Chinese restaurant
Range, 89.7345.9 g/m3; highest concentrations in the
Japanese restaurant
Formaldehyde
Pan et al.
(2008),
Taiwan,
China
23 Chinese
restaurants
Cross-sectional
study;
measurements in
kitchens and
dining areas
Airborne PM and PAHs

Urinary 1hydroxypyrene (1-OHP)
Urinary 8-hydroxy-2'deoxyguanosine (8OHdG)
Airborne PM and PAH levels in kitchens significantly

exceeded those in dining areas.
Geometric mean: kitchen staff, 4.5 g/g creatinine; service
staff, 2.7 g/g creatinine (significantly higher)
Geometric mean: kitchen staff, 7.9 g/g creatinine; service
staff , 5.4 g/g creatinine (significantly higher)
Urinary 1-OHP level, work in kitchens, gender and work
hours per day were four significant predictors of urinary 8OHdG levels after adjustments for covariates.
Reference,
location
Table 1.11. (contd)

Reference,
location
Setting
Study design/
samples
Main results
Yeung & To
(2008),
Hong Kong,
China
Commercial
cooking settings
Survey during
commercial
cooking
processes
Size distributions of the

aerosols
Log normal distribution; mode diameter of aerosols increased

with increasing cooking temperature, especially in the size
range between 0.1 and 1.0 m.
PAH, polycyclic aromatic hydrocarbon; PM, particulate matter
329
Setting
Study design/
samples
Main results
To et al.
(2007),
Hong Kong,
China
Commercial kitchens of
Chinese restaurants,
western restaurants and
food servicing areas
Territorial-wide
survey on the
quantification of
cooking fumes
discharged from
commercial
kitchens
Organic compounds (nalkanes, PAHs, fatty acids

and aromatic amines)
Wide spectrum of organic compounds including nalkanes, PAHs, fatty acids and aromatic amines
PAHs: no statistically significant difference in the
composition of fumes between restaurants;
n-alkanes: mean concentrations in fumes from exotic
food servicing areas significantly higher than those
for Chinese or western restaurants (p<0.05)
Samples from
kitchen exhausts
trans,trans-2,4-decadienal
(t,t-2,4-DDE)
Emission factor (g/customer): barbecue, 1990 >

Chinese, 570 > Western, 63.8.
Yang et al.
16 restaurants with 3
(2007),
types of cooking:
Taiwan, China Chinese, western and
barbecue
Reference,
location
330
Table 1.12. Environmental exposure to cooking emissions from commercial restaurants
Table 1.12. (contd)

Setting
Study design/
samples
Main results
Zhao et al.
(2007a),
Guang Zhou,
China
1 commercial westernstyle fast food

restaurant
Sampling from
exhaust
Chemical composition of
particulate organic matter
(POM)
The total amount of quantified compounds of per mg

POM in western-style fast food cooking is much
higher than that in Chinese cooking. The predominant
homologue is fatty acids, accounting for 78% of total
quantified POM, with the predominant one being
palmitic acid. Dicarboxylic acids display the second
highest concentration in the quantified homologues
with hexanedioic acid being predominant, followed
by nonanedioic acid. C-max of n-alkanes occurs at
C25, but they still appear at relatively higher
concentrations at C29 and C31. The relationship of
concentrations of unsaturated fatty acids (C16 and
C18) with a double bond at C9 position and C9 acids
indicates the reduction of the unsaturated fatty acids
in the emissions could form the C9 acids. Moreover,
the non-linear fit indicates that other C9 species or
other compounds are also produced, except for the C9
acids. The potential candidates of tracers for the
emissions from western-style fast food cooking could
be: tetradecanoic acid, hexadecanoic acid,
octadecanoic acid, 9-octadecenoic acid, nonanal,
lactones, levoglucosan, hexanedioic acid and
nonanedioic acid.
Reference,
location
331
332
Table 1.12. (contd)

Reference,
location
Setting
Study design/
samples
Zhao et al.
(2007b),
Guang Zhou,
China
Sampling from
4 Chinese restaurants:
Cantonese style, Hunan exhaust
style, Sichuan style and
Dongbei style
Main results
Chemical composition of
POM in PM2.5
The quantified compounds account for 510% of total

POM in PM2.5. The dominant homologue is fatty
acids, constituting 7385% of the quantified
compounds. The emissions of different compounds
are impacted significantly by the cooking ingredients.
The candidates of organic tracers used to describe and
distinguish emissions from Chinese cooking in
Guangzhou are tetradecanoic acid, hexadecanoic acid,
octadecanoic acid, oleic acid, levoglucosan,
mannosan, galactosan, nonanal and lactones.
1.5
333
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2. Studies of Cancer in Humans

2.1
Introduction
Since the 1970s, a total of 17 casecontrol studies have explored the relationship
between exposure to cooking fumes and the risk for lung cancer. These studies were
conducted in Chinese populations residing in China (including Taiwan and Hong Kong
Special Administrative Region) and Singapore. While active tobacco smoking is a wellestablished major cause of lung cancer in Chinese men and women, a relatively high
proportion of lung cancer in Chinese women, many of whom are nonsmokers, can not be
explained by active smoking. Thus, one motivation for these studies was to investigate the
role of other lifestyle factors, including indoor air pollution from cooking oil fumes, in the
etiology of lung cancer in Chinese women.
Exposure assessment of cooking practices and cooking oil fumes varied substantially
(Tables 2.1 and 2.2). Two aspects related to cooking oil fumes have been investigated: (i)
the types of oil used and practices of high-temperature cooking, including frequency, stirfrying, deep-frying and pan-frying, and (ii) cooking practices, including the availability of
a separate kitchen, ventilation in the kitchen based on the number and size of windows,
the use of a fume extractor, personal assessment of ventilation, such as frequency of eye
irritation during cooking and smokiness in the kitchen, duration of exposure (years of
cooking) and susceptible time of exposure (age started to cook). In four studies (Lan et
al., 1993; Dai et al., 1996; Shen et al., 1996; Wang et al., 1996), results were based on a
single variable that represented some aspect of cooking practices. In contrast, exposure
assessment was more comprehensive in seven studies (Gao et al., 1987; Ko et al., 1997;
Zhong et al., 1999; Ko et al., 2000; Lee et al., 2001; Metayer et al., 2002; Yu et al.,
2006). In several studies, the authors specified that past cooking practices or those
experienced earlier in life (Seow et al., 2000) or at a particular age or time period in life
(Ko et al., 1997, 2000; Lee et al., 2001) were investigated. Behaviours related to the type
of cooking oil used most often and the frequency of high-temperature cooking (stirfrying, pan-frying, deep-frying) were also frequently examined. However, in most of the
studies, no discussion was included regarding the timing of exposure or whether the
information collected was related to current, usual or past cooking practices. Other factors
included frequency of eye irritation during cooking, frequency of smokiness in the house,
location of the kitchen, windows in the kitchen and the presence of fume extractors; these
are viewed as indirect measures to assess the severity of exposure to cooking fumes and
general household ventilation. Greater attention was paid to the measures of exposure that
were considered to be more objective and whether duration, frequency and intensity of
exposure to cooking oil fumes were assessed.
Of the 17 casecontrol studies that have investigated the relationship of exposure to
cooking oil fumes and lung cancer, one was a study of lung cancer mortality (Lei et al.,
338
Table 2.1. Assessment of cooking practices/fumes included in the published casecontrol studies of lung cancer
Cooking in
separate
kitchen
Windows in
kitchen/size
Fumes visible
Smokiness in
kitchen
Eye
irritation
No. of meals
cooked/day
Age started
cooking
Years of cooking
MacLennan et al.
(1977)
No/yes (cooking)
Gao et al. (1987)
Never to
frequent
Xu et al. (1989)
Cooking in
bedroom (yrs)
Wu-Williams et al.
(1990)
Never to
frequent
Liu et al. (1991)
10 vs. >15 yrs
30, 3144, 45
Ger et al. (1993)
Ventilation
(no/yes)
01, 2, 3
Lan et al. (1993)
Liu et al. (1993)
No/yes
Size; chimneys
Dai et al. (1996)
Koo et al. (1996)
<25, 2640, 41
Lei et al. (1996)
Size kitchen
Infrequent, 20,
2040, >40
Shen et al. (1996)
No/yes
Times/week
(no results)
Wang et al. (1996)
No/yes
Ko et al. (1997)
Fume extractor
(no/yes)
720 vs. 21 yrs
Zhong et al. (1999)
No/yes
Area of
window
No/yes
None to
considerable
Never to
frequent
Reference
Table 2.1. (contd)

Reference
Cooking in
separate
kitchen
Windows in
kitchen/size
Fumes visible
Smokiness in
kitchen
Eye
irritation
No. of meals
cooked/day
Ko et al. (2000)
<2 vs. 2, size

of opening:
small or
medium, large
Fume extractor
Ventilation
Poor/good
Rarely vs.
frequently
Daily (no/yes) 20 vs. 20 yrs

meals (1, 2, 3)
120, 2140, 40
Seow et al. (2000)
<Daily/daily
Zhou et al. (2000)
(location)
Separate
Living room,
Bedroom
Medium/heavy
vs slight
None, slight,
medium, heavy
Never to
frequent
Age started
cooking
Years of cooking
Fume extractor
20 vs. 20 yrs
Metayer et al. (2002)
No to
considerable by
oil type
Ever to
frequent by
oil type
2 vs. 3
13, 1416, 17
yrs
29, 3039,
4049, 50
Chan-Yeung et al.
(2003)
Shi et al. (2005)
Fuel smoke,
cooking oil
smoke
Yu et al. (2006)
Fume extractor/
exhaust fan
Lee et al. (2001)
339
340
Table 2.2. Assessment of cooking practices/fumes by type of oil, type of frying and type of fuel included in the
published casecontrol studies of lung cancer
Rapeseed oil
Other type of
oil
Amount of
oil
No. of times
stir-frying
No. of times
deep-frying
No. of times
pan-frying
No. of
times
boiling
Fuel for
cooking
Fuel for
heating
MacLennan et al.
(1977)
Gas
Kerosene
Gao et al. (1987)
Never to
frequent
Never to
frequent
2030/wk
03/wk
312/wk Coal/gas/
wood
Xu et al. (1989)
Gas
Coal
Wu-Williams et al.
(1990)
03/mo
Coal
Coal
Liu et al. (1991)
Coal
Wood
Ger et al. (1993)
No/yes
No/yes
No/yes
No/yes
Coal
Lan et al. (1993)
Never vs.
often
Coal
Liu et al. (1993)
Coal/gas/
wood
Dai et al. (1996)
5 vs.
5/mo*
5 vs. 5/mo*
Coal
Kerosene
Koo & Ho (1996)
Gas
Kerosene
Lei et al. (1996)
Preferred/
average/not
preferred
Shen et al. (1996)
Use per mo
(no results)
Solid/non- Coal
solid fuel
Wang et al. (1996)
Reference
Table 2.2. (contd)

Rapeseed oil
Other type of
oil
Amount of
oil
No. of times
stir-frying
Ko et al. (1997)
No/lard/
vegetable oil
Zhong et al. (1999)
Used
frequently
Ko et al. (2000)
Seow et al. (2000)
No. of times
deep-frying
No. of times
pan-frying
No. of
times
boiling
Fuel for
cooking
Fuel for
heating
04 vs. 5/wk 04 vs.

5/wk
04 vs. 5/mo
Gas/coal/
wood
Soya bean
used frequently
<7, 7, >7/wk
1 vs. >1/wk
1 vs. >1/wk
Coal/coal
gas/gas
No/yes after
fumes, fume
extractor
No/yes after
fumes, fume
extractor
No/yes after
fumes, fume
extractor
Coal
Gas
Unsaturated
vs. saturated
oil
Not daily vs.

daily
Zhou et al. (2000)
01 vs. 2/wk
Lee et al. (2001)
Lard/vegetable
oil
No/yes after
fumes, fume
extractor
No/yes after
fumes, fume
extractor
No/yes after
fumes, fume
extractor
Gas/coal/
wood
Metayer et al.
(2002)
No/yes
Linseed/
perilla/
hempseed oil
Catty/mo
36
153/mo
13/mo
Coal/wood
Chan-Yeung et al.
(2003)
No exposure
<3.5/wk
3.57/wk
>7/wk
Yu et al. (2006)
Never/seldom, Peanut/corn oil

sometimes,
always
50 dishyears
51100
101150
151200
>200
50
51100
101150
151200
>200
50
51100
101150
151200
>200
341
deep-frying and pan-frying combined
Reference
342
1996); the other studies included six population-based (Gao et al., 1987; Xu et al., 1989;
Wu-Williams et al., 1990; Lan et al.., 1993; Zhong et al., 1999; Metayer et al., 2002) and
10 hospital-/clinic-based studies of incident lung cancers (Ger et al., 1993; Dai et al.,
1996; Shen et al., 1996; Wang et al., 1996; Ko et al., 1997, 2000; Seow et al., 2000; Zhou
et al., 2000; Lee et al., 2001; Yu et al., 2006). Twelve studies included only women (Gao
et al., 1987, Wu-Williams et al., 1990; Lan et al., 1993; Dai et al., 1996; Wang et al.,
1996; Ko et al., 1997; Zhong et al., 1999; Ko et al., 2000; Seow et al., 2000; Zhou et al.,
2000; Metayer et al., 2002; Yu et al., 2006), seven of which studied only nonsmokers
(Lan et al., 1993; Dai et al., 1996; Wang et al., 1996; Ko et al., 1997; Zhong et al., 1999;
Ko et al., 2000; Yu et al., 2006). Men and women, smokers and nonsmokers were
included in the other five studies (Xu et al., 1989; Ger et al., 1993; Lei et al., 1996; Shen
et al., 1996, Lee et al., 2001).
These studies used heterogeneous methodologies and included different sources of
cases, types of controls, methods of data collection and use of surrogate respondents; the
degree of pathological confirmation of lung cancer diagnoses also differed. Relevant
information regarding each of the casecontrol studies (i.e. study population, study
period, sources of cases and controls, number of cases and controls, response rate, number
of proxy interviews, percentage of pathologically/cytologically confirmed cases) and
selected results are shown in Table 2.3.
2.2
Casecontrol studies
2.2.1
Northern China
Two large population-based casecontrol studies carried out in industrial areas in

northern China during the late 1980s provided information on cooking practices and the
risk for lung cancer. The main objectives of these two studies were to examine the role of
active and passive smoking, and pollution from industrial and domestic sources. Xu et al.
(1989) studied men and women who had lung cancer in Shenyang while Wu-Williams et
al. (1990) examined the pattern of risk for lung cancer among women in Harbin and
Shenyang.
The study in Shenyang included 1249 lung cancer cases (729 men, 520 women) and
1345 population-based controls (788 men, 557 women); 86% of male cases and 70% of
male controls were smokers; the corresponding figures in women were 55% of cases and
35% of controls (Xu et al., 1989). Nearly 80% (85.1% in men, 75.0% in women) of the
lung cancers were pathologically/cytologically confirmed; 31% of these were
adenocarcinoma of the lung. After adjusting for age, education and active smoking, the
risk for lung cancer was higher when cooking took place in the bedroom or entry corridor
to the bedroom than in a separate kitchen or elsewhere in the house. In men, the adjusted
odds ratios were 1.0, 1.2 and 2.1 in relation to cooking in the bedroom for 0, 129 and
30 years, respectively (p trend <0.05); the corresponding adjusted odds ratios in women
were 1.0, 1.5 and 1.8 (p trend <0.05).
Table 2.3. Casecontrol studies of cooking practices/fumes and lung cancer in China
Characteristics
of controls
Data collection,
response rate
Exposure categories
Gao et al.
(1987),
Shanghai,
198486
735 frequencymatched by age

and selected
from the general
population of
Shanghai; 130
smokers
Response rate:
cases, 672/765
(88.0%);
controls,
735/802
(91.3%)
Oil used
Soya bean
Rapeseed
Stir-frying (dishes/week)
20
2024
2529
30
Deep-frying
(dishes/week)
0
1
2
3
Boiling (dishes/week)
3
47
811
12
Eye irritation/
smokiness
Never/none
Never/considerable
Frequent/none
Frequent/considerable
672 women; 81% HC;

61% ADC; 22% SqCC;
6% SCLC; 11% other;
236 smokers; aged 35
69 years permanent
residents of the area,
Shanghai Cancer
Registry
ICD-9 (162)
No. of
cases
Relative risk
(95% CI)
269
322
1.0
1.4 (1.11.8)
336
198
48
34
1.0
1.2 (0.91.5)
1.2 (0.81.9)
2.6 (1.35.0)
502
85
21
8
1.0
1.5 (1.02.1)
1.6 (0.83.2)
1.9 (0.56.8)
96
390
63
67
1.0
1.0 (0.71.3)
1.8 (1.13.0)
2.2 (1.33.7)
244
55
212
109
1.0
1.6 (1.02.5)
1.6 (1.22.1)
2.6 (1.83.7)
Adjustment
factors
Comments
(covariates
considered)
Age, education, Study

population and
smoking
exposure
indices defined
clearly; use of
coal/gas was
unrelated to
risk
Reference,
Characteristics of
study location, cases, histological
period
confirmation (HC),
cell type (%)
343
344
Table 2.3. (contd)

Characteristics of
Reference,
period
confirmation (HC),
cell type (%)
Wu-Williams
et al. (1990),
Shenyang,
198587
Data collection,
response rate
Exposure categories
No. of
cases
1249 (729 men, 520

women); 79% HC;
31% ADC; 43% SqCC;
16% SCLC; 10%
other; 86% men and
55% women smoked;
aged 3069 yrs; newly
diagnosed with
primary lung cancer;
Shenyang Cancer
Registry
ICD-9 (162)
1345 (788 men,

557 women)
population
controls,
frequencymatched on age
and sex; 70%
men and 35%
women smoked
Response rate:
cases,
1249/1318
(94.8%);
controls, 100%
Cooking in bedroom
0 year
129 yrs
30 yrs
p for trend
Men
570
75
84
965 women (520 from

Shenyang, 445 from
Harbin); 74% HC; 44%
ADC; 28% SqCC; 16%
SCLC; 12% other; 545
smokers (56.7%); aged
3069 years; Shenyang
Cancer Registry; 729
men from Shenyang
959 female (555

from Shenyang,
404 from
Harbin)
population
controls,
frequencymatched by age;
357 smokers
(37.2%); 788
male controls
from Shenyang
Response rate:
cases, 962/1049
(92.7%);
controls, 100%
0 year
129 yrs
30 yrs
p for trend
Deep-frying
(times/month)
0
1
2
3
Eye irritation
Never/rarely
Occasionally
Frequently
Burning kangs
0
120
21+
Women
503
25
29
Relative risk
(95% CI)
Adjustment
factors
1.0
1.2
2.1
<0.05
Age, education, CIs not

smoking
reported; coal
use was not
adjusted for in
the analysis
1.0
1.5
1.8
<0.05
324
326
170
121
1.0
1.2 (1.01.5)
2.1 (1.52.8)
1.9 (1.42.7)
647
218
89
1.0
1.6 (1.21.8)
1.8 (1.32.6)
677
106
173
1.0
1.2 (0.91.7)
1.5 (1.12.0)
Age, education,
smoking, study
area
Comments
(covariates
considered)
Xu et al.
(1989),
Shenyang,
198587
Characteristics
of controls
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Ger et al.
(1993), Taipei,
Taiwan,
199091
524 (262 hospital,

262
neighbourhood)
matched to cases
on age, sex,
insurance status/
residence; 229
nonsmokers (111
hospital controls,
118
neighbourhood
controls)
In-person
interview;
response rate:
cases, 131/143
(92%); hospital
controls, 88%;
neighbourhood
controls, 83%
ADC
Frying
No
Yes
Stir-frying
No
Yes
Deep-frying
No
Yes
Boiling
No
Yes
SqCC-/SCLC
Frying
No
Yes
Stir-frying
No
Yes
Deep-frying
No
Yes
Boiling
No
Yes
131 hospital patients

(92 men, 39 women);
100% HC; 50% ADC;
27% SqCC; 14%
SCLC; 48 nonsmokers
No. of
cases
Relative risk
(95% CI)
46
26
1.0
0.71 (0.361.39)
28
44
1.0
1.19 (0.582.44)
63
9
1.0
0.63 (0.261.55)
38
34
1.0
1.75 (0.993.12)
44
15
1.0
0.93 (0.372.32)
33
26
1.0
1.00 (0.472.14)
51
8
1.0
1.22 (0.423.52)
36
23
1.00
1.26 (0.612.60)
Adjustment
factors
Comments
(covariates
considered)
Results shown
were based on
neighbourhood controls.
Matched
analysis:
variables
included were
not specified.
Definition of
cooking
practices was
not presented.
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
345
346
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Lan et al.
(1993), Xuan
Wei County,
198890
139 female farmers;

39.6% HC; 49.1%
ADC; 36.4% SqCC;
14.6% NOS with
all nonsmokers
139 female
farmers from the
general
population
matched 2
years; all
nonsmokers
In-person
interview;
response rate
not reported
Rapeseed oil
Never
Occasional
Often
Dai et al.
(1996),
Harbin,
199293
120 women with

100% HC; 100% ADC;
aged 3069 years;
Harbin resident at least
10 years; all
nonsmokers
120 population
1:1 matched by
age (5 yrs); all
nonsmokers
In-person
Pan-fried and deepinterview in the fried
hospital or at
5 times/month
home; response
>5 times/month
rate not reported
No. of
cases
Relative risk
(95% CI)
24
106
9
Age, length of
1.00
menstrual cycle,
1.26 (0.682.63) menopause age,
4.58 (0.5637.08) family history
of lung cancer
1.0
9.20 (1.5355.3)
p=0.152
Adjustment
factors
Income, area of
resident, years
of coal use in
bedroom, years
of coal heating,
exposure to
coal, intake of
carrot, family
history of
cancer
Comments
(covariates
considered)
Coal use was

not adjusted
for in the
analysis.
Definition of
occasional use
was not
provided.
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
No. of
cases
Lei et al.
(1996),
Guangzhou,
1986
792 (563 men,

229 women); 1:1
matched on sex,
age ( 5 years),
year of death,
block of
residence; no
history of
respiratory
disease; 422
smokers (361
men, 61 women)
In-person
interview with
next of kin;
response rate,
792/831
(95.3%); home
interviews with
spouses or
relatives
Men
Kitchen space
<1
12
2
Cooking activity
Infrequent
20 yrs
2040 yrs
>40 yrs
Cooking frying
Preferred
Average
Not preferred
Women
Kitchen space
<1
12
2
Cooking activity
Infrequent
20 yrs
2040 yrs
>40 yrs
Cooking frying
Preferred
Average
Not preferred
Deaths
792 (563 men, 229

women) who died from
lung cancer; 0% HC;
no information on cell
type; 566 smokers (443
men, 123 women)
Relative risk
(95% CI)
18
66
431
1.0
[0.70]
[0.78]
339
83
79
30
1.0
[0.92]
[1.10]
[1.00]
192
177
177
1.0
[0.72]
[0.89]
6
28
179
1.0
[1.20]
[1.82]
29
28
83
62
1.0
[0.72]
[0.88]
[0.75]
55
93
77
1.0
[0.88]
[1.06]
Adjustment
factors
Comments
(covariates
considered)
Crude analysis
was presented;
odds ratios
were
calculated
based on the
data presented.
Definition of
frying was not
provided.
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
347
348
Table 2.3. (contd)

Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
Exposure categories
No. of
cases
Relative risk
(95% CI)
Lin et al.
122 cases of
(1996), Harbin adenocarcinoma;
City
nonsmokers aged 30
69 years
122 matched
controls by
gender and age;
non-smokers
>3 times per month

frying
NR
3.00 (1.356.69)
Age adjusted
Shen et al.
(1996),
Nanjing,
198693
263 (men and women); 263 general

100% HC; 20 years
population;
old
healthy residents
of Nanjing,
matched on age
(5 years), sex,
neighbourhood
In-person
interview;
response rate
not reported
Cooking fumes
SqCC
No
Yes
Active
smoking,
chronic
1.0
3.81 (1.0613.73) bronchitis,
family history
of cancer, coal
1.0
stove for
2.99 (1.685.34) heating, fuel
index.
Many
limitations in
the study
methodsno
information on
gender,
smoking or
other factors
135 newly diagnosed

cases of lung cancer;
57% HC; 100% HC;
54.5% ADC; 20%
SCLC; 16.4% SqCC;
9.1% other; aged 35
69 years; all
nonsmokers;
ICD-9 (162)
In person
interview;
response rate
not reported
135 general
population
matched on age
(5 years), sex,
lifetime
nonsmoking
status
ADC
No
Yes
Exposed to cooking
fumes
No
Yes
Yes (adjusted)*
77
Adjustment
factors
* All study
variables were
considered in
1.0
3.79 (2.296.27) multivariate
4.02 (2.386.78)* analysis, but
results on
cooking fumes
were adjusted
for coal smoke
during cooking
Comments
(covariates
considered)
Data collection,
response rate
Wang et al.
(1996),
Shenyang,
199294
Characteristics
of controls
Table 2.3. (contd)

Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
117 female cases with
64.8% ADC; 17.1%
SqCC; 15.2% SCLC;
2.9% LCC; 106
nonsmokers included
in analysis
ICD-9 (162)
Data collection,
response rate
Exposure categories
117 hospital
controls matched
on age (2
years), date of
interview,
nonsmokingrelated disease
Personal
interviews;
response rate:
cases, 117/128
(91.4%);
controls,
117/125
(93.6%)
Use of fume extractor

Stir-frying
04/week
5/week
Pan-frying
04/week
5/week
Deep-frying
04/month
5/month
Age when first cooking
21 yrs
720 yrs
Before 20 yrs of age
Yes
No
At 2040 yrs of age
Yes
No
No (adjusted)*
After 40 yrs of age
Yes
No
No. of
cases
Relative risk
(95% CI)
14
91
1.0
2.4 (1.15.2)
29
76
1.0
2.3 (1.24.6)
82
23
1.0
0.9 (0.51.9)
36
67
1.0
1.6 (0.83.0)
7
60
1.0
5.3 (1.125.6)
25
78
1.0
6.4 (2.914.1)
8.3 (3.122.7)*
76
22
1.0
2.3 (1.15.1)
Adjustment
factors
Comments
(covariates
considered)
Social class,
residential area,
and education
were adjusted
in all analysis.
*Additional
adjustment for
tuberculosis,
cooking fuels,
living near
industrial
district
Coal use not

significant
Wood/charcoal
use was
significant
40 yrs
Cooking fuel
use was only
adjusted for in
selected
analysis.
Ko et al.
(1997),
Kaohsiung,
Taiwan,
199293
Characteristics
of controls
349
350
Table 2.3. (contd)

Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
Data collection,
response rate
Exposure categories
Cooking oils
No cooking
Lard
Vegetable oil
At 2040 yrs of age
No cooking
Lard
Vegetable oil
After 40 yrs of age
No cooking
Lard
Vegetable oil
No. of
cases
Relative risk
(95% CI)
38
51
16
1.0
1.6 (0.83.1)
2.0 (0.84.8)
2
38
65
1.0
1.4 (0.82.6)
2
7
91
1.0
0.5 (0.12.2)
Adjustment
factors
Comments
(covariates
considered)
Ko et al.
(1997) (contd)
Characteristics
of controls
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Zhong et al.
(1999),
Shanghai,
199294
601 nonsmoking
general
population
frequencymatched to age
distribution by
5-year age
intervals; 74
smokers
excluded from
analyses
In-person
interview at
hospital, home
or work;
response rate:
cases, 649/706
(91.9%) (for
smokers and
nonsmokers);
controls, 84%
High-temperature
cooking
No
Yes
Most frequently used oil
Soya bean oil
Rapeseed oil
Both oils
Stir-frying (no./week)
<7
7
>7
Pan-frying (no./week)
1
>1
Deep-frying (no./week)
1
>1
Smokiness in kitchen
None
Somewhat
Considerable
Eye irritation
Never
Rarely
Occasionally
Frequently
504 nonsmoking
women ~77% HC;
76.5% ADC; 12.4%
SqCC; 1.8% SCLC;
0.3% LCC; 9.0%
mixed cells; aged 35
69 years; permanent
residents of the area;
Shanghai, China
Cancer Registry; 145
smokers excluded from
analysis
No. of
cases
Relative risk
(95% CI)
339
165
1.0
1.64 (1.242.17)
444
49
11
1.0
1.84 (1.123.02)
0.92 (0.372.28)
40
434
30
1.0
0.38 (0.190.75)
2.33 (0.687.95)
464
40
1.0
2.09 (1.143.84)
469
35
1.0
1.88 (1.063.32)
177
241
86
1.0
1.67 (1.252.21)
2.38 (1.583.57)
338
49
74
43
1.0
1.49 (0.912.43)
1.75 (1.162.62)
1.68 (1.022.78)
Adjustment
factors
Age, education,
income, intake
of vitamin C,
respondent
status, exposure
to passive
smoking,
family history
of lung cancer,
employment in
high-risk
occupation
Comments
(covariates
considered)
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
351
352
Table 2.3. (contd)

