Basic Environmental Health
Basic Environmental Health
Basic Environmental Health
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UNEP
BASIC
ENVIRONMENTAL
HEALTH
BAS IC
ENVIRONMENTAL
HEALTH
Annalee Yassi
lord Kjellström
Theo de Kok
Tee L. Guidotti
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OXFORD
UNIVERSITY PRESS
2001
OXFORD
UNIVERSITY PRESS
98765432
Printcd in the United States of America
on acid-free paper
PREFACE
V
The problem solving exercises in the Teacher's Guide can be used to adjust
the level of complexity of the course for individual students or the class as a
whole. In interdisciplinary classes, for example, the teachcr may require more
in-depth research from students in the areas of their OWfl disciplines compared
to others in different disciplines, who would in turn focus on areas of their own
expertise. This permits each student to achieve a maximum learning experience
while contributing optimally to the group. It also simulates the real world sce-
nario in which professionals in different disciplines are expected to understand
each other, while depending on each other for the more complex details.
The text and teaching kit are part of a sustained effort by WHO, UNEP,
UNESCO, and CRE to promote strengthened teaching in environmental health
for a wide variety of students at university level.
vi Preface
ACKNOWLEDGMENTS
This text was developed with the assistance of the United Nations Environment
Programme (UNEP), Conference of European University Rectors (CRE), and the
United Nations Educational Scientific and Cultural Organisation (UNESCO), and
under the overall auspices of the Office of Global and Integrated Environmental
Health of the World Health Organisation (WHO). It was tested at workshops in
Visby, Sweden; Budapest, Hungary; Cape Town, South Africa; and Amman, Jor -
dan where valuable comments were provided by the participants. Comments re-
ceived in meetings of reviewers held in Geneva in June 1994 and November
1995, and by many others were also incorporated.
Dr. Theo de Kok (University Maastricht, The Netherlands), the third author
of the book, has been developing distance learning materials, in conjunction with
this text. Merri Weinger (education specialist, WHO) is the primary author of the
Teacher's Guide.
There are many people who have made valuable contributions to this text to
date; these and others will hopefully continue to contribute by supplying case
studies from which others could learn. Among the many contributors, several
stand out for specific mention.
Dr. Jerry Spiegel (formerly of Manitoba Environment, Winnipeg, Canada and
now with the Liu Centre for the study of Global Issues at the University of British
Columbia, Vancouver, Canada) served as the major editor of the book and con-
tributed substantially to the chapter on risk management. He also wrote a large
section of the industry chapter and extensively rewrote other parts of the text.
Dr. Alan Pinter (Johan Bela National Institute of Health INIHI, Budapest, Hun-
gary), and Dr. Evert Nieboer (McMaster University, Hamilton, Canada) both had
substantial input to the book, particularly to the toxicology sections, and Dr.
Avrum Regenstreif had major input to the chapter on settlements and urban de-
velopment. The following individuals (listed in alphabetical order) also served as
reviewers and contributed valuable comments and materials:
Dr. Pedro Más Bermejo, Director, National Institute of Hygiene Epidemiology and
Microbiology, La Hahana, Cuba
Dr. Helen Dolk, London School of Hygiene and Tropical Medicine, London, UK
Professor Hunay Evliya, Cukurova University, Turkey
Professor Maria Alvim Ferraz, University of Oporto, Portugal
Professor H.N.B. Gopalan, UNEP, Nairobi, Kenya
VII
Dr. Steve Hrudey, University of Alberta, Canada
Dr. Steven Markowitz, Mount Sinai School of Medicine, New York, USA
Dr. S. Miyagawa, Division of Food and Nutrition, WHO, Geneva
Dr. Monica Nordberg, Karolinska Institute, Stockholm, Sweden
Dr. Peter Orris, Cook County Hospital, Chicago, USA
Dr. Peri Pamir, CRE, Geneva
Dr. David Rapport, University Guelph, Canada
Dr. Yasmin von Schirnding, Environmental Health, Johannesburg, South Africa
Dr. Cohn Soskolne, University of Alberta, Canada
Dr. Carl-Einar Stalvant, Stockholm University, Sweden
Ms. Adrienne Taylor, Auckland, New Zealand
Professor Dr. Henk van de Plas, Copernicus Steering Committee, The Netherlands
Dr. Susan van de Vynckt, UNESCO, Paris
and others.
viii Acknowledgments
CONTENTS
Introduction, 1
Birth, Life, Death, and the Environment, 2
Health and the Environment, 3
Historical Perspective, 10
Basic Requirements for a Healthy Environment, 14
Measuring Environmental Quality, Human Exposure, and
Health Impact, 18
Patterns of Illness Throughout the World, 21
Impact of Environmental Factors on Health, 35
Links Between Environmental and Occupational Health, 38
Obstacles to and Opportunities for Resolving Environmental
Health Problems, 41
Role of the Environmental Health Professional, 46
Air, 180
Overview of Air Pollution, 180
Common Health Effects of Ambient Air Pollution, 188
Health Effects of Specific Air Pollutants, 190
Industrial Air Pollution, 198
Air Pollution and the Community, 201
x Contents
Industrial Pollution and Chemical Safety, 332
Extent of Industrial Pollution, 333
Public Exposure From Industrial Sources, 333
Hazards by Industry, 340
Major Chemical Contaminants of Concern in the General
Environment and the Workplace, 344
The Social Context of Occupational Health and Safety, 350
Dimensions and Types of Occupational Health Problems, 354
Industrial Environmental Accidents, 362
Approaches to Prevention, 363
Index, 421
CONTENTS xi
BASIC
ENVIRONMENTAL
HEALTH
1
INTRODUCTION
LEARNING OBJECTIVES
CHAPTER CONTENTS
Birth, Life, Death, and the Environment Safe and Sufficient Water
Health and the Environment Adequate and Safe Food
An Ecosystem Perspective Safe and Peaceful Settlements
Definitions of Health and Stable Global Environment
Environment Measuring Environmental Quality,
Human Interaction with the Human Exposure, and Health Impact
Environment Measuring Environmental Quality
Human Ability to Adapt Measuring Human Exposure to
Supportive Environments for Environmental Hazards
Health Determining Health Elfects and
Historical Perspective Risks in Human Populations
Economic and Industrial Develop- Environmental Health Monitoring
ment and Environmental Health Patterns of Illness Throughout
The First Environmental Crisis the World
The Second Wave of Environmen- Demographic and Epidemiological
tal Concern Transitions
The Third Wave of Environmental Mortality Trends
Concern Burden of Disease
Basic Requirements for a Healthy Vulnerable Groups
Environment Impact of Environmental Factors
Clean Air on Health
Links Between Environmental and Obstacles to and Opportunities for
Occupational Health Resolving Environmental Health
Importance of the Workforce Problems
Linked Environmental and Demographic Issues
Occupational Health Hazards Poverty
Common Approaches and Human Consumption Patterns
Resources Macroeconomic Policies
The Workplace as a Sentinel for Role of the Environmental Health
Environmental Hazards Professional
The Total Exposure Concept You Can Make a Difference
Consistency in Setting Standards The Multidisciplinary Team
Incentives for Prevention
• the constant search for sufficient food and drinking water while avoiding plants
that contained natural toxins (like poisonous toadstools) or rancid infected
meat
• infections and parasites that spread from person to person or animal to per-
son, often through food, drinking water, or insect vectors
• injuries from falls, fires, and animal attacks
• cold and hot temperatures, rain, snow, natural disasters, and other adverse
conditions.
These health hazards all occurred in the natural environment. In some soci-
eties the "traditional hazards" listed above still dominate environmental health
concerns. However, as human beings brought these hazards under control in
some regions, "modern hazards" caused by technological and industrial devel-
opment took over as the primary threat to health and well-being.
Over the last few decades, life expectancy has increased significantly in most
countries, as examples of survival curves show (Fig. Li). Some investigators say
that this is largely due to improvements made in the living environment. Oth-
ers say that improvements in nutrition are an essential reason for longer lives.
Still others say that the changes could not have happened without improved
medical diagnosis and treatment of illnesses. All of these statements are proba-
bly correct. Progress in health has gone hand in hand with improvements in en-
vironmental quality, nutrition, and medical care. People who are sick now are
more likely to survive because of improved medical care, and the much greater
number who are healthy at any given time are likely to stay healthy and fit be-
cause of improved nutrition and control of environmental health hazards. Pro-
0,
60 60
0 o 50
50
a) a)
0) 0)
Ca 40 40
0 0
a)
U 30 30
a) a)
0 20 o 20
10 10
0 0
0 5 10152025303540455055606570758085+ 0 5 10152025303540455055606570758085+
Age Age
Figure 1.1 Survival curves, 1955-2025. From WHO, 1998a, with permission.
jections of survival and world population through to year 2025 indicate a con-
tinual improvement of life expectancy (Fig. 1.1).
Environmental health science is essentially about two things: hazards in the
environment, their effects on health, and the variations in sensitivity to expo-
sures within populations; and the development of effective means to protect
against hazards in the environment. This book will describe the major environ-
mental hazards that can affect health, show how these hazards can be assessed,
and demonstrate how the resulting adverse health effects can be reduced or
avoided. The roles of various professionals in protecting health will be explored
and the fundamental principles that all environmental health professionals need
to understand, regardless of where they work, will be described.
INTRODUCTION 3
pox 1.1
James Lovelock, a British atmospheric scientist, advanced the hypothesis that the
earth and all its components (including the geosphere and the water, gas, nutrients,
energy cycles, and all living organisms) constitute a global homeostatic mechanism
that ensures constancy of the environment. This hypothesis is known as the Gaia
hypothesis, as the word Gala comes from the Greek goddess Mother Earth. Lovelock
contends that the global biosphere acts in a self-regulating manner, using feedback
mechanisms to counter externally imposed disturbances. For example, the heat out-
put of the sun has increased by about 30% since our planet was formed. Yet the
earth has maintained a relatively constant temperature. This is believed to be due
to the increased solar energy stimulating an increase in photosynthesis, which re-
duces carbon dioxide levels in the atmosphere. This in turn reduces the "green-
house" capacity of the atmosphere, causing it to cool and thereby compensate for
more heat from the sun. Similarly, the Gaia hypothesis suggests that oxygen has
accumulated in the atmosphere to a level that is optimal for biological life on Earth,
reflecting the balance of positive and negative feedback from the variety of inter-
dependent living organisms. These changes have taken place very slowly over thou-
sands or millions of years, while the currently debated increase in greenhouse gases
has taken place in a few decades.
The controversy surrounding the Gaia hypothesis is due in part to the fact that
it cannot be scientifically tested. Additionally, the hypothesis is seen by some in-
vestigators to imply that nature acts in a purposeful manner, a concept that does
not fit comfortably with the mechanistic view of the world that prevails in con-
temporary Western civilization. Nonetheless, the Gala hypothesis has stimulated
awareness of the interdependencies within ecosystems and the balance of nature,
which, within limits, serve to sustain the planet's life support systems.. It has also
provtded a powerful vision or analogy for treating the Earth with the same respect
one would show a mother.
Source: Lovelock, 1988; see also McMichael, 1993.
INTRODUCTION 5
As noted in the book Our Planet, Our Health (WHO, 1992a), the responsibil-
ity for protecting and promoting good health extends to all groups in society. No
longer is good health the responsibility of only traditional health care profes-
sionals, such as doctors, nurses, sanitary engineers, and safety officers, who seek
to cure disease, care for the sick, remove pathogens, and reduce injuries. Human
well-being is now clearly the responsibility of planners, architects, teachers, em-
ployers, industrial managers, and all others who influence the physical or social
environment. That is why this book is geared for teaching people in many pro-
fessions. Naturally, health professionals have a special role in environmental
health, but they need to work with all groups in society to promote good health.
The ability to work in teams and adopt a transdisciplinary approach is key to be-
ing able to solve environmental health problems (Somervile and Rapport, 2000).
7/ HEALTH
INTRODUCTION 7
Sometimes there is an ethical dilemma between promoting human health and
protecting the environment. One extreme position is that any control limiting
the exploitation of resources may inhibit an individual's or a community's at-
tempts to enhance their standard of living, therefore infringing on their rights
and freedoms as well as decreasing their ability to maintain health. At the other
extreme is the position that any action to protect the environment and maintain
the integrity of the ecosystem is justified regardless of the impact on human ac-
tivity and health. The United Nations has stated that ensuring human survival
should be taken as a first-order principle, one that takes precedence over all oth-
ers. The first order assigned to meeting human survival is consistent with the
United Nations Universal Declaration of Human Rights (UN, 1948), which states
that "all people have the right to a standard of living adequate for the health and
well-being of themselves and their family, including food, clothing, housing,
health care, and the necessary social services." Respect for nature and control of
environmental degradation is a "second-order" principle, which should guide all
human activities, except when these activities conflict with the first principle. In
reality, most such conflicts are more apparent than real and arise from a faulty
understanding of the human-environment interaction, or a dysfunctional social
and economic system.
Sustainable development implies that everyone eventually must have access to
the environmental resources that meet their needs. This must also be done with
a continuous commitment to improve general understanding of how the envi-
ronment and health are linked. It must be done without overwhelming the fi-
nite absorptive capacities of the global ecosystem.
• industrial pollution
• poor services of drinking water and sanitation
• poor housing and town planning
• lax control over eating establishments or food industry
• the role of local environmental factors in the healthy development of the com-
munity
• an approach that enables and promotes health, as well as protects from environ-
mental hazards
• creation of equity in health within a community
• the importance of sustainable development as a health issue
• people's understanding of environment in a broad sense
• people's sense of involvement and personal interest in restoring or creating a
healthy environment.
Source: Haglund et cii., 1992.
INTRODUCTION 9
HISTORICAL PERSPECTIVE
Economic and Industrial Development and Environmental Health
While it is well known that biological agents and naturally occurring chemical and
physical hazards have existed throughout human history, there is also a long his-
tory of environmental pollution from anthropogenic sources (human activities).
Even in ancient times, sites of production and manufacturing were contaminated
with pollution. A good example is lead contamination in the area around smelters
centuries ago and the horrible odor and water pollution associated with tanneries.
By modern standards, the scale of most of these enterprises was very small, how-
ever. The technology was that of the individual artisan using traditional work prac-
tices that had not substantially changed for centuries. The resulting pollution was
usually restricted to the immediate area. Pollution from human waste was con-
sidered more of a problem, as it effectively limited the size of cities. As great a prob-
lem as pollution was occupational health and safety, as workers were subjected to
intense exposure to a variety of hazards at the workplace.
The Industrial Revolution marked a dramatic turning point in the interaction
between economic activity and the environment. Industrial pollution was first
identified as an obvious and serious issue in the early 1 800s, when it became ob-
vious that production on an industrial scale, using the breakthrough technology
of the time, resulted in pollution on a scale never before seen. This pollution was
largely the result of the energy requirements of a technology based on iron and
steel, which led to more widespread air pollution as well as local concentrations
of pollution near the factory site.
The United Kingdom, home of the Industrial Revolution, was the first coun-
try to suffer from industrial pollution on a massive scale. It became particularly
obvious during the later years of the reign of Queen Victoria (the Victorian era).
Mass production led to the recruitment of hundreds of thousands of new work-
ers into a wage-earning class. These workers soon became consumers themselves.
Production soared and the profits created a pool of capital that was then rein-
vested in further industrial expansion. The new industrial cities became infa-
mous. A well-studied example was the city of Manchester, but the export of new
technology created many other examples in the British Isles, Europe, and else-
where. At that time much of what is now the developing world was under colo-
nialism. It would be many years before these areas would suffer similar prob-
lems in the course of their own economic development. The colonial system
restricted most manufacturing to the colonizing country, which sold manufac-
tured goods in the colonies and bought raw materials and food from them.
Industrial pollution may have been a serious problem in the Victorian era,
but it was not high on the list of social priorities of the day. Considered much
more important at that time were social issues, such as child labor, class-based
poverty, alcohol and drug abuse (mostly gin and opium), welfare services (or the
absence thereof), corruption, and prostitution. All of these issues were related to
the urbanization that accompanied the recruitment of an industrial work force.
The principal health concerns of the day were communicable diseases, which
were out of control in the squalid, densely populated cities. These problems be-
came a national crisis in England and Scotland and it soon became obvious that
INTRODUCTION 11
sector. Synthetic rubbers, solvents, plastics, and pesticides became available and
were often more effective and cheaper to produce than the older products. Many
of these new synthetic chemicals were based on chlorine chemistry. A large num-
ber of them turned out to be difficult to break down by natural processes and,
as a result, persisted in the environment. Changes in technology and a greater
demand from consumers in North America, Japan, and Europe also led to huge
increases in the volume of hazardous materials. In the postwar years, production
expanded massively, along with a well-documented increase in industrial pollu-
tion that led to a public outcry in the 1960s and 70s in many countries.
1798 Thomas Maithus developed his theories on resource allocation and popula-
tion
1848 Public Health Act passed by British Parliament
1895 Svante Arrhenius describes the greenhouse effect
1899 First international convention to ban chemical weapons
1956 British Clean Air Act passed
1962 Publication of Rachel Carson's book Silent Spring draws attention to pesticides
and the environment
1969 First international agreement on cooperation in case of marine pollution
(North Sea region)
1972 United Nations Conference on Human Environment, Stockholm; DDT banned
in the United States
1982 Multilateral Conference on Acidification of the Environment starts process
leading to fornial recognition of transregional pollution and need for inter-
national controls
1986 First International Conference on Health Promotion; produced the Ottawa
Charter, which defined health promotion as enabling people to take control
of the determinants of their health.
1987 Our Common Future (the Brundtland Commission Report) calls for "sustain-
able development"; Montreal Protocol on limiting emissions to air of chioro-
fluorocarbons to reduce depletion of stratospheric ozone layer
1992 Earth Summit (United Nations Conference on Environment and Develop-
ment), Rio de Janeiro
1994 International Conference on Population and Development, Cairo
1995 UN World Summit for Social Development, Copenhagen
1996 UN Conference on Human Settlements (I-IABJTAT II), Istanbul
1997 UN Framework Convention on Climate Change, IKyoto
1980s, even though scientists had given warnings about their toxic effects much
earlier (see Box 1.3). These chemicals have since become a major environmen-
tal concern.
The Third Wave of Environmental Concern
In the 1980s and into the 1990s, the accelerated rate of economic development,
combined with a substantial increase in world population, introduced a critical
new factor into the environmental equation. Until the 1980s the levels of pro-
duction in the developing world were relatively low compared to those in the
developed countries. As a consequence, industrial pollution in developing coun-
tries tended to be confined to local areas, as it had been in Europe and America
in earlier times. Recently, however, production levels in these countries have in-
creased very rapidly along with the demand for goods and the capacity for di-
INTRODUCTION 13
Yect trading among countries because of the globalization of trade. Much of the
production in this new sector is relatively undercapitalized and therefore it is of-
ten based on expedient, cheaper technologies. There are usually few controls
over effluents and emissions, and the result is increases in industrial pollution.
Since 1987 and the publication of the seminal report Our Common Future
(WCED, 1987), environmental planning and economic development have be-
come oriented toward "sustainable development." the level of production and
activity that can be undertaken in one generation without compromising envi-
ronmental integrity or depleting the resources to support the next generation.
This concept, which is roughly equivalent to the idea in biology of living within
the carrying capacity of the ecosystem for a society, has entered the mainstream
of economic thought and environmental management. It represents a way of
thinking about development that takes into account resource management, pol-
lution, social development, and human health.
New environmental concerns continue to emerge. Some toxicologists are fo-
cusing on chemicals that disrupt the endocrine system and are persistent in the
environment (see Chapter 2). Certainly the concerns about global environmen-
tal change (see Chapter 11) have generated renewed interest in the environment
that will likely persist for decades to come.
INTRODUCTION 15
Adequate and Safe Food
Food provides the energy for our bodies to function. The equivalent of about
1000 to 2000 calories is required each day for a person to stay alive, depending
on a person's body weight and level of physical activity. Without food, most pco-
pie would die after about 4 weeks. Food also provides essential vitamins and trace
elements, without which people develop deficiency diseases.
The output of the world's food-producing systems has matched the population
growth over the last few decades (Fig. 1.3). There is no global shortage of food or
lack of capacity to produce it at this time. Nonetheless, the success in global agri-
culture has not been shared equally. Asia and Latin America have substantially in-
creased their per-capita food production, while Africa's food production has not
kept pace with population growth, and the countries of the former Soviet Union
have had a dramatic decrease in fod production. For a large part of the world's
population, undernutrition and the infections associated with it remain a major
cause of ill health and premature death. Foodborne pathogens cause millions of
cases of diarrheal disease each year, including thousands in the developed world.
Poor food distribution and its utilization are the main culprits in this situation.
Rapid degradation of land and watcr resources also pose an important threat to
future food production. To make matters worse, because of economic pressures to
develop exports of agricultural products, increasingly, the best land is not being
used for local food production. In many situations, food intake is the most impor-
tant route of exposure for chemical environmental contaminants.
There are many health effects, other than foodborne diseases, that result from
an inadequate diet, including starvation under disaster conditions, excess num-
bers of premature and underweight births, and nutrition so marginal as to weaken
immune systems and deny millions of children proper growth and development.
Food contaminated by toxins from plants and molds or those present in fish and
shellfish can also be a serious problem, as is food contaminated directly by agri-
180
Agricultural -
6' 160 production
140
— Population
120
0)
'T 100
CD per capita
80
60
a)
C)
40
20
0 -
1970 1975 1980 1985 1990 1995
Year
Figure 1.3 Trends in world food production and food production per capita. From WHO,
1997, with permission.
INTRODUCTION 17
house gases, and eventual global warming (McMichael et al., 1996) may also
threaten a stable global environment that protects health.
The United Nations Environmental Programme (UNEP) launched the Global
Environmental Project in 1995, a participatory process involving experts from
over 100 countries. Its recent publication, GEO-2000 (UNEP, 2000) noted that
global emissions of CO 2 continue to rise, with an annual increase over the past
decade of 1.3%, with the level in 1996 being almost four the 1950 total. GEO-
2000 urges that alternative policies be swiftly implemented to avoid major envi-
ronmental disasters.
INTRODUCTION 19
situations where the illness of interest is chronic in nature, is indistinguishable
from normally endemic illnesses, or involves long latency periods. In such settings,
disease rates may need to he studied in relatively large population units (countries,
provinces) over extended periods of time. After defining the cases and the popu-
lation at risk, the number of cases and persons at risk can be used to calculate rates
of disease occurrence (either as incidence rates or prevalence rates). The observed
incidence (or prevalence) of the disease must be compared with disease occurrence
in some reference (or control) population, with appropriate adjustments so that
rates are compared using equivalent populations distributed by age, gender, and
other similar aspects and according to similar case definitions. In this manner, in-
vestigators can determine whether there is indeed an increase in the health effects
of concern and can gather information to isolate what might have caused it.
Environmental Health Monitoring
To quantify health effects by monitoring the health of populations, appropriate
health indicators must be selected, monitoring methods must be developed, and
data quality needs to be evaluated. Through standardization of health indicators and
harmonization of sampling and measurement techniques, it is possible to compare
data between jurisdictions. Health-monitoring strategies involve the application of
different methods to get results in the most cost-effective way (see Table 11).
Monitoring strategies are dependent on available health care infrastructure.
Use of records from hospital and medical services is more feasible in countries
with national medical care services and centralized administrations than in coun-
tries where most services are provided by independent health care agencies and
TABLE 1.1
CHARACTERISTICS OF SELECTED APPROACHES TO HEALTH MONITORING
Sample Population Data Providers Potential for Quantification
of Environmental Impact
National Entire population Health care personnel Large, provided that health
registers of country Hospital records data are ]inked with good
Laboratory records exposure data; confounding
needs to be avoided
Local Entire population Health care personnel Large, provided that health
registries of smaller Hospital records data are linked with good
administrative Laboratory records exposure data; conclusions
entities can be generalized only if
the population studied is
representative
Sentinel Population Selected praciitioners, Only if relevant exposure data
networks covered by laboratories, hospitals are concurrently collected
data providers and the population studied
is representative
Periodic ideally randomly Specifically trained survey Only if relevant exposure data
health drawn from team are concurrently collected or
surveys population are available from other
sources
WORKERS
INTRODUCTION 21
low–birth rate situation in which few cases of communicable diseases have occurred.
This shift, which started in the last century and has continued to the present time,
has been called the demographic transition (see Fig. 1.4), as it relates mainly to the
crude birth rate and death rate. When both rates were high, the populations stayed
stable. In those countries where they are now both low, the populations have again
stayed stable, as in the Scandinavian countries. During the transition from high to
low rates there is a period when death rates lower while the birth rate stays high;
during this period the population will grow. The more the death rates decrease
while birth rates remain stable, the more rapid is the growth of the population, a
phenomenon that can be found in most developing countries. Many developed
countries have more or less completed their demographic transition. The death rate
in such countries now principally reflects diseases associated with aging.
The high pretransition death rates are very much linked to a high level of
communicable disease, so the transition in death and birth rates is accompanied
by a change in the pattern of the causes of death—less communicable disease
and more chronic noncommunicable disease. This change in disease pattern over
time has been called the epidemiological transition. Figure 1.5 shows how the mor-
tality patterns changed in the United States in the twentieth century.
This pattern of change has been shown in all countries to follow economic
development, as improvements in housing, sanitation, and community infra-
structure reduce the risk of communicable disease. It is not just the improving
economy itself that protects citizens' health but the improvements to water sup-
ply, shelter, and nutrition, which are part of the development of community ser-
vices. As these improvements take place, chronic noncommunicable diseases be-
come a more important factor, largely because of the longer life expectancy and
increasing proportion of old people in communities.
C
0
Cu
75a- Stage 1 Stage 2 Stage 3
0
a.
0
0
0
lit 40
a- ——
a) Population
- (absolute
.0 30 numbers)
a)
'O - Birth rate
'O
(a
20
el
10
a)
'O
sj
14
50 - 100
Time (years)
Figure 1.4 The demographic transition. From Kjellstriirn and Rosenstock, 1990, with per-
mission.
MM
0
E 60
(U
0
0
U)
C)
CU 40
U)
0
U)
0
0
1900 1910 1920 1930 1940 1950 1960 1970
Year
Figure 1.5 The epidemiological transition as it has occurred in the United States. From
Beaglehole et al., 1993, with permission.
Mortality Trends
In many developing countries crude death rates are declining while in developed
regions they remain steady. The data on life expectancy, which are a better mea-
sure of trends, as it takes into consideration differences in age structure, show
that improvements in levels of health have been made throughout the world, al-
though life expectancies are still much lower in developing countries than in de-
veloped regions.
Age-standardized mortality figures are generally riot available for developing
countries. Table 1.3 provides estimates of the proportion of deaths from various
causes as a percentage of the total number of deaths. Although this gives a pro-
file of what people in each country are dying of, it does not indicate which groups
are dying at what age or at what rate. The differences between the two patterns
shown in Table 1.3 reflect in part a different age composition in the two groups
of ciuntries. But this difference does not go far to explain the 10-fold disparity
in mortality from infectious diseases in general or the 20-fold difference in
mortality from tuberculosis. Such statistics are dramatic evidence of the pretran-
sinorl state of the developing world.
As an unambiguous event, death is a good indicator for statistical compar-
isons of health situations in countries. Mortality rates, nonetheless have their
limitations. They tell us little about suffering and loss of productivity related to
morbidity; direct information on the incidence and prevalence of diseases would
INTRODUCTION 23
TABLE_1.3
CAUSES OF DEATH IN DEVELOPED AND DEVELOPING COUNTRIES, 1993
Deaths from all Causes (%)
Cause of Death Developed Countries Developing Countries
Infectious and parasitic diseases 1.2 41.5
Chronic lower respiratory diseases 7.8 5.0
Malignant neoplasms 21.6 8.9
Diseases of the circulatory system 46.7 10.7
Maternal causes 0 1.3
Perinatal and neonatal conditions 0.7 7.9
External causes of mortality 7.5 7.9
Other and unknown causes 14.5 16.8
Source: WI-tO, t995a
be a better indicator. But this information is only available from surveys of lim-
ited temporal and geographic scope. Systems for registering cases of important
communicable diseases, such as AIDS, yellow fever, leprosy, and cholera, exist
in most countries. Annual data on cancer incidence are reported to the Interna-
tional Agency for Research on Cancer (IARC) from participating countries'
registries.
At an individual level, the risk (%) of dying between the ages of 15 and 60
years from noncommunicable disease does not increase during the epidemiologic
transition, it decreases (see Fig. 1.6). These transitions are also accompanied by
a change in the types of environmental hazards to which people are exposed. In
the pretransition stage, the dominant hazards are what we know to be the tra-
ditional hazards of poverty: unsafe drinking water, lack of sanitation, poor shel-
ter, indoor air pollution from stoves and fireplaces, and injury hazards from poorly
constructed buildings. As economic development and the epidemiologic transi-
(I)
- - —
15 Non-communicable
C) diseases
o 10 Communicable
diseases
Injuries
Oh-
1955 1960 1965 1970 1975 1980 1985
Year
Figure 1.6 The epidemiological transition as it has occurred in Chile. From Murray et al.,
1992, with permission.
Burden of Disease
Many conditions that do not lead to people's deaths are still responsible for a high
prevalence of illness or disability. Burden of disease measures the impact of ill health
on communities (World Bank, 1993; Murray and Lopez, 1996; the term public
health impact was used previously). Included in this concept is the impact of both
morbidity and mortality on normal life and work capacity. Often the unit of cal-
culation is in terms of life years lost, which statistically converts the duration and
timing of illness and disability into a comparable scale, equivalent to the years that
might have been lost from a fatal disease. Insurance companies apply the same ap-
proach when calculating compensation for permanent injury, e.g., 25% of death
compensation for the loss of a limb, 50% compensation for blindness, etc.
Attempts have been made to express the burden of disease in a single num-
ber, namely the overall life-years-lost equivalent. This number has been given
different names, such as quality-adjusted life years (QALYs) or disa bility- adjusted life
years (DALYs). Each is based on a number of very uncertain assumptions and
judgments about how a disease or disability period should be translated into
number of disease free or disability free years lost prior to death. Thus, the final
numbers need to be interpreted with caution. Although it is convenient to have
a single number for burden of discasc, ii may be misleading, particularly when
comparing disease patterns over time or between geographic regions, for which
the impact of disease on well-being and productivity is not constant. For exam-
ple, improved rehabilitation, technologies for mobility, and access policies have
made physical disabilities much less of a handicap in some countries than they
used to he. To assume that a particular type of disability is equivalent to a par-
ticular number of life-years-lost in every country at any time may seriously bias
the interpretation of what these calculations mean.
The burden of disease can also be described as a series (or matrix) of num-
bers of mortality, morbidity, and disability. Although this description is more
complex than using just one number, it offers the opportunity to highlight spe-
cific aspects of the burden, such as the impact on the use of health services. A
"burden of disease matrix" would also make it possible to better identify the con-
tributions to this burden of disease from specific environmental hazards, with-
out the need to translate ill health into death. For instance, it has been estimated
in Sweden that about 400,000 people are disturbed in their homes by traffic noise
INTRODUCTION 25
BOX 1.4
The Disability-Adjusted Life Year Concept
To show how the calculations have been made for one specific example of burden
of disease measurement, the DALY concept will he described here. The WHO and
the World Bank undertook a joint exercise to attempt to quantify the extent of
"healthy life" lost due to various diseases and conditions. Diseases were classified
into 109 categories on the basis of the international classification of diseases (ninth
revision). Using the recorded cause of death where available and expert judgment
when records were not available, the study assigned all deaths in 1990 to these cat -
egories by age, gender, and demographic region. For each death, the number of
years of life lost was defined as a difference between the actual age at death and
the expectation of life at that age in a low-mortality population. The disability, and
the incidence of cases by age, gender, and geographic region were estimated on the
basis of community surveys or expert opinion. The number of years of healthy life
lost was then obtained by multiplying the expected duration of the condition by a
severity weight that measured the severity of the disability in comparison with loss
of life. Diseases were grouped into six classes of severity or disability. The death and
disability losses were then combined. As shown in Figure 1.7, the value of each year
of life lost, shown on the left, rises steeply from 0 at birth to a peak at age 25 and
then declines gradually with increasing age. The age weights reflected a consensus
judgment, but other patterns could he used. Through using the combination of dis-
counting (reducing by 3% SC) that future use of healthy life is valued at progres-
sively lower levels) and age weights (e.g., using uniform age weight, with each year
of life having the same value, therefore increasing the relative importance of child-
hood diseases), a pattern of DALYS lost by death at each age could be seen. As shown
on the right, the death of a newborn girl represents a loss of 32.5 DALYs; a female
death at age 30 means the loss of 29 DALYs; and a female death at age 60 repre-
sents 12 lost DALYs.
Source: World Bank, 1993.
and about 100 people die from lung cancer due to residential radon exposure in
their homes. Is it possible to make a comparison of the health impact of noise
disturbance and death with a common measurement unit? Would that be needed
to guide decisions about financial input into prevention of different health risks?
The methods for the measurement of the burden of disease (discussed further in
Box 1.4) will need further development to produce useful information for deci-
sion making and priority setting for environmental hazards control. Two of the
key issues are whether deaths in the future should be discounted using an eco-
nomic analysis approach, and whether deaths at different ages should be given
different values (Fig. 1.7). Considerable work is now being done to atfempt to
quantify the value of reducing health risks (Tengs et at. 1999) using economic
methods such as contingent valuation, and comparing the results using various
techniques (Spiegel, 2000). This type of analysis may be very useful for decision-
makers.
The sum of disease across all ages, conditions, and regions is referred to as
the global burden of disease (GBD). Table 1.4 shows the GBD by cause and regional
burden of disease in four of the eight World Bank regions.
Vulnerable Groups
By far the greatest risk factor for poor health is poverty. Particularly vulnerable
groups include children, women, elderly people, racial minorities, disabled peo-
plc, and indigenous peoples, all of whom are often vulnerable because they are
not empowered to change their Physical environments. Smaller body size, pre-
existing diseases, pregnancy, and nutritional deficiencies are several factors that
may also increase their vulnerability. Often we do not know how specific haz-
ards affect subgroups of the population. The effects of the hazard on groups in
populations that are in a minority or underrepresented in detailed studies may
not be identified. There may also be subgroups that are more vulnerable because
of where they live or work, because of personal illness (e.g., asthma), or because
of biological factors of susceptibility as described below. (As noted in Chapter 3,
levels of safe exposure to a contaminant for the general population are often ad-
justed to account for these vulnerable groups.)
INTRODUCTION 27
TABLE 1.4
GLOBAL DISTRIBUTION OF DALY-LOSS BY DISEASE, 1990A
Latin Formerly
America Socialist Established
Sub-Saha ran and the Economies Market
Cause World Africa Caribbean of Europe Economies
Population 5267 510 444 346 796
iiiillious)
respiratory rate, for example, is proportionately greater and they breathe in much
more air pollution in relation to their body weight than an adult in similar cir-
cumstances. Children also have a grealer chance of experiencing chronic effects
of exposure to environmental hazards than adults, because when they are ex-
posed to a carcinogen, the chances are mitch higher that they will live beyond
the latency period (the years that it takes for a cancer to develop after exposure).
The physical environment of children is dillerent from those of adults, even
in the same home. Newborns remain in cribs and are not able to remove them-
Women The rapid increase in problems arising from the destruction of natural
resources, rapid industrialization and urbanization, pollution and population pres-
sures has a special impact on women (Sims, 1994). Women have less privileged
status in society and less access to resources, although they are often obliged to
fulfil multiple roles and function as producers, reproducers, and home managers.
Of the 1.3 billion people living in poverty, 70% are women (UNDP, 1995).
INTRODUCTION 29
Women may be at a disadvantage from birth onward because of inadequate
nutrition, lack of education, heavy workloads, early marriage, and early and fre-
quent pregnancies. In some countries, women who have no partners are at par-
ticularly high risk of poor health and are forced into poverty or prostitution be-
cause of insufficient opportunities to earn a living by themselves. Prostitution has
grown to immense proportions in some developing countries (this applies to girls
and boys as well as women). In addition, women suffer discrimination at the
workplace and are often subjected to the worst working conditions. In rural ar-
eas, women have particularly heavy workloads, as they are responsible for gath-
ering fuel, collecting water, and foraging.
Women's vulnerability during pregnancy and childbirth is evident from the
very high levels of maternal mortality in most developing countries. In many low-
income communities, there is a significantly higher incidence of certain diseases
among women, because they spend more time in its contaminated environments.
Women suffer more from diseases associated with inadequate water and sanita-
tiori and from respiratory problems associated with smoke in living environments
where cooking or heating is on open fires or poorly designed stoves using coal
or wood. An anthology entitled Women, Health and the Environment (Sims, 1994),
published by the WHO, provides further examples and details in this area. The
role of women in sustainable development has received increasing attention. In
many societies, women have greater influence than men on rates of population
growth, infant mortality, and various aspects of health and environmental degra-
dation. Thus any socioeconomic pressures that are detrimental to women are
detrimental to society as a whole and the global ecosystem.
im
a)
-
> • :
: . •. -
a)
Ca
0
Ca
E0
4
a)
0
••
U)
. ••. •
IQ 2
. . . .
0 I I I I I
0 10 20 30 40 50 60 70 80 90 100
Percent of adult females who are literate
Figure 1.8 Fertility rate by female literacy, 1990. From WRI, 1994, with permission.
350
'so I U
. 1
250 I
-U
() U
U
2 200 U •
U I U
U •u
ci) . S
C. • .
U
.0
150 . •1
.
'a
• •. U
U
we U •
I
•
•
I
I U
U
. U
• I U
•. U
U
50 U
I.
•
U
•
U.S •••
• a
løI I I
0 10 20 30 40 50 60 70 80 90 100
Percent of adult females who are literate
Figure 1.9 Mortality rate for children under 5 by female literacy, 1990-91. From WRI,
1994, with permission.
INTRODUCTION 31
be combined with basic health services, expanded economic opportumties, and
enforced civil rights. Many multilateral organizations, including many United Na-
tions agencies, have been working together to recommend national and inter-
national actions toward these ends. One publication by the United Nations Pop-
ulation Fund, published as part of Investing in Women: The Focus of the '90's (Nafis,
1990), urges governments and international nongovernmental organisations to
do the following:
Elderly People The world is aging. This simple fact has immense implications for
the provision of shelter, health care, and social support. Elderly persons are at
an increased risk of having diseases. They are more likely to be malnourished
than younger adults, for a variety of social, economic, and physiological reasons
(including early dementia), and are therefore more vulnerable to many diseases.
Especially important are diseases that decrease the body's ability to cope with
hazardous exposures. Examples of such disabling conditions that are common in
the elderly include emphysema, kidney disease, congestive heart failure, de-
mentia, and diabetes. As with children, elderly persons with respiratory diseases
are not able to tolerate air pollution. The elderly are more likely to have had a
long exposure to a given toxin simply because they have been living longer. An
older body also has less mass, and often metabolizes toxins at a slower rate. As
in children, therefore, smaller doses of a given substance will have a greater ef-
fect on the elderly than on younger adults.
Recent rapid changes in lifestyles in many societies has led to changes in cul-
tures that once had more respect for elders. As a result, the elderly are often im-
poverished without the social support of extended families, and are subject to
some of the same patterns of vulnerabilities as children.
Disabled People It is estimated that there are 500 million disabled people in the
world today, and this number is expected to double in the early part of the
twenty-first century. Four out of five disabled people live in developing coun-
tries, and one third of them are children. Few countries are able to provide mean-
ingful assistance, support, rehabilitation, and protection, thus many disabled peo-
ple are particularly impoverished and subject to exploitation and chronic illness.
Chronic psychiatric conditions, including addictions to alcohol or drugs, may also
lead to malnutrition, self-mutilation, and depression. These conditions may de-
crease the body's ability to cope with environmental hazards.
Disabled people often have difficulty finding meaningful jibs that pay them
an adequate living. They are often forced to take unwanted and dangerous jobs
or face unemployment and poverty. The disabled, therefore, are sometimes at
increased risk from environmental hazards because of their cultural milieu, in
addition to their vulnerability as a result of their disability.
180
1I.
.(/1 140
120
0
(I)
80
a)
C
60
40
Olt
Countries
Figure 1.10 Infant mortality rates in different countries and aniong aboriginal populations
in Canada. A, most sub-Saharan African countries, Afghanistan, Bangladesh, Haiti; B,
some North African countries, India, Central America, Brazil; C, Venezuela, Argentina,
China, some Asian and Middle Eastern countries; D, Korea, Malaysia, Chile, Panama,
Uruguay, Romania, former USSR; E, Costa Rica, Cuba, Jamaica, Greece, Portugal, East-
ern Europe; F, Western Europe, North America, Australiasia, tsrael, Japan, Hong Kong.
From Waldram et al., 1995, with permission.
INTRODUCTION 33
250
200
\ NWT Inuit
\
.0 \
cc
150 \
cc
cc \
100
\
Registered \
Indians N
49
ce
Figure 1.11 Infant mortality
rate among Canadian registered
Canadians Indians, Northwest Territories
Inuit, and all Canadians. From
1956-601961-65 1966-70 1971-5 1976-80 1981-5 1986-90
Waidram et al., 1995, with per-
Year 1IIiSSiO11.
respiratory tract are more common among aboriginal communities. Various hous-
ing surveys have documented the high proportion of aboriginal dwellings char -
acterized by overcrowding, inadequate heating, and poor ventilation (Clatwor-
thy and Stevens, 1987). These factors contribute to the high risk of respiratory
infections.
Of particular concern is the increase in chronic diseases and the high preva-
lence of obesity in many aboriginal groups. Among the most serious health prob-
lems now affecting aboriginal peoples are injuries sustained as a result of acci-
dents and violence. The high level of morbidity and mortality from such injuries
has been attributed to the prevailing economic conditions and social stress that
aboriginal peoples experience. For example, in Canadian aboriginal communities
a high number of residential tires have occurred, which have been linked to per-
sonal behaviors such as smoking, drinking, leaving children unattended, and hav-
ing suicidal intent. Contributing social environmental factors that are largely at-
tributable to poverty include disconnection of electricity because the utility bill
hasn't been paid, alcoholism, lack of fire protection in the community, mrnad-
herence to building codes, lack of child care, and mental health problems. More-
over, acts of violence are intimately related to the mental health of individuals
and the social health of a community. Suicide, which is particularly high among
young adult males, is indicative of the alienation and despair occurring in these
corn mun i ties.
Many aboriginal people recognize that these problems must be resolved
through a healing process undertaken by the communities themselves. The
reestablishment of individual and community self-esteem has been actively pur-
sued through the enhancement of positive traditional values and customs. A land-
mark conference entitled "Healing Our Spirit Worldwide" in Edmonton, Canada
in 1992 brought together aboriginal groups from around the world who shared
their experience in healing the wounds of violence and substance abuse. Such
INTRODUCTION 35
TABLE 1.5
ESTIMATED GLOBAL BURDEN OF DISEASE FROM SELECTED ENVIRONMENTAL
THREATS, 1990, AND POTENTIAL WORLDWIDE REDUCTIONS THROUGH
INTERVENTION IN THE WORKPLACE AND AMBIENT ENVIRONMENT
Reduction Burden Averted
Achievable by Feasible Burden
Type of Burden from Through Interventions Averted
Environment These Diseases Feasible (millions of per 1000
and Principal (millions of Interven tions b DALYs/year) Population
Related Diseases° DALYs/year) (%) year) (DALYs/year
OCCUPATIONAL 318 - 36 7.1
Cancers 79 5 4 0.8
Neuropsychiatric 93 5 5 0.9
Chronic respiratory 47 5 2 0.5
Musculoskeletal 18 50 9 1.8
Unintentional injury 81' 20 16 3.1
Acute respiratory
infections 123 5 6 1.2
Chronic respiratory
diseases 47 5 2 0.5
ROAD TRANSPORT
INTRODUCTION 37
TABLE 1.7
PROPORTION OF GLOBAL DALYS ASSOCIATED WITH ENVIRONMENTAL
EXPOSURES, 1990
% of all DALI's
Global Environmental
DALYs Environmental DALYs All Age Age 0-14
(thousands) fraction (%) (thousands) Groups Years
Acute respiratory 116,696 60 70,017 5.0 4.50
infections
Diarrheal diseases 99,633 90 89,670 6.5 6.10
Vaccine-preventable 71,173 10 7117 0.5 0.49
infections
Tuberculosis 38,426 10 3843 0.3 0.04
Malaria 31,706 90 28,535 2.1 1.80
Unintentional injuries 152,188 30 45,656 3.3 1.60
Intentional injuries 56.459 NE NE
Mental health 144,950 10 14.495 1.1 0.08
Cardiovascular 133.236 10 13,324 1.0 0.12
diseases
Cancer 70,513 25 17,628 1.3 0.11
Chronic respiratory 60.370 50 30,185 2.2 0.57
diseases
Total these diseases 975,350 33 320,470 23.0 15.40
Other diseases 403,888 NE NE
Total all diseases 1,379,238 23) (320,470)
NE, to It est mat ed
Source; WHO, 1997; DALY data front Miirrar and Lopez. 1996
INTRODUCTION 39
The Total Exposure Concept
It is not cnough to assess the exposure to a hazard from just one source. The sum
of all exposures needs to he measured to assess health impacts and establish dose-
response relationships. Pesticide exposure is a classic example where occupational
exposure may he supplemented by substantive environmental exposure. This may
come through food and water source contamination and through nonoccupational
airborne exposure. In Central America, for example, some cotton growers using pes-
ticides not only have little access to protective clothing but live very close to the cot-
ton fields; many live in temporary housing with no walls for protection from aerial
pesticide spraying. Workers also wash in irrigation channels containing pesticide
residues, resulting in increased exposure (Michaels et al., 1985). Thus to understand
the relationship between their pesticide exposure and the health effects that may
be reported, all sources of exposure to pesticide should be taken into consideration.
Other examples of exposure that may occur at the workplace as well as in the am-
bient environment are exposure to particulate matter from engine emissions (from
industrial machines or traffic), benzene (as a solvent or from cigarette smoke), and
polycyclic aromatic hydrocarbons (from products containing tar or from diet).
TABLE 1.8
COMPARISON BETWEEN WHO HEALTH-BASED GUIDELINES FOR AIR
IN THE WORKPLACE AND IN THE GENERAL ENVIRONMENT (WHO AIR
QUALITY GUIDELINES)
Chemical Workplace Guideline General Environment Guideline
,ug/m 3 (8-hr mean) ,ag/m 3 (annual mean)
Lead 30-60 0.5-1.0
Cadmium 10 0.01-0.02
Manganese 300 1
Mercury 50 1
Formaldehyde 500 100 (24 hours)
Nitrogen dioxide 900 150 (24 hours)
Sulfur dioxide 1300 50
Source: WHO, 1 987a and several Technical Report Series issues
Demographic Issues
The impact of people on the environment is related to the size of the population
and to the level of consumption. Both expand independently and both lead to
increasing pressure on the environment as both a supplier of resources and a
repository of waste. Limited resources have made development in the poorest
countries of the world difficult, with increasing demand for water, food, and en-
ergy for domestic use being in direct proportion to the number of users. Mean-
while, more people are moving to urban areas where the infrastructures are rarely
able to keep up with the influx of new citizens. In temperate and sub-Arctic
countries, energy needs may be greater than in other parts of the world because
of the climate. Countries in these areas are generally highly developed, and the
high level of consumption accompanying their affluence (which until recently,
in many countries, was not accompanied by much genuine concern for the
environment or the need br conservation of resources) has magnified global
problems
Different areas of the world have different rates of population growth. The
global annual increase is thought to have stabilized, with an increase of about
81 million people added each year for 1990-95 (WRI, 2000). Nevertheless, the
world population, which was 5.3 billion in 1990, and more 5.9 billion in 1999
is expected to be between 7.7 and 11.2 billion by the year 2050 (WRI, 2000).
Because of the dillerences in rates of increase, the proportion of the world's pop-
ulation in North America and Europe has been shrinking while in other parts of
the world it has been expanding or has remained stable (see Fig. 1.12). These
projections are based on expected trends in birth and death rates, and adjust-
ments to the projections will he necessary as new information becomes available.
Improvements in the provision of health care may alter the pattern of mortality,
and the AIDS pandemic will have a major influence on population growth, es-
pecially in Africa, where children and young adults are most affected. Changes
INTRODUCTION 41
10
7 -
TABLE 1.9
WORLD BANK ESTIMATES OF THE SCALE OF POVERTY 4 IN DEVELOPING
COUNTRIES, 1985
Net
Under-S Primaiy
Head- Mortalityd School
Number of count Poverty (per Life Enrollment
Poor Index b Gapc thousand Expectancy Rate
(millions) (%) (%) born) (years) (%)
Sub-Saharan 180 47 Il 196 50 56
Africa
East Asia 280 20 1 96 67 96
China 210 20 3 58 69 93
South Asia 520 51 10 172 56 74
India 420 55 12 199 57 81
Eastern Europe 6 8 5 23 71 90
East em 60 31 2 148 61 75
Mediterranean
and North Africa
Latin America 70 19 1 75 66 92
and the
Can hbcan
All developing 1116 33 3 121 62 83
countries
The poverty tine in international dolls rs (using Pu rctasing power parities) is $370 per capita a year for the
poor.
The headcount index is defined as the percentage of the poputation below the poverty line
The poverty gap is defined as the aggregate rncnme shortfall of the poor as a percentage of aggregate con-
sUrnption
Undcr —5 mortality rates are for I 980--85, e\ccpt for Chmna and South Asia, where the period is 1975-80.