Characteristics of
Reference,
period
confirmation (HC),
cell type (%)
131 women with
primary carcinoma of
the lung; 100% HC;
19.8% SqCC; 62.6%
ADC; 13.7% SCLC;
2.3% LCC; 1.5% NOS;
>40 years of age;
nonsmokers
ICD-9 (162)
Data collection,
response rate
Exposure categories
252 hospital eye

or orthopaedic
patients, or in for
check-ups
(diseases
unrelated to
smoking); 262
community, agematched
randomly
selected from a
computerized
population
database.;
matched for age
and date of
interview;
nonsmokers
Personal
interviews;
response rate:
cases, 131/148
(88.5%);
hospital
controls,
252/281
(89.7%);
community
controls,
262/294
(89.1%)
Daily cooking
No
Yes
Age cooking started
>20 yrs
20 yrs
Yrs cooking at home
120
2140
40
Meals cooked/day
1
2
3
Windows in kitchen
<2
2
Ventilation of kitchen
Poor
Good
No. of
cases
Relative risk
(95% CI)
1
130
1.0
5.9 (0.753.6)
47
83
1.0
1.5 (0.92.4)
36
74
20
1.0
1.3 (0.62.6)
1.0 (0.42.9)
13
71
46
1.0
3.1 (1.66.2)
3.4 (1.67.0)
62
69
1.0
1.3 (0.82.1)
71
60
1.0
0.9 (0.61.4)
Adjustment
factors
Comments
(covariates
considered)
Socio-economic
status,
occupation,
previous lung
disease, passive
smoking
Results shown
are based on
comparison
with
community
controls.
Role patterns
were similar
for hospital
controls
Ko et al.
(2000),
Kaohsiung,
Taiwan,
199396
Characteristics
of controls
Table 2.3. (contd)

Characteristics of
Reference,
confirmation (HC),
period
cell type (%)
Data collection,
response rate
Exposure categories
Eye irritation
Rarely
Frequently
Stir-fry after fumes
emitted
No
Yes
Yes
No
Aged 2040 yrs
Yes
No
Aged >40 yrs
Yes
No
No. of
cases
Relative risk
(95% CI)
84
46
1.0
2.1 (1.33.5)
22
108
1.0
2.4 (1.4 4.2)
40
43
1.0
0.9 (0.42.0)
85
45
1.0
2.2 (1.33.8)
114
12
1.0
1.3 (0.62.8)
Adjustment
factors
Comments
(covariates
considered)
Ko et al.
(2000) (contd)
Characteristics
of controls
353
354
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Seow et al.
(2000),
Singapore,
199698
765 hospital
controls,
frequencymatched for age,
hospital, date of
admission; no
history of cancer,
heart chronic
disease or renal
failure; 100
smokers, 663
nonsmokers
In-person
interview within
3 months of
diagnosis;
response rate:
cases, 361/380
(95.0%);
controls,
765/789
(96.9%)
Smokers
Stir-frying
25
Less than daily
97
Daily
21
Less than daily with
meat
Lifetime nonsmokers
Stir-frying
52
Less than daily
122
Daily
41
meat
Smokers
46
Stir-frying meat less
than daily
Daily with meat
75
23
meat with fume-filled
kitchen
Daily with meat with
52
fume-filled kitchen
Lifetime nonsmokers
Stir-frying meat less
93
than daily
Daily with meat
76
34
meat with fume-filled
kitchen
Daily with meat with
42
fume-filled kitchen
303 women; 100% HC;

54.8% ADC; 18.5%
SqCC; 6.9% SCLC;
15.2% LCC; 4.6%
NOS; aged <90 years;
127 smokers, 176
nonsmokers
No. of
cases
Relative risk
(95% CI)
1.0 ref
2.0 (1.03.8)
1.0 (0.52.4)
1.0 ref
1.0 (0.71.5)
0.9 (0.61.5)
1.0 ref
2.7 (1.35.5)
1.7 (0.73.9)
3.7 (1.87.5)
1.0 ref
0.9 (0.61.4)
1.1 (0.71.7)
1.0 (0.61.4)
Adjustment
factors
Comments
(covariates
considered)
Age ,
birthplace,
family history
of cancer,
intake of fruits
and vegetables.
For smokers,
odds ratios
were
additionally
adjusted for
duration of
smoking (in
years) and
number of
cigarettes
smoked/day.
Current and
ex-smokers
grouped
together
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Zhou et al.
(2000),
Shenyang,
199195
72 general
population, age
1:1 matched
(5 years) to
cases;
23 smokers
In person
interview;
response rate
not reported
Eye irritation from

smoke
Never
Slight
Medium
Heavy
p for trend
Location of kitchen
Separate
In living room
In bedroom
p for trend
Cooking oil fumes
Slight
Medium/heavy
Deep-fried (no./week)
01
2
Extent of smoke when
cooking
None
Slight
Medium
Heavy
p for trend
72 women with
100% HC; 100% ADC;
aged 3569 years;
20 smokers
No. of
cases
6
63
3
30
42
5
67
19
15
35
3
Relative risk
(95% CI)
Adjustment
factors
Comments
(covariates
considered)
Multivariate
odds ratio
1.0
1.58 (0.624.03)
11.45 (3.1042.4)
3.41 (0.5222.5)
0.002
Crude odds ratio
1.00
1.40 (0.414.88)
1.00 (0.118.93)
0.83
Income, family
history of lung
cancer, number
of live births
Fuel use for

cooking/
heating was
not considered
in the analysis.
1.0
4.53 (2.099.94)
1.0
1.68 (0.456.84)
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
1.0
0.73 (0.281.90)
2.71 (1.096.80)
1.32 (0.189.50)
0.027
355
356
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Lee et al.
(2001),
Kaohsiung,
Taiwan,
199399
407 hospital
patients;
matched to cases
on sex, age
(2 years);
~2 controls per
case; smoking in
female controls
not reported
In-person
interview;
response rate
(presented for
men and women
combined):
cases, 527/574
(91.8%);
controls,
805/883
(91.2%)
Kitchen with fume

extractor
Yes
No
Cooking oils
Lard
Vegetable oil
Age first cooked (yrs)
>20
20
Stir-frying after fumes
No
Yes
Pan-frying after fumes
No
Yes
Deep-frying after fumes
No
Yes
236 male, 291 female;

only women with
ADC, SqCC and SCLC
retained for this
analysis; 100% HC;
55.7% ADC; 20.3%
SqCC; 8.6% SCLC;
2.1% LCC; 5.5% BA;
7.9% NOS; aged 18
83 years
No. of
cases
Relative risk
(95% CI)
Adjustment
factors
Comments
(covariates
considered)
SqCC/SCLC
Residence area
(urban,
suburban,
rural),
educational
levels, socioeconomic status
(high, medium
low), smoking
(cumulative
packyears)
Wood/charcoal
use was a
significant risk
factor; this was
not adjusted
for in the
analysis.
51
31
1.0
3.0 (1.37.1)
28
54
1.0
0.7 (0.31.4)
27
55
1.0
1.5 (0.73.1)
23
59
1.0
0.9 (0.41.9)
24
58
1.0
0.8 (0.41.5)
44
38
1.0
1.0 (0.52.0)
Characteristics of
Reference,
period
confirmation (HC),
cell type (%)
Table 2.3. (contd)

Reference,
Characteristics of
confirmation (HC),
period
cell type (%)
Characteristics
of controls
Lee et al.
(2001) (contd)
Exposure categories
No. of
cases
Kitchen with fume

extractor
Yes
84
No
74
Cooking oils
Lard
50
Vegetable oil
108
Age first cooked (yrs)
>20
65
20
93
Stir-frying after fumes
No
29
Yes
29
Pan-frying after fumes
No
20
Yes
138
Deep-frying after fumes
68
No
90
Yes
233 women; 37% HC;
cell type distribution
not presented; aged
3075 years; 27
smokers
Type of oil (ever use)

In-person
Linseed
interview;
Rapeseed
response rate:
Rapeseed + linseed
cases, 233/238
(98%); controls, Perilla + hempseed
459/509 (90%) Stir-fying (times/month)
<15
1529
30
31
p for trend
Adjustment
factors
Comments
(covariates
considered)
ADC
1.0
3.9 (2.36.6)
1.0
1.2 (0.71.9)
1.0
1.1 (0.71.7)
1.0
2.0 (1.23.3)
1.0
2.6 (1.54.5)
1.0
1.6 (1.02.6)
80
53
90
5
1.0
1.65 (0.83.2)
1.70 (1.02.8)
3.25 (0.814.0)
71
60
52
45
1.0
1.96 (1.13.5)
1.73 (1.03.1)
2.24 (1.14.5)
<0.05
Age, Prefecture,
socio-economic
factors,
respondent
type.
357
459 randomly
selected from
1990 population
census list of
study areas;
frequencymatched by age
( 5 years),
Prefecture; 47
smokers
Relative risk
(95% CI)
Metayer et al.
(2002), Gansu
Province,
199498
Data collection,
response rate
358
Table 2.3. (contd)

Reference,
Characteristics of
confirmation (HC),
period
cell type (%)
Metayer et al.
(2002) (contd)
Characteristics
of controls
Data collection,
response rate
Exposure categories
Relative risk
(95% CI)
70
86
38
1.0
0.82 (0.51.3)
0.83 (0.51.5)
52
76
65
29
1.00
1.26 (0.62.8)
2.51 (0.96.8)
2.46 (0.87.9)
63
85
80
1.0
0.69 (0.41.1)
0.69 (0.41.2)
193
36
1.0
1.36 (0.82.4)
72
100
54
1.0
1.37 (0.82.2)
2.82 (1.65.0)
<0.01
49
155
23
1.0
0.90 (0.61.5)
0.76 (0.41.6)
Adjustment
factors
Comments
(covariates
considered)
Deep-frying
(times/month)
Never/<1
12
3
Years of cooking
29
3039
4049
50
Age started cooking (yrs)
13
1416
17
No. of meals cooked/day
2
3
Eyethroat irritation
Never
Occasionally/seldom
Frequently
p for trend
Home smokiness
No
Some/little
Considerable
No. of
cases
Table 2.3. (contd)

Characteristics
of controls
Data collection,
response rate
Exposure categories
Chan-Yeung
et al. (2003),
Hong Kong,
19992001
331 in- and outpatients without

cancer; matched
for age, sex
Personal
interviews for
cases and
controls;
response rates
not given
Frying foods
Men
No or <2 yrs
<3.5 yrs
3.57 yrs
>7 yrs
Women
No or <2 yrs
<3.5 yrs
3.57 yrs
>7 yrs
Shi et al
(2005),
Shenyang,
20002002
331 histologically or
cytologically proven
cases of lung cancer
618 newly diagnosed

female patients with
primary lung cancer
Randomly
Face-to-face
selected from the interviews
general
population in
urban districts
Cooking oil smoke
No. of
cases
Relative risk
(95% CI)
146
27
22
13
1.0
0.69 (0.321.49)
0.83 (0.381.80)
1.22 (0.383.99)
34
37
27
21
1.0
1.08 (0.502.32)
1.05 (0.462.42)
1.54 (0.574.13)
4.11 (2.147.89)
Adjustment
factors
Comments
(covariates
considered)
Place of birth,
educational
status, family
history of lung
cancer,
smoking (in
men);
educational
status, smoking
status (in
women)
In multivariate
analysis
cooking oil
smoke
remained
statistically
significant but
fuel smoke did
not remain
significant
Reference,
Characteristics of
period
confirmation (HC),
cell type (%)
359
360
Table 2.3. (contd)

Reference,
Characteristics of
confirmation (HC),
period
cell type (%)
291 women newly
diagnosed with
primary carcinomas;
96% participation rate;
68.5% ADC; aged 30
79 yrs; 67 smokers
Data collection,
response rate
Exposure categories
661 randomly
sampled
residents from
same districts as
cases; frequency
matched 10
years; 322
(48.7%
participation
rate)
In-person
interviews
Total dishyears
50
51100
101150
151200
>200
Heating a wok to high
temperatures
Never/seldom
Sometimes
Always
Never
Ever
Use of peanut oil
Seldom/sometimes
Always
Use of corn oil
Seldom/sometimes
Always
Use of canola oil
Seldom/sometimes
Always
No. of
cases
Relative risk
(95% CI)
1.0
1.31 (0.812.11)
2.80 (1.525.18)
3.09 (1.416.79)
8.09 (2.5725.45)
25
37
131
1
1.02 (0.512.06)
1.97 (1.063.65)
12
183
1
0.73 (0.291.87)
70
125
1
1.36 (0.872.15)
146
49
1
1.27 (0.762.10)
181
14
1
1.40 (0.593.30)
Adjustment
factors
Comments
(covariates
considered)
Age, education,
employment
status, previous
lung diseases
and history of
lung cancer in
first degree
relatives (for
model 1
regarding total
dish-years);
age, history of
lung cancer in
first degree
relatives, intake
of dark green
vegetables,
yellow orange
vegetables,
meat, coffee
drinks,
multivitamins,
total dishyears
ADC, adenocarcinoma; BA, basal-cell cancer; CI, confidence interval; ICD, International Classification of Diseases; LCC, large-cell carcinoma; NOS, not otherwise
specified; SqCC, squamous-cell carcinoma; SCLC, small-cell cancer
Yu et al.
(2006)
Hong Kong
Characteristics
of controls
361
The report by Wu-Williams et al. (1990) was based on 965 female lung cancer cases in
northern China (445 in Harbin, 520 in Shenyang) and 959 female controls (404 in Harbin,
555 in Shenyang); 417 cases and 602 controls were nonsmokers. Seventy-four per cent
(714/965) of the lung cancers were histologically/cytologically confirmed of which 44%
were adenocarcinoma of the lung. Cases and controls were compared in terms of deepfrying practices. Compared with no deep-frying, the adjusted odds ratios were 1.2, 2.1 and
1.9 for deep frying once, twice and more than three times per month, respectively. Cases
reported that their homes became smoky during cooking more often than controls and that
they had irritated eyes more frequently during cooking. Compared with women who
never or rarely experienced eye irritation during cooking, the risk was increased among
those who occasionally (odds ratio, 1.6; 95% CI, 1.21.8) or frequently (odds ratio, 1.8;
95% CI, 1.32.6) reported such irritation. The authors noted that results were similar for
squamous-/oat-cell cancers and adenocarcinomas and for smokers and nonsmokers.
Pollution from coal burning for heating was a major risk factor in this area in northern
China; in a multivariate analysis, deep-frying and eye irritation remained significant risk
factors after adjusting for active smoking, previous lung diseases and coal burning (i.e.
use of kangs). [The Working Group noted that, although coal heating was adjusted for in
the multivariate analysis, the risk associated with frequent eye irritation may be due to
fuel smoke and cooking smoke. The assessment of cooking practices was relatively
limited in these two studies.]
Two small studies were conducted in Harbin (Dai et al., 1996) and Shenyang during
the early 1990s (Wang et al., 1996; Zhou et al., 2000). The study by Dai et al. (1996)
included 120 nonsmoking women who had adenocarcinoma of the lung and an equal
number of nonsmoking controls; all were long-term (at least 10 years) residents of
Harbin. The risk for adenocarcinoma of the lung was significantly influenced by
frequency of frying food; women who pan-fried and deep-fried more than five times per
month experienced a more than ninefold increased risk (adjusted odds ratio, 9.20; 95%
CI, 1.5355.28) after adjustment for various covariates including exposure to coal
burning. [The Working Group noted that the prevalence of frying was not presented; the
wide confidence interval is a concern. It is unclear whether these questions related to
current or usual frying practices and whether other questions on cooking practices were
asked. One Chinese study by Lin et al. (1996) evaluated the exposure to cooking oil
fumes and the risk of lung adenocarcinoma among female nonsmokers. An age-adjusted
increased risk of lung cancer (odds ratio, 3.0; 95% CI, 1.356.69) was observed for those
who reported to fry food more than 3 times per month.
In a hospital-based study conducted in Shenyang, Wang et al. (1996) compared the
experiences of 135 female lifetime nonsmokers who had been diagnosed with primary
lung cancer and an equal number of nonsmoking female population controls. Of the lung
cancers included, 57.2% were diagnosed pathologically or cytologically, 54.5% of which
were adenocarcinoma. The risk for lung cancer increased significantly in association with
some or frequent exposure to cooking fumes (odds ratio, 3.79; 95% CI, 2.296.27). In a
multivariate analysis, exposure to cooking fumes remained a significant risk factor
362
(adjusted odds ratio, 4.02; 95% CI, 2.386.78) after adjusting for exposure to coal smoke
and other factors. [The Working Group noted that this study was small and the exposure
was limited to dichotomized (no/yes) assessment. The specific variables that were
included in the multivariate analysis were not described. Coal use and exposure to coal
smoke were reported in this study and may confound the findings related to cooking
fumes. The validity of a diagnosis of adenocarcinoma is questionable because the authors
stated that determination of the histological cell type was based on relevant medical
record, chest X-rays, CT films and cytological and histological slides.]
Zhou et al. (2000) published another report on a subset of women from the hospitalbased study in Shenyang (Wang et al., 1996). Specifically, 72 women (52 nonsmokers)
who had been diagnosed with adenocarcinoma of the lung between 1991 and 1995 were
compared with an equal number of control women (49 nonsmokers). A nonsignificant
increased risk was observed in relation to deep-frying; the crude odds ratio was 1.68 (95%
CI, 0.456.84) for deep-frying two or more times per week compared with none or once a
week. The risk for adenocarcinoma increased significantly among women who reported
that they experienced medium/heavy exposure to cooking fumes (crude odds ratio, 4.53;
95% CI, 2.099.94) or had frequent eye irritation and exposure to smoke during cooking.
The risk for lung cancer was not significantly associated with whether cooking was
carried out in a separate kitchen or in the living-room or bedroom. In a multivariate
regression analysis, frequent eye irritation from smoke had an independent impact on risk.
Compared with women who reported no eye irritation from smoke, those who reported
slight, medium and heavy eye irritation showed elevated risks; the respective adjusted
odds ratios were 1.58, 11.45 and 3.41 for (p for trend=0.002). [The Working Group noted
that most of the lung cancer cases and controls included in the analysis by Zhou et al.
(2000) represented a select subgroup of subjects reported by Wang et al. (1996) and the
selection criteria were not described. This study was small and the confidence intervals
were very wide.]
2.2.2
Other parts of China and Singapore
One of the first studies of exposure to cooking oil fumes and the risk for lung cancer
was a large population-based casecontrol study conducted in the mid-1980s in Shanghai
that was designed to examine lifestyle factors and lung cancer (Gao et al., 1987). The
study included 672 women who had lung cancer and 735 population controls, of whom
436 cases and 605 controls were nonsmokers. Eighty-one per cent (542/672) of the lung
cancers were diagnosed histologically or cytologically. Questions on cooking practices
included type of oil used most often, frequency of frying, smokiness in the kitchen during
cooking and frequency of eye irritation during cooking. Several measures of cooking
practices were associated with an increased risk for lung cancer after adjusting for age,
education and tobacco smoking. Compared with women who most frequently used soya
bean oil, those who used rapeseed oil had an increased risk for lung cancer (adjusted odds
ratio, 1.4; 95% confidence interval [CI], 1.11.8). The increased risk associated with the
363
use of rapeseed oil existed at each level of reported frequency of eye irritation when
cooking. However, the increased risk associated with frequent eye irritation when cooking
was found among both women who used soya bean oil and those who used rapeseed oil,
although the highest risk was found in women who used rapeseed oil and frequently
experienced eye irritation (adjusted odds ratio, 2.8; 95% CI, 1.84.3). There was a
stepwise increase in risk associated with smokiness in the house. Specifically, women
who reported occasional/frequent eye irritation and a considerable amount of smokiness
in the house showed a more than twofold increased risk (adjusted odds ratio, 2.6; 95% CI,
1.83.7). Risk increased with increasing number of dishes prepared by stir-frying
(adjusted odds ratios, 1.0, 1.2, 1.2 and 2.6 for 20, 2024, 2529 and 30 times per week,
respectively) and deep-frying (adjusted odds ratios, 1.0, 1.5, 1.6 and 1.9 for 0, 1, 2 and 3
times per week, respectively). The risk patterns were similar for adenocarcinoma and
squamous-cell/oat-cell carcinoma of the lung. [The Working Group noted that this was
one of the first well-conducted population-based studies on this topic and had many
strengths. The Working Group also noted that the increased risk was found with
increasing number of dishes prepared by boiling food. Since it should produce less oil
vapour than stir-frying and deep-frying, the comparably high odds ratios associated with
boiling food were unexpected, although the authors suggested that oil was also added
during boiling.]
In the 1990s, Zhong et al. (1999) conducted another study in Shanghai that used study
methods similar to those used by Gao et al. (1987) and included a total of 649 women
who had been diagnosed with incident lung cancer during 199294 and 675 population
controls. Subjects who had smoked at least one cigarette a day for at least 6 months (145
cases, 74 controls) were excluded from the analyses. Thus, results on cooking practices
were based on 504 cases and 601 controls who were lifetime nonsmokers. Seventy-seven
per cent (387/504) of the lung cancers were diagnosed histologically or cytologically;
76.5% (296/387) of these were adenocarcinoma. Women who did not cook in a separate
kitchen experienced a small increased risk (adjusted odds ratio, 1.28; 95% CI, 0.981.68).
Risk for lung cancer was higher among those who had used rapeseed oil most frequently
compared with those who had used soya bean oil (adjusted odds ratio, 1.84; 95% CI,
1.123.02). However, the risk was not elevated when both types of oil had been used
(adjusted odds ratio, 0.92; 95% CI, 0.372.28). Risk also increased with higher frequency
of frying. Compared with women who deep-fried once a week or less often, those who
deep-fried more than once a week had a nearly twofold increased risk (adjusted odds
ratio, 1.88; 95% CI, 1.063.32). Similarly, compared with women who pan-fried food
once a week or less often, those who pan-fried food more than once a week had a
significantly increased risk (adjusted odds ratio, 2.09; 95% CI, 1.143.84). However, the
risk pattern in relation to stir-frying was less consistent. Compared with stir-frying less
than seven times a week, women who stir-fried seven times a week had a reduced risk
(adjusted odds ratio, 0.38; 95% CI, 0.190.75), but those who stir-fried more than seven
times a week showed an increased risk (adjusted odds ratio, 2.33; 95% CI, 0.687.95).
Women exposed to visible fumes from high-temperature frying had an increased risk
364
(adjusted odds ratio, 1.64; 95% CI, 1.242.17). This risk more than doubled for women
who reported considerable smokiness (i.e. smokiness affected vision during cooking)
from cooking oil or fumes (adjusted odds ratio, 2.38; 95% CI, 1.583.57) compared
with those who reported no smokiness. There was also a trend of increasing risk with
increasing frequency of self-reported eye irritation; the adjusted odds ratio was 1.68 (95%
CI, 1.022.78) for women who reported frequent (5 times per week) eye irritation
compared with those who reported no eye irritation. Risk patterns related to Chinese-style
cooking were generally similar in analyses that were restricted to all self-respondents
(400 cases, 581 controls) or to self-respondents with histologically confirmed lung cancer
(308 cases, 581 controls). Results were also comparable for women who had
adenocarcinomas (296 cases), non-adenocarcinomas (91 cases) or unknown cell type (i.e.
diagnosed clinically/radiologically) of lung cancer (117 cases). In a multivariate
regression analysis, cooking temperature, smokiness in the kitchen during cooking, type
of cooking oil and the frequency of stir-frying and of pan-frying displayed independent
effects on the risk for lung cancer after adjustment for variables on ventilation (e.g. area of
windows, cooking in a separate kitchen). Frequency of eye irritation and frequency of
deep-frying were correlated with the other variables and did not exhibit independent
effects on risk. [The Working Group noted several strengths in this population-based
study: it was conducted among lifetime nonsmokers, the assessment of cooking practices
was comprehensive and the analyses were thorough. Results were generally consistent
across various subgroup analyses by histological and respondent type. The type of fuel
used for cooking (coal, gas) was not significantly associated with risk and was not
adjusted for in the multivariate analysis. It should be noted that the distribution of stirfrying was skewed and the confidence intervals were wide for stir-frying. The prevalence
of use of rapeseed oil was 7.2% among controls in this study compared with 47.2% in
Shanghai in the mid-1980s. The reason for the large differences in the pattern of use of
rapeseed oil was not discussed but may be due to differences in the questions asked in the
two studies.]
Two other studies were conducted in urban areas of China to examine the relationship
between exposure to cooking oil fumes and risk for lung cancer. Shen et al. (1996)
investigated potential risk factors for lung cancer among long-term (at least 20 years)
residents of Nanjing in a hospital-based, casecontrol study that included 263 cases of
lung cancer and an equal number of population controls. Only histologically confirmed
lung cancers were studied (83 squamous-cell carcinomas, 180 adenocarcinomas).
Exposure to cooking fumes was associated with an increased risk for squamous-cell
carcinoma (adjusted odds ratio, 3.81; 95% CI, 1.0613.73) and adenocarcinoma (adjusted
odds ratio, 2.99; 95% CI, 1.685.34) of the lung. [The Working Group noted that the
study had serious limitations. The report lacked details regarding the study design (e.g.
response rate) and characteristics of the study population (e.g. gender distribution, active
smoking history). The source of information on exposures was not presented. Only
significant results were presented; risk patterns in relation to the amount of oil used in
cooking and frequency of cooking per week were not presented.]
365
Cooking practices and lung cancer mortality were investigated in a casecontrol study
in Guangzhou (Lei et al., 1996). Using registered deaths that occurred in this city in 1986,
the analysis was based on 792 (562 men, 229 women) lung cancer deaths reported in
long-term (at least 10 years) Guangzhou residents. The comparison group included other
registered decedents who were matched to cases on gender, age (5 years) and residence
and whose cause of death was unrelated to cancer or respiratory disease. A standardized
interview administered to spouses or cohabiting relatives of the decedents collected
information on active smoking, exposure to secondhand smoke, living conditions,
cooking facilities, exposure to coal dust and dietary habits. In analyses conducted
separately in men and women, cases and controls did not differ significantly in their
preference of frying, years of cooking (infrequent, 20, 2040, >40 years) or size the of
kitchen (<1, 12, 2 m2 per household). Similarly, living conditions (type of building,
location of residence, interior dimensions of residence) and average size of the living area
did not differ significantly between lung cancer cases and controls. [The Working Group
noted that the study had several deficiencies. The quality of information on cooking
practices obtained from next of kin is questionable; a considerable amount of information
was missing; the data analysis was confined to crude analysis; and the accuracy of lung
cancer diagnosis based on reviewed death records is not known for China.]
In addition to the above-mentioned studies that were conducted largely in urban areas
of China, two studies were conducted in more rural parts of China: one in Xuan Wei
County, Yunnan Province (Lan et al., 1993), an area where mortality rates for lung cancer
are very high among women, and one in Gansu Province, a rural area in northwestern
China (Metayer et al., 2002).
The study in Xuan Wei County, Yunnan Province, investigated the use of rapeseed
oil in the study population and was based on 139 incident female lung cancers that were
diagnosed between 1988 and 1990 and 139 age-matched controls (Lan et al., 1993). Of
the lung cancer cases, 55 (39.6%) were diagnosed cytologically/pathologically. All cases
and controls were nonsmokers. Compared with women who never used rapeseed oil,
those who used it occasionally or frequently showed an increased risk; the respective
adjusted odds ratios were 1.26 (95% CI, 0.682.63) and 4.58 (95% CI, 0.5637.08) after
adjusting for age, length of menstrual cycle, age at menopause and family history of lung
cancer. [The Working Group noted that coal use was prevalent in this study population
and was not considered in the analysis on cooking oil. In addition, the definition of
occasional or frequent use of rapeseed oil was not provided. Few subjects (2.2% of
controls) were frequent users of rapeseed oil and the confidence limits were wide. It is
unclear whether other questions related to cooking practices were asked.]
Metayer et al. (2002) conducted a population-based casecontrol study that was
designed to examine the association between cooking oil fumes and other sources of
indoor air pollution and lung cancer in Gansu Province. The study included 233 female
lung cancer cases and 459 control subjects; 206 cases and 411 controls were nonsmokers.
Thirty-seven per cent of the cases were cytologically or histologically confirmed.
Smokers (27 cases, 47 controls) were included in the analysis on cooking practices.
366
Compared with women who only used linseed oil, an elevated risk was associated with
the use of rapeseed oil alone (adjusted odds ratio, 1.65; 95% CI, 0.83.2), rapeseed and
linseed oil in combination (adjusted odds ratio, 1.70; 95% CI, 1.02.5) and
perilla/hempseed oil (adjusted odds ratio, 3.25; 95% CI, 0.814.0). The risk for lung
cancer was unrelated to the frequency of deep-frying (adjusted odds ratio, 1.0, 0.82 and
0.83 for never/less than once a month, 12 times per month and 3 times per month,
respectively). However, there was a significant exposureresponse of increased risk with
increasing frequency of stir-frying (adjusted odds ratios, 1.00, 1.96, 1.73 and 2.24, for stirfrying <15, 1529, 30 and 31 times per month; p for trend=0.03). Risk tended to
increase with decreasing age when started to cook (adjusted odds ratio, 0.69 for started
cooking at age 17 versus 13 years), with increasing number of meals cooked per day
(adjusted odds ratio, 1.36 for 3 meals versus 2 meals) and with increasing years of
cooking (adjusted odds ratio, 1.0, 1.26, 2.51 and 2.46 for 29, 3039, 4049 and
50 years) (p for trend <0.09). Although women who reported frequent eyethroat
irritation showed a significantly increased risk (adjusted odds ratio, 2.82; 95% CI, 1.6
5.0) compared with those who never experienced such irritation (p trend <0.01), the
general level of indoor smokiness was unrelated to risk. Risk for lung cancer was not
elevated among women who reported considerable home smokiness (odds ratio, 0.76;
95% CI, 0.41.6) compared with those who reported no smokiness. The authors
hypothesized that, as underground cave dwellings in Gansu Province reported high
ventilation rates as measured by air exchanges per hour, this may explain the lack of any
risk associated with general smokiness. The positive associations with stir-frying, years of
cooking and eye irritation were found in women who cooked with linseed oil only
(80 cases, 247 controls) and in those who cooked with rapeseed oil (148 cases,
205 controls). In addition, the authors reported that the results were generally similar
when the analyses were restricted to self-respondents or to histologically confirmed lung
cancer cases. [The Working Group noted that this study included a comprehensive
assessment of cooking practices and conditions. Coal use for heating/cooking was not
significantly associated with lung cancer risk in this population. Although coal use was
not considered in the analysis on cooking practices, it is unlikely to confound the findings.
The results suggest that fumes from all types of oil may have deleterious effect. This
study is limited by a relatively large number of only clinically/radiologically diagnosed
lung cancers and because interviews were conducted with next-of-kin respondents for
123 cases (53%) and 20 controls (4%).]
Shi et al. (2005) conducted a casecontrol study that included nonsmoking women
who had been newly diagnosed with lung cancer between June 2000 and December 2002
in city hospitals of urban Shenyang. Eighty-four per cent of cases were diagnosed
pathologically or cytologically. Controls were randomly selected from the general female
population of urban areas and matched on age (within 2 years). Information on
demographic factors, exposure to cooking oil smoke, types of fuel used, exposure to coal
smoke, use of heated kangs, passive smoking, history of lung disease and other factors
was obtained. Risk for lung cancer increased significantly in association with exposure to
367
cooking oil smoke (odds ratio, 3.18; 95% CI, 2.553.97) and fuel smoke (odds ratio, 2.56;
95% CI, 1.834.55) after adjusting for education and social class. Risk was unrelated to
the use of kangs (odds ratio, 1.12; 95% CI, 0.911.39). In a multivariate analysis, the
increased risk associated with cooking oil smoke remained statistically significant
(adjusted odds ratio, 4.11; 95% CI, 2.147.89) but the risk associated with fuel smoke
was no longer statistically significant. [The Working Group noted that, although the
finding on cooking oil smoke was adjusted for fuel smoke, it is difficult to rule out
residual confounding in this study.]
Seven studies on cooking practices and the risk for lung cancer have been conducted
in other parts of China, including one study in Hong Kong Special Administrative Region
(Yu et al., 2006), four in Taiwan (Ger et al., 1993; Ko et al., 1997, 2000; Lee et al., 2001)
and two in Singapore (MacLennan et al., 1977; Seow et al., 2000).
(a)
Hong Kong Special Administrative Region
Chan-Yeung et al. (2003) conducted a casecontrol study in Hong Kong Special

Administrative Region during the late 1990s which included 331 Chinese residents
(212 men, 119 women) who had been diagnosed with a histologically confirmed primary
lung cancer in a large teaching hospital. An equal number of age- and gender-matched
residents identified from the same hospital who had non-malignant respiratory diseases
were used as controls. Most of the women were nonsmokers (106 cases, 113 controls)
while many of the men were smokers (160 cases, 116 controls). All cases and controls
were interviewed by one interviewer and were asked about regular exposure to cooking
fumes from frying in the house. Years of regular exposure to frying food was not
significantly related to the risk for lung cancer in men or women. For women with no or
less than 2 years of exposure, the respective odds ratios associated with <3.5 years, 3.5
7 and >7 years of exposure to frying food were 1.08 (95% CI, 0.502.32), 1.05 (95% CI,
0.462.42) and 1.54 (95% CI, 0.574.13) after adjustment for demographic factors and
smoking habits. The corresponding risk estimates in men were 0.69 (95% CI, 0.321.49),
0.83 (95% CI, 0.381.80) and 1.22 (95% CI, 0.383.99). [The Working Group noted that
this study included a single measure of exposure to frying in the house. Control subjects
had non-malignant respiratory diseases and may have had risk factor profiles that are
more similar to the lung cancer patients than control subjects selected from the general
population. Thus, estimates of risk associated with exposure to frying may be
underestimated.]
Yu et al. (2006) conducted a casecontrol study in Hong Kong Special
Administrative Region during the early 2000s that included 200 nonsmoking Chinese
women who had been diagnosed with a histologically confirmed primary lung cancer in a
large oncology centre and 285 population controls. All but 12 participants (six cases, six
controls) were interviewed in person using a standardized structured questionnaire that
asked extensive questions about lifetime cooking habits since childhood and included
number of years of cooking, the frequencies of stir-frying, pan-frying and deep-frying, the
types of cooking oils used, the use of a fume extractor or exhaust fans and the habit of
368
heating up a wok to high temperatures. The risk for lung cancer increased significantly
with increasing total cooking dishyears, a composite index that was constructed to
account for both the frequency and the duration of cooking. The odds ratios were 1.00,
1.31, 2.80, 3.09 and 8.09, respectively, for 50, 51100, 101150, 151200 and 200
total frying dishyears after adjusting for age, education, employment status, previous
lung disease and family history of lung cancer. The results remained significant after
further adjustment for factors that may contribute to indoor air pollution (e.g. radon,
exposure to environmental tobacco smoke, use of kerosene, use of firewood, burning of
incense and use of mosquito coils) and dietary factors. In addition, a trend of increasing
risk with heating a wok to high temperature was observed; the odds ratio was 1.0, 1.02
and 1.97 in relation to never/seldom, occasionally and always engaging in such cooking
habits. Risk (per 10 dishyears) was highest for deep-frying (odds ratio, 2.56; 95% CI,
1.315), intermediate for pan-frying (odds ratio, 1.47; 95% CI, 1.271.69) and lowest for
stir-frying (odds ratio, 1.12; 95% CI, 1.071.18). However, risk was not significantly
associated with the use of a particular type of oil (peanut oil, corn oil, canola oil) for
cooking or with using a fume extractor. A pattern of risk associated with total cooking
dishyears was observed for adenocarcinoma and for non-adenocarcinoma, although the
results were stronger for adenocarcinoma of the lung, which represented 69% of the lung
cancer cases included in this study. [The Working Group noted that this study included a
comprehensive assessment of lifetime cooking habits. Duration and frequency of
exposure was captured by a composite index, total cooking dishyears, which permitted
a quantitative assessment of cumulative exposure. While the confidence interval for the
highest exposure category (>200 dishyears) was wide, there was a monotonic increase in
risk with increasing exposure. It should be noted that this index was computed based on
the number of dishes cooked by the three cooking methods (stir-frying, pan-frying and
deep-frying). Although the response rate among controls was modest (~50%), few
differences between cases and controls were noted for demographic factors except for a
higher rate of employment among controls (88%) compared with cases. Elevated risks
associated with moderate to high levels of cooking (>100 dishyears) remained after
further adjustment for employment status.]
(b)
Taiwan (China)
Four hospital-based casecontrol studies of lung cancer from Taiwan investigated the
role of cooking practices. The main type of oil used in Taiwan is vegetable oil (mainly
peanut or soya bean oil).
Ger et al. (1993) conducted a hospital-based casecontrol study in Taipei, Taiwan,
that included 131 primary lung cancers (92 men, 39 women) identified between 1990 and
1991. All were histologically confirmed. Two control groups were interviewed;
262 hospital controls were matched to cases on sex, date of birth (5 years), date of
interview (4 weeks) and insurance status and 262 neighbourhood controls were matched
to cases on age, sex and residence of case at the time of diagnosis. In total, 48 cases and
229 controls (111 hospital controls, 118 neighbourhood controls) were nonsmokers. Risk
369
for adenocarcinoma and squamous-/small-cell cancers in men and women combined was
unrelated to cooking style; cases and controls did not differ in pan-frying, stir-frying,
deep-frying or boiling practices after adjusting for active smoking and other covariates.
Risk for adenocarcinoma increased significantly in persons who reported that they were
professional cooks (adjusted odds ratio, 5.54; 95% CI, 1.4920.65); no increased risk was
found for squamous-cell cancer (adjusted odds ratio, 1.16; 95% CI, 0.32422). [The
Working Group noted that this study included few female lung cancer patients. Results
were based on dichotomized cooking variables (e.g. no/yes frying) that were not defined.]
Three hospital-based casecontrol studies were conducted in Kaohsiung, a heavily
industrialized city in Taiwan (Ko et al., 1997, 2000; Lee et al., 2001). The designs of
these studies were similar. The first study included 117 female lung cancer cases
identified between 1992 and 1993 who were compared with 117 hospital controls who
were admitted for a health check-up (55 controls) or for eye diseases (62 controls) (Ko et
al., 1997). Active smokers (11 cases, three controls) were excluded so that the analysis
was based on 105 casecontrol pairs who were nonsmokers. In a univariate analysis, risk
for lung cancer increased with increased frequency of stir-frying (odds ratio, 2.4; 95% CI,
1.15.2 for 5 versus 04 times per week), pan-frying (odds ratio, 2.3; 95% CI, 1.24.6
for 5 versus 04 times per week) but not with deep-frying (odds ratio, 0.9; 95% CI, 0.5
1.9 for 5 versus 04 times per month). Risk also increased with younger age when
started to cook (odds ratio, 1.6; 95% CI, 0.83.0 for started at ages 720 versus after age
21 years). Risk for lung cancer was elevated in women who cooked in a kitchen without a
fume extractor; this was found at different ages of cooking including before age 20 years
(odds ratio, 5.3; 95% CI, 1.125.6), between the ages of 20 and 40 years (odds ratio, 6.4;
95% CI, 2.914.1) or after 40 years of age (odds ratio, 2.3; 95% CI, 1.15.1). The risk for
lung cancer was not significantly related to types of cooking oil (lard versus vegetable
oil). In a multivariate analysis, use of a fume extractor during cooking between the ages of
20 and 40 years remained statistically significant (adjusted odds ratio, 8.3; 95% CI, 3.1
22.7). [The Working Group noted that, while there was no increased risk associated with
cooking with coal, the risk increased significantly in relation to cooking with wood or
charcoal before 20 years of age and between the ages of 20 and 40 years. These
investigators examined the combined effects of frying and use of fume extractors between
the ages of 20 and 40 years. The increased risks associated with stir-frying and pan-frying
remained regardless of use of fume extractors.]
A second study conducted by the same group of investigators was based on 131 lung
cancer cases identified between 1993 and 1996, 252 hospital controls and 262 community
controls; all participants were nonsmokers (Ko et al., 2000). All lung cancers were
histologically confirmed; 63% were adenocarcinoma of the lung. Of the more than
10 variables related to cooking practices that were investigated, risk for lung cancer was
associated with five. There was a significant trend of increasing risk with number of
meals cooked per day (adjusted odds ratios, 1.0, 3.1 and 3.4 for cooking 1, 2 and 3 meals
per day, respectively). Risk was also elevated for women who cooked between the ages of
20 and 40 years without a fume extractor (adjusted odds ratio, 2.2; 95% CI, 1.33.8). In
370
addition, women who reported frequent eye irritation (odds ratio, 2.1; 95% CI, 1.33.5)
showed significantly elevated risks. Subjects who usually waited until fumes were
emitted from the oil and then stir-fried, pan-fried or deep-fried also experienced about a
twofold increased risk that was statistically significant. In contrast, years of cooking at
home, general ventilation in the kitchen, number of windows in kitchen (<2 versus 2)
and size of openings (windows) to the outside did not differ between cases and controls.
The risk estimates presented above were obtained when cases were compared with
community controls, and risk patterns were generally similar when lung cancer cases
were compared with hospital controls. [The Working Group noted that use of coal and
wood/charcoal was not reported. However, since this study overlapped with the earlier
study (Ko et al., 1997), the same comments relating to cooking fuel are applicable.]
A further expansion of the previous two studies included lung cancer patients
diagnosed between 1993 and 1999 (Lee et al., 2001). Women who had been diagnosed
with squamous-/small-cell (84 cases) cancer or adenocarcinoma of the lung (162 cases)
and 407 corresponding controls were included in the analysis. Women who had other
lung cancer cell types (45 cases) and men who had lung cancer were excluded from the
analysis of cooking practices. Prevalence of smoking in female controls was not presented
but, among female cases, 96.9% of those with adenocarcinoma of the lung and 81.6% of
those with squamous-/small-cell lung cancer were nonsmokers. Risk was significantly
higher for those who cooked in a kitchen without a fume extractor; the adjusted odds ratio
was 3.0 (95% CI, 1.37.1) for squamous-/small-cell cancer and 3.9 (95% CI, 2.36.6) for
adenocarcinoma of the lung. Women who stir-fried, pan-fried or deep-fried only when
fumes were emitted from the oil showed significantly higher risk for adenocarcinoma
(respective odds ratios, 2.0, 2.6 and 1.6) but not for squamous-/small-cell cancer of the
lung (respective odds ratios, 0.9, 0.8 and 1.0). Risk for either cell type of lung cancer was
not significantly influenced by age when first started to cook (>20 versus 20 years) or
type of cooking oils (lard versus vegetable oils). In a multivariate regression analysis,
cooking in a kitchen that was not equipped with a fume extractor remained a significant
risk factor for both squamous-/small-cell lung cancer and adenocarcinoma of the lung; the
respective adjusted odds ratios were 3.3 (95% CI, 1.29.2) and 3.8 (95% CI, 2.16.8). In
addition, waiting to fry until the cooking oil has reached a high temperature was
associated with an increased risk for adenocarcinoma of the lung (adjusted odds ratio, 2.1;
95% CI, 1.13.0) but not for squamous-/small-cell lung cancer. [The Working Group
noted that there was an overlap of cases and controls in the three reports by Ko and
colleagues. An advantage of the second report (Ko et al., 2000) is that a group of
population controls was also included and most of the risk patterns were similar compared
with both control groups. It should be noted that use of wood/charcoal, a significant risk
factor for both cell types of lung cancer, was not adjusted for in the analysis on cooking
practices.]
(c)
371
Singapore
Seow et al. (2000) conducted a hospital-based casecontrol study in Singapore during

the late 1990s; 303 women who had been diagnosed with a pathologically confirmed
primary lung cancer (56% were adenocarcinoma of the lung) and 765 hospital controls
were compared. Analyses were conducted separately for smokers (former and current
smokers combined; 127 cases, 100 controls) and lifetime nonsmokers (176 cases,
663 controls). All participants were interviewed in person using a standardized
questionnaire that asked extensive questions on diet, reproductive history, exposure to
secondhand smoke and cooking practices. Specifically, questions included the frequency
of stir-frying, types of oil used and usual cooking practice 2030 years before diagnosis.
Subjects were also asked how often the air in their kitchen became filled with oily
smoke during frying. For each of these cooking exposures, there were six possible
responses ranging from never/less than yearly, less than monthly, to daily and more than
once a day. Among smokers, the risk for lung cancer doubled in association with daily
stir-frying (adjusted odds ratio, 2.0; 95% CI, 1.03.8) after adjusting for a large number of
potential confounders. This increase in risk was confined to those who stir-fried meat on a
daily basis (adjusted odds ratio, 2.7; 95% CI, 1.35.5). Compared with smokers who stirfried meat less frequently than daily, risk was intermediate for those who stir-fried meat
less than daily in a fume-filled kitchen (adjusted odds ratio, 1.7; 95% CI, 0.73.9) and
was highest for those who stir-fried daily and reported a smoke-filled kitchen (adjusted
odds ratio, 3.5; 95% CI, 1.86.9). Women who stir-fried meat daily and primarily used
unsaturated oils had the highest risk (adjusted odds ratio, 4.6; 95% CI, 1.613.0), while
risk was intermediate for those who stir-fried daily but did not use unsaturated oils
exclusively (adjusted odds ratio, 2.2; 95% CI, 1.24.2). In contrast, the risk for lung
cancer in nonsmokers was unrelated to stir-frying (adjusted odds ratio, 1.0; 95% CI, 0.7
1.5) or stir-frying meat daily (adjusted odds ratio, 0.9; 95% CI, 0.61.4). Risk for lung
cancer in nonsmokers was not affected by smokiness of kitchen or types of oil used. [The
Working Group noted that this study presented no data on pan-frying or deep-frying.
Although fuel use was not considered in this analysis, it is unlikely to be an important
confounder because gas/kerosene is usually used (MacLennan et al., 1977). However, this
was one of the few studies that described the questions that were asked regarding cooking
practices and that specifically addressed cooking practices during the period 2030 years
before cancer diagnosis/interview. Reasons for the differences in findings by smoking
status are not apparent but the sample size of smokers was modest. The risk estimates
presented in the tables were slightly different from the numbers presented in the text; the
numbers presented in the tables are those given in this Monograph.]
2.3
Meta-analysis
Feng & Ling (2003) carried out a meta-analysis on casecontrol studies among
nonsmoking women that were published between 1992 and 2002 in the English and
372
Chinese literature and examined the relationship between exposure to cooking oil fumes
and lung cancer. Six studies (two in English and four in Chinese) were conducted in
mainland China and two (in English) in Taiwan. All studies reported significantly
increased odds ratios ranging from 2.10 to 9.20. The combined odds ratio using a fixed
effects model was 2.94 (95% CI, 2.433.56). [The Working Group noted that the two
studies in Taiwan had some overlap in their study subjects. Two reports by the same
group of authors in China (Wang et al., 1996), one in English and one in Chinese,
essentially overlap one another. The exposure metrics were not uniform and the rationale
for selecting certain odds ratios out of a range in each paper was not entirely clear.
2.4
References
Chan-Yeung M, Koo LC, Ho JCM et al. (2003). Risk factors associated with lung cancer in Hong
Kong. Lung Cancer, 40:131140 doi:10.1016/S0169-5002(03)00036-9. PMID:12711113
Dai XD, Lin CY, Sun XW et al. (1996). The etiology of lung cancer in nonsmoking females in
Harbin, China. Lung Cancer, 14 Suppl. 1;S85S91 doi:10.1016/S0169-5002(96)90213-5.
PMID:8785670
Feng SD, Ling HY (2003). Meta analysis of female lung cancer associated with cooking oil fumes.
J Environ Health, 20:353354.
Gao YT, Blot WJ, Zheng W et al. (1987). Lung cancer among Chinese women. Int J Cancer,
40:604609 doi:10.1002/ijc.2910400505. PMID:2824385
Ger LP, Hsu WL, Chen KT, Chen CJ (1993). Risk factors of lung cancer by histological category
in Taiwan. Anticancer Res, 13 5A;14911500. PMID:8239527
Ko YC, Cheng LS, Lee CH et al. (2000). Chinese food cooking and lung cancer in women
nonsmokers. Am J Epidemiol, 151:140147. PMID:10645816
Ko YC, Lee CH, Chen MJ et al. (1997). Risk factors for primary lung cancer among non-smoking
women in Taiwan. Int J Epidemiol, 26:2431 doi:10.1093/ije/26.1.24. PMID:9126500
Koo LC, Ho JH (1996). Diet as a confounder of the association between air pollution and female
lung cancer: Hong Kong studies on exposures to environmental tobacco smoke, incense, and
cooking fumes as examples. Lung Cancer, 14 Suppl.;4761.
Lan Q, Chen W, Chen H, He XZ (1993). Risk factors for lung cancer in non-smokers in Xuanwei
County of China. Biomed Environ Sci, 6:112118. PMID:8397894
Lee CH, Ko YC, Cheng LS et al. (2001). The heterogeneity in risk factors of lung cancer and the
difference of histologic distribution between genders in Taiwan. Cancer Causes Control,
12:289300 doi:10.1023/A:1011270521900. PMID:11456224
Lei YX, Cai WC, Chen YZ, Du YX (1996). Some lifestyle factors in human lung cancer: a casecontrol study of 792 lung cancer cases. Lung Cancer, 14 Suppl.;S121S136
doi:10.1016/S0169-5002(96)90218-4.
Lin CY, Sun XW, Lin YJ et al. (1996). Indoor air pollution and lung adenocarcinoma in nonsmoking women. Cancer Research on Prevention and Treatment, 23:4749.
Liu Q, Sasco AJ, Riboli E, Hu MX (1993). Indoor air pollution and lung cancer in Guangzhou,
Peoples Republic of China. Am J Epidemiol, 137:145154. PMID:8452118
Liu ZY, He XZ, Chapman RS (1991). Smoking and other risk factors for lung cancer in Xuanwei,
China. Int J Epidemiol, 20:2631 doi:10.1093/ije/20.1.26. PMID:2066232
373
MacLennan R, Da Costa J, Day NE et al. (1977). Risk factors for lung cancer in Singapore
Chinese, a population with high female incidence rates. Int J Cancer, 20:854860
doi:10.1002/ijc.2910200606. PMID:591126
Metayer C, Wang Z, Kleinerman RA et al. (2002). Cooking oil fumes and risk of lung cancer in
women in rural Gansu, China. Lung Cancer, 35:111117 doi:10.1016/S0169-5002(01)004123. PMID:11804682
Seow A, Poh WT, Teh M et al. (2000). Fumes from meat cooking and lung cancer risk in Chinese
women. Cancer Epidemiol Biomarkers Prev, 9:12151221. PMID:11097230
Shen XB, Wang GX, Huang YZ et al. (1996). Analysis and estimates of attributable risk factors
for lung cancer in Nanjing, China. Lung Cancer, 14 Suppl.;S107S112 doi:10.1016/S01695002(96)90216-0.
Shi H, He Q, Dai X, Zhou B (2005). Study on risk factors of lung cancer in non-smoking women.
Chinese J Lung Cancer, 8:279282.
Wang TJ, Zhou BS, Shi JP (1996). Lung cancer in nonsmoking Chinese women: A casecontrol
study. Lung Cancer, 14 Suppl.;S93S98 doi:10.1016/S0169-5002(96)90214-7.
Wu-Williams AH, Dai XD, Blot W et al. (1990). Lung cancer among women in north-east China.
Br J Cancer, 62:982987. PMID:2257230
Xu ZY, Blot WJ, Xiao HP et al. (1989). Smoking, air pollution, and the high rates of lung cancer
in Shenyang, China. J Natl Cancer Inst, 81:18001806 doi:10.1093/jnci/81.23.1800.
PMID:2555531
Yu ITS, Chiu Y-L, Au JSK et al. (2006). Dose-response relationship between cooking fumes
exposures and lung cancer among Chinese nonsmoking women. Cancer Res, 66:49614967
doi:10.1158/0008-5472.CAN-05-2932. PMID:16651454
Zhong L, Goldberg MS, Gao YT, Jin F (1999). A case-control study of lung cancer and
environmental tobacco smoke among nonsmoking women living in Shanghai, China. Cancer
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Zhou BS, Wang TJ, Guan P, Wu JM (2000). Indoor air pollution and pulmonary adenocarcinoma
among females: a case-control study in Shenyang, China. Oncol Rep, 7:12531259.
PMID:11032925
374
3. Studies of Cancer in Experimental Animals

3.1
Cooking oil fumes

(a)
Mouse
Four groups of 3032 male and 3032 female Balb/c mice (weighing 153 g) [age
unspecified] were exposed to air heated at 2230C (control) or ~9, 21 and 39 mg/m3
cooking oil fumes for 30 min per day for 2 months, then every other day for a period of
6 months (150 times overall) after which time they were killed. Oil fumes were generated
by heating an unspecified volume of unrefined rapeseed oil at a temperature of 2705C
in a steel container with an electric heating element. Fumes were directed into a
cylindrical 1-m3 exposure chamber. The incidence of lung tumours in both sexes
combined was 0.0 (0/61), 15.09 (8/53; p<0.05), 20.00 (10/50; p<0.05) and 22.00%
(11/50; p<0.05) for the control, low-, mid- and high-dose groups, respectively. The
incidence in females was 0.00 (0/31), 12.00 (3/25; p<0.05), 25.00 (5/20; p<0.05) and
25.92% (7/27; p<0.05), respectively, and that in males was 0.00 (0.30), 17.86 (5/28;
p<0.05), 16.67 (5/30; p<0.05) and 17.39% (4/23; p<0.05), respectively. The lung tumours
were mainly adenocarcinomas (Zhang et al., 2003; Chen et al., 2005).
(b)
Rat
Four groups of 3035 male and 3035 female Sprague-Dawley rats (weighing
~127 g) [age unspecified] were exposed to air or ~7, 15 and 35 mg/m3 cooking oil fumes
for 30 min every other day for 12.5 months after which they were killed. Oil fumes were
generated by heating 250 mL unrefined rapeseed oil to a temperature of 260C in steel
container with an electric heating element. Fumes were directed into a cylindrical 2.2-m3
exposure chamber. The incidence of lung carcinoma in both sexes combined was 0.0
(0/70), 6.56 (4/61), 8.96 (6/67) [p<0.05] and 12.70% (8/63) [p<0.005] for the control,
low-, mid- and high-dose groups, respectively. The incidence in females was 0.0 (0/35),
6.45 (2/31), 11.76 (4/34) and 19.35% (6/31) [p<0.01], respectively, and that in males was
0.0 (0/35), 6.67 (2/30), 6.06 (2/33) and 6.25% (2/32), respectively (Long et al., 2005).
3.2
References
Chen F, Zhang ZH, Long LL (2005). [Experimental study of potential carcinogenesis of cooking
oil fumes.] J Environ Occup Med, 22:287290.
Long LL, Chen F, He XP, Li FH (2005). Experimental study on lung cancer induced by cooking
oil fumes in SD rats. J Environ Health, 22:114116.
375
Zhang ZH, Chen F, Tan Y et al. (2003). [Pulmonary carcinoma pathological change caused by
COF in Balb/c mouse.] Chinese J Public Health, 19:14551457.
376
4. Mechanistic and Other Relevant Data

4.1
Toxicokinetics
See the monograph on Household use of solid fuels.
4.2
Mechanisms of carcinogenesis
4.2.1
Polycyclic aromatic hydrocarbons (PAHs)

Siegmann and Sattler (1996) detected a variety of genotoxic PAHs (e.g.
benzo[a]anthracene, chrysene, benzo[a]pyrene) in vegetable oils (rapeseed, corn and
peanut) heated to above 260C (1.122.8 g/m3 PAHs). Wu et al. (1998) detected a
variety of mutagenic PAHs (e.g. benzo[a]pyrene) and nitro-PAHs (e.g. 1,3-dinitropyrene)
in fumes of lard, soya bean oil and peanut oil heated to above 250C; the emission of
PAHs and nitro-PAHs were reduced upon addition of the antioxidant catechin.
4.2.2
Particles