Source: World Bank, 1990.
INTRODUCTION 43
within countries are such that some people with income well above the poverty
line may have inadequate living standards while someone living below the
poverty line may have adequate standards.
A better way of calculating the number of people living in poverty is to eval-
uate the number that lack a minimum standard of living including adequate food,
safe and sufficient supplies of water, secure shelter, access to education and health
care, and, in high-density settlements, provision for the removal of domestic
wastes. With these criteria it has been estimated that 2200 million people live in
poverty in the developing world. According to the United Nations Development
Program (UNDP) 1300 million live in absolute poverty. 840 million are under-
nourished (UNDP. 1997); 1400 million lack safe drinking water (UNICEF, 1997)
and 900 million are illiterate (UNESCO, 1996), as discussed by the World Re-
sources Institute (WRI, 2000).
In most cities in developing countries, between one-third and two-thirds of
all inhabitants live in informal settlements with inadequate or no infrastructure
or services. Even in the richest countries, a proportion of the population suffers
the adverse health effects of physical deprivation and social exclusion. Particular
cities or districts within cities that suffer most have not only high levels of
unemployment, particularly among young people, but also high levels of poor-
quality housing and social problems. They also tend to have significantly higher
than average infant mortality rates and a lower life expectancy.
At the beginning of the chapter the overall increase in life expectancy was
noted. But the gap in life expectancy between the least developed (43 years) and
most developed (78 years) countries is widening; by the year 2000 the gap is
projected to be 37 years. Also, even if improvements are made globally, chang-
ing conditions could result in dramatic setbacks in specific countries. The most
striking example is the reduction in life expectancy in Russia following 1990
(WRI, 1996).
Consumption Patterns
One important obstacle to progress in resolving environmental health prchlems
is the major difference in consumption patterns between different countries and
between different groups within countries. The very high consumption of energy
and natural resources by the richest countries and the richest groups within coun-
tries cannot be sustained. If the people of China achieved the same density of au-
tomobiles per capita as that in the United States, for example, the production of
greenhouse gases, air pollution, and other traffic-related problems would create a
major health crisis. Greenhouse gases also vastly increase the global problem of
climate change (see Chapter 11, Climate Change and the Greenhouse Effect).
Rees and Wackernagel (1992) characterized the land area necessary to sus-
lain current levels of resource consumption and waste discharge by a population
as its ecolog wal footprint. The ecological footprints of high income cities are hun-
dreds of times larger than their politic or geographical area and are much larger
than the ecological footprints of lower income communities.
Development is often seen as the poor reaching toward the lifestyle and eco-
nomic level of the rich. Clearly, large gaps in health and well-being between pop-
Macroeconomic Policies
Macroeconomic policies have important direct and indirect effects on health and
the environment. They influence the use and degradation of natural resources
because they can affect consumer demand and the prices of natural resources.
The effect of macroeconomic policies are felt most directly at the level of an in-
dividual's purchasing power. For example, they permit improvements in the qual-
ity and quantity of food and thus in nutritional status and susceptibility to dis-
ease. in an economic crisis, they may result in sharply diminished purchasing
power and a lack of adequate nutrition.
Global economic changes, adverse changes in the terms of trade for Some
countries, and an increased debt burden driven by the rise of real interest rates
have all contributed to periodic decline in the word economy. The International
Monetary Fund (IMF) has required many countries to implement "structural ad-
justment programs" (usually cuts in public expenditures, including health and
related services) before it provides loans to developing countries. Public works
such as piped water supplies, sewers, and drains, which require a large capital
investment, often receive the largest cuts. For example, in sub-Saharan Africa
the social services budget fell by 26% between 1980 and 1985 and in Latin Amer-
ica by 18%. Health spending per person has declined in most countries Since
1980. Most experts recognize that there may be adverse effects on nutrition and
health. However, there is much uncertainty about the actual impact, and it is
generally acknowledged that structural adjustment may adversely affect the en-
vironment and health.
Despite this pessimistic picture, there have been shorter periods of real growth,
such as 1995-1998. The effect of macroeconomic policies cannot he considered
in isolation. Trends in the global economy may also dictate personal income and
what is possible for a country to attempt to do with macroeconomic policies. It
should he kept in mind, however, that countries with better health status have
more equitable social policies (Kawachi ci a]., 1999). It is not wealth per se but
the distribution of prosperity in the society that seems to he the link between
health and the social environment (Hertzman et a]., 1994).
INTRODUCTION 45
ROLE OF THE ENVIRO1"MFNTAT. HEAlTH PRflFFSS1CNAT
INTRODUCTION 47
related conditions or events in defined populations. Epidemiologists need not he
medically qualified, but they need to be able to creatively link their work with
that of other disciplines, including medicine, biology, and the social sciences. Epi-
demiologists must be able to optimize the use of observational data and routinely
collected information. In practice, the functions of the epidemiologist are broad
and may include health and injury surveillance, collaborative research with clin-
ical medical specialists and heldwork, and the study of health-related behaviors
in the home and at wcrk.
INTRODUCTION 49
diseases (see Chapter 10). The work also involves health education of workers and
management, the evaluation of occupational hazards, the recommendation of
safety precautions, and statistical analysis of epidemiological data.
Toxicologist Toxicologists are biological scientists who study the adverse effects
of chemical agents on living organisms. The specialist toxicologist acquires knowl-
edge over many years and is often required to interpret animal experimental data
and other laboratory-generated data for the purpose of predicting adverse hu-
man effects following exposure to toxin(s). Research toxicologists have skills in
animal husbandry and handling, and in in vivo and in vitro testing and experi-
mental design. Regulatory toxicologists advise government authorities on the reg-
ulation of public and occupational exposures. Often toxicologists are involved in
risk assessment in field settings as well.
1. What proportion of people horn in your country in the same year as you
have already died, and what was the major cause of death?
INTRODUCTION 51
2
NATURE OF ENVIRONMENTAL
HEALTH HAZARDS
LEARNING OBJECTIVES
CHAPTER CONTENTS
52
Physical Hazards Vulnerable Groups
Types of Physical Hazards Injury Settings
Noise and Vibration Occupational Injuries and
Ionizmg Radiation Ergonomics
Nonionizing Radiation Traffic-Related Injuries
Light and Lasers Home- and Recreation-Related
Pressure Inj uries
Extremes of Temperature Intentional Injury
Concepts in Injury Prevention
Mechanical Hazards
Understanding Mechanical Hazards Psychosocial Hazards
Impact of Injury on the Individual Psychosocial Hazards and Stressors
and Society Health Effects of Stress
One can study environmental health hazards in various ways. Examining the
nature of the hazard, which can be biological, chemical, physical, mechanical, or
psychosocial, is one approach. Biological hazards can be divided into viruses, bac-
teria, parasites, etc. Route of exposure is also a useful organizing principle, e.g., via
air, water, land. Each route can he further subdivided for purposes of separate
discussion—e.g., indoor versus outdoor air, or groundwater versus surface wa-
ter versus drinking water. Another approach is to focus on the setting where the
hazard occurs, for example, home, work, school, hospitals, or by community.
Table 2.2 provides one conceptual framework of biological, chemical, and phys-
ical hazards by routes of exposure and related factors.
Because environmental health is a huge field, it tends to be taught in frag-
ments. (The nature-of-the-hazard approach is classic in academic settings. Mi-
crobiologists tend to teach the characteristics of biological hazards; toxicologists
discuss the health effects of chemicals; health physicists teach the implications of
radiation on human health; crgononhists discuss biomechanical hazards; and psy-
chologists discuss psychosocial issues. It is, in fact, essential to have some un-
derstanding of the basic microbiological, toxicological, health physics, ergonomic,
and psychosocial sciences in the practice of environmental health. To develop
the public health perspective it may also be useful to focus on routes of expo-
sure. Air pollution, for example, tends to be assessed and managed by a differ-
ent group of public health professionals than water pollution or hazardous waste.
This latter approach lends itself best to advocacy in the community at large. The
middle chapters of this book present the hazards according to their routes of ex-
posure (air, water, food).
The different hazards can also be described in the context of agriculture, set-
tlements, and industry. This approach allows environmental issues to be dealt
with as problems in community and economic development. The later chapters
in the book analyze the health impacts and prevention methods of environmental
issues in relation to settings and development issues (urbanization, energy use,
industrialization, global concerns). This chapter introduces environmental health
concerns according to the nature of the hazards, and outlines the basic issues in
these areas. (The basic physiology needed to understand the effects of environ-
mental hazards on human health can be found in standard physiology texts.)
AIR
WATER
LAND
BIOLOGICAl. HAZARDS
TABLE 2.3
ESTIMATED GLOBAL NUMBER OF DEATHS FROM INFECTIOUS AND
PARASITIC_DISEASES, 1993
Disease/Condition Number of Deaths (thousands)
Acute lower respiratory infections under age 5 years 4110
Diarrhea under age 5, including dysentery 3010
Tuberculosis 2709
Malaria 2000
Measles 1160
Hepatitis B 933
AIDS 700
Whooping cough 360
Bacterial meningitis 210
Schistosomiasis 200
Leishmaniasis 197
Congenital syphilis 190
Tetanus 149
Hookworm diseases 90
Amoehiasis 70
Ascariasis (roundworm) 60
Atrican trypanosomiasis (sleeping sickness) 55
American trypanosomiasis (Chagas disease) 45
Onchocerciasis (river blindness) 35
Meningitis 35
Rabies 35
Yellow fever 30
Dengue/dengue hemorrhagic fever 23
Japanese encephalitis 11
Foodhorne trernatodes 10
Cholera 6.8
Poliomyelitis 5.5
Diphtheria 3.9
Leprosy 2.4
Plague 0.5
TOTAL 16,445
Source: WHO, 1995a.
Investigation Methods
Microbiologists have developed laboratory methods to identify and quantify the
occurrence of most viruses, bacteria, and parasites in any medium. These tools
are constantly being refined on the basis of new knowledge about the mi-
CHEMICAL HAZARDS
Inorganic Substances Halogens are elements that form a salt by direct union with
a metal. They include fluorine, chlorine, bromine, and iodine. At standard tem-
perature and pressure, fluorine and chlorine are gases, bromine is a liquid, and
iodine is a solid. When placed in water, reactions occur, yielding acids that irri-
tate tissues. As individual elements and compounds, the halogens have their own
Estrogens form a class of steroid hormones synthesized both in males and females.
These hormcnes play an important role in human reproduction, including sexual dif-
ferentiation, development of female secondary sex characteristics, and development
and functioning of the testes. Hormones exert their action by binding to a specific re-
ceptor. When a hormone hinds to a cellular receptor to form a hormone-receptor
complex, a number of reactions take place that eventually result in a physiological ef-
fect. To develop and function normally, hormonal blood levels have to be regulated
very accurately. This regulation of hormone levels is determined by the rate of syn-
thesis and elimination by metabolism. This mechanism of regulation can be disturbed,
however, when humans or other organisms are exposed to environmental chemicals
that are also capable of binding to the estrogen receptor. In principle, there are two
possible reactions. (I) The binding of the environmental compound to the estrogen
receptor results in the same cellular response; this is called an estrogen-mimicking effect.
(2) Binding to the receptor does not result in the normal response. This may indicate
that the xenoestrogen, not normally present in the body, has (permanently) blocked
the receptor, making it unable to interact with endogenous estrogens.
Humans may be exposed to xenoestrogens in many different ways. The human
diet may contain large amounts of phytoestrogens such as lignans and isoflavones.
Estrogen-blocking effects have been demonstrated in women who ate a iscflavones-
enriched diet. However, most phytoestrogens are metabolized and excreted in urine
in the same way as endogenous estrogens and therefore do not accumulate in the
body. The opposite holds true, however, for some other xenoestrogens, including poly-
chlorinated biphenyl (PCB5), dioxins, and furans. Exposure to some PCB congeners
has been correlated with reduced sperm motility and density. Furthermore, after in
utero exposure, increased fetal loss, reduced birth weight, and behavioral and devel-
opmental effects were reported after severe poisoning accidents in Japan and Taiwan,
Occupational exposures to estrogenic compounds (like Kepone) have also resulted in
decreased sperm count and motility, and abnormal sperm morphology.
Other xenoestrogens to which humans can be exposed are alkylphenols,
phthalate esters, and bisphenol-A. Considerable concern about these compounds has
HO
Estrogen (Estradiol) Testosterone
cl
ci_ O__O_ c
CI-C-C)
OH_O-C = C_O_OH
OH 2 OH2
ci OH 3 OH3
DDT Diethyistilbestrol
been raised because they are So pervasive in the environment. In particular, intake
of phthalates, which may amount to several hundreds of ig/kgIday, mainly by con-
sumption of food, may result in estrogenic elfects. The most obvious exposure to
xenoestrogens is, of course, the direct administration of synthetic hormones, such
as diethylstilbestrol (DES), the effects of which are well documented in the offspring
of women who took it. In some countries, the same hormones may be preseru in
incat and dairy products. The similarities in chemical structure between endogenous
estradiol and the xenoestrogens DES and dichlorodiphenyl-trichloroethane (DDT),
are shown in Figure 2.1
Whether xenoestrogens in the environment are having an effect on people in
general is unknown and certainly unproven. The data on falling sperm counts among
men are not consistent from one place to the next and there is little evidence of a
rise in breast cancer rates among women when age and birth history is taken into
account. The risks associated with environmental xenoestrogens are better docu-
mented for animals than for people. For example, it is not clear that exposure to
xenoestrogens, which tend to he weakly estrogenic in environmental exposure, can
match the direct exposure to estrogen that women have today from living longer
and healthier.
drocarhon chain bends around so that the last carbon molecule is attached to the
first to form a circle. In general, the longer the carbon chain (whether saturated,
unsaturated, or cyclic), the more lipid (fat) soluble. Unsaturated hydrocarbons
are more reactive and usually more toxic than saturated ones. The aromatic hy-
drocarbons are also circular molecules containing one or more benzene rings. A
benzene ring is a circular six-carbon hydrocarbon with alternating single and dou-
ble bonds.
For various reasons, a berizene ring is a very stable structure (i.e., a lot of en-
ergy is needed to break a benzene ring). This category of chemicals is further
classified depending on the number of benzene rings and the type of linkage be-
tween them in the molecule. These groups are (1) benzene and its aliphatic and
alicyclic derivatives; (2) polyphenyls, i.e., two or more noncondensed rings; and
(3) polycyclic ring.c, or two or more condensed rings. Examples of aromatic com-
pounds include benzcnc, toluene, styrene, and naphthalene. Aromatic hydrocar-
bons act as primary irritants to the mucous membranes and cause central ner-
vous system depression. In addition, some have particularly toxic and carcinogenic
properties. For example, benzene has long been known for its toxicity to the
hematopoietic (i.e., blood) system and its ability to cause leukemia. In general,
the more benzene rings in the molecule, the less soluble and more persistent it
is in the environment (i.e., it doesn't break down easily). Because of these last
two features, these chemicals are more likely to be carcinogenic or ecotoxic, al-
though other characteristics of the molecule (such as its three-dimensional shape)
may also contribute to its toxicity.
Certain types of organic compounds have estrogen-like activity (see Box 2.1).
Such action by exogenous chemicals is believed to occur because of the spatial
(geometric) resemblance between the toxicant and the natural (endogenous) es-
trogen hormone. Links to breast cancer and male infertility have been hypoth-
esized for these estrogen-like substances (Davies et al., 1995; Sharpe and Skakke-
ylene). Some of these compounds, such as benzene and toluene, are also pres-
ent in combustion products of organic material, such as when tires are burned.
Paints used to include organic or inorganic hydrobarbon solvents, but increas-
ingly, water is being used as a solvent, which has significantly reduced the health
risks of painters.
Routes of Exposure
Chemicals can be released into the environment in many different ways. These
include the naturally occurring chemicals released during natural geological
processes and from mining and dredging, as well as wastes from many indus-
trial, agricultural, coirimcrcial, domestic, and manufacturing sources. Chemical
pollution may also occur by the unintentional release of chemicals during pro-
duction, storage, and transportation of products such as household products. Air,
soil, fresh waters, and oceans are all subject to chemical pollution. Contamina-
tion of food involves absorption of chemical residues in the food chain as well
as the use of chemicals in food processing. Natural toxins (aflaloxins, ochratox-
ins, pyrrolizidne alkaloids) also cause a variety of illnesses.
Exposure to chemical hazards may occur via all types of exposure: inhalation,
oral ingestion, absorption through the skin, absorption through the eyes, pla-
cental transfer from a pregnant woman to the fetus, inoculation and direct pen-
etration to target organs, and from mother to child lhrough breastfeeding. In the
nonoccupational environment, ingestion of substances containing chemicals is
Exposure
Media I Air, water,
dirt, etc. Air
Food, water,
I drugs
exfoliation
Transport and
Distribution f
I' 1 ( organs
Other i Blood T~ Liver
Kidney
Maj or
'S - _,
I
excretory ( Sweat ' Hair '
I
'I Urine ' i Feces'
I
pathways - - - - - - ' S -
external contamination
Figure 2.2 Routes of absorption, distribution, and excretion of potentially toxic substances.
Dotted lines indicate materials potentially useful for biological monitoring. Modified from
Clarkson et al., 1988, with permission.
Bioactivation of Benzene
Many carcinogenic chemicals require hioactivation for their action. For instance,
during metabolism of aflatoxins, vinyl chloride, benzo al pyrene, and benzene, highly
reactive intermediates, epoxidi's, are formed. These epoxides exist for only a very
short period of time because of their high instability and reactivity. Since the epox-
ides are electrophilic, they react with nucleophilic groups, including those in bio-
macromolecules like proteins and DNA. As a result of this reaction, cellular processes
can be disturbed and the generic code may be modified. As will be discussed later,
changes in the genetic code may eventually result in tumor formation and cancer.
The chemical formation of the epoxide from henzene is illustrated, in Figure 2.3.
After the formation of phenol, this end product of the phase I reaction is conju-
gated (coupled) with glucuronic acid, an endogenous compound, to form phenyl-
glucuronide during phase II. To show the structtiral resemblance between different
types of chemicals that are converted to reactive epoxide intermediates during phase
I reactions, the structures of vinyl chloride as well as its epoxide are also shown in
Figure 2.3.
Phase I Phase U
—(O
—>
mono-oxygenase
0 U <0 — OH . Gluc
H H mono-oxygenase H 0 H
/ ___ ___
c=c c—c etc.
/ \ /
H Cl H Cl
Figure 2.3 Formation of epoxides during the metabolism of henzene (A) and vinyl
chloride (B). Modified from Niesink et al., 1996, with permission.
phase I
(bioactivation or inactivation)
oxidation, reduction, hydrolysis
lar
phase II
(bioinactivation) conjugation
hydrophilic
extracellular mobilization
may also create allergic diseases through altering the immunologic system, or they
may alter the DNA to cause cancer or birth defects. Whether the toxic effects are
systemic or local, they can he acute or chronic, and temporary or permanent.
• Svstenuc toxicity. Toxic effects that result front absorption of a chemical and its
spread to different body syslenis. Examples of common systemic toxicity include
the serious, sometimes fatal, poisoning that may occur from contact with certain
organophosphate pesticides parathion and inhalation of organic solvents.
Orqcin-specijic toxicity. Certain chemicals have a target organ specificity (i.e., they
harm a certain organ rather tliamì others) often because of biotratisforniation or
bioconcentration. The route of exposure niight also be responsible for specific or-
gan injury.
Liter toxicity. Most chemicals are metabolized in the liver. Therefore, the liver be-
comes the target organ for many chemicals. Organic solvents (CC I. chloroforni, I
ethanol) and certain trace metals (copper, cadnuum) may cause extensive liver
damage, characterized by fatty changes, necrosis, fibrosis, and alteration of the
structure.
Kidney toxicity. Many xenobiotics are removed by glomertilar filtration and tubu-
lar excretion, while essential elements are reabsorbed in the tubuli. Chemicals
with kidney toxicity include metals (e.g., mercury, cadmium, lead).
Skin toxicity. Skin rashes are a coinnion reactioti to chemicals. Allergic reactions
can occur in sensitive individuals whereas skiii irritatioil can occur in anyone ex-
posed to a wide variety of irritatilig chemicals. Certain chieitticals produce a char-
acteristic type of skiii reaction, which provides a clue as to the exposure the pt'r-
son may have experienced. Most, however, do not.
Neiin, toxicitv. Most toxic substances act on the central or peripheral nervous sys-
tem. Futictional or organic alterations of iietirotransmitters can cause excitative I
symptoms or paralysis (through exposure to organophosphates, chloritiated or-
ganic compounds. metals).
7 Inimunotoxicity. The function of the iitiiituiie system ensures (1) nonspecific de-
tense mnechaiiisins against agents for which no previous sensitization has oc-
curred, and (2) specific, adaptive mechanisms directed against specific agents to
winch the organism has previously been sensitized or with which it has been iii-
fected. The body has very complicated mechanisms to defend itself against attack
by viruses and bacteria and these can be inipaired by exposure to certain chem-
icals. One result of such exposure may be a subtle increase in the frequency of
viral illnesses, such as influenza or colds. Impaired immunological reactions can
lead to allergy. Molecules can react with other body components, altering their
properties and hence their biological functions. This may result in the immune
system treatitig these components as foreign. Antibodies may be produced that
bind to abnormally altered body components and trigger inflamniatioti, tissue
breakdown, and other harniful effects.
codes and information. This complex process involves gene mutation, chromo-
somal alteration (structural and numerical), and/or gene rearrangements, all oh
which are described briefly in Box 2.5.
Cancer arises as a consequence of multiple genetic and noilgenetic events that
IlIuIIuIIIuIIIIIIuII
Brain
Heart - uIuuuuuuuu,IuIIuuIIII
(Usually not
Limbs susceptible IuuIuuIuuIuIIIIIuuuIuII
to teratogens)
Eyes uIIuu'uI.IIIIuIIu.uuu.,IIuIII
Ear uuIuIuuIIu'IuIIIuIuIuIu,IIIIuuIuIIuIlI
Teeth IJuIIuJu.uuuI,uIuuI
Palate uIuIIuuuIIuIuIIIuIuuII,-
External
Genitalia II I I II I II I I I I I I I I
Prenatal
death Major Morphological Abnormalities Physiological
Defects and
Minor Morphological
Anomalies
ui.. highly sensitive period - continued development, but less sensitivity to teratogens
Figure 2.5 Critical periods of fetal development by organ system. From Jedrychowski and
Krzyzanowski, 1995, with permission.
There are three different types of genotoxic effects, which are the result of changes
induced in the genetic material:
Gene mutation is the result of single or multiple base pair changes (substitutions,
deletions, insertions) in the DNA, which alter the information encoded in the
DNA's genome. Normally, the cell defense mechanisms can repair DNA damages,
recreating the original structure. Repair can be faulty, however, leading to her -
itable changes.
Chromosomal alterations may occur through damage by genotoxic agents, lead-
ing to structural aberrations (breaks, deletions, translocations), and through loss
or gain of one or more chromosomes and sometimes changes in the number of
chromosomes. Results of these changes might also lead to cell death or profound
genetic changes.
Gene rearrangements are characterized by altered gene expression (gene ampli-
fication, loss of activity). The underlying causes might he translocations or in-
versions of large parts of chromosomes.
contributed by A. Pinter, Johan Bela Institute, Budape.ct.
state, as the damage is not expressed as a new phenotype. However, the dam-
age will be converted to a permanent change unless the DNA is rapidly repaired.
Promotion A promoter is a substance that does not cause tumor development it-
self but which, by its action, transforms the initiated cell into an abnormal, ac-
tivated cell that may be the first cell of a tumor. This transformation results in
local cell proliferation leading to usually benign tumor formation. As with every-
thing in toxicology, dose and duration of exposure are key factors, so under cer-
tain circumstances, a promoter can also he tumorigenic in and of itself. At this
stage, the tumor is not yet malignant. Some tumors may be benign, but others
take the next stage of progression and become malignancies.
Progression In this stage, the tumor cells become malignant and the unrestricted
proliferation results in invasion of adjacent tissues and rnetastases. Metastases oc-
cur when cells from the tumor break off and arc transported elsewhere in the
body to give rise to new tumor masses. These may grow even more rapidly than
the original tumor, which is called the primary tumor.
Acute Toxicity Studies Acute animal studies are most commonly used to predict
human effects of short-term, high-lcvel exposures, such as may occur following an
TABLE 2.4
CARCINOGENIC CATEGORIZATION BY THE INTERNATIONAL AGENCY
FOR RESEARCH ON CANCER
Accepted Categories
1. There is sufficient evidence for carcinogenicity in humans
An agent is probably carcinogenic to humans
An agent is possibly carcinogenic to humans
There is inadequate evidence for carcinogenicity to humans
Not carcinogenic
accident, and these studies can provide a measure of the toxic potential of dif-
ferent compounds. Metabolic and pharmacokinetic studies arc used to determine
the absorption, distribution, and elimination of the test compound, its biotrans-
formation, and the rates in which these processes occur.
When toxicity is described in quantitative terms, the concepts lethal dose at
50% (LD 50 ) and effective dose at 50% (ED 50 ) are often used. The ED 50 is the
dose that would cause the effect in SO% of the lest population; the LD 50 is the
close that would kill 50%. The LD 50 or ED 50 is determined according to the
dose—response relationship. Lefhal doses by inhalation of chemicals in the form
of a gas or vapor can also he tested. In this case, the concentration of gas or va-
por that kills half the animals is known as the lethal concentration for 50% (LC50).
Although the LD 50 and the LC 50 only give information about the death of ani-
mals, they are very widely used as an index of toxicity. The criteria in Table 2.6
are often used for purposes of classification of acute toxic effects in animals.
The LD 50 and LC 50 are relatively reliable and in most cases correlate with lev-
els of human toxicity. However, they are not sufficient to fully characterize the
toxicity of chemicals, and it is impossible to assess health risks on the basis of
Suhchronic toxicity Often used to determine a dose without effect, generally of 28 or 90 days
duration; also referred to as subacute studies
Chronic toxicity Generally of approximately 2 years duration when rodents are used. May
be designed as carcinogenicity studies, chronic toxicity studies, or both
types combined.
SPECIALIZED STUDIES
TABLE 2.6
CLASSIFICATION SYSTEM FOR ACUTE TOXIC EFFECTS IN ANIMALS
Oral LU50 Rat Dermal LU50 Rat Inhalation LU50 Rat
(mg/kg) or Rabbit (mg/kg) (mg/rn 3 hr)
Very toxic <25 <50 <500
Toxic 25-200 50-400 500-2000
Harmful 200-2000 400-2000 21,000-20,000
Subchronic Tests In subchronic toxicity tests, animals are usually exposed re-
peatedly to a given chemical over a relatively long period (28 days or longer),
normally lO% of the lifetime of the selected animal. This means that inhalation
or ingestion studies last about 90 clays for rats and approximately 1 year for a
dog. Crude studies simply call for examination of the general condition of the
animals based on weight, food intake, activity and behavior, as well as exami-
nation of the organs for gross abnormalities to the naked eye. More sophisticated
studies include functional tests such as kidney and liver function, histopatho-
logical examination of organs and other tissues, and chemical analysis of blood
or urine samples.
Human Studies Information on toxic effects in humans can be obtained from ei-
ther clinical studies or epidemological studies that investigate health effects after
exposure in occupational settings or other environments. Clinical studies usually
focus on the detailed study of individual cases of disease, whereas experimental
studies are carefully controlled experiments in healthy humans, using low doses
otherwise considered to be safe. In view of the ethical aspects, only relatively mi-
nor and reversible health effects, such as subtle changes in reaction time, be-
havioral functions, and sensory responses, can be studied in experiments. Epi-
demiological research methods and the use in the health risk assessment process
will be discussed in Chapter 3.
Structure—Activity Relationships For many years it has been hoped that by ap-
plying knowledge of the physical structure and chemical characteristics of a
substance one could predict its biological activity. Much information has been
collected for various classes of compounds on the correlation between chemi-
cal structure, in terms of functional groups and special orientation, and para-
meters of toxicity. Short-term tests for assessing toxicity and maximum per-
missible concentraticns for occupational and ambient air pollutants have been
developed on the basis of such studies. However, the toxicological mechanism
of all chemical structures is not understood and there are many compounds
that do not react as expected, based on the structure—activity relationship. At
the current level of knowledge, structure—activity relationships are useful indi-
cators of potential toxicity and may hell) to priorize toxicological research, but
they require corroborating evidence and should not be relied on solely in the
decision-making process.
Information on Toxicity
Product identity is, of course, crucial in hazard identification. A product may have
a common trade name that is used for advertising and marketing purposes. The
Chemical Abstracts Service (CAS), a section of the American Chemical Society, as-
signs a CAS registry number to every chemical. Most product information sheets
contain CAS numbers, which are useful in researching the toxicity of the chem-
ical in question. The Registry of Toxic Effects of Chemical Substances (RTEC) number
is also important, as it is linked to a list of scientific articles on the health effects
of chemicals. This registry is operated by the National Institute for Occupational
Safety and Health (NIOSH) in the United States.
PHYSICAL HAZARDS
Not combustible but enhanses NO contact with all combustible Shut off supply it not possible and
FIRE combustion of other substances materials including clothing. no risk to surroundings, let the fire
Supports combustion of carbon, burn itself out: in other cases
pI'iosphorus and sulfur, exsnguish with powder. dry chemical
Elevated temperature may In case of fire: keep cylinder cool by
EXPLOSION spraying with water, Combat fire out
cause cylinders to explode,
of sheltered posit ion
Cough, headache. nauxea: symptoms Ventilation, local exhaust. Fresh air, rest, half-upright position,
Inhalation and refer for medical attention
may be delayed: see Notes or breathing protection
Protective gloves, protective Remove contaminated clothes, rinse
Skin Redness clothing when liquefied gas. and then wash skin with water and
soap, and refer for medical attention.
Safety goggles, or, when First rinse with plenty of water for several
Eyes Redness. pain, liquefied gas, face shield, minutes (remove contact lenses if easily
or eye protection in combination possible), then take to a doctor
with breathing protection
Evacuate danger area, consult an expert, ventilation Separate from combustible. UN baz class: 2.3
use water spray to knack down vapour, neutralize organic oxidizable substances: UN subsidiary risksi 5 1
running water with chalk or soda, do NOT absorb in ventilation along the floor.
saw-dust or other combustible absorbents (extra FURTHER INFORMATION ON LABELLING
personal protection: complete protective clothing Consult national legislation
including self-contained breathng apparatus).
ENVIRONMENTAL
DATA
NOTES
The commercial brown liquid under pressure is called nitrogen tetroxide. Transport Emergency Card,
Actually this is an equilibrium mixture of NO2 and the colourless N 2 0 4 TEC (R(-109
Nonirritunt concentration may cause lung oederna. The symptoms of lung
oedema sometimes do not become manifest until 24 -36 hours have passed NFPA Code: H 3: F 0 R 0 ray
and they are aggravated by physical effort. Rest and medical observation are
therefore essential. Turn leaking cylinger with the leak up to prevent escape
of gas in liquid state. Corrosive to steel when wet, but may be stored in steel
cylinders when moisture content is 0_1 1/, or lens
Figure 2.6 International chemical safety card. Source: International Program on Chenii-
cal Safety, WHO, Geneva.
The atom is the simplest unit into which matter can be broken down yet still retain
its identity as a distinct element, including all of its chemical characteristics. Each
atom consists of two components: a nucleus (containing protons and neutrons) and
orbiting electrons. The number of protons in the nucleus of the atom, also indicated
as the atomic number, determines the identity of element. There is an equivalent
number of electrons in the atom unless it is ionized or incorporated into a molec -
ular bond. The atomic number determines the chemical characteristics of the ele-
ment—how many electrons, how they are arranged, and how atoms of the element
bond to one another and other elements.
Unstable atoms, which possess too many or too few neutrons, try to become
more stable by emitting particulate and/or electromagnetic radiation (energy). The
type of radiation emitted (alpha, beta, or gamma radiation) depends on the type of
instability. When alpha or beta particles are emitted, the atoms of one element ac-
tually convert to atoms of another element. The emission of radiation from an un-
stable atom is called decay or disintegration. Each type of unstable atom has a known
half-life, which represents the length of time required for half the atoms to decay,
to emit radiation. Examples of half-lives are as follows:
For example, X-rays are machine-made gamma rays, whereas cosmic rays are
gamma rays from space.
4. Neutron radiation. Free neutrons can he a form of radiation when they are re-
leased from the atomic nucleus. They can induce significant cell damage by ion-
izaflon because the heavy particle carries a high amount of energy. Material
through which they pass may become radioactive, absorbed by nuclei of atoms
in the material, which then become unstable and decay themselves; this is called
neutron activation.
Ionizing Radiation
Radiation hazards can be divided into those from ionizing and nonionizing radi-
ation. (Nonionizing radiation and light as one specific form of nonionizing radi-
ation are discussed in Noniodizing Radiation, and Light and Lasers, below.) The
basic principles and the different types of radiation are described in Box 2.7. Ion-
izing radiation emerges when an electron is removed from a neutral atom and a
pair of ions are produced—a negatively charged electron and a positively charged
atom. It is the ionizaticn of atoms in the human body that causes harmful bio-
logical effect. The ions are highly reactive and damage critical cell structures, in-
cluding proteins and DNA. Ionizing radiation is, in fact, defined as electromag-
netic radiation (see next section for definition) with sufficient energy to displace
an electron from an atom.
Knowledge about the nature and probability of adverse health effects of ion-
izing radiation is based on animal experiments and observations of the effects of
human exposures at high doses, such as the studies of survivors of the atomic
bombings of Japan and of people exposed in radiation accidents. Studies of pa-
tients exposed to radiation for medical treatment as well as occupational health
Nonionizing Radiation
All forms of nonionizing radiation are part of the electromagnetic spectrum. Elec-
tromagnetic radiation is a form of energy that consists of an electric and a mag-
netic component. The energy is transported by the propagation of disturbances
in electric and magnetic fields that are always at right angles to each other. The
two fields vary in phase with one another in the form of a wave motion.
The waves travel at the speed of light, which is in vacuum approximately 3
io rn/sec. Figure 2.7 shows the complete electromagnetic spectrum, which spans
from wavelengths shorter than 10 1 ° ( gamma rays) meter to longer than 1 me-
ter (up to 100 km) for radiowaves. Electromagnetic radiation with a wavelength
above 10 10 meter does not have enough energy to cause ionizations. Therefore,
this part of the spectrum is referred to as nonionizing radiation.
As indicated in Figure 2.7, nonionizing radiation includes UV radiation from
the sun, which can cause eye cataracts that in turn can lead to blindness, as well
as skin cancer and immune system damage. In recent years, there has been con-
siderable concern about this hazard, because the depletion of stratospheric ozone
layer has led to an increase in UV radiation exposures (see Chapter 11 and WHO,
1994a). Another type of nonionizing radiation to which millions of people are
exposed is electromagnetic fields (EMF). These develop around electric power lines,
electric machinery, electric installations in home radio transmitters, and portable
telephones. In most situations the doses are too low to cause any adverse health
effects. However, a number of suspected adverse health impacts, including can-
cer, have been reported, but research data have not given a clear picture yet.
Light is in itself a type of radiation that can cause blindness if the eye is directly
exposed to very high—intensity light, such as when a person looks straight at the
sun for too long (see Light and Lasers. below).
t
microwaves
-1011
-1010
10 -2
10-1
- 10 1 meter (m)
I
- 10 8 -101
- 10 102
-106 - 10 kilometer (km)
- 10 10
radiowaves
- 10
10
Exposure to UV radiation occurs mainly from sunlight, but it can also occur
from electric welding arcs and from UV lights used in laboratories. Sunlight con-
tains UV-A, UV-B, and UV-C, but normally only UV-A reaches the earth's sur-
face in significant amounts. UV-B and UV-C are more damaging to health but
they are normally reflected away from the earth by the stratospheric ozone layer.
In case of damage to the ozone layer, which has now been shown to occur be-
cause of contamination of the atmosphere with chiorofluorocarbon (CFC) chem-
icals, people may be exposed to an increasing intensity of UV-B. UV-C does not
reach the earth's surface.
The most well-documented health effect of UV radiation exposure is skin can-
cer. People with light skin are at greater risk, particularly if they work outside in
occupations that do not provide much protection from the sun. An example is
the very high risk of skin cancer among outdoor workers (including farmers) in
Australia and New Zealand. Excessive sun-bathing is another exposure that adds
to the risk of skin cancer. Skin cancer is now becoming increasingly common in
countries with light-skinned people, such as the United Kingdom and Scandi-
na via.
Another important health effect of UV radiation is cataract (lens opacity) of
the eye. Cataracts may lead to blindness and are increasingly common at older
ages. This effect is caused by direct exposure of the lens to UV radiation. In In-
Pressure
Barometric pressures above or below one atmosphere (the normal pressure at
sea level) are part of the conditions of work in special environments, such as un-
Extremes of Temperature
Hazards associated with extremes of temperature can be divided into exposure
to heat and exposure to cold. In most countries, the climate changes from cold
to warm once a year, or a change in seasons brings torrential rainfall or hurri-
canes. Heat and cold affect the well-being and health of millions of people each
year. Adaptation to the climate, and type of housing, clothing, and other pre-
cautions will determine the impact on health.
Internal temperature regulation in the presence of temperature variation in
the environment is necessary for human life. Problems arise when one of three
conditions occurs: (1) temperature variations are so extreme that they exceed
the considerable ability of the body to adapt; (2) mechanisms of adaptation, such
as vasodilatation or sweating, arc impaired; or (3) exposure to extremes of tem-
perature is concentrated on a particular body part, as in frostbite or thermal burns.
The human body regulates temperature through the central nervous system from
a control center in the hypothalamus, a small structure in the center of the brain.
This center receives neural impulses from thermal receptors on the skin and re-
ceptors sensing the temperature of blood in deep body structures. It responds by
activating mechanisms controlled by the autonomic nervous system that dissi-
pate heat (vasodilatation and sweating) or that increase the internal generation
of heat (shivering) and conserve heat (vaso). It also sends signals to the cortex
of the brain that make one aware of being hot or cold, initiating behavioral
changes, such as changes in dress, seeking shelter, or modifying activity. This
MECHANICAL HAZARDS
Vulnerable Groups
Children, the elderly, and disadvantaged groups have higher rates of injury than
the overall population. Peak ages for fatal injuries are ages 1-4, 15-25, and over
70. Deaths in the 15-25 year range are mostly motor vehicle related. At all ages,
males have higher injury death rates than females.
The rates of child injury mortality have been falling in maiiy countries over
the last few decades; since 1960 injury mortality in boys aged 5-14 years has
fallen 60% in Australia, 53% in Canada, and 33% in the United States (Pless,
1994). However, these figures have not decreased at the same rate as deaths from
Injury Settings
Historically, injuries that occur at work and injuries that occur in other settings
have been considered separately, more for practical reasons than for conceptual
reasons. Work environments often present a high level of exposure to mechan-
ical hazards both in terms of the magnitude of risk (working with dangerous ma-
chinery) and the length of exposure (40 hr a week for 30 years). Legislation has
been passed in many jurisdictions to control and regulate the workplace for the
protection of workers, as discussed further in Chapter 10. In some jurisdictions,
compensation systems exist to cover the financial burden of injury on the worker
through payment generally charged back, at least partially, to the employer where
the injury occurred. The cost of workers' compensation to employers has added
further incentive to explore preventive options. The emphasis on injury preven-
tion has also contributed to the training of physicians, nurses, ergonomists, and
other professionals with expertise in the prevention and treatment of work-
related injuries. The work and research of these professionals have greatly ad-
vanced the understanding of injuries in the workplace.
In contrast, injuries that occur elsewhere, such as in the home, on the road,
and in various places of recreation, have not received an equal amount of at-
tention. The situations in which injuries occur are diverse, and no one health
professional or body has been charged with the overall responsibility of com-
Traffic-Related Injuries
Motor vehicle–related crashes are by far the leading cause of serious injuries in
most countries. Unfortunately, high rates of injuries are usually tolerated by so-
ciety and accepted as an unavoidable cost of transportation. This is quite unnec-
essary as injuries can be prevented by improved design of roads, improved de-
use) whereas passive strategies lie at the opposite end of the continuum—little or
no action is required (such as automobile airhags). The consensus within the in-
jury prevention field is that passive strategies should he employed wherever avail-
able, and when active strategies are necessary, they are most effective when man-
dated. The need for a flexible combination of strategies has been recognized.
Another key tool in injury prevention is the Haddon matrix, which is based on
the concept that injury events can be broken down into preinjury, injury, and postin-
jury phases. This phase concept is combined with the traditional causation concepts
of host, agent, and environment, resulting in a way of breaking down an injury sit-
uation and thinking about possible points of intervention. This matrix approach has
been embraced by injury prevention researchers and applied in various forms to
numerous injury prevention situations. An example of how this can be used is
shown in Table 2.9, where Haddon's matrix is applied to analysis of motor vehicle
injuries. It is generally accepted that control programs that modify the vehicles, vec-
tors, or environment are more effective than those that modify the host.
A further contribution to injury prevention analysis is Haddon's ten coun-
termeasure strategies for reducing injuries. These are generic measures that can
be applied to any type of injury prevention initiative, including the physical haz-
ards discussed previously. These are listed in Table 2.10 in abbreviated form.
Safety measures should he integrated into a comprehensive package so that
they are mutually reinforcing, hacked by public policy, specific to local hazards,
TABlE 2 10
HADDON'S TEN COUNTERMEASURE STRATEGIES FOR REDUCING INJURIES
Injury Reduction Strategy
Prevent the creation of the hazard in the lirsi place.
Reduce the am()utit of hazard brought into being.
Prevent the release of an existing hazard,
Modify the rate or spatial distribution of release of the hazard from its source.
Separate, in time or in space, the hazard and that which is to be protected.
Separate the hazard and that which is to be protected by interposition of a material harrier.
Modify the basic qualities of the hazard.
Make that which is to he protected more resistant to damage from the hazard.
Counter damage already done by the environmental hazard.
Stabilize, repair, and provide rehabilitative and cosmetic surgery.
Source: Haddoii, 1980.
PSYCHOSOCIAL HAZARDS
alld 1nfl c
CHAPTER CONTENTS
The Health Risk Assessment and Risk Relationship Between Dose and Health
Management Framework Outcome
Epidemiological Methods Dose—Effect and Dose—Response
Steps in Epidemiological Field Relationships
Investigations Calculating Risks for Threshold
Study Methods Effects
Quantifying Risks Thresholds and Other Important
Study Difficulties and the Benchmarks
Determinates of Causation Uncertainty Factors in Establishing
Cluster Investigations and Thresholds
Ecological Studies Calculating Risks for
Non-Threshold Effects
Hazard Identification in the Field
Occupational Environment Human Exposure Assessment
General Environment Options in Approach
104
Personal Exposure Monitoring Errors and Quality Assurance
Biological Monitoring of Exposure Ensuring Adequate Sample Size
or Effect Health Risk Characterization
Indirect Approaches to Estimation General Approach
ol Exposure Specific Health Risk Assessments
Estimating Inhalation Exposure in Field Situations
Estimating Ingestion Exposure
Health in Environmental Impact
Estimating Skin Exposure and
Assessment
Doses
Principles of Population Sampling
tems are obtained, when possible, to assess the environmental quality. If no mea-
surement data are available, emissions may be calculated or estimated at the
source and exposure levels may be estimated on the basis of mathematical mod-
els showing how these emissions are carried by air, water, or in the ground. In-
tegration of these data provides an estimation of the most likely exposure levels
for individuals who may come into contact with the contaminants. This part of
the risk assessment process is addressed in greater detail in the section Human
Exposure Assessment.
Risk characterization is the integration of the first three steps in the risk as-
sessment process. Ideally, it should produce a quantitative estimate of the risk in
the exposed population, or estimates of the potential risk under different plau-
sible exposure scenarios. Typically, a range of estimates is developed, using dif-
ferent assumptions and statistical methods that determine how sensitive the es-
timates are to basic assumptions in the model. If diffetcnt health effects arc likely
to occur, the risk of each should be characterized. Other exposures or factors con-
tributing to the health effects should also be characterized. This process will be
described in the section Health Risk Characterization.
The literature on environmental health risk assessment can be confusing, as
the same terms are used to refer to both generic risk assessments (often regula-
tory agency—based) and specific field risk assessments. Generic risk assessments
characterize a hazard in general scientific terms on the basis of anticipated ex-
posures and hypothetical population characteristics. However, when there is sus-
picion of a risk in a specific situation, it must be ascertained if people really are
sufficiently exposed for health effects to occur.
Risk assessment has its limitations. In practice, crucial data are frequently lack-
ing, and reasonable assumptions are made to arrive at a quantitative risk esti-
mation. Most risk assessments contain one or more of the many sources of un-
certainties that may accompany a risk assessment, listed in Table 3.1, and it is
essential to evaluate their impact on the assessment. This process, usually re-
ferred to as sensitivity analysis, may be quite complex.
In many situations, only a qualitative risk assessment may be appropriate. In
this approach, reasoned judgment is used, taking into account what information
EPIDEMIOEOGICAL METHODS
Data from epidemiological studies may be used directly to identify hazards and
dose—response relationships. The types of studies used in epidemiology each have
their own benefits and limitations.
Figure 3.2 Logical development of epidemiological field investigations. From WHO, 1991 a,
with permission.
Study Methods
Epidemiological study types differ considerably in their strengths and weaknesses.
Table 3.2 summarizes the main features of the traditional types of epidemiolog-
ical studies. Note that in each of these types of studies, the individual person is
the unit of analysis. Ecological studies, in which the community or region is the
unit of analysis, will be discussed later.
Descriptive studies may be longitudinal (often) or cross-sectional. Historical
studies provide trends over time in an exposure or in the health effects of inter-
est. Cross-sectional descriptive studies provide a snapshot of the exposure or the
effects at a given time, or both. Researchers conducting descriptive studies do not
try to draw associations between an environmental exposure and a health prob-
lem; instead, they simply try to describe the ways things have been or currently
are. However, both historical and cross-sectional studies can compare an expo-
sure or an environmental exposure prevalence to a health problem's prevalence
in a study group and a control group, to establish whether a link may exist be-
tween a risk factor and an outcome. The study designs used most often in ana-
lytical epidemiology are cohort studies and case—control studies. These two study
designs differ fundamentally from each other because they approach the ques-
tions of causation (or more precisely, association) from opposite ends of the cause-
.- --
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TIME
direction of inquiry
•*. disease
People Exposed
without disease
ation... disease
the
disease
Not exposed__f...*.Iro_disease
Figure 3.3 Design of a cohort study. From Beaglehole ci al., 1993, with permission.
and-effect spectrum. Cohort studies start with a population that has been exposed
to the risk factor, then the frequencies of disease in the exposed and unexposed
populations are compared as they occur over time (see Fig. 3.3). ('ase-control stud-
ies start with people who have the disease, then frequencies of exposure that oc-
curred in the past in the population with the disease and the population with-
out the disease are compared (see Fig. 3.4). Researchers using analytical
epidemiology must look out for bias in the information, or confounders, factors
that are not causal but may be associated with the exposure and the disease for
other reasons.
Case-control studies can provide powerful and accurate estimates of risk ra-
tios and are usually economical in terms of both cost and study duration. An ex-
ample of the use of a case-control study in testing the association between an
acute epidemic disease and a particular exposure is the toxic food oil syndrome
investigation that took place in Spain (see Box 3.1). Case-control studies can also
be used in examining chronic, long-latency, hyperendemic problems and are es-
pecially useful in studying rare diseases, as noted in Table 3.2.
Cohort studies have the advantage of being able to directly measure the risk
of a disease and calculate the actual population illness rate, the occurrence of ill-
TIME
direction of inquiry
..
Start with:
Figure 3.4 Design of a case-control study. From Beaglehole et al., 1993, with permission.
In a similar fashion, within case families, the estimated amount of oil consumed per
person correlated with the severity of the symptoms of the disease. The syndrome
became known as toxic oil syndrome (TOS) and was probably caused by imidazoline-
thiol components, derivatives of isothiocyanate.
This is an example of a case—control study, as investigators started with indi-
viduals with and without the disease, and looked for an association to exposure be-
fore the symptoms started, in this case, ingestion of the cooking oil. Case—control
studies can he used in this manner to investigate the cause of an unknown disease
epidemic. If there is a statistically higher level of exposure in the cases than in the
controls, then the exposure may be the causative agent. (In this situation, with 100%
of cases having consumed the oil, and O% of cases not having consumed it, the odds
ratio, as discussed in the section Quantifying Risks, would be infinity.)
Within 2 months of the date when the initial case was recorded, the number of
persons contracting the syndrome had reached its peak and the incidence declined.
This decline corresponded with public education about the oil and the replacement
of the oil with uncontaminated cooking oil.
Source: WHO. 1990c.
The vinyl chloride monomer (VCM) is a gas produced largely through chlorination
of ethylene, a product of the petroleum industry. When polymerized, it forms
polyvinyl chloride (PVC), one of the major polymer plastics widely used today. It
has been produced commercially since the 1930s and its production has steadily in-
creased. It is widely used in floor tiles, seat covers, toys, water pipes, and other com-
mon products. Once considered a relatively inert gas, VCM was widely used for a
time as a propellant in spray cans.
In 1967, the U.S. National Institute for Occupational Safety and Health (NIOSH)
was notified that 4 cases of a rare liver cancer, angiosarcoma of the liver (ASL), had
occurred in a workforce of only 500 workers. Shortly thereafter, further observa-
tions were reported, including an Italian study on rats, that supported the associa-
tion between VCM and the development of ASL. The NIOSH decided to conduct a
historical cohort mortality study of workers at PVC polymerization plants to com-
pare observed cause-specific mortality rates among these workers with that expected
in the U.S. population. Four plants were selected for the study based on length of
operation, accessibility of records, and probable ease of follow-up. The total person-
years at risk for disease were calculated. Follow-up was virtually complete (1287
out of 1294 workers) with 10-year latency. Thirty-five cases of cancer had occurred.
Expected numbers of deaths were calculated according to the ages of the people at
risk. From the expected number of deaths in this workforce by age category and
the standardized mortality ratio (SMR) (for the workers with 10-year latency), it
can be seen that the cancer mortality is significantly increased. As the numbers are
small, only the excess in liver tumors is statistically significant. Excess numbers for
leukemia and lung and brain cancer should be noted as deserving further study.
95 016 confidence
Cause of death Observed Expected SMR intervals
Cardiovascular 57 54.7 104 79-135
Cancer 35 23.5 149* 104-207
Pulmonary 12 7.7 156 80-272
Liver/hiliary 7 0.6 1 167** 467-2404
Leukemia/Iyinphoma 4 2.5 160 51-386
Brain 3 0.9 333 85-907
Other 9 11.8 76 35-145
Cirrhosis of liver 2 4.0 50 8-165
Pulmonary disease 6 3.4 176 64-384
(excluding cancer)
Violent deaths 13 14.2 92 49-157
All other causes 22 26.5 85 52-126
Unknown cause
TOTAL 136 126.3 108 90-127
*p = 0.05; ** p = 0.01.
Source; Falk and Heath, 1986
Quantifying Risks
There are a few standard equations used in epidemiology to determine if the
study population is at an increased risk or has an increased number of cases of
the disease in question compared to a standard population. The rate of disease,
the most fundamental measure (Fig. 3.5), can he measured in terms of incidence
(new cases) or prevalence (existing cases). To determine if the observed rate is
excessive, a risk ratio, or relative risk should be calculated. These are usually cal-
culated from cohort studies.
A risk ratio of 1.0 means that the rate of the problem (or outcome of inter-
est) in the group being studied is not different from the rate of the occurrence
in the general population. A risk ratio of >2 or 3 is usually considered evidence
of an important risk. For example, a risk ratio of 5 would mean that the popu-
lation with the risk factor (e.g., those who are exposed to asbestos) are five times
RATE OF DISEASE: Number of cases of disease in population at dsk
Number of persons in population at risk
Example: 50 Cases = 20
2500 persons at risk 1000
Expressed as A numerical ratio (1.5, 3.0 etc. indicating that risk of disease
in the exposed (or at risk) population is 1.5, 3.0, etc. times
greater than that in the unexposed (or not at risk) population
Figure 3.5 Definition and calculation of rates of disease and risk ratios.
SMR = Observed number of deaths (or events) in the study population X 100%
Expected number of deaths (or events) if the study population had the
same age and gender specific death rates as the comparison
(e.g., national) population
The denominator of the SMR (e.g., the expected number of deaths) is computed
as follows:
l• A calculation is made of the person-years at risk in the cohort for each agel
gender group (the sum of the number of years that each individual in the co-
hort has been followed).
The figure obtained is multiplied by the expected age/gender specific mortal-
ity rate for the disease(s) being ccnsidered based on national health statistics.
The expected number of cases is the sum of cases in the age/gender groups.
An SMR of 130 for a particular cause of death indicates that there was a 30%
greater mortality of that disease found than was actually expected.
Since these measurements of risk are statistical, we cannot be sure that the
observations in a study did not occur by chance. The statistical variation of these
measures is usually expressed as the confidence interval. The 95% confidence in-
terval is the range within which the true value lies, with 95% probability. The
where U = incidence (or mortality) in the unexposed group; E = incidence (or mor-
tality) in the exposed group; p = prevalence of exposure at a designated time preva-
lence in the total population; 1= incidence in the total population; and RR = risk
ratio.
When the size of the total population at risk is not known, e.g., in case—control
studies, the RR can he estimated by calculating the odds ratio (OR). Consider the
following notation for the distribution of a binary exposure and a disease in a pop-
ulation divided into four groups: individuals with disease and exposed (A), with dis-
ease and unexposed (C), without disease and exposed (B), and without disease and
unexposed (D). The OR would be calculated as follows:
Disease
Exposed Yes No
Yes A B
No C D
Thus
OR = Lc
B/C
true effect is most likely to be the mean or central tendency of the confidence
interval but it may be larger or smaller; 95% of the time, however, it will fall
within the range calculated as the confidence interval. There is also a 5% chance
that the true value lies outside the confidence interval; that is, it is higher or
lower than either extreme valtie of the confidence interval. The width of the con-
fidence interval depends on the number of cases observed, the size of the pop-
ulation in the study, and the variability of the comparison or expected rates.
These issues are discussed at greater length in Basic Epidemiology (Beaglehole et
al., 1993) and other standard epidemiology texts.
TABLE 3.3
TESTS OF CAUSATION
Temporal relation: Does the cause precede the cifect? (essential)
Plausibility: Is the association consistent with either knowledge?
Mechanism of action: Is there evidence from experimental animals?
Consistency: Have similar results been shown in other studies?
Strength: What is the strength of the association between the cause and the elfect? (relative risk)
Dose—response relationship: Is increased exposure to the possible cause associated with increased
effect?
Reversibility: Does the removal of a possible cause lead to reduction of disease risk?
Study design: Is the evidence based on a strong study design?
Judging the evidence: How many lines of evidence lead to the conclusion?
Source: Bcaglehole et at., 1993 (these are modified criteria of causation from those originally developed by
Bradford Bitt).
rural community using well water contaminated with pesticides. The increased
occurrence of respiratory problems during a summer smog period can be seen as
a cluster in time. An increased occurrence of lung disease in workers at a par-
ticular workshop is a cluster in the population.
Clusters thought to relate to environmental factors sometimes receive a lot of
publicity. However, many clusters are actually not real, because the presumed
diagnoses are incorrect or misunderstood. Others are just chance events. For other
clusters, there may be explanations other than a common environmental expo-
sure because the exposure cannot account for the cluster.
A basic approach has been developed to investigate reported clusters as effi-
ciently as possible. The objective is to verify expediently (1) if a cluster truly ex-
ists or if it is a coincidence or merely false; (2) if human exposure to a possible
environmental hazard actually exists; and (3) if the relationship between these
two merits further investigation and/or action. Even if the answer to the first
two questions is yes, it still remains to be determined whether there is a causal
relationship between the increased number of diseased individuals and the rel-
atively high exposure levels. Each question nccds to be pursued independently,
because each requires further action if positive, even if the other is negative.
An ecological study is one in which the unit of analysis is the population group
or region, rather than the individual. Typically, regions involve persons living in
a geographic area such as a census tract, country, or province. For each group
or region the average exposure level to the agent in question and the rate of dis-
ease in question are determined independently. It is not known whether the in-
dividuals who have been exposed are the same individuals who developed the
disease. Because the exposure levels of individuals are not linked to the disease
occurrence in the same individuals, ecological designs are incomplete as evidence
for causal association, although they may be very useful for generating new hy-
potheses or proposed associations that can be tested in other studies. Ecological
studies arc also an inexpensive option for linking available health data sets or
record systems to environmental data. Other important variables are often avail-
able in these studies, such as sociodemographic and other census variables. Fig-
ure 3.6 illustrates the findings of an ecological study of the relationship between
C)
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3.5 4 4.5 5 5.5 6 6.5 7 7.5 8 8.5 9 9.5 10 10.5
Salt sold (kg / person I year)
Figure 3.6 Study of the relationship between salt sold in Chinese counties and esophageal
cancer mortality rates. From Beaglehole et al., 1993, with permission.
salt sold in a county (local government area) and escphageal cancer mortality
rates. Ecological studies can be classified into five basic design types that differ
according to the method of study selection and methods of analysis: exploratory
studies, space—time cluster studies, multiple groups studies, time trend studies,
and mixed studies.
Occupational Environment
In the workplace it can be relatively easy to make an inventory of all potential
hazards. This is made easier by an accurate registration or tracking system of all
chemicals that are frequently used or stored, which unfortunately is not always
available. To make an inventory of chemical hazards, product identity is, of
course, crucial. From knowledge of which product is used, one may then learn
what is in it and what constituents are hazardous. Identifying the chemicals in
100
80
Z- 60
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cr
20
Death
Unconsciousness
Nausea,
blackouts
Headache,
dizziness
Slight
headache
0 10 20 30 40 50 60 70 80
Carboxyhaemoglobin in blood (%)
Figure 3.8 Dose-effect relationship. From Beaglehole et al., 1993, with permission.
population) (Fig. 38). A hicrarchy of effects on health can be identified for most
hazards, ranging from acute illness and death to chronic and lingering illnesses,
from minor and temporary ailments to temporary behavioral or physiological
changes, as shown in Table 3.5. Dose-response relationships are considerably dif-
ferent for non-carcinogens (thought to have a threshold) and carcinogens
(thought to be non-threshold) as discussed further below.
Calculating Risks for Threshold Effects
Many environmental hazards have a specific effect on individuals only when the
dose reaches a certain level, i.e., a threshold for that effect. Figure 3.9 illustrates
the dose-respunse relationship for various health effects of lead concentrations
in blood in children. Sometimes the number of years of exposure has to be used
as an indicator of dose, when duration and levels of exposure are not known.
When concentration and dose are known, a dose index can be calculated. This
was done for workers in a Swedish battery factory (Kjellström, 1986b). Figure
3.10 illustrates how increased years of exposure to cadmium and average expo-
sure level (mg/rn 3 ) relate to high levels of 2 -microglobulin in the urine (>290
rg/liter), a measure of kidney dysfunction.
Dose-response relationships can also be obtained for physical hazards. Figure
3.11 illustrates the relationship between sound levels at work and the percent-
age of those with impaired hearing according to the age of the vvorkforcc. This
figure shows that the dose-response relationship is different in the different age-
groups.
100
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80
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36 Figure 3.10 Dose—response re-
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50
sure and prevalence of high uri-
U)
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c
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ted line indicates a maximum
25
possible response if all retired
26 and deceased workers with
65 dose index above 12.5 had a
0 I high 132 -microglobulin. From
0.5 1 2 5 10I 20
I 50 100 Kjellström, 1986b, with per-
Dose index (mg I day) x years mission.
(see Fig. 3.14). A no observed effect level (NOEL) is the level at which no effect, ei-
ther good or bad, is detected.
Because all individuals are constantly exposed to certain levels of environ-
mental chemicals, the question to address is what levels of exposure to these
chemicals are likely to affect human health. This analysis is usually done by of-
ficial agencies (e.g., the Environmental Protection Agency in the United States),
by applying animal and epidemiological studies. From these studies, an acceptable
daily intake (ADI), or tolerable daily intake (TDI) (depending on the jurisdiction),
is calculated. These values indicate the maximal daily intake of a chemical that
VLsI
• Factory workers
[;I.1 o General population
Age
50
55 - 59
40
(0 40-46
E
30
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0)
0
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35
30
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U-
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10 /
/
,x
Figure 312 Dose—response re- 5 x Non-fatal injuries
lationship between speed of a //BELTED
car in a collision and risk of dri-
ver injury for seat belt use and 0
0 25 50 75 100 112
non-use. From Beaglehole et
al., 1993, with permission. Speed (km / h)
is not expected to result in adverse health effects after a lifelong exposure. The
ADI is usually the NOAEL (or LOAEL) divided by uncertainty factors (UF) (which
are discussed below):
The ADIs can then be used as reference values in establishing guidelines to pro-
tect individuals. Note that time and dosimetry factors (such as body weight, sur-
face area, and absorption rate) must be specified for an ADI. For example, an
ADI is often prepared for a person of 70 kg who is exposed to a chemical for 3
hr/day. The ADI5 and TDI5 are often revised over dine, as new information is
discovered through further studies. Examples of TDIs are given in Table 3.6.
70
/1
60 /
/
/
USEPA(1973)
0
50
>
U)
0
/
C /
CU
/
40 /
I
0)
/
/ Schultz et al. (1976)
/
30 ,
,
,
,
20 ,
,
/
,
10
I-
000
0
40 50 60 70 80 90
Day time L eq or L dn (dB(A))
Figure 3.13 Dose—response relationship between outdoor noise level and annoyance. From
WHO, 1980a, with permission.
No Threshold
Response ,
I
Threshold
Response
LOAEL
NOAEL
Figure 3.14 No observed adverse effect level (NOAEL): the level of exposure to a chemical
at which no adverse effects were observed during studies with animals. Lowest observed
adverse effect level (LOAEL): the lowest level of exposure to a chemical at which adverse
effects were observed during studies with animals. From HC, 1993, with permission.
TABLE 3.7
SAFETY OR UNCERTAINTY FACTORS
Factor Comments
lOX factor Applied to data from valid experimental studies on prolonged human intake.
This protects the Sensitive members of the population.
lOOX factor Applied when experimental results from studies of human intake are not avail-
able, or are inadequate but there are valid results from low-dose intake stud-
ies on one or more species of experitnental animals. This accounts for species-
to-species extrapolation.
1000)< factor Applied when there are no low-dose or acute human data and only scanty
results on experimental animals. This is applied to account for spectes to
species extrapolation, from high dose to low dose, and from short-term to
long-term effects, as well as protecting sensitive members of the population.
One hundred is the safety factor appropriate for use with a NOAEL from animal
studies with no comparable human data; ten is an additional safety factor because
the duration of exposure in the experiment was significantly less than a lifetime.
As no data were available on the contributions of food and air to exposure, an
arbitrary designation of 20% was chosen as the maximum allocation from drinking
water. If the daily water intake per person is assumed to be 2 liters per day, the al-
located ADI (AADI) for water is:
by a multiple dosing experiment. Curves AB, AD, and AE are possible dose-
response curves at lower doses, with points B, D, and E being the respective
threshold for adverse effects in the human population. In setting an ADI con-
centration (point C), a selected safety or uncertainty factor is applied to the dose
at point A. If the curve AB is the true effect curve, then the calculated ADI value
will be lower than the threshold dose, thus indicating that the safety factor was
appropriate. However, if AD or AE is the true dose—effect curve, then the calcu-
lated ADI will be too high and the safety factor too small. In this case, some in-
CE
dividuals in the population will suffer adverse effects. The size of the gap be-
tween points C and B is also of interest, because if it is large, expenditure on
control methods may be greatly in excess of what is needed.
Once the threshold dose for a toxic substance has been determined for the
normal and healthy population, consideration must be given to high-risk groups
such as infants, young children, elderly people, pregnant women and their fe-
tuses, the nutritionally deprived, the ill, individuals with genetic disorders, and
those exposed to other environmental health hazards. There are many examples
of the susceptibility of these high-risk groups. The increased susceptibility of fe-
tuses and infants has been well documented. For example, several Japanese chil-
dren born to mothers exposed to methylmercury in fish in Minamata suffered
congenital malformations even though the mothers showed few or no symptoms
of mercury poisoning at all. The fact that nutritional deficiencies increase suscep-
tibility is also well documented. Dietary deficiencies of calcium and iron signifi-
cantly intensify the toxicity of lead. Individuals who suffer from kidney disease,
for example, will experience greater effects from exposure to toxic metabolites
that require excretion through the kidneys, and impaired liver function affects the
inctabolic conversion, particularly detoxification of certain pollutants or their ex-
cretion in bile. Individuals suffering from cardiovascular or respiratory disease are
at greater risk from the effects of carbon monoxide or sulfur dioxide. It may there-
fore be necessary to apply an additional safety factor to the dose that is toxic to
the general population, in an effort to protect susceptible groups.
Emissions
I __
Environmental Concentration
N \ / -Z
Exposure
External Exposure
$
Absorbed Dose
$
Target Organ Dose
Health Effects wk
tack the target organ. Internal dose refers to the amount of the contaminant ab-
sorbed in body tissues upon inhalation, ingestion, or absorption. The biologically
effective dose is the amount of the absorbed or deposited contaminants that con-
tributes to the dose at the target site where the adverse effect occurs. Total dose
is the term used to indicate the sum of all doses received by a person of a con-
taminant over a given time interval from interaction with all media.
Because the dose is difficult to measure, the parameter usually considered is
the exposure. Therefore, regulators usually establish rules and regulations that
are directly linked to reducing exposure, as opposed to dose. Estimates can then
be made of the dose, based on the exposure, various assumptions, and animal
models. While such estimates often have large uncertainties, it is a more practi-
cal parameter than dose. In any case, it has to be clear that measuring exposure,
not just environmental concentration, is the critical parameter since it is more
directly related to health effects. To put it simply, if someone is not inhaling, in-
gesting, or absorbing the pollutant, there is no exposure and hence no adverse
health effect is possible. In all such investigations the total exposure from all
sources must be assessed and not just the concentration in the medium or cir-
cumstance of concern. Exposure is usually measured for just one medium at a
time. Risk assessment that is intended to optimize mitigation strategies must es-
Indirect
Direct Methods
Methods
Pharmacokinetics and
Pharmacodynamic models
Exposure
Models
Figure 3.17 Direct and indirect approaches for the analysis of exposures. From NRC, 1991,
with permission.
tablish the relative risks associated with absorption from all media and routes of
entry in order to gain a clear picture of which is more important.
Monitoring may be direct and indirect, as indicated in Figure 3.16. Personal
environmental monitoring and biological monitoring are considered direct ap-
proaches; environmental area monitoring as well as questionnaires, diaries, and
mathematical models are considered indirect.
Assessment of exposure can be made in different ways, as illustrated by the var-
ious points along the continuum described in Figure 3.17. Environmental monitoring
irieasures concentrations of contaminants to which individuals may be exposed. Bi-
ological monitoring usually measures dose, or more specifically, body burden at a point
in time. Each of these can be further subdivided into area sampling, which measures
concentrations without taking into account the extent of actual exposure, and per-
sonal sampling, which measures more directly the concentrations to which an indi-
vidual is exposed throughout a period of time. Similarly, biological monitoring can
also be further subdivided to reflect the extent to which the biological marker being
sampled is a measure of dose, a marker of effect, or a marker of susceptibility.
Personal Exposure Monitoring
Personal air-monitoring devices provide direct measurements of concentrations
of air contaminants in the breathing zone of an individual. Generally, samplers
worn by subjects record time-integrated concentrations, reading concentrations
directly, or they collect time-integrated samples that require lab analysis. Sam-
plers may either be active, requiring a pump to move air, or passive, requiring
no pump and collecting the airborne contaminant by diffusion.
For watcrbornc contaminants, a direct measurement entails sanipling from
the water source, such as a drinking tap, or from the water actually drunk. To
measure food contaminants, duplicate meals are analyzed. In this method, an in-
dividual must collect a second portion of everything consumed. This duplicate
meal is then homogenized and analyzed for the compounds of interest.
TABLE 3.8
EXAMPLES OF USEFUL MARKERS OF EXPOSURE
Substance Biological Marker
Carbon monoxide COHb in blood
Cadmium Cadmium in urine
Lead Lead in blood
Methyl-mercury (in fish) Mercury in hair
PCP PCP in urine
Alcoholic beverages Ethanol in exhaled breath
Organic so]vents Mttaboliies in urine
VOCs VOCs in exhaled breath
Tobacco smoke Colinine in urine
COi{tj, cart, xyhemoglobtn; PCP, pdntkht()111c1iot SOCs, volatile or-
'anics.
The first value represents straight tap Water only', the secoitd includes tap water—based beverages such as tea,
coffee, and reconstituted soft drinks. Exclosivel breast-led infants (BFi do not require additional liquids. Estimates
for non—breast-fed infants NBF) are based on volume consumed as drinking water and on consumption of 750
mi/day of Ii irroula made from p iwdered formula and tapwater for total drinking water.
Source: HC, 1992.
are given in Table 3.9. Other factors influencing the volume of air breathed in-
clude temperature, altitude body weight, smoking habits, history of heart dis-
ease, and possibly background air pollution. The absorbed dose is dependent on
the deposition of the chemical in the respiratory tract and the absorption of the
deposited chemical into the bloodstream.
Soil Soil can he eaten unintentionally when soil sticks to hands or to food. Soil
can also be ingested when other objects are put in the mouth or swallowed. All
children do this to some extent. The frequency that children swallow and put
objects in their mouths varies. Children between the ages of 1 and 3 years, and
children with iron deficiency or certain mental disorders develop a habit of swal-
lowing objects more often than other children (known as pica). Standard values
for the daily ingestion of soil by children who do not swallow objects regularly
and by adults are presented in Table 3.9. To calculate the soil ingestion dose, it
is assumed that 100% of the contaminant ingested with soil is absorbed. The
equation, however, should convert the concentration of the contaminant in the
soil (C) from ,ag/kg of soil to pg/kg of soil, so that the units for soil concentra-
tion are the same as those for soil ingestion.
The area of the skin that is exposed will he influenced by the activity being per-
formed and the season of the year. To estimate the absorption of a contaminant
in water through the skin, a permeability ccnstant (P) should be used. However,
such constants have been established for only a few chemicals. Even for chem-
icals that have been tested, the value of the constant can depend to a very large
degree on the design of the experiment used to test the chemical. Box 3.5 sum-
marizes the information needed to calculate estimated daily intake (EDT) via in-
gestion and skin absorption.
Principles of Population Sanip ling
In the selection of a population sample for human exposure assessment, a sam-
pling frame should be established, which should include (a) all the people in the
target population. or (b) areas and the approximate number of people linked to
each area. If the people in the target population are mobile, they may have to
be linked to the areas where they eat or sleep. Developed countries usually have
a central statistical bureau that maintains registries or conducts a population cen-
sus, which may form an ideal frame for sampling from the general population.
As these listings are rarely complete, sampling frames often need to be conducted
in stages, as discussed below, with these data constituting a sampling frame for
the initial stages of a multistage sample. In developing countries, where census
data are generally not available, special efforts may be needed to estimate the
population linked to the areas to construct a sampling frame.
....................
Urban Block
it1
Neighborhood
ic -
2.
- ......................
•\jJA1
Househqld
General ApproaL
Risk characterization brings together the first three components of the risk assess-
ment process: hazard identification, dose–response assessment, and exposure as-
sessment. The incidence and severity of potential adverse effects are estimated
as well. The major assumptions, scientific judgments, and uncertainties are de-
scribed in detail to fully understand the validity of the estimated risk. Risk char-
acterization (or risk estimation as it is also known) may be subdivided into four
different steps as indicated in Table 3.10.
The first equation of total exposure combines the concentration of pollutants
(by direct measurement through sampling and analysis, modeling, analysis of bi-
ological markers, and questionnaires) with the duration of exposure, expressed ac-
cording to the health effects of concern. For carcinogenic effects, the total time
(hours or days) of exposttre during a person's lifetime is the principal concern (cx-
posure every day over a lifetime would be 25,550 days, assuming a 70-year life-
time). For noncarcinogenic effects, short-term exposures at elevated concentrations
are targeted, therefore a duration of hours or even minutes may he important. For
chronic exposure, an average daily pollutant concentration is usually used with
the assumption that it is relatively constant over a lifetime. For children, epore
periods are generally divided into age categories, e.g., 0-6 months, 6 months to 5
years, and 5 years to 12 years, because of their differing body weights.
The second equation combines the exposure information with dosimetry fac-
tors in a simple model to estimate the average dose per day over a lifetime. These
factors include absorbed rate, average body weight, average lifetime, and others,
as relevant. Dose is usually expressed as pollutant mass per kilogram of body
weight per day. It should also include exposures from all media (air, water, soil,
direct skin contact, etc.), such that the total dose is the sum of all of the indi-
vidual doses.
The third equation integrates this exposure assessment with the dose—response
relationship. As discussed in the section Relationship Between Dose and Health
Outcome, it incorporates uncertainty factors (and any other modifying factors
that reflect professional judgment regarding scientific uncertainties of the entire
database) with the NOAEL. This creates a benchmark against which to evaluate
the significance of the dose with respect to its implication for health. The U.S.
EPA has estimated potency factors that can be applied for many carcinogens.
(Methodologies to estimate the chance of toxic outcomes other than cancer are
less developed.) The reference dose, or recommended maximum concentration in some
jurisdictions, is the NOAEL divided by the uncertainty factors multiplied by any
modifying factors of concern. The lifetime individual risk is therefore the prod-
uct of the dose multiplied by these response factors. For cancer, this is expressed
as the lifetime excess risk of cancer for an individual exposed at the given life-
time exposure. For noncarcinogenic agents, it is usually assumed that there is a
threshold below which there is no effect. The ratio of the exposure level to the
estimated threshold dose gives some indication of the likelihocd that adverse
health effects will result from exposure to the toxic substance.
One of the greatest water-related projects in Turkey, known as the Lower Seyhan
trrigation Project, was started in the Cukurova regicn in the early 1950s. The ac-
tivities in the project included the construction of a dam on the Seyhan river to
store water for hydroelectric and agricultural purposes; the establishment of a spill-
way for excess water; construction of irrigation canals to distribute the water
throughout the plain and for irrigation of fields; and construction of drainage canals
for excess water from the fields.
The Cukurova authorities did not consider it a danger when malaria-infected
workers arrived from the southeastern part of Turkey (where malaria transmission
still occurred). It was thought that the disease was totally under control because of
the very Imv number of malaria cases reported from the entire country. The con-
sequences of the project can be listed as follows:
I. Populations from areas to be covered by water were resettled around newly ir-
rigated areas.
Productivity of irrigated lands increased.
Insects and different kinds of insecticides were introduced into the area, creat-
ing vector resistence to insecticides.
Irrigation expanded the number of arabic fields, creating an increase in the need
for laborers.
People moved from poorer parts of the country (most of them came from ar-
eas where unnoticed malaria epidemics still occurred) to he seasonal workers
in the newly developing areas.
Seasonal workers settled along the canals (attracted by vegetation and slopes of
less than t%), where water collections became efficient breeding places for
malaria vectors.
Malaria parasites were introduced to the local mosquito vector (An satharovi),
which has a great capacity for transmitting the disease.
S. Industries increased their work on local products because of the agricultural de-
velopment.
The increase in industrial activity created increased demand for workers.
Workers and families gravitated toward industrial activities, resulting in an in-
crease in the population of the Ctikurova region.
if. Unhealthy settlements were established around towns for the incoming popu-
lation.
New, high-rise apartment buildings were built to meet the housing needs of the
newcomers. The underground floors of these buildings became new breeding
places for vectors because of the high level of the water table and deep base-
ment excavation.
Malaria parasites were transmitted to nonimmune local people.
Finally, there was a resurgence of malaria in the area. During 1970, the num-
ber of cases reported in the Cukurova region increased from 49 to 149.
Source: WHO/CEMP, 1992.
ucstions
I. Consider all information that is needed to assess human exposure to a spe-
cific hazard. Consider how this information could be gathered.
What are the advantages and disadvantages of environmental and biolog-
ical monitoring?
Which of the consequences indicated in Box 3.6 are directly or indirectly
related to health? Which of these impacts on human health can be expected to
be positive or negative? Which of these aspects would have to be taken into ac-
count in an EHIA, and what specific information would be needed to assess quan-
titative health risks prior to the onset of the project? What would be needed to
assess quantitative health risks prior to the onset of the project?
CHAPTER CONTENTS
143
THE APPROACH TO MANAGTNG RISK
Risk management brings together the evaluation and perception of risk to con-
trol exposure to hazards (Fig. 4.1). It is partly a scientific, quantitative exercise
in which the results of a risk assessment (Chapter 3) are compared to standards,
guidelines, or comparable risks. Having made this comparison, and knowing the
assumptions, extrapolations, and estimates that go into the two numbers in the
comparison (as discussed in Chapter 3), an environmental health professional
can determine whether a significant risk is present. But the perception of the risk
by the individuals or community facing the risk must also be taken into account.
Of course, the manner in which the risk evaluation is communicated will also
affect risk perception, as will the effectiveness of communicating the plans for
and results of exposure control.
After the risk is evaluated and the exposure is controlled as appropriate, the
risk must be monitored to ensure that it remains under control. Although some-
times the problem can be solved, usually the process is an iterative one in which
the risk must be reassessed and community perception reevaluated on a contin-
ual basis. In reality, this interactive process means that the different steps in risk
assessment and management may be carried out simultaneously.
jcj< FVALUATION
Risk Assessment
Hazard identification
Dose-response assessment
Exposure assessment
+ Risk Management
00 5. Risk evaluation
Risk Characterization 6. Risk perception and communication
Control of exposure
Risk Monitoring
Figure 4.1 Risk assessment and management framework.
Risk Perception
Environmental health professionals often disccvcr that the public perception of
an environmental health risk differs widely from that of scientists. The level of
public outrage toward an environmental health hazard plays a major role in the
acceptability of the risk associated with this hazard. In past decades, it was often
thought that if the public were educated about the risks associated with the haz-
ard, people would find the hazard more acceptable. It is now known that un-
derstanding the risk is only one of many dimensions that affect risk perception
and acceptance. Moreover, this has been shown to be a fairly minor factor rela-
tive to other dimensions. Some of the more important dimensions that affect en-
vironmental health risk perception and the strategies for risk management and
communication in light of these dimensions are shown in Table 4.1. Aside from
these (e.g. voluntarism, attribute of blame, understanding), risks that have de-
layed health effects and those that affect future generations are accepted less
readily than those that are immediately apparent.
Coping Strategies
Many factors influence how people respond to environmental health risks. As dis-
cussed above, one person's perception of a risk may be completely different from
another person's perception. In addition, individuals have different coping strategies
to deal with perceived risk, or stress in general. A distinction can be made between
coping strategies that concentrate on either the individual emotional response, called
emotion-focused coping, or eliminating or reducing the observed hazard, problem-focused
coping. These strategies may involve both direct action and mental processes.
Most of this text addresses problem-focused responses to risks. Viewing an indi-
vidual's health problems in terms of emotion-focused coping may lead the environ-
mental health professional to attribute them to the emotional stress of a situation
(e.g., Chernobyl; see Chapter 9) or to the person's own actions, inability to cope, or
other personal characteristics. This may inadvertently lead to victim blaming, which
in turn may obscure the real threat that a risk imposes and in any case does not help
the professional address the individual in an effective manner. Nonetheless, it is im-
portant for environmental health professionals to have some understanding of cop-
ing strategies to manage environmental health risks appropriately.
Cognitive coping strategies are characterized by the use of thought processes
aimed at the reduction of experienced stress. These mental strategies take many
different forms:
Problem denial. The individual tries to convince himself or herself that the health
risk is exaggerated by others or by the media, and that the authorities will ex-
ercise their responsibility to protect the community.
Coping strategies may lead to direct action-based strategies. These include the
following:
Action aimed at risk reduction. This could be achieved by trying to influence the
decision-making process, for example by demonstrating against a given situation
or organizing action groups.
Searching for information. This could result in a better understanding of the risk
and may be a valuable strategy since unfamiliarity usually relates to overesti-
mation of the risk.
Searching for help. This would include contacting environmental action groups that
can give advice or practical assistance in reducing the risk. Working oil one's feel-
ings in discussion groups is another active form of coping.
Active search for distraction. Immersing oneself in sports, hobbies, or other activi-
ties and avoiding thinking about the problem would characterize this type of ac-
tion.
Emotional modification. Use of tobacco, alcohol, or drugs can be seen as a form of
emotional modification. These coping strategies, however, involve exposure to
health hazards and may result in disrupted social structures, violence, and crim-
inal behavior.
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TABLE 4.2
THE U.S. ENVIRONMENTAL PROTECTION AGENCY'S
SEVEN CARDINAL RULES OF RISK COMMUNICATION
Accept and involve the public as a lcgitiniatc partner.
Plan carefully and evaluate your efforts.
Listen to the public's specific concerns.
Be honest, frank, and open.
Coordinate and collaborate with other credible sources.
Meet the needs of the media.
Speak clearly and with compassion.
Source; Covello and Allen, 1988.
a significant risk of which they may be unaware, or (b) to calm concerns about
a small risk that the public or decision makers perceive as serious.
With increased public concern over various environmental health risks, in-
creasing demands are placed on environmental health professionals to provide
information that explains the nature of risk in clear, comprehensible terms and
that conveys credibility and trustworthiness. Increasing attention has been paid
to risk communication to respond not only to the publics desire to be informed
but also to the need to overcome opposition to decisions and to develop effec-
tive alternatives to direct regulatory control. Such alternatives can require greater
accountability on the part of individuals, agencies, or private corporations.
It must be stressed that merely disseminating information without relying on
communication principles can lead to ineffective messages regarding risk and in-
advertantly convey ineffective control of a hazard. The U.S. Environmental Pro-
tection Agency (EPA) has articulated seven cardinal rules of risk communication
(Table 4.2) to prevent such nuscommunications. In addition to these rules, it
must be emphasized that to provide effective risk communication, the health pro-
fessional must understand the appropriate technical information that may arise.
Because in some countries the public obtains much of the environmental health
risk information from the news media, the guidelines for dealing with the me-
dia in Box 4.1 are wcrth considering.
I. Don't take the questions personally. If you sound defensive the media will pick
that up and push to find out "what you are hiding."
Never say "no comment." This is often interpreted by journalists as an admission
of guilt. Instead, say why you are unable to comment (e.g., "We are currently in-
vestigating the situation and are unable to comment on our findings at this time").
Always tell the truth. If there is a problem for which you share in the responsi-
bility (e.g., errors in judgement were made), explain it, but remember to list
many positive aspects so that the negative ones will be outweighed (e.g., "We
initially had difficulty with our communication procedures, but they have since
been corrected and following this tire, the entire emergency plan will be reviewed
and improved").
Never speculate. Only comment on the facts; the rest is "under investigation,"
"unconfirmed," or "not known."
Don't speak off the record. Unless you have good reasons to believe you can trust
the journalist to honor an agreement to allow you to speak off the record, you should
consider any comments you make to be fair game in the pursuit of a good story.
Substitution
Engineering controls
General ventilation
Exhaust ventilation
Protective harriers
SECONDARY PREVENTION
such as training, or even biological measures, such as immunization. The final inca-
sure of controlling a hazard is secondaiy prevention, i.e., early detection of effects of
exposure and subsequent remediation. The hierarchy of methods for controlling a
hazard is shown in Table 4.3. The same hierarchy of controls can also he used in
environmental health hazard control and in setting standards (Fig. 4.2).
Product Product
standards quality
control Biological
standards
Residue
Product Pro3 I Transformation standards
in tissue
Metabolism
Environmental quality
Emission goals and standards
control Interior
Absorption
Source Emission Dispersion
Figure 4.2 Pollutant pathway showing possible points at which standards may be set. From
de Koning, 1987, with permission.
Product Standards If a substance does not have a known threshold level or has
not been adequately tested, it may make sense to redesign the product to mini-
mize the amount of the substance required, or search for a substitute. Govern-
ments can ban the use of a substance for specific purposes. Sweden, for exam-
ple, banned the use of cadmium except in electroplating, pigments, and stabilizers
for plastics (and soldering if the product does not come into contact with drink-
ing water or food). Governments may also encourage the use of substitutes by
imposing strict labeling requirements.
Emission Standards Emission limits on industrial discharges to air and water, and
more recently to soil, have been in place for decades in many jurisdictions. These
standards may be expressed in terms of the permissible concentration of a pollutant
in units of air emitted or wastewater discharged by a source or in terms of a total
load of pollutant per time, unit of production, or unit of energy or materials input.
Emission or effluent standards may also be expressed in terms of danger to health
or the environment, with a preferred method of control being specified. In this ap-
proach, the best available and economically feasible control technology is used.
Standards can also relate to operating practices, including maintenance mea-
sures to avoid spills, and measures to promote prompt clean-up, careful storage,
and segregation of wastes. They may stipulate rules for cleaning and maintenance
Exhaust hood
Baffles to improve
efficiency
Welding
rod
Shielding
gas inlet
duct
Exhaust -
outlet duct
Work
Exhaust flow requirements must be
determined for each welding operation
and welding gun configuration by
experimental testing with air contaminant
sampling and analysis
Figure 4.3 Examples of local exhaust ventilation for welding. Source: Fact Sheet From
1-lamilton, Ontario, with permission. Canadian Center for Occupational Health and Safety
(CCOHS).
tors, gloves, rubber boots, protective clothing, goggles and safety glasses, hard
hats, and hearing protection. Table 4.4 summarizes the steps and resources re-
quired for a PPE program. Figure 4.4 shows a uranium miner with PPE and mon-
itoring equipment. The International Program on Chemical Safety (IPCS) has pro-
vided guidelines for using PPE and for choosing the proper equipment (see How
to Use the IPCS Health and Safety Guides, UNEP/ILO/WHO, 1993).
Other measures at the level of the target or exposed individual include im-
munization against infectious hazards. Guidelines regarding which workers
Problem analysis: characterizing the relationship between the health problem and
human behavior.
Behavior determinants: identifying the factors that determine specific behaviors.
Options for changing behavior. assessing the relative importance of such determi-
nants and the extent to which they can be changed
Intervention plan: determining how behavior can be changed most successfully
Intervention implementation: carrying out the intervention to change behavior
Evaluation: ascertaining the effect of the intervention.
When the relationship between the health problem and human behavior is not
well established, or when behavior is only of minor influence on the extent of
the problem, an intervention plan for changing behavior is not likely to improve
public health significantly.
badge
Gloves stripes
i meter
ty belt
Radio
Radon /
pump
)veralls
boots
?quired
Figure 4.4 Miner with PPE and personal monitoring equipment. From Carneco, 1996,
with permission.
Attitude
Skills
paints are not available in that town (lack of the alternative option), or they are
too expensive (financial barrier).
Other conceptual models have also been developed to help health promotion
professionals to carry out their duties. One model, which builds upon the
Ottawa Charter's definition of health promotion as activities that enable people
to increase control over the determinants of their health, is known as the
PRECEDE—PROCEED model (Green and Kreuter, 1999). It uses educational ap-
proaches to influence the predisposing factors to unhealthy choices through di-
rect communication, the reinforcing factors through promoting changes in val-
ues that support lifestyle choices, and the enabling factors to permit these changes
through training and organization. While the PRECEDE part of the model ad-
dresses the predisposing, reinforcing and enabling constructs in educational and
ecological diagnosis and evaluation, the PROCEED part addresses the policy, reg-
ulatory, and organizational constructs in educational and environmental devel-
opment. Box 4.3 elaborates on this model and how it relates to the DPSEEA
framework used elsewhere in this text.
The figure below illustrates the PRECEDE—PROCEED model (Green and Kreuter, 1999),
indicating that the place to start is to conduct a social assessment in a community, as-
certaining the perspectives of the community members, their hopes, aspirations and
concerns. Next, an epidemiological assessment is conducted to ascertain the health prob-
lems and risk factors. Phase 3 involves identifying the health-related behavioral as well
as physical environmental factors that may he predisposing (e.g., knowledge, attitude,
values of the individuals concerned), reinforcing (e.g., attitude and behavior of deci-
sion-makers) and enabling factors (e.g., availability of resources and skills) underlying
the concerns identified. Phase 4 focuses on assessing the policy and administrative is-
sues that must be addressed, and phases 6 through 9 are the implementation, process
evaluation, impact evaluation, and outcome evaluation steps.
PRECEDE
4 Phase 3 1 Phase 2 Phase 1
Behavioural & Epidemialogical Social
Environmental
aiTeJ Assessment LAssessment AssessI1(J
reuter 1999
shading in
r and dab-
Force -Pres -
•e then cor-
relating to
regulatory,
then corre-
it, whereas
xperts. The
decade or
ming to re-
Jerry Spiegel
RISK MONITORING AND IJSF OF INDI1ATORc
The test must he sensitive and specific. Sensitivity refers to the proportion of dis-
eased persons in the population who are correctly identified by the test. Speci-
fic/tv refers to the proportion of nondiseased individuals who are correctly iden-
tilied as such by the test. (An insensitive but specific test may yield many
false-negative results (c), whereas a sensitive but nonspecific test may give many
false positives (h(. Note that a posit/ic predictive value refers to the proportion of
persons who have a positive test and are truly diseased. A neqative predictive value
refers to the proportion of persons who have a negative test and are not diseased.
These two indices depend on the sensitivity and specificity of the test and the
prevalence of the disease. They are quoted less often than the sensitivity and
specificity of a test, but should he considered when discussing the usefulness of
a screening test.
The test must he simple and inexpensive.
The test must he safe. The test must have a very high degree of salety as it is
meant to he applied to a large number of normal people who likely have only a
very small risk of the condition in question.
The test must he acceptable. The test cannot be inconvenient, time consuming,
ttncomlortable, or unpleasant to the sttbjects beit1g offered the screening.
Source: Fletcher et al., 1982.
4.5. In this case, only when biological tTH)flitoring for occupational lead poisoning
through centralized reporting of blood lead results was combined with industrial
hygiene controls and enforcement of lead in air criteria did a sustained decrease
in occupational lead poisoning occur (Yassi et al., 1991, 1996).
An analysis was conducted of 16,199 blood lead samples from employees of nine
high-risk workplaces in Manitoba, 1979-94, as part of an integrated regulated oc-
cupational surveillance system. Adjusted median blood lead levels were analyzed,
as was the proportion of levels above the regulatory target over the years. Trends
in individual workers and in each of the targeted firms were also examined.
It was found that a 1979 government regulation specifying the maximum al-
lowable lead in blood as 3.38 Mmol/liter (70 j.rg/dl) was followed by a drop in blood
lead concentrations; the 1983 order to reduce maximum allowable blood lead con-
centrations to below 2.90 mol/liter (60 .rg/dl) was not followed by such a decrease.
Longitudinal analysis by individual worker suggested that companies were comply-
ing by using administrative control—i.e., removing workers to lower-lead areas un-
til blood lead levels had fallen, then returning them to high-lead areas.. In 1987 a
further order was issued that required removal of workers from a site when their
blood lead level was 2.40 j.rrnol/liter (50 ig/dl) and limited environmental expo-
sure to 50 g/m 3 . This new integrated approach succeeded in bringing about a sig-
nificant reduction in blood lead concentrations overall as well as in most of the high-
risk companies. Moreover, this seems to have been accomplished in most companies
without their having to rely on worker rotation.
50
45
40
-J
- 35
-
C)
,?; 30 .- .
-D
25 /N.
Reduce
20 blood Pb to
0
0
15 <70.tgIdL Reduce
blood Pb to Reduce
it. <60pg/dL
blood Pb to
<501.tg/dL
The study concluded that while having an appropriately stringent blood lead tar-
get is essential, focusing upon blood lead as the sole criterion for compliance is in-
effective. Regulations must specifically require environmental monitoring and ex-
posure controls, with biological surveillance serving to ensure effectiveness of these
nteasures. The analysis that was conducted illustrates the usefulness of a compre-
hensive, centralized surveillance system linked to inspections and enforcement, as
it was invaluable in targeting preventive measures and ensuring the effectiveness
of regulatory efforts.
Source: Yassi et al., 1991, 1996.
The linkage between environmental indicators and health indicators is key to ac-
curate monitoring of environmental or occupational health risks (Briggs ef al., 1 996;
Corvalan et al., 1997). To visualize these linkages, Corvalan and Kjellström (1995)
developed the driving force—pressure—state—exposure—effect—action (DPSEEA) frame-
work (Fig. 4.6) as an adaptation of the pressure—state—response (PSR) framework
used by the Organization for Economic Cooperation and Development (OECD) and
the United Nations in the development of indicators for sustainable development
monitoring. The environmental indicators listed in Table 4.5 are primarily state in-
dicators and some of the proxy/surrogate indicators are pressure or driving-force in-
dicators. Figure 4.5 highlights the importance of exposure in environmental health
risk monitoring and the need to include action indicators in monitoring risk man-
agement implementation. A recent example of use of the DPSEEA framework by a
community to assist in developing indicators to evaluate interventions aimed at im-
proving health in an urban ecosystem is provided by Yassi et al. (1999).
Clean
technologies
Cleane
[PRESSURE Production Consumption Waste
produchon:
release
waste
Figure 4.6 Framework for environmental health indicators. Modified from Corvalan and
with permission.
Kjellstrom, 1995,
Step 1: Evaluate The Problem The major role of the health practitioner at this
step is as an advisor and resource for technical information. To perform this role,
the health professional needs the most accurate possible information on the fol-
lowing:
This information may change constantly during a real episode. In a typical inci-
dent, there are innumerable false reports, doubts, and updates. The practitioner
involved must be prepared to be flexible.
Correct identification of the substances involved is essential. Labels on drums
may be misleading because drums are often recycled. Samples should he taken
by an environmental health specialist or industrial hygienist who wears suitable
personal protective equipment. Unless there is a compelling reason to act, such
as during a fire or a rapid leak, it is usually wise to let the material rest where
it is until the material is identified and suitable precautions can be taken. If an
emergency forces action before the material is identified, the only prudent move
is to assume the worst unless one has evidence that the material is not highly
toxic. Unidentified materials usually turn out to be fairly benign. Until they are
identified, however, they often cause great anxiety by requiring the use of full
protective gear by emergency response personnel. Once the identity of a mate-
rial is known, the hazard potential must be determined. There are a number of
sources of information on the toxicology and safety hazard of common indus-
trial and commercial chemicals.
Users of hazardous materials are required by law in many jurisdictions to keep
on file a Material Safety Data Sheet (MSDS) prepared by the manufacturer (sec
Chapter 3). The MSDSs usually give reasonable information on the safety haz-
ard of chemical formulations, but they are almost always incomplete in their de-
scriptions of the compound's toxic ellects and are usually weak or missing in-
formation on chronic effects. Many chemical formulations are proprietary
mixtures, thus their formulations are considered trade secrets and the MSDS may
not identify specific chemicals or their proportions. The MSDSs in the files of
many companies are also often incomplete, and not all pertinent MSDSs may be
available on short notice.
Other sources of information, such as medical libraries, are familiar to physi-
cians for clinical information. Law libraries also often have information On tox-
icology. Both usually carry the standard reference works in toxicology and can
order computerized literature searches for users. Many familiar medical texts have
• International Registry for Potentially Toxic Chemicals (TRPTC) toxicity profiles and
legal titles
The IPCS is a joint program of the World Health Organization. the International Labor
Organization (1LO), and the United Nations Enviromnent Program (UNEP).
Not everyone in the community will actually be exposed, of course, and for pur-
poses of planning a medical response, it is important to consider the character-
istics of the persons who may actually come into contact with the material. Chil-
dren may develop skin rashes from direct contact: fumes may he merely annoying
to the young and healthy, but could be troublesome or life threatening to the
elderly, those who have cardiovascular or pulmonary diseases, to infants, or to
asthmatics. Pregnant women require special attention to protect mother and foe-
tus. Knowledge of the community at risk allows health authorities to warn sus-
ceptible individuals to take protective measures or to leave the area.
Step 2: Contain the Problem The next step in managing an environmental health
emergency is to establish control over the situation to minimize the potential of
exposure. This requires teamwork among police, fire, and public health author-
ities and obviously varies with the nature of the incident. The physician still serves
as an advisor in this step. In more complex situations, coordination among and
with local authorities is essential. Fire departments are usually best equipped to
handle safety hazards but often need advice and assistance in dealing with toxic
materials. The most difficult situations, such as fires involving multiple toxic sub-
stances, known and unknown, pose serious threats to public safety personnel
and may require on-site medical presence.
In extreme situations, evacuation may be unavoidable. The mental health
consequences of evacuation arc great and this extreme step should ncver be taken
without good reason. Large-scale population evacuations carry a high cost in
stress and safety, as well as the potential for violence.
An important aspect of containing the problem is to prevent public overre-
action. An incident like this provokes rumors and misinformation that must be
set straight to avoid panic or misguided interference in public safety measures.
Early establishment of a rumor control committee, a hotline, and good working
relations with the media can be very valuable. It is particularly important to fun-
nel all public information, whenever pcssiblc, through a single spokesperson.
Otherwise, slight differences of opinion, interpretation, and understanding may
look like confusion, uncertainty, and rivalry among responsible authorities.
Step 3: Manage the Health Effects Most practitioners feel uncertain and over-
whelmed when called on to deal with complex toxic exposures. Although these
cases are admittedly complex, there are certain guidelines that can be folk wed.
There are two separate problems that the health practitioner faces: evaluation of
The use of benefit-cost analysis (BCA) in managing environmental health risks has
expanded rapidly in recent years. Basically, in this analytical technique the
present value of benefits is compared with the present value of the costs to de-
termine the net present value of the management option under review. Cost-
effectiveness analysis (CEA) is similar to BCA in its treatment of costs, however, the
consequences of interventions (i.e., results, impacts, effects, outcomes) are not
valued. Instead, the PUoSC of this analysis is merely to determine the costs in
relation to the benefit achieved, measured in terms of natural units, e.g., addi-
tional years of life, case of disease incidence, etc.
BCA 6- CEA provide practical techniques for determining whether resources
are being allocated efficiently in achieving objectives. In this regard they provide
powerful tools for planning 6- evaluating alternative programs related to envi-
roninental health risks.
In BCA the value of the benefits is compared with the value of the costs, with
each of these measurements entailing three steps: (I) identification of the type of
elfects, (2) quantification in concrete terms, and (3) valuation. First, all items of
cost must be identified, uninhibited by potential measurement difficulties. The
costs to be considered include the initial design and implementation of the pro-
TABLE 4.7
SUMMARY OF STEPS INVOLVED IN CONDUCTING BENEFIT-COST AND
COST-EFFECTIVENESS ANALYSES
Define the study scope and objectives.