4.2.3
Genetic and related effects

(a)
Humans
Cherng et al. (2002) used the reverse-transcription polymerase chain reaction to

investigate expression of human 8-oxoguanine DNA glycosylase 1 (HOGG1), a repair
enzyme that removes 8-hydroxydeoxyguanine (8-OHdG) from damaged DNA, in the
peripheral blood lymphocytes of 94 professional cooks and 43 home cooks exposed to
cooking oil emissions. The results showed that HOGG1 expression in cooking oil
emissions-exposed cooks was significantly higher than that in 111 control subjects. Odds
ratios, adjusted for age, sex and smoking and drinking status, for home cooks versus
controls and professional cooks versus controls were 3.94 (95% CI, 0.9516.62) and
10.12 (95% CI, 2.8336.15), respectively. Furthermore, significant induction of HOGG1
expression was confirmed in vitro in human lung adenocarcinoma CL-3 cells after
exposure to cooking oil emissions extracts.
(b)
377
Experimental systems
(i)
Experimental animals
Glaser et al. (1989) reported that flow cytometric analyses of lung cells from Wistar
rats exposed to emissions (20 mg/m3) from fish frying in fat for 28 days showed
alterations in the structure and content of nuclear DNA. In comparison with the control
group, samples from exposed animals showed a significant shift and broadening of the G1
peak, which may be caused by loss of chromosomal fragments or by chromosomal
aberration during cell division.
Several studies have documented clastogenic effects, genotoxic effects and oxidative
stress in experimental animals exposed to cooking oil fumes.
Intraperitoneal injection of male Kunming mice with condensates of emissions from
rapeseed oil heated to 270C (doses of 800, 1600, 2400 or 3200 mg/kg body weight [bw])
induced a significant dose-dependent increase in the frequency of micronucleated
polychromatic erythrocytes in the bone marrow. The addition of the antioxidant butylated
hydroxyanisole to the oil reduced the magnitude of the effect (Chen et al., 1988; Qu et al.,
1992). Two studies have shown induction of bone-marrow cell micronuclei in mice
exposed to cooking oil fumes. Chen et al. (1992) reported a time- and dose-dependent
increase in bone-marrow micronuclei in male Swiss mice exposed by inhalation to
rapeseed oil fumes for 3 h per day, 6 days per week for 4 weeks. Liu et al. (1987) showed
an increase in the frequency of bone-marrow cell micronuclei in mice exposed by
inhalation for 5 days to 1/16 of the LD50 of cooking oil fumes from soya bean oil heated at
250270C. A subsequent study by Li et al. (1998) showed that intratracheal instillation
of refined vegetable oil (heated to 270280C)-fume condensate into Sprague-Dawley
rats (doses of 225, 450 or 900 mg/kg bw) elicited a significant increase in bone-marrow
cell micronuclei.
Chen et al. (1996) revealed significant induction of chromosomal aberrations in
diploid male germ cells (diakenesis/meiosis I) of ICR mice exposed to rapeseed oil
emissions condensate (270280C) by daily intraperitoneal injections of 100, 400 or
1600 mg/kg bw for 5 days.
Zhang et al. (2001) observed significant increases in DNA damage in peripheral
blood lymphocytes (comet assay) of Balb/c mice following inhalation exposure for
8 months to 9.139 mg/m3 fumes of heated rapeseed oil.
Kawai et al. (2006) showed that 4-oxo-2-hexenal (4-OHE), a mutagenic substance
formed by the peroxidation of -3 polyunsaturated fats such as linolenic acid, was present
in a condensate of smoke released during fish frying. In an earlier study, Kasai et al.
(2005) noted that oral administration of 4-OHE to mice induced an increase in the levels
of DNA adducts (4-OHE-deoxycytosine, 4-OHE-deoxyguanosine, and 4-OHE-5-methyldeoxycytosine) in the gastrointestinal tract (i.e. oesophagus, stomach and intestine). They
also showed that 4-OHE, which was detected in the volatile emissions of heated perilla oil
(from Perilla frutescens, a member of the mint family) and broiled fish, seems to be
produced by the oxidation of -3 fats (e.g. linolenic acid). Xi et al. (2003) showed that
378
intratracheal instillation of heated cooking oil emissions condensate into Wistar rats
induced a dose- and time-dependant increase in the frequency 8-OHdGDNA adducts in
lung tissue. Li et al. (1998) also noted a decrease in superoxide dismutase activity and an
increase in malondialdehyde (an indicator of oxidative stress) in lung tissue. Similarly,
significantly decreased superoxide dismutase activity and increased malondialdehyde
content in lung tissue was reported in Sprague-Dawley rats exposed by inhalation to
43 mg/m3 fumes from cooking oil heated to 270280C for 2060 days (Rang et al.,
2000).
Rang et al. (2000) showed in the study above that lung tissue samples showed high
P53 protein content. Using immunohistochemical methods, Liu et al. (2005) also
observed overproduction of P53 and a decrease in P16 protein in lung tissues of SpragueDawley rats exposed by inhalation to 43.9 mg/m3 fumes from cooking siritch oil [i.e.
Chinese Hu-Ma oil or linseed oil] (heated to 200220C) for 2060 days. Long et al.
(2005) showed that Sprague Dawley rats exposed by inhalation to fumes from rapeseed
oil heated to 260C (6.935 mg/m3 for 30 min every other day for 12.5 months)
developed pulmonary carcinoma in addition to enhanced production of P53 and a
decrease in fragile histidine triad protein in lung (bronchial epithelia) tissue sections.
A study that used the Drosophila melanogaster sex-linked recessive lethal assay
showed that exposure to a condensate of a cooking oil fume (110, 320 and 960 mg/L in
food) induced heritable mutations (Li et al., 1999). Wang et al. (1995) revealed that
tracheal epithelial cells removed from Wistar rats exposed to rapeseed oil condensate by
three intratracheal instillations of 0.1 or 1.5 mg/kg bw displayed a high frequency of cell
transformation in vitro. Finally, Zhang et al. (1999) showed that exposure of female
Kunming mice to cooking oil emissions condensates from rapeseed oil, soya bean oil and
salad oil by subcutaneous injection (1.12.3 g/kg) caused an inhibition of the delayed
hypersensitivity response and of the activity of natural killer cells in comparison with
controls.
(ii) In-vitro exposure of human cells
Several studies investigated the effect of cooking oil emissions condensates on
cultured human lymphocytes. Jin and Cu (1997) noted significant induction of
unscheduled DNA synthesis in cultured human lymphocytes exposed to cooking oil
emissions condensate (200C) from rapeseed oil and soya bean oil. Similarly, Shen et al.
(1998) reported that fume condensates from heated rapeseed oil collected in Nanjing,
China, induced unscheduled DNA synthesis in human peripheral blood lymphocytes with
and without metabolic activation. Hou et al. (2005) reported that cooking oil emissions
condensate significantly increased chromosomal aberrations but not micronucleus
frequency in human peripheral blood lymphocytes.
32
P-Postlabelling was used to show dose-dependent induction of DNA adducts in
human lung adenocarcinoma CL-3 cells exposed to extracts of cooking oil fumes from
fish fried in soya bean oil. Subsequent liquid chromatography/mass spectrometry
confirmed that the DNA adduct in CL-3 cells induced by exposure to cooking oil
379
emissions extract was benzo-[a]pyrene-7,8-diol-9,10-epoxide-N2-deoxyguanosine (Yang

et al., 2000). In addition, the comet assay showed induction of DNA damage (DNA
strand breaks) in human lung adenocarcinoma CL-3 cells following exposures to
100 g/mL cooking oil emissions condensate from fried fish (Lin et al., 2002). Dosedependent induction of DNA damage, measured using the comet assay, was also
observed in human lung carcinoma A549 cells treated with extracts of fumes from heated
peanut oil (Wu & Yen, 2004), sunflower oil, soya bean oil and lard (Dung et al., 2006).
Dung et al. (2006) determined in the study above that trans-trans-2,4-decanedial (t,t2,4-DDE), which is a by-product of lipid peroxidation and is one of the most abundant
and potent mutagens identified in cooking oil fumes to date (Wu et al. 2001), was present
in all three condensate samples, and induced a significant increase in the level of 8-OHdG
adducts. It is also thought to induce intracellular formation of reactive oxygen species and
has been shown to induce a dose-dependent increase in 8-OHdG in CL-3 cells (Cherng et
al., 2002). Chang et al. (2005) also studied oxidative stress in human bronchial epithelial
BEAS-2B cells, and confirmed that t,t-2,4-DDE induced a concentration-dependent
increase in the production of reactive oxygen species and a decrease in the reduced
glutathione/oxidized glutathione ratio (glutathione status). The data also suggest that t,t2,4-DDE leads to cell proliferation, significant increases in unscheduled DNA synthesis
(measured by bromodeoxyuridine incorporation), as well as induction of tumour necrosis
factor- and interleukin-1 gene expression and release of the corresponding cytokines in
cultured BEAS-2B cells. Co-treatment of BEAS-2B cells with the antioxidant Nacetylcysteine prevented t,t-2,4-DDE-induced release of cytokines and concomitant cell
proliferation.
(iii) Other in-vitro systems
Several studies have shown that exposure of Chinese hamster V79 cells to rapeseed
oil cooking fumes induced a marked increase in the frequency of sister chromatid
exchange (Zhu et al., 1990; Chen et al., 1992) and, moreover, the magnitude of the
genotoxic effect was inversely related to the degree of hydrogenation of the cooking oil
(Zhu et al., 1990). Qu et al. (1992) noted that exposure of V79 cells to an extract of
cooking fumes from heated unrefined rapeseed oil and heated refined rapeseed oil
induced a significant increase in sister chromatid exchange frequency; however, fume
condensate from unrefined rapeseed oil supplemented with the antioxidant butylated
hydroxyanisole (0.02%) failed to induce a concentration-dependent significant increase in
sister chromatid exchange frequency. Additional analyses of fumes from hydrogenated
rapeseed oil samples also failed to induce a significant increase in sister chromatid
exchange frequency. Wu et al. (1999) noted a concentration-related increase in sister
chromatid exchange frequency, both with and without exogenous metabolic activation, in
Chinese hamster ovary (CHO-K1) cells exposed to condensates of fumes from lard or
soya bean oil. The same condensates have also been shown to induce DNA damage (SOS
Chromotest) in Escherichia coli PQ37.
380
Pu et al. (2002) noted a time-dependent increase in DNA cross-links and single-strand

breaks in rat type II lung cells exposed to cooking oil emissions condensates. A reduction
in cytotoxicity, DNA cross-links and strand breaks following pretreatment with the
antioxidant N-acetylcysteine suggested that cooking oil fumes induced oxidative stress in
exposed cells. Similarly, Zhang et al. (2002) noted a concentration-related increase in
DNA damage, as measured by the comet assay, in rat type II pneumocytes exposed to a
condensate of cooking fumes (obtained from a kitchen ventilator) at concentrations up to
10 g/mL. Yin et al. (1998) also noted a significant increase when these cells were
exposed to cooking oil emissions condensate from vegetable oil heated to 2705C.
Finally, three studies demonstrated that cooking oil fumes induced DNA damage in
calf thymus DNA. Wu et al. (1992) demonstrated that exposure to rapeseed oil (heated to
280C)-fume condensate can induce adducts in naked calf thymus DNA without
metabolic activation, and Yin et al. (1997) demonstrated that exposure to rapeseed and
soya bean oil (heated to 270C)-fume condensates can induce cross-links in calf thymus
DNA. Xi et al. (2003) demonstrated that exposure to cooking oil emissions condensates
can induce 8-OHdG formation in calf thymus DNA.
Cooking oil emissions emissions were also investigated in several cell transformation
assays. A dose-dependent increase in the frequency of morphological transformation was
observed in BALB/c3T3 cells exposed to condensates of cooking fumes (Shen et al.,
1998). Zhao et al. (2000) observed dose-dependent malignant transformation in KMB-17
diploid human embryo lung cells exposed to a condensate of cooking oil fumes. The
transformed cells showed a variety of distinct features, including loss of density
inhibition, loss of contact inhibition, growth at low serum concentration, agglutination at
low concentrations of concanavalin A, aneuploidy and deviation from diploid status and
loss of anchorage dependence (Zhao et al. 2002).
(iv) Salmonella reverse mutation assay
Studies have related mutagenic activity in Salmonella to a host of indoor activities,
including cooking (e.g. Sexton et al., 1986; Teschke et al., 1989). A wide range of sourcespecific studies has confirmed the mutagenic activity in Salmonella of emissions from
heated cooking oil (e.g. Qu et al., 1992; Nardini et al., 1994; Shields et al., 1995; Chiang
et al., 1997, 1998; Wu et al., 2001) and highlighted that these sources are significant
contributors to the mutagenic activity of indoor air. Moreover, several studies have noted
a positive empirical relationship between the mutagenic activity of indoor air (in
revertents/m3) in Salmonella and the concentration of airborne PM (Mumford et al., 1987;
Chiang et al., 1999). This relationship is not unexpected because combustion emissions
are composed of PM, and several researchers (e.g. Maertens et al., 2004, 2008) have
commented on the tendency for mutagens in combustion emissions, such as PAHs, to
adsorb to particulate material and solid surfaces (e.g. upholstery, carpets). Chiang et al.
(1999) noted particle concentration levels as high as 28 mg/m3 in dwellings that were
filled with cooking oil fumes.
381
Table 4.1 provides a summary of studies that have used the Salmonella assay to
investigate the mutagenic activity (in revertants/m3) of indoor air particulates from hightemperature frying. The data indicate that organic extracts of indoor air particulate
material collected from areas without any obvious source of contamination have
mutagenic potency values in Salmonella in the 1 and 10 TA98 revertants/m3 range. Table
4.2 provides a summary of studies that investigated the mutagenic potency (in
revertants/mg) in Salmonella of source-specific particulate emissions from hightemperature frying.
The mutagenic potency values reached several hundreds of TA98 revertants/m3 and
several thousands of TA98 revertants/mg of particle with or without exogenous metabolic
activation (Sexton et al., 1986; Lfroth et al., 1991; Wu et al., 2001). It is interesting to
note that two studies (Qu et al., 1992; Xu et al., 1995) described a relationship between
the mutagenicity of cooking oil emissions condensates and heating temperature. Qu et al.
(1992) noted that condensates of fumes from unrefined rapeseed oil did not elicit a
significant response unless the oil was heated to 270C (TA98 with metabolic activation).
Similarly, Xu et al. (1995) only detected a significant mutagenic response (TA98 with
metabolic activation) when the rapeseed oil was heated to 230C or 280C.
Several studies have used bioassay-directed fractionation methods to identify
mutagenic agents in condensates of cooking oil fumes. Wu et al. (2001) determined that
the mutagenic activity in Salmonella TA98 of methanolic extracts from heated peanut oil
fumes without metabolic activation is contained within a neutral fraction. Detailed
chemical analyses of the neutral fraction resulted in the identification of four direct-acting
alkenals: t,t-2,4-DDE, trans-trans-2,4-nonadienal, trans-2-decenal and trans-2-undecenal.
The most potent agent, t,t-2,4-DDE, elicited 385 revertants/g in TA100 and
18 revertants/g in TA98 (without metabolic activation). Qu et al. (1992) hypothesized
that the mutagenic agents in condensates of heated rapeseed oil are the oxidized products
of unsaturated fatty acids such as linoleic and linolenic acid, and noted contrasting levels
of mutagenic activity between unsaturated oil samples and highly hydrogenated samples.
Unsaturated rapeseed oil samples with 10 and 12% linolenic and linoleic acid,
respectively, elicited significant positive responses, whereas highly hydrogenated samples
without either acid failed to elicit a positive response. Moreover, complete elimination of
mutagen formation by the addition of 0.1% butylated hydroxyanisole supported this
hypothesis. In addition, Shields et al. (1995) showed that mutagenic activity in TA98
(with metabolic activation) was induced when unsaturated fatty acids such as linoleic acid
and linolenic acid were heated to 240C. Moreover, the mutagenic activity (TA98 with
metabolic activation) of condensates from heated Chinese rapeseed oil (275280C),
heated peanut oil (260265C) and heated soya bean oil (260265C) was positively
related to the content of linolenic acid. The presence of several other mutagens in the
condensates of heated oils was also confirmed. These included 1,3-butadiene, benzene,
acetaldehyde and acrolein.
382
Table 4.1. Mutagenicity in Salmonella of organic extracts of indoor air particulate matter from hightemperature frying (in revertants/m3)
Source
Particle concentration
(g/m3)
Mutagenic potency in revertants/m3

Without metabolic
activation
With metabolic
activation
Reference
Italy
Canada
Canada
USA
31600
US
US
US
329
618
617
50
108
ND
ND
220

Teschke et al. (1989)
Teschke et al. (1989)
Sexton et al. (1986)
USA
US
960
1180
Sexton et al. (1986)

a
Type of cooking oil not specified
TA98
Olive oil
Deep frya
Woka
Frying hamburgera
TA100
Frying hamburgera
Country
Table 4.2. Mutagenicity in Salmonella of organic extracts of particulate emissions from high-temperature
frying (in revertants/mg)
Source
(g/m3)

Without metabolic
activation
With metabolic
activation
Reference
China
China
US
US
ND
neg.
[46.1]
[62.2]
Xu et al. (1995)
Qu et al. (1992)
China
US
neg.
[123.9]
Qu et al. (1992)
China
China
China
China
China
Italy
China
China
China
China
China
China
China
China
China
China
US
US
25.1
26.8
28.3
31600
26.2
US
US
US
US
US
28.5
US
US
US
ND
ND
[19.6]
[12.5]
[8.1]
10
neg.
neg.
35
61
82
43
neg
neg.
ND
neg.
[282.5]
[109.7]
[62.4]
neg.
[21]
3
[180]
54
101
180
236
122
[80]
82
[45.6]
[101]
Shields et al. (1995)

Xu et al. (1995)
Chiang et al. (1999)
Shields et al. (1995)
Qu et al. (1992)
TA98
Rapeseed oil 230C
Rapeseed oil
(unrefined) 270C
Rapeseed oil (refined)
270C
Rapeseed oil 275C
Rapeseed oil 280C
Sunflower oil 300C
Refined lard 300C
Vegetable oil 300C
Olive oil
Lard
Lard 100C
Lard 200C
Lard 200C
Lard 300C
Lard 300C
Soya bean oil
Soya bean oil 200C
Soya bean oil 260C
Soya bean oil 270C
Country
383
384
Table 4.2. (contd)

Source
Country
(g/m3)

Without metabolic
activation
With metabolic
activation
Reference
China
China
China
China
China
Sweden
Sweden
US
US
27.1
US
US
US
US
neg.
42
neg.
neg.
[12600]
ND
ND
61
112
[40]
66
[11600]
7400
800

Wu et al. (2001)
Lfroth et al. (1991)
Lfroth et al (1991)
Sweden
Sweden
US
US
ND
ND
15
25
Lfroth et al (1991)
Lfroth et al (1991)
TA98NR
Olive oil b
Italy
31600
10
ND
TA100
Peanut oil
China
US
[21000]
[18030]
Wu et al. (2001)
ND, no data; neg., negative; US, unspecified

a
type of cooking oil not specified
b
spilled on a hot plate
TA98 (contd)
Soya bean oil 300C
Soya bean oil 300C
Peanut oil
Peanut oil 300C
Peanut oil
Lean pork, minceda
Commercial pork,
minceda
Pork chops
Baltic herringa
4.3
385
Genetic susceptibility
4.4
Mechanistic considerations
The mutagenicity of emissions from high-temperature frying may be due to PAHs

and lipid peroxidation products, among other compounds. Unlike emissions from the
combustion of wood and coal, for which extensive, positive genotoxicity data have been
generated almost exclusively in humans in vivo, nearly all of the mutagenicity data for
emissions from high-temperature frying have been generated in experimental animals and
in cells in vitro. The large number of genotoxic end-points and largely positive results,
especially in experimental animals, provide plausible evidence that a carcinogenic
mechanism similar to that described for coal emissions also applies to emissions from
high-temperature frying.
4.5
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389
5. Summary of Data Reported

5.1
Exposure data
A large proportion of the emissions generated during cooking is steam from the water
contents of the food. However, during frying (with oil), fatty acid esters that make up
edible oils and fat can decompose and produce volatile organic compounds, as well as
semi-volatile compounds that can condense to form particles. A wide variety of organic
compounds have been identified in cooking emissions, including alkanes, alkenes,
alkanoic acids, carbonyls, polycyclic aromatic hydrocarbons and aromatic amines. The
main volatile compounds generated during frying were aldehydes, alcohols, ketones,
alkanes, phenols and acids. Of particular concern in relation to carcinogenicity are
polycyclic aromatic hydrocarbons, heterocyclic amines and aldehydes. The contribution
of commercial cooking operations to outdoor levels of polycyclic aromatic hydrocarbons
can be substantial.
Cooking also increases the concentrations of fine and ultrafine particles.
The chemical composition of cooking emissions varies widely depending on the
cooking oils used, the temperature, the kind of food cooked, and the method and style of
cooking adopted.
5.2
Human carcinogenicity data
To examine the potential association between emissions from cooking oil and the risk
for lung cancer, the Working Group considered studies to be more informative when
cooking-related effects were separated from fuel-related effects and when the studies
reported results on the exposureresponse relationships between high-temperature frying
(i.e. stir-frying, deep-frying and pan-frying) and lung cancer. Studies that only collected
information on cooking habits (e.g. age at starting to cook, years of cooking), ventilation
in the kitchen or frequency of eye irritation due to cooking or smokiness in the kitchen
were considered to be less informative because they did not allow the effects of emissions
from cooking oil to be distinguished from those of combustion products of cooking fuels.
On this basis, four casecontrol studies were considered to be the most informative.
The study conducted in Hong Kong Special Administrative Region used a composite
index that accounted for both the frequency and the duration of all three types of hightemperature frying; it found a significant threefold increased risk for lung cancer
associated with moderate to high categories of exposure (>150 total dishyears) and an
eightfold increased risk associated with the highest category (>200 total dishyears).
In the other three informative studies in Shanghai (two studies) and Gansu, China, the
risk for lung cancer increased generally with increasing frequency of stir-frying, deepfrying and pan-frying and a nearly twofold increased risk was associated with the highest
390
frequency of high-temperature frying. In the study conducted in Gansu, however, the risk
for lung cancer increased significantly with increasing frequency of stir-frying but not of
deep-frying. However, potential confounding by solid cooking fuel could not be ruled out
with reasonable confidence in these three studies. In the study from Hong Kong that
compared risk (per 10 dishyears) for the three types of high-temperature frying, the
magnitude of risk was highest for deep-frying, intermediate for pan-frying and lowest for
stir-frying, but all were associated with a significantly elevated risk for lung cancer. In the
studies in Shanghai and Gansu, the effects of the different types of frying were not
mutually adjusted for and, because of the substantial differences in the frequency of stirfrying and deep-frying, a direct comparison of the risk estimates associated with an
individual type of frying could not be made.
These four studies also provided information on the specific type of cooking oil.
There was no significant difference in risk estimates for lung cancer with use of any
particular type of cooking oil (peanut oil, corn oil or canola oil a type of rapeseed oil)
in the study in Hong Kong. In the three other studies, risk was higher for women who
cooked with canola oil most frequently. Some increased risk was associated with cooking
with linseed oil in the population-based casecontrol study conducted in Gansu and with
cooking with soya bean oil in the study in Shanghai.
In summary, results from the four most informative studies demonstrate an exposure
response relationship between increased frequency of or cumulative exposure (frequency
and duration) to high-temperature frying and increased risk for lung cancer. These four
studies were conducted in different populations in Hong Kong, urban Shanghai (two
studies) and rural Gansu where study characteristics differed, and where cooking practices
and other co-factors may also have differed. However, confounding by cooking fuel could
not be ruled out with reasonable confidence in the latter three studies. Furthermore, all
epidemiological evidence was based on casecontrol studies and recall bias may have
contributed to the positive findings in some of these studies.
5.3
Animal carcinogenicity data
Inhalation of high concentrations of emissions from high-temperature frying of

unrefined rapeseed oil caused an increase in the incidence of lung carcinomas (mainly
adenocarcinomas) in male and female mice in one study and female rats in another study.
5.4
See also Section 5.4 in the monograph on household use of solid fuels.
The available information on the genotoxic and mutagenic activity of cooking oil
fumes includes data from professional and home cooks that show the induction of 8oxoguanine DNA glycosylase 1, which is a DNA repair enzyme that removes 8hydroxydeoxyguanine. In experimental animals, cooking oil-fume condensates from
rapeseed and soya bean oils induced micronuclei in the bone marrow of both mice and
391
rats, oxidative DNA damage, enhanced transformation of tracheal epithelia and

accumulation of TP53 protein. Cooking oil-fume condensate also induced chromosomal
aberrations in the diploid male germ cells of mice. In cultured human or animal cells,
cooking oil fumes from a variety of oils induced DNA adducts, DNA damage (comet
assay), oxidative damage, sister chromatid exchange, chromosomal aberrations,
unscheduled DNA synthesis and DNA cross-links. Cooking oil fumes induced DNA
damage in naked calf thymus DNA.
Extracts or condensates of emissions from cooking oil fumes are mutagenic in
Salmonella. In strain TA98, in the presence or absence of a metabolic activation system,
the mutagenic potency in terms of revertants per milligram of particle reached several
thousands or in terms of revertants per cubic metre of air reached several hundreds.
Several studies showed that the mutagenicity of cooking fumes in Salmonella was
positively correlated with heating temperature, the extent of unsaturation and the
concentration of unsaturated fatty acids. Polycyclic aromatic hydrocarbons and lipid
peroxidation products also contribute to the mutagenic activity of cooking oil fumes.
392
6. Evaluation and Rationale

There is limited evidence in humans for the carcinogenicity of emissions from hightemperature frying.
There is sufficient evidence in experimental animals for the carcinogenicity of
emissions from high-temperature unrefined rapeseed oil.
Overall evaluation
Emissions from high-temperature frying are probably carcinogenic to humans
(Group 2A).
Rationale
Among the studies of cancer in humans, four were considered most informative
because they allowed the effects of cooking-oil emissions to be distinguished from those
of the fuels used for heating the stove. These studies, in four different populations,
consistently showed an increased risk for lung cancer and showed an exposureresponse
relationship between increased frequency or duration of high-temperature frying and
increased risk for lung cancer. Confounding by the fuel used to heat the stove could be
ruled out with reasonable confidence in only one of these studies.
These epidemiological results are supported by the evidence from studies in
experimental animals. Although positive results in experimental animals were observed
only for unrefined rapeseed oil heated to high temperatures, positive results for
mutagenicity were observed in virtually every category of in-vivo test. These
mutagenicity data would have been enough to support an evaluation of Group 2A if the
evidence of carcinogenicity in experimental animals had been less than sufficient or the
evidence of carcinogenicity in humans had been less than limited. The mechanistic data
also show that lipid peroxidation is an important mechanism that leads to carcinogenesis
by these mixtures, although there may also be a contribution from the mechanisms by
which polycyclic aromatic hydrocarbons induce cancer (see Volume 92).
The evaluation was made for emissions from high-temperature frying. This wording
was determined after considering several aspects of the available data.
The available studies involved frying at high temperatures. Emissions from lowtemperature cooking methods can be considerably different from those studied. Data
indicate that cooking oil has little mutagenic potential when heated below 100oC and high
mutagenic potential when heated above 230oC.
No differences were apparent between stir-frying, deep-frying and pan-frying when
these methods were investigated separately. Other high-temperature cooking methods
393
(e.g. baking) were not included because the Working Group reasoned that their emissions
could be considerably different from those of frying.
The epidemiological data are not detailed enough to distinguish between different
cooking oils and fats and experimental animal data were available for unrefined rapeseed
oil only, although data are available that indicate a higher mutagenic potency for
unsaturated fats.
The epidemiological data do not permit the risk to be attributed to a specific chemical
compound or to the cooking oil alone. Some risk could be attributable to the food being
cooked, to emissions from the heated stove or cooking vessel itself or to the fuel used to
heat the stove. Nevertheless, it might be reasonable to attribute some risk to cooking oils,
because in-vivo and in-vitro data indicate that emissions from some oils heated to high
temperatures are mutagenic.
LIST OF ABBREVIATIONS
ABC
ADC
AhR
AKR
Asymp. sig.
ATP
AUC
avg.
BA
BAL
B(a)P
Bcm
BP
bw
CI
CIN
CO
COPD
CV
CYP
DBA
DMBA
DMSO
ELISA
ENT
GC
GM
GSH
GST
HOGG1
HPLC
HPV
HSCU
ICD
LC
LPG
adenosine triphosphate binding cassette

adenocarcinoma
aryl hydrocarbon receptor
aldo-keto reductase
asymptote significance
adenosine triphosphate
area under the curve
average
basal-cell cancer
bronchioalveolar lavage
benzo[a]pyrene
billion cubic metres
benzo[a]pyrene
body weight
confidence interval
cervical intraepithelial neoplasia
carbon monoxide
chronic obstructive pulmonary disease
coefficient of variation
cytochrome P450
dibenz[a]anthracene
7,12-dimethylbenz[a]anthracene
dimethyl sulfoxide
enzyme-linked immunosorbent assay
ear, nose and throat
gas chromatography
geometric mean
glutathione
glutathione S-transferase
human 8-oxyguanine DNA glycosylase 1
high-performance liquid chromatography
human papilloma virus
heavy smoky coal user
International Classification of Diseases
liquid chromatography
liquefied petroleum gas
395
396
Max.
MDM2
MS
Mt
N
NADPH
ND
NG
NOS
NOx
NPC
NS
8-OHdG
4-OHE
PAH
Pap
PARP
PCB
PCDD
PCDF
PCR
PJ
PM
QMS
S
SCC
SD
SD
SE
SM
SNP
SO2
SPM
SULT
t,t-2,4-DDE
TLC
TPA
TSP
TWA
TWh
UFP
US
maximum
murine double minute 2
mass spectrometry
million tones
number
nicotinamide adenine dinucleotide phosphate
not detected
not given
not otherwise specified
nitrogen oxide
nasopharyngeal carcinoma
not significant
8-hydroxydeoxyguanine
4-oxo-2-hexenal
polychlorinated aromatic hydrocarbon
Papanicolaou
poly(ADP-ribose)polymerase
polychlorinated biphenyl
polychlorinated dibenzo-para-dioxin
polychlorinated dibenzofuran
polymerase chain reaction
peta joules
particulate matter
quadruple ion-trap mass spectrometry
significant
squamous-cell carcinoma
standard deviation
standard deviation
standard error
small-cell cancer
single nucleotide polymorphisms
sulfur dioxide
suspended particulate matter
sulfotransferase
trans,trans-2,4-decadienal
thin-layer chromatography
12-O-tetradecanoylphorbol-13-acetate
total suspended particles
time-weighted average
terawatt hours
ultrafine particles
unspecified
CUMULATIVE CROSS INDEX TO IARC MONOGRAPHS ON

THE EVALUATION OF CARCINOGENIC RISKS TO HUMANS
The volume, page and year of publication are given. References to corrigenda are given in
parentheses.
A
A--C
Acenaphthene
Acepyrene
Acetaldehyde
40, 245 (1986); Suppl. 7, 56 (1987)

92, 35 (2010)
92, 35 (2010)
36, 101 (1985) (corr. 42, 263); Suppl. 7, 77
(1987); 71, 319 (1999)
Acetaldehyde formylmethylhydrazone (see Gyromitrin)

Acetamide
Acetaminophen (see Paracetamol)
Aciclovir
Acid mists (see Sulfuric acid and other strong inorganic acids,
occupational exposures to mists and vapours from)
Acridine orange
Acriflavinium chloride
Acrolein
Acrylamide
Acrylic acid
Acrylic fibres
Acrylonitrile
Acrylonitrile-butadiene-styrene copolymers
Actinolite (see Asbestos)
Actinomycin D (see also Actinomycins)
Actinomycins
Adriamycin
AF-2
Aflatoxins
7, 197 (1974); Suppl. 7, 56, 389 (1987);

71, 1211 (1999)
76, 47 (2000)
16, 145 (1978); Suppl. 7, 56 (1987)

13, 31 (1977); Suppl. 7, 56 (1987)
19, 479 (1979); 36, 133 (1985); Suppl. 7,
78 (1987); 63, 337 (1995) (corr. 65, 549)
39, 41 (1986); Suppl. 7, 56 (1987); 60, 389
(1994)
19, 47 (1979); Suppl. 7, 56 (1987); 71,
1223 (1999)
19, 86 (1979); Suppl. 7, 56 (1987)
19, 73 (1979); Suppl. 7, 79 (1987); 71, 43
(1999)
19, 91 (1979); Suppl. 7, 56 (1987)
Suppl. 7, 80 (1987)
10, 29 (1976) (corr. 42, 255)
10, 43 (1976); Suppl. 7, 82 (1987)
31, 47 (1983); Suppl. 7, 56 (1987)
1, 145 (1972) (corr. 42, 251); 10, 51
(1976); Suppl. 7, 83 (1987); 56, 245
(1993); 82, 171 (2002)
Aflatoxin B1 (see Aflatoxins)