Define and measure the outcomes or effects of each option under analysis.
Identify, measure, and valtte all costs.
Identify, measure, and value all benefits.
Compare the costs with benefits, along with sensitivity tests of the magnitude of the costs and
benefits where uncertainty may exist regarding measures of outconhe or its value.
Define the implications of the results for presentation to decision makers.
In the 1950s and 1960s Japan experienced a period of rapid industrialization and
economic growth, but little attention was paid to the environmental consequences.
The result was high levels of pollutants in the air, water, and soil in some areas and
several infamous outbreaks of diseases. Strong corrective action was taken in the
1970s and 1980s to redress the most severe problems. Three conclusions emerge
from the examples given below: allowing the release of toxic substances into the
environment can lead to serious health consequences and economic losses; pre-
venting the problem, as Japan is doing now, is less costly than cleaning it up; and
taking corrective action now is less costly than allowing problems to persist.
Between 1956 and 1973 one of Japan's largest petrochemical complexes was con-
structed at Yokkaichi City. By 1960 air pollution was causing local concern, and by
1963 1-hr average sulfur dioxide levels exceeded 2800 rg/m 3 , far above the WHO's
suggested maximum of 350 rg/m. In 1967 local residents successfully sued six com-
panies, claiming medical costs and compensation for lost income. Seven percent of
the total population of the district was certified to have been medically affected by
ambient air pollution. Increasingly stringent pollution measures were introduced in
1970, and by 1976 sulfur dioxide levels were in compliance with local standards.
Air pollution control costs since 1971, including technical installations and their
operauon, monitoring, and creation of environmental buffer zones, have been $114
million a year. Without this investment, however, medical expenses and compen-
sation would have been more than $160 million a year.
At the turn of the century, Minamata was a scenic coastal town of 12,000 people
who made their living from wood products, oranges, and fish. In 1908 a fertilizer
plant was established that eventually became the Chisso Corporation, one of Japan's
largest manufacturers of chemicals. By the 1920s compensation for damage to fish-
eries had already become an issue, and in 1956 patients with a severe neurological
affliction, later to be called Minarnata disease, were observed.
In 1968, following extensive research, the disease was linked to the ingestion of
seafood containing high concentrations of methylmercury, a compound discharged
into Minamata Bay by the Chisso Corporation as a by-product of the manufacture
of acetaldehyde. The discharge of methylmercury peaked in 1959; it ended in 1968
when the company ceased production of acetaldehyde, but by then the floor of the
bay and its aquatic life had become heavily contaminated. Starting in 1974, 1.5 mil-
lion cubic meters of polluted sediment were dredged and removed.
By 1991, 2248 people (1004 of whom had died) had been certified as suffering
from Minamata disease and were eligible for compensation. An additional 2000 peo-
ple were pursuing claims for compensation. Had the discharge of mercury contin-
ued, the estimated annual costs of the damage, including paneni treatment and com-
pensation, sediment dredging, and losses to fisheries, would have been $97 million
a year. If acetaldehyde production had continued, pollution abatement through in-
plant waste recycling would have cost only $1 million a year.
Oflhj1ii, 1)
174 Basic Environmental Health
(continued)
CASE 3: CADMIUM IN THE SOIL
In the late 1940s a disease characterized by extreme generalized pain, kidney dam-
age, and loss of bone strength appeared in the Jinzu River Basin. The disease, which
primarily afflicted women, was called itai-itai ("It hurts, it hurts!") after the cries of
the sufferers. After two decades of research in 1968 the conclusion was drawn that
the cause was chronic cadmium poisoning, which was traced to the effluent from
the Mitsui Mining and Smelting Company located in the upper reaches of the basin.
The route for the cadmium poisoning was from river water to irrigation water to
129 people had been certified as itai-itai sufferers, and 116 of
soil to rice. By 1991,
them had died.
A major program of soil restoration was initiated in 1979. By 1992, 36 9% of the
contaminated area of 1500 hectares had been treated. Had the further release of
cadmium not been prevented, the annual costs from medical compensation, agri-
cultural losses, and soil restoration would have been $19 million a year. The costs
of prevention were $5 million a year.
Soutie: World Bank, 1993.
of different health stales where known probabilities can be used to assess the rel-
ative willingness to pay for improved health risks. (Details of these methodolo-
gies are beyond the scope of this basic text.) Similar techniques may he applied
to determine preferences among different health states SO that quality-adjusted
life-years can be used as a common denominator to compare the benefits of dif -
ferent risk reduction interventions.
The SCOC of the study is also important to define. Typically BCA studies are
microeconomic in focus and assume prices where quantities of other goods or
services remain unchanged as a consequence of the project or policy interven-
tion. Generally, for occupational health and safety interventions or relatively lo-
calized air or water pollution interventions, this assumption is reasonable. Flow-
ever, in the case of assessing the environmental health impacts of rapid population
growth, OZOflC depletion, and related global warming, the BCA framework may
be difficult to apply. Box 4.8 presents three cases in Japan that illustrate how
prevention would have been cheaper than the costs involved in treating and
compensating those affected by pcllution.
Increasing numbers of articles and textbooks are addressing BCA and CEA in
environmental health decision making. Principal issues in the use of economic
analyses in the environmental health field include the definition of options, the
perspective of the analysis, valuation, issues of benefit cost distribution, and the
scope of the study. Each of these will he addressed briefly below.
With respect to defining the options, it is generally accepted that a BCA or
CEA is not complete until an assessment is conducted for more than one op-
tion or alternative. In the environmental health area, this may entail alterna-
tive approaches, e.g., using alternative technology, regulation capacity, or in-
formation monitoring. The following example of residential radon exposures
illustrates how BCA can be applied by environmental health authorities to de-
termine the economic it1lplications of taking steps to reduce residential expo-
sure to radon gas.
The Potential Health Risk In the case of radon, risk assessment evidence on the
health risks are well documented—by case studies, animal tests, and epidemio-
logical investigations. As early as 1556, excess deaths attributed to an unusual
and fatal chest disease were noted among Central European miners. Over the
years, as knowledge expanded, such disease became clearly linked to exposure
to radon and its radioactive decay products. Over 20 case–control studies of oc-
cupational cohorts have confirmed the association between exposure and lung
cancer. The International Agency for Research on Cancer (IARC) confirmed radon
as a lung carcinogen in 1988 (see Chapters 2 and 9 for discussion of radiation
and its health effects).
In 1988, a blue ribbon panel of experts organized by the (U.S.) National Re-
search Council's Committee on Biological Effects of Ionizing Radiation (BEIR-IV)
developed a consensus position on a dose–response model, with implications that
residential exposure could constitute a serious hazard. Epidemiological studies,
however, have not produced conclusive results. Nevertheless, while consensus
on this issue has not been reached, the suspicions about a connection between
radon and lung cancer have more evidence to back them up than other recog-
nized hazards have.
The Potential for Exposure Radon is a naturally occurring inert gas formed by
the radioactive decay of radium-226, which itself is a product of the decay of
uranium-238. It is present at varying levels of concentration in all rock, soil, and
water. While present in ambient air at low levcls, concentrations can he consid-
erably higher in closed structures (such as houses) if the gas is allowed to infil-
trate. Testing has confirmed that the distribution of radon in homes within a re-
gion tends to be log-normal (that is, most homes have low levels, whereas a small
number produce high readings). The levels observed, particularly at the higher
end, correspond to a range of exposures where a health effect would be expected,
especially considering the large numbers of people who arc potentially exposed.
The Cost of Prevention Although radon occurs naturally, the level to which hu-
mans is exposed is influenced by the technologies used in housing construction
and operation. Research has confirmed the effectiveness of various methods to
reduce exposure in new and existing homes—from better construction techniques
to active ventilation systems for blocking the entry of soil gas into a hime. The
costs, originally estimated from experimental work in the 1970s
at approximately
$7500 (Canadian) per home, have been revised downward substantially.
Step 1. Define the Study Scope and Objectives A Canadian study (Letourncau Ct
al. 1992), considered five different program options to reduce radon exposure
• estimating the relative benefits of different residential radon risk reduction op-
tions
• identifying the conditions (e.g., implications of acting at different exposure lev-
els that would result in the greatest benefit in relation to the costs.
Step 2. Select the Most Appropriate Outcome Measurement Because lung cancer
is the health outcome of concern, measures for determining cost-effectiveness
would include such things as cost per cancer case averted, cost per life saved,
and cost per additional life-year, or cost per radiation exposure reduction. These
measurements provide a way to summarize how much money would have to he
spent for each unit of benefit produced. This avoids ethical issues and other con-
troversies that must be encountered in estimating the value of each unit of ben-
efit (in other words, placing a dollar value on a life).
Step 3. Identify, Measure, and Value all Costs Costs were explicitly identified for
each program option under review, based on current practices and technologies
(notably at levels well below those that had been originally estimated from ex-
perimental remcdiation research). For example, the cost of a screening test was
set at $35, the cost of sub-slab depressurization for an existing home at $1 500,
etc. As costs in the options under review are incurred over a 10-year period,
these must be discounted (at a designated interest rate) to allow options to be
estimated at present values.
Step 4. Identify, Measure, and Value all Benefits Benefits were based on estimates
of the effectiveness of the mitigation in reducing exposure (measured in working
level months IWLMI of radiation exposure) and then estimating the health ben-
Step 5. Compare Costs with Benefits (and Apply Sensitivity Tests) Results of the
Canadian study are provided in Table 4.8. At a national level (based on the results
of national testing conducted in 19 different cities to determine levels of exposure),
the greatest cost-effectiveness ($33,000 per WLM reduced) was determined to he
associated with the option of testing at point of sale and mitigating if concentra-
tions exceed the Canadian "action level" guideline of 800 Becquerels/m 3 .
Comparison of the right column with the left column shows that lowering
the action level (to 150 Bq/m 3 , which is in effect in the United States) for these
options nationally would make the cost-effectiveness more attractive—for ex-
ample, the cost-effectiveness ratio would be reduced to $15,000 per WLM re-
duction. (Sensitivity tests conducted to consider the implications of varying the
interest rate used to discount future costs indicated that the adoption of a 1 0%
discount rate would lower the cost-effectiveness ratio further—to $9000 per WLM
reduced.)
Comparison of estimates for a program to reduce radon risk in cities with high
and low mean levels of exposure showed that there can be dramatic differences
in the cost-effectiveness of preventing lung cancer cases. The two cities chosen
for comparison are a city with high exposure (Winnipeg) and one with lower
exposure (Vancouver). Analysis of BEIR-IV and others of the dose–response data
showed that for every exposure reduction of one WLM, four cancer cases could
he avoided. It would cost $8000 to avert one case of radon-induced lung cancer
in Winnipeg, but over $50,000,000 in Vancouver; Vancouver has high screen-
ing (testing) costs and very little mitigation, whereas in Winnipeg, a smaller city
with high exposures, there are much smaller screening costs and considerably
more mitigation.
T,BTE 4.8
COST-EFFECTIVENESS RATIOS FOR RADON MITIGATION OPTIONS IN CANADA
Cost-Effectiveness Ratio
($1 0001WLM Reduced)
National Application of Various Options @800 Bq/m 3 @150 Bq/m 3
Mitigate existing homes 54 25
Change building codes 75 -
Retrotit to changed building codes 74 64
Screen point of sale and mitigate 33 15
Screen point 01 sale and mitigate, and change building code 74 65
WLM, working level months, a unit ot radiation exposure
Stud9uestinnc
The construction of a depot for chemical waste is planned near a residen-
tial area. Several residents perceive this new situation as threatening to their
health and that of their families. Give examples of possible coping strategies that
can be characterized as emotion focused or problem focused.
Consider the advantages and disadvantages of a "best practical means" ap-
prcach as compared to an emission or effluent standard. Which best preserves
environmental quality in nonpolluted areas? Which best encourages the devel-
opment of new abatement technology? Which is most related to actual health
effects?
Think of an example of the use of immunization in an occupational health
context and consider the advantages and disadvantages of this practice. Should
this immunization be mandatory? Why or why not?
Consider whether you agree with the statement that personal protective
equipment should he a last resort. Why or why not? Under what circumstances?
Consider to what extent the control measures at the person, indicated for
the occupational environment, could also be effective to control for ambient
exposures. Indicate if you regard such control options desirable for the general
public.
CHAPTER CONTENTS
Overview of Air Pollution Industrial Air Pollution
Aerosols Types of Industrial Air Pollutants
Gases Air Pollution from Industrial Acci-
Inhalation dents
Common Health Effects of Ambient Air Air Pollution in the Workplace
Pollution Air Pollution and the Community
Health Effects of Specific Air Pollutants Magnitude and Sources of Ambi-
Ozone ent Air Pollution
Sulfur Dioxide Ambient Air Quality Standards and
Oxides of Nitrogen Guidelines
Particles Control of Ambient Air Pollution
Carbon Monoxide Indoor Air Pollution
Volatile Organic Compounds
Trace Metals
IVIII
human, plant, and animal health. For example, there is good evidence that the
health of about I billion urban dwellers is compromised daily because of high
levels of ambient air sulfur dioxide concentrations (see the section Control of
Ambient Air Pollution, below; WHO, 1997). Air pollution affects health most
clearly when compounds accumulate to relatively high concentrations, produc-
ing an adverse effect on the body, e.g., bronchoconstriction or other asthmatic
symptoms. Recent studies have shown that even low levels of exposure to fine
particles can produce illness and deaths in a community. Often, this effect is not
visible against the greater number of cases of illness or deaths caused by other
factors, such as hot weather. Air pollution can also affect the properties of ma-
terials (such as rubber), visibility, and the quality of life in general.
Although people have caused air pollution ever since they learned how to
use fire, anthropogenic air pollution has increased rapidly since industrialization
began. In addition to the common air pollutants, many volatile organic com-
pounds, inorganic compounds, and trace metals are emitted into the atmosphere
by human activities. Worldwide, almost 100 million tons of sulfur oxides (SO s ),
IF7190
may receive emissions for days on end. When conditions are right, usually in the
1970
SOx 1980 OECD countries
1990
r —i rest of world
NO 1980
990
1 190
SPM
19701
Co 19801
____i1 990
Figure 5.1 Anthropogenic emissions of air pollutants. From UNEP, 1992a, with permis-
sion.
AIR 181
morning or when there is descent of air from higher altitudes, a special atmo-
spheric condition is created that is called an inversion. In an inversion, the tem-
perature rises with increasing altitude rather than falling, which is normally the
case. An inversion layer is a mass of air with an inverted temperature gradient
(warmer above, cooler below). The motion of air in an inversion layer is sup-
pressed and it limits the mixing and dilution of air pollution. Inversions are very
common, especially in valleys and coastlines. The worst episodes of air pollution
usually occur when inversions stay in place for days on end and the atmosphere
underneath receives air pollution day after day with no mixing or wind to di-
lute it.
Air pollution is a very complicated physical and chemical system. It can he
thought of as gases and particles that are dissolved or suspended in air respec-
tively. Many air pollutants interact with one another to produce their effects. The
severity of air pollution changes with the season, with daylight, with industrial
activity, with changes in traffic, with the prevailing winds, and with precipita-
tion (rain or snow), among many relevant factors. The composition of air pollu-
tion, theretore, is not constant from day to day or even week to week, but tends
to cycle. Average levels go up and down fairly consistently depending on the
time of year, but the actual levels are highly variable from one day to the next.
Aerosols
Small solid or liquid particles (line drcps or droplets) that are suspended in air
form a mixture called aerosols. Forming are complex systems in air pollution.
Aerosols often consist of a mixture of solid-phase particles, combined solid- and
liquid-phase particles, and sometimes liquid droplets suspended in air. Even
aerosols that are predominantly solid may contain absorbed water. On the coast,
some aerosols are formed by salt water droplets.
Dust consists of particles in the solid phase. The term is usually used for the
particles themselves or the accumulation of particles after they have settled or
have been deposited. When they arc up in the air, the particles are called sus-
pended particulate matter. This term is usually reserved for particles that are cre-
ated by dry pri cesses and are chemically and physically unchanged from the orig-
inal material except for their size. Smoke consists of particles in both the solid and
sometimes liquid phase and the associated gases that result from combustion.
Smoke is very complicated chemically and varies in composition depending on
what has been burned. Tobacco smoke and air pollution are both examples of
smoke and both undergo chemical transformations over time as they age. Ash is
the solid phase of smoke, particularly after it settles into a fine dust.
The most important characteristics of aerosols that determine their behavior
are size and composition. Size affects how the particle will travel in air and com-
position determines what will happen when it settles or lands on something. The
range in size of common particles associated with different constituents of air
pollution and occupational exposures is shown in Figure 5.2.
The individual particles in aerosols may he relatively uniform in size, or
monodispersed, or highly variable in size, or polydispersed. In nature, all aerosols
are polydispersed. Monodispersed aerosols are most commonly created for re-
search and for certain medications where it is important for the droplet or par-
Figure 5.2 Range of particle diameters from airborne dusts and fumes. Adapted from Levy
and Wegman, 1988, with permission.
AIR 183
especially fine particles are mostly caused by certain types of combustion, asso-
ciated with diesel exhausts, power plants, and other forms of rapid, hot com-
bustion. Small particles of around 10 ,im may also be formed by the aggregation
of fine particles, around 2.5 Am. Fine particles generally consist of a matrix of
carbonaceous compound, and dissolved or abscrbed or solid-phase sulfate, ni-
trate, and trace metals and some water. The effects of small particles on the body
are different from those produced by larger particles and are considered more
toxic. The composition of an aerosol determines the chemical reactivity of its par-
ticles and their density.
From the human health perspective, however, the most important aspect of
particle size relates to how a particle behaves in the respiratory tract. In discus-
sions of health a special measure of size, the aerodynamic diameter, is used, which
is different from the actual measurement of the particle and reflects the behav-
ior of a particle more accurately than a physical measurement would. The aero-
dynamic diameter of a particle is defined as the diameter of a sphere with a den-
sity of 1. This means that if the particle in question had the density of water they
would both settle at the same velocity. This measure allows one to compare par-
ticles that are different in shape, density, or mass. For example, a piece of fluff
(e.g., cotton) has a relatively large surface but a low density and will therefore
be easily suspended or carried away by the wind. Thus it has a small aerody-
namic diameter whereas its geometric diameter is relatively large. From this point
on in the text, the size of particles will be expressed in terms of the aerodynamic
diameter measured in micrometers. Larger particles have more mass and thus
more inertia; they are less likely to make it through the twists and turns of the
human respiratory tract.
The effect of particles on the body reflects the efficiency with which they pen-
etrate all the way to and within the lung and their chemical reactivity and tox-
icity once they arrive. Larger particles carry much more substance but are much
less likely to have an effect on the body because they do not penetrate into the
lower respiratory tract (belcw the first division of the windpipe, or trachea). The
largest particles, visible to the naked eye as specks of dust, are mostly filtered out
in the nose. Particles above 100 Am may be sources of irritation to the mucous
membranes of the eyes, nose, and throat but they do not get much further. Those
particles below this cutoff make up the inhalable fraction because they can be in-
haled into the respiratory tract. Particles larger than about 20 Am generally do
not enter the lower respiratory tract, below the throat (trachea). Those particles
below 20 im comprise the thoracic fraction because a high proportion can pene-
trate into the lungs. Particles below 10 Am enter the airways with greatest effi-
ciency and may be deposited in the alveoli, or airspaces, that are the deepest
structures of the lungs. Particles between 10 Am and 2.5 .tm are called coarse
particles. Particles below 2.5 lm are deposited in the alveoli with very high ef-
ficiency and are called "fine particles." Particles below 0.1 jm are called "ultra-
fine particles." Air pollution is predominantly in the coarse and fine range.
Notwithstanding the efficiency of penetration, ultrafine particles, smaller than
about 0.1 Am, tend to remain suspended in air and be breathed out again un-
less they carry an electrostatic charge. Thus, as a practical matter, the greatest
penetration and retention of particles is in the range 10.0 to 0.1 tm, which is
100
20
Primary bronchi
10
ondary bronchi
Terminal
bronchioles
called the respirable range. This is because particles in this range can be inhaled
all the way to the deepest structures of the lung. These patterns of deposition are
shown graphically in Figure 5.3.
Once in the lung, particles may have different effects, depending on their size.
Particles predominantly in the size range between 10 and 20 jim are more likely
to have effects on the airways. A large proportion of particles below 10 jim but
above 0.1 jim may be retained in the lungs. When they accumulate in large num-
bers and the lung responds to their presence, they may cause a type of disease
called pneumoconiosis; this is seen following high exposures, usually over several
years, in occupational settings. Pneumoconiosis is not a consequence of ambient
air pollution where the effects tend to be on airways rather than alveoli.
In air quality studies, the total aerosol suspended in air once was measured
as total suspended particles (TSP) or an optical measurement known as "British
Smoke." This measurement reflects the perception of smoke in the air and di-
minished visibility. These measurements are comparatively easy compared to
measurements of coarse and fine particles. PM 10 and PM2.5 have become the pre-
ferred measurements of particulate air pollutiin. Ultrafine particles are very dif-
ficult to measure.
Although disregarded for purposes of measuring the size of the particle, shape
is important in determining the effects of a particle. The human body handles
longer and thinner particics, called fibers, somewhat differently from particles that
are more rounded in shape because fibers are more difficult to remove from the
lungs by natural protective mechanisms. The very long and thin shape of fibres
of asbestos are particularly damaging to the lung and can cause lung cancer and
mesothelioma of the pleura. Fibers are described by the ratio of their length to
their width. A particle at least five times longer than it is wide is considered to
be a particle.
Liquid constituents of air pollution exist as aerosols, either as liquid-phase
particles, which are droplets, or in association with solid-phase particles. Liquids
that are constituents of air pollution are always aqueous, or water-based, because
AIR 185
droplets of more volatile organic compounds evaporate to the gaseous phase very
quickly. A cloud or dense collection of droplets is called a mist.
Small solid-phase particles also contain a small amount of absorbed water.
Both liquid- and gas-phase constituents of air pollution are often attracted to and
ride on the surface of solid particles; this is called adsorption (not to be confused
with absorption, in which the liquid or gas is actually taken into the particle).
The humidity in the atmosphere is an important determinate of the water
content of particles; the lower the humidity, the faster the water evaporates. A
particle may be reduced to a solid phase, which is called a droplet nuclei. Droplet
nuclei are small and easily inhaled and are particularly important in the spread
of some infectious diseases such as tuberculosis, when they come from an in-
fected person who coughs. Dry particles may also take on water when they are
released into a humid atmosphere. Small particles typically absorb large amounts
of water if it is available in the atmosphere; these are said to be hygroscopic.
Through this absorption mass is added to the particle and its capacity to carry
other dissolved constituents may be increased. Air pollution from the same types
of sources may therefore be different in humid climates and dry climates.
There are processes in the atmosphere through which liquid is converted to
gas and hack again or liquid is converted to solid. Volatile liquids may evaporate
to become gases. The evaporated compound in the gas phase is called a vapor and
behaves like a gas in air pollution. Droplets may also form from condensation of
vapor in a saturated atmosphere. Fog is a familiar example of an aerosol of liq-
uid water droplets that forms from condensation in an atmosphere saturated with
water vapor. Droplets may also form from ocean spray. Droplets often form by
condensation of liquid around a small solid particle. In coastal areas, the droplets
of seawater may evaporate to form solid-phase particulates that contain salt (this
is an important source of PM 10 near oceans).
Precipitation, in the form of rain and snow, reduces air pollution by dissolv -
ing soluble gases and by attracting and holding small airborne particles, bringing
theni down to the ground. The air may then be much cleaner, but the con-
stituents of air pollution in the rainwater or snow may present a serious prob-
1cm (acid rain; see Chapter 11, Acid Precipitation). Acid-forming compounds,
such as sulfates and oxides of nitrogen, reduce the pH in exposed lakes and soils
(surface water acidification), which if it exceeds the buffering capacity of the wa-
ter may lead to fish deaths and other ecological damage.
Gases
Air pollution can also consist of gaseous constituents, the iroperties of greatest
importance being solubilitv in water and chemical reactivity. At concentrations found
in air pollution, solubility is a major determining factor of the health effects of
gases. Relatively soluble constituents of air pollution include nitrogen oxides or
sulfur dioxide, which may be ionized in water and which in the atmosphere may
coalesce to form ultrafine particles and fine particles. In addition, a number of
gases occurring more commonly as occupational exposures are water-soluble, in-
cluding hydrochloric acid vapor and ammonia. Other gases, such as ozone, hy-
drogen sulfide, and organic compounds are less soluble.
Solubility for gases is much like size for particles; it is a characteristic that de-
Inhalation
Inhalation of toxicants often constitutes the most rapid avenue of entry into the
body because of the intimate association of air passages in the lungs with the cir -
culatory system. On inhalation, soluble gases tend to dissolve into the water sur-
face of the pulmonary tract; insoluble gases generally penetrate to the alveolar
level. Because the alveoli bring the blood into very close and direct proximity to
air, gases may pass directly across the alveolar membrane and into the blood-
stream very efficiently. Particles, once deposited in the alveoli, may dissolve and
release their constituent compounds. The degree to which they enter the blood,
are circulated, and delivered to the body's tissues depends on the concentration
inhaled, duration of exposure, solubility in blood and tissue, reactivity of the
compound, and the respiratory rate. (The respiratory rate determines how much
air is breathed in and therefore the total amount taken into the body.) Unlike
many toxic substances that are ingested and therefore passed through the liver
and metabolized, inhaled compounds are not significantly metabolized prior to
circulation throughout the body. They may therefore have a direct and immedi-
ate effect, not unlike direct injection into the bloodstream. To understand the
health problems associated with airborne contaminants it is essential to have at
least a basic understanding of the structure and function of the respiratory tract.
Anything that decreases the partial pressure of oxygen in the alveoli reduces
the oxygen available for exchange and thus deprives the body of oxygen. At high
altitude, the partial atmospheric pressure is lower than at sea level and the cor-
AIR 187
responding pressure of oxygen in alveoli air also decreases, reducing the satura-
tion of blood with oxygen. When the oxygen in air is displaced by another gas,
so that there is not enough to support life, or when a person is prevented from
breathing, it is called asphyxiation. Substances that dilute or displace the oxygen
in air without any other effect are simple asphyxiants. Examples include carbon
dioxide, nitrous oxide, nitrogen, or hydrocarbons, such as natural gas. Com-
pounds that block the transfer of oxygen to the tissues or the utilization of oxy-
gen once it reaches the tissues are called chemical asphyxiants. The two most com-
mon examples of such inhibitors of oxygen uptake or utilization are carbon
monoxide (CO), which blocks the site on hemoglobin that binds and transports
oxygen, and hydrogen cyanide (HCN), which (in the form of cyanide) blocks the
pathway by which the tissues utilize oxygen. Carbon monoxide is particularly
common as a hazard resulting from incomplete combustion of fuels (such as in
automobile exhaust or open-flame heaters): It is especially dangerous because it
has no odor and thus gives no warning of exposure.
Chemical agents that irritate the lung may also impair oxygen uptake by other
means. Irritants may inflame the respiratory tract, causing bronchitis or provok-
ing an asthmatic attack or causing the lungs to be lilled with fluid (pulmonary
edema), a process much like drowning.
Respiratory symptoms are the most common adverse health effects from air pol-
lution (Table 51). Common symptoms include cough (which may produce spu-
tum), nose and throat irritation, and mild shortness of breath. These respiratory
symptoms are often associated with eye irritation and a sense of fatigue. Exac-
erbation of allergic symptoms is typical. Athletes often report that their perfor-
mance is off and that they become tired more rapidly when exercising dtiring
periods of high pollution levels. Asthmatics and patients with chronic obstruc-
tive pulmonary disease (COPD) often experience worsening of their symptoms
during air pollution episodes. Recent studies suggest a close association between
frequency and severity of asthma attacks and atmospheric oxidant and sulfate
levels. People with bronchitis may also experience more coughing due to in-
creased irritation of the bronchial mucosa. Acute upper and lower respiratory
tract infections also appear to occur more frequently in residents of areas with
higher pollution levels. Fever is not a feature of air pollution exposure alone and
suggests a possible infection.
Direct cardiovascular effects of air J)ollution are associated primarily with CO,
which is known to reduce oxygen delivery to the myocardium and suspected to
aggravate the process of atherosclerosis. These effects may occur in normal indi-
viduals who have no unusual susceptibility, but they are particularly severe
among people with existing heart disease.
Respiratory effects of air pollution, particularly in people who suffer from
chronic bronchitis, may place an additional strain on the heart as well. Air poi-
jurion is associated with increased risk of death from heart disease and lung dis-
ease, even at levels below those known to be acutely toxic to the lungs or heart.
It is thought that the compromise in lung function places an additional burden
on the heart, which cannot tolerate this. The stimulation of nerve rellcxes con-
necting the heart and the lung may cause additional problems in a diseased heart.
Mucosal irritation in the form of acute or chronic bronchitis, nasal tickle, or
conjunctivitis is characteristic of high levels of air pollution, although individu-
als vary considerably in their susceptibility to such effects. Eye irritation is par-
ticularly severe in the setting of high levels of particulates (which need to he in
the respirable range described and may be quite large soot particles) or of high
concentrations of pholochemical oxidants and especially aldehydes.
The link between cancer associated with the organic contents of air pollution
has always been a concern but an association has not been proven for ambient
urban air pollution, of the types described. There is little evidence to suggest that
community air pollution is a significant cause of cancer except in unusual and
extreme cases. Examples of cancer associated with community air pollution in-
clude point-source emissions from some poorly controlled smelters that release
arsenic, which can cause lung cancer. There are also important examples of in-
door air pollution in homes (radon) and workplaces (asbestos) that are linked to
AIR 189
lung cancer. Tobacco smoking is more carcinogenic than arsenic, radon, or as-
bestos in the air, multiplying the lung cancer risk from these toxins.
Central nervous system effects, and possibly learning disabilities in children,
may result from accumulated body burdens of lead. Air pollution contributes a
large fraction of exposure in many countries because of lead additives in gaso-
line. Even in countries where lead has been removed from gasoline the lead re-
mains in the environment as one source of exposure.
There are several documented occurences in which severe mortality from
many causes is associated with short-term exposure to fine particles. Air pollu-
tion has been associated in several severe episodes of high mortality, usually
among persons with pulmonary or cardiovascular disorders. Recent studies have
shown an association between particulates in urban air pollution and mortality
from a wide variety of causes, not just lung diseases. This finding was unexpected,
as the levels studied were much lower than those that had been previously linked
to increased mortality. The reason for the newer findings is probably that the
methods of statistically analyzing large populations are much better and the meth-
ods of measuring exposures, such as PM 25 , are much more refined than those
used earlier.
Ozone
Ozone is a highly reactive compound that irritates airways in the lungs and in-
terferes with host defense mechanisms in the body. It also has an unusual effect
on breathing patterns as the result of changes in the reflex breathing mechanism.
In the lower atmosphere, oxygen, with light from the sun as a source of en-
ergy, reacts with nitrogen compounds and volatile hydrocarbons to create ozone.
This occurs especially in stagnant weather conditions and inversions under con-
ditions of sunshine, where there is ample time for the photochemical reactions
to take place. Ozone is chemically unstable and will react with a variety of sub-
stances. (The effects of ozone depletion in the upper atmosphere are discussed
in Chapter 11.) Ozone appears to trigger a reflex response in the lungs that al-
ters breathing patterns. People without asthma cannot inhale as deeply and will
have small changes in airflow.
Studies using pulmonary function testing have found that healthy persons
can experience adverse effects from ozone exposure. This is especially true when
they have an increased respiratory rate, for example when they are involved in
AIR 191
a 100
C
o Upper respiratory symptoms
0 90 • Non respiratory symptoms
A Lower respiratory symptoms
E 80
0
0
E>. 70
60
Cs
5)
E 50
0.
:3
0
40
C)
5) 30
Cs
C) 20
a
C)
C) 10 __o-- Figure 5.4 Effect of ozone on
0 respiratory symptoms. From
0 1000 2000 3000 4000 5000 Kleinman ci al., 1989, with
Effective Ozone Dose (micrograms detvered in 2 hr) permission.
stquaresfit 0
tolerant to ozone and have fewer symptoms. Their breathing becomes more nor-
mal, but persons with asthma may still develop airflow obstruction. Within a
brief period, the inflammation produced by the irritant effect of ozone results in
a reduction of airflow and a worsening of asthma. Ozone also appears to make
persons whose asthma is triggered by allergies more susceptible to the allergen.
Ozone may provoke asthmatic attacks in people who already have asthma, al-
though ozone does not appear to cause the disease in the first place. The attacks
tend to occur 1 or 2 days after the ozone concentration is at its highest, not dur-
>
ing the peak.
20
A 0.1 ppm
• 0.2 ppm
• 0.3 ppm
o 0.4 ppm
15
0
>
Ui
U-
. 10
a
C)
0
Cs
.0
0
5
0
The demand for hospital beds increased on December 8, and the central Lon-
don hospitals issued an Emergency Bed Warning that they had sufficient beds for
fewer than 850/ of applicants. The mortality rate in certain parts of London in-
creased dramatically during this time (see Fig. 5.6). The mayor causes of death were
a variety of respiratory-related illnesses, cardiac illness, and ill-defined illnesses. At
least a few deaths were caused by injuries and a few people drowned when they
could not see and fell into the Thames River. In addition, many animals )e.g., cat-
tle) had to he slaughtered because of illness during this time, likely because of the
fog.
Based on the epidemiological data collected during the London smog episodes,
it was felt at the time that the increased number of deaths in London during the
fog was more closely related to the particulate matter in the air, rather than the
SO 2 . A reanalysis later, though, suggested that the acid aerosols (e.g., sulfur diox-
ide) were the major factor in causing the increased mortality.
Adapted by A. Marliarn; from Kjcllstrd;n and Kicks, 1991.
Sulfur Dioxide
Sulfur dioxide (SO 2 ) has been a serious problem in air pollution since the earli-
est days of industrialization. II has been the major problem in reducing (see sec-
tion Industrial Air Pollution, below) or acidifying air pollution during the period
of rapid economic growth in many countries. It was one of the major cornpo-
nents of the so-called London Fog, which had serious direct health effects, as il-
lustrated in Box 5.1 and Figure 5.6.
Soon after the London Fog incident experimental studies of the effects of sul-
fur dioxide on humans showed that, at least in acute exposures, concentrations
of up to 8 ppm caused respiratory changes that were dose dependent. Later stud-
ies revealed that the main effect of sulfur dioxide is bronchoconstniction (closing
AIR 193
90
80 /
/ \\LAC
70
0
/
o 60 /
0
0
o 50 /
40
30 I/OR
0
—————
20
10
0
8 15 22 29 6 13 20 27 3 10
Nov Nov Nov Nov Dec Dec Dec Dec Jan Jan
Date
Figure 5.6 Weekly death rates in London Administration County (LAC) and the outer
ring (OR) 1 November 1952-10 January 1953. From WHO, 1998b, with permission.
Oxides of Nitrogen
As mentioned above, nitrogen compounds, especially nitrogen dioxide, are in-
volved in the formation of ozone at ground level. The oxides of nitrogen also
produce adverse health effects and are important air pollutants in their own right.
Nitric oxide (NO) is produced by combustion. Nitrogen dioxide (NO 2 ), which
has greater health effects, is a secondary pollutant created by the oxidation of
NO under conditions of sunlight, or it may be formed directly by higher-
temperature combustion in power plants or indoors from gas stoves. The direct
Particles
Particulate matter in the air (aerosols) is associated with an elevated risk of mor-
tality and morbidity (including cough and bronchitis), especially among popula-
tions such as asthmatics and the elderly. As indicated earlier, they arc released
from fireplaces, wood and coal stoves, tobacco smoke, diesel and automotive ex-
haust, and other sources of combustion.
In recent years we have learned a great deal about the health effects of par-
ticles. As noted above, fine particulates in urban air pollution, below 2.5 /.rrn in
diameter, differ in their chemical composition from larger particles. Larger par-
ticulates that are included in PM 10 (particulates 10 rm and smaller) consist mostly
of carbon-containing material and are produced from combustion; some fraction
of these is produced by wind blowing soil into the air. These larger particulates
do not seem to have as much effect on human health as the smaller particulates.
Particulates in the fraction PM25 (2.5 rm and below) contain a proportionately
larger amount of water and acid-forming chemicals such as sulfate and nitrate,
as well as trace metals. These smaller particulates penetrate easily and completely
into buildings and are relatively evenly dispersed throughout urban regions where
they are produced. Unlike other air contaminants that vary in concentration from
place to place within an area, PM 25 tends to be rather uniformly distributed.
AIR 195
The health effects of PM25 CO. sulfate, and ozone cannot be easily separated
because they tend to occur togethcr in urban air pollution. Recent research
strongly suggests that at least PM2 , 5 and sulfate, and probably ozone as well, are
associated with an increase in deaths in affected cities. The higher the air pollu-
tion levels for these specific contaminants, the more excess deaths seem to oc-
cur on any given day, above the levels that would be expected for the weather
and the time of year. Likewise, depending on the time of the year and the
weather, there are more hospital admissions for various conditions when these
contaminants are high. Ozone in particular is linked with episodes of asthma,
but all three elements seem to be associated with higher rates of deaths from and
complaints about lung disease and heart disease. It is not yet known which is
the predominant factor in the cause of these health effects; some combination of
each may be responsible for some effects.
At the much higher concentrations of CO, sulfate, and ozone encountered in
many developing countries, the health effect is likely to be proportionately
greater. There are many factors that complicate such studies in developing coun-
tries. The very high rates of respiratory disease during the winter among even
nonsmokers in some northern Chinese cities, for example, have been attributed
to air pollution, and although this is likely to be true, cigarette smoking, indoor
air pollution from coal-fired stoves, crowded conditions, and the risk of viral in-
fections may also be important factors.
Carbon Monoxide
Carbon monoxide is produced primarily by the incomplete burning of fossil fu-
els—for example, by cars and other gasoline-powered engines and by charcoal
or oil heaters. As it is odorless, cokrless, and slightly heavier than air, it tends
to collect in confined spaces and affects people without warning. The written his-
tory of CO goes back centuries, as Roman records discuss deaths associated with
fires in enclosed spaces.
Basically, as CO concentrations go up, the oxygen-carrying capacity of the
blood goes down, because oxygen molecules are literally being replaced by CO
molecules and the ability of hemoglobin (carboxy-hemoglobin [COHb]) to bind
oxygen depends on 02 binding at neighboring sites. The CO molecule's bond to
hemoglobin is 200-300 times stronger than the hemoglobin-oxygen bond, so CO
TABLE 5.4
PREDICTED CARBOXYHEMOGLOBIN LEVELS FOR SUBJECTS ENGAGED IN
DIFFERENT TYPES OF WORK
Carbon Monoxide
Concentration Predicted COHb Level for those Engaged in
Exposure
(ppm) (mg1rn3 ) Time Sedentary Work Light Work Heavy Work
100 115 15 min 1.2 2.0 2.8
50 57 30 inin 1.1 1.9 2.6
25 29 1 hr 1.1 1.7 2.2
tO 11.5 8 In 1.5 1.7 1.7
is not cleared easily from the circulatory system. Exposure to short periods of
high-concentration CO is just as bad as long periods of low concentrations. Car-
bon monoxide is also a messenger molecule in the human nervous system and
some of its effects may be direct
Normal amounts of CO in the blood are in the range of 1%. Smokers can have
higher concentrations, around 3%-5%, and if one were to exercise at rush hour
in heavy traffic (at 10-15 ppm), levels of 3%_4% could be expected. Different pre-
dicted COHb levels for subjects engaged in different types of work are shown in
Table 5.4. Different lowest observed adverse effect levels (LOAELs) are shown in
Table 5.5. Exercise tolerance does not seem to be decreased until after a level of
about 5% is reached in healthy subjects. People at increased risk include thcse with
heart and lung problems. Follinsbee (1992) found that "for every 1% increase in
COHh there was a 4 0% decrease in time to ischaernic changes." At low levels of CO
exposure, symptoms include fatigue, headaches, and dizziness, but higher concen-
trations of around 3%-5% can lead to impaired vision, disturbed coordination, nau-
sea, and eventually death. To prevent COHb levels from exceeding a 2.5% to 3%
level in the nonsmoker, the following guidelines have been proposed: a maximum
permitted exposure of 100 mg/rn 3 for <15 mm; 60 mg/rn 3 (50 ppm) for <30 mm;
30 mg/m 3 (25 ppm) for <60 mm, and 10 mg/rn 3 (9 ppm) for 8 hr (WHO, 1987a).
AIR 197
cur in the environment at very low levels, some are highly reactive. Like nitro-
gen compounds, they cause indirect effects (such as helping to create ozone) as
well as having direct human physiological effects. They may originate from house-
hold products such as painting supplies, dry cleaning establishments, refineries,
gasoline stations, and many other sources. They can cause irritation to the res-
piratory tract (from increased rhinitis, or runny nose, to asthma) as well as
headaches and other nonspecific complaints. At high concentrations, VOCs have
markedly toxic effects, some of which vary by compound, but which include
neurological effects in all cases. Direct toxicity from VOCs is primarily an indoor
air pollution problem and an occupational hazard, as levels indoors and in the
workplace can reach many times that of outdoor levels.
Trace Metals
The trace metals include cadmium, mercury, zinc, copper, lead, and a dozen oth-
ers. These are called trace elements because they are present in the environment
or body only in small amounts. Human activity has led to the increase in release
of these elements into the environment. Trace metals may have direct health ef-
fects on the nervous and respiratory systems, such as liver and skin.
Lead is the best studied of these trace metals. It is known to be a highly toxic
substance that particularly causes nerve damage. In children, this can result in
learning disabilities and neurobehavioral problems. An estimated 80%_901% of lead
in ambient air is thought to be derived from the combustion of leaded petrol. Be-
cause of its effects on the behavior and learning abilities of children even at low
levels of exposure, efforts throughout the world are being directed at removing
lead from gasoline and consumer products such as house paint. The WHO guide-
lines value for long-term exposure to lead in the air is 0.5-1.0 tg/m 3 /year (WHO,
1987a). Lead is discussed further in Chapter 10 as an occupational hazard.
Other trace metals that occur in air pollution include mercury, vanadium, and
iron; all at very low concentrations.
Photocliemical air pollution, much newer in human history, results from com-
plicated chemical reactions in the atmosphere that are driven by the energy in
sunlight. In photochernical smog, emissions rich in oxides of nitrogen and hy -
drocarbons undergo reactions to produce ozone, specific compounds of nitrogen,
and aldehydes—all of which are highly reactive and chemically oxidizing. This
type of smog is caused primarily by automobile traffic, to which are added emis-
sions from stationary sources, such as hydrocarbons from gasoline and dry clean-
ing solvents and oxides of nitrogen from power plants. Many cities have been
able to bring reducing air pollution under control. However, as automotive traf-
fic has increased worldwide, photochemical smog became a problem. This type
of air pollution may occur in settings that do not have a concentration of in-
dustry, if there is enough motor vehicle traffic. It is most common, and usually
most severe, where the sunlight is strong and temperatures are warm because
these conditions favor the chemical reactions that are characteristic of this form
of air pollution. Because these characteristic chemical reactions takes time, pho-
tochemical air pollution is often worse downwind of the source and several hours
after peak emissions.
A third type of industrial air pollution is point-source emissions, which affects
the immediate vicinity of the plant but does not usually involve atmospheric re-
actions to any great extent. Examples include lead in the vicinity of a smelter,
hydrogen sulfide from a sour gas plant, pesticides from agricultural application,
and concentrated fumes from a spill or tank rupture. Such emissions arc fre-
quently the result of accidents, particularly those related to transporting haz-
ardous substances by truck or train.
AIR 199
BOX .S.2
Bhopal: Case Study of an International Disaster
the United States in 1948 (Donora, Pennsylvania), one in Mexico in 1950 (Poza
Rica), two in England in 1952 and 1962 (both in London; see Box 5.1), and one
in India in 1984 (Bhopal). The Bhopal incident is presented in Box 5.2.
CO, and hydrocarbons, as well as ozone and other photochemical oxidants and
lead in many jurisdictions. Attempts to control emissions, primarily through the
introduction of catalytic converters and more fuel-efficient engines, have largely
been outstripped by growth in motor vehicle traffic (see Mage and Zali, 1992).
Meanwhile, in many developing countries, rapid urbanization has resulted in a
duplication of many of the problems faced by developed countries. In certain
countries, heavy reliance on coal and oil for fuel means that urban SO 2 and SPM
levels remain high. In addition, rapid economic development has meant that
emissions from industry and motor vehicles are increasingly causing air quality
problems (Table 5.7). These issues are discussed further in Chapters 8 and 9.
AIR 201
TABLE 5.7
RELATIVE CONTRIBUTION OF DIFFERENT EMISSIONS AND RESPECTIVE
POLLUTANTS IN SÃO PAULO, BRAZIL
Particulate Matter Sulfur Oxides Carbon Monoxide Nitrogen Oxides
(%) (%) (%) (%)
Vehicles 40 64 94 92
Industry 10 36 3 7
Other 50 0 3 1
Urban air pollution at extremely high levels is implicated in acute and chronic
lung diseases, heart disease, and neurological damage. In the past decade, some
of the highest air pollution levels (for SO 2 ) have been found in cities in devel-
oping countries (seven of the world's ten worse cities were in developing coun-
tries). Today, the worst megacitics for SO 2 pollution are in developing countries.
More than a billion people live in urban areas with unacceptable air quality con-
ditions. Some of the most severe situations of air pollution are in these mega-
cities, such as Mexico City and São Paulo (Brazil).
NO2 0053 ppm (100 p_g/m t ) Annual (arithmetic Increased respiratory infections,
mean) risk of acute lung disease
in the region that the jurisdiction responsible cannot allow to be exceeded. Some-
times the penalty for this is withholding of funds from the national government
or some administrative penalty. Ambient air quality is monitored in various places
within the region; an exceedance occurs when the level of a particular pollutant is
exceeded. The number of exceedanccs, the average levels of air pollution, and the
peak levels during 1 hr may all be used as indicators in air quality standards or
guidelines. Ambient air quality standards may include a nondegradation policy, which
TABLE 5.9
WHO AIR QUALITY GUIDELINES FOR EUROPE, REVISED 1999
Compound Guideline Value Averaging Time
Carbon motinxide 1 ' 100 tng/m 1 (90 ppm) 5 15 mm
60 mg/m 1 (50 PP°')" 30 mm
30 mg/ni 1 (25 ppm) 1 hr
10 mg/m 1 (10 pPt)1) 8 hr
AIR 203
means that not only should air pollution not exceed certain levels but it cannot be
permitted, on average, to get worse over time even within the allowable levels.
Studies of human exposures to air pollutants from motor vehicles have revealed the
following:
• Concentrations of some air pollutants inside motor vehicles and along roadsides
are typically higher than those recorded simultaneously at fixed-site monitors.
• Exposures tend to be higher inside automobiles than in buses and other vehicles
used in public transit.
• Priority lanes used to afford speed advantages to buses and car pools tend to re-
duce air pollutant exposures.
• Concentrations of air pollutants in enclosed settings are similar to outdoor con-
centrations in the absence of indoor sources, but tend to lag behind the peak con-
centrations observed outdoors. (A notable exception is commercial buildings at-
tached to inadequately ventilated parking garages.)
• Concentrations of motor vehicle air Pollutants decline with greater distance from
the road, suggesting that passengers and vehicles are at greatest risk, followed by
pedestrians and street merchants along roadsides, and then the general urban pop-
ulation.
AIR 205
200
150
• 2 100
1)
0
C
0
0
50
0
(I)
Figure 5.7 Trends in sulfur dioxide concentrations in selected cities around the world.
Froin UNEP, 1992a, with permission.
Due to growing public concern, many nations initiated air quality monitor-
ing in the 1960s. In 1973, the WHO set up a global program to assist countries
in operational air pollution monitoring. This project, which became a part of
UNEP's Global Environmental Monitoring System in 1976, covers some 50 coun-
tries, and data from this project suggest that nearly 900 million people living in
urban areas around the world are exposed to unhealthy levels of SO 2 and more
than one billion people are exposed to excessive levels of particulate matter (see
Figure 5.7 for trends in SO 2 concentrations in selected cities around the world).
uestions
Draw a diagram showing how the physical forms are related and how sub-
stances may change from one form to another.
Describe the specific composition of particulates and gaseous constituents
of (1) wood smoke, (2) cigarette smoke, (3) automobile exhaust, and (4) emis-
sions from a coal-fired power plant. Which has the most matter? Which is pre-
dominantly gas? Which is most complicated chemically? Which is likely to be
most dangerous?
Is air pollution a problem in your area? What are the main sources? What
control measures are being used to reduce air pollution at the source? along the
path? at the level of the person?
How have criteria for developing air quality been developed? What are the
scientific and nonscientific issues in setting standards for air quality?
Air quality management may involve controlling sources of emissions from
industry, transportation, and homes. What effect on air quality may be expected
from a national transportation policy that favors automotive transportation over
mass transit? What may be expected from a national energy policy that favors
the burning of fossil fuels over hydroelectric or nuclear energy? Does the eco-
nomic base and structure of the community have any implications for air qual-
ity in the region? What role does city and regional planning play in influencing
air quality? Use your home community as an example of these issues, then com-
pare the situation in another city, town, or village in your country. A number
AIR 207
of initiatives and suggestions for better management of air resources have been
discussed in this chapter. Try to develop other initiatives that could be used to
promote air quality conservation—these could be economic, social, legal, or phys-
ical in nature. (Chapter 8 will return to the issue of air quality as it relates to ur-
banization; Chapter 9 will discuss it with respect to energy policy; and Chapter
10 will discuss it with respect to industry.)
6. Is indoor air pollution a problem in your home? What are the main sources?
How do you maintain air quality?
CHAPTFP. CONTENTS
Why Water is Essential Acceptable Daily Intake and
Water Quality, Sanitation, and Health Guideline Values for Chemicals
Communicable Diseases Associated Drinking-Water Supply and Monitoring
with Water The Source
Chemical and Radioactive Con- Treatment of Drinking water
stituents of Water Distribution and Storage
Other Aspects of Water Quality Place of Use
Adequacy of Freshwater Supply to Sanitation
Meet the World's Needs Control of Water Pollution
Adequacy of Supply Industrial Pollution
Global Trends Wastewater Treatment and Reuse
Determining Quality of Fresh
Recreational Water Quality Guidelines
Water
Ensuring a Safe and Sufficient
Drinking -Water Quality Criteria
Water Supply
Monitoring Contaminants
The Water Decade, 1981-1990
Microbiological Standards
Water Resources Management
WHY ATERISSSENTIAT
Water (or liquids based on water) is essential for basic survival (see Chapter 1).
When a person has nothing else to drink, even poor-quality water must be con-
sumed to stave off death through dehydration. The relief may only be tempo-
rary since contaminated water can spread disease and cause poisoning. People
209
and animals drink water but they also bathe in it and depend on it to grow crops.
Every person on earth requires about 2 liters of clean drinking water each day,
which amounts to 12 million m 3 /day for the world's population. Animal con-
sumption is considerably larger, but animals do not require the same quality of
water needed for human consumption. Most of the world's fresh water is used
for irrigation: 70% of fresh water is used daily. As the world population increases,
the demand for drinking water and irrigation will grow. Water is also used in
the generation of hydroelectric and thermoelectric power. Dammed reservoirs
provide the gravity-driven force that turns turbines to produce electricity (ener-
gize dynamos). Water also acts as a coolant for nuclear and coal/oil power sta-
tions. Industry uses significant amounts of water, particularly in the production
of paper, petroleum, chemicals, and primary metals. Attempts have been made
in these industries to cut back on water consumption through reuse of water, as
well as through new processing methods. Water is used for the transportation of
goods and people, as a means of recreation through swimming and boating, and
as a natural habitat for many forms of fish and wildlife. Seawater is also used to
produce salt. The quality requirements for different water uses vary and the im-
pact on water quality varies with the type of use (see Box 6.1).
This chapter will emphasize the health hazards related to contaminated drink-
ing water and lack of proper sanitation. Lack of good-quality water is a key prob-
lem in economic development in many parts of the world. In dry parts of the
world, lack of water sources is complicated by the poor quality of what is avail-
able. The term water privation diseases comprises those health problems that oc-
cur because of lack of water.
Uses less or not at all affected by water quality, and with usually less impact on wa-
ter quality:
A flowing body of water partially cleans itself. Dissolved oxygen, clay and soil
particles, and living organisms in the water all play an important role in the
process. Flowing water can dilute, oxidize, and remove pathogens as long as its
capacity is not exceeded and sufficient time elapses before water is withdrawn
downstream for human use. When the population density of a given area places
intense pressure on water resources, this self-purifying capability of water is ex-
ceeded. Bodies of water that have their natural flowing properties removed, as,
for example, through damming, are much less able to cleanse themselves.
According to Agenda 21, the United Nations Program of Action from the Rio
Conference in 1992 (UN, 1993), 80% of all diseases and over one-third of deaths
in developing countries are caused by consumption of contaminated water. As
much as one-tenth of every person's productive time is sacrificed to water-
related diseases (UN, 1993). An estimated 1.4 billion people still do not have ac-
cess to safe drinking waler and 2.9 billion do not have access to adequate sani-
tation (UN 1997), and according to the World Resources Institute (WRI, 1998)
this inadequate access to water and sanitation contribute to 2.5 million child-
hood deaths each year from diarrhea. Most pathogens come from animal or hu-
man feces, a result of insanitary excreta disposal. Inadequate water supply plays
an equally important role in the spread of disease. Most diseases that are water-
Water-Based Diseases In these diseases, water provides the habitat for interme-
diate host organisms in which some parasites pass part of their life cycle. These
parasites are later the cause of disease in people as their infective larval forms in
fresh water find their way back to humans, either by boring through wet skin
or by being ingested with water plants, minute water crustacea, or raw or inad-
equately cooked fish. Schistosomiasis is an example of a water-based disease.
Water-Related Diseases Water may provide a habitat for insect vectors of water-
related diseases. Mosquitoes breed in water and the adult mosquitoes may trans-
mit parasite diseases, such as malaria, and virus infections, such as dengue, yel-
low fever, and Japanese encephalitis.
Water-Dispersed Infections The disease categories listed above are primarily prob-
lems in developing countries. A fifth category of diseases associated with water
is emerging in developed countries—infections whose pathogens can proliferate
in freshwater and enter the body through the respiratory tract. Some freshwa-
ter amoebae that are not usually pathogenic can proliferate in warm water, and
if they enter the host in large numbers, they can invade the body along the ol-
factory tracts and cause fatal meningitis. These bacteria can be dispersed as
aerosols from air-conditioning systems; an example of this type of disease is Le-
gionella (WHO, 1992a).
Cholera is one of humankind's oldest diseases and one of the best-known water-
borne diseases. Drinking water that has been contaminated at the source or during
storage is the most common source of infection. Any foods that have been taken
from contaminated water (fish, shellfish) or washed with it (fruit, vegetables) are
also important sources of infection. Severe diarrhea and vomiting are the main symp-
toms of cholera. The diarrhea is so severe and rapid that patients suffer severe loss
of liquid. The main treatment is therefore intravenous or oral liquid rehydration,
which prevents the patient from becoming fatally dehydrated. About 90% of cholera
cases are mild and difficult to distinguish clinically from other types of acute diar-
rhea.
The first cholera epidemic in Latin America since the turn of the century began
in Peru and quickly spread to a number of neighboring Latin American countries,
spreading as far north as the United States. Peru was hardest hit by the disease with
a total of close to 300,000 cases reported by January 1992. The spread of disease
during the initial period, by February 1992, and by March 1993, is shown in Fig-
ure 6.1.
In assessing what had led to the devastating cholera outbreak in Peru, a num-
ber of factors were identified: (a) urban water supplies were operated on an inter-
mittent basis and thus subject to contamination from leaks, back siphoning, and
* Initial epidemics
January 1991
- August 1991
- February 1992
March 1993
00
Figure 6.1 Geographic extent of the Latin American cholera epidemic over time.
From Hug and Colwell. 1996, with permission. continued)
Arsenic Arsenic is naturally ljresent in all lead, copper, and gold ores. Ground-
water enriched through the weathering of arsenic-bearing minerals is generally
the most important source of arsenic in drinking water. There are several geo-
logical areas in Asia, North America, and Latin America where derinatological
effects were the first manifestation of groundwater enrichment of arsenic. At
chronic poisoning levels, various effects are observed, such as vascular disease,
liver disease, skin lesions, skin cancer, and neurological disorders.
Fluoride Fluoride is naturally present in some foods as well as in water, but for
the most part, it is the amount provided by drinking water that determines the
daily intake. Since fluoride is an important component in bone and tooth struc-
ture, it is considered an essential element. It is also a toxic chemical. Only a mel-
Iodine Water is one of the main sources of dietary intake of iodine. In areas
where there is very low concentration of groundwater iodine, resident popula-
tions suffer from iodine deficiencies resulting in an enlargement of the thyroid
gland (goiter) and, in severe cases, mental retardation and cretinism.
E;3
U,
- 6
z
0)
E
C
0
C
a)
0
C
0
(-)
a, 2
CU
a, CU
z 0
Measured at mouth or downstream frontier of rivers
Figure 6.2 Nitrate concentrations in selected rivers: 1970, 1975, 1980, and late 1980s.
From WHO, 1992a, with permission.
Taste and Odor Taste and odor originate from natural and biological sources,
from contamination by chemicals, or as a side effect of water disinfection. Taste
and odor may develop during storage and/or distribution. Any deviations in taste
and odor may indicate some sort of pollution or malfunction with the storage or
distribution systems.
Adequacy of Supply
Freshwater quality and quantity are inextricably linked. There is sufficient fresh-
water worldwide to meet human demands at present and in the foreseeable fu-
ture, but because of uneven distribution of groundwater, surface water, and rain-
fall, many and and semi-arid parts of the world lack reliable sources. Of all the
world's water, 97% is in oceans or lakes. Of the remaining 2.53 0%. by far the
largest part, 69%, is in the form of snow and ice. The available liquid fresh sur-
face water upon which most communities depend accounts for only 0.008
(2.53% X 0.34) (see Fig. 6.3).
Sources of freshwater include rivers, lakes, and groundwater. The last three
centuries have witnessed a significant growth in the volume of water being with-
drawn from these sources, an increase of more than 35 times compared to a sev-
enfold increase of the population. In recent decades, there has been a further in-
crease in water withdrawal, with the highest rates of growth occurring in
developing countries. The main increase in water withdrawal is for agricultural
purposes (see Fig. 6.4).
Access to water is at least as important a problem for health as water contam-
ination. Water is distributed very unevenly around the world and those areas
with less access have had much greater problems with hygiene and quality of
water. The tropics and the mid-level of the Northern Hemisphere has much more
potential freshwater available than other parts of the world.
Rivers,
Lakes,
Swamps
Permafrost and Other
Freshwater 0.86% 0.34%
Other Reserves Groundwater
0.97% 2.53% 30.1%
Figure 6.3 Global total water and freshwater reserves. From Shiklomanov, 1993, with
permission.
3,500
3,000 Agriculture
• 1
2,500
/
• 1
2,000
/
. 1,500 Industry
0
1,000 I-
/ Domestic
500 Municipa
Figure 6.4 Global water with-
0 drawal by sector, 1900-2000.
1900 1920 1940 1960 1980 2000 From Shiklomanov, 1993,
Year with permission.
DRINKING-WATER_QUALITY CRTTERIA
The WHO Guidelines for Drinking Water Quality (WHO, 1993d) are comprehensive
in scope and intended to be used as a basis for the development of national stan-
dards. Through use of the WHO Guidelines, each country can develop its own
standards based on a risk-benefit approach. Standards that are too stringent may
have the effect of reducing or limiting available water supplies in some parts of
the world. The Guidelines are therefore designed to be realistic, adaptable, and
advisory. The overriding priorities in the Guidelines are (in priority order):
ACIDIFICATION
EUTROPHICATION
DIRECT DISCHARGE
ALEXANDRIA, EGYPT
Most industries in Alexandria discharge untreated liquid wastes into the sea or into
Lake Maryut. In the past decade, fish production in Lake Maryut declined by some
80% because of the direct discharge of industrial and domestic effluents. The lake
has also ceased to be a prime recreational site because of its poor condition. Simi-
lar environmental degradation is taking place along the seafront due to the discharge
of untreated wastewater from poorly located sewage pipe outfalls. The paper, tex-
tile, and food industries contribute most to the organic load.
BOGOTA, COLOMBIA
The Tunjuelito, a tributary of the Bogota River, is highly polluted. Many tanneries
and plastic-processing plants pour untreated wastes into it and the dissolved oxy-
gen in the water is almost depleted. The wastes include heavy metals such as lead
and cadmium. Other rivers are not so heavily polluted with chemical wastes but re-
ceive large volumes of untreated sewage.
KARACHI, PAKISTAN
The Lyan River, which runs through Karachi, Pakistan's largest industrial city, is an
open drain, from both the chemical and the microbiological points of view, for a
mixture of raw sewage and untreated industrial effluents. Most industrial effluents
come from an industrial estate with some 300 major industries and almost three
times as many small units. Three-flfths of the units are textile mills. Most other in-
dustries in Karachi also discharge untreated effluent into the nearest water body.
SHANGHAI, CHINA
Some 3.4 M3 of industrial and domestic waste pour into the Suzhou Creek and the
Huangpu River, which flows through the heart of the city. Less than 5% of the city's
wastewater is treated, and these rivers have become the main open sewers for the
city. Most of the waste is industrial since few houses possess flush toilets. The
Huangpu has essentially been dead since 1980. The normally high water table also
means that a variety of toxins from industrial plants and local rivers find their way
into groundwater and contaminate wells, which also contribute to the water
supply.
Source: WHO, 1992a.
isms are present in high numbers in the feces of humans and warm-blooded an-
imals and are readily detectable by simple methods. They do not grow in
water itself. The major indicator organisms of fecal pollution are Escherichia coli,
thermotolerant and other coliform bacteria, the fecal streptococci and sulfite-
reducing clostridia. No water intended for human consumption should contain
E. coli or therniotolerant coli orm bacteria Must not he detectable in any 100 ml sample
E. coil or thermotolerant coliform bacteria Must not be detectable in any 100 ml sample
Total colilorm bacteria Must not be detectable in any 100 ml sample
TREATED WATER IN
DISTRIBUTION SYSTEM
E. co/i or thermotolerant colilorm bacteria Must not be delectable in any 100 ml sample
Total colilorm bacteria Must not be detectable in any 100 ml sample.
In the case of large supplies where suffi-
cient samples are examined, must not be
present in 95% of samples taken through-
- out any 12-month period
E. coli in any 100 ml sample. taken. Treated water should not contain total col-
iform bacteria in any 100 ml sample (Table 6.1). The indicators may or may not
be associated with the disease themselves. For example, most E. co/i do not cause
human disease, although some do. The presence of E. co/i, however, is a reliable
indicator of potential contamination by pathogens.
Monitoring Contaminants
It is not practical or necessary to monitor water for all possible chemical con-
taminants and pathogens. While it is possible to detect the presence of many
pathogens in water, the methods of isolation and enumeration are often com-
plex and time consuming. Therefore, rather than monitoring water for every pos-
sible pathogen, the more logical approach is to detect organisms normally pre-
sent in the feces of humans and other warm-blooded animals as indicators
of fecal pollution (see Table 6.1). The strategy that works is one that (a) identi-
fies episodes of contamination that might carry a significant risk and (b) closely
monitors a few specific contaminants (such as arsenic) that could cause serious
trouble.
The WHO has identified contaminants that are potentially hazardous to hu-
man health and those detected relatively frequently and in relatively high con-
centrations in drinking water. Certain indicator organisms and some 128 chem-
ical contaminants can now be assessed through comparison with guideline values.
The Guidelines for Drinking Water Quality (WHO, 1993d) apply the following prin-
ciples:
Microbiological Standards
Most of the disease agents that contaminate water and food are biological and
come from animal or human feces. The contaminants come in the form of path-
ogenic bacteria, viruses, protozoa or parasites. Those that can be transmitted via
the fecal-oral route by drinking water are listed in Table 6.2, together with a
summary of their health significance and main properties. These pathogens pre-
sent a serious risk of disease whenever they are present in drinking water. Many
of these pathogens are also a hazard in food (these are described further in Chap-
ter 7) and include Salmonella spp., Shigella spp., pathogenic E. co/i, Vibrio cholerae,
Yersinia enterocolitica, Campylobacter jejuni, C. co/i, the viruses listed in Table 6.2,
and the parasites Giardia, Cryptosporidiuni, Entamoeba histolytica, and Dracunculus
VIRUSES
PROTOZOA
HELMINTHS
where bw = body weight (60 kg for adults, 10 kg for children, 5 kg for infants),
P = fraction of the ADI allocated to drinking water, and C = daily drinking-
water consumption (2 liters for adults, I liter for children 0.75 liters for infants).
DfflNKING-WATERSUPPLYANDMONITORIN___
The Source
Proper selection and protection of water sources are critical for the provision
of safe water. It is always better to protect water from contamination than to
treat it after it has been contaminated. Before determining that a source of wa-
ter will be used as a drinking-water supply, it is important to ensure that the
quality of the water is satisfactory or treatable and that the quantity available
is sufficient to meet continuing water demands. Seasonal variations and p0-
tential growth of the community must be taken into account to ensure that
there are no shortages. Sources of groundwater such as springs and wells should
be sited and constructed so they are protected from surface drainage and flood-
ing. Areas of groundwater abstraction should be fenced in and kept clear of
garbage.
The protection of surface water is more problematic. Surface water such as
streams, rivers, and lakes are more vulnerable to pollution. The water source should
be protected from human activities. If possible, the source should be isolated and
there should be control over polluting activities in the area, such as dumping of
hazardous wastes, mining, and agricultural use of fertilizers and pesticides. Recre-
ational activities should be limited so that they are not likely to introduce conta-
mination. While it may be possible to protect a reservoir from major human ac-
tivity, this may be more difficult to enforce in the case of a river. Often it is necessary
to accept existing uses of a lake or river and design treatment accordingly.
In areas where drinking water is collected from roofs it is important to avoid
contamination from paint on the roof or in the storage tanks. In addition, an in-
crease in air pollution may add to poor-quality roof water.
The United Nations Environment Program's Earthwatch office and the Global En-
vironment Monitoring System (GEMS), in association with the WHO, UNESCO, and
the World Meteorological Organization, have developed a global water quality mon-
itoring network, called GEMS/Water. Initiated in 1977, the network includes 344
monitoring stations-240 river stations, 43 lake stations, and 61 groundwater sta-
tions. Rivers such as the Rhine, the Nile, and the Ganges, and lakes, from Lake Tal
in China to the North American Great Lakes, are routinely sampled and analyzed.
Groundwater, crucial for drinking-water supplies, is sampled in Africa and the Mid-
dle East, particularly in areas where no perennial rivers flow. More than 50 water
variables are measured, providing information on the suitability of water for hu-
man consumption, and for agricultural, commercial, and industrial uses. All data
are stored and processed at the GEMS/Water global data bank at the National Wa-
ter Research Institute in Canada, and summaries of the data are published every 3
years. In 1990. the GEMS/Water Program broadened its scope to include not only
monitoring but data interpretation, assessment of critical water quality issues, and
management option analysis.
Whereas guideline values have been set for drinking water itself, no firm re-
quirements can be formulated for the source of such water (WHO/UNEP, 1989).
Waler quality monitoring, however, is in place in several countries through the
GEMS project (Box 6.6).
Drinking water can also be produced froin seawater through desalination. This
is common in countries with little rainfall and large oil supplies, e.g., Bahrain
and Curaçao. The process of removal of salt from seawater involves boiling, dis-
tillation, or reverse osmosis, all technologies with high energy requirements.
A typical water treatment facility, as may be found in large cities in Canada, is shown
in Figure 6.5. After water is drawn from a source, large debris is removed via a
screen. A disinfectant is then added to reduce bacteria. The process of coagulation,
flocculation, sedimentation, and filtration constitutes the treatment process. Through
coagulation and flocculation particulate impurities are removed; adding a coagulant
causes the particles to clump, whereas flocculation is a slow stirring process during
which the particles gather together to form larger particles. Sedimentation is used
to remove suspended solids that have been preconditioned by the coagulation-
flocculation process, following which a filter completes the process of removing sus-
pended solids. Sometimes a disinfectant is added before the distribution of treated
water. -
Trihalomethanes (THMs) result from the reaction of chlorine with organic pre-
cursors during the water treatment process. Several ecological studies have exam-
med the relationship between THM5 and cancer. These studies have generally sug-
gested that there is an association between THMs and cancer of the bladder and
colon. Some of the studies have also reported that incidence of cancers of the rec-
tum, stomach, breast, lung, pancreas, and kidney and non-Hodgkin's disease may
increase in association with THM5. Some case—control studies have also suggested
significant associations for cancers of the bladder, colon and rectum. The sum of the
available evidence points to a small increased risk of some cancers associated with
consuming water with high levels of THMs.
Characteristics of the treatment process affect the amount of chlorine compounds
and organic precursors in treated water. The stage at which disinfection is performed
is important in determining the THM level, since other treatment procedures will
affect the level of organic precursors available to react with chlorine. For example,
when chlorine compounds are added before any treatmeni, the largest levels of
THM5 result. This effect is tempered by using activated carbon later in the process,
as it has the potential to remove volatile organic compounds. The amount of chlo-
rine by-products in treated water can also be reduced with dechlorination.
It is important to recognize that disinfection is an important component of wa-
ter treatment. While measures should be followed to reduce cancer risk to a mini-
mum, the health risks associated with failing to chiorodisinfect water lar exceed the
risks of chlorination, according to current knowledge.
Source: Marrett and King, 1995.
Guidelines document (WHO, 1993d). One of the basic elements of the treatment
methods is sedimentation of larger particles in reservoirs, where special screens
can further reduce the amount of organic matter in the water. Predisinfection
with chlorine compounds can also be used in this process if the water is known
to be polluted by sewage. In the coagulation step, aluminium or iron compounds
are added, which react with impurities in the water to cause flocculation (cre-
ation of slimy particles, called floes, in the water). These flocs will attach to bac-
teria and other remaining organic material in the water, and the flocs can be sep-
Figure 6.5 Diagram of a water treatment process. From Marrett and King, 1995, with per-
mission.
arated from the water by sedimentation or flotation. To ensure that all floes and
most bacteria are removed from the water, the next step includes filtration in
sand, The longer distance of sand the water filters through, the more efficient
the filtration. Normally, bacterial counts can be reduced by a factor of about 1000
by a suitable sand filter.
Even after thorough sand liltration, some bacteria and viruses may remain,
so a final disinfection is extremely important. The most commonly used meth-
ods involve the addition of chlorine or hypochlorite to the water. Disinfection
can also be achieved with chloramines, chlorine dioxide, ozone, and ultraviolet
(UV) radiation. The latter method has been applied in small-scale solar-powered
disinfection units, and this may he the method of choice for remote areas with
much sunlight. The chlorination process makes it possible to maintain a certain
level of free residual chlorine in the water during its transport through the dis-
tribution system. This reduces the buildup of bacterial and algae growth inside
the pipes, and it maintains some protection from contamination of the water dur-
irig transport. In large population supply systems, the water source is often prone
to contamination and the storage and distribution systems can be contaminated.
Chlorine is preferred because it continues to act downstream. In Box 6.7 chlori-
nation of drinking water is discussed further.
In some countries, fluoridation of drinking water is as an approach to increase
the daily intake of fluoride to levels that prevent caries in teeth. This practice has
been controversial because excessive intake of fluoride can have detrimental health
effects and can discolcr teeth (see Chemical and Radioactive Constituents of Water,
above). Individual intake is diflicult to control. Fluoride in toothpaste provides sig-
nificant exposure for people who use such toothpaste. The fluoridation of water sup-
plies is nonetheless promoted as an essential intervention for preventive oral health.
Distribution and Storage
Where high-quality piped water is readily available in the home, monitoring of
water quality can be done directly at the time of use. According to the WHO's
Place of Use
As discussed in Chapter 4, Factors Affecting the Perception and Acceptance of
Risk, many organisms present in water have no real health significance but may
be important indicators of other problems with either the water supply or the
water distribution system. Consumers cannot usually assess the safety of their
water systems themselves but their attitude toward their water supply and wa-
ter suppliers will certainly be affected by what they can perceive themselves. The
provision of water that is not only safe but physically acceptable is important to
a community (see Other Aspects of Water Quality, above).
Heat kills bacteria and protozoa and destroys viruses. Boiling water is a very
effective means of treating water for biological contamination but it is ineffective
for controlling chemical contamination. It is also very expensive, especially where
fuel is in scarce supply. Water can also be filtered at the place of use. For small
volumes, disinfection chemicals can be used to treat highly contaminated water.
Small-scale systems based on solar UV radiation as a disinfectant have been de-
veloped.
cANTTATTON
Throughout this chapter numerous references have been made to sewage, cx-
creta, or fecal contamination. The prevalence of waterborne diseases resulting
from this type of contamination raises the obvious question of what can be done
to improve sanitation. In the 1970s, international agencies began to look at al-
ternative low-cost sanitation technologies for rural and low to medium-density
urban settlements. There are now over 20 different excreta disposal systems that
offer varying degrees of convenience and protection. One such system, the ven-
tilated improved pit (VIP) latrine, is outlined in Box 6.8 and Figure 6.6. Larger-
scale sewage systems for urban areas are described in the section Wastewater
Treatment and Reuse, below. Concerted efforts during the 1980s brought im-
proved water and sanitation services to many of the world's poorest people. Al-
though the target of the International Drinking Water Supply and Sanitation
Decade (IDWSSD), discussed in the last section of this chapter, was to provide
safe drinking water and sanitation to underserved urban and rural communities
by 1990, the progress of the decade was not enough.
Most urban centers in Africa and Asia have no sewage system at all, includ-
ing many cities with a million or more inhabitants (WHO, 1992a). In 1994 at
A ventilated improved pit latrine (VIP) is an improved version of the traditional pit
latrine. The main difference between a VIP and a pit latrine is that a VIP has a vent
pipe with a fly screen at the top. The vent pipe and fly screen together have two
effects: increased ventilation and fly control. The vent pipe creates a flow of fresh
air through the cubicle and pit. As wind blows over the top of the vent pipe, it sucks
air up the pipe and out of the pit. Fresh air is then drawn from outside, through
the cubicle, and down into the pit. The toilet itself is therefore odorless (see Fig.
66a). Flies approaching the latrine are attracted to the odors coming from the pipe,
but cannot pass the screen to enter the pit. Flies escaping from the pit are attracted
to the light coming down the pipe, but are trapped by the screen and cannot leave.
Thus far fewer flies are attracted to and able to breed in the toilet (see Fig. 6.6b).
FIGURE 6.6 Ventilated improved pit (VIP) latrine. In addition to the vent pipe and fly-
screen, the following are other important features of a VIP toilet: (1) Apart from the holes
for the vent pipe and the toilet seat, the pit should be completely sealed by the slab to
prevent odors (B) and flies (A) from escaping. (2) In soft ground the pit should be lined,
to prevent the toilet from collapsing. If the ground is solid, it may only be necessary to
line the top part of the pit. (3) The superstructure interior must be shaded (i.e., light niust
not be allowed to enter it directly), as this attracts flies from the pit. (4) The toilet must
be well maintained and kept clean for it to work properly. Contributed by D. Carter, The
MVULA Trust.
SANITATION
least 220 million people still lacked an easily accessible source of potable water
(see Table 6.3) (WRI, 1996). Figures for water supply and sanitation often un-
derstate the problem because they do not take into account the quantity of wa-
ter needed by a household for proper hygienic practices. Moreover, figures given
for clean water sources or adequate sanitation facilities in a comtnunity may also
conceal some problems. If people have to wait in long lines for their water, they
often reduce their water consumption below what is needed for good health
(WHO, 1992a). People who have to walk long distances to use a latrine may end
up defecating where it is most convenient to save effort. Improving sanitation
will only work if other factors such as personal hygiene and adequate water sup-
ply are addressed simultaneously. Improving access to water and sanitation fa-
cilities alone can reduce the incidence of diarrheal disease by at least 20% (WRI,
1996).
As noted in Our Planet Our Health (WHO, 1992a), capital costs alone are not
a sufficient basis for determining the cost of a system because some systems
are more expensive than others to operate and maintain. The total discounted
capital, operation, and maintenance costs for each household must be calcu-
lated to determine the charge that must be levied for the service and establish
whether households can afford to pay for the service. If the monthly cost of
providing sanitation exceeds 5% of the family income, it may be considered
unaffordable. Most low-cost sanitation alternatives come within this range,
even for the poorest of communities. Table 6.4 outlines typical sanitation fa-
cilities and their costs. Costs are a crucial factor in the choice of sanitation sys-
tems, but a number of other determinants such as settlement and population
density, ground conditions, and social and cultural practices will also play a
role.
Domestic sewage, stormwaler runoff, and industrial wastes have all been men-
tioned in this chapter as significant contributors to water quality degradation. A
few decades ago, it was considered economically acceptable to turn over some
water courses entirely to waste disposal, with other water bodies being reserved
for drinking water. However, this is no longer acceptable practice. The increase
of population density in urban areas, the concern for environmental protection,
the g7reater understanding of the links between the environment and health, and
a better assessment of the economic damage of water pollution have all served
to motivate an improvement in pollution control practices (Hespanol and Helmer.
1993).
As highlighted in Bcx 6.5, many of the rivers that flow through the devel-
oping world's major cities are little more than open sewers. Untreated industrial
and municipal wastes add pollution loads far beyond the rivers' self-purifying ca-
pacities. While these rivers and other surface water bodies are highly visible signs
of pollution, less visible but equally dangerous is the contamination taking place
in groundwater. The attraction of groundwater as a supply source has led to over-
expkntation. This in turn has led to a number of quality problems. As the nat-
ural water table falls, saline water is drawn in to replace the fresh water. Seep-
age through the soil can contaminate groundwater with pathogens from sewage,
as well as a wide variety of potentially toxic compounds dumped by industry.
Improvements in sanitation, wastewater treatment and reuse, and in the regu-
lation of industrial pollution need to he priority areas for controlling the pollu-
tion of both surface and groundwater sources.
• stabilization ponds
• activated sludge
• trickling filters and towers
• aerated lagoons
• upflow anaerobic sludge blanket reactors (UASBR).
The choice of treatment depends on such factors as land availability, power re-
quirements, and availability of skilled operators. The UASBR5 have low power
and land requirements. Stabilization ponds require large amounts of land but arc
simple and inexpensive to operate. Activated sludge plants require considerable
amounts of power as well as skilled operation.
Wastewater is a valuable resource that plays an important role in the man-
agement of water resources (WHO, 1980b). Worldwide, water withdrawal for ir-
rigation accounts for nearly 70% of all use. By using wastewater for irrigation,
particularly in and or semi-arid parts of the world, high-quality water currently
being used for agriculture could instead be made available for drinking. Reuse of
• Wastewater treatment, to ensure that the wastewater applied to crops has low
levels of pathogenic organisms
Wastewater application techniques, such as drip irrigation, that avoid wastewater
coming into contact with the edible parts of crops
o Crop selection, to limit the use of wastewater for irrigating crops that are not
consumed directly (industrial and fodder crops) or that grow well above the
ground (tomatoes and chili), or crops not eaten raw (potatoes)
Human exposure control, by advising farm workers, crop handlers, and consumers
of potential hazards through programs of health education, by immunizations,
by providing treatment and adequate medical facilities to treat diarrheal dis-
eases
100
F_ • 1970
O 1980
0 1990
80
a)
>
a)
0)
0
60
a-
0
a-
540
20
South Africa had a long history of racial discrimination and inequality. The coun-
try had its first democratic elections in 1994. South Africa was left with a huge
legacy of inequalities, among them unequal environmental conditions. The chal-
lenge of providing the entire country's population with a basic and sustainable level
of water supply and sanitation service is enormous. The Mvula Trust is a non-
governmental organization (NGO) dedicated to improving water supply and sanita-
lion services to disadvantaged, poor, and marginalized rural communities. It pro-
vides funds mainly to villages that are remote and have low incomes. Local
government structures in South Africa are very new, with little capacity to main-
tain service infrastructure. Overcoming these difficulties to achieve sustainability re-
quires innovative approaches to all aspects of project design and implementation.
The technologies installed must be easy for the community to maintain, and they
must be affordable. However, the most important element in sustainability is that
the community must have a sense of ownership and responsibility for the scheme.
For this reason a community-centred approach to project design and implementa-
tion is essential. The Mvula Trust has developed an approach based on the follow-
ing principles.
DEMAND DRIVEN
The Trust only responds to requests for assistance from communities. It does not
search for projects, nor does it respond to proposals from consultants unless they
are in support of a community application. Without effective, gentnne demand for
the service and for the level at which it is to be installed, there is unlikely to he a
commitment to the smooth implementation of the project and, more importantly,
to the maintenance of the scheme.
CONCEPT OF OWNERSHIP
The Trust approach stresses community ownership of the process and the product
of the project. The Trtist only enters into a contract with the association represent-
ing the community, which is then expected to open a bank account, procure ma-
terials, employ labor, pay consultants, and set up a tariff collection systeni.
In order for the community to take an active interest in the ongoing maintenance
of the scheme, it is essential that the facilities effectively serve their needs. Key de-
cisions regarding the design of the system and the implementation of the project
must therefore be niade by the community, within a set of clear guidelines, such as
the policies of the funding agency. Without this, there is a risk that an inappropri-
ate system will be installed.
COST SHARING
The principle of paying for services is basic to the South Afrkan government's re-
construction and development program, which the Trust supports. The Trust ex-
pects the community to start contributing cash to a special fund as soon as the pro-
ject starts. The process through which the association must go to raise the contri-
butions to this fund sets a precedent for the collection of operation and rnainte-
nance fees.
CAPACITY BUILDING
A key element in promoting sustainability is to develop the skills needed to take re-
sponsibility for the scheme. All Trust-funded projects have a large training compo-
nent, and the community is given the opportunity to put their training into prac-
tice during the course of the project. This develops a strong sense of self-reliance
needed to run the project after completion.
The government Department of Water Affairs and the Trust have entered into
an innovative agreement. The Trust receives most of its funding from the Depart-
ment but it is allowed to be separately accountable for public funds. This enables it
to retain a flexible NGO structure that can implement rapid, demand-driven
processes to support community empowerment.
Contributed by I. Wilson, Mvula Trust.
• The ability of communities to run and maintain their own sanitation and wa-
ter systems needs to be strengthened.
• There needs to he greater emphasis on the connections between improvements
in water and sanitation and improvements in hygiene and primary health care.
• It is important to involve local populations in decisions regarding design, costs,
and management of projects.
• Disease risk and socioeconomic conditions must be considered in the design
and delivery of water and sanitation services.
Economic instruments used to put this principle into practice include effluent
charges, subsidies to pollution control works, financial enforcement incentives,
tax rebates, and budgetary and fiscal mechanisms. Financial incentives that as-
sist polluters to protect the environment, although not universally accepted, are
in widespread use. Grants, low-interest loans, and tax credits are incentives given
to encourage remedial measures. Financial assistance can he a powerful instru-
mert in environmental protection programs, particularly in developing countries
(Hespanol and Helmer, 1993).
Significant progress cannot be made in ensuring water supply and proction
without a strong commitment at the governmental level, as large expenditures
Study uesti2Is
What factors need to be considered to develop an effective strategy to im-
prove sanitation in a rural community of a developing country? Of an urban
community?
A number of initiatives and suggestions for better management of water
resources have been discussed in this chapter. Try to develop other initiatives
that could be used to promote water conservation. These could be economic, so-
cial, legal, or physical in nature. Think about how these may be implemented.
Make a list of ten tips to reduce water consumption in a community af-
fected by water shortage.
CF[APTER CONTFTS
242
Global Food Production Capacity and Production and Use of Pesticides
Food Security Populations at Risk for Exposure
World Food Situation to Pesticides
Crucial Conditions for Food Toxic Effects of Pesticides
Production Integrated Pest Management
Environment and Food Security Fertilizers
Global Trends Modern Intensive Farming
Environmental and Occupational Health Methods
Hazards in Agriculture Prevention and Control
Physical Injuries and Infections
(continued)
MINERALS
all essential nutrients. These food groups are considered arbitrary by some in-
vestigators, and there is controversy about alleged cultural biases in the recom-
mendations. Many people do not consume products from each of these groups
and yet are still in good health. As Table 7.1 indicates, there is a great deal of
flexibility when choosing foods that give all the nutrients required. Box 7.1 out-
lines an example of feod consumption that differs radically from the North Amer-
ican model while still providing everything a person requires. Apart from the cul-
tural influences on the dietary composition, factors such as availability, taste,
smell, appearance, cost, and convenience are important determinants of food
choice.
The Inuit are an indigenous people living in northern North America. Their tradi-
tional diet consists mainly of sea mammals (seal, walrus, whale, polar bear), cari-
bou, and marine fish, with occasional berries and shellfish. This diet is high in pro-
tein and also has high amounts of polyunsaturated lipids (from the phytoplanktori
consumed by the fish). It has very low levels of carbohydrates and relatively high
levels of overall fats, exceeding the recommended amount. Despite these problems
and the limited variety in their diet, the Inuit have traditionally experienced good
health. Studies of the composition of their marine diet indicate that the animals are
extremely rich food sources providing all of the required vitamins and minerals that
normally would be achieved only by combining a wide variety of fruits and veg-
etables. It is gradually becoming clear that native foods can provide all nutritional
needs without supplementation.
Traditionally, health risks related to vitamins are associated with deficiencies. How-
ever, the relation between health and the intake of vitamins shows an optimum.
Excessive vitamin intake, either through diet or through high supplementation, may
result in toxic effects. The margin between physiological need and toxic dose is dif-
ferent for two distinct groups of vitamins: lipophilic (fat-soluble) vitamins (A, D, E,
and K) and hydrophilic (water-soluble) vitamins (vitamins B and C, biotin, niacin,
pantothenic acid, and folate). For the lipohilic vitamins this margin may he rela-
tively narrow compared to that of the water-soluble vitamins. Whereas vitamin A
deficiency may cause xerophthalia or (night) blindness, high doses of vitamin A may
result in several other adverse health effects including headache, vomiting, liver
damage, and hone abnormalities (see Fig. 7.1 for the health effects of vitamin A de-
ficiency and high dosage). Furthermore, a high incidence of spontaneous abortions
and birth defects has been observed among fetuses of women receiving therapeu-
tic doses of 500 to 1500 rg of 13-cis retinoic acid per kg body weight. Although the
natural content of the diet is not likely to induce toxic effects, it is increasingly im-
portant to regulate the standards set for vitamin intake because of the trend toward
vitamin supplementation and the use of vitamins as naturally occurring antioxi-
dants in food processing. This is most relevant for the lipophilic vitamins A and D
since they may accumulate in the body during long-term consumption of high doses.
- *
death
hepatotoxicity
bone factures
> hemorrhages
0 alopecia
0 eczema
night normal
ness
>
0 keratinization
0
Figure 7.1 Clinical symptoms death
as a result of vitamin A defi-
ciency and from vitamin A
10 100 1,000 10,000 100,000
toxicity. From Rutten, 1997
with permission. vitamin A intake jig I kg body wt I day
Other Deficiencies Other nutritional deficiencies are also widespread in some ar-
eas of the world. Fluoride deficiencies can lead to dental caries. Rickets and other
bone abnormalities are attributable to a combination of insufficient exposure to
sunlight and lack of vitamin D in the diet, causing calcium disorders similar to
osteoporosis. Ascorbic acid deficiency still occurs in some drought-affected areas,
particularly Africa. Vitamin B 12 deficiency can cause anemia and neurological
disorders. People on vegetarian diets that contain no food of animal origin are
particularly at risk for B 12 deficiency.
Foodborne illnesses are a common and serious health problem. Statistics under-
estimate the number of cases of foodborne illness because not everyone affected
visits a doctor, and doctors may not report all cases to public health authorities.
Some cases of foodborne illness may not be documented because they are not
recognized as such. In various developed countries up to 60% of cases may be
caused by poor food handling techniques and by contaminated food served in
food service establishments. Similar problems exist in the developing world.
Biological contaminants
Biological hazards in food that are of concern to public health include pathogenic
strains of bacteria, viruses, parasites, helminths, protozoa, algae, and certain toxic
products they may produce (WHO, 1992b). The following four categories sum-
marize the concerns about biological contaminants.
Bacterial Contaminants Biological hazards may act through two general mech-
anisms in causing human illness. One mode of action is the production of tox-
ins that may cause adverse health effects ranging from mild symptoms of short
duration to severe intoxications that can be life threatening or induce long-term
health consequences. These toxins arc complex enzymes that can destroy pro-
tein and tissues. The second mode of action is the production of pathological re-
sponses that result from ingestion of viable organisms capable of infecting the
host (see Box 7.3). Generally, for foodborne illness to occur, one of the follow-
ing events must take place: (1) bacteria present in the original food source sur-
vive food production, including harvesting, storage, and processing stages; (2)
bacteria enter the food preparation area via the food source or food handler and
contaminate other foods that are ready to eat; (3) (bacteria in food multiply and
are present in sufficient quantities when consumed; and (4) bacteria produce a
toxin when they multiply and a sufficient level of the toxin is present.
In the case of food poisoning induced by bacterial toxins, threshold levels of
concern are much easier to establish than with illnesses resulting from infections.
Dose—response data can be obtained and health risks can be assessed by follow-
ing the quantitative risk assessment paradigm proposed for chemicals (see Chap-
ter 3). To characterize risks from invasive strains of pathogenic bacteria, how-
ever, dose—response data only apply to the quantity of bacteria needed to start
an infection, and this may vary for the following reasons:
SA LMONELLAE
The bacteria may reach food either directly or indirectly through such channels as
animal excreta, human excreta, or water polluted by sewage. The symptoms include
diarrhea, abdominal pain, vomiting, and fever. In recent years the contamination
of poultry has been a major source of salnionellosis. Other incriminated foods in-
clude dairy products, shellfish, and vegetables. This is a classic example of a food-
borne infection.
STAPHYLOCOCCI
lems arise in many parts of the world where meat and/or fish are eaten raw or
undercooked and where people drink untreated water or use it in food prepa-
ration. The best protection from parasitic diseases is a safe water supply and ad-
equate cooking and refrigeration temperatures (Jacob, 1989). Two of the most
widespread parasitic foodborne diseases are giardiasis and trichinellosis (some-
times called trichinosis) (see Box 7.4 and Fig. 7.2).
Mycotoxins Mycotoxins are secondary metabolites of fungi that can exert vari-
ous types of adverse health effects, including teratogenicity, carcincgenicity, mu-
tagenicity, as well as oestrogenic effects. At this moment several hundred myco-
toxins have been docutnented, and many of them are produced by the genera
Aspergillus. Penicillium, and Fusarium. Although toxic syndromes associated with
exposure to mycotoxins, also indicated as mycotoxicoses, have been known for
many centuries, it was not until the discovery of the aflatoxins in the early 1960s
that these dietary risk factors were fully appreciated. Mycotoxin contamination
of food items depends on the environmental conditions that may allow mold
growth and production of toxins. As with bacterial food intoxication, the absence
of live molds in foods does not imply that mycotoxins have not been produced,
or vice versa. Toxins may have been formed in earlier stages or during produc-
non or storage and, as a result of their chemical stability, may still be present af-
ter cooking or other forms of food processing. The aflatoxins, now regarded as
the most important mycotoxins, are produced by the molds Aspergillusfiavus and
A. parasiticus. Allatoxins reveal high carcinogenic activity. Before they are bio-
logically active, they have to be metabolized. Aflatoxin Bi, the most prevailing
Giardiasis cysts
in intestine
Encysted worms
I
in pork meat
Gia
Transfer lemolN
to mouth excreted
\
I Water used
for washing
Trichinella \Cs
spiralis
worms in ra t intcton 'Pig eats
/ rat excretions
t!;4
vegetables
Figure 7.2 Mode of transmission of giardiasis and trichinellosis. From Jacob, 1989, with
permission.
form, followed by Gi, B2, and G2, has been shown to be a potent hepato-
carcingen. Particularly in combination with hepatitis B virus infection, aflatox-
ins may lead to primary liver cancer. Allatoxins are produced both pre- and post-
harvest, at relatively high moisture contents and relatively high temperatures.
The fungi involved in the production grow best at approximately 25°C and with
a relative air humidity of over 80%. Aflatoxins occur on several food products,
including oilseed (groundnuts), grains (maize), and figs. Aflatoxin Ml can be
found in low concentration in milk samples. Discouraging fungal growth is the
most effective way to achieve prevention of aflatoxin contamination. Particularly,
adequate post-harvest crop drying is essential to reduce the chance of fungal
growth.
Chemical Contaminants
There are many sources of chemical contaminants (see Fig. 7.3). Vehicle exhausts
and emissions are a common cause of air pollution, and hazardous airborne el-
ements can be deposited onto and absorbed into various crops. Industrial and
mining activities that produce poisonous wastes can contaminate plant and soil
alike. Because of the complex interrelationships between air, water, land, and
plants, the contamination of any one element—from, for example, a chemical
leak or a nuclear accident—will have serious implications for the others. Contam-
inants are often found in animals, particularly as a result of modern farming
methods. Drugs used to prevent disease and promote growth in these animals
have to be carefully regulated to ensure that levels in meat are safe for human
consumption.
Contamination can also occur during food storage. Coatings containing poly-
chlorinated biphenyls (PCB5) have been used inside silos and have resulted in
high levels of PCBs in milk. Food processing allows another potential period for
chemical contamination. Some processing plants have witnessed instances of heat
cu
crops
processing
(cadmium,
agricultural practice1.J.. lead, PCBs)
(pesticides, cadmium, p p
PCBS) f114 cooking
livestock
LJ L I
landfills (PCBs, lead)
storage
seafood (aflatoxins)
industrial
emissions and
effluents (lead,
cadmium, mercury, PCB5)
Figure 7.3 Pathways to food for selected chemical contaminants. From UNEP/GEMS. 1992,
with permission.
0.07
0.06 Japan
p.9/kg
0.05
\/ \"
bw/day d
0.04
\ /
/
0.03
United States
0.02
0.01
Figure 7.4 Average daily intake of
PCBs in adults in the United States
1977 1979 1981 1983 1985 1987 and Japan (p.g/kg bodyweight/day).
From UNEP/GEMS, 1992, with per
Year n-li SSI ()fl.
though there have been reports of high levels in some breakfast cereals, a result
of contamination by packing materials. Generally, of all types of foods monitored,
fish contain the highest levels of PCBs. As a result, diets consisting of high lev-
els of fish consumption may have a high PCB intake, as seen in Figure 7.4, which
shows the difference between average dietary intake of PCBs in the United States
and that in Japan, where large amounts of fish are consumed.
Lead Lead produces adverse effects on blood forming tissues, the digestive and
nervous systems, and the kidneys (also see Chapter 2). Lead is naturally present
in the soil and is introduced into the environment through industry and through
exhaust fumes of leaded gas used in vehicles. Lead is found in batteries, solder,
dyes, and insecticides and can be transferred to food either directly through per-
sonal contact or indirectly through environmental contamination. Lead may be
present in drinking water where lead pipes are used for domestic plumbing or
where lead-based solder is used on copper pipes. It may also he found in the
enamel used for kitchenware, in the glazes used for pottery, and in the solder
used for cans containing food or drink.
Fish and shellfish generally have a higher concentration of lead than other
foodstuffs; however, in regions where there is extensive industry and mining,
vegetables also show significantly high concentrations. Vegetables, grains, and
Cadmium Cadmium is a cumulative poison that affects the kidneys even at rel-
atively low levels of exposure. It also affects placental function, liver function,
testes, and formation of bone tissue. In addition, cadmium is a suspected human
carcinogen. The main sources of cadmium in foods are industrial emissions and
fertilizers. In Japan in the 1950s a number of areas with cadmium-contaminated
rice were identified, and similar problems have been found more recently in
China. Other potential sources of cadmium in food are kidneys (especially from
animals that roam wild), cadmium-lined metal equipment used in commercial
food processing, kitchen enamel, pottery glazes, and some plastics.
The established PTWI for cadmium is 7 pg/kg body weight. Data show that
average levels were lowest in dairy products, vegetables, fruit, cereals, meat, and
fish, whereas a sharp increase in cadmium concentration was found in molluscs
and crustaceans and in animal kidneys. Populations in industrial areas showed
significantly higher concentrations of cadmium in their bodies.
Mercury Mercury has been used for many centuries and is still commonly used
today. It can be found in thermometers, batteries, fluorescent lights, and in many
industrial processes including the production of fungicides and paints. Mercury has
toxic effects on animals and people. Pregnant women, nursing mothers, and chil-
dren are particularly susceptible to mercury poisoning. The most toxic form of mer-
cury is methylmercury, which causes damage to the central nervous system.
The PTWI for mercury is 5 [hg/kg body weight, of which no more than 3.3
gfkg should be methylmcrcury. Methylmercury is often found in fish because
of the industrial effluents containing mercury that are discharged into rivers or
seas and converted by bacteria into methylmercury (see Box 7.5). The Mediter-
ranean area accounts for half the world's production of mercury and accordingly,
mercury levels in fish from this area have been found to be very high. (Aston et
al., 1985; Bosnir et al., 1999)
Other areas of naturally high mercury discharge are the mid—north Atlantic
ocean and some river systems in North America. Some tributaries of the Ama-
zon have been contaminated by mercury from the use of the metal in gold ex-
traction in primitive gold mining operations. Flooding caused by hydroelectric
dams is another source of increased levels of mercury in fish (see Chapter 11,
Deforestation and Descrtification).
Radioactive Contaminants
On the basis of the non-threshold concept, radionuclides may present carcino-
genic, mutagenic, and teratogenic hazards. Several radionuclides have special,
Poisoning from organic niercurial compounds results in a wasting brain disease and
lcss of control of the motor nerves. This form of poisoning became known as Mi-
namata disease because one of the worst outbreaks occurred in Minamata, Japan in
the early 1950s. This outbreak alerted the world to the dangers of chemical conta-
nhination.
People in the small fishing town suffered progressive weakening of the muscles,
loss of vision, and eventual paralysis and coma. Minamata seabirds and household
cats that, like the fishermen and their families, subsisted on fish also showed signs
of the disease. Several hundred people__40% of those affected—died, and others
suffered from permanent damage from the poisoning.
Concentrations of metbylmercury were discovered in fish and shellfish taken
from the local bay, and in 1968 mercury was officially identified as the cause of the
poisoning. The source of the mercury compounds was traced to the effluent dis-
charged from a local chemical company.