Aflatoxin B2 (see Aflatoxins)
Aflatoxin G1 (see Aflatoxins)
Aflatoxin G2 (see Aflatoxins)
Aflatoxin M1 (see Aflatoxins)
Agaritine
31, 63 (1983); Suppl. 7, 56 (1987)
397
398
Alcohol drinking
Aldicarb
Aldrin
Allyl chloride
Allyl isothiocyanate
Allyl isovalerate
Aluminium production
Amaranth
5-Aminoacenaphthene
2-Aminoanthraquinone
para-Aminoazobenzene
ortho-Aminoazotoluene
para-Aminobenzoic acid
4-Aminobiphenyl
2-Amino-3,4-dimethylimidazo[4,5-f]quinoline (see MeIQ)
2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline
(see MeIQx)
3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole
(see Trp-P-1)
2-Aminodipyrido[1,2-a:3,2-d]imidazole (see Glu-P-2)
1-Amino-2-methylanthraquinone
2-Amino-3-methylimidazo[4,5-f]quinoline (see IQ)
2-Amino-6-methyldipyrido[1,2-a:3,2-d]imidazole (see Glu-P-1)
2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (see PhIP)
2-Amino-3-methyl-9H-pyrido[2,3-b]indole (see MeA--C)
3-Amino-1-methyl-5H-pyrido[4,3-b]indole (see Trp-P-2)
2-Amino-5-(5-nitro-2-furyl)-1,3,4-thiadiazole
2-Amino-4-nitrophenol
2-Amino-5-nitrothiazole
2-Amino-9H-pyrido[2,3-b]indole (see A--C)
11-Aminoundecanoic acid
Amitrole
Ammonium potassium selenide (see Selenium and selenium
compounds)
Amorphous silica (see also Silica)
Amosite (see Asbestos)
Ampicillin
Amsacrine
Anabolic steroids (see Androgenic (anabolic) steroids)
Anaesthetics, volatile
Analgesic mixtures containing phenacetin (see also Phenacetin)
Androgenic (anabolic) steroids
Angelicin and some synthetic derivatives (see also Angelicins)
44 (1988)
53, 93 (1991)
5, 25 (1974); Suppl. 7, 88 (1987)
36, 39 (1985); Suppl. 7, 56 (1987); 71,
1231 (1999)
36, 55 (1985); Suppl. 7, 56 (1987); 73, 37
(1999)
36, 69 (1985); Suppl. 7, 56 (1987); 71,
1241 (1999)
34, 37 (1984); Suppl. 7, 89 (1987); 92, 35
(2010)
8, 41 (1975); Suppl. 7, 56 (1987)
16, 243 (1978); Suppl. 7, 56 (1987)
27, 191 (1982); Suppl. 7, 56 (1987)
8, 53 (1975); Suppl. 7, 56, 390 (1987)
8, 61 (1975) (corr. 42, 254); Suppl. 7, 56
(1987)
16, 249 (1978); Suppl. 7, 56 (1987)
1, 74 (1972) (corr. 42, 251); Suppl. 7, 91
(1987)
27, 199 (1982); Suppl. 7, 57 (1987)
7, 143 (1974); Suppl. 7, 57 (1987)

57, 167 (1993)
57, 177 (1993)
16, 43 (1978); Suppl. 7, 57 (1987)
31, 71 (1983); Suppl. 7, 57 (1987)
39, 239 (1986); Suppl. 7, 57 (1987)
7, 31 (1974); 41, 293 (1986) (corr. 52,
513; Suppl. 7, 92 (1987); 79, 381 (2001)
42, 39 (1987); Suppl. 7, 341 (1987); 68, 41

(1997) (corr. 81, 383)
50, 153 (1990)
76, 317 (2000)
11, 285 (1976); Suppl. 7, 93 (1987)
Suppl. 7, 310 (1987)
Suppl. 7, 96 (1987)
40, 291 (1986)
CUMULATIVE INDEX
Angelicin plus ultraviolet radiation (see also Angelicin and some
synthetic derivatives)
Angelicins
Aniline
ortho-Anisidine
para-Anisidine
Anthanthrene
Anthophyllite (see Asbestos)
Anthracene
Anthranilic acid
Anthraquinones
Antimony trioxide
Antimony trisulfide
ANTU (see 1-Naphthylthiourea)
Apholate
para-Aramid fibrils
Aramite
Areca nut (see also Betel quid)
Aristolochia species (see also Traditional herbal medicines)
Aristolochic acids
Arsanilic acid (see Arsenic and arsenic compounds)
Arsenic and arsenic compounds
Arsenic in drinking-water
Arsenic pentoxide (see Arsenic and arsenic compounds)
Arsenic trioxide (see Arsenic in drinking-water)
Arsenic trisulfide (see Arsenic in drinking-water)
Arsine (see Arsenic and arsenic compounds)
Asbestos
Atrazine
Attapulgite (see Palygorskite)
Auramine (technical-grade)
Auramine, manufacture of (see also Auramine, technical-grade)
Aurothioglucose
Azacitidine
5-Azacytidine (see Azacitidine)
Azaserine
Azathioprine
Aziridine
2-(1-Aziridinyl)ethanol
Aziridyl benzoquinone
Azobenzene
AZT (see Zidovudine)
399
Suppl. 7, 57 (1987)
Suppl. 7, 57 (1987)
4, 27 (1974) (corr. 42, 252); 27, 39 (1982);
Suppl. 7, 99 (1987)
27, 63 (1982); Suppl. 7, 57 (1987); 73, 49
(1999)
27, 65 (1982); Suppl. 7, 57 (1987)
32, 95 (1983); Suppl. 7, 57 (1987); 92, 35
(2010)
32, 105 (1983); Suppl. 7, 57 (1987); 92, 35
(2010)
16, 265 (1978); Suppl. 7, 57 (1987)
82, 129 (2002)
47, 291 (1989)
47, 291 (1989)
9, 31 (1975); Suppl. 7, 57 (1987)
68, 409 (1997)
5, 39 (1974); Suppl. 7, 57 (1987)
85, 39 (2004)
82, 69 (2002)
82, 69 (2002)
1, 41 (1972); 2, 48 (1973); 23, 39 (1980);
Suppl. 7, 100 (1987)
84, 39 (2004)
2, 17 (1973) (corr. 42, 252); 14 (1977)

(corr. 42, 256); Suppl. 7, 106 (1987) (corr.
45, 283)
53, 441 (1991); 73, 59 (1999)
1, 69 (1972) (corr. 42, 251); Suppl. 7, 118
(1987)
Suppl. 7, 118 (1987)
13, 39 (1977); Suppl. 7, 57 (1987)
26, 37 (1981); Suppl. 7, 57 (1987); 50, 47
(1990)
10, 73 (1976) (corr. 42, 255); Suppl. 7, 57
(1987)
26, 47 (1981); Suppl. 7, 119 (1987)
9, 37 (1975); Suppl. 7, 58 (1987); 71, 337
(1999)
9, 47 (1975); Suppl. 7, 58 (1987)
9, 51 (1975); Suppl. 7, 58 (1987)
8, 75 (1975); Suppl. 7, 58 (1987)
400
B
Barium chromate (see Chromium and chromium compounds)
Basic chromic sulfate (see Chromium and chromium compounds)
BCNU (see Bischloroethyl nitrosourea)
11H-Benz[bc]aceanthrylene
Benz[j]aceanthrylene
Benz[l]aceanthrylene
Benz[a]acridine
Benz[c]acridine
Benzal chloride (see also -Chlorinated toluenes and benzoyl
chloride)
Benz[a]anthracene
Benzene
Benzidine
Benzidine-based dyes
Benzo[b]chrysene
Benzo[g]chrysene
Benzo[a]fluoranthene
Benzo[j]fluoranthene
Benzo[ghi]fluoranthene
Benzo[a]fluorene
Benzo[b]fluorene
Benzo[c]fluorene
Benzofuran
Benzo[ghi]perylene
Benzo[c]phenanthrene
Benzo[a]pyrene
Benzo[e]pyrene
1,4-Benzoquinone (see para-Quinone)
1,4-Benzoquinone dioxime
Benzotrichloride (see also -Chlorinated toluenes and benzoyl
chloride)
Benzoyl chloride (see also -Chlorinated toluenes and benzoyl
chloride)
92, 35 (2010)
92, 35 (2010)
92, 35 (2010)
32, 123 (1983); Suppl. 7, 58 (1987)
3, 241 (1973); 32, 129 (1983); Suppl. 7, 58
(1987)
29, 65 (1982); Suppl. 7, 148 (1987); 71,
453 (1999)
3, 45 (1973); 32, 135 (1983); Suppl. 7, 58
(1987); 92, 35 (2010)
7, 203 (1974) (corr. 42, 254); 29, 93, 391
(1982); Suppl. 7, 120 (1987)
1, 80 (1972); 29, 149, 391 (1982); Suppl. 7,
123 (1987)
Suppl. 7, 125 (1987)
92, 35 (2010)
92, 35 (2010)
92, 35 (2010)
3, 69 (1973); 32, 147 (1983); Suppl. 7, 58
(1987); 92, 35 (2010)
3, 82 (1973); 32, 155 (1983); Suppl. 7, 58
(1987); 92, 35 (2010)
32, 163 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
32, 171 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
32, 177 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
32, 183 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
32, 189 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
63, 431 (1995)
32, 195 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
32, 205 (1983); Suppl. 7, 58 (1987); 92, 35
(2010)
3, 91 (1973); 32, 211 (1983); (corr. 68,
477); Suppl. 7, 58 (1987); 92, 35 (2010)
3, 137 (1973); 32, 225 (1983); Suppl. 7, 58
(1987); 92, 35 (2010)
29, 185 (1982); Suppl. 7, 58 (1987); 71,
1251 (1999)
29, 73 (1982); Suppl. 7, 148 (1987); 71,
453 (1999)
29, 83 (1982) (corr. 42, 261); Suppl. 7, 126
(1987); 71, 453 (1999)
CUMULATIVE INDEX
Benzoyl peroxide
Benzyl acetate
Benzyl chloride (see also -Chlorinated toluenes and benzoyl
chloride)
Benzyl violet 4B
Bertrandite (see Beryllium and beryllium compounds)
Beryllium and beryllium compounds
Beryllium acetate (see Beryllium and beryllium compounds)
Beryllium acetate, basic (see Beryllium and beryllium
compounds)
Beryllium-aluminium alloy (see Beryllium and beryllium
compounds)
Beryllium carbonate (see Beryllium and beryllium compounds)
Beryllium chloride (see Beryllium and beryllium compounds)
Beryllium-copper alloy (see Beryllium and beryllium
compounds)
Beryllium-copper-cobalt alloy (see Beryllium and beryllium
compounds)
Beryllium fluoride (see Beryllium and beryllium compounds)
Beryllium hydroxide (see Beryllium and beryllium compounds)
Beryllium-nickel alloy (see Beryllium and beryllium compounds)
Beryllium oxide (see Beryllium and beryllium compounds)
Beryllium phosphate (see Beryllium and beryllium compounds)
Beryllium silicate (see Beryllium and beryllium compounds)
Beryllium sulfate (see Beryllium and beryllium compounds)
Beryl ore (see Beryllium and beryllium compounds)
Betel quid with tobacco
Betel quid without tobacco
BHA (see Butylated hydroxyanisole)
BHT (see Butylated hydroxytoluene)
Biomass fuel (primarily wood), indoor emissions from household
combustion of
Bis(1-aziridinyl)morpholinophosphine sulfide
2,2-Bis(bromomethyl)propane-1,3-diol
Bis(2-chloroethyl)ether
N,N-Bis(2-chloroethyl)-2-naphthylamine
Bischloroethyl nitrosourea (see also Chloroethyl nitrosoureas)
1,2-Bis(chloromethoxy)ethane
1,4-Bis(chloromethoxymethyl)benzene
Bis(chloromethyl)ether
Bis(2-chloro-1-methylethyl)ether
Bis(2,3-epoxycyclopentyl)ether
401
36, 267 (1985); Suppl. 7, 58 (1987); 71,
345 (1999)
40, 109 (1986); Suppl. 7, 58 (1987); 71,
1255 (1999)
11, 217 (1976) (corr. 42, 256); 29, 49
(1982); Suppl. 7, 148 (1987); 71, 453
(1999)
16, 153 (1978); Suppl. 7, 58 (1987)
1, 17 (1972); 23, 143 (1980) (corr. 42,
260); Suppl. 7, 127 (1987); 58, 41 (1993)
37, 141 (1985); Suppl. 7, 128 (1987); 85,

39 (2004)
37, 141 (1985); Suppl. 7, 128 (1987); 85,
39 (2004)
95, 41 (2010)
9, 55 (1975); Suppl. 7, 58 (1987)
77, 455 (2000)
9, 117 (1975); Suppl. 7, 58 (1987); 71,
1265 (1999)
4, 119 (1974) (corr. 42, 253); Suppl. 7, 130
(1987)
26, 79 (1981); Suppl. 7, 150 (1987)
15, 31 (1977); Suppl. 7, 58 (1987); 71,
1271 (1999)
15, 37 (1977); Suppl. 7, 58 (1987); 71,
1273 (1999)
4, 231 (1974) (corr. 42, 253); Suppl. 7, 131
(1987)
41, 149 (1986); Suppl. 7, 59 (1987); 71,
1275 (1999)
47, 231 (1989); 71, 1281 (1999)
402
Bisphenol A diglycidyl ether (see also Glycidyl ethers)

Bisulfites (see Sulfur dioxide and some sulfites, bisulfites and
metabisulfites)
Bitumens
Bleomycins (see also Etoposide)
Blue VRS
Boot and shoe manufacture and repair
Bracken fern
Brilliant Blue FCF, disodium salt
Bromochloroacetonitrile (see also Halogenated acetonitriles)
Bromodichloromethane
Bromoethane
Bromoform
1,3-Butadiene
1,4-Butanediol dimethanesulfonate
2-Butoxyethanol
1-tert-Butoxypropan-2-ol
n-Butyl acrylate
Butylated hydroxyanisole
Butylated hydroxytoluene
Butyl benzyl phthalate
-Butyrolactone
-Butyrolactone
71, 1285 (1999)
35, 39 (1985); Suppl. 7, 133 (1987)

26, 97 (1981); Suppl. 7, 134 (1987)
16, 163 (1978); Suppl. 7, 59 (1987)
25, 249 (1981); Suppl. 7, 232 (1987)
40, 47 (1986); Suppl. 7, 135 (1987)
16, 171 (1978) (corr. 42, 257); Suppl. 7, 59
(1987)
71, 1291 (1999)
52, 179 (1991); 71, 1295 (1999)
52, 299 (1991); 71, 1305 (1999)
52, 213 (1991); 71, 1309 (1999)
39, 155 (1986) (corr. 42, 264); Suppl. 7,
136 (1987); 54, 237 (1992); 71, 109
(1999); 97,45 (2008)
4, 247 (1974); Suppl. 7, 137 (1987)
88, 329
88, 415
39, 67 (1986); Suppl. 7, 59 (1987); 71, 359
(1999)
40, 123 (1986); Suppl. 7, 59 (1987)
40, 161 (1986); Suppl. 7, 59 (1987)
29, 193 (1982) (corr. 42, 261); Suppl. 7, 59
(1987); 73, 115 (1999)
11, 225 (1976); Suppl. 7, 59 (1987); 71,
1317 (1999)
11, 231 (1976); Suppl. 7, 59 (1987); 71,
367 (1999)
C
Cabinet-making (see Furniture and cabinet-making)
Cadmium acetate (see Cadmium and cadmium compounds)
Cadmium and cadmium compounds
Cadmium chloride (see Cadmium and cadmium compounds)
Cadmium oxide (see Cadmium and cadmium compounds)
Cadmium sulfate (see Cadmium and cadmium compounds)
Cadmium sulfide (see Cadmium and cadmium compounds)
Caffeic acid
Caffeine
Calcium arsenate (see Arsenic in drinking-water)
Calcium carbide production
Calcium chromate (see Chromium and chromium compounds)
Calcium cyclamate (see Cyclamates)
Calcium saccharin (see Saccharin)
Cantharidin
Caprolactam
Captafol
2, 74 (1973); 11, 39 (1976) (corr. 42, 255);

Suppl. 7, 139 (1987); 58, 119 (1993)
56, 115 (1993)

51, 291 (1991)
92, 35 (2010)
10, 79 (1976); Suppl. 7, 59 (1987)

19, 115 (1979) (corr. 42, 258); 39, 247
(1986) (corr. 42, 264); Suppl. 7, 59, 390
(1987); 71, 383 (1999)
53, 353 (1991)
CUMULATIVE INDEX
Captan
Carbaryl
Carbazole
3-Carbethoxypsoralen
Carbon black
Carbon electrode manufacture
Carbon tetrachloride
Carmoisine
Carpentry and joinery
Carrageenan
Cassia occidentalis (see Traditional herbal medicines)
Catechol
CCNU (see 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea)
Ceramic fibres (see Man-made vitreous fibres)
Chemotherapy, combined, including alkylating agents (see
MOPP and other combined chemotherapy including alkylating
agents)
Chimney sweeps and other exposures to soot
Chloral (see also Chloral hydrate)
Chloral hydrate
Chlorambucil
Chloramine
Chloramphenicol
Chlordane (see also Chlordane/Heptachlor)
Chlordane and Heptachlor
Chlordecone
Chlordimeform
Chlorendic acid
Chlorinated dibenzodioxins (other than TCDD) (see also
Polychlorinated dibenzo-para-dioxins)
Chlorinated drinking-water
Chlorinated paraffins
-Chlorinated toluenes and benzoyl chloride
Chlormadinone acetate
Chlornaphazine (see N,N-Bis(2-chloroethyl)-2-naphthylamine)
Chloroacetonitrile (see also Halogenated acetonitriles)
para-Chloroaniline
Chlorobenzilate
Chlorodibromomethane
3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone
Chlorodifluoromethane
Chloroethane
403
30, 295 (1983); Suppl. 7, 59 (1987)
12, 37 (1976); Suppl. 7, 59 (1987)
32, 239 (1983); Suppl. 7, 59 (1987); 71,
1319 (1999)
40, 317 (1986); Suppl. 7, 59 (1987)
3, 22 (1973); 33, 35 (1984); Suppl.7, 142
(1987); 65, 149 (1996); 93, 2010
92, 35 (2010)
1, 53 (1972); 20, 371 (1979); Suppl. 7, 143
(1987); 71, 401 (1999)
8, 83 (1975); Suppl. 7, 59 (1987)
25, 139 (1981); Suppl. 7, 378 (1987)
10, 181 (1976) (corr. 42, 255); 31, 79
(1983); Suppl. 7, 59 (1987)
15, 155 (1977); Suppl. 7, 59 (1987); 71,
433 (1999)
92, 35 (2010)
63, 245 (1995); 84, 317 (2004)
63, 245 (1995); 84, 317 (2004)
9, 125 (1975); 26, 115 (1981); Suppl. 7,
144 (1987)
84, 295 (2004)
10, 85 (1976); Suppl. 7, 145 (1987); 50,
169 (1990)
20, 45 (1979) (corr. 42, 258)
Suppl. 7, 146 (1987); 53, 115 (1991); 79,
411 (2001)
20, 67 (1979); Suppl. 7, 59 (1987)
30, 61 (1983); Suppl. 7, 59 (1987)
48, 45 (1990)
15, 41 (1977); Suppl. 7, 59 (1987)
52, 45 (1991)
48, 55 (1990)
Suppl. 7, 148 (1987); 71, 453 (1999)
6, 149 (1974); 21, 365 (1979); Suppl. 7,
291, 301 (1987); 72, 49 (1999)
71, 1325 (1999)
57, 305 (1993)
5, 75 (1974); 30, 73 (1983); Suppl. 7, 60
(1987)
52, 243 (1991); 71, 1331 (1999)
84, 441 (2004)
41, 237 (1986) (corr. 51, 483); Suppl. 7,
149 (1987); 71, 1339 (1999)
52, 315 (1991); 71, 1345 (1999)
404
1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (see also

Chloroethyl nitrosoureas)
1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (see also
Chloroethyl nitrosoureas)
Chloroethyl nitrosoureas
Chlorofluoromethane
Chloroform
Chloromethyl methyl ether (technical-grade) (see also
Bis(chloromethyl)ether)
(4-Chloro-2-methylphenoxy)acetic acid (see MCPA)
1-Chloro-2-methylpropene
3-Chloro-2-methylpropene
2-Chloronitrobenzene
Chlorophenols (see also Polychlorophenols and their sodium
salts)
Chlorophenols (occupational exposures to)
Chlorophenoxy herbicides
Chlorophenoxy herbicides (occupational exposures to)
4-Chloro-ortho-phenylenediamine
4-Chloro-meta-phenylenediamine
Chloroprene
Chloropropham
Chloroquine
Chlorothalonil
para-Chloro-ortho-toluidine and its strong acid salts (see also
Chlordimeform)
4-Chloro-ortho-toluidine (see para-chloro-ortho-toluidine)
5-Chloro-ortho-toluidine
Chlorotrianisene (see also Nonsteroidal oestrogens)
2-Chloro-1,1,1-trifluoroethane
Chlorozotocin
Cholesterol
Chromic acetate (see Chromium and chromium compounds)
Chromic chloride (see Chromium and chromium compounds)
Chromic oxide (see Chromium and chromium compounds)
Chromic phosphate (see Chromium and chromium compounds)
Chromite ore (see Chromium and chromium compounds)
Chromium and chromium compounds (see also Implants,
surgical)
Chromium carbonyl (see Chromium and chromium compounds)
Chromium potassium sulfate (see Chromium and chromium
compounds)
Chromium sulfate (see Chromium and chromium compounds)
Chromium trioxide (see Chromium and chromium compounds)
Chrysazin (see Dantron)
26, 137 (1981) (corr. 42, 260); Suppl. 7,

150 (1987)
Suppl. 7, 150 (1987)
Suppl. 7, 150 (1987)
41, 229 (1986); Suppl. 7, 60 (1987); 71,
1351 (1999)
1, 61 (1972); 20, 401 (1979); Suppl. 7, 152
(1987); 73, 131(1999)
4, 239 (1974); Suppl. 7, 131 (1987)
63, 315 (1995)

63, 325 (1995)
65, 263 (1996)
65, 263 (1996)
65, 263 (1996)
Suppl. 7, 154 (1987)
41, 319 (1986)
Suppl. 7, 156 (1987)
41, 357 (1986)
27, 81 (1982); Suppl. 7, 60 (1987)
27, 82 (1982); Suppl. 7, 60 (1987)
19, 131 (1979); Suppl. 7, 160 (1987); 71,
227 (1999)
12, 55 (1976); Suppl. 7, 60 (1987)
13, 47 (1977); Suppl. 7, 60 (1987)
30, 319 (1983); Suppl. 7, 60 (1987); 73,
183 (1999)
16, 277 (1978); 30, 65 (1983); Suppl. 7, 60
(1987); 48, 123 (1990); 77, 323 (2000)
77, 341 (2000)
21, 139 (1979); Suppl. 7, 280 (1987)
41, 253 (1986); Suppl. 7, 60 (1987); 71,
1355 (1999)
50, 65 (1990)
10, 99 (1976); 31, 95 (1983); Suppl. 7, 161
(1987)
2, 100 (1973); 23, 205 (1980); Suppl. 7,

165 (1987); 49, 49 (1990) (corr. 51, 483)
CUMULATIVE INDEX
Chrysene
Chrysoidine
Chrysotile (see Asbestos)
CI Acid Orange 3
CI Acid Red 114
CI Basic Red 9 (see also Magenta)
CI Direct Blue 15
CI Disperse Yellow 3 (see Disperse Yellow 3)
Cimetidine
Cinnamyl anthranilate
CI Pigment Red 3
CI Pigment Red 53:1 (see D&C Red No. 9)
Cisplatin (see also Etoposide)
Citrinin
Citrus Red No. 2
Clinoptilolite (see Zeolites)
Clofibrate
Clomiphene citrate
Clonorchis sinensis (infection with)
Coal, indoor emissions from household combustion of
Coal dust
Coal gasification
Coal-tar distillation
Coal-tar pitches (see also Coal-tars)
Coal-tars
Cobalt[III] acetate (see Cobalt and cobalt compounds)
Cobalt-aluminium-chromium spinel (see Cobalt and cobalt
compounds)
Cobalt and cobalt compounds (see also Implants, surgical)
Cobalt[II] chloride (see Cobalt and cobalt compounds)
Cobalt-chromium alloy (see Chromium and chromium
compounds)
Cobalt-chromium-molybdenum alloys (see Cobalt and cobalt
compounds)
Cobalt metal powder (see Cobalt and cobalt compounds)
Cobalt metal with tungsten carbide
Cobalt metal without tungsten carbide
Cobalt naphthenate (see Cobalt and cobalt compounds)
Cobalt[II] oxide (see Cobalt and cobalt compounds)
Cobalt[II,III] oxide (see Cobalt and cobalt compounds)
Cobalt sulfate and other soluble cobalt(II) salts
Cobalt[II] sulfide (see Cobalt and cobalt compounds)
Coffee
Coke production
Combined estrogenprogestogen contraceptives
Combined estrogenprogestogen menopausal therapy
405
3, 159 (1973); 32, 247 (1983); Suppl. 7, 60
(1987); 92, 35 (2010)
8, 91 (1975); Suppl. 7, 169 (1987)
57, 121 (1993)
57, 247 (1993)
57, 215 (1993)
57, 235 (1993)
50, 235 (1990)
16, 287 (1978); 31, 133 (1983); Suppl. 7,
60 (1987); 77, 177 (2000)
57, 259 (1993)
26, 151 (1981); Suppl. 7, 170 (1987)
40, 67 (1986); Suppl. 7, 60 (1987)
8, 101 (1975) (corr. 42, 254); Suppl. 7, 60
(1987)
24, 39 (1980); Suppl. 7, 171 (1987); 66,
391 (1996)
21, 551 (1979); Suppl. 7, 172 (1987)
61, 121 (1994)
95, 43 (2010)
68, 337 (1997)
34, 65 (1984); Suppl. 7, 173 (1987); 92, 35
(2010)
92, 35 (2010)
35, 83 (1985); Suppl. 7, 174 (1987)
35, 83 (1985); Suppl. 7, 175 (1987)
52, 363 (1991)
86, 37 (2006)
86, 37 (2006)
86, 37 (2006)
51, 41 (1991) (corr. 52, 513)
34, 101 (1984); Suppl. 7, 176 (1987); 92,
35 (2010)
Suppl. 7, 297 (1987); 72, 49 (1999); 91, 39
(2007)
Suppl. 7, 308 (1987); 72, 531 (1999); 91,
203 (2007)
406
Conjugated equine oestrogens

Conjugated oestrogens (see also Steroidal oestrogens)
Continuous glass filament (see Man-made vitreous fibres)
Copper 8-hydroxyquinoline
Coronene
Coumarin
Creosotes (see also Coal-tars)
meta-Cresidine
para-Cresidine
Cristobalite (see Crystalline silica)
Crocidolite (see Asbestos)
Crotonaldehyde
Crude oil
Crystalline silica (see also Silica)
Cycasin (see also Methylazoxymethanol)
Cyclamates
Cyclamic acid (see Cyclamates)
Cyclochlorotine
Cyclohexanone
Cyclohexylamine (see Cyclamates)
4--Cyclopenta[def]chrysene
5,6-Cyclopenteno-1,2-benzanthracene
Cyclopropane (see Anaesthetics, volatile)
Cyclophosphamide
Cyclosporine
Cyproterone acetate
72, 399 (1999)

21, 147 (1979); Suppl. 7, 283 (1987)
15, 103 (1977); Suppl. 7, 61 (1987)
32, 263 (1983); Suppl. 7, 61 (1987); 92, 35
(2010)
10, 113 (1976); Suppl. 7, 61 (1987); 77,
193 (2000)
35, 83 (1985); Suppl. 7, 177 (1987); 92, 35
(2010)
27, 91 (1982); Suppl. 7, 61 (1987)
27, 92 (1982); Suppl. 7, 61 (1987)
63, 373 (1995) (corr. 65, 549)

45, 119 (1989)
42, 39 (1987); Suppl. 7, 341 (1987); 68, 41
(1997) (corr. 81, 383)
1, 157 (1972) (corr. 42, 251); 10, 121
(1976); Suppl. 7, 61 (1987)
22, 55 (1980); Suppl. 7, 178 (1987); 73,
195 (1999)
10, 139 (1976); Suppl. 7, 61 (1987)
47, 157 (1989); 71, 1359 (1999)
92, 35 (2010)
32, 269 (1983); Suppl. 7, 61 (1987); 92, 35
(2010)
92, 35 (2010)
9, 135 (1975); 26, 165 (1981); Suppl. 7,
182 (1987)
50, 77 (1990)
72, 49 (1999)
D
2,4-D (see also Chlorophenoxy herbicides; Chlorophenoxy
herbicides, occupational exposures to)
Dacarbazine
Dantron
D&C Red No. 9
Dapsone
Daunomycin
DDD (see DDT)
DDE (see DDT)
DDT
Decabromodiphenyl oxide
Deltamethrin
15, 111 (1977)

26, 203 (1981); Suppl. 7, 184 (1987)
50, 265 (1990) (corr. 59, 257)
8, 107 (1975); Suppl. 7, 61 (1987); 57, 203
(1993)
24, 59 (1980); Suppl. 7, 185 (1987)
10, 145 (1976); Suppl. 7, 61 (1987)
5, 83 (1974) (corr. 42, 253); Suppl. 7, 186

(1987); 53, 179 (1991)
48, 73 (1990); 71, 1365 (1999)
53, 251 (1991)
CUMULATIVE INDEX
Deoxynivalenol (see Toxins derived from Fusarium
graminearum, F. culmorum and F. crookwellense)
Diacetylaminoazotoluene
N,N-Diacetylbenzidine
Diallate
2,4-Diaminoanisole and its salts
4,4-Diaminodiphenyl ether
1,2-Diamino-4-nitrobenzene
1,4-Diamino-2-nitrobenzene
2,6-Diamino-3-(phenylazo)pyridine (see Phenazopyridine
hydrochloride)
2,4-Diaminotoluene (see also Toluene diisocyanates)
2,5-Diaminotoluene (see also Toluene diisocyanates)
ortho-Dianisidine (see 3,3-Dimethoxybenzidine)
Diatomaceous earth, uncalcined (see Amorphous silica)
Diazepam
Diazomethane
Dibenz[a,h]acridine
Dibenz[a,j]acridine
Dibenz[a,c]anthracene
Dibenz[a,j]anthracene
7H-Dibenzo[c,g]carbazole
Dibenzodioxins, chlorinated (other than TCDD) (see Chlorinated
dibenzodioxins (other than TCDD))
Dibenzo[a,e]fluoranthene
13H-Dibenzo[a,g]fluorene
Dibenzo[h,rst]pentaphene
Dibenzo[a,e]pyrene
Dibenzo[a,h]pyrene
Dibenzo[a,i]pyrene
Dibenzo[a,l]pyrene
Dibenzo[e,l]pyrene
Dibenzo-para-dioxin
Dibromoacetonitrile (see also Halogenated acetonitriles)
1,2-Dibromo-3-chloropropane
407
8, 113 (1975); Suppl. 7, 61 (1987)