Source. Environment Agency, 1975.
strong affinities for specific organs or tissues, resulting in a relative dose that may
be several times higher than the ingested or absorbed dose. These affinities may
result in accumulation over time. There is no detoxification or elimination mech-
anism for radionuclides except for excretion or spontaneous decay.
The radionuclides of interest in food safety are the so-called internal emitters
that enter the body by ingestion. Naturally occurring internal emitters that con-
tribute to the total radioactive dose in the diet are potassium-40, radium-226,
uranium-228, carhun-14, tritium, rubidiurn-87, lead-21 0, and polonium-2 10. In
addition to this natural radioactivity, the environment (and therefore also food)
can he contaminated with a number of human-made radioactive elements. Small
amounts of these elements may be released in the environment by emission from
nuclear reactors through their effluents (see below). Furthermore, radioactivity
may come from fallout from atmospheric testing of nuclear devices, spills from
reactor accidents, and nuclear warfare.
Since the first nuclear reactor was constructed in 1954 in the United States,
many other nuclear power plants have been built all over the world. Although
relatively small amounts of radionucleides are emitted through the effluents of
these reactors into the environment, they are generally considered to be safe. By
contrast, the release of radioactive products following a reactor malfunction or
explosion is a much bigger concern. Unfortunately, such events have occurred
on several occasions, including the accident in the Windscale reactor in the
northwest of England (October 1957) and the Three Mile Island reactor in Penn-
sylvania in the United States on March 28, 1979. Following the Windscale acci-
dent, iodine- I 31 was found in milk prodticed in the surrounding areas. (Dunser
et al., 1959). There was no contamination found in milk or other foodstuffs with
Oi'ervieit'
The quality and safety of the food supply is a topic of continual interest to the
media and the general public. The word quality has many different meanings and
interpretations. The average consumer associates quality with personal prefer-
ences and may therefore subjectively interpret the term as indicating whether
the food is liked or disliked, good or poor. In addition to these psychological fac-
tors, sensory stimulations such as flavor, color, texture, visual appearance, and
packaging are important. Also, new developments in food supply prompt dis-
cussions about the scientific evidence for safety and the use of suitable control
measures. Food quality from a more scientific point of view also includes a num-
ber of safety aspects such as the presence of environmental contaminants, pes-
ticide residues, use of food additives, microbial contamination, and nutritional
quality. Thus, food quality is determined by four main categories of qualitative
properties: (1) organoleptic aspects (how it affects the senses; its taste and smell),
(2) nutritional value, (3) functional properties, and (4) hygienic properties. A
given characteristic of a food is often relevant to more than one of these cate-
gories. For instance, a longer shelf life is an important quality relevant to food
retailers, as it makes stock management easier. It is also of interest to consumers,
as it keeps prices lower and prolongs home storage periods. These advantages re-
fer primarily to functional properties, but they also affect the hygienic proper-
Safety Standards for Natural Toxins and Food Contaminants Natural toxins and
contam-inants are undesirable and uiiintentionally present in food. These food
constituents form a large and very diverse group of chemicals, some of which
have already been discussed in previous sections. Again, acceptable intake is based
on the toxicological profile of the component in question, defined in a way sim-
• prctection of the health of the consumer and the safeguarding of fair practice
in food trade
• coordination of all food regulatory activities carried out by international gov-
ernmental and nongovernmental organizations
• establishment of priorities for the preparation of provisional standards
• finalizing of provisional standards that will be published in a Codex Alimen-
tarius
• amendment of already published standards, if necessary.
The Codex standards (FAQ/WHO, 1989) have been shown to be of great value
in bringing food standards into accord, even though the Codcx standards have
no legal status (see Box 7.6). The Commission's system is unique in that it pro-
vides industry leaders the possibility to participate in pre-Codex meetings and to
join the debate, although industry representatives have no voting rights in these
meetings. Furthermore, industry representatives are offered the opportunity to
comment on decisions made about safety evaluation during specially organized
JECFA, JMPR, or European Community (EC) hearings.
The harmonization of food standards is also one of the objectives of the EC.
Within the EC the safety evaluation of food additives or other substances in food
is formally carried out by several working groups of the Commission of the Eu-
ropean Communities. Once a proposal is enforced by the Council of Ministers,
it is mandatory for the regulatory authorities in the member countries.
To ensure high quality of the food supply, a number of parties must play spe-
cific roles. The main actors include the government, consumers, and the food in-
dustry. The government is responsible for the establishment of standards or codes
of practice as well as the enforcement of laws and regulations. Furthermore, it
should encourage the food industry to undertake voluntary measures to improve
fcod safety, such as providing advice and guidancc. Consumers in turn should
be well aware of the quality of the food they buy, prepare, and consume and
should adopt appropriate practices of food handling at home. At the industry
level, all segments, including agriculture, should establish some systcm for safety
assurance of their products and employ appropriate procedures and technologies.
The flow of raw food materials to actual consumption is schematically pre-
sented in Figure 7.5, including the accompanying hazards and risks. In principle,
the same flow scheme applies to both the food indusiry and to locally produced
Like many developing countries in tropical regions, Thailand has had a great po-
tential for improving its food export business. This Southeast Asian country grows
pineapple and other tropical fruits, cashew nuts, mans types of mushrooms and
baby corn. It also harvests shrimp and other marine products, and its rice is con-
sidered by man't to he the best in the world. Since the establishment of its National
Codex Alimentarius Committee in 1969, Thailand has seen its food export grow
nearly 12-fold to more than U.S. $4000 million. However, the growth has been hap-
hazard: exports increased by about 30°c between 1980 and 1981 but then dropped
back to less than the 1980 level for the next 4 years as food products were contin-
ually rejected by foreign countries. Noting that products were being refused because
of contamination and improper labeling, the country called upon the Food and Agri-
cultural Organization (FAQ) and the United Nations Development Program for help.
Experts from the FAQ were sent to the country, as they often are upon request. Us-
ing Codex Alimentarius standards and guidelines, they set up a pilot export control
program, trained inspectors, designed voluntary inspection systems, and brought in
laboratory people to train Thai workers. Video programs were developed for train-
ing projects, and a Memorandum of Understanding ensuring inspection and certi-
fication procedures for monitoring and sampling was signed with one of the world's
major importing countries. At the same time, WHO experts assisted Thailand in
building up its domestic food safety capabilities. Thailand's food exports grew from
U.S. $2000 million to U.S. $4800 million between 1985 and 1989, contributing
greatly to the country's 10% economic growth rate during the period
Source. (FAÜ/ WHO, 1994).
foods for private consumption, although in the latter case the food processing,
storage, and transport stages will be relatively short. In such a situation, adequate
monitoring of food quality is usually more difficult to achieve. All steps in this
process and possible preventive measures for ensuring food quality at various
stages are briefly presented here.
Hazards:
Food reaction products
Processing • contaminants
I • additives
Hazards:
Storage chemical contamination
and Transport • microbial contamination
Hazards:
Food • chemical contamination
Preparation • microbial contamination
Risks:
Food • intoxication by chemical contaminants Figure 7.5 Flow scheme of
Consumption • foodborne infections food production to food con-
food poisoning
sumption.
netically engineered foods may include new toxins and the plants may grow in
uncontrolled ways creating new weeds. More research on the safety of these ge-
netically engineered crops is needed. These biotechnological methods for food
production have been challenged on ethical grounds, as genetic engineering can
he seen as the development of unnatural plant species with unpredictable eco-
logical consequences.
Food Processing
Greater demands are being made on the food-processing industry as a result of in-
creasing urbanization. As consumers continue to move further away from the
sources of production, they will require an effective and safe food distribution sys-
tem. This separation of the consumer from the production sector also means a loss
of the traditional methods used by the consumer to ensure the safety of food.
Substantial losses of food by contamination and spoilage can be prevented
through the use of carefully controlled technology and well designed food pro-
cessing infrastructure. In addition, modern technologies can he used to prevent
or reduce the formation or use of chemicals in food. For example, crops can be
dried to prevent mold growth and production of mycotoxins during storage. Ir-
radiation can replace the use of potentially harmful chemicals used for disinfec-
tion and inhibition of sprouting. Traditional approaches to food safety, hygiene,
protection, and sanitation have their limitations and do not always guarantee re-
ductiori to the desired level of reported foodborne diseases, even in developed
countries. The potential formation of reaction products from irradiation has not
been fully investigated, however, and new health risks cannot be entirely ex-
cluded.
The mainstay of microbiological food safety programs has been inspection. In-
spection programs have serious limitations, however, as they sometimes over-
look critical factors that are not part of the inspection protocol. Inspection ser-
vices are usually inadequate or nonexistent in developing countries, where
inspectors, scientists, and regulatory authorities arc sorely lacktng. Industrialized
countries need to standardize regulations to ensure the free flow of food among
all the countries of the world (WHO, 1992b).
A different approach to safety in mcdern industrial food production is the
Hazard Analysis and Critical Control Point (HACCP) system, which is attempt-
ing to make a significant impact on the prevention of Ioodbornc diseases. The
HACCP system consists of a series of interrelated actions that should be taken to
ensure the safety of all processed and prepared foods at critical points during the
stages of production, storage, transport, processing, preparation, and service. The
elements of the HACCP system are summarized in Table 7.2. The applications of
this system are discussed in Microorganisms in Food (1988 International Commis-
sion on Microbiological Specifications for Food, the Hazard Analysis Critical Con-
trol Point Manual published in 1989 by the Food Marketing Institute of the U.S.
Bryan, 19891, as well as in a WHO report, Bryan, 1992).
100
60
62.8
-- 1
Danger
zone
40.0
37.7
37.0
- -- / Bacteria
4multiply
rapidly
Bacteria
'multiply
P.
Bacteria
multiply
36.1 0000 slowly
15.0 --
-p'
---J
10
7.2—.
Most bacteria cease
0 to multiply but
donotdie
Fresh food, cooked and eaten while still hot, will not cause foodborne inlec-
tiOfl. Even though many raw foods are contaminated with pathogenic bacteria
when they are purchased, thorough cooking should kill the bacteria. If the cook-
ing is not thorough enough, bacteria can incubate within the food and produce
foodborne infections. Some bacteria give rise to SOCS that can survive cooking
and will develop into bacterial growth if the food is cooled too slowly or if it is
stored at kitchen temperature for too long.
The chemical risks in food preparation at home are the same as those present
during food processing. The general public should be made aware of these risks,
such as frying at high temperatures (grill or barbecue), which results in toxic re-
action products. Consumers should be advised not to use utensils that may con-
tain toxic materials, e.g., lead -glazed containers.
Strcel foods can he defined as ready-to-ear foods and beverages prepared and/or sold
by vendors outside and in other public places (WHO, 1992c). Such street foods are
an affordable source of nourishment for people on low incomes and in many coun-
tries these people would be worse off if these foods were not available. The street
food industry has undergone remarkable expansirn particularly in Asian, African,
and South American countries. Although this industry employs 6%-25% of the
workforce, authorities remain hesitant to recognize it as a formal sector of the food
industry. As a consequence, this route of food supply may be ignored in food con-
trol programs and specific regulatory structures remain to be developed. Health haz-
ards related to street foods comprise all types of hazards discussed earlier in this
chapter. Cholera, hepatitis A, typhoid, and other diseases of microbiological origin
can be transmitted through such foods. In principle, foods that are thoroughly cooked
and consumed on the spot are safe, whereas precooked foods stored at ambient tem-
peratures of 5°-40°C for more than 4 hr present a considerable microbiological risk.
Hazardous chemicals and additives, notably unauthorized colorants and preser-
vatives, have been found in street-vended foods. Regulation of street-vended foods
should aim at ensuring safe, wholesome, reasonably priced food at convenient places,
without diminishing the economic, employment, and other benefits of this trade.
All extensive list of essential safety requirements for street foods has been estab-
lislied (WHO, 1992h), including recommendations regarding raw material and in-
gredients, place of preparation and sale, water, waste disposal, and preparation and
processing. Perhaps the most crucial point is the training of handlers, which has the
potential to be a more successful means of safeguarding food quality than punish-
ment of vendors, and should therefore receive more attention.
suit, the emphasis of quality control is often placed on the quality of the incoming
product, leaving a wide gap between the initial phase of quality control and ser-
vice to the consumer. Street foods arc particularly prone to lapses in safe food
preparation, as discussed in Box 7.7.
While the worlds most profound nutritional emergency is visibly exhibited in only
I or 2% of the world's children, an estimated 190 million children under age five
are chronically malnourished. The causes of malnutrition are complex—many
households run short of food between harvests, or amid drought and war. Many
malnourished children, however, live in homes with adequate food supplies and
need only a very small proportion of a family's intake to remain adequately fed. of-
ten low birth weight and specific practices such as bottle feeding contribute to mal-
nutrition in these cases. However, the main cause is the pattern of disease, espe-
cially diarrhoea, that thrives in poor communities lacking proper water and
sanitation (see Chapter 6).
When nourishment runs low, the body makes concessions to keep itself going.
These compromises may be invisible—the only outward sign is lethargy, as the body
attempts to conserve energy. To compensate for fewer nutrients, the body's ineta-
bolic rate drops, as does blood pressure. If body fat is low, it borrows from its re-
serves, thereby depleting niuscle instead of fat and damaging bone growth. Malnu-
trition amplifies all other illnesses and the risk of dying from some other disease is
doubled for mildly malnourished children and tripled for moderately malnourished
children. Good nutrition, by contrast, is excellent protection against disease.
Source: UNICEF, 1994.
tween the developed and the developing countries (3399 and 2434 calories per
capita, respectively). There are also wide gaps between and within developing
countries (UNEP, 1992a). Some people have too much food and suffer from an
unbalanced diet, whereas other people do not have enough to eat and suffer
from malnutrition. For a large part of the world's population, malnutrition re-
mains the major cause of mortality and morbidity (Box 7.8) and significant per-
centages of the world's populations remain undernourished (Table 73).
food, storage facilities and distribution systems should be improved. Three ele-
ments must be in place for the production of food: land, water, and fertilizers.
The total area of potential arabic land in the world is about 3.2 billion hectares,
about 46% of which is already under cultivation. Although large areas of new
land could he brought under cultivation, unused arabic land is not always avail-
able to those who need it most, and opening up new areas is an expensive means
of increasing agricultural production. Soil that was once fertile is being degraded
through erosion, salinization, and pollution. In areas where fertile land exists,
water is often too scarce to properly irrigate it.
Worldwide, about 2700 cubic kilometers of water were withdrawn for irri-
gation in 1990, or about 70% of freshwater usc. As discussed in Chapter 6, fresh-
water resources are becoming more scarce, requiring increased wastewatcr reuse
and better maintenance of irrigation systems. In and and semi-arid zones, the
problem of water scarcity for food production is particularly acute.
The increased application of fertilizers to supply plant nutrients (nitrogen,
phosphorus, and potassium) is an essential component of modern agriculture.
Worldwide consumption of fertilizers has been increasing over the last two
decades (UNEP, 1992a).
Despite the appearance of global focd sufficiency, the global economic climate
has changed for the worse so that for some countries the corning years will bring
a deteriorating food situation. In every country, there are both rich and poor,
urban and rural, and industrialized and agrarian communities; even where na-
tional food supplies are adequate, large sections of the population may still not
have enough food for their needs. Over the next two decades, food production
will have to keep pace with an increasing world population. The challenge for
governments and food producers will be to ensure food and nutrition security
without placing undue pressure on the environment and perpetuating different
types of health problems (WHO, 1 992b). Estimates of possibilities for increased
food production are shown in Figure 7.7.
Sub-Saharan Africa
Eastern Mediterranean
North Africa
Figure 7.7 Possibilities of
increased food production. Asia
1982184-2000, I Yield in- (excluding China)
creases; 123 arabic land in-
Latin America
creases; fl increases in
cropping intensity. From
WHO, 1992b, with permis- 0 20 40 60 80 100
Si On. Increase (%)
Global Trends
The most important factors that influence consumption and demand for food and
agricultural products are population growth, income distribution, and increased
urbanization. Most of the changes in consumption of food and agricultural prod-
ucts are due to growth in population and incomes. At constant per-capita in-
DEFORESTATION
DESERTIFICATION
About one-third of the planet's land surface is either semi-arid or arid. Because of
the stress from drought, these areas have very low productivity. With prudent irri-
gation, productivity in these areas can be increased; however, these lands tend to
be very vulnerable to further degradation. The loss of vegetation can occur because
of natural climatic shifts. It may also be induced by human activities, such as tree
felling, inappropriate agricultural practices, or overgrazing by goats or cattle.
EROSION
Wind and water erosion strip away nutrient-rich topsoil, leaving the land less pro-
ductive. Erosion is nearly always caused by a decrease in the vegetative cover of the
soil by deforestation, overgrazing, and/or agricultural practices. Loss of topsoil
through water erosion is the most common form of soil degradation; however, wind
erosion is widespread in semi-arid climates.
Source. WHO, 19921,.
comes, the demand for loud and agricultural products was expected to increase
at about 1.7% annually during the 1990s. The greater part of this increase was
to occur in developing countries, with sub-Saharan Africa showing the largest
percentage increase (WHO, 1992h).
Only in recent decades have research findings confirmed the suspicion that
dietary preferences may influence the onset of many diseases, particularly those
attributed to the so-called affluent diet, a diet consisting of large quantifies of
high-fat and high-sugar foods. Examples of these diseases include obesity, heart
disease, and certain types of cancer. With about two-thirds of all energy coming
from vegetable sources and one-third from foods of animal origin, the developed
market economies have reached a level at which no further substitution between
the two groups is desired.
The use of inorganic chemicals to control insects has a long history, possibly
dating back to classical Greece and Rome. In the middle of the nineteenth cen-
tury, modern pesticides began to be introduced. They replaced older plant-
derived pesticides, such as nicotine, and other chemical pesticides, including the
salts of arsenic. Many of the older compounds were highly toxic and their use
by the public was restricted in many countries. The introduction of dichloro-
diphenyl-trichioroethane (DDT), which was first synthesized in Switzerland dur-
ing World War II, seemed to be full of promise because of its wide spectrum of
activity and relatively low human toxicity. DDT is an organochlorine pesticide
that was followed by organophosphorus compounds and the carhamatcs. The
benefits of their use for agriculture seemed remarkable, as both the quantity and
quality of crops rose as a result of their use. Eventually, the health and envi-
ronmental pesticides to the agricultural workers became a major concern (see
Boxes 7.10 and 7.11). A wide range of insecticides, fungicides, molluscicides, hac-
TABLE 7.4
GENERAL CATEGORIES OF PESTICIDES
Pesticide Used Against Category Examples
insecticides Insects and related organophosphorons Malathion, parathion,
species COiiipoti nds dichlorvos
Carbaniate compounds Aldicarp, carbaryl, metliotnyl
Organochlorine compounds Aldrin, dieldrin, endrin, DDT
Pvrethroid compounds Bioallethnn, cvhalothrin
Rodenticides Rats, mice, and Ant icoagulants Wariarin and derivati es
other rodents Others Zinc phosj)liide, thallium
Herbicides Weeds Dipyridyl derivatives Paraquat, diquat
Phenol derivatives Pentachlorophenol
Fungicides Fungi and molds Dithioca rbamates Arasan, thirantid
Phta lami des Captan
Motluscicides Snails M eta Ide hyde
Fumigants Gases used to Ethylene (libr()nmmde
sterilize products Methyl bromide
DDT, an organochiorine pesticide, was used widely from the 1940s to the 1960s.
DDT persists in plants and soil, passes along the food chain, and can thus be pres-
ent in food for human consumption. In the 1970s, these dangers were recognized
and the use of DDT was restricted in many countries. It is still, however, one of the
major pesticides in India and is widely used in developing countries to kill mosqui-
toes and thereby combat malaria. Like other organochiorine pesticides. DDT accu-
mulates in fatty tissue and is therefore found in food with a high fat content, par-
ticularly milk and dairy products.
Acute exposure to DDT (or other organochlorine pesticides) causes central ner-
vous system excitation (irritability, excitability, headache, disorientation, twitching).
High doses can damage the liver and are suspected to be carcinogenic and may in-
duce xenooestrogenic effects. Apart from its use to increase quality and quantity of
crops, DDT has also been widely used to combat malaria. After several years of suc-
cess in fighting this disease, resulting in significant benefits for human health, the
mosquito carrying the malaria developed resistance to the chemical.
Source.' UNEP/GEMS. 1992.
These substances are the most common cause of acute pesticide intoxication. The
organophosphares (e.g., parathion, dichiorvos, malathion) and the carbamares (e.g.,
aldicarb, carbofuron, carbaryl) share a common mechanism of toxicity—cholinesrerase
inhibition. The nerve transmitter, acetyicholine, is normally itiactivated by an en-
zyme called acetvlcholinesterase. The action of this enzyme is blocked through the for-
mation of a pesticide–enzyme complex. The clinical presentation following acute
poisoning is easily recognized: neuromuscular paralysis, central nervous system dys-
function, and depression of red cell and plasma cholinesterase activity. The charac-
ter, degree, and duration of the illness depend on the degree and rate of accumu-
lation of aceryicholine. (Characteristic symptoms include blurred vision, tearing,
salivation, nausea, diarrhea, headache) Chronic effects may include dermatitis as
well as mood lability, fatigue, and impaired concentration. A delayed neuropathy,
rapid-onset distal symmetric sensory motor neuroparhy, may also occur.
Pesticide manufacturers
/ /term, very high'\
level exposure
formulators, misers,
applicators, and pickers / Long-term
high level exposure
All population /
groups
The general population may be exposed to pesticides in several ways, the main
routes being ingestion via food and drinking water, inhalation via air and dust, and
skin absorption via clothing or direct contact. The most common cases of acute ac-
cidental poisoning by pesticides are those in which grain coated in pesticides has
been eaten. Other accidents have occurred when insecticides that are effective
against one type of pest were used incorrectly against other types, such as bedbugs
and lice. The use of old pesticide containers for household food and water storage
is another source of poisoning. Pesticides that are improperly stored have been con-
sumed by unknowing children. Studies of any link between pesticides and cancer
in the general population are difficult because generally the exposure levels are low.
In addition to the toxic elfects listed in Table 7.5, effects on human repro-
duction have been shown for a number of pesticides, including sterility, fetal
death, fetal toxicity, and teratogenicity (fetal malformations). Other recognized
effects of certain pesticides include cataract formation, cellular proliferation in
the lungs, and damage to the immune system.
Integrated Pest Manaqement
Pest management may consist of many different methods ranging from routine
applications of pesticides to measures for ecological management. Pest control
based solely on the application of pesticides is now increasingly rejected in most
countries. Instead, many approaches that can control pests while reducing pes-
ticide use are employed. In a pest management system, all suitable techniques
and methods are used in as compatible a manner as possible, and the pest pop-
ulation is maintained at levels below those causing economic losses (WHO,
1990a). Approaches that minimize pesticide use include plant disease forecasting
methods to minimize use; better formulation and placement of chemicals so that
smaller amounts are used; alternative farming systems to minimize pest attacks;
and repeated field visits to determine whether pest levels necessitate spraying.
A number of other pest control strategies are also increasing in significance,
including the use of biological insecticides based on insect pathogens; the release
or encouragement of predators of pests; release of sterile male insects to limit the
reproducticn of pests; planting of crop varieties that are resistant to pests; and
planting of trap crops to lure pests away from the principal crop (WRI, 1992).
Furthermore, modern biotechnological techniques offer the possibility to trans-
fer genes from one species to another, making crops more resistant to plagues.
For instance, it is well known that the bacterium Bacillus thuringiensis priduces
a toxin that kills larvae and insects. Using DNA recombination techniques, the
gene coding for the bacterial toxin has been isolated and transferred to tobacco
plants, where it is expressed. When insects eat from such a transgenic plant, they
die rapidly. However, these techniques are not yet widely accepted by society
and there is considerable reluctance to accept genetic engineering because of fears
of unanticipated effects and cultural concerns about the ethics of manipulating
life.
Study ,ectrnc
How can the HACCP concept he used to reduce the formation of Maillard
reaction products?
Many different actions can be taken to improve the safety and quality of
our food. Prepare a summary of these actions, indicating (a) the level at which
this action should be taken and (Li) the type of contaminant (biological or chem-
ical) involved.
CHAPTER CONTENTS
The Nature and Requirements of Development and Ownership of
Human Settlements Land
Human Settlements as Ecosystems Conservative/Traditional Values
Basic Health Requirements of Mixed Implications of
Settlements Environmental Protection
Housing and Health Urbanization and Health
Housing, Communicable Diseases, The Urban Poor
and Infections Infrastructural Requirements of
Home Accidents and Toxic Urbanization
Exposures Air Pollution
Psychosocial Problems Noise
Factors Causing Increased Urbanization Motor Vehicle Accidents
Trends in Urbanization The "Healthy Cities" Approach
Migration to Urban Centers to Prevention
Rural Economic and Social Promoting Urban Health
Development Characteristics of a Healthy Cities
Differences of Time and Space Program
Dependence on Primary Industries From Program to Movement
Healthy City Actions
281
THE NATURE AND RFOIJIRFMFNTS OF HUMAN SFTTTFMFNTS
As humans have become more alienated from their natural environment, the
biofeedback mechanisms that throughout time have regulated human–ecosystem
interactions have become more obscured. To provide a comprehensive explanation
of the intimate relationship between humans and their surrounding life-supporting
environment, a holistic transdisciplinary "ecosystem health" approach must take into
account the circumstances of these rapidly expanding built environments.
Urban settlements, ecosystems created by and inhabited by humans, consist of
both the built and human-modified physical environment. Thus they include the
processes of social aggregation, migration, modernization and industrialization, and
the circumstances of urban hying. These human-created urban ecosystems exist within
a larger frame of reference—the bio-regionai and planetary "natural" ecosystems that
ultimately provide fundamental life support. The social and economic development
that has played a central role in improved population health historically is built upon
those natural ecosystems, their resources and the "free" eco-services they provide.
Human health, thus, cannot he maintained if ecosystem health is not sustained.
DIMENSIONS TO CONSIDER
The relationship between the built environment, the natural environment, and hu-
man health is closely intertwined. Analysts such as Trevor Hancock (Hancock, 2000)
have drawn attention to six distinct dimensions of urban ecosystem health:
Health status of the urban human population in terms of its physical and men-
tal well-being, including health equity, the distribution of health, and well-
being across the different segments of the community;
Social well-being within the urban community, including social, economic, and
cultural conditions, the effectiveness of the processes of governance (including
education, participation, and access to decision-making power), and social eq-
uity, the distribution of these and other determinants of health;
Quality of the built environment, including aspects of housing quality, trans-
portation, sewage and water supply, roads and public transport systems, parks
and recreation facilities, and other civic amenities;
Ambient environmental quality within the urban environment in terms of air,
water, soil and noise pollution;
Health of the biotic community, including aspects of habitat quality and genetic
and species diversity;
Impact of the urban ecosystem on the wider natural ecosystems of which it is a
part, as measured by environmental sustainability concepts such as the urban
"ecological footprint."
c_
-- -
zz C
E zz -
- )p--
E
E
- z
fl
Iz
—),-
r 1Ic
(continued)
In the developed world, the long-term sustainability of current patterns of re-
source consumption has been repeatedly called into question and questions of eco-
toxicity (e.g., endocrine disruptors, persistent and cumulative exposures) have been
frequently raised. Nevertheless, improvements in environmental protection achieved
over the last quarter of the twentieth century have contributed to create generally
ljveable conditions, albeit with threats to viability and sustainability. However, in
the developing world, there are many indicators of distress—and the ability to pro-
vide liveable and viable conditions is tinder considerable strain. Frameworks devel-
oped to assist decision-makers understand the relationship of human-ecosystem in-
teractions are especially valuable in understanding dynamic relationships between
driving forces, pressures, states, exposures, and effects (DPSEEA) within this envi-
ronment. The figure in this box builds upon Hancock's urban ecosystem dimensions
(Hancock, 2000), utilizing the DPSEEA framework discussed elsewhere in this text.
It shows how each dimension ultimately impacts human health, albeit mediated by
different pathways and determinants.
One example of how this framework is being applied within an urban ecosys-
tem community is in Centro Habana, Cuba, in which an extensive series of health
interventions were implemented in an inner-city community to try to improve the
quality of life and ecosystem health. The interventions addressed areas that the com-
munity perceived as being of highest risk, including housing conditions, environ-
mental sanitation, lifestyle concerns, social environment issues and immediate
threats to health. The results to date indicate the strong capacity-building nature of
applying such approaches (Yassi ci al., 1999; Fernandez ci at., 2000). In fact, the
development of analytical indicators collahoratively with the community is itself a
principle that has received recognition as an element consistent with an ecosystem
analysis (Spiegel et al. 2001).
Contributed by Dr. Jer7y SpkqeL
and public transportation, and the production and distribution of consumer goods
like food and clothing. They also enable the provision of services such as educa-
tion, health, and law enforcement, as well as provide infrastructure and support
for cultural, religious, and recreational activities. Settlements also give assistance
to vulnerable groups, such as elderly people.
In effect, a symbiotic relationship exists between family dwellings and com-
munity settlements, in which the values of both enhance each other. The fam-
ily dwelling is not just a place in which to eat and sleep but is also where peo-
ple store their possessions, relax, study, procreate, nurture and educate their
children, and often die. It is usually the most important focus of a person's life.
Settlements provide an umbilical cord of support for families and individuals.
Shelter requirements are to a large degree dependent on climate. For exam-
ple, in extreme northern and southern latitudes, shelter from cold is of central
importance, while in hotter regions protection from heat is essential. In low-
lying coastal or tropical regions, hurricanes, monsoons, and tidal waves are seri-
ous problems for communities, while in some inland regions, sandsiorms, tor-
nadoes, and blizzards present different problems. In regions where seismic ac-
tivities are possible, volcanoes and earthquakes pose a potential threat to
communities. Each of these conditions has inspired different designs for both
dwellings and settlements with regard to ideal infrastructure and housing needs.
BOX 8.2
Examples of Environmental Health Indicators
DRtVING FORCES
PRESSURES
LOCAL HAZARDS
EXPOSURES
EFFECTS
ACTIONS
TABLE 8.1
HOUSING FACTORS INFLUENCING HEALTH
Sale and adequate water supply
Sanitary disposal of human and animal excreta
Efficient drainage of surface water
Appropriate solid waste disposal and storage
Personal and domestic hygiene
Safe food preparation
Housing structure and maintenance
addition, inadequate humidification can cause dry air (a known cause of irrita-
tion to eyes, skin, and throat), static electricity, and temperature fluctuations.
Sources of environmental contamination include ofi-gassing from new furni-
ture or carpeting, cleaning materials, chemicals from adjacent offices, unclean
ducts, fibreglass, and cigarette smoke. Virtually all dusts, vapors and aerosols that
can react with proteins can cause an allergic rcacticn. Generally considerable ex-
posure is required to become sensitized. However, once the individual has be-
come sensitized to any of these, allergic reactions may be elicited after only a
brief and low-concentration exposure.
Psychosocial Problems
Reducing psychosocial stress is a vital role of proper housing, as the link between
a good psychological environment at home and health is strong. Poor psycholog-
ical health makes pecple generally more susceptible to many ccmmunicable and
chronic diseases and there are numerous other health problems that accompany
poor psych( logical health (e.g., psychosomatic illnesses, substance abuse, mental
illness, and violent behaviors). Increasingly, housing in urban settings fails to serve
the role of psychosocial haven, as overcrowding and the stresses of urban life pro-
duce exactly the opposite effect. Urban housing, with its model of individual fam-
ily homes (transplanted from the developed world to communities all over the
globe), often tends to break down traditional community structures that existed in
rural environments, increasing individual alienation. The urban poor have the ad-
ditional burden of living in insecure tenant situations and being subject to ex-
ploitation in their housing environments. All of these problems arc experienced
most keenly by those making the transition from rural to urban life. The trend to-
ward urbanization makes this problem urgent. Many factors involved in housing
can reduce these problems to a minimum, some of which are listed in Table 8.4.
TABI.E 9.4
FACTORS AFFECTING CONTROL OF PSYCHOSOCIAL PROBLEMS
Living space should he sufliciently large and reasonably Irivate and comfortable.
The housing environment must he safe and couducive to community interaction.
Recreational space must he available to neighborhood residents.
Neighborhoods should be protected against traffic noise and industrial pollution.
Parks, l)laygrouflds, and other community amenities should he easily available.
Housing should he easy to maintain and keel) clean.
Trends in Urbanization
Urbanization, the process by which an increasing proportion of the population
comes to live in urban areas, has become a worldwide problem. Urbanization is a
reflection of population growth and opportunities in cities. A population can grow,
only through increase in births, decrease in deaths (the natural increase); or in-
creased immigration. Decreased emigration may reduce the loss of population if
the rate of immigration does not also fall. Urban areas of the world are now ex-
periencing both a natural increase and an increase in net migration to the cities.
in 1999 the world's population reached 6000 million people—more than three
times the population of 100 years ago. A 30% rise is predicted by the year 2010.
Of this predicted growth, 90 0% is expected to occur in countries that are presently
classified as developing countries. Urbanization is also occurring at a dramatic
pace. The urban populations of developing countries will double in the 20 years
from 1990, which means that by 2010, well over half the world's population will
he in urban centers, or about 4000 million people UNEPIWHO, 1992c). By 2025
it is expected that more than 5000 million will live in urban areas, as shown in
Figure 8.1 (WRI, 1996). Urbanization has been growing in developing countries
at a much faster rate than in developed countries. It is estimated that by 2010,
60 1VO of the developing countries' urban population will be living in shanty towns
or informal settlements.
Of special concern in this global trend of urbanization is the growth of mega-
cities, or cities with a ptpulation of 8 million or more; it is projected that by 2015
there will he 36 megacities (UN, 1997). The largest cities are listed in Table 8.5.
Megacities warrant concern because their sheer size creates great challenges to
human health and the environment.
1101
(I)
0
6
.0
=
C
0
4
75
0
0
0
Figure 8.1 Urban population growth. 1950-2025. From UNDP. 1995, with permission.
TABT.F. 9.6
FACTORS AFFECTING REGIONAL URBANIZATION
Changes in a region's economic or employment base often lead to increased employment opportu-
nities in urban centers.
Areas with unequal income distribution, where only a few individuals are affected by economic
growth, experience signiticantly diflerent urbanization patterns than areas where many people
have access to economic l)enefits.
Political structures can affect the distribution of poverty and hence urban developnient areas.
Government niacroecononlic policies may favor urban centers, and thus increase urbanization
rates.
World markets, which intlitence national economics, necessarily influence urban systems.
Casablanca
Kinshasa
Bogota
Calcutta
Buenos Aires
Mexico City
Bombay
Manila
Bangkok
0 20 40 60 80 100
Percentage
Figure 8.2 Percentage of people living in slums and squatter settlements in some urban
centers (1988). From UNEP, 1992a, with permission.
uid waste management, and housing and transportation networks. All of these
are energy-expensive but they must be met, at least to some degree, to ensure
a minimum standard of health. The rapid pace of urbanization in many areas has
virtually outstripped the ability of local governments to provide these services
adequately. Additionally, promotion of economic growth has led to industrial ex-
pansion that frequently overwhelms the existing urban services. Several of the
health-promoting housing design features listed in Tables 8.1 to 8.4 relate di-
rectly to urban infrastructure.
Air Pollution
As discussed in Chapter 5, air pollution is one of the many problems modern cities
experience, no matter what their level of economic development. In the past, air
pollution was often considered a matter of aesthetics and quality of life, but not
of survival or health. Increasing scientific evidence has shown that the effects of
air pollution on health are considerable, even in developed countries where the
levels of air pollution have been largely controlled. This has led to a reexamina-
tion of the need for air quality management. The negative effects of air pollution
are now taken much more seriously. The annual sulfur dioxide (SO 2 ) and sus-
pended particulate matter (SPM) levels in cities involved in the Global Environ-
mental Monitoring System (GEMS) are shown in Figures 8.3 and 8.4.
The principal sources of emissions into the air are the direct products of ceo-
nomic activity in cities: transportation, power production, home heating and
cooking, and industrial production. The costs imposed by air pollution are most
Key
1 Milan Ran
2 Shenyang ItA
3 Tehran
4 Seoul
5 Rio de Janeiro
6 S8o Paulo
7 Xian
8 Paris
9 Beijing
10 Madrid
11 Manila
12 Guangzhou
13 Glasgow
14 Fankturt
15 Zagreb
16 Santiago
17 Brussels
18 Calcutta
19 London
20 New York City
21 Shanghai
22 Hong Kong
23 Dublin
24 St. Louis
25 Medellin
26 Montreal
27 New Delhi
28 Warsaw
29 Athens
30 Wroclaw
31 Tokyo
32 Caracas
33 Osaka
34 Hamilton
35 Amsterdam
36 Copenhagen
37 Bombay
38 Christchurch
39 Sydney
40 Lisbon
41 Helsinki
42 Munich
43 Kuala Lumpur
44 Houston
45 Chicago
46 Bangkok
47 Toronto
48 Vancouver
49 Bucharest
50 Tel Aviv
51 Call
52 Auckland
53 Melbourne
54 Craiova
WHO Guideline 40 - 60 pg m3
Figure 8.3 Annual SO 2 measures in GEMS/Air cities, 1980-84. From UNEP/WHO, 1987b,
with pern1ission.
Key
1 Kuwait Range of individual site
2 Shenyang annual averages
3 Xian
4 New Delhi
5 Beijing I I I
6 Calcutta
7 Tehran f
Combined site
8 Jakarta
9 Shanghai average 1980-84
10 Guangzhou
11 Illigan City
12 Bangkok
13 Bombay
14 Kuala Lumpur
15 Zagreb
16 Rio de Janeiro
17 Bucharest
18 Acera
19 Lisbon
20 Manila
21 Chicago
22 Caracas
23 Birmingham
24 Helsinki
25 Hamilton
26 Sydney
27 Houston
28 Cralova
29 Toronto
30 Melbourne
31 Medellin
32 Chattanooga
33 Fairfield
34 Montreal
35 Vancouver
36 New York City
37 Tokyo
38 Osaka
39 Cali
40 Copenhagen
41 Frankfurt
WHO Guideline 60— 90g m3
Figure 8.4 Annual SPM measures in GEMS/Air cities, 1980-84. Front UNEP/ WHO, 1987h,
with permission.
In recent years, it has become obvious that pour comn)unities tend to he inore
affected by air pollution than those with higher average incomes. This observa-
tion has been followed by a number of studies that have shown that exposure
to pollution tends to accompany pcverty, marginalization from society, and lack
of access to social services and health care. The 1ikely explanation for this is that
people who have access to personal resources are more likely to live together,
a oiding unhealthy or unpleasant neighborhoods. However, there is also evi-
dence that factories, power plants, or other facilities that may be sources of poi-
lution are more likely to be built in or near poor communities in the first place.
The problem of equity in environmental risk, called environmental justice, is an is-
sue of serious concern in discussions and policies regarding air pollution, Con-
taminated water supplies, and hazardous waste disposal.
Noise
The major sources of noise arc road and air traffic, Construction, industry, and
people. These types of noises are generally on the rise as urban centers become
more dense, industry expands, and the need for transportation increases. Noise
is of most direct concern in the workplace, where hearing loss most commonly
occurs. (Industrial noise and its control are also discussed in Chapters 2, 4, and
In many countries of the world, governments have actively promoted bicycle com-
muting. For example:
• In China, where 50%_80% of urban trips are by bicycle, the government offers
subsidies to those who bicycle to work. It has also allocated extensive urban street
space to bicycle traffic.
• Prompted by Cuba's petroleum crisis, car traffic has been reduced in Havana by
35% and bus traffic by SOC/u, and bicycle use has been actively encouraged. Now,
one of every three trips in Havana is made by bicycle. The city government re-
duced car speeds to improve safety conditions, and in addition to offering bicy-
clists subsidies, has constructed bike lanes.
• In developed countries, Denmark and The Netherlands have done a great deal to
promote bicycle use. The Dutch National Transportation Plan aims to increase the
amount of cycling by 30% by 2010, by providing new bicycle routes, parking at
railway stations and bus and tram stops, and additional safety measures, despite
the fact that bicycle use is already very high in this country.
• In several cities in Canada and Australia, extensive bicycle paths have been in-
troduced.
• In Seattle, all buses in the Metropolitan Transit System are now equipped with
bicycle racks.
These examples illustrate how, if properly promoted and encouraged, bicycles can
provide access to shopping, schools, and work. This can help reduce air pollution
and the other problems associated with motorized vehicles described in this chap-
ter. In addition, bicycle use is a form of active transport that gives much-needed
physical exercise to sedentary populations of developed countries.
Source: WRI, 1996.
10.> However, as rates of urbanization all over the globe exceed the ability of
city planners to protect residents from noise, increasingly it has become a gen-
eralized urban problem.
As discussed in Chapter 2, noise may cause physical, physiological, and psy-
chological effects in humans. The physical effect of sound waves against the ear
drum resulting in hearing loss is sometimes referred to as a direct effect. The phys-
iological changes that may register cognitively include sleep disturbance and psy-
chological damage, and are considered indirect effects. The dose—response rela-
tionship between noise and hearing loss was discussed in Chapter 2.
Environmental noise, (also called community noise) is often complex (Ry-
lander, 1992; Berglund ci al., 1999). Acoustical patterns are traditionally ex-
pressed as the summation of sound energy over a certain period of time. Vari-
ous methods of calculating an average have been developed, such as the noise
pollution level, the average day and night level, and the equivalent sound level
Noise may affect health by inducing nuisance. Nuisance is a difficult concept to mea-
sure objectively and has many of the characteristics of psychosocial hazards dis-
cussed in Chapter 2. For instance, the extent to which a person is aggravated is not
merely determined by the type and intensity of the noise but also by personal char -
acteristics or circumstances. Nuisance may he rather specific—for instance, when a
conversation is interrupted by a passing train, but it can also be nonspecific and give
a general feeling of annoyance, discontent, or even fear. Apart from the intensity
of the noise, other physical characteristics such as frequency and rhythm (impulse
versus nonimpulse sounds) are of relevance. Noise with low frequency components,
for example, require lower guideline values. For impact noise, both the maximum
sound pressure and number of noise events must be considered.
During the day, few people are annoyed at noise levels below 50 dB(A). How-
ever, sound levels during the evening and night should be 5-10 dB lower. A WHO
expert panel (Bergiund et al., 1999) developed the guidelines in Table 8.7 for com-
munity noise in specific environments.
therefore relate to the extent of the impact on the population, i.e., the propor-
tion the population suffering from serious sleep disturbance, the most serious ad-
verse effect of noise. According to the principles of risk assessment, health effect
data constitute the necessary background information for the formulation of stan-
dards. The WHO suggests that from a medical point of view, the proportion of
very annoyed people in the population of urban centers should not exceed 5%
(Rylander, 1992). Politicians and administrators who are responsible for setting
noise standards should bear this suggestion in mind, as well as the guidelines in
Table 8.7.
Many things can be done to alleviate noise-related problems. Residents can
be protected from industrial noise by zoning laws that prohibit the mixing of in-
dustry with residential areas. (This is particularly important for informal settle-
ments, which are often forced to develop in industrial areas because these areas
are the only viable option for the very poor.) Zoning laws can also separate res-
idential areas from major transportation routes and airports. Municipal bylaws
can prevent people from making unnecessary or excessive noise. Regulations can
also place restrictions on motor vehicles, specifying that they must be in good
running condition and that they must have appropriate mufflers. The difficulty
with all of these solutions is that they require active participation on the part of
government. Large-scale changes in laws are notoriously difficult and slow to be
implemented.
There is little residents can do independently to reduce the amount of noise
in their lives. Hearing protectors can be worn to reduce the likelihood of direct
hearing loss, and they may reduce sleeplessness due to background noise. But
this solution does not address the real cause of the problem and brings new prob-
lems of its own (discomfort, inability to hear important low-intensity noise).
tween 1960 and 1989, compared to 2.1% per year, respectively. By early next
century, if current trends continue, the rapidly developing areas of the world (es-
pecially Asia, Eastern Europe, and Latin America) and the Organization of Eco-
nomic Cooperation and Development (OECD) Pacific region will have as many
vehicles as North America and Western Europe, although per-capita rates will
remain substantially lower. Figures 8.5 and 8.6 show the 1993 per-capita num-
ber of passenger cars in selected regions and projected trends in worldwide mo-
tor vehicle ownership, respectively.
In 1993 an estimated 885,000 people died in traffic accidents (WHO. 1995a).
Globally, this makes traffic accidents the second-leading cause of death for peo-
ple aged 5 to 44. With the majority (70%) of these deaths occurring in devel-
oping countries, in some places it is the number-one killer for this age-group.
For example, in Nigeria, motor vehicle accidents account for one-half of the to-
tal deaths for this age-group.
In developed countries, the mortality rate for motor vehicle accidents has been
dropping over the last 70 years, even as the rate of vehicle ownership has dra-
matically increased. This has been attributed to the gradual improvement of road
conditions, the establishment of higher vehicle safety standards, and increased
driver training. In developing countries, however, the opposite has occurred. The
rate of fatal injuries per registered vehicle climbed to 300% since 1968 in Africa.
One reason for this is that each incident frequently affects many people—for ex-
ample, when a motor vehicle accident involves a crowded bus. Moreover, mo-
900
800
700
600
500
400
300
200
Figure 8.6 Worldwide motor 100
vehicle ownership, 1970-2010. 0
1970 1980 1990 2000 2010
From WRI, 1996, with permis-
sion. Year
All of the above indicated actions (political decisions, intersectoral action, com-
munity participation, and innovation) contribute to the outcome of a program:
a heahhy public policy. The success of a Healthy Cities program is reflected in
the degree to which policies that create settings for health are in effect through-
out the city. Program participants have achieved their goals when homes, schools,
workplaces, and other parts of the urban environment become healthier settings
in which to live.
From Program to Movement
The dissemination of Healthy Cities strategies has been greatly accelerated by the
growth of national and subnational networks. Although the Healthy Cities pro-
gram was introduced in Europe, the influence of the program extends beyond
the boundaries of this region. Regional networks have been developed in Aus-
tralia, Canada, the Maghreb region (Northern Africa), Iran, Malaysia, the United
States, and Middle and South America. Participation in Healthy Cities programs
in developing countries is also encouraging (WHO, 1995b). Through the success
of the developed networks, the number of communities cooperating with the of-
ficial programs is becoming a sort of movement that is growing far more rapidly
than expected.
In 1996 World Health Day was dedicated to the Healthy Cities program and
about 1000 cities committed themselves to urban health promotion. In addition,
a Safe Communities Network has grown up as well, and the United Nations En-
Study ()liecOnfls
Is urbanization occurring in your area? If so, why? If not, why not, and
do you think it will occur in the near future?
Is noise a problem in your area? If so, what are the main sources?
Outline what you would do to decrease the incidence of road injuries in
your jurisdiction.
. I-low would you apply the principles of' Healthy Cities" in your jurisdic-
tion?
CHAPTER CONTENTS
311
TABLE 9.1
SUMMARY OF ENERGY NEEDS
Basic human needs (heating, lighting, cooking)
Agriculture (irrigation, mechanization)
Urbanization (basic Services)
Transportation
industrial production
The patterns of energy use and production are key characteristics of all soci-
eties. The challenge is to produce the amount of energy needed while imposing
the least possible health risk and environmental detonation. The availability of
energy often determines the nature of a region's sicloeconomic development.
For development to be sustainable, energy sources must also be dependable, safe,
and environmentally sound.
It is widely accepted that an assessment of the total risk of an energy source
must include an evaluation of all the risks across the energy cycle: (a) material ac-
quisition and construction, (b) emissions from material acquisition and energy
production, (c) operation and maintenance, (d) energy back-up systems, (e) en-
ergy storage systems, (f) transportation, and (g) waste management.
350
300 oa
250
.----
- 200
OECD countries
>< 150
ID
Developing
100 countries
50 — Transition countries
(tormer Soviet Union & Central Europe)
OF- Figure 9.1 Trends in energy
1973 1978 1983
11 1988 1993 Consumption. 1973-1993. From
Year WRI, 1996, with permission.
80
60
C
a
>< Gas
.- 40
Hydro — —
011
Figure 9.2 Commercial energy —
•- Nuclear
———
consuniptmn by source, indus-
trialized countries, 1971-91.
1974 1978 1982 1986 1990
From WRI, 1994, with permis- 1970
Si OIl. Year
slant since 1965, although some current projections suggest that the energy con-
sumption growth rate will be highest in the developing countries over the next
several decades (4.5% per year versus 1.5% per year in developed countries)
(UNEP, 1992a). In fact, according to the U.S. Office of Technology Assessment,
commercial energy use in developing countries could triple over the next 30 years.
In some countries demand is growing more than 10 11% annually (OTA, 1992).
With industrialization, there is a trend away from reliance on biomass and other
renewable energy sources and toward dependence on fossil fuels, which are non-
renewable. About 100 years ago, noncommercial sources of fuel (fuel wood, agri-
culture [e.g., dung]) accounted for about 50% of the total energy used in the world.
Today, this type of fuel only comprises about 12% of the total energy use in the
world, although about two billion people depend on noncommercial products for
their fuel. This percentage has remained constant since about 1970 (UNEP, 1992a).