16, 293 (1978); Suppl. 7, 61 (1987)
12, 69 (1976); 30, 235 (1983); Suppl. 7, 61
(1987)
16, 51 (1978); 27, 103 (1982); Suppl. 7, 61
(1987); 79, 619 (2001)
16, 301 (1978); 29, 203 (1982); Suppl. 7,
61 (1987)
16, 63 (1978); Suppl. 7, 61 (1987)
16, 73 (1978); Suppl. 7, 61 (1987); 57, 185
(1993)
16, 83 (1978); Suppl. 7, 61 (1987)

16, 97 (1978); Suppl. 7, 61 (1987)
13, 57 (1977); Suppl. 7, 189 (1987); 66, 37

(1996)
7, 223 (1974); Suppl. 7, 61 (1987)
3, 247 (1973); 32, 277 (1983); Suppl. 7, 61
(1987)
3, 254 (1973); 32, 283 (1983); Suppl. 7, 61
(1987)
32, 289 (1983) (corr. 42, 262); Suppl. 7, 61
(1987); 92, 35 (2010)
3, 178 (1973) (corr. 43, 261); 32, 299
(1983); Suppl. 7, 61 (1987); 92, 35 (2010)
32, 309 (1983); Suppl. 7, 61 (1987); 92, 35
(2010)
3, 260 (1973); 32, 315 (1983); Suppl. 7, 61
(1987)
32, 321 (1983); Suppl. 7, 61 (1987); 92, 35

(2010)
92, 35 (2010)
3, 197 (1973); Suppl. 7, 62 (1987); 92, 35
(2010)
3, 201 (1973); 32, 327 (1983); Suppl. 7, 62
(1987); 92, 35 (2010)
3, 207 (1973); 32, 331 (1983); Suppl. 7, 62
(1987); 92, 35 (2010)
3, 215 (1973); 32, 337 (1983); Suppl. 7, 62
(1987); 92, 35 (2010)
3, 224 (1973); 32, 343 (1983); Suppl. 7, 62
(1987); 92, 35 (2010)
92, 35 (2010)
69, 33 (1997)
71, 1369 (1999)
15, 139 (1977); 20, 83 (1979); Suppl. 7,
191 (1987); 71, 479 (1999)
408
1,2-Dibromoethane (see Ethylene dibromide)

2,3-Dibromopropan-1-ol
Dichloroacetic acid
Dichloroacetonitrile (see also Halogenated acetonitriles)
Dichloroacetylene
ortho-Dichlorobenzene
meta-Dichlorobenzene
para-Dichlorobenzene
3,3-Dichlorobenzidine
trans-1,4-Dichlorobutene
3,3-Dichloro-4,4-diaminodiphenyl ether
1,2-Dichloroethane
Dichloromethane
2,4-Dichlorophenol (see Chlorophenols; Chlorophenols,
occupational exposures to; Polychlorophenols and their sodium
salts)
(2,4-Dichlorophenoxy)acetic acid (see 2,4-D)
2,6-Dichloro-para-phenylenediamine
1,2-Dichloropropane
1,3-Dichloropropene (technical-grade)
Dichlorvos
Dicofol
Dicyclohexylamine (see Cyclamates)
Didanosine
Dieldrin
Dienoestrol (see also Nonsteroidal oestrogens)
Diepoxybutane (see also 1,3-Butadiene)
Diesel and gasoline engine exhausts
Diesel fuels
Diethanolamine
Diethyl ether (see Anaesthetics, volatile)
Di(2-ethylhexyl) adipate
Di(2-ethylhexyl) phthalate
1,2-Diethylhydrazine
Diethylstilboestrol
Diethylstilboestrol dipropionate (see Diethylstilboestrol)
Diethyl sulfate
N,N-Diethylthiourea
77, 439 (2000)

63, 271 (1995); 84, 359 (2004)
71, 1375 (1999)
39, 369 (1986); Suppl. 7, 62 (1987); 71,
1381 (1999)
7, 231 (1974); 29, 213 (1982); Suppl. 7,
192 (1987); 73, 223 (1999)
73, 223 (1999)
7, 231 (1974); 29, 215 (1982); Suppl. 7,
192 (1987); 73, 223 (1999)
4, 49 (1974); 29, 239 (1982); Suppl. 7, 193
(1987)
15, 149 (1977); Suppl. 7, 62 (1987); 71,
1389 (1999)
16, 309 (1978); Suppl. 7, 62 (1987)
20, 429 (1979); Suppl. 7, 62 (1987); 71,
501 (1999)
20, 449 (1979); 41, 43 (1986); Suppl. 7,
194 (1987); 71, 251 (1999)
39, 325 (1986); Suppl. 7, 62 (1987)

41, 131 (1986); Suppl. 7, 62 (1987); 71,
1393 (1999)
41, 113 (1986); Suppl. 7, 195 (1987); 71,
933 (1999)
20, 97 (1979); Suppl. 7, 62 (1987); 53, 267
(1991)
30, 87 (1983); Suppl. 7, 62 (1987)
76, 153 (2000)
5, 125 (1974); Suppl. 7, 196 (1987)
21, 161 (1979); Suppl. 7, 278 (1987)
11, 115 (1976) (corr. 42, 255); Suppl. 7, 62
(1987); 71, 109 (1999)
46, 41 (1989)
45, 219 (1989) (corr. 47, 505)
77, 349 (2000)
29, 257 (1982); Suppl. 7, 62 (1987); 77,
149 (2000)
29, 269 (1982) (corr. 42, 261); Suppl. 7, 62
(1987); 77, 41 (2000)
4, 153 (1974); Suppl. 7, 62 (1987); 71,
1401 (1999)
6, 55 (1974); 21, 173 (1979) (corr. 42,
259); Suppl. 7, 273 (1987)
4, 277 (1974); Suppl. 7, 198 (1987); 54,
213 (1992); 71, 1405 (1999)
79, 649 (2001)
CUMULATIVE INDEX
Diglycidyl resorcinol ether
Dihydrosafrole
1,2-Dihydroaceanthrylene
1,8-Dihydroxyanthraquinone (see Dantron)
Dihydroxybenzenes (see Catechol; Hydroquinone; Resorcinol)
1,3-Dihydroxy-2-hydroxymethylanthraquinone
Dihydroxymethylfuratrizine
Diisopropyl sulfate
Dimethisterone (see also Progestins; Sequential oral
contraceptives)
Dimethoxane
3,3-Dimethoxybenzidine
3,3-Dimethoxybenzidine-4,4-diisocyanate
para-Dimethylaminoazobenzene
para-Dimethylaminoazobenzenediazo sodium sulfonate
trans-2-[(Dimethylamino)methylimino]-5-[2-(5-nitro-2-furyl)vinyl]-1,3,4-oxadiazole
4,4-Dimethylangelicin plus ultraviolet radiation (see also
Angelicin and some synthetic derivatives)
4,5-Dimethylangelicin plus ultraviolet radiation (see also
2,6-Dimethylaniline
N,N-Dimethylaniline
Dimethylarsinic acid (see Arsenic and arsenic compounds)
3,3-Dimethylbenzidine
Dimethylcarbamoyl chloride
Dimethylformamide
1,1-Dimethylhydrazine
1,2-Dimethylhydrazine
Dimethyl hydrogen phosphite
1,4-Dimethylphenanthrene
Dimethyl sulfate
3,7-Dinitrofluoranthene
3,9-Dinitrofluoranthene
1,3-Dinitropyrene
1,6-Dinitropyrene
1,8-Dinitropyrene
Dinitrosopentamethylenetetramine
2,4-Dinitrotoluene
2,6-Dinitrotoluene
3,5-Dinitrotoluene
1,4-Dioxane
2,4-Diphenyldiamine
Direct Black 38 (see also Benzidine-based dyes)
Direct Blue 6 (see also Benzidine-based dyes)
409
11, 125 (1976); 36, 181 (1985); Suppl. 7,
62 (1987); 71, 1417 (1999)
1, 170 (1972); 10, 233 (1976) Suppl. 7, 62
(1987)
92, 35 (2010)
82, 129 (2002)

24, 77 (1980); Suppl. 7, 62 (1987)
54, 229 (1992); 71, 1421 (1999)
6, 167 (1974); 21, 377 (1979))
15, 177 (1977); Suppl. 7, 62 (1987)
4, 41 (1974); Suppl. 7, 198 (1987)
39, 279 (1986); Suppl. 7, 62 (1987)
8, 125 (1975); Suppl. 7, 62 (1987)
8, 147 (1975); Suppl. 7, 62 (1987)
7, 147 (1974) (corr. 42, 253); Suppl. 7, 62
(1987)
Suppl. 7, 57 (1987)
Suppl. 7, 57 (1987)
57, 323 (1993)
57, 337 (1993)
1, 87 (1972); Suppl. 7, 62 (1987)
12, 77 (1976); Suppl. 7, 199 (1987); 71,
531 (1999)
47, 171 (1989); 71, 545 (1999)
4, 137 (1974); Suppl. 7, 62 (1987); 71,
1425 (1999)
4, 145 (1974) (corr. 42, 253); Suppl. 7, 62
(1987); 71, 947 (1999)
48, 85 (1990); 71, 1437 (1999)
32, 349 (1983); Suppl. 7, 62 (1987); 92, 35
(2010)
4, 271 (1974); Suppl. 7, 200 (1987); 71,
575 (1999)
46, 189 (1989); 65, 297 (1996)
46, 195 (1989); 65, 297 (1996)
46, 201 (1989)
46, 215 (1989)
33, 171 (1984); Suppl. 7, 63 (1987); 46,
231 (1989)
11, 241 (1976); Suppl. 7, 63 (1987)
65, 309 (1996) (corr. 66, 485)
65, 309 (1996) (corr. 66, 485)
65, 309 (1996)
11, 247 (1976); Suppl. 7, 201 (1987); 71,
589 (1999)
16, 313 (1978); Suppl. 7, 63 (1987)
29, 295 (1982) (corr. 42, 261)
29, 311 (1982)
410
Direct Brown 95 (see also Benzidine-based dyes)

Disperse Blue 1
Disperse Yellow 3
Disulfiram
Dithranol
Divinyl ether (see Anaesthetics, volatile)
Doxefazepam
Doxylamine succinate
Droloxifene
Dry cleaning
Dulcin
29, 321 (1982)

48, 139 (1990)
8, 97 (1975); Suppl. 7, 60 (1987); 48, 149
(1990)
12, 85 (1976); Suppl. 7, 63 (1987)
13, 75 (1977); Suppl. 7, 63 (1987)
66, 97 (1996)
79, 145 (2001)
66, 241 (1996)
63, 33 (1995)
12, 97 (1976); Suppl. 7, 63 (1987)
E
Endrin
Enflurane (see Anaesthetics, volatile)
Eosin
Epichlorohydrin
1,2-Epoxybutane
1-Epoxyethyl-3,4-epoxycyclohexane (see 4-Vinylcyclohexene
diepoxide)
3,4-Epoxy-6-methylcyclohexylmethyl 3,4-epoxy-6-methylcyclohexane carboxylate
cis-9,10-Epoxystearic acid
Epstein-Barr virus
d-Equilenin
Equilin
Erionite
Estazolam
Ethinyloestradiol
Ethionamide
Ethyl acrylate
Ethylbenzene
Ethylene
Ethylene dibromide
Ethylene oxide
Ethylene sulfide
Ethylenethiourea
2-Ethylhexyl acrylate
Ethyl methanesulfonate
N-Ethyl-N-nitrosourea
Ethyl selenac (see also Selenium and selenium compounds)
5, 157 (1974); Suppl. 7, 63 (1987)

15, 183 (1977); Suppl. 7, 63 (1987)
11, 131 (1976) (corr. 42, 256); Suppl. 7,
202 (1987); 71, 603 (1999)
47, 217 (1989); 71, 629 (1999)
11, 147 (1976); Suppl. 7, 63 (1987); 71,

1441 (1999)
11, 153 (1976); Suppl. 7, 63 (1987); 71,
1443 (1999)
70, 47 (1997)
72, 399 (1999)
72, 399 (1999)
42, 225 (1987); Suppl. 7, 203 (1987)
66, 105 (1996)
6, 77 (1974); 21, 233 (1979); Suppl. 7, 286
(1987); 72, 49 (1999)
13, 83 (1977); Suppl. 7, 63 (1987)
19, 57 (1979); 39, 81 (1986); Suppl. 7, 63
(1987); 71, 1447 (1999)
77, 227 (2000)
19, 157 (1979); Suppl. 7, 63 (1987); 60, 45
(1994); 71, 1447 (1999)
15, 195 (1977); Suppl. 7, 204 (1987); 71,
641 (1999)
11, 157 (1976); 36, 189 (1985) (corr. 42,
263); Suppl. 7, 205 (1987); 60, 73 (1994);
97, 185 (2008)
11, 257 (1976); Suppl. 7, 63 (1987)
7, 45 (1974); Suppl. 7, 207 (1987); 79, 659
(2001)
60, 475 (1994)
7, 245 (1974); Suppl. 7, 63 (1987)
1, 135 (1972); 17, 191 (1978); Suppl. 7, 63
(1987)
12, 107 (1976); Suppl. 7, 63 (1987)
CUMULATIVE INDEX
Ethyl tellurac
Ethynodiol diacetate
Etoposide
Eugenol
Evans blue
Extremely low-frequency electric fields
Extremely low-frequency magnetic fields
411
12, 115 (1976); Suppl. 7, 63 (1987)
6, 173 (1974); 21, 387 (1979); Suppl. 7,
292 (1987); 72, 49 (1999)
76, 177 (2000)
36, 75 (1985); Suppl. 7, 63 (1987)
8, 151 (1975); Suppl. 7, 63 (1987)
80 (2002)
80 (2002)
F
Fast Green FCF
Fenvalerate
Ferbam
Ferric oxide
Ferrochromium (see Chromium and chromium compounds)
Fluometuron
Fluoranthene
Fluorene
Fluorescent lighting (exposure to) (see Ultraviolet radiation)
Fluorides (inorganic, used in drinking-water)
5-Fluorouracil
Fluorspar (see Fluorides)
Fluosilicic acid (see Fluorides)
Fluroxene (see Anaesthetics, volatile)
Foreign bodies
Formaldehyde
2-(2-Formylhydrazino)-4-(5-nitro-2-furyl)thiazole
Frusemide (see Furosemide)
Frying, emissions from high-temperature
Fuel oils (heating oils)
Fumonisin B1 (see also Toxins derived from Fusarium
moniliforme)
Fumonisin B2 (see Toxins derived from Fusarium moniliforme)
Furan
Furazolidone
Furfural
Furniture and cabinet-making
Furosemide
2-(2-Furyl)-3-(5-nitro-2-furyl)acrylamide (see AF-2)
Fusarenon-X (see Toxins derived from Fusarium graminearum,
F. culmorum and F. crookwellense)
Fusarenone-X (see Toxins derived from Fusarium graminearum,
Fusarin C (see Toxins derived from Fusarium moniliforme)
16, 187 (1978); Suppl. 7, 63 (1987)

53, 309 (1991)
12, 121 (1976) (corr. 42, 256); Suppl. 7, 63
(1987)
1, 29 (1972); Suppl. 7, 216 (1987)
30, 245 (1983); Suppl. 7, 63 (1987)
32, 355 (1983); Suppl. 7, 63 (1987); 92, 35
(2010)
32, 365 (1983); Suppl. 7, 63 (1987); 92, 35
(2010)
27, 237 (1982); Suppl. 7, 208 (1987)
26, 217 (1981); Suppl. 7, 210 (1987)
74 (1999)
29, 345 (1982); Suppl. 7, 211 (1987); 62,
217 (1995) (corr. 65, 549; corr. 66, 485);
88, 39 (2006)
7, 151 (1974) (corr. 42, 253); Suppl. 7, 63
(1987)
95, 309 (2010)
45, 239 (1989) (corr. 47, 505)
82, 301 (2002)
63, 393 (1995)

31, 141 (1983); Suppl. 7, 63 (1987)
63, 409 (1995)
25, 99 (1981)
50, 277 (1990)
412
G
Gallium arsenide
Gamma ()-radiation
Gasoline
Gasoline engine exhaust (see Diesel and gasoline engine exhausts)
Gemfibrozil
Glass fibres (see Man-made mineral fibres)
Glass manufacturing industry, occupational exposures in
Glass wool (see Man-made vitreous fibres)
Glass filaments (see Man-made mineral fibres)
Glu-P-1
Glu-P-2
L-Glutamic acid, 5-[2-(4-hydroxymethyl)phenylhydrazide]
(see Agaritine)
Glycidaldehyde
Glycidol
Glycidyl ethers
Glycidyl oleate
Glycidyl stearate
Griseofulvin
Guinea Green B
Gyromitrin
86, 163 (2006)

75, 121 (2000)
45, 159 (1989) (corr. 47, 505)
66, 427 (1996)
58, 347 (1993)
40, 223 (1986); Suppl. 7, 64 (1987)

40, 235 (1986); Suppl. 7, 64 (1987)
11, 175 (1976); Suppl. 7, 64 (1987); 71, 1459

(1999)
77, 469 (2000)
47, 237 (1989); 71, 1285, 1417, 1525, 1539
(1999)
11, 183 (1976); Suppl. 7, 64 (1987)
11, 187 (1976); Suppl. 7, 64 (1987)
10, 153 (1976); Suppl. 7, 64, 391 (1987); 79,
289 (2001)
16, 199 (1978); Suppl. 7, 64 (1987)
31, 163 (1983); Suppl. 7, 64, 391 (1987)
H
Haematite
Haematite and ferric oxide
Haematite mining, underground, with exposure to radon
Hairdressers and barbers (occupational exposure as)
Hair dyes, epidemiology of
Halogenated acetonitriles
Halothane (see Anaesthetics, volatile)
HC Blue No. 1
HC Blue No. 2
-HCH (see Hexachlorocyclohexanes)
HC Red No. 3
HC Yellow No. 4
Heating oils (see Fuel oils)
Helicobacter pylori (infection with)
Hepatitis B virus
Hepatitis C virus
Hepatitis D virus
Heptachlor (see also Chlordane/Heptachlor)
Hexachlorobenzene
1, 29 (1972); Suppl. 7, 216 (1987)

Suppl. 7, 216 (1987)
1, 29 (1972); Suppl. 7, 216 (1987)
57, 43 (1993)
16, 29 (1978); 27, 307 (1982)
52, 269 (1991); 71, 1325, 1369, 1375, 1533
(1999)
57, 129 (1993)
57, 143 (1993)
57, 153 (1993)

57, 159 (1993)
61, 177 (1994)
59, 45 (1994)
59, 165 (1994)
59, 223 (1994)
5, 173 (1974); 20, 129 (1979)
20, 155 (1979); Suppl. 7, 219 (1987); 79, 493
(2001)
CUMULATIVE INDEX
Hexachlorobutadiene
Hexachlorocyclohexanes
Hexachlorocyclohexane, technical-grade (see
Hexachlorocyclohexanes)
Hexachloroethane
Hexachlorophene
Hexamethylphosphoramide
Hexoestrol (see also Nonsteroidal oestrogens)
Hormonal contraceptives, progestogens only
Human herpesvirus 8
Human immunodeficiency viruses
Human papillomaviruses
Human T-cell lymphotropic viruses
Hycanthone mesylate
Hydralazine
Hydrazine
Hydrochloric acid
Hydrochlorothiazide
Hydrogen peroxide
Hydroquinone
1-Hydroxyanthraquinone
4-Hydroxyazobenzene
17-Hydroxyprogesterone caproate (see also Progestins)
8-Hydroxyquinoline
8-Hydroxysenkirkine
Hydroxyurea
Hypochlorite salts
413
20, 179 (1979); Suppl. 7, 64 (1987); 73, 277
(1999)
5, 47 (1974); 20, 195 (1979) (corr. 42, 258);
Suppl. 7, 220 (1987)
20, 467 (1979); Suppl. 7, 64 (1987); 73, 295

(1999)
20, 241 (1979); Suppl. 7, 64 (1987)
15, 211 (1977); Suppl. 7, 64 (1987); 71, 1465
(1999)
Suppl. 7, 279 (1987)
72, 339 (1999)
70, 375 (1997)
67, 31 (1996)
64 (1995) (corr. 66, 485); 90 (2007)
67, 261 (1996)
13, 91 (1977); Suppl. 7, 64 (1987)
24, 85 (1980); Suppl. 7, 222 (1987)
4, 127 (1974); Suppl. 7, 223 (1987); 71, 991
(1999)
54, 189 (1992)
50, 293 (1990)
36, 285 (1985); Suppl. 7, 64 (1987); 71, 671
(1999)
15, 155 (1977); Suppl. 7, 64 (1987); 71, 691
(1999)
82, 129 (2002)
8, 157 (1975); Suppl. 7, 64 (1987)
21, 399 (1979) (corr. 42, 259)
13, 101 (1977); Suppl. 7, 64 (1987)
10, 265 (1976); Suppl. 7, 64 (1987)
76, 347 (2000)
52, 159 (1991)
I
Implants, surgical
Indium phosphide
Inorganic acids (see Sulfuric acid and other strong inorganic acids,
occupational exposures to mists and vapours from)
Inorganic lead compounds
Insecticides, occupational exposures in spraying and application of
Insulation glass wool (see Man-made vitreous fibres)
Involuntary smoking
Ionizing radiation (see Neutrons, - and X-radiation)
IQ
Iron and steel founding
Iron-dextran complex
74, 1999
3, 229 (1973); 32, 373 (1983); Suppl. 7, 64
(1987); 92, 35 (2010)
86, 197 (2006)
Suppl. 7, 230 (1987); 87 (2006)

53, 45 (1991)
83, 1189 (2004)
40, 261 (1986); Suppl. 7, 64 (1987); 56, 165
(1993)
34, 133 (1984); Suppl. 7, 224 (1987)
2, 161 (1973); Suppl. 7, 226 (1987)
414
Iron-dextrin complex
Iron oxide (see Ferric oxide)
Iron oxide, saccharated (see Saccharated iron oxide)
Iron sorbitol-citric acid complex
Isatidine
Isoflurane (see Anaesthetics, volatile)
Isoniazid (see Isonicotinic acid hydrazide)
Isonicotinic acid hydrazide
Isophosphamide
Isoprene
Isopropanol
Isopropanol manufacture (strong-acid process)
(see also Isopropanol; Sulfuric acid and other strong inorganic
acids, occupational exposures to mists and vapours from)
Isopropyl oils
Isosafrole
2, 161 (1973) (corr. 42, 252); Suppl. 7, 64

(1987)
2, 161 (1973); Suppl. 7, 64 (1987)

10, 269 (1976); Suppl. 7, 65 (1987)
4, 159 (1974); Suppl. 7, 227 (1987)

26, 237 (1981); Suppl. 7, 65 (1987)
60, 215 (1994); 71, 1015 (1999)
15, 223 (1977); Suppl. 7, 229 (1987); 71,
1027 (1999)
Suppl. 7, 229 (1987)
15, 223 (1977); Suppl. 7, 229 (1987); 71,

1483 (1999)
1, 169 (1972); 10, 232 (1976); Suppl. 7, 65
(1987)
J
Jacobine
Jet fuel
Joinery (see Carpentry and joinery)
10, 275 (1976); Suppl. 7, 65 (1987)

45, 203 (1989)
K
Kaempferol
Kaposis sarcoma herpesvirus
Kepone (see Chlordecone)
Kojic acid
31, 171 (1983); Suppl. 7, 65 (1987)

70, 375 (1997)
79, 605 (2001)
L
Lasiocarpine
Lauroyl peroxide
Lead acetate (see Lead and lead compounds)
Lead and lead compounds (see also Foreign bodies)
Lead arsenate (see Arsenic and arsenic compounds)

Lead carbonate (see Lead and lead compounds)
Lead chloride (see Lead and lead compounds)
Lead chromate (see Chromium and chromium compounds)
Lead chromate oxide (see Chromium and chromium compounds)
Lead compounds, inorganic and organic
Lead naphthenate (see Lead and lead compounds)
Lead nitrate (see Lead and lead compounds)
10, 281 (1976); Suppl. 7, 65 (1987)

36, 315 (1985); Suppl. 7, 65 (1987); 71, 1485
(1999)
1, 40 (1972) (corr. 42, 251); 2, 52, 150
(1973); 12, 131 (1976); 23, 40, 208, 209, 325
(1980); Suppl. 7, 230 (1987); 87 (2006)
Suppl. 7, 230 (1987); 87 (2006)
CUMULATIVE INDEX
Lead oxide (see Lead and lead compounds)
Lead phosphate (see Lead and lead compounds)
Lead subacetate (see Lead and lead compounds)
Lead tetroxide (see Lead and lead compounds)
Leather goods manufacture
Leather industries
Leather tanning and processing
Ledate (see also Lead and lead compounds)
Levonorgestrel
Light Green SF
d-Limonene
Lindane (see Hexachlorocyclohexanes)
Liver flukes (see Clonorchis sinensis, Opisthorchis felineus and
Opisthorchis viverrini)
Lucidin (see 1,3-Dihydro-2-hydroxymethylanthraquinone)
Lumber and sawmill industries (including logging)
Luteoskyrin
Lynoestrenol
415
25, 279 (1981); Suppl. 7, 235 (1987)

25, 199 (1981); Suppl. 7, 232 (1987)
25, 201 (1981); Suppl. 7, 236 (1987)
12, 131 (1976)
72, 49 (1999)
16, 209 (1978); Suppl. 7, 65 (1987)
56, 135 (1993); 73, 307 (1999)
25, 49 (1981); Suppl. 7, 383 (1987)

10, 163 (1976); Suppl. 7, 65 (1987)
21, 407 (1979); Suppl. 7, 293 (1987); 72, 49
(1999)
M
Madder root (see also Rubia tinctorum)
Magenta
Magenta, manufacture of (see also Magenta)
Malathion
Maleic hydrazide
Malonaldehyde
Malondialdehyde (see Malonaldehyde)
Maneb
Man-made mineral fibres (see Man-made vitreous fibres)
Man-made vitreous fibres
Mannomustine
Mate
MCPA (see also Chlorophenoxy herbicides; Chlorophenoxy
MeA--C
Medphalan
Medroxyprogesterone acetate
Megestrol acetate
MeIQ
MeIQx
Melamine
Melphalan
6-Mercaptopurine
Mercuric chloride (see Mercury and mercury compounds)
82, 129 (2002)

4, 57 (1974) (corr. 42, 252); Suppl. 7, 238
(1987); 57, 215 (1993)
Suppl. 7, 238 (1987); 57, 215 (1993)
30, 103 (1983); Suppl. 7, 65 (1987)
4, 173 (1974) (corr. 42, 253); Suppl. 7, 65
(1987)
36, 163 (1985); Suppl. 7, 65 (1987); 71, 1037
(1999)
12, 137 (1976); Suppl. 7, 65 (1987)
43, 39 (1988); 81 (2002)
9, 157 (1975); Suppl. 7, 65 (1987)
51, 273 (1991)
30, 255 (1983)
40, 253 (1986); Suppl. 7, 65 (1987)
9, 168 (1975); Suppl. 7, 65 (1987)
6, 157 (1974); 21, 417 (1979) (corr. 42, 259);
Suppl. 7, 289 (1987); 72, 339 (1999)
Suppl. 7, 293 (1987); 72, 49 (1999)
40, 275 (1986); Suppl. 7, 65 (1987); 56, 197
(1993)
40, 283 (1986); Suppl. 7, 65 (1987) 56, 211
(1993)
39, 333 (1986); Suppl. 7, 65 (1987); 73, 329
(1999)
9, 167 (1975); Suppl. 7, 239 (1987)
26, 249 (1981); Suppl. 7, 240 (1987)
416
Mercury and mercury compounds

Merphalan
Mestranol
Metabisulfites (see Sulfur dioxide and some sulfites, bisulfites
and metabisulfites)
Metallic mercury (see Mercury and mercury compounds)
Methanearsonic acid, disodium salt (see Arsenic and arsenic
compounds)
Methanearsonic acid, monosodium salt (see Arsenic and arsenic
compounds)
Methimazole
Methotrexate
Methoxsalen (see 8-Methoxypsoralen)
Methoxychlor
Methoxyflurane (see Anaesthetics, volatile)
5-Methoxypsoralen
8-Methoxypsoralen (see also 8-Methoxypsoralen plus ultraviolet
radiation)
8-Methoxypsoralen plus ultraviolet radiation
Methyl acrylate
5-Methylangelicin plus ultraviolet radiation (see also Angelicin
and some synthetic derivatives)
2-Methylaziridine
Methylazoxymethanol acetate (see also Cycasin)
Methyl bromide
Methyl tert-butyl ether
Methyl carbamate
Methyl-CCNU (see 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)1-nitrosourea)
Methyl chloride
1-, 2-, 3-, 4-, 5- and 6-Methylchrysenes
N-Methyl-N,4-dinitrosoaniline
4,4-Methylene bis(2-chloroaniline)
4,4-Methylene bis(N,N-dimethyl)benzenamine
4,4-Methylene bis(2-methylaniline)
4,4-Methylenedianiline
4,4-Methylenediphenyl diisocyanate
2-Methylfluoranthene
3-Methylfluoranthene
Methylglyoxal
58, 239 (1993)

9, 169 (1975); Suppl. 7, 65 (1987)
6, 87 (1974); 21, 257 (1979) (corr. 42, 259);
Suppl. 7, 288 (1987); 72, 49 (1999)
79, 53 (2001)
26, 267 (1981); Suppl. 7, 241 (1987)
5, 193 (1974); 20, 259 (1979); Suppl. 7, 66
(1987)
40, 327 (1986); Suppl. 7, 242 (1987)
24, 101 (1980)
Suppl. 7, 243 (1987)
19, 52 (1979); 39, 99 (1986); Suppl. 7, 66
(1987); 71, 1489 (1999)
Suppl. 7, 57 (1987)
9, 61 (1975); Suppl. 7, 66 (1987); 71, 1497
(1999)
1, 164 (1972); 10, 131 (1976); Suppl. 7, 66
(1987)
41, 187 (1986) (corr. 45, 283); Suppl. 7, 245
(1987); 71, 721 (1999)
73, 339 (1999)
12, 151 (1976); Suppl. 7, 66 (1987)
41, 161 (1986); Suppl. 7, 246 (1987); 71, 737

(1999)
32, 379 (1983); Suppl. 7, 66 (1987); 92, 35
(2010)
1, 141 (1972); Suppl. 7, 66 (1987)
4, 65 (1974) (corr. 42, 252); Suppl. 7, 246
(1987); 57, 271 (1993)
27, 119 (1982); Suppl. 7, 66 (1987)
4, 73 (1974); Suppl. 7, 248 (1987)
4, 79 (1974) (corr. 42, 252); 39, 347 (1986);
Suppl. 7, 66 (1987)
19, 314 (1979); Suppl. 7, 66 (1987); 71, 1049
(1999)
32, 399 (1983); Suppl. 7, 66 (1987); 92, 35
(2010)
32, 399 (1983); Suppl. 7, 66 (1987); 92, 35
(2010)
51, 443 (1991)
CUMULATIVE INDEX
Methyl iodide
Methylmercury chloride (see Mercury and mercury compounds)
Methylmercury compounds (see Mercury and mercury compounds)
Methyl methacrylate
Methyl methanesulfonate
2-Methyl-1-nitroanthraquinone
N-Methyl-N-nitro-N-nitrosoguanidine
3-Methylnitrosaminopropionaldehyde [see 3-(NNitrosomethylamino)-propionaldehyde]
3-Methylnitrosaminopropionitrile [see 3-(N-Nitrosomethylamino)propionitrile]
4-(Methylnitrosamino)-4-(3-pyridyl)-1-butanal [see 4-(NNitrosomethyl-amino)-4-(3-pyridyl)-1-butanal]
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone [see 4-(NNitrosomethyl-amino)-1-(3-pyridyl)-1-butanone]
N-Methyl-N-nitrosourea
N-Methyl-N-nitrosourethane
N-Methylolacrylamide
Methyl parathion
7-Methylpyrido[3,4-c]psoralen
Methyl red
Methyl selenac (see also Selenium and selenium compounds)
Methylthiouracil
Metronidazole
Microcystin-LR
Microcystis extracts
Mineral oils
Mirex
Mists and vapours from sulfuric acid and other strong inorganic acids
Mitomycin C
Mitoxantrone
MNNG (see N-Methyl-N-nitro-N-nitrosoguanidine)
MOCA (see 4,4-Methylene bis(2-chloroaniline))
Modacrylic fibres
Monochloramine (see Chloramine)
Monocrotaline
Monuron
MOPP and other combined chemotherapy including
alkylating agents
Mordanite (see Zeolites)
Morinda officinalis (see also Traditional herbal medicines)
Morpholine
5-(Morpholinomethyl)-3-[(5-nitrofurfurylidene)amino]-2oxazolidinone
417
15, 245 (1977); 41, 213 (1986); Suppl. 7, 66
(1987); 71, 1503 (1999)
19, 187 (1979); Suppl. 7, 66 (1987); 60, 445

(1994)
7, 253 (1974); Suppl. 7, 66 (1987); 71, 1059
(1999)
27, 205 (1982); Suppl. 7, 66 (1987)
4, 183 (1974); Suppl. 7, 248 (1987)
1, 125 (1972); 17, 227 (1978); Suppl. 7, 66

(1987)
4, 211 (1974); Suppl. 7, 66 (1987)
60, 435 (1994)
30, 131 (1983); Suppl. 7, 66, 392 (1987)
32, 405 (1983); Suppl. 7, 66 (1987); 92, 35
(2010)
40, 349 (1986); Suppl. 7, 71 (1987)
8, 161 (1975); Suppl. 7, 66 (1987)
12, 161 (1976); Suppl. 7, 66 (1987)
7, 53 (1974); Suppl. 7, 66 (1987); 79, 75
(2001)
13, 113 (1977); Suppl. 7, 250 (1987)
94 (2010)
94 (2010)
3, 30 (1973); 33, 87 (1984) (corr. 42, 262);
Suppl. 7, 252 (1987)
5, 203 (1974); 20, 283 (1979) (corr. 42, 258);
Suppl. 7, 66 (1987)
54, 41 (1992)
10, 171 (1976); Suppl. 7, 67 (1987)
76, 289 (2000)
19, 86 (1979); Suppl. 7, 67 (1987)

10, 291 (1976); Suppl. 7, 67 (1987)
12, 167 (1976); Suppl. 7, 67 (1987); 53, 467
(1991)
Suppl. 7, 254 (1987)
82, 129 (2002)

47, 199 (1989); 71, 1511 (1999)
7, 161 (1974); Suppl. 7, 67 (1987)
418
Musk ambrette
Musk xylene
Mustard gas
65, 477 (1996)

65, 477 (1996)
9, 181 (1975) (corr. 42, 254); Suppl. 7, 259
(1987)
Myleran (see 1,4-Butanediol dimethanesulfonate)
N
Nafenopin
Naphthalene
1,5-Naphthalenediamine
1,5-Naphthalene diisocyanate
Naphtho[1,2-b]fluoranthene
Naphtho[2,1-a]fluoranthene
Naphtho[2,3-e]pyrene
1-Naphthylamine
2-Naphthylamine
1-Naphthylthiourea
Neutrons
Nickel acetate (see Nickel and nickel compounds)
Nickel ammonium sulfate (see Nickel and nickel compounds)
Nickel and nickel compounds (see also Implants, surgical)
Nickel carbonate (see Nickel and nickel compounds)

Nickel carbonyl (see Nickel and nickel compounds)
Nickel chloride (see Nickel and nickel compounds)
Nickel-gallium alloy (see Nickel and nickel compounds)
Nickel hydroxide (see Nickel and nickel compounds)
Nickelocene (see Nickel and nickel compounds)
Nickel oxide (see Nickel and nickel compounds)
Nickel subsulfide (see Nickel and nickel compounds)
Nickel sulfate (see Nickel and nickel compounds)
Niridazole
Nithiazide
Nitrate or nitrite, ingested, under conditions that result in endogenous
nitrosation
Nitrilotriacetic acid and its salts
Nitrite (see Nitrate or nitrite)
5-Nitroacenaphthene
5-Nitro-ortho-anisidine
2-Nitroanisole
9-Nitroanthracene
7-Nitrobenz[a]anthracene
Nitrobenzene
6-Nitrobenzo[a]pyrene
4-Nitrobiphenyl
6-Nitrochrysene
Nitrofen (technical-grade)
24, 125 (1980); Suppl. 7, 67 (1987)

82, 367 (2002)
27, 127 (1982); Suppl. 7, 67 (1987)
19, 311 (1979); Suppl. 7, 67 (1987); 71, 1515
(1999)
92, 35 (2010)
92, 35 (2010)
92, 35 (2010)
4, 87 (1974) (corr. 42, 253); Suppl. 7, 260
(1987)
4, 97 (1974); Suppl. 7, 261 (1987)
30, 347 (1983); Suppl. 7, 263 (1987)
75, 361 (2000)
2, 126 (1973) (corr. 42, 252); 11, 75 (1976);

Suppl. 7, 264 (1987) (corr. 45, 283); 49, 257
(1990) (corr. 67, 395)
13, 123 (1977); Suppl. 7, 67 (1987)

31, 179 (1983); Suppl. 7, 67 (1987)
94 (2010)
48, 181 (1990); 73, 385 (1999)
16, 319 (1978); Suppl. 7, 67 (1987)
27, 133 (1982); Suppl. 7, 67 (1987)
65, 369 (1996)
33, 179 (1984); Suppl. 7, 67 (1987)
46, 247 (1989)
65, 381 (1996)
33, 187 (1984); Suppl. 7, 67 (1987); 46, 255
(1989)
4, 113 (1974); Suppl. 7, 67 (1987)
33, 195 (1984); Suppl. 7, 67 (1987); 46, 267
(1989)
30, 271 (1983); Suppl. 7, 67 (1987)
CUMULATIVE INDEX
3-Nitrofluoranthene
2-Nitrofluorene
Nitrofural
5-Nitro-2-furaldehyde semicarbazone (see Nitrofural)
Nitrofurantoin
Nitrofurazone (see Nitrofural)
1-[(5-Nitrofurfurylidene)amino]-2-imidazolidinone
N-[4-(5-Nitro-2-furyl)-2-thiazolyl]acetamide
Nitrogen mustard
Nitrogen mustard N-oxide
Nitromethane
1-Nitronaphthalene
2-Nitronaphthalene
3-Nitroperylene
2-Nitro-para-phenylenediamine (see 1,4-Diamino-2-nitrobenzene)
2-Nitropropane
1-Nitropyrene
2-Nitropyrene
4-Nitropyrene
N-Nitrosatable drugs
N-Nitrosatable pesticides
N-Nitrosoanabasine (NAB)
N-Nitrosoanatabine (NAT)
N-Nitrosodi-n-butylamine
N-Nitrosodiethanolamine
N-Nitrosodiethylamine
N-Nitrosodimethylamine
N-Nitrosodiphenylamine
para-Nitrosodiphenylamine
N-Nitrosodi-n-propylamine
N-Nitroso-N-ethylurea (see N-Ethyl-N-nitrosourea)
N-Nitrosofolic acid
N-Nitrosoguvacine
N-Nitrosoguvacoline
N-Nitrosohydroxyproline
3-(N-Nitrosomethylamino)propionaldehyde
3-(N-Nitrosomethylamino)propionitrile
4-(N-Nitrosomethylamino)-4-(3-pyridyl)-1-butanal
419
33, 201 (1984); Suppl. 7, 67 (1987)
46, 277 (1989)
7, 171 (1974); Suppl. 7, 67 (1987); 50, 195
(1990)
50, 211 (1990)
7, 181 (1974); Suppl. 7, 67 (1987)
1, 181 (1972); 7, 185 (1974); Suppl. 7, 67
(1987)
9, 193 (1975); Suppl. 7, 269 (1987)
9, 209 (1975); Suppl. 7, 67 (1987)
77, 487 (2000)
46, 291 (1989)
46, 303 (1989)
46, 313 (1989)
29, 331 (1982); Suppl. 7, 67 (1987); 71, 1079
(1999)
33, 209 (1984); Suppl. 7, 67 (1987); 46, 321
(1989)
46, 359 (1989)
46, 367 (1989)
24, 297 (1980) (corr. 42, 260)
30, 359 (1983)
37, 225 (1985); Suppl. 7, 67 (1987); 89, 419
(2007)
37, 233 (1985); Suppl. 7, 67 (1987); 89, 419
(2007)
4, 197 (1974); 17, 51 (1978); Suppl. 7, 67
(1987)
17, 77 (1978); Suppl. 7, 67 (1987); 77, 403
(2000)
1, 107 (1972) (corr. 42, 251); 17, 83 (1978)
(corr. 42, 257); Suppl. 7, 67 (1987)
1, 95 (1972); 17, 125 (1978) (corr. 42, 257);
Suppl. 7, 67 (1987)
27, 213 (1982); Suppl. 7, 67 (1987)
27, 227 (1982) (corr. 42, 261); Suppl. 7, 68
(1987)
17, 177 (1978); Suppl. 7, 68 (1987)
17, 217 (1978); Suppl. 7, 68 (1987)
37, 263 (1985); Suppl. 7, 68 (1987); 85, 281
(2004)
37, 263 (1985); Suppl. 7, 68 (1987); 85, 281
(2004)
17, 304 (1978); Suppl. 7, 68 (1987)
37, 263 (1985); Suppl. 7, 68 (1987); 85, 281
(2004)
37, 263 (1985); Suppl. 7, 68 (1987); 85, 281
(2004)
37, 205 (1985); Suppl. 7, 68 (1987)
420
4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK)
N-Nitrosomethylethylamine
N-Nitroso-N-methylurea (see N-Methyl-N-nitrosourea)
N-Nitroso-N-methylurethane (see N-Methyl-N-nitrosourethane)
N-Nitrosomethylvinylamine
N-Nitrosomorpholine
N-Nitrosonornicotine (NNN)
N-Nitrosopiperidine
N-Nitrosoproline
N-Nitrosopyrrolidine
N-Nitrososarcosine
Nitrosoureas, chloroethyl (see Chloroethyl nitrosoureas)
5-Nitro-ortho-toluidine
2-Nitrotoluene
3-Nitrotoluene
4-Nitrotoluene
Nitrous oxide (see Anaesthetics, volatile)
Nitrovin
Nivalenol (see Toxins derived from Fusarium graminearum,
NNK (see 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone)
NNN (see N-Nitrosonornicotine)
Nodularins
Nonsteroidal oestrogens
Norethisterone
Norethisterone acetate
Norethynodrel
Norgestrel
Nylon 6
37, 209 (1985); Suppl. 7, 68 (1987); 89, 419

(2007)
17, 221 (1978); Suppl. 7, 68 (1987)
17, 257 (1978); Suppl. 7, 68 (1987)

17, 263 (1978); Suppl. 7, 68 (1987)
17, 281 (1978); 37, 241 (1985); Suppl. 7, 68
(1987); 89, 419 (2007)
17, 287 (1978); Suppl. 7, 68 (1987)
17, 303 (1978); Suppl. 7, 68 (1987)
17, 313 (1978); Suppl. 7, 68 (1987)
17, 327 (1978); Suppl. 7, 68 (1987)
48, 169 (1990)
65, 409 (1996)
65, 409 (1996)
65, 409 (1996)
31, 185 (1983); Suppl. 7, 68 (1987)
94 (2010)
Suppl. 7, 273 (1987)
6, 179 (1974); 21, 461 (1979); Suppl. 7, 294
(1987); 72, 49 (1999)
72, 49 (1999)
6, 191 (1974); 21, 461 (1979) (corr. 42, 259);
Suppl. 7, 295 (1987); 72, 49 (1999)
6, 201 (1974); 21, 479 (1979); Suppl. 7, 295
(1987); 72, 49 (1999)
19, 120 (1979); Suppl. 7, 68 (1987)
O
Ochratoxin A
Oestradiol
Oestradiol-17 (see Oestradiol)
Oestradiol 3-benzoate (see Oestradiol)
Oestradiol dipropionate (see Oestradiol)
Oestradiol mustard
Oestradiol valerate (see Oestradiol)
Oestriol
Oestrogen replacement therapy (see Post-menopausal oestrogen
therapy)
Oestrogens (see Oestrogens, progestins and combinations)
Oestrogens, conjugated (see Conjugated oestrogens)
Oestrogens, nonsteroidal (see Nonsteroidal oestrogens)
10, 191 (1976); 31, 191 (1983) (corr. 42,

262); Suppl. 7, 271 (1987); 56, 489 (1993)
6, 99 (1974); 21, 279 (1979); Suppl. 7, 284
(1987); 72, 399 (1999)
9, 217 (1975); Suppl. 7, 68 (1987)

6, 117 (1974); 21, 327 (1979); Suppl. 7, 285
(1987); 72, 399 (1999)
CUMULATIVE INDEX
Oestrogens, progestins (progestogens) and combinations
Oestrogens, steroidal (see Steroidal oestrogens)
Oestrone
Oestrone benzoate (see Oestrone)
Oil Orange SS
Opisthorchis felineus (infection with)
Opisthorchis viverrini (infection with)
Oral contraceptives, sequential (see Sequential oral contraceptives)
Orange I
Orange G
Organic lead compounds
Organolead compounds (see Organic lead compounds)
Oxazepam
Oxymetholone (see also Androgenic (anabolic) steroids)
Oxyphenbutazone
421
6 (1974); 21 (1979); Suppl. 7, 272(1987); 72,
49, 339, 399, 531 (1999)
6, 123 (1974); 21, 343 (1979) (corr. 42, 259);
Suppl. 7, 286 (1987); 72, 399 (1999)
8, 165 (1975); Suppl. 7, 69 (1987)
61, 121 (1994)
61, 121 (1994)
8, 173 (1975); Suppl. 7, 69 (1987)
8, 181 (1975); Suppl. 7, 69 (1987)
Suppl. 7, 230 (1987); 87 (2006)
13, 58 (1977); Suppl. 7, 69 (1987); 66, 115
(1996)
13, 131 (1977)
13, 185 (1977); Suppl. 7, 69 (1987)
P
Paint manufacture and painting (occupational exposures in)
Palygorskite
Panfuran S (see also Dihydroxymethylfuratrizine)
Paper manufacture (see Pulp and paper manufacture)
Paracetamol
Parasorbic acid
Parathion
Patulin
Paving and roofing with coal-tar pitch
Penicillic acid
Pentachloroethane
Pentachloronitrobenzene (see Quintozene)
Pentachlorophenol (see also Chlorophenols; Chlorophenols,
salts)
Permethrin
Perylene
Petasitenine
Petasites japonicus (see also Pyrrolizidine alkaloids)
Petroleum refining (occupational exposures in)
Petroleum solvents
Phenacetin
Phenanthrene
Phenazopyridine hydrochloride
47, 329 (1989)

42, 159 (1987); Suppl. 7, 117 (1987); 68, 245
(1997)
24, 77 (1980); Suppl. 7, 69 (1987)
50, 307 (1990); 73, 401 (1999)
10, 199 (1976) (corr. 42, 255); Suppl. 7, 69
(1987)
30, 153 (1983); Suppl. 7, 69 (1987)
10, 205 (1976); 40, 83 (1986); Suppl. 7, 69
(1987)
92, 35 (2010)
10, 211 (1976); Suppl. 7, 69 (1987)
41, 99 (1986); Suppl. 7, 69 (1987); 71, 1519
(1999)
20, 303 (1979); 53, 371 (1991)
53, 329 (1991)

32, 411 (1983); Suppl. 7, 69 (1987); 92, 35
(2010)
31, 207 (1983); Suppl. 7, 69 (1987)
10, 333 (1976)
45, 39 (1989)
47, 43 (1989)
13, 141 (1977); 24, 135 (1980); Suppl. 7, 310
(1987)
32, 419 (1983); Suppl. 7, 69 (1987); 92, 35
(2010)
8, 117 (1975); 24, 163 (1980) (corr. 42, 260);
Suppl. 7, 312 (1987)
422
Phenelzine sulfate
Phenicarbazide
Phenobarbital and its sodium salt
Phenol
Phenolphthalein
Phenoxyacetic acid herbicides (see Chlorophenoxy herbicides)
Phenoxybenzamine hydrochloride
Phenylbutazone
meta-Phenylenediamine
para-Phenylenediamine
Phenyl glycidyl ether (see also Glycidyl ethers)
N-Phenyl-2-naphthylamine
ortho-Phenylphenol
Phenytoin
Phillipsite (see Zeolites)
PhIP
Picene
Pickled vegetables
Picloram
Piperazine oestrone sulfate (see Conjugated oestrogens)
Piperonyl butoxide
Pitches, coal-tar (see Coal-tar pitches)
Polyacrylic acid
Polybrominated biphenyls
Polychlorinated biphenyls
Polychlorinated camphenes (see Toxaphene)
Polychlorinated dibenzo-para-dioxins (other than
2,3,7,8-tetrachlorodibenzodioxin)
Polychlorinated dibenzofurans
Polychlorophenols and their sodium salts
Polychloroprene
Polyethylene (see also Implants, surgical)
Poly(glycolic acid) (see Implants, surgical)
Polymethylene polyphenyl isocyanate (see also 4,4Methylenediphenyl diisocyanate)
Polymethyl methacrylate (see also Implants, surgical)
Polyoestradiol phosphate (see Oestradiol-17)
Polypropylene (see also Implants, surgical)
Polystyrene (see also Implants, surgical)
Polytetrafluoroethylene (see also Implants, surgical)
Polyurethane foams (see also Implants, surgical)
Polyvinyl acetate (see also Implants, surgical)
Polyvinyl alcohol (see also Implants, surgical)
Polyvinyl chloride (see also Implants, surgical)
Polyvinyl pyrrolidone
24, 175 (1980); Suppl. 7, 312 (1987)

12, 177 (1976); Suppl. 7, 70 (1987)
13, 157 (1977); Suppl. 7, 313 (1987); 79, 161
(2001)
47, 263 (1989) (corr. 50, 385); 71, 749 (1999)
76, 387 (2000)
9, 223 (1975); 24, 185 (1980); Suppl. 7, 70
(1987)
13, 183 (1977); Suppl. 7, 316 (1987)
16, 111 (1978); Suppl. 7, 70 (1987)
16, 125 (1978); Suppl. 7, 70 (1987)
71, 1525 (1999)
16, 325 (1978) (corr. 42, 257); Suppl. 7, 318
(1987)
30, 329 (1983); Suppl. 7, 70 (1987); 73, 451
(1999)
13, 201 (1977); Suppl. 7, 319 (1987); 66, 175
(1996)
56, 229 (1993)
92, 35 (2010)
56, 83 (1993)
53, 481 (1991)
30, 183 (1983); Suppl. 7, 70 (1987)
19, 62 (1979); Suppl. 7, 70 (1987)
18, 107 (1978); 41, 261 (1986); Suppl. 7, 321
(1987)
7, 261 (1974); 18, 43 (1978) (corr. 42, 258);
Suppl. 7, 322 (1987)
69, 33 (1997)
69, 345 (1997)
71, 769 (1999)
19, 141 (1979); Suppl. 7, 70 (1987)
19, 164 (1979); Suppl. 7, 70 (1987)
19, 314 (1979); Suppl. 7, 70 (1987)
19, 195 (1979); Suppl. 7, 70 (1987)
19, 218 (1979); Suppl. 7, 70 (1987)
19, 245 (1979); Suppl. 7, 70 (1987)
19, 288 (1979); Suppl. 7, 70 (1987)
19, 320 (1979); Suppl. 7, 70 (1987)
19, 346 (1979); Suppl. 7, 70 (1987)
19, 351 (1979); Suppl. 7, 70 (1987)
7, 306 (1974); 19, 402 (1979); Suppl. 7, 70
(1987)
19, 463 (1979); Suppl. 7, 70 (1987); 71, 1181
(1999)
CUMULATIVE INDEX
Ponceau MX
Ponceau 3R
Ponceau SX
Post-menopausal oestrogen therapy
Potassium arsenate (see Arsenic and arsenic compounds)
Potassium arsenite (see Arsenic and arsenic compounds)
Potassium bis(2-hydroxyethyl)dithiocarbamate
Potassium bromate
Potassium chromate (see Chromium and chromium compounds)
Potassium dichromate (see Chromium and chromium compounds)
Prazepam
Prednimustine
Prednisone
Printing processes and printing inks
Procarbazine hydrochloride
Proflavine salts
Progesterone (see also Progestins; Combined oral contraceptives)
Progestins (see Progestogens)
Progestogens
Pronetalol hydrochloride
1,3-Propane sultone
Propham
-Propiolactone
n-Propyl carbamate
Propylene
Propyleneimine (see 2-Methylaziridine)
Propylene oxide
Propylthiouracil
Ptaquiloside (see also Bracken fern)
Pulp and paper manufacture
Pyrene
Pyridine
Pyrido[3,4-c]psoralen
Pyrimethamine
Pyrrolizidine alkaloids (see Hydroxysenkirkine; Isatidine; Jacobine;
Lasiocarpine; Monocrotaline; Retrorsine; Riddelliine;
Seneciphylline; Senkirkine)
423
8, 189 (1975); Suppl. 7, 70 (1987)
8, 199 (1975); Suppl. 7, 70 (1987)
8, 207 (1975); Suppl. 7, 70 (1987)
Suppl. 7, 280 (1987); 72, 399 (1999)
12, 183 (1976); Suppl. 7, 70 (1987)

40, 207 (1986); Suppl. 7, 70 (1987); 73, 481
(1999)
66, 143 (1996)

50, 115 (1990)
26, 293 (1981); Suppl. 7, 326 (1987)
65, 33 (1996)
26, 311 (1981); Suppl. 7, 327 (1987)
24, 195 (1980); Suppl. 7, 70 (1987)
6, 135 (1974); 21, 491 (1979) (corr. 42, 259)
Suppl. 7, 289 (1987); 72, 49, 339, 531 (1999)
13, 227 (1977) (corr. 42, 256); Suppl. 7, 70
(1987)
4, 253 (1974) (corr. 42, 253); Suppl. 7, 70
(1987); 71, 1095 (1999)
12, 189 (1976); Suppl. 7, 70 (1987)
4, 259 (1974) (corr. 42, 253); Suppl. 7, 70
(1987); 71, 1103 (1999)
12, 201 (1976); Suppl. 7, 70 (1987)
19, 213 (1979); Suppl. 7, 71 (1987); 60, 161
(1994)
11, 191 (1976); 36, 227 (1985) (corr. 42,
263); Suppl. 7, 328 (1987); 60, 181 (1994)
7, 67 (1974); Suppl. 7, 329 (1987); 79, 91
(2001)
40, 55 (1986); Suppl. 7, 71 (1987)
25, 157 (1981); Suppl. 7, 385 (1987)
32, 431 (1983); Suppl. 7, 71 (1987); 92, 35
(2010)
77, 503 (2000)
40, 349 (1986); Suppl. 7, 71 (1987)
13, 233 (1977); Suppl. 7, 71 (1987)
Q
Quartz (see Crystalline silica)
Quercetin (see also Bracken fern)
para-Quinone
31, 213 (1983); Suppl. 7, 71 (1987); 73, 497

(1999)
15, 255 (1977); Suppl. 7, 71 (1987); 71, 1245
(1999)
424
Quintozene
5, 211 (1974); Suppl. 7, 71 (1987)
R
Radiation (see gamma-radiation, neutrons, ultraviolet radiation,
X-radiation)
Radionuclides, internally deposited
Radon
Refractory ceramic fibres (see Man-made vitreous fibres)
Reserpine
Resorcinol
Retrorsine
Rhodamine B
Rhodamine 6G
Riddelliine
Rifampicin
Ripazepam
Rock (stone) wool (see Man-made vitreous fibres)
Rubber industry
Rubia tinctorum (see also Madder root, Traditional herbal medicines)
Rugulosin
78 (2001)
43, 173 (1988) (corr. 45, 283)
10, 217 (1976); 24, 211 (1980) (corr. 42,
260); Suppl. 7, 330 (1987)
15, 155 (1977); Suppl. 7, 71 (1987); 71, 1119
(1990)
10, 303 (1976); Suppl. 7, 71 (1987)
16, 221 (1978); Suppl. 7, 71 (1987)
16, 233 (1978); Suppl. 7, 71 (1987)
10, 313 (1976); Suppl. 7, 71 (1987); 82, 153
(2002)
24, 243 (1980); Suppl. 7, 71 (1987)
66, 157 (1996)
28 (1982) (corr. 42, 261); Suppl. 7, 332
(1987)
82, 129 (2002)
40, 99 (1986); Suppl. 7, 71 (1987)
S
Saccharated iron oxide
Saccharin and its salts
Safrole
Salted fish
Sawmill industry (including logging) (see Lumber and
sawmill industry (including logging))
Scarlet Red
Schistosoma haematobium (infection with)
Schistosoma japonicum (infection with)
Schistosoma mansoni (infection with)
Selenium and selenium compounds
Selenium dioxide (see Selenium and selenium compounds)
Selenium oxide (see Selenium and selenium compounds)
Semicarbazide hydrochloride
Senecio jacobaea L. (see also Pyrrolizidine alkaloids)
Senecio longilobus (see also Pyrrolizidine alkaloids, Traditional)
herbal medicines)
Senecio riddellii (see also Traditional herbal medicines)
Seneciphylline
2, 161 (1973); Suppl. 7, 71 (1987)

22, 111 (1980) (corr. 42, 259); Suppl. 7, 334
(1987); 73, 517 (1999)
1, 169 (1972); 10, 231 (1976); Suppl. 7, 71
(1987)
56, 41 (1993)
8, 217 (1975); Suppl. 7, 71 (1987)

61, 45 (1994)
61, 45 (1994)
61, 45 (1994)
9, 245 (1975) (corr. 42, 255); Suppl. 7, 71
(1987)
12, 209 (1976) (corr. 42, 256); Suppl. 7, 71

(1987)
10, 333 (1976)
10, 334 (1976); 82, 153 (2002)
82, 153 (1982)
10, 319, 335 (1976); Suppl. 7, 71 (1987)
CUMULATIVE INDEX
Senkirkine
Sepiolite
Sequential oral contraceptives (see also Oestrogens, progestins
and combinations)
Shale-oils
Shikimic acid (see also Bracken fern)
Shoe manufacture and repair (see Boot and shoe manufacture
and repair)
Silica (see also Amorphous silica; Crystalline silica)
Silicone (see Implants, surgical)
Simazine
Slag wool (see Man-made vitreous fibres)
Sodium arsenate (see Arsenic and arsenic compounds)
Sodium arsenite (see Arsenic and arsenic compounds)
Sodium cacodylate (see Arsenic and arsenic compounds)
Sodium chlorite
Sodium chromate (see Chromium and chromium compounds)
Sodium cyclamate (see Cyclamates)
Sodium dichromate (see Chromium and chromium compounds)
Sodium diethyldithiocarbamate
Sodium equilin sulfate (see Conjugated oestrogens)
Sodium fluoride (see Fluorides)
Sodium monofluorophosphate (see Fluorides)
Sodium oestrone sulfate (see Conjugated oestrogens)
Sodium ortho-phenylphenate (see also ortho-Phenylphenol)
Sodium saccharin (see Saccharin)
Sodium selenate (see Selenium and selenium compounds)
Sodium selenite (see Selenium and selenium compounds)
Sodium silicofluoride (see Fluorides)
Solar radiation
Soots
Special-purpose glass fibres such as E-glass and 475 glass fibres
(see Man-made vitreous fibres)
Spironolactone
Stannous fluoride (see Fluorides)
Static electric fields
Static magnetic fields
Steel founding (see Iron and steel founding)
Steel, stainless (see Implants, surgical)
Sterigmatocystin
Steroidal oestrogens
Streptozotocin
Strobane (see Terpene polychlorinates)
Strong-inorganic-acid mists containing sulfuric acid (see Mists and
vapours from sulfuric acid and other strong inorganic acids)
Strontium chromate (see Chromium and chromium compounds)
425
10, 327 (1976); 31, 231 (1983); Suppl. 7, 71
(1987)
42, 175 (1987); Suppl. 7, 71 (1987); 68, 267
(1997)
Suppl. 7, 296 (1987)
35, 161 (1985); Suppl. 7, 339 (1987)
40, 55 (1986); Suppl. 7, 71 (1987)
42, 39 (1987)
53, 495 (1991); 73, 625 (1999)
52, 145 (1991)
12, 217 (1976); Suppl. 7, 71 (1987)
30, 329 (1983); Suppl. 7, 71, 392 (1987); 73,