Figures 9.2 and 9.3 show how the use of various energy sources has changed
between 1971 and 1991 in the industrialized countries, and developing countries
50
40
30
a)
=0
a Solids
20
Liquids
•. -—
10
BIOMASS FUELS
40 20
-D
30 15
Par5cuiates
per standard a
U) CD
a \me&
CO per
5 20 standard 10
a
.5 - mea 2
0 Sn
CD
0
10 05
a
Figure 9.4 Amount of indoor a
TART F Q 2
ADVERSE EFFECTS OF BIOMASS FUEL PRODUCTION AND COLLECTION
ON HUMAN HEALTH
Function Possible Health Effects
Processing/preparing dung cakes Fecal/orallenteric infection
Skin infection
Charcoal production CO/smoke poisoning
Burns/trauma
Cataracts
Gathering fuel Trauma
Reduction in infant/child care
Bites from venomous snakes, spiders, leeches, insects
Allergic reactions
Fungus infections
Severe fatigue
Source; WEtO, 199 lb.
FOSSIL FUELS
TABlE 0 4
HAZARDS ASSOCIATED WITH FOSSIL FUEL EXTRACTION AND PROCESSING
Fuel Location Hazards and Effects -
Coal Underground mines Coal workers' pncumoconiosis (CWP( or "black
lung," silicosis, fires/explosions, injuries
Open-pu mines Industrial tironchitis, chronic cough, accidents
(mining, transport)
Oil Oft-shore developments Accidents caused by weather, explosions
Land oil fields Dermatitis (from long-term expostire to crude oil),
accidents/explosions
Refineries Exposure to hydrocarbons (known carcinogens)
Natural gas Deposits Hydrogen sulfide exposure, accidents/explosions
Refineries Exposure to hydrocarbons (known carcinogens),
accidents/explosions
In November 1979, the Swedish Government commissioned the Swedish Power Board
to investigate and report on how the health and environmental problems arising from
an increased use of coal in Sweden could be solved. The project's investigators ana-
lyzed the various stages of the use of coal and the disturbances that can arise from such
use. The emission of sulfur and nitrogen oxides, toxic metals, and dust is, of course,
not peculiar to coal, but can occur to varying degrees in the burning of other fuels.
Large resources of coal, including the much-desired low-sulfur coal, are avail-
able in many parts of the world, including the United States, Poland, the former So-
viet Union, western Canada, Australia, and Colombia. Coal, like peat and wood, is
not homogeneous, but rather contains a varying content of trace elements. Mer-
cury is one of the most iniportant toxicologically.
The occupational hazards associated with coal are well known. Dustiness oc-
curring in the transport and handling of coal can occur particularly in warm and
windy weather conditions. The risks of harmful dust can be eliminated or strongly
reduced by rational working methods and technical solutions. This also applies to
the transport and handling of waste products. Special care must he taken at the
point loading takes place at the installation and when loading the products at the
dump (see Fig. 9.5). Dry ash should be handled in fully enclosed systems.
The Swedish Project concluded that adverse effects on the respiratory system
were not expected to occur with the burning of coal in Sweden, given the use of
modern and effective techniques. Investigations into the content of mutagenic and
carcmogenic substances in the emissions have shown that the large modern, well-
run, coal-fired and oil-fired installations emit only a small quantity of rnutagenic
materials. However, emissions per energy unit of mutagenic substances can be con-
siderably greater from small installations.
The Power Board considered that the use of coal, which involves replacement
of oil, affecied the level of methylmercury in fish to a small degree. There is a risk
of increased levels in fish in acid-sensitive lakes close to large point sources, such
as a coal-fired powered station, if prudent measures are not taken. Siting, local con-
ditions, and the measures taken in such cases determine the extent to which an in-
creased risk occurs. It was noted that tighter regulations in this area can very well
prove essential to bring down mercury risks to acceptable levels.
On the assumption that fly ash with too high a radioactivity is not used in build-
ing materials for residences, and that drinking-water wells are not situated in the vicin-
ity of waste dumps, the techniques available for transport and disposal of waste prod-
ucts from the combustion of coal were deemed to be sufficient to avoid risks of negative
results. The project concluded that coal can he used as replacement for oil in district
heating and power stations and within industry, in a way that is acceptable for health
concerns, if coal is used in well-maintained installations that are big enough to make
it feasible to use environmentally safe technology. The production of electricity in coal-
fired powered stations was similarly judged to be acceptable. It was noted that special
investigations into local and regional conditions should he conducted at each site be-
fore deciding the extent of electricity production that is possible.
Coal, like other fossil fuels, contains comprunds of an undesirable nature that
are released during combustion. Many of these may affect health. Apart from the
annoyance of people, local effects on the respiratory tract, effects on other organ
systems, and genotoxic effects (e.g., cancer) can occur. Impurities in effluent from
refuse dumps, particularly metals, can lead to systemic effects.
SOUrCe. SCHEP, 1983.
320
Radionuclides
MEMEN
ME Iiit4 I
.I
Beneficiation Plant ' Truck Utility Ash Sludge
F bou r
plant waste
%
I %
I
''
rA'
,
I
I
Train
I
I • Barge II
I
I • I
I I
I I
•
I I
I l Slurry A I
pipeline :
I •
I I I
I I I I
I
I I I
WATER I
:
Figure 9.5 Various stages in the handling of coal in Sweden and the environniental dis-
turbances that can occur. From SCHFP, 1983, with permission.
that are the most hazardous. Leaks of crude oil are generally less dangerous than
leaks of refined petroleum products, such as gasoline, which can cause explo-
sions, fires and contamination of ground water. Sour gas, which is natural gas
containing a relatively high content of sulfur is particularly hazardous because it
may contain high levels of hydrogen sulfide, a toxic gas.
Large power stations can convert coal, oil, and, to a lesser extent, natural gas
into electricity with fewer incomplete combustion products than can individual fires.
HYDROPOWER
Electricity These possible risks associated with the use of electricity are, of course,
independent of the way in which the electricity is generated. Electricity is dis-
tributed at high voltage to communities and then stepped down in voltage be-
fore delivery to homes. The transformers that convert voltage used PCBs in the
past and were a source of heavy exposure for workers. Now, the PCB5 have been
replaced with mineral oils in most countries. Wiring and appliances must be safety
designed and maintained to prevent injury from shock or damage from fires.
An additional concern is that a number of studies have linked electromagnetic
fields from the power lines that carry the electricity that is generated, to a num-
ber of different types of cancer. These studies have been under recent scrutiny,
however, as some researchers question their methodology and conclusions.
NUCLEAR PoWER
Safety Approaches
The United States was one of the first countries to commit to a large-scale pro-
gram of nuclear power. The costs of building in safeguards and the difficulty in
insuring the facilities have essentially stopped the building of new reactors in that
country. While these facilities attracted strenuous public opposition, proponents
of nuclear energy point out that past problems have been problems of reactor
design and that newer nTlOdels are much safer. However, the extent of public
concern in many countries makes it unlikely that fission nuclear power will ever
become as widespread as its proponents originally hoped.
As a result of the Chernobyl accident, attention has been focused on the safety
of operating older types of reactors. Considerable effort is currently being un-
dertaken to backfit older operating reactors to achieve safety levels compatible
with current international standards. Mitigation strategies for nuclear power
plants focus on prevention, i.e., building safer reactors. These built-in safety fac-
tors include barriers to prevent releases, backup systems for system failures, and
quality assurance.
Another major debate concerns radioactive waste. Different stages of the nu-
clear fuel cycle produce radioactive wastes. At present, there are two approaches
to the management of irradiated reactor fuel. These are the temporary or per -
manent storage of spent fuel and the reprocessing of spent fuel. The latter en-
tails the subsequent recycling of uranium in thermal reactors (WHO, 1992d).
Ccnsiderations for radioactive waste disposal can be divided as follows.
Low- and Intermediate-Level Waste Disposal Safe methods for the management
and disposal of low- and intermediate-level wastes arc well established and op-
erational. Essentially safe disposal is ensured by the establishment of effective
barriers, preventing significant transfer of radionuclides into the environmental
pathways that might lead to excessive human exposures. Typical disposal strate-
gies involve shallow-ground disposal with or without a concrete liner, near-sur-
face engineered structures, or an underground rock cavity repository. Doses to
the general public from such waste disposal are likely to be extremely low.
ALTERNATIVE_ENERGY SOURCES
A number of energy sources have been developed as alternatives to the previously
mentioned sources. The most promising ones include wind, solar, and geo-thermal
power. These particular alternatives, are promising because they are generally re-
newable. They are generally thought to be prohibitively expensive, although as
shown in Box 9.2, this need not necessarily he the case. Nonetheless, these sources
will not be viable global energy sources for many years to come and still cause
health-related problems (see Table 9.6). One of the major problems with solar-
derived energy is that the generating facilities are individually small and too decen-
tralized for an effective power grid. However, they can be a very useful local power
source, meeting local needs relatively cost-effectively, as noted in Box 9.2.
As with any energy source, there are also disadvantages to these technolo-
gies. Not all countries have the necessary environmental conditions for their im-
BOX 9.2
The Potential for Cost-Effective Electricity from
Alternative Energy Sources
Considerable gains in the use of alternative energy sources have been made, despite
the lack of commitment on the part of energy planners, technical failures attribut-
able to poor capacity for local maintenance, and the high costs associated with these
new technologies. Field experience and technical developments widened the appli-
cation of wind turbines and solar photovahaic (PV) arrays in developing countries.
These are already cost-effective at many remote sites (Foley, 1992). (Several case
examples are provided in World Resources 1994-1995 [WRI, 1994].) As shown in Fig-
ure 9.6, the price of wind energy dropped by two-thirds over the last decade, and
some 20,000 electricity-generating wind turbines, as well as large number of wind-
powered water pumps, have been installed worldwide (WRI, 1994).
Solar power has also become more cost-effective. The detnand for PV assemblies
is growing steadily, and prices are expected to fall further. Smaller solar applica-
tions, including water heaters, cookers, kilns, and crop dryers, have been success-
ful in India and China.
plementation. Both wind and solar power are considered to be very environ-
mentally friendly, but the use of geothermal power (tapping into the earth's core)
requires pollution control measures for the release of hot, mineral-filled under-
ground water to avoid a negative environmental impact, including mercury con-
tamination of fish, arsenic contamination of drinking water, and the effects of
heated water on ecosystems.
0.3
0.25
0.2
j
75
o9:5
- Percent
6 Percent - -
0.05
COMPZ\RTNG RTSIKc
Throughout the 1970s and 1980s, comparisons of risk from different energy
sources were investigated. However, these comparisons tended to account short-
term local health and environmental effects only and discount the more diffi-
cult-to-measure effects, such as the effect of increased CO 2 emissions, which could
have global implications. It is also difficult to account for all the health risks that
occur across the energy production cycle and to all stakeholders involved.
Unquestionably, reducing fossil fuel consumption will require raising the price
of these fuels. Electricity, natural gas and coal are subsidized in most countries;
petroleum consumption is subsidized in oil-exporting developing countries (WRI,
1998). The recognition that energy, like water, is a vital resource, underlies these
policies. Refrigeration, for example, saves lives from foodborne illness. If prices
are changed, the immediate benefits must be weighed against the risks.
The perception of the risk associated with a source of energy is usually more
important in the minds of decision makers than the actual risk. A nuclear power
station is more likely to be perceived as posing a higher risk than a more com-
mon source of energy, e.g., biomass fuels, even though the former has actually
caused less mortality than the latter. The factors influencing the perception of
risk were discussed in Chapter 4. The subjective perceptions of the risks involved
with any given energy source must be taken into account by all those involved.
The first two problems "involve very large groups of people (hundreds of mil-
lions) of all ages, mostly, but not exclusively, in developing countries, who are
exposed to significant health hazards requiring intensive mitigating action, now."
udtiw
What energy sources are used most heavily in your home town?
What do you know about the hazards associated with them?
Are there alternatives that should be promoted?
What issues/difficulties can you think of in your country concerning the
control of the energy-related factors listed above?
You are the environmental health officer on duty. You receive a call that
there has been a small spill of irradiated water from the nuclear power plant. Us-
ing the approach outlined in Chapters 3 and 4, describe the steps you would take
to address this problem.
('14APTFR CflNTPr'JTS
332
FXTFNT OF TNDTTTRTAJ POT JTTTTON
or that uses less polluting technologies may produce less air pollution. This may
involve increasing the efficiency of combustion, physically trapping particles be-
fore they go into the smokestack, and chemically trapping or scrubbing airborne
emissions before they are released into the atmosphere. Much industrial air pol-
lution comes from combustion of coal, oil, or gas. The specific pollution, there-
fore, often includes particulate matter and sulfur dioxide (SO7). In addition, mans'
industries emit other specific toxic subslances and odcrs, as discussed in the sec-
tion Hazards by Industry below.
One of the most effective ways of controlling air pollution at the local level
has been to build higher smokestacks at stationary sources (see Chapter 5). De-
pending on the stack height and the temperature of the emissions, the emissions
from the source rise higher in the atmosphere, travel further, become more highly
diluted in the atmosphere, and are less likely to affect the local community. The
problem with this strategy is that it sends air pollution long distances away from
the source. Air movements high in the atmosphere can transport air pollution
long distances, allowing the pollutants to fall with rain or snow at locations far
away from the source. This is to he one of the more important causes of acid de-
position, which has become a problem in recent years (see Chapter 11).
Despite these problems, air quality has improved in many cities of the world
(see Chapter 8) and serious air pollution crises, such as occurred in London in
the 1950s, are much less common today. However, the control of air pollution
is difficult and expensive. It is especially difficult in plants that have not been
properly designed in the first place, such as older plants. The cost of air pollu-
4tQ~
'__C_ Lake trout
4.83 ppm
Rainbow smelt
1.84 ppm
Zooplankton
0.123 ppm
Phytoplankton
0.0025 ppm
Figure 10.1 Bioaccumulation and hiomagniticatiori of PCBs in the Canadian Great Lakes
aquatic food chain. From Environment Canada, 1987, with permission.
• The number and hazardous nature of toxic substances in common use has
changed dramatically. Since World War II, research and development in or-
ganic chemistry and chemical engineering have introduced thousands of new
compounds into widespread commercial use, including such persistent com-
pounds as the PCBs and more potent pesticides, accelerators, and plasticizers
with unusual and poorly understood effects. Compounds for which there has
been little time to evaluate are in common use today.
• The production of chemicals has risen dramatically. In 1941 production of all
synthetic organic compounds in the United States alone was less than one mil-
lion tons; since then it has increased 100-fold. Many of these substances are
toxic and degrade very slowly, resulting in accumulation in the environment.
The environment contains much greater quantities of these toxic chemicals
than ever before.
• Toxic chemicals are much more intrusive in daily life. Many chemical plants
or disposal sites that were once isolated or on the edge of town have become
incorporated into urban areas by suburban growth. Communities now lie in
closer proximity to the problem than they have in the past. Some communi-
ties are built directly over old disposal sites.
People come into contact with tcxic substances in many ways. Exposure may
occur at several points in the life cycle of the substance. Some people work in
Multiple chemical sensitivity (MCS) is the common name for a set of symptoms that
occur in the setting of chemical exposure. These symptoms are often vague and
nonspecific and do not correspond to the known toxic effects of these chemicals.
The symptoms may include fatigue, confusion (called brain fog by some advocates,
loss of appetite, headache, and nausea. They may occur after the patient has expe-
rienced exposure to very low levels of a chenmical, well below the levels known to
cause toxic reactions. Sometimes they seem to occur at times when exposure is un-
likely but sufferers feel that they have been exposed. Some people believe that MCS
represents a generalized allergic reaction to all chemicals. The workings of the im-
mune system, however, are highly specific and one normally reacts only to partic-
ular chemicals or classes of chemicals. Sufferers of MCS often respond to chemicals
of many different types, regardless of chemical composition. The most common
chemicals that trigger this reaction seem to be perfumes, pesticides., solvents, to-
bacco smoke, and food additives. Research on the problem has resulted in many
theories, but little firm evidence for a mechanisni.
Patients with this disorder may come from all walks of life but most are female,
young, relatively affluent, and either work at home or work in office jobs. To de-
termine the cause of their syniptotns, they cornnionly consult practitioners of al-
ternative medicine, some of whom may give them the diagnosis of MCS. The effect
of the diagnosis of MCS on them is often quite dramatic. The diagnosis becomes a
central feature of their lives. They may withdraw from their usual daily life, quit
work, change their diet, change their housing, and require visitors to avoid bring-
ing any chemical into their surroundings, even freshly washed clothes. Many times
these changes are very radical and have the effect of isolating them from family,
friends, and society. Often they show features of depression or obsessive-compul-
sive behavior, although it is controversial whether this is a cause or a result of their
condition. Alternative treatments are long, involved, and costly, and there is no ev-
idence that they work. Because conventional medicine does not recognize the dis-
order, there is no obvious medical treatment. Psychotherapy seems to he the most
effective form of treatment available. Most patients refuse this, however, and many
react angrily to suggestions that their condition may have a psychosomatic dinien-
sion.
One of the problems in investigating MCS is that the definition and the terms
used change frequently. The leading advocates for the existence of MCS as a dis-
tinct clinical disorder once called themselves clinical ecologists, and now call them-
selves environmental medicine practitioners. In the past, MCS itself has gone by the
names of chemical sensitivity, twentieth-century disease, and environmental hype rsens itivity
disorder. Some of these practitioners believe that MCS covers a wide variety of seem-
ingly related illnesses, such as sick building syndrome (which occurs when people
working in a building with poor ventilation feel ill; see Chapter 8), chronic fatigue
syndrome (another nonspecific diagnosis possibly related to a viral infection), and
more conventional allergies and toxicity conditions. Most mainstream medical prac-
titioners strongly disagree that this entity has a distinct pathophysiological basis and
believe that a MCS-associated behavior pattern may represent a psychological dis-
turhance on the part of some patients. Some believe that what appears to be MCS
is actually a psychosomatic, behavioral response to chemicals in the environment.
Others, however, believe that there may be unknown toxicological or immunolog-
ical responses that underlie the response of some patients to chemicals at low 1ev-
els but that the responses are not yet understood by current scientific knowledge
and, in any case, need not be disabling.
There are many examples in the past of disorders that were once thought to be
particular diseases that are now considered psychological responses to stress. These
have included hysteria, neurasthenia, and catalepsy—all diagnoses now discarded
by the medical profession. (The term hysteria, comes frorn the Latin word for uterus.
It is pejorative to svomen because it implies that women are biologically prone to
be emotionally unstable, and thus the term should not be used.) Some physicians
feel that MCS, chronic fatigue syndrome, and multiple personality disorder are mod-
ern examples of this type of condition. Others feel that some of these patients may
well have disorders that medicine cannot yet explain. It is possible that in a few
years MCS will cease to be a commonly used medical term and that some cases now
called MCS will be found to reflect conventional allergies and tcxicities, some will
be clearly psychological in origin, and some will remain difficult to explain. Sparks
et al. (1994) have provided a useful case definition, and summarized the theories
of paihogenesis, diagnostic testing, treatment, and social consideration.
Source: Various summaries produced bt' the Association of Occupational
and Environmental Clinics; See also Sparks, 2000.
humans appear to he more resistant to the effects of these compounds than other
species. Even so, these are dangerous compounds to the environment and must
be controlled for ecological reasons. We still do not know many of their more
subtle effects on humans and it is only prudent that we minimize exposure to
humans as well.
Pesticides are particularly dangerous in hazardous waste, especially the rela-
tively toxic class known as the orqanophosphates. Fires involving pesticide storage
areas are a particularly dangerous situation, as the pesticides may be converted
into even more highly toxic combustion products and substantial amounts of en-
vironmentally damaging dioxins and furans may be generated.
Strong acids and strong alkali are commonly found at waste sites and are dan-
gerous if there is a possibility of direct contact or inhalation of fumes. They may
cause serious skin and eye burns on contact. Some acids may generate clouds of
fumes that may cause lung injury. If mixed together, the acids and alkali may
generate intense, possibly explosive heat and substantial dangerous fumes. Two
acids that are particularly dangemus are nitric acid and hydrofluoric acid. Nitric
acid releases nitrogen dioxide, which may cause pulmonary edema and bronchial
irritation. Hydrofluoric acid is used for etching in the electronics industry and is
exceedingly dangerous when inhaled or when it touches skin or mucous mem-
branes. On contact with skin or eyes, it causes deeply penetrating burns.
Cyanide is present in some situations, especially gold-plating solutions. In-
haled cyanide fumes from the solution are highly toxic. Cyanide can be released
by mixing the plating solution with a strong acid, such as those often found at
hazardous waste sites.
A major unresolved issue in municipal solid waste handling is contamination
by hazardous waste disposed of by accident or intent. This can be minimized by
diverting such disposal into a separate waste stream. Other means have been
"A7AR,Dc, BY INDUSTRY
This brief summary can only give a snapshot of the types of health hazards that
may be related to industry. Information about the specific health hazards and
preventive approaches for each industry can be found in publications of the In-
ternational Labor Office (ILO), particularly the ILO Encyclopedia of Occupational
Health and Safety (ILO, 1998), as well as documents from the United Nations En-
vironment Program (UNEP) Industry and Environment Office in Paris. A num-
ber of major occupational health hazards occur in each of these industries (see
section Dimensions and Types of Occupational Health Problems, below).
Materials Extraction
This type of industry is sometimes called primary industry and represents the first
step in the process of creating manufactured products. It includes mining for met-
als and minerals, coal and oil extraction, forestry, agriculture, and fishing. Out-
puts of this type of industry include ore or metal concentrate, coal, oil, sand,
wood, fibres (cotton, wool, hemp), grains, and fish. Issues related to the food and
agriculture industry are examined in Chapter 7. These primary industries can be
found in all countries, but as countries develop they usually tend to represent a
decreasing proportion of the overall economy.
The types of pollution and hazards related to the mining industry include dust
in air and water pollution from the processes that use water to transport, wash,
or concentrate the raw materials. Mines and quarries also create physical scars
in the local environment and can cause major emergency pollution risks when
tailings dams (accumulations of debris that trap water behind them) burst or over-
flow. Often processing plants for concentration or refining of metals arc located
together with the mine itself, and these plants can cause major sulfur dioxide or
metals pollution, as has happened in a number of places. The sulfur dioxide pol-
lution occurs because the ores of many metals contain large amounts of sulfur.
Special problems accompany uranium mining as radioactive compounds can be
released to the environment.
Coal extraction is similar to metal mining, except that the coal mines are of-
ten colocated with coal power plants, which emit large amounts of particulates
(dust), sulfur dioxide, and toxic metals included in the raw coal (see Chapter 9).
The amount of pollution will depend on the quality of the coal and pollution
control measures. Dramatic air pollution situations related to coal extraction ex-
ist, for instance, around coal mines in central Europe, India, and China. Oil ex-
traction involves direct surface oil pollution from spillages, as well as air pollu-
tion from the burning (flaring) of excess gas combined with oil or from power
stations or petrochemical industries colocated with the oil field.
Processing Industries
Industries that process extracted raw materials into concentrated intermediate
products are potentially large sources of environmental impact because of the
scale and nature of their operations. The metals industries, including iron and
steel production, transform metal ores to metal ingots, sheets, and pipes, and can
generate considerable air, water, and land pollution. Some metals, such as lead
and cadmium, are very toxic, and many incidents of poisoning in populations
living around such industries have taken place. Particular problems occur in in-
dustries that recycle scrap metal products, as the content of the scrap is not al-
ways well known, and a mixture of toxic chemicals may be emitted to the air or
water. Lead has been a particular problem in this regard.
Petrochemical industries have already been mentioned. They process oil prod-
ucts into bulk raw materials for the production of plastics and chemicals. These
raw materials themselves, e.g., benzene, may be highly toxic. Sulfur dioxide is a
common pollutant, as most raw petroleum oil contains sulfur. These industries
involve major fire risks, and when a fire occurs, the smoke will contain a mix-
ture of very toxic chemicals. Depending on the wind direction and town plan-
ning, population groups may be highly exposed. In some countries, such as the
United States and Canada, industry has attempted to address these problems with
comprehensive voluntary risk management programs that include public con-
sultation.
The major pollution source in the processing of forestry products is the pulp
and paper industry. Large amounts of water are used to prepare the pulp and
process it into paper. The lignin (a natural glue that holds together wood fibers)
in the wood gets washed out with the water as well as the remains of various
chemicals used in the processing. This pollution can seriously affect the water
quality as measured by the biolQqical oxygen demand (BOD). The BOD is an in-
dicator of the amount of oxygen required to hiodegrade all the organic material
in water and is the fundamental measurement used to monitor water quality.
Mercury fungicides were used in the past to keep the paper pulp from growing
moldy. Some of these fungicides ended up in the wastewater and have caused
long-lasting pollution of lakes, particularly in Sweden. The sulfate and sulfide
processes in the paper pulp industry lead to air pollution of mercaptans and other
extremely smelly chemicals. Odor pollution is common, but is often more no-
ticed by people traveling past a plant than those living close to it all the time,
because the nose adapts to smells. Another problem in the forest industry is the
pesticide treatment of timber or wood products, often carried out under primi-
Service Industries
An increasing proportion of overall economic activity is based on the provision
of services, in contrast to the production of goods. This is often referred to as ter-
tiary industry and includes restaurant and hotel services, health services, personal
services (such as hairdressing), entertainment, travel, tourism, public adminis-
trative services, telecommunications, and the new high-tech industries (such as
software production). Generally they do not produce much environmental pol-
lution, although all establishments at which large numbers of people are assem-
bled create increased pressures on sanitation and waste management, e.g., tourist
resorts create greater needs for sewage treatment. Hospitals and medical lahora-
tories have particular problems with medical waste, which can contain infectious
agents and radioactive materials.
Another issue related to concentrations of people is disturbing noise. The travel
and transportation industry causes a fair amount of noise around airports, mo-
Lead Lead is one of the oldest environmental hazards known to society. There
are many sources of exposure to lead, with residents in urban areas tending to
have lead levels that are higher than those in rural areas. Lead enters the body
primarily through the inhalation of tiny particles that contain it or through in-
gestion of food or beverages that contain it. Absorption of tetraethyl lead gaso-
line additive through the skin does occur, but such exposures have rarely caused
lead poisoning. Petrol sniffing among youth in certain communities has caused
significant poisoning problems. Lead remains a serious environmental hazard as
well as a serious occupational health and safety problem.
Lead was used long before the tndustrial Revolution for making pipes, pig-
Cadmium Another metal that has been used in a number of industrial applica-
ticns is cadmium. It is used as an anti-corrosive coating on steel, and in recharge-
able electric batteries. Cadmium compounds have also been used as pigments in
plastics, but in some countries restrictions on its use have been regulated to rc-
ducc the possibility of environmental contamination by cadmium.
SoLvents
Solvents are liquids at room temperature that can dissolve other substances with-
out necessarily reacting with them chemically. While water is by far the most
common solvent, there are numerous other compounds that are used in indus-
try as cleaners, degreasing agents, extraction solvents, viscosity modifiers, con-
stituents of glues and paints, and paint or coating removers. These mostly or-
The field of occupational health and safety relates to the analysis and control of
hazards in particular workplaces. Occupational health primarily deals with haz-
ards of a chemical, physical, or biological nature; occupational safety primarily
addresses hazards of a mechanical nature. With increasing recognition that er-
gonomic factors can cause not only acute trauma but also repetitive strain in-
juries (e.g. occupational overuse syndrome, carpal tunnel syndrome, tendonitis,
and epicondylitis), occupational health professionals must consider biomechani-
cal factors within their realm of expertise as well. Psychosocial hazards of work
(e.g., stress, burnout, harassment) are also issues that occupaticnal health pro-
fessionals must address. (The WHO and the ILO have developed many impor-
tant documents in this area; the ILO's Encyclopedia of Occupational Health and Safety
[ILO, 1998] is an excellent source of information on the issues in this field.)
Although there is a great deal of variation worldwide in the nature and sever-
ity of occupational health and safety problems and the resources available to con-
trol them, there are many more issues in common. At the beginning of devel-
opment, whether historically among developed nations or currently among
developing nations, occupational health and safety tend to be a low priority be-
cause of a perceived need to develop at all costs. This is unfortunate, because at
this stage of development, a relatively small investment in worker protection may
yield great benefits in improved worker health.
As societies become increasingly developed, the field of occupational health and
safety tends to become an increasing priority. Often, a series of well-publicized ac-
cidents forces citizens to address this issue. Sometimes, trade unions force em-
Workers' Compensation
Beyond a certain level of development, societies tend to introduce an insurance
scheme for their workers to minimize the disruption that occupational injuries
can cause and to control the costs. In particular, the cost of lawsuits associated
with injuries and illnesses may rapidly grow out of control. The response to this
situation may take the form of social security programs that operate as a com-
prehensive health care system for workers and their families. Some countries
have used this to phase in more universal coverage for health services for their
population. It may also take the form of workers' compensation, a no-fault insur-
ance system funded by employers that compensates workers for health care and
lost earnings from work-related injuries or illnesses. Some jurisdictions also pro-
vide an impairment award, based on measurable loss of function, regardless of
whether the worker can continue working.
Workers have often had to give up their right to sue their employers in ex-
change for a comprehensive workers' compensation system, which is adminis-
tered by an impartial board responsible to government, e.g., as in Canada. The
Workers' Compensation Board (WCB), having obtained information from the
employer, the worker, and the worker's attending physician, decides if the
worker's health problem is work related and the extent to which it disables the
worker. The system tends to work reasonably well for injuries but less well for
diseases, many of which are mullifactorial in origin.
Some workers are particularly disadvantaged as they have to deal with racism
and sexism at work in addition to the health hazards of work. Particular prob-
lems facing women in the workplace arc discussed in the next section.
The Global Estimates for Health Situation Assessments and Pro fections has suggested
that there were 32.7 million occupational injuries and 146,000 occupational
Ox 10. 3
Common Occupational Lung Diseases
PNEUMOCONIOSIS
The pneumoconioses are diseases characterized by the deposition of dust in the lungs
and the pulmonary response to its presence. The degree of fibrosis (scarring) that
results varies with the properties of the dust. Silica and the fibrous silicates, such as
asbestos or zeolite, cause intense fibrotic reactions. Carbon black or iron oxide pro-
vokes only small and localized reactions. Even relatively benign dusts may be asso-
ciated with more serious responses when combined with other exposures, such as
toxic gases or carcinogens that may adsorb on the surface of particles.
Ashestosis, often called white lung, is a common and serious pneumoconiosis re-
suIting from the inhalation of large quantities of asbestos fibers. The disease is a risk
for shipyard workers, plumbers and pipe titters, insulation workers, members of the
building trades, and many others working where asbestos had been used heavily
and without tight control. The natural history of the disease is progression of the
restrictive impairment, sometimes to total disability, and a very high risk of cancer.
The disease is not associated with smoking, but smoking clearly makes the symp-
toms worse and the management more difficult once the disease appears. Asbestos
exposure also causes lung cancer and the risk of this disease increases dramatically
in asbestos workers who smoke.
Silicosis is an ancient disease that continues today in numerous occupations. Sil-
ica exposure is a hazard of mining and quarrying, older techniques of sandblasting
and etching, foundry work, industrial and artisan ceramics, and innumerable occu-
pations in which finely pulverized silica flour is employed as a filler material. When
combined with tuberculosis, the resulting condition of silicotuberculosis can he a
devastating, swiftly progressive fibrotic process that resembles a malignancy. The
complication of silicosis by tuberculosis is common and may be devastating. The im-
paired lung cannot contain the tuberculosis infection and the result is an acceler-
ated fibrotic process that may require lifelong treatment with anti-tuberculosis mcd-
ication to control. Individuals with silicosis are predisposed to initial infection by the
TOXIC INHALATION
Toxic inhalation is a general term for the serious pulmonary toxicity of a variety of
gases presenting similar clinical patterns, including ozone, phosgene, chlorine, ni-
trogen dioxide, hydrogen fluoride, and many others. Exposure to these gases at the
levels required to produce this condition is usually the result of accidental release,
uncontrolled chemical reactions, or fires. Certain of these gases, particularly phos-
gene, chlorine, and nitrogen dioxide, are generated when plastic furnishings and in-
terior design fixtures burn, as in a hotel fire. In such combustion situations, cyanide
and carbon monoxide are also released and contribute to toxicity.
OCCUPATIONAL ASTHMA
Asthma is a complex of symptoms and signs resulting from reversible obstruction
of air flow. Usually asthma presents as wheezing and shortness of breath, occurring
repeatedly in isolated episodes, often immediately following exposure to a recog-
nizable allergen. In a few cases of asthma, cough may he the major symptom. In
occupational asthma, the agent may be difficult to identify and the pattern of air-
ways obstruction may he unusual or delayed. The easiest agents to identify are those
that are highly sensitizing and that trigger the familiar immediate hypersensitivity
reaction. Such conventional allergic sensitizers include animal secretions, ethylene
diamine, grain dusts, detergent enzymes, epoxy resin curing agents, and virtually
any organic or small-molecular-weight compounds, including metals such as plat-
inum salts.
A few produce reactions by mechanisms that are not typical of the common im-
mediate hypersensitivity reaction, such as grain dust, wood dust, formaldehyde,
pharmaceutical agents, and toluene diisocyanate (TDI), a particularly potent sensi-
tizing chemical used in the production of polyurethane plastics. Isocyanates in gen-
eral, and TDI in particular, are among the most common chemicals in industry, pre-
sent in most paints, coatings, and finishing preparations. Isocyanate-induced asthma
is particularly common in autobody shops because of the use of binders containing
isocyanates in fibrous glass repair work. In such cases, the responses may be mixed
with immune, irritant, and pharmacologic mechanisms playing some role. iso-
cyanates are both potent sensitizers and irritants, with either mechanism promot-
ing airway reactivity.
HYPERSENSITIVITY PNEUMONITIS
INDUSTRIAL BRONCHITIS
Workers in dusty occupations, particularly steelworkers and grain handlers, may de-
velop a nonspecific chronic bronchitis (see Becklake, 1985; 1989). Cigarette smok-
ing may aggravate the bronchitis.
FUME FEVERS
There are two common types of fume fever, both involving mixed pulmonary and
systemic reactions to inhaled toxic agents. Metal fume fever results from exposure to
hot metal fumes, particularly zinc, cadmium, and copper. The illness is a self-
limited but highly unpleasant reaction, similar to influenza, developing an hour or
so after exposure and consisting of nausea, fever and chills, malaise, myalgias, and
leukocytosis. Metal fume fever lasts only 1 or 2 days and should not be confused
with toxic inhalation, which may result from exposure to high concentrations of
cadmium or nickel fumes or from high concentrations of volatilized mercury, or
with acute lead poisoning. Metal fume fever is most often seen when inexperienced
welders try to weld or cut metal that is galvanized or of mixed composition.
Polymer fume fever is a similar influenza-like reaction resulting from the pyroly-
sis products of Teflon and related polymers when particles settle on cigarettes and
burn, and the fumes are inhaled. Polymer fume fever can he prevented by banning
cigarette smoking in workplaces where products containing these polymers are fab-
ricated. Polymer fume fever should not he confused with "meat-wrappers asthma,"
a problem of bronchospasm and an irritant bronchitis resulting from the inhalation
of fumes generated when polyvinyl chloride film wrapping is cut using a hot wire.
This used to he a common problem in supermarkets but has since been solved by
adjusting the temperature of the hot wire.
Some chemicals affect the reproductive system in either men or women and
can cause sterility, miscarriages, or birth defects. Table 10.1 lists agents that have
been reported to adversely affect reproductive capacity. Table 10.2 summarizes
known or highly suspect carcinogens in the workplace.
Neurotoxicity is another serious problem associated with both heavy metals
and solvents, as described in the sections above, and with other chemicals. Like-
wise, liver and kidney toxicity are common responses to chemical exposure. Re-
cently, there has been much attention given to the effect of chemical CXOSUC
on the immune system. It seems likely that research in this field will yield many
insights into subtle health effects that are currently not known in detail.
Physical Hazards
Physical hazards are also very common at worksites. Noise is by far the most
widespread of the occupational hazards, and the high incidence of noise-induced
hearing loss worldwide demonstrates that it remains one of the most poorly con-
trolled. (Chapter 4 provided an example of an occupational noise control pro-
Aluminum, arsenic, beryllium, hora nes, boron, cadmium, cobalt, lead (inorganic and Organic),
manganese, mercury (inorganic and organic), molybdenum, nickel, selenium, silver, uranium, zinc
INSECTICIDES
HERBICIDES
RODENTICIT) ES
INDUSTRIAL CHEMICALS
MISCELLANEOUS
gram.) In son-ic countries, excessively hot or cold working environments are corn-
mon. There are also sources of ultraviolet irradiation outdoors and in some work-
places that have effects like those described in Chapter 11. Ionizing radiation, is
a familiar type of exposure because it is common in health care settings and is a
risk in the nuclear industry, as noted in Chapter 9. Although laser light (because
it is so concentrated) is a serious physical hazard in some technical settings, lasers
used in applications such as supermarket checkout counters are too low in en-
ergy to induce injuries.
Mechanical Hazards
Mechanical hazards may be of two general types: unsafe working conditions and
ergonomic hazards. The science of ergonomics generally includes the control of
hazards that may result in acute injury as well as chronic disorders usually of
the musculoskeletal system, as noted in Chapter 2. Unsafe working conditions
are those that may allow a sudden release of energy (such as an overly pressur-
ized gas cylinder) that can cause injury or that place the worker at risk of injury.
Sewage is a mixture of liquids and solids of domestic and industrial origin that varies
in composition from sewer to sewer and from hour to hour. Workers processing
sewage and maintaining sewage systems are exposed to a variety of biological haz-
ards. An increased risk of self-limited diarrheal diseases has been reported in sewage
treatment workers employed in various jurisdictions. Leptospirosis is a well-known
occupational disease of sewage workers. Giardiasis has also been reported as a risk.
Some but not all studies have revealed increased evidence of hepatitis A infection
in sewage workers. In communities where there has been epidemics of hepatitis A,
occupational transmission of this infection has been reported.
Contributed by A. Kraut, University of Manitoba. Canada.
such as a fall, laceration, or a sprain. The key to controlling unsafe working con-
ditions is to reduce the amount of energy that could be released and to build in
guards, harriers, and other devices that protect the worker.
Ergonomic hazards result from a mismatch between the worker's body and
the design of the workstation. The result is a disproportionate strain that is placed
on an intrinsically weak part of the body—e.g., a chair fails to support the hack
properly or a work station is designed in such a way that the worker must stretch
to perform a common task. The usual result is an injury that results from the cu-
mulative effect of the strain, not a single injury event. Repetitive strain injuries
among typists and keyboard operators, assembly line workers using vibrating
tools for prolonged periods, or supermarket checkout clerks who handle items
with repetitive motion at the wrist are examples of ergonomic hazards (see Yassi,
1997; 2000 for a review of this topic).
Biological Hazards
Biological hazards are most obviotis in health care and agriculture but may oc-
cur in many other industries. Infection with one or more viruses that cause he-
patitis is another major concern. Tuberculosis (TB) is a serious problem among
hospital workers. Infection with the human immunodeficiency virus (HIV) (the AtDS
virus), or with the hepatitis B virus can occur from needlestick injuries or blood
contact and, understandably, is widely feared. Leptospirosis, a bacterial infection
spread by contact with rat urine, occurs in some occupations and is a risk in the
sugar cane industry. Brucellosis is another disease of farmers and slaughterhouse
workers and is caused by contact with cows, pigs, and goats. Sewage workers
are at risk for some of these infectious diseases (although not TB or AIDS; see
Box 10.4).
Problems associated with allergies and reactions to organic products are com-
mon in agriculture. Enctunters with poisonous or otherwise hazardous species
Psychological Hazards
As discussed in Chapter 2, it is now generally accepted that stress at work is as-
sociated with lack of control over the working environment and with high work-
place demands. Such stress-producing circumstances, however, are precisely what
has been created in the workplace as a result of economic restructuring. In this
vein, expectations of behavior in the workplace that show commitment and a
drive for increased productivity may be seen as positive to managers and stress-
ful by workers. The psychological stress from being unemployed can also be se-
vere. Generally, it is difficult to separate out stress at work from stress in daily
life.
Table 10.3 lists examples of the major environmental disease outbreaks that re-
sulted in a substantial number of reported deaths or severe illness. Numerous
other incidents have been reported with fewer reported cases of illness, often
because of effective management of the mishap. The accidents listed in the table
include only chemical poisoning outbreaks in the community around an in-
dustry or in the community consuming certain contaminated food products.
Some of these have been due to sudden accidental releases of chemicals, such
as the Bhopal case, and others have involved long-term low-level pollution that
finally reached danger levels, such as the Toyama case. These major poisoning
TABLE 103
APPROACHFS TO PREVENTiON
CHAPTER CONTENTS
368
We live in a time of rapid change on a global scale. Many of these changes hold
the promise of positive developments in quality of life and international cooper-
ation. Improved communication, rapidly expanding trade, and new technologies
that conserve energy and resources are just a few of the changes that have a
worldwide impact on society and may make tomorrow's world better than to-
day's. However, not all global developments are likely to he positive. Global ccc'-
logical changes, including those related to stratospheric ozone depletion, the green-
house effect, deforestation and desertification, loss of biodiversity, interregional
transport of pollution, and large-scale resource depletion, are having a major im-
pact on communities worldwide. The implications of environmental trends for
weather, human habitation, and food supply suggest serious trouble ahead. To
these environmental hazards, which are largely due to industrial development
or economic pressures on agriculture, must be added the environmental conse-
quences of intentional destruction from war. Willful destruction for military or
political advantage has become one of the major issues in global ecological change.
In the past, most of these environmental hazards and the effects of environ-
mental pollution were treated as local issues and were generally handled on a
local level by public health authorities. In recent years, however, the scope of
environmental issues has broadened considerably and there is no clear dividing
line between problems that used to be considered public health problems and
those that involve large-scale ecological change. The degradation of the envi-
ronment has become a major global problem, outstripping its local public health
dimensions and becoming a serious threat, perhaps even to human survival. We
begin this chapter by examining the intentional destruction that occurs in war -
fare, both because of its own damaging effects and because it interleres with the
international and regional cooperation needed to solve the other problems.
The general outline of the global ecological crisis is clear: rapid technological
development in the developed world introduces new potential hazards in a so-
ciety in which environmental degradation is historically severe but coming un-
der relative control. Rapid population growth and industrial development, based
largely on obsolete technologies in the developing world, accelerates existing en-
vironmental degradation. This is aggravated by poverty, urbanization without ad-
equate infrastructure, rural development policies that do not strengthen local
economies, and a limited economic base that is too often dependent on com-
modity prices. The problem of environmental degradation has become global in
three distinct senses:
There is now imbalance on the level of entire global systems, such as climate.
The distribution of familiar environmental problems, such as air pollution,
has become much more widespread and regionalized until these problems are
encountered worldwide and not just in areas of development and urban growth.
The economic and political systems that operate to create and sustain these
problems (but that might also hold the key to some of the solutions) have be-
come global to the extent that the world is rapidly becoming one large market
economy, beyond the capacity of governments to regulate effectively. Much of
this change deals with drastic increases in consumption levels of resources and
consumer goods, and rising expectations for consumption among developing
societies.
The most destructive human activity is warfare. As noted by Garfield and Neugut
(1997), the 1960s expression "war is not healthy for children and other living
things" is so understated that one hesitates to attempt to define how unhealthy
war is. Not only is war intentionally destructive between the sides engaged in
fighting, but when modern warfare is practiced, the environment is another cas-
ualty. The first and most tragic consequence of war is the direct casualties, the sol-
diers and civilians who die or are maimed in the fighting, and their loved ones
who must carry on. Table 11. 1, with all the limitations and inaccuracies in data
collection of this sort, indicate that mortality rates from war rose dramatically in
the twentieth century. This was largely attributable to large increases in mortal-
ity during World Wars I and II. Prior to World War II, more war-related deaths
occurred due to disease than to battlefield deaths.
The need to support a war effort and the care required by those who are
wounded but survive place a burden on the society supporting the fighting. Mod-
ern warfare also strikes directly at the economic and logistical ability of the soci-
ety to make war, often by targeting the environment directly. Garfield and Neugut
(1997) suggest that civilian deaths compose 90% of all deaths in twentieth-
century wars.
In War and Public Health (Levy and Sidel, 1997), the impact of war on public
health is documented and suggestions of what health professionals could do to
prevent war and minimize its consequences are offered. With respect to the Gulf
War, for example, studies have shown that the war and trade sanctions caused
a threefold increase in mortality among Iraqi children under 5 years of age (As-
cherio et al., 1992). The suggestion that by using high-precision weapons with
strategic targets the Allied forces were producing only limited damage to the civil-
ian population was shown to be false, confirming that the casualties of war still
extend far beyond those caused directly by warfare.
Modern Conventional Warfare
The primary purpose of modern warfare is to defeat or debilitate the enemy's so-
ciety and support systems to control a strategic resource and thereby impose or
avoid political domination. This is in contrast to warfare in earlier societies, when
battles tended to be fought by smaller armies with limited force and the fighting
TABLE 11.1
ESTIMATED AVERAGE ANNUAL MILITARY DEATHS IN WARS, WORLDWIDE,
BY CENTURY
Average Annual Military
Average Annual World Mid-Century Deaths per Million
Century Military Deaths Population in Millions Population
17th 9500 500 19.0
18th 15,000 800 18.8
19th 13,000 1200 10.8
20th 498,000 2500 183.2
Source: Levy and SkId, 1997
Chemical Warfare
Chemical warfare, introduced on a large scale in World War I, involves the con-
trolled release of toxic chemicals, usually nerve toxins or intensely irritating agents.
When used in the field, these poisons are indiscriminate in their actions and may
affect civilians or troops on either side, as well as wildlife and domestic animals.
These agents can cause considerable local damage and may wipe out entire vil-
lages. As a consequence, they are often considered to be weapons of terror and
civilian intimidation rather than effective military measures. The agents that have
actually been used in recent years do not seem to be very persistent in the envi-
ronment, perhaps because armed forces that use them kncw that they may have
to enter and occupy the same area later. The storage of chemicals used for chem-
People who are suddenly displaced by the events of war and forced to migrate usually
take their belongings with them. Such refugees are forced to depend on foster assis-
tance to meet their most basic needs, such as food, shelter, medical care, and water.
In assesstng what public health measures are appropriate, officials in refugee/displaced
person camps must consider the following: the types of make-shift shelters being used,
the physical environment, the demographic profile of the people in the camp, and the
extent and type of disease circulating in the population. The goal of the resulting pub-
lic health measures should be primarily to prevent the occurrence and spread of the
diseases favored by this situation. The process of identifying needs and setting priori-
ties requires an immediate assessment of the population's health and nutritional sta-
tus, as well as a rapid environmental health assessment of the available accommoda-
non. A monitoring and reporting system should be established to assess the effectiveness
of the measures, and to ensure the timely detection of newly developed risks. Envi-
ronmental health measures taken should include the following:
• The site should be selected according to the facilities needed to provide hygienic
and healthy conditions. Flood areas and natural foci of infection must be avoided,
• The accommodation site should afford an adequate protection against inclement
weather conditions.
• Overcrowding should be avoided.
WATER SUPPLY
• Ensure that water is adequate in quantity and quality (consider access to water
treatment and cooking facilities), and protect the source of water and water sup-
ply facilities from pollution.
REFUSE DISPOSAL
• Distribute dried and preserved foods. Prepare food individually. Place storerooms
(if they exist) and community feeding facilities under health surveillance, and
provide hygienic food preparation courses.
In addition, provisions must be made for child immunization, health education, pa-
dent treatment, drug supply, medical personnel, and a health service scheme, in-
cluding a system for referrals to inpatient facilities.
Prvi'ided by Krui toslat' 7apak, Croatian National Institute of Public Health.
372
ical warfare has sometimes created a hazard, particularly over many years when
the containers begin to disintegrate. Although chemical weapons have been out-
lawed for a very long time by an international agreement known as the Hague De-
claration, there have been many documented instances of their use and many more
suspected incidents in which absolute proof has been lacking or controversial.
Biological Warfare
Biological warfare, which is even more difficult to control, involves targeted re-
lease of pathogeris such as viruses and bacteria. In the few instances in which it
has been tried, there have been limited outbreaks of disease involving local res-
idents and wildlife. The effects of biological weapons are short term and unpre-
dictable, but certain agents, are transmissible and could cause widespread epi-
demics. Because the weapons perform poorly in the battlefield and are unreliable
against civilians, biological warfare has been used only rarely, although it has
been often alleged. In recent years, world concern over biological weapons has
focused chiefly on the testing and development of these weapons and the use of
biological agents in laboratories released into the environment during studies to
develop protective measures. These weapons have been outlawed by the Geneva
Protocol since 1925. This was strengthened by a further Convention in 1972, to
which 100 countries subscribe. In recent years there have been fears that ter-
rorist groups would use biological agents.
Nuclear Warfare
The ultimate extension of ecological warfare is, of course, nuclear war, where
the target is both the people and the region. The massive destructive power of
nuclear weapons led to an impasse that dominated the latter half of this century:
both sides held such massive military power that any attempt by either side to
use nuclear weapons assured their mutual destruction. This climate of fear is
thought to guarantee that neither side would use these weapons, a terrifying ba-
sis for peace but, to many, an effective one. Since the collapse of the Soviet Union,
there is little immediate prospect of total nuclear war, but the proliferation of
nuclear weapons to other countries carries a grave risk that they will be used in
regional conflicts. Should a nuclear exchange ever occur, the regional devasta-
tion it would bring would be inconceivable: sudden death, fire, massive de-
struction, and slow death by radiation sickness for those survivors at the pe-
riphery. However, this would be only part of the impact. Release of radiation,
potentially carried many miles by wind and water, disruption and contamination
of food supplies, shortages of medical services and supplies, and the susceptibil-
ity to infection of tnalnourished and irradiated survivors would result in massive
casualties well beyond the initial blast zone. It is also possible that a massive ex-
change would propel huge quantities of debris into the atmosphere, creating dust
clouds that would block sunlight and cause a prolonged cooling of the earth's
surface called nuclear winter (see Robock, 1991).
The testing and production of nuclear weapons continue to pose a threat of ac-
cidental release and local contamination. The sites of several nuclear weapons plants
are reported to be seriously contaminated and radionuclides have been detected
in groundwater downstream from at least one plant in the United States, although
Ultraviolet Radiation
Ultraviolet radiation carries much energy and causes tissue damage in human be-
ings and animals (see Chapter 2, Physical Hazards). There are three types of UV ra-
diation, all of which differ in wavelength (see Fig. 11.1). The longest wavelength,
UV-C, carries the most energy but is almost completely absorbed by the upper at-
mosphere so it does not reach the earth's surface; UV-C will not be discussed fur-
ther here. Ozone in the stratosphere in particular absorbs UV radiation completely
in the UV-C range (200-290 nm) and a large proportion in the UV-B range (290-320
nm). This serves as a shield, reducing exposure at the earth's surface below the ozone
layer. UV-A carries relatively low energy and is less harmful. UV-B carries somewhat
more energy and causes skin damage and tanning in lighter-skinned people.
10 0 - 10 6
DNA Solar
damage ('action radiation at
spectrum') ground level I
CD
105
CD
a) Cr
Cu 0•
Mouse
(skin 0
10 2 cancer (action)
104
6
pectrY a)
cc
CD
cc CD
C)
> 1 o- 103 •0
CD
Cl)
C 0
a) C
C 100-fold I)
a) difference C
1 o- in biological 10 2
C))
0 effect 0
0 between x, y CD
w ><
I I 0
Cl)
1 -5 LL —— —— — y 10 1 C
CD
II
10 -6 100
Figure 11.1 wavelength composition of solar ultraviolet radiation at the Earth's surface,
and relative biological effect. From McMichael, 1993, with permission.
dust in the atmosphere, so that at any one location there may be considerable
variability in measurements from moment to moment and from year to year.
Carbon dioxide accumulation and increased cloud cover tend to offset ozone de-
pletion, introducing another set of variables that are poorly understood. Ozone
depletion may not be the only significant factor to take into account in project-
ing future UV-B radiation at ground level. All of these factors complicate the pro-
jections that scientists make regarding future trends.
Despite these technical problems the overall pattern is clear. Ozone levels in
the stratosphere are decreasing at several locations, most particularly at the North
and South Poles, and UV irradiation at the earth's surface appears to he increas-
ing in the areas beneath the thinning ozone ("ozone holes") (National Academy
of Sciences, 1992). This interpretation fits with the facts as we now know them.
There are early suggestions of a consistent increase in ground-level UV-B irradi-
ation in readings in the Alps, although the areas of maximal increase are over
the Poles and particularly the southern oceans where regular reduction in strato-
spheric ozone seems to have been most marked. It is expected that the first cv-
25
a)
=
0)
Ca
20
0
0
, 15
=
a)
0
a 10
[]
65N 55N 45N 35N 25N 15N 5N 5S 15S 25S 35S 45S 55S 65S
Latitude
Figure 11.2 Estimated relationship between increases in stratospheric ozone depletion and
skin cancer induction by latitude. Front McMichael et al., 1996, with permission.
Global climate change will occur as a result of changes in the balance of heat
taken on and retained by the planet. An increase in heat may lead to global
warming and chaotic weather conditions, and a decrease in heat may lead to
cooling, longer winters, and an increase in water trapped in the polar ice caps.
Human activity, primarily reflecting changes in industry and agriculture, causes
an increase in the amount of heat retained by the planet. This leads to an aver-
age warming of the earth's surface but with a great deal of local variation, which
makes it difficult to predict changes for local areas. Changes in climate of the
magnitude that is predicted may lead to many health problems related to heat
stress, natural weather disasters, changes in the distribution of vectors causing
human and animal diseases, new infectious disease patterns, unreliable crop pro-
duction, local food shortages, and flooding. Many of the health problems are
likely to he indirect, resulting from the social and economic consequences of these
effects (Leaf, 1989; Mungall and McLaren, 1990; Chivian et al., 1993; McMichael
et al., 1996; UNEP, 2000). The Intergovernmental Panel on Climate Change (IPCC),
which represents the concensus of the international scientific community (WRI,
1998), estimates that current emission patterns are likely to increase the average
temperature 1°C to 3.5°C by 2100, and raise sea levels 15-19 centimeters (IPCC,
1996). The effects could be devastating.
Solar radiation
by
~~ S
Absorption
Troposphere water vapor,
clouds and aerosois
/
Most incoming radiation Long-wave infrared
is absorbed by Earth's Earth radiation is emitted
surface and warms it from Earth's surface
lion in sunlight, so the radiation passes through and warms the plants and inte-
rior of the greenhouse. However, the glass also insulates the greenhouse, trap-
ping the heat that is created when the infrared radiation is absorbed Likewise,
infrared radiation from the sun passes through the earth's atmosphere, but the
carbon dioxide and some other gases in the atmosphere tend to insulate the earth,
trapping heat. The greenhouse effect normally contributes to stability of the
world's temperature and maintains the biosphere within a temperature range
conducive to life—the earth absorbs a certain amount of heat and loses the same
amount by radiation; the carbon dioxide and water vapor in the atmosphere keep
the average temperature higher than it otherwise would have been.
Until recently, the earth's heat budget was said to be in balance, i.e., its av-
erage temperature remained stable. However, in recent years there has been an
accumulation of gases in the atmosphere that upset this balance. Certain atmo-
spheric gases trap too much heat from infrared radiation, so global temperature
rises. The exaggerated greenhouse effect and resultant global warming may re-
sult in changes in regional climate and weather patterns. The accumulation of
greenhouse gases appears to have raised average global temperature by an esti-
mated /2 to 1 0 Celsius from 1930 to 1990. These changes in average tempera-
ture have occurred more rapidly in the last 10 years than in any earlier period.
A warming trend has been apparent since 1980, and 1998 was the warmest year
ever recorded up to that time. Rises of several degrees more are predicted in the
corning century. In fact, an overall global temperature rise of 3°-4C degrees in
the next 50 years is predicted by some experts. This increase may seem small,
but on a global scale this average masks marked extremes of temperature and
that has substantial implications (Mungall and McLaren, 1990; WHO, 1992a; Chi-
xi
0.4
0
0.2
E
0
c
C
0.0
ci)
cci
0
E
ci)
cci
-Q -0.4
0
-0.6
-0.8 I I I
1860 1880 1900 1920 1940 1960 1980 2000
Year
Figure 11.4 Combined land and sea temperatures, 1861-1994. From McMichael et al.,
1996, with permission.
350
El Average temperature
300 • Deaths 27 >
CD
250 26 co
Cl)
C
CZ
200 3
25 CD
Cs
a)
r 150 CD
0 24
a)
.o 100
E
23 cD
0,
50
22 C -)
I
1979 1980 1981 1982 1983 1984 1985 1986 1981 1988
Year
Figure 11.5 Annual fluctuations in average summer temperature and heat-related health
in Missouri, USA, 1979-88. From McMichael, 1993, with permission.
This species is responsible for major fish kills in Maryland, North Carolina and off
the Florida coast.
In Asia, there has long been an association between the seasonal appearance of
cholera and the yearly blooms of algae, zooplankton, and sea plants in coastal wa-
ters. Recently discovered is the nonculturable form of V cholerae in a wide range of
marine life (research by International Center for Diarrheal Diseases Research,
Bangladesh). In unfavorable conditions, V. cholerae assumes spore-like, quiescent
forms; with proper nutrients, pH, and temperature, the bacteria revert to a readily
transmissible and infectious state. V. cliolerae and V. vulnificus are present in coastal
waters of the United States. The latter is associated with a 67% case-fatality rate
among those with preexisting liver disease.
Both viral and bacterial diseases from the marine environment are on the increase.
Hepatitis A and bacterial diseases such as salmonella and campylobacter infections
continue to be major health problems throughout the world. A recent multistate
outbreak of viral gastroenteritis was related to the consumption of oysters from a
few U.S. states.
contributed by D. Rapport. See also Epstein and Rapport, 1996.
servation in and regions. The endemic zones of diseases currently limited to the
tropics are likely to extend into currently temperate zones. It is also possible that
such diseases will extend their ranges vertically to higher altitudes, especially in
the tropics (WHO, 1990b; Chivian et al., 1993; McMichael Ct al.. 1996; WRI,
1996).
Even a change in only several degrees in temperature, along the lines predicted by
the Inter-Governmental Panel On Climate Change (McMichael et al., 1996) can
have major effects on the vectors that transmit infectious diseases. In Rwanda, tem-
peratures increased greatly between 1961 and 1990, reaching a peak in 1987. In
the mid-I 980s, malaria became established in areas where it had previously been
rare or absent. Among people in high altitude zones, the incidence of malaria in-
creased more than 500%. Experts feel that the high temperatures and large amounts
of rainfall accounted for 80% of the difference in the monthly incidents. It is fur -
ther estimated that there will he an increase in the number of malaria cases from
the current 400 million annually to about 500 million annually by the year 2100,
based on the global climate change models and the substantial geographical widen-
ing of the malaria zone associated with a 3°C increase in global mean temperatures.
For example, in southern Honduras, erosion from grazing and farming, coupled with
a severe increase in temperature between 1972 and 1990, forced many Hondurans
into recently deforested regions in the north. The new migrants tended to be non-
immune to malaria. The surge in population, coupled with heavy rains, caused the
number of malaria cases in the northern region to more than quadruple.
Souri: WRJ, 1996. See also McMichael et al,, 1996.
and water vapor, into the earth's atmosphere. The increase in the release of these
gases exaggerates the greenhouse effect (see section The Greenhouse Effect), but
the underlying reason for this increase is intensive industrial and agricultural de-
velopment and increasing consumption of fossil fuels. The rapid rise in concen-
tration of these greenhouse gases is occurring in the troposphere. Carbon diox-
ide is increasing at 0.4% per year, methane at about 1% per year, CFCs until
recently at about 5% per year, and oxides of nitrogen at 0.3% per year; the con-
centration of ozone and a miscellaneous group of other gases is also on the rise.
This increase is mostly the result of industrial and transport development, espe-
daily the use of internal combustion engines and coal-burning electric power
generators. Methane also comes from agriculture, landfills, and other sources,
such as the decomposition of rotting vegetation and from the digestive tracts of
plant-eating animals like cattle. Water vapor, another important greenhouse gas,
has not been increased as much by human activity and does not seem to be ris-
ing (Mungall and McLaren, 1990; National Academy of Sciences, 1992).
Of these greenhouse gases, carbon dioxide is the most important, accounting
for half of the effect. It is also particularly difficult to control, because it is gen-
erated by any form of combustion and is inevitable in the burning of fossil fu-
els. By contrast, the CFCs are no longer increasing in concentration. A world-
wide moratorium on their manufacture and distribution in new products was
negotiated when they were identified as the principal cause of stratospheric ozone
depletion (see section Stratospheric Ozone Depletion, above).
Ticks belonging to the Ixodidae family have a wide geographical distribution range,
including parts of the subarctic regions. These ticks are vectors for several diseases,
such as Lyme disease and tick-borne encephalitis (TBE). Several animals, such as
birds, rodents, and deer, act as hosts for the tick. They may be infected with the
pathogen and can pass it on to humans through a blood-sucking tick. Ticks as well
as their host animals and habitat are all dependent on changes in local weather con-
ditions. A future climatic change would affect the complicated ecological interac-
tions associated with the transmission of tick-borne diseases. As a result, tick-borne
diseases may spread into new areas that are located at higher northern latitudes and
altitudes than present endemic regions.
Contributed Lw E. Lindgren, Sweden.
Human activity has changed the face of the earth considerably. Only remnants
now remain of the huge forests that once covered Europe, the Middle East, and
China. Central Europe was once a dense forest and in Roman limes the cedar
groves of Lebanon were famous. North America used to be much more heavily
forested along the East Coast than it is tcday, although the forest is coming back
in many areas of the East Coast. Large tracts of forest remain in protected areas
in North America, in the mountains of the West, along the Pacific Northwest,
and in the far North. Southeast Asia, South America, and Africa still have vast
expanses of rain forest but through the clearing of huge areas for agriculture and
industrial development, the total area of forest coverage has been rapidly re-
duced.
Clearance is usually undertaken on a piecemeal basis for agriculture. Often,
as in the Amazon Basin and Indonesia, woodlands are cleared by fire. Some-
times, as in northern Africa and China, forests are consumed for firewood. The
resulting depletion of forests can result in serious ecological consequences.
Forests also play a critical role in the removal, storage, and release of carbon
dioxide from the atmosphere, as discussed earlier. Throughout history, at least
since the last Ice Age, it would appear that the global sinks for carbon dioxide
have had sufficient capacity to absorb any excess caused by volcanic eruption or
forest fires. As a result, the content of carbon dioxide in the atmosphere remained
relatively stable. Today, however, production of carbon dioxide exceeds the ca-
pacity of the global sinks, and the concentration of the gas in the atmosphere is
steadily increasing, leading ultimately to the exaggerated greenhouse effect de-
scribed above (see McMichael et al., 1996).
Defcrestation reduces the capacity of the world's forests to serve as a carbon
dioxide sink. Burning forested areas aggravates the global accumulation of car-
bon dioxide in the atmosphere. When forests are cut down for firewood or catch
on fire, the stored carbon in the wood and brush is released into the atmosphere
again. Even when wood is used for building construction and other purposes,
some carbon dioxide is eventually released. Another, and quite unexpected, con-
sequence of deforestation is mercury contamination, as described in Box 11.5.
Reforestation, on the other hand, takes carbon dioxide out of the atmosphere
and traps it in biomass. That is why one response to the challenge of global cli-
mate change has been to encourage the planting of trees and the reforestation
of forests.
As mentioned in the section Solutions to the Problem, the most significant
sinks for carbon dioxide appear to be in the Amazon rain forest and the tem-
perate zones of the northern hemisphere. Large-scale destruction of the Ama-
zonian forests and, potentially, the boreal forest in Canada and Siberia will re-
duce the capacity of the biosphere to remove carbon dioxide and act as a
Gold mining in the Amazon, originally thought to he the only cause of the mercury
pollution of some of the rivers, began approximately three decades ago when thou-
sands of impoverished miners, known as garimpeiros, swept into the jungle to mine
gold using a mercury mining method they use to this day (see Chapter 10). About
half of the approximately 130 tons of mercury per year used is emitted into the air
while the other half seeps into the water, contaminating fish.
The team of Canadian and Brazilian scientists investigating the mercury conta-
mination and its health effects on the villagers (see Lebel et al., 1995) began to sus-
pect that there was too much methylmercury in the Amazon to be the result solely
of garimpeiros activities. Everywhere they collected river sediment samples they
recorded 1.5 to 3 times more mercury than there had been 40 years ago, even 400
kilometers downstream from the gold mining. They soon found that deforestation
was the other source. When impoverished people from northern Brazil colonize the
Amazon jungle they usually clear the forest in a 10 to 20 kilometer area on both
sides of a river and burn the remaining rubble. Following deforestation, heavy rains
wash out nutrients from the soil into the waterways. As the Amazon basin has con-
siderable natural mercury in its soil, mercury released into the water contaminates
the fish to cause mercury poisoning in people consuming large quantities of fish.
The Canadian team had a particular interest in mercury because in the north-
ern area of two Canadian provinces, high mercury exposure occurred in the abo-
riginal community from a similar process: hydroelectric dams and reservoirs raised
water levels, the water inundated ancient soils, which then degraded and released
their naturally occurring mercury.
Although Brazil has officially banned the use of mercury for mining, this tech-
nique is still occurring. Moreover, the reforms instituted have not added the prob-
lem of landless settlers burning trees and destroying the soil, thereby releasing mer-
cury into the Amazon. In the meanwhile, in discussing the results with the
community, it was advised that they vary their diet so as to eat more "fish that do
not eat other fish."
Contributed by D. Mergler
stabilizing mechanism to climate change. Thus much attention has been given to
the development of the Amazon Basin and concern expressed over the clearing
of rain forests in South America and the northern hemisphere (Canada and
Siberia). Not surprisingly, the few countries with large forested areas remaining
have been singled out for criticism, notably Brazil. This issue has led to a con-
flict over the right of a particular country to pursue its short-term development
strategy and the right of the world as a whole to be protected from massive
change in the long term that will affect everyone. Forests in many parts of the
world, such as Brazil, are being cleared in remote areas for agriculture and eco-
nomic development by people who have limited economic opportunities and are
B IODIVER SITY
Biodiversity refers to the multiplicity of species of plants and animals in a biolog-
ical community and the many ecological niches that they may occupy. It is a
fundamental principle of ecology that diversity in animal and plant species leads
to greater stability of the ecosystem. The ecosystem functions more efficiently,
with different species occupying more niches and extracting full benefit from the
energy and nutrients available. More complicated systems have greater adapt-
ability in the face of environmental changes and the ecological niches occupied
by different species may partly overlap and allow substitutions if one or more
are lost. Loss of biodiversity therefore means a less stable, less adaptable, less self-
restoring ecosystem (Chivian et al., 1993).
Biological Siqnificance of Biodiversitv
Biodiversity is also a means of preserving genetic diversity. Each species and sub-
species contain within their genes the result of hundreds of thousands, even mil-
lions of years of evolution. This genetic constitution is written onto DNA, the
molecule that conserves the genetic code. It constitutes a library of 'blueprints'
for living beings and for biological adaptation. For all groups of organisms rec-
ognized as species, there is a basic genetic constitution consisting of characteris-
tics common to all members of the species, and a set of variations that have been
introduced by mutations, random changes in the gene pool introduced by mis-
takes in replication of DNA or the effect of ionizing radiation on DNA. Most of
such mutations are harmful and do not survive; a few confer new traits that may
or may not be useful to the individual that carries them. The variation in ge-
netically determined traits among individual members of any species or subspecies
is what drives evolution: natural selection favors some variants and not others,
SO that some traits survive and others do not. Many of the variants represent
traits that survived because they were useful; the individuals who carried the
traits could adapt to new conditions or exploit new ecological niches. Loss of bin-
diversity means that even if the species as a whole survives, the variation within
Loss of Biodiversitv
Ecosystems can lose hiodiversity in many ways. Individual species may become
extinct through hunting, habitat loss, or reduction in the species that they de-
pend on for food. Entire ecosystems or large areas of larger ecosystems may he
changed or lost by urbanization and agricultural clearance. Particular habitats of
individual species with limited ranges may be lost in the same way: the essen-
tial area lost might relate to feeding requirements, territoriality, or breeding.
Sometimes foreign species are introduced into a stable ecosystem, preying on and
reducing the numbers of the local species that give the ecosystem stability. Of-
ten all of these mechanisms occur at the same time (Chivian ci al., 1993).
Even ecosystems that appear to be healthy may suffer loss of biodiversity.
Old-growth forests, for example, are forests that have not been cut down and
that maintain a much richer diversity of species and considerably more stable
ecosystems than new-growth forests, which arise by ecological succession after
earlier forests have been cut down. Even though the forest may look the same,
appearances can be very deceiving.
Loss of biodiversity is an important indicator of the magnitude of these trends.
It shows the extent to which the ecosystem is being simplified. Because the sta-
bility of ecosystems depends on complexity and variability, simplification is nec-
essarily environmental degradation, regardless of what else is happening in the
environment. That is why it is a mistake to concentrate too narrowly on the eco-
logical or economic importance of a particular species when it comes to local is-
sues of conservation and ecosystem protection. The loss of a particular species or
subspecies is important in and of itself, but it is also another thread that is cut
in the ecological web and reflects a trend toward an increasingly simplified and
unstable ecosystem. Biodiversity is a critical part of the network of ecological re-
lationships that supports human society. Loss of biodiversity is both a serious
problem in its own right and a sensitive sign of the deterioration of the envi-
ronment as a whole.
ACID PRECIPITATION
Acid precipitation (acid rain) occurs when rainwater, snow, and other forms of
precipitation have a lower than natural pH as a result of dissolved acidic chem-
icals that occur from air pollution. This is caused by increased production of acid-
ifying emissions from industrial sources, principally sulfates and nitrates, and air -
borne transport of these pollutants. Often, these pollutants are carried very long
distances and fall as acid precipitation hundreds or even thousands of kilometers
away from the original site of production. When the precipitation reaches the
ground, it can change the pH of small lakes and the soil, causing ecological dam-
age. This is particularly a problem in areas where there is little natural buffering
capacity in the soil or water (WHO, 1992a).
In recent years, surveys of soil and water acidity in the Northern Hemisphere
tries are often willing partners because of the money the importation of haz-
ardous waste brings in the form of fees, facilities, and, sometimes, bribes. How-
ever, these countries usually have no effective means of controlling hazardous
waste once it arrives. In some cases, the waste is simply dumped where it may
pollute groundwater, the oceans, or land. In a few cases, the wastes may be chem-
ically treated and disposed of in a manner that is similar to good practices in the
developed world but without the stringent supervision and monitoring that is
needed to ensure that the material does not pollute the environment.
Such practices are not confined to the developing world. Some of the worst
incidents documented recently have involved the former East Germany and the
former Soviet Union. Developing countries arc particularly vulnerable to this
form of "toxic blackmail." Since 1989 an international protocol on the move-
ment of hazardous waste, the Base! Convention, has governed the transboundary
movement of hazardous wastes, on the basis of the six principles paraphrased in
Table 11.2.
DISASTERS
Emergency Actions
Depending on the magnitude of the disaster and its extent, disasters can overwhelm
the health care system in the area and disrupt the operations of fire, transporta-
tion, and rescue services. In the first few hours following a disaster, the first prior-
TABLE 11.3
PERCEIVED DIFFERENCES BETWEEN NATURAL AND TECHNOLOGICAL DISASTERS
Natural Disasters Technological Disasters
Nature of disaster Clean, unavoidable Dirty, contaminated
Responsibility No agent Culpable party
Objective magnitude of loss Often great Usually less
Perceived magnitude ol loss Usually minimized Usually maximized
Community support for those affected Nonjudgmenta] - Highly judgmental, ambiguous
Study Oliestions
Your health minister has been invited to attend a special cabinet meeting
to discuss your country's response to recent reports regarding climate change.
She has been told that there are no major health impacts in your jurisdiction,
therefore it is not necessary for her to prepare a detailed report. She has asked
you if you think that she ought to attend. Formulate a memo of no more than
two pages offering her advice. Discuss how global warming could affect health
in your country.
What are the most serious global health concerns? Prioritize and justify
your list.
Summarize the areas of greatest debate and state why these debates exist.
What are the obstacles to overcome in addressing global health problems?
What strategies exist to address these obstacles?
CHAPTER (ONTENJTS
399
What is not so clear is what to do about them. Many individuals and many
political groups have their own ideas about radical changes that would correct
specific problems at what they perceive to be their root causes. However, the
root cause for some people (for example, overpopulation) may be seen as a sec-
ondary phenomenon by others (as, for example, the lack of education and em-
powerment of women). Radical solutions are easy to conceive but very difficult
to implement. It is clear that the world does not have much more time to de-
bate these issues before the damage to the environment will be permanent, ir-
reversible, and sufficiently advanced to constrain the life choices and freedoms
of the next generation. Regardless of their view of the causes of the problems,
however, many thoughtful and conscientious people are arriving at a common
point of view regarding the most urgent changes that are needed to give society
and the environment breathing room. At least the outline of a consensus is emerg-
ing in countries around the world on the minimal steps necessary to deal with
the issues. These are summarized in Table 12.1, not necessarily in any order of
fundamental importance.
If there is an emerging consensus on the minimum that must be done, the next
question is who should do it. Clearly, many of these actions have a practical, tech-
nical component that must be handled by trained professionals. However, these pro-
fessionals cannot act in isolation. There must be support from the people who are
directly affected, from national leaders, from institutions, and from leaders at the lo-
TABlE 12.1
COMPONENTS TO ADDRESSING ENVIRONMENTAL HEALTH CONCERNS
Pollution control, to prevent the release of pollution into the environment in the first place, and the
economic and regulatory structures that support vigilance in pollution control
Remediation, to clean up polluted areas and to restore them to the extent feasible to their nat ural
or at least an acceptable state
Resource conservation, including recycling and reuse, to reduce the amount of raw materials needed
by industry and increase the efficiency of use of these resources
Ecosvcteoi conservation, to ensure that habitats for the world's species will be preserved in full pro-
ductivity and that appropriate human uses can be sustained
Cenintitnient to end extreme povi'rt'c and support of national efforts to achieve a sustainable ec000nly,
to provide for most of the world's peoples at least a comparable level of economic security and
personal wealth to that in the developed world today
Technology transfer, to allow the developing world to industrialize with the advantage of the more
efficient, less hazardous, and less polluting technologies
Sustainable economic systems that base their economic productivity on what can be extracted from
the environment without permanent damage over the long ternl
Control of population growth, with a concomitant commitment to improved quality of lamily life and
individual security
Acceptance of some deqree of risk as part of daily life, along with a ommittnent by society to moderate
the effects of risk on its citizens throttgh education, regulation, and economic incentives so that
the hazards of life are not constant preoccupations
Prevention of conventional and nuclear war to the fullest extent that ho ma ii institutions can manage,
and the redirection of funds spent for armaments for peaceful purposes, including environmen-
tal reconstruction
The environmental health professional must make many decisions in daily work
that involve not only technical-scientific issues but also issues of ethics. The ba-
sic ethical principles in environmental health work follow the same ethical prin-
ciples as have been developed for other health work, except that these guide-
lines ask environmental health professionals to pay even greater attention to the
broader social consequences of their work. Table 12.2 provides the ethical guide-
lines that have been developed for environmental epidemiologists. They apply to
other members of the environmental health team as well.
At the personal level the application of ethical principles involves how one's
own lifestyle and resource consumption reflect the environmental health con-
cerns that have been outlined in this hook. Ultimately, every environmental
health professional must strike a balance between his or her own convictions
and personal commitment and what is required to be professional. Some useful
guidelines are shown in Table 12.3.
In the broader global context, the environmental health professional also has
responsibilities in promoting and facilitating community application of a precau-
tionary environmental health approach. As a member of an interdisciplinary
team, strengthening one's specialized knowledge in one's own profession will
help contribute to the solution of environmental health problems. The following
section outlines these roles more specifically.
Technical Expertise
The first and most obvious role of the environmental health professional is to
master the technical details and context of environmental problems. In order to
solve a problem, it is usually necessary to understand what caused it, and it is
always necessary to understand what perpetuates it. This textbook will help
achieve this level of mastery, but it is not sufficient in and of itself. Further de-
OBLIGATIONS TO SOCIETY
Avoid partiality
Distinguish one's role as scientist from that of advocate
The public interest always lakes precedeisce over any other interest
Be objective in disseminating research findings and he understandable in public discussions
tnvolve communities being proposed for study throughout all stages of the research and its
rep i rt ii g
Engage with other disciplines to advance and maximize the public utility of environmental
epidemiology
Consider the broader social consequences, including psychosocial and physical health outcomes
Consider both eqenty and remediation in the allocation of resources applied to environmental epi-
demiology research across the different areas of research, social strata, and jurisdictions
Environmental epidemiology findings arc based on uncertainty and as such must he used appro-
priately in their application to, for example, the development of risk analyses, policy, and
interven I ions
Be diligent in exectiting professional responsibilities
Ensure that both researcher and sponsor/eniplover are apprised of one another's respective re-
sponsibilities and expectations
Emphasize obligations to other parties
Protect privileged information, but release research methodv procedures and results
OBLIGATIONS TO COLLEAGUES
veloprncnt of knowledge and skills will be required. In fact, the learning process
continues throughout one's professional life. This process will be more effective
if every problem faced is seen as an opportunity to understand better how to
solve the next problem. To become an effective professional in this field, one
needs to keep up-to-dale with the technical-scientific knowledge, as well as de-
velop skills to do things and skills in working as a team member with other pro-
fessionals and the community.
The in-service learning process can be greatly facilitated by structured dis-
cussions and reviews of experiences in handling environmental health problems.
If a program for such discussions does not exist in your workplace, consider tak-
ing the initiative to get it started. The program could include regular reviews of
particularly interesting cases you and your colleagues have dealt with. It could
include all colleagues reading selected articles in scientific or professional jour-
nals or chapters in selected textbcoks, and discussing their content and the im-
plications for your work.
Formal higher-level training in environmental health topics is another way
to develop one's knowledge and skills,. The availability of such training varies
from country to country. National professional societies in the field usually main-
tain information about these types of courses. Courses promoted at the interna-
tional level can be found, for instance, in the inventories and databases provided
by the WHO.
The environmental health professional who wishes to be truly effective must
be committed to a lifelong effort of reading, thinking, and analysis to understand
the problems and the possible solutions. Above all, a capacity for sound judg-
ment is needed to know what will work in the real world, what will not work,
and how to achieve a workable solution in an imperfect world.
Professional Practice
Closely related to the role of environmental health professionals as technical ex-
pert is the skill that they show as practitioners. Professional practice as an envi-
ronmental health practitioner depends on the job and the setting but typically
requires mastery of a certain number of health indicators and standardized lab-
oratory tests (for example, to determine water quality) and an ability to inter-
pret the results and draw conclusions about the problem. These are basic skills
in technical proficiency, and environmental health professionals are expected to
Advocacy
A critically important role of environmental health professionals is to serve as
advocates for environmentally sound policies and practices, much akin to the
role of physician as the patient's advocate. This role overlaps the responsibilities
mentioned earlier for public education and implies attempting to influence deci-
sion makers to adopt enlightened policies.
Within the environmental health professional's role as a technical expert, it
is appropriate to advocate a preferred or scientifically rational solution to re-
solving a question after presenting an overview of the potential solutions and
their implications. It generally works best if the pro's and con's of each poten-
tial solution are spelled out and a justification is given as to why one option is
superior to the others. For narrowly technical problems, this is usually enough.
The analysis by the experts will decide the matter. However, most major deci-
sions are complicated by issues of cost, local history, public perception, political
acceptability, and interrelation with other problems in the community. For bet-
ter or for worse, it is up to the political decisk n-making bodies to decide on the
best course of action that takes all of these factors into account.
Although the decision as to how far to go in attempting to influence decision
makers is a personal isstie for each environmental health professional, it is part
of the professional's role to guide society in seeking the most appropriate solu-
tion. Depending on the country and political system, this may or may not be
easy to do. One approach is to form or join professional associations and soci-
eties and to work within them to develop recommendations and policies that will
influence decision makers. Often a statement on an issue prepared by a large or-
ganization carries much more weight than the opinion of an expert. It also shows
Networking
A very effective way for environmental health professionals to enhance their role
and to increase their contribution to society is to network, by forming relation-
ships between themselves and their organizations. Networks can be formal or in-
formal, personal or institutionalized. They are created whenever colleagues keep
in touch and share ideas and resources. A professional in a network is in a much
stronger position than a prolessional in isolation.
Networks expand the range of options for dealing with a problem because
they enable professionals to get good ideas, share or loan needed resources, learn
about and adapt good ideas or inncvative methods, and continuously stay edu-
cated about developments in the field and in the region. Interdisciplinary net-
works can also be effective in keeping the various members aware of new de-
velopments in their fields of expertise. The simplest network is the set of
colleagues and friends in the field that environmental health professionals may
have and the organizations to which they belong. More sophisticated networks
may include WHO initiatives such as the Global Environmental Epidemiology
Network (GEENET) and the Global Environment and Health Libraries Network
(GELNET), which provide access to educational and practical tools by mail and
electronic mail.
Although national and international networks are very useful and important,
local or community networks may be exceptionally powerful when one needs
to solve a local environmental problem. It is very helpful to be able to draw on
community leaders, business representatives, scientists, and engineers as needed
to solve a particular problem, and because they know the community that they
live in, the solutions are likely to be more practical and feasible than solutions
proposed by colleagues who do not live there. There is also likely to be greater
support for proposed solutions.
Study Questions
Assuming that you agree that professionals should get involved, in the issues
they study, what can you do with respect to each of the categories discussed in
the section Role of Environmental Health Profession? Be as concrete as possible,
with specific examples of actions that you might take.
ACOHOS. (1983) Principles and Procedures for the Interpretation of Epidemiological Studies. Ad-
visory Memorandum 82-V to the Minister of Labor, Toronto, Ontario, Canada.
Ad Hoc Population Dose Assessment Group. (1979) Population Dose and Health Impact of the
Accident at Three Mile Island Nuclear Station. Washington, DC: U.S. Environmental Pro-
tection Agency, and National Research Council.
Ajzen I. (1991) The theory of planned behaviour. Organ Behav Hum Decision Processes 50:
179-211.
Ames BN, Gold LS. (1990). Dietary carcinogens, environmental pollution, and cancer:
some misconceptions. Med Oncol Tumor Pharniacotlter 7(2-3):69-85.
Anderson DM. (1992) The fifth international conference on toxic marine phytoplankton:
a personal perspective. Harmful Algae News (Suppl. to lot Marine Sci 62:6-7).
Ascherio A, Chase R, Cote T, Dehaes G, Hoskins F, Laaquej J, Passey M, Qaderi 5,
Shuqaider S, Smith MC, Zaidi S. (1992) Effect of the Gulf War on infant and child
mortality in Iraq. N Enqi I Med 327:931-936,
Ashton SR, Fowler SW. (1985) Mercury in the open Mediterranean: evidence of conta-
mination? Sci Total Environ 43(1-2(:13-26.
410
ATSDR. (1992) Public Health Assessment Guidance Manual. MI: Lewis Publishers.
Baker D, Landrigan P. (1993) Occupational exposures and hunian health. In: Critical Con-
dition: Human Health and the Environment. Chivian E. McCally M, Hu R, Homes A. (eds).
Cambridge, MA: MIT Press.
Baker SP, O'Neill B. Karpf FS. (1984) The Injury Fact Book. Lexington: D.C. Health.
Bearer C. (1995) How are children different from adults?' Environ Health Perspect 103,
(Suppi 6: 7-12).
Beaglehole R, Bonita R, Kjellström T. (1993) Basic Epidemiology. Geneva: World Health Or-
gani zation.
Becklake MR. (1985) Chronic airflow limitation: its relationship to work in dusty occu-
pations. Chest 4:608-6 17.
Becklake MR. (1989) Occupational exposures: evidence for a causal association with
chronic obstructive pulmonary disease. Am Rev Respir Dis 140:S85—S91.
Beneson AS (ed). (1995) Control of Communicable Diseases Manual. United Book Press Inc.,
Baltimore, MD.
Berdén M, Nilsson SI, Rosen K, Tyler G. (1987) Soil Acidification: Extent, Causes, and 'onse-
quences. Solna, Sweden: National Swedish Environment Protection Board.
Bisson JI, Jenkins PL, Alexander J, Bannister C. (1997) Randomised controlled trial of
psychological debriefing for victims for acute burn trauma. Br J Psychiatry 171:78-81.
Bosnir J, Puntaric D, Smit Z, Capuder Z. (1999) Fish as an indicator of eco-syslem con-
tamination with mercury. Croat Med J 40(4):546-549.
Briggs D, Corva]an C. Nunninen M. 1996) Linkage Methods jér Environment and Health Analv-
sis. General Guidelines, Document WHOIEHGI95.26. Geneva: World Health Organization.
Brooks 5, Gochfeld M, Herzstein J, Jackson R, Schenker MB. (1995) Environmental Medi-
cine. St Louis: C.M. Mosby.
Bryan FL. (1989) HACCP: Hazard Analysis Critical Control Point Manual, Washington, DC:
Food Marketing Institute.
Bryan FL. (1992) Hazard Analysis Criticial Control Point Evaluations. Geneva: World Health
Organization.
Capuder Z. (1999) Fish as an indicator of eco-system contamination with mercury. Croat
Med J 40)4):546-549.
Carson R. (1962) Silent Spring. Boston: Houghton Mifflin.
Cameco. (1996) McArthur River Mining Development Environmental Impact Statement. Saska-
toon: Cameco Corporation.
Chivian F, McCally M, Hu R, Ilaines A. (1993) Human Health and the Environment. Cam-
bridge, MA: MIT Press.
Ctarkson TW, Friherg L. Nordberg GE, Sager PR (eds). (1988) Biological Monitorinq of Toxic
Metals. New York: Plenum Press,
Clatworthy S. Stevens H. (1987) An Overview of the Housing Conditions in Registered Indians
in Canada. Ottawa: Department of Indian Affairs and Northern Development.
Codex Aliinentarius Commission, Joint FAO/WHO, Food Standard Programme. (1989).
Colborn T, Dumanoski I), Peterson Myers J. (1996) Our Stolen Future. New York: Penguin.
Corvaldn C, Kjellstrdm T. (1995) Health and environment analysis for decision making.
World Health Stat Q 49(2):7I-77.
Corvalãn C, Nurminen M, Pastides H. (1997) Linkage Mt'thod.c for Environment and Health
Analysis. Technical Guidelines, Document. WHO/EHG/ 97.11. Geneva: World Health
Organization.
Covello VT. (1989) Informing people about risks froni chemicals, radiation, and other toxic
substances: a review of obstacles to public understanding and effective risk communi-
cation. In: Prospects and Problems in Risk Communication. Leiss W (ed). Canada: Univer-
sity of Waterloo Press, Waterloo.
Covello VT, Allen FW. (1988) Seven Cardinal Rules of Risk Communication. Washington, DC:
U.S. Environmental Protection Agency.
Davies DL, Bradlow HL, Wolff M, Woodruff T, Hoe! DG, Anton-Culver H. (1995) Med-
ical hypothesis: xenoeslrogens as preventable cause of breast cancer. Environ Health
Perspect 101:372-377.
REFERENCES 411
Dean K, Hancock T. (1992) Supportive Environments for Health. Copenhagen: World Health
Organization.
Dejoy DM. (1984) A report on the status of research on the cardiovascular effects of noise.
Noise Control Engineering J 23:32-39.
de Koning HW. (1987) Setting Environmental Standards. Guidelines for Decision-Making.
Geneva: World Health Organization.
Dhara R, Dhara yR. (1995) Bhopal----a case study of international disaster. mt .1 Occup En-
viron Health l(i):58-69.
Dunser HJ, Howells H, Templeton WL. (1959) District surveys following windscale inci-
dent in October 1959. In: Proceedings of the Second United Nations International Conference
on the Peaceful Uses of Atomic Energy (Sept. 1-13, 1958). Geneva: United Nations.
Elinder CG, Friberg L, Kjellström I, Nordberg G, Oherdoerster G. (1994) Biological Moni-
toring of Metals. WHO Document WHO/EHG!94.2. Geneva: World Health Organization.
Environmental Agency (1975). Studies on the Dealt/i Effects of Alkylmercury in Japan. Tokyo,
Japan: Environmental Agency.
Environment Canada. (1976) Criteria for Air Quality Objectives. Report for the Federal!
Provincial Committee on Air Pollution. Ottawa: Environment Canada.
Environment Canada. (1987) The Great Lakes: An Environmental Atlas and Resource
Book. Toronto, Ont: Environment Canada, in collaboration with US Environmental
Protection Agency, Chicago, Illinois, as cited in Environment Canada (1991) State of
the Environment Report. Ministry, Supply and Services, Ottawa, Canada.
Epstein PR, Rapport DJ. (1996) Changing coastal marine environments and human health.
Ecosystem Health 2)3): 166-176.
Ewetz L, Camner P (eds). (1983) Motor Vehicles and Cleaner Air: Health Risks Resulting from
Exposure to Motor Vehicle Exhaust. A report to the Swedish Government Committee of
Automotive Air Pollution Stockholm National Institute of Environmental Medicine.
Stockholm, Sweden.
Falk H, Heath C. (1986) Vinyl chloride and cancer. In: Teaching Epidemiology in Occupa-
tional Health. Atlanta: U.S. National Institute for Occupational Safety and Health and
World Health Organization.
FAO!WHO. (1994) CodexAlimentarizes. Rome and Geneva: Food and Agricultural Organi-
zation! World Health Organization.
Federspiel JF. (1983) The Ballad of Typhoid Mary. New York: E.P. Dutton.
Fernández N, Tate RB, Bonet M, Cañizares M, Mas P. Yassi A. (2000) Health-risk per-
ception in the inner city commutlity of Centro Hahana, Cuba. Tnt J Occup Environ Health
6(1 ):34-43.
Fletcher RG, Fletcher SW, Wagner PH. (1982) Clinical Epidemiology—The Essentials. Balti-
more: Williams & Wilkins.
Foley G. (1992) Renewable energy in third world energy assistance. Energy Policy
20(4) :335-361.
Folinsbee U. (1992) Human health elfects of air pollution. Environ Health Perspect
100:45-56.
Franklin CA, Burnett RT, Paolini RJ, Raizenne ME. (1985) Health risks from acid rain: a
Canadian perspective. Environ Health Perspect 63:1 5 5-68.
Garfield M, Neugut A (1997) The hutnan consequences of war. in: War and Public Health.
Levy BS, Sidel VW (eds). New York: Oxford University Press, pp. 27-38.
Goldman LR. (1995) Children—unique and vulnerable: Environmental risks facing chil-
dren and recommendations for response. Environ Health Perspect 103(Suppl 6): 13-18.
Goyer RA, Bachmann J, Clarkson TW, Ferris BG, Graham J, Mushak F, Perl DP, Schlesinger
R, Sharpe W. (1985) Potential human health effects of acid rain: report of workshop.
Environ Hea It/i Perspect 60:355-368.
Green LW, Kreuter M. (1999) Health Promotion Planning: An Educational and EcologicalAp-
proach (3rd ed). Mountain View, CA: Mayfield.
Gregory K. (1992) The earth summit: opportunity for energy reform. Energy Policy
20) 6) : 547.
REFERENCES 413
tnhaher H. (1979) Risk with energy from conventional and nonconventional sources. Sci-
ence 23;203(4382):718-723.
Intergovernmental Panel on Climate Change. (1996). Climate Change 1995: The Science of
Climate Change Cambridge, U.K.: Cambridge University Press, p. 4.
Jacob M. (1989) Safe Food Handling: A Training Guide for Managers of Food Service Establish-
ments. Geneva: World Health Organization.
JBMC. (1995) Report of Activities 1994-1 995. Montreal: James Bay Mercury Committee.
Jedrychowski W, Krzyzanowski M (eds). (1995) Host Factors in Enviromnental Epidemiology.
Proceedings of the Conference and Workshop, Cracow, June 11-14, 1995. Central and
Eastern European Chapter of ISEE/ISEA, WHO
Jeyaratnam J (ed.) (1992) Occupational Health in Developing Countries. Oxford: Oxford Uni-
versity Press.
Jones RR. (1987) Ozone depletion and cancer risk. Lancet 11:443-445.
Jones TS, Liang AP, Kilbourne EM, Griffin MR, Patriarca PA, Wassilak SG, Mullan RJ,
Herrick RF, Donnell HD Jr., Choik Thacker SB. (1982) Morbidity and mortality asso-
ciated with the July 1980 heat wave in St. Louis and Kansas City, Mo. JAMA
247:3327-3331.
Kaferstein FK, Miyagishima K, Miyagawa S, Motarjemi Y, Moy G. (1995) What is food
quality and safety? In: Proceedings of Food Session, 39th EOQ Annual con qress. Hochschul-
verlag.
Kalimo R, El-Batawi MA, Cooper CL (eds). (1987) Psychosocial Factors at Work and Their Re-
lation to Health. Geneva: World Health Organization.
Kawachi I. (1999) Social capital and community effects on population and individual
health. Ann N YAcad Sci 896:120--30.
Kjellström T, (1986a) Itai-itai disease. In: Cadmium and Health, Vol. 2. Friberg L, Elinder
CG, Kjellstrom T, Nordberg G. et al. (eds). Boca Raton, FL: CRC Press
Kjellström T. (1986b) Critical organs, critical concentrations, and whole body dose-
response relationships. In: cadmium and Health, Vol. 2. Friberg L, Elinder CG, Kjell-
strom I, Nordberg G (eds). Boca Raton, FL: CRC Press.
Kjellström T, Hicks N. (1991) Atmospheric fog in greater London. In: Problem-Based Train-
ing Exercises for Environmental Epidemiology. WHO Document WHOIPEP/92 .05-A.
Geneva: World Health Organization.
Kjellströrn T, Rosenstock L. (1990) The role of environmental and occupational hazards
in the adult health transition. World Health Stat Q 43:188-196.
Kjellström T, Yassi A. (1998) Linkages between environmental and occupational health.
In: Encyclopaedia of Occupational and Safety, 4th ed. Stellman JM (ed). Geneva: Interna-
tional Labour Organization, pp. 532-534.
Kleinman MT, Phalen RF, Mautz WJ, Mannix RC, McCltire TR, Crocker TT. (1989) Health
effects of acid aerosols formed by atmospheric mixtures. Environ Health Perspect 79:
137-145.
Kraus JF, Robertson LS. (1992) Injuries and the public health. In: Public Health and Pre-
ventive Medicine. 13th ed. Last JM. Norwalk )eds). New York: Appleton-Century-Crofts.
Kusiac RA, Ritchie AC, Muller J, Springer J. (1993) Mortality from lung cancer in On-
tario uranium miners. Br J md Med 50(10(:920-928.
Last JM. (1992) Global environment, health, and health services. In: Public Health and Pre-
ventive Medicine, 13th ed. Last JM, Norwalk (eds). New York: Appleton-Century-Crofts.
Last JM (ed). (1995) A Dictionary of Epidemiology, 3rd ed. New York: Oxford University
Press.
Leaf A. (1989) Potential health effects of global climatic and environmental changes. N
EnglJMed 321:1577-1583.
Lehel J, Mergler D, Lucotte M, Amonim M, Dolbec J, Miranda D, Arantes G, Rheault 1,
Pichet P. (1996) Evidence of early nervous system dysfunction in Amazonian popula-
tions exposed to low levels of methylmercury. Neurotoxicology 17:157-168.
Lemeshov 5, Hosmer DW, KIar J, Lwange SK. (1990) Adequacy of Sample Size iii Health
Studies. New York: John Wiley & Sons.
REFERENCES 415
NIOSH. (1995) Cumulative Trauma Disorders in the Workplace: Bibliography. Cincinnati: Na-
tional Institute for Occupational Safety and Health.
Noguiera DP. (1987) Prevention of accidents and injuries in Brazil. Ergonomics 30:387-393.
Norman R, Wells R. (2000) Ergonomic interventions for reducing musculoskeletal disor-
ders. In: Sullivan T (ed). Injury and the Nest' World, Vancouver, UBC Press, pp. 115-139.
NRC. (1991) Human Exposure Assessment forAirborne Pollutants. Washington, DC: National
Research Council.
NRC. (1999) Biological Effects of Ionizing Radiation (BEIR) VI Report. The Health Affects
of Exposure to Indoor Radon. NRC. National Academy of Sciences: 28 May 1999.
(http:/lwww.ruderserv.comldiscussion).
OECD. (1991) State of the Environment Report. Paris: Organization for Economic Coopera-
tion and Development.
O'Grady J. (2000) Joint Health and Safety Committees: finding a balance. In: Sullivan T
(ed). Injury and the New World, Vaiicouver, UBC Press, pp. 162-197.
Ong CN, Jeyaratnam J, Koh D. (1993) Factors influencing the assessment and control of
occupational hazards in developing countries. Environ Res 60:112-123.
Ostro B. (1996) A Methodology for Estimating Air PollutionHealth Effects. WHO Document
WHO/EHG/96.5 Geneva: World Health Organization.
OTA. (1992) Fueling Development: Energy Technology for Developing Countries. Washington,
DC: Office of Technology Assessment.
Pandey MR. (1984) Domestic smoke pollution and chronic bronchitis in a rural commu-
nity of the hill region of Nepal. Thorax 39:339-339.
Pandey MR, Boleij JS, Smith KR, Wafula EM. (1989) Indoor air pollution in developing
countries and acute respiratory infection in children. Lancet 25;(8635):427-429.
Pisaniello DL, McMichael AJ, Woodward A. (1993) Guidelines on Planning Education and
Training for the Control of Environmental Health Hazards: A Contribution to Capacity-Build-
ing at National and Sub-National Levels. Geneva: World Health Organization.
Pless M. (1994) Editorial. Unintentional childhood injury—where the btick should stop.
Am I Public Health 84:537-539.
Polanyi M, Frank J, Shannon H, Sullivan T, Lavis J. (2000) Promoting the determinants
of good health in the workplace. In: Poland B, Green L, Rootman I. (eds.). Settings for
Health Promotion: Linking Theory and Practice. Newbury Park, CA: Sage, pp. 138-160.
Putnam RD. (1993) Making Democracy Work. New Jersey: Princeton University Press.
Rapport DJ. (1995a) Ecosystem health: exploring the territory. Ecosystem Health 1:5-13.
Rapport DJ. (1995b) Ecosystem health: an emerging integrative science. In: Evaluating and
Monitoring the Health of Large-Scale Ecosystems. Rapport DJ, Gaudet CL, Calow P (eds).
NATO ASI Series 1. Global Environmental Change Vol 28 Springer-Verlag, Berlin, Ger-
many.
Rapport DJ. (1998) Editorial: ecosystem health as an ecotone. Ecosystem Health, 4(1):1-2.
Rapport DJ. (1997) The dependency of human health on ecosystem health. Ecosystem Health