451 (1999)
55 (1992)
3, 22 (1973); 35, 219 (1985); Suppl. 7, 343
(1987)
24, 259 (1980); Suppl. 7, 344 (1987); 79, 317

(2001)
80 (2002)
80 (2002)
1, 175 (1972); 10, 245 (1976); Suppl. 7, 72

(1987)
Suppl. 7, 280 (1987)
4, 221 (1974); 17, 337 (1978); Suppl. 7, 72
(1987)
426
Styrene
Styrene-acrylonitrile copolymers
Styrene-butadiene copolymers
Styrene-7,8-oxide
Succinic anhydride
Sudan I
Sudan II
Sudan III
Sudan Brown RR
Sudan Red 7B
Sulfadimidine (see Sulfamethazine)
Sulfafurazole
Sulfallate
Sulfamethazine and its sodium salt
Sulfamethoxazole
Sulfites (see Sulfur dioxide and some sulfites, bisulfites and
metabisulfites)
Sulfur dioxide and some sulfites, bisulfites and metabisulfites
Sulfur mustard (see Mustard gas)
Sulfuric acid and other strong inorganic acids, occupational
exposures to mists and vapours from
Sulfur trioxide
Sulphisoxazole (see Sulfafurazole)
Sunset Yellow FCF
Symphytine
19, 231 (1979) (corr. 42, 258); Suppl. 7, 345

(1987); 60, 233 (1994) (corr. 65, 549); 82,
437 (2002)
19, 97 (1979); Suppl. 7, 72 (1987)
19, 252 (1979); Suppl. 7, 72 (1987)
11, 201 (1976); 19, 275 (1979); 36, 245
(1985); Suppl. 7, 72 (1987); 60, 321 (1994)
15, 265 (1977); Suppl. 7, 72 (1987)
8, 225 (1975); Suppl. 7, 72 (1987)
8, 233 (1975); Suppl. 7, 72 (1987)
8, 241 (1975); Suppl. 7, 72 (1987)
8, 249 (1975); Suppl. 7, 72 (1987)
8, 253 (1975); Suppl. 7, 72 (1987)
24, 275 (1980); Suppl. 7, 347 (1987)
30, 283 (1983); Suppl. 7, 72 (1987)
79, 341 (2001)
24, 285 (1980); Suppl. 7, 348 (1987); 79, 361
(2001)
54, 131 (1992)

54, 41 (1992)
54, 121 (1992)
8, 257 (1975); Suppl. 7, 72 (1987)
31, 239 (1983); Suppl. 7, 72 (1987)
T
2,4,5-T (see also Chlorophenoxy herbicides; Chlorophenoxy
Talc
Talc, inhaled, not containing asbestos or asbestiform fibres
Talc-based body powder, perineal use of
Tamoxifen
Tannic acid
Tannins (see also Tannic acid)
TCDD (see 2,3,7,8-Tetrachlorodibenzo-para-dioxin)
TDE (see DDT)
Tea
Temazepam
Teniposide
Terpene polychlorinates
Testosterone (see also Androgenic (anabolic) steroids)
Testosterone oenanthate (see Testosterone)
Testosterone propionate (see Testosterone)
2,2,5,5-Tetrachlorobenzidine
2,3,7,8-Tetrachlorodibenzo-para-dioxin
15, 273 (1977)

42, 185 (1987); Suppl. 7, 349 (1987)
93 (2010)
93 (2010)
66, 253 (1996)
10, 253 (1976) (corr. 42, 255); Suppl. 7, 72
(1987)
10, 254 (1976); Suppl. 7, 72 (1987)
51, 207 (1991)

66, 161 (1996)
76, 259 (2000)
5, 219 (1974); Suppl. 7, 72 (1987)
6, 209 (1974); 21, 519 (1979)
27, 141 (1982); Suppl. 7, 72 (1987)

15, 41 (1977); Suppl. 7, 350 (1987); 69, 33
(1997)
CUMULATIVE INDEX
1,1,1,2-Tetrachloroethane
1,1,2,2-Tetrachloroethane
Tetrachloroethylene
2,3,4,6-Tetrachlorophenol (see Chlorophenols; Chlorophenols,
salts)
Tetrachlorvinphos
Tetraethyllead (see Lead and lead compounds)
Tetrafluoroethylene
Tetrakis(hydroxymethyl)phosphonium salts
Tetramethyllead (see Lead and lead compounds)
Tetranitromethane
Textile manufacturing industry, exposures in
Theobromine
Theophylline
Thioacetamide
4,4-Thiodianiline
Thiotepa
Thiouracil
Thiourea
Thiram
Titanium (see Implants, surgical)
Titanium dioxide
Tobacco
Involuntary smoking
Smokeless tobacco
Tobacco smoke
ortho-Tolidine (see 3,3-Dimethylbenzidine)
2,4-Toluene diisocyanate (see also Toluene diisocyanates)
2,6-Toluene diisocyanate (see also Toluene diisocyanates)
Toluene
Toluene diisocyanates
Toluenes, -chlorinated (see -Chlorinated toluenes and benzoyl
chloride)
ortho-Toluenesulfonamide (see Saccharin)
ortho-Toluidine
Toremifene
Toxaphene
T-2 Toxin (see Toxins derived from Fusarium sporotrichioides)
427
41, 87 (1986); Suppl. 7, 72 (1987); 71, 1133
(1999)
20, 477 (1979); Suppl. 7, 354 (1987); 71, 817
(1999)
20, 491 (1979); Suppl. 7, 355 (1987); 63, 159
(1995) (corr. 65, 549)
30, 197 (1983); Suppl. 7, 72 (1987)

19, 285 (1979); Suppl. 7, 72 (1987); 71, 1143
(1999)
48, 95 (1990); 71, 1529 (1999)
65, 437 (1996)
48, 215 (1990) (corr. 51, 483)
51, 421 (1991)
51, 391 (1991)
7, 77 (1974); Suppl. 7, 72 (1987)
16, 343 (1978); 27, 147 (1982); Suppl. 7, 72
(1987)
9, 85 (1975); Suppl. 7, 368 (1987); 50, 123
(1990)
7, 85 (1974); Suppl. 7, 72 (1987); 79, 127
(2001)
7, 95 (1974); Suppl. 7, 72 (1987); 79, 703
(2001)
12, 225 (1976); Suppl. 7, 72 (1987); 53, 403
(1991)
47, 307 (1989); 93 (2010)
83, 1189 (2004)
37 (1985) (corr. 42, 263; 52, 513); Suppl. 7,
357 (1987); 89, 39 (2007)
38 (1986) (corr. 42, 263); Suppl. 7, 359
(1987); 83, 51 (2004)
19, 303 (1979); 39, 287 (1986)
19, 303 (1979); 39, 289 (1986)
47, 79 (1989); 71, 829 (1999)
39, 287 (1986) (corr. 42, 264); Suppl. 7, 72
(1987); 71, 865 (1999)
16, 349 (1978); 27, 155 (1982) (corr. 68,

477); Suppl. 7, 362 (1987); 77, 267 (2000)
66, 367 (1996)
20, 327 (1979); Suppl. 7, 72 (1987); 79, 569
(2001)
428
Toxins derived from Fusarium graminearum, F. culmorum and

F. crookwellense
Toxins derived from Fusarium moniliforme
Toxins derived from Fusarium sporotrichioides
Traditional herbal medicines
Tremolite (see Asbestos)
Treosulfan
Triaziquone (see Tris(aziridinyl)-para-benzoquinone)
Trichlorfon
Trichlormethine
Trichloroacetic acid
Trichloroacetonitrile (see also Halogenated acetonitriles)
1,1,1-Trichloroethane
1,1,2-Trichloroethane
Trichloroethylene
2,4,5-Trichlorophenol (see also Chlorophenols; Chlorophenols,
salts)
2,4,6-Trichlorophenol (see also Chlorophenols; Chlorophenols,
salts)
(2,4,5-Trichlorophenoxy)acetic acid (see 2,4,5-T)
1,2,3-Trichloropropane
Trichlorotriethylamine-hydrochloride (see Trichlormethine)
T2-Trichothecene (see Toxins derived from Fusarium
sporotrichioides)
Tridymite (see Crystalline silica)
Triethanolamine
Triethylene glycol diglycidyl ether
Trifluralin
4,4,6-Trimethylangelicin plus ultraviolet radiation (see also
2,4,5-Trimethylaniline
2,4,6-Trimethylaniline
4,5,8-Trimethylpsoralen
Trimustine hydrochloride (see Trichlormethine)
2,4,6-Trinitrotoluene
Triphenylene
Tris(aziridinyl)-para-benzoquinone
Tris(1-aziridinyl)phosphine-oxide
Tris(1-aziridinyl)phosphine-sulphide (see Thiotepa)
2,4,6-Tris(1-aziridinyl)-s-triazine
Tris(2-chloroethyl) phosphate
1,2,3-Tris(chloromethoxy)propane
Tris(2,3-dibromopropyl) phosphate
11, 169 (1976); 31, 153, 279 (1983); Suppl. 7,

64, 74 (1987); 56, 397 (1993)
56, 445 (1993)
31, 265 (1983); Suppl. 7, 73 (1987); 56, 467
(1993)
82, 41 (2002)
26, 341 (1981); Suppl. 7, 363 (1987)
30, 207 (1983); Suppl. 7, 73 (1987)
9, 229 (1975); Suppl. 7, 73 (1987); 50, 143
(1990)
63, 291 (1995) (corr. 65, 549); 84 (2004)
71, 1533 (1999)
20, 515 (1979); Suppl. 7, 73 (1987); 71, 881
(1999)
20, 533 (1979); Suppl. 7, 73 (1987); 52, 337
(1991); 71, 1153 (1999)
11, 263 (1976); 20, 545 (1979); Suppl. 7, 364
(1987); 63, 75 (1995) (corr. 65, 549)
20, 349 (1979)
20, 349 (1979)
63, 223 (1995)
77, 381 (2000)

11, 209 (1976); Suppl. 7, 73 (1987); 71, 1539
(1999)
53, 515 (1991)
Suppl. 7, 57 (1987)
27, 177 (1982); Suppl. 7, 73 (1987)
27, 178 (1982); Suppl. 7, 73 (1987)
40, 357 (1986); Suppl. 7, 366 (1987)
65, 449 (1996)
32, 447 (1983); Suppl. 7, 73 (1987); 92, 35
(2010)
9, 67 (1975); Suppl. 7, 367 (1987)
9, 75 (1975); Suppl. 7, 73 (1987)
9, 95 (1975); Suppl. 7, 73 (1987)
48, 109 (1990); 71, 1543 (1999)
15, 301 (1977); Suppl. 7, 73 (1987); 71, 1549
(1999)
20, 575 (1979); Suppl. 7, 369 (1987); 71, 905
(1999)
CUMULATIVE INDEX
Tris(2-methyl-1-aziridinyl)phosphine-oxide
Trp-P-1
Trp-P-2
Trypan blue
Tussilago farfara L. (see also Pyrrolizidine alkaloids)
429
9, 107 (1975); Suppl. 7, 73 (1987)
31, 247 (1983); Suppl. 7, 73 (1987)
31, 255 (1983); Suppl. 7, 73 (1987)
8, 267 (1975); Suppl. 7, 73 (1987)
10, 334 (1976)
U
Ultraviolet radiation
Underground haematite mining with exposure to radon
Uracil mustard
Uranium, depleted (see Implants, surgical)
Urethane
40, 379 (1986); 55 (1992)

1, 29 (1972); Suppl. 7, 216 (1987)
9, 235 (1975); Suppl. 7, 370 (1987)
7, 111 (1974); Suppl. 7, 73 (1987)
V
Vanadium pentoxide
Vat Yellow 4
Vinblastine sulfate
Vincristine sulfate
Vinyl acetate
Vinyl bromide
Vinyl chloride
Vinyl chloride-vinyl acetate copolymers
4-Vinylcyclohexene
4-Vinylcyclohexene diepoxide
Vinyl fluoride
Vinylidene chloride
Vinylidene chloride-vinyl chloride copolymers
Vinylidene fluoride
N-Vinyl-2-pyrrolidone
Vinyl toluene
Vitamin K substances
86, 227 (2006)

48, 161 (1990)
26, 349 (1981) (corr. 42, 261); Suppl. 7, 371
(1987)
26, 365 (1981); Suppl. 7, 372 (1987)
19, 341 (1979); 39, 113 (1986); Suppl. 7, 73
(1987); 63, 443 (1995)
19, 367 (1979); 39, 133 (1986); Suppl. 7, 73
(1987); 71, 923 (1999); 97, 445 (2008)
7, 291 (1974); 19, 377 (1979) (corr. 42, 258);
Suppl. 7, 373 (1987); 97, 311 (2008)
7, 311 (1976); 19, 412 (1979) (corr. 42, 258);
Suppl. 7, 73 (1987)
11, 277 (1976); 39, 181 (1986) Suppl. 7, 73
(1987); 60, 347 (1994)
11, 141 (1976); Suppl. 7, 63 (1987); 60, 361
(1994)
39, 147 (1986); Suppl. 7, 73 (1987); 63, 467
(1995); 97, 459 (2008)
19, 439 (1979); 39, 195 (1986); Suppl. 7, 376
(1987); 71, 1163 (1999)
19, 448 (1979) (corr. 42, 258); Suppl. 7, 73
(1987)
39, 227 (1986); Suppl. 7, 73 (1987); 71, 1551
(1999)
19, 461 (1979); Suppl. 7, 73 (1987); 71, 1181
(1999)
60, 373 (1994)
76, 417 (2000)
W
Welding
Wollastonite
49, 447 (1990) (corr. 52, 513)

42, 145 (1987); Suppl. 7, 377 (1987); 68, 283
(1997)
430
Wood dust
Wood industries
62, 35 (1995)
25 (1981); Suppl. 7, 378 (1987)
X
X-radiation
Xylenes
2,4-Xylidine
2,5-Xylidine
2,6-Xylidine (see 2,6-Dimethylaniline)
75, 121 (2000)

47, 125 (1989); 71, 1189 (1999)
16, 367 (1978); Suppl. 7, 74 (1987)
16, 377 (1978); Suppl. 7, 74 (1987)
Y
Yellow AB
Yellow OB
8, 279 (1975); Suppl. 7, 74 (1987)

8, 287 (1975); Suppl. 7, 74 (1987)
Z
Zalcitabine
Zearalenone (see Toxins derived from Fusarium graminearum,
Zectran
Zeolites other than erionite
Zidovudine
Zinc beryllium silicate (see Beryllium and beryllium compounds)
Zinc chromate (see Chromium and chromium compounds)
Zinc chromate hydroxide (see Chromium and chromium compounds)
Zinc potassium chromate (see Chromium and chromium compounds)
Zinc yellow (see Chromium and chromium compounds)
Zineb
Ziram
76, 129 (2000)
12, 237 (1976); Suppl. 7, 74 (1987)

68, 307 (1997)
76, 73 (2000)
12, 245 (1976); Suppl. 7, 74 (1987)

12, 259 (1976); Suppl. 7, 74 (1987); 53, 423
(1991)
List of IARC Monographs on the Evaluation of Carcinogenic Risks to Humans*

Volume 1
Some Inorganic Substances,
Chlorinated Hydrocarbons,
Aromatic Amines, N-Nitroso
Compounds, and Natural
Products
1972; 184 pages (out-of-print)
Volume 2
Some Inorganic and Organometallic Compounds
Volume 3
Certain Polycyclic Aromatic
Hydrocarbons and Heterocyclic
Compounds
Volume 4
Some Aromatic Amines,
Hydrazine and Related
Substances,
N-Nitroso Compounds and
Miscellaneous Alkylating
Agents
Volume 5
Some Organochlorine
Pesticides
Volume 6
Sex Hormones
Volume 7
Some Anti-Thyroid and Related
Substances, Nitrofurans and
Industrial Chemicals
Volume 8
Some Aromatic Azo
Compounds
Volume 9
Some Aziridines, N-, S- and
O-Mustards and Selenium
Volume 10
Some Naturally Occurring
Substances
Volume 11
Cadmium, Nickel, Some
Epoxides, Miscellaneous
Industrial Chemicals and
General Considerations on
Volatile Anaesthetics
Volume 12
Some Carbamates, Thiocarbamates and Carbazides
Volume 13
Some Miscellaneous
Pharmaceutical Substances
1977; 255 pages
Volume 14
Asbestos
Volume 15
Some Fumigants, the Herbicides
2,4-D and 2,4,5-T, Chlorinated
Dibenzodioxins and
Miscellaneous Industrial
Chemicals
Volume 16
Some Aromatic Amines and
Related Nitro CompoundsHair
Dyes, Colouring Agents and
Miscellaneous Industrial
Chemicals
1978; 400 pages
Volume 17
Some N-Nitroso Compounds
1978; 365 pages
Volume 18
Polychlorinated Biphenyls and
Polybrominated Biphenyls
Volume 19
Some Monomers, Plastics and
Synthetic Elastomers, and
Acrolein
Volume 20
Some Halogenated
Hydrocarbons
Volume 21
Sex Hormones (II)
1979; 583 pages
Volume 22
Some Non-Nutritive Sweetening
Agents
1980; 208 pages
Volume 23
Some Metals and Metallic
Compounds
Volume 24
Some Pharmaceutical Drugs
1980; 337 pages
Volume 25
Wood, Leather and Some
Associated Industries
1981; 412 pages
Volume 26
Some Antineoplastic and
Immunosuppressive Agents
Volume 27
Some Aromatic Amines,
Anthraquinones and Nitroso
Compounds, and Inorganic
Fluorides Used in Drinkingwater and Dental Preparations
Volume 28
The Rubber Industry
Volume 29
Some Industrial Chemicals and
Dyestuffs
Volume 30
Miscellaneous Pesticides
Volume 31
Some Food Additives, Feed
Additives and Naturally
Occurring Substances
Volume 32
Polynuclear Aromatic
Compounds, Part 1: Chemical,
Environmental and
Experimental Data
Volume 33
Compounds, Part 2: Carbon
Blacks, Mineral Oils and Some
Nitroarenes
Volume 34
Compounds, Part 3: Industrial
Exposures in Aluminium
Production, Coal Gasification,
Coke Production, and Iron and
Steel Founding
Volume 35
Compounds, Part 4: Bitumens,
Coal-tars and Derived Products,
Shale-oils and Soots
1985; 271 pages
Volume 36
Allyl Compounds, Aldehydes,
Epoxides and Peroxides
1985; 369 pages
Volume 37
Tobacco Habits Other than
Smoking; Betel-Quid and ArecaNut Chewing; and Some Related
Nitrosamines
Volume 38
Tobacco Smoking
1986; 421 pages
Volume 39
Some Chemicals Used in Plastics
and Elastomers
Volume 40
Some Naturally Occurring and
Synthetic Food Components,
Furocoumarins and Ultraviolet
Radiation
Volume 41
Some Halogenated Hydrocarbons
and Pesticide Exposures
Volume 42
Silica and Some Silicates
1987; 289 pages
Volume 43
Man-Made Mineral Fibres and
Radon
Volume 44
Alcohol Drinking
1988; 416 pages
Volume 45
Occupational Exposures in
Petroleum Refining; Crude Oil
and Major Petroleum Fuels
1989; 322 pages
Volume 48
Some Flame Retardants and
Textile Chemicals, and
Exposures in the Textile
Manufacturing Industry
1990; 345 pages
Volume 49
Chromium, Nickel and Welding
1990; 677 pages
Volume 50
Pharmaceutical Drugs
1990; 415 pages
Volume 51
Coffee, Tea, Mate,
Methylxanthines and
Methylglyoxal
1991; 513 pages
Volume 52
Chlorinated Drinking-water;
Chlorination By-products; Some
Other Halogenated Compounds;
Cobalt and Cobalt Compounds
1991; 544 pages
Volume 53
Insecticide Application, and
Some Pesticides
1991; 612 pages
Volume 54
Occupational Exposures to
Mists and Vapours from Strong
Inorganic Acids; and Other
Industrial Chemicals
1992; 336 pages
Volume 46
Diesel and Gasoline Engine
Exhausts and Some Nitroarenes
1989; 458 pages
Volume 55
Solar and Ultraviolet Radiation
1992; 316 pages
Volume 47
Some Organic Solvents, Resin
Monomers and Related
Compounds, Pigments and
Paint Manufacture and Painting
Volume 56
Some Naturally Occurring
Substances: Food Items and
Constituents, Heterocyclic
Aromatic Amines and
Mycotoxins
1993; 599 pages
Volume 57
Occupational Exposures of
Hairdressers and Barbers and
Personal Use of Hair
Colourants; Some Hair Dyes,
Cosmetic Colourants, Industrial
Dyestuffs and Aromatic Amines
1993; 428 pages
Volume 58
Beryllium, Cadmium, Mercury,
and Exposures in the Glass
Manufacturing Industry
1993; 444 pages
Volume 59
Hepatitis Viruses
1994; 286 pages
Volume 60
Some Industrial Chemicals
1994; 560 pages
Volume 61
Schistosomes, Liver Flukes and
Helicobacter pylori
1994; 270 pages
Volume 62
Wood Dust and Formaldehyde
1995; 405 pages
Volume 63
Dry Cleaning, Some Chlorinated
Solvents and Other Industrial
Chemicals
1995; 551 pages
Volume 64
Human Papillomaviruses
1995; 409 pages
Volume 65
Printing Processes and Printing
Inks, Carbon Black and Some
Nitro Compounds
1996; 578 pages
Volume 68
Silica, Some Silicates, Coal Dust
and para-Aramid Fibrils
1997; 506 pages
Volume 69
Polychlorinated Dibenzo-paraDioxins and Polychlorinated
Dibenzofurans
1997; 666 pages
Volume 70
Epstein-Barr Virus and Kaposis
Sarcoma Herpesvirus/Human
Herpesvirus 8
1997; 524 pages
Volume 71
Re-evaluation of Some Organic
Chemicals, Hydrazine and
Hydrogen Peroxide
1999; 1586 pages
Volume 72
Hormonal Contraception and
Post-menopausal Hormonal
Therapy
1999; 660 pages
Volume 73
Some Chemicals that Cause
Tumours of the Kidney or Urinary
Bladder in Rodents and
Some Other Substances
1999; 674 pages
Volume 74
Surgical Implants and Other
Foreign Bodies
1999; 409 pages
Volume 75
Ionizing Radiation, Part 1,
X-Radiation and -Radiation,
and Neutrons
2000; 492 pages
Volume 66
Some Pharmaceutical Drugs
1996; 514 pages
Volume 76
Some Antiviral and
Antineoplastic Drugs, and Other
Pharmaceutical Agents
2000; 522 pages
Volume 67
Human Immunodeficiency
Viruses and Human T-Cell
Lymphotropic Viruses
1996; 424 pages
Volume 77
Some Industrial Chemicals
2000; 563 pages
Volume 78
Ionizing Radiation, Part 2,
Some Internally Deposited
Radionuclides
2001; 595 pages
Volume 79
Some Thyrotropic Agents
2001; 763 pages
Volume 80
Non-Ionizing Radiation, Part 1:
Static and Extremely LowFrequency (ELF) Electric and
Magnetic Fields
2002; 429 pages
Volume 81
Man-made Vitreous Fibres
2002; 418 pages
Volume 82
Some Traditional Herbal
Medicines, Some Mycotoxins,
Naphthalene and Styrene
2002; 590 pages
Volume 83
Tobacco Smoke and Involuntary
Smoking
2004; 1452 pages
Volume 84
Some Drinking-Water
Disinfectants and
Contaminants, including
Arsenic
2004; 512 pages
Volume 85
Betel-quid and Areca-nut Chewing
and Some Areca-nut-derived
Nitrosamines
2004; 334 pages
Volume 86
Cobalt in Hard Metals and
Cobalt Sulfate, Gallium
Arsenide, Indium Phosphide
and Vanadium Pentoxide
2006; 330 pages
Volume 87
Inorganic and Organic Lead
Compounds
2006; 506 pages
Volume 88
Formaldehyde, 2-Butoxyethanol
and 1-tert-Butoxypropan-2-ol
2006; 478 pages
Volume 89
Smokeless Tobacco and Some
Tobacco-specific NNitrosamines
2007; 626 pages
Volume 90
Human Papillomaviruses
2007; 670 pages
Volume 91
Combined EstrogenProgestogen Contraceptives and
Combined Estrogen-Progestogen
Menopausal Therapy
2007; 528 pages
Volume 92
Some Non-heterocyclic
Polycyclic Aromatic
Hydrocarbons and Some Related
Exposures
2010; 853 pages
Volume 95
Household Use of
Solid Fuels and Hightemperature Frying
2010; 430 pages
Volume 96
Consumption of Alcoholic
Beverages and Ethyl
Carbamate (Urethane)
(in preparation)
Volume 97
1,3-Butadiene, Ethylene Oxide
and Vinyl Halides (Vinyl
Fluoride, Vinyl Chloride and
Vinyl Bromide)
2008; 510 pages
Supplement No. 1
Chemicals and Industrial
Processes Associated with
Cancer in Humans (IARC
Monographs, Volumes 1 to 20)
Volume 93
Carbon Black, Titanium
Dioxide and Non-Asbestiform
Talc
(in preparation)
Supplement No. 2
Long-term and Short-term
Screening Assays for
Carcinogens: A Critical
Appraisal
(updated as IARC Scientific
Publications No. 83, 1986)
Volume 94
Ingested Nitrates and Nitrites,
and Cyanobacterial Peptide
Toxins
(in preparation)
Supplement No. 3
Cross Index of Synonyms and
Trade Names in Volumes 1 to 26
of the IARC Monographs
Supplement No. 4
Chemicals, Industrial Processes
and Industries Associated with
Cancer in Humans (IARC
Monographs, Volumes 1 to 29)
Supplement No. 5
Supplement No. 6
Genetic and Related Effects:
An Updating of Selected IARC
Monographs from Volumes 1
to 42
Supplement No. 7
Overall Evaluations of
Carcinogenicity: An Updating of
IARC Monographs Volumes
142
Supplement No. 8

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WORLD HEALTH ORGANIZATION

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER

IARC Monographs on the Evaluation of

WORLD HEALTH ORGANIZATION

IARC Monographs on the Evaluation of

Household Use of Solid Fuels and

This publication represents the views and expert opinions

International Agency for Research on Cancer, 2010

(NLM Classification: W1)

IARC MONOGRAPHS VOLUME 95

2. Studies of Cancer in Humans................................................................................ 144

3. Studies of Cancer in Experimental Animals ........................................................ 374

NOTE TO THE READER

IARC MONOGRAPHS ON THE EVALUATION OF

Lyon, 1017 October 2006

IARC MONOGRAPHS VOLUME 95

David M. DeMarini, Environmental Carcinogenesis Division (B-143-06), U.S.

IARC MONOGRAPHS VOLUME 95

IARC MONOGRAPHS ON THE EVALUATION OF

A. GENERAL PRINCIPLES AND PROCEDURES

IARC MONOGRAPHS VOLUME 95

In the Monographs, an agent is termed carcinogenic if it is capable of increasing the

IARC MONOGRAPHS VOLUME 95

3. Selection of agents for review

IARC MONOGRAPHS VOLUME 95

B. SCIENTIFIC REVIEW AND EVALUATION

IARC MONOGRAPHS VOLUME 95

General information on the agent

Analysis and detection

An overview of methods of analysis and detection of the agent is presented, including

Production and use

Occurrence and exposure

Information on the occurrence of an agent in the environment is obtained from data

IARC MONOGRAPHS VOLUME 95

Regulations and guidelines

Statements concerning regulations and guidelines (e.g. occupational exposure limits,

Types of study considered

Several types of epidemiological study contribute to the assessment of carcinogenicity

Quality of studies considered

IARC MONOGRAPHS VOLUME 95

Meta-analyses and pooled analyses

Use of biomarkers in epidemiological studies

Criteria for causality

IARC MONOGRAPHS VOLUME 95

IARC MONOGRAPHS VOLUME 95

IARC MONOGRAPHS VOLUME 95

Toxicokinetics refers to the absorption, distribution, metabolism and elimination of

Data on mechanisms of carcinogenesis

IARC MONOGRAPHS VOLUME 95

aneuploidy. The concentrations employed are given, and mention is made of

Other data relevant to mechanisms

A description is provided of any structureactivity relationships that may be relevant

Individuals, populations and life-stages may have greater or lesser susceptibility to an

Data on other adverse effects

IARC MONOGRAPHS VOLUME 95

Data are summarized, as appropriate, on the basis of elements such as production,

Cancer in experimental animals

Data relevant to an evaluation of carcinogenicity in animals are summarized. For each

Mechanistic and other relevant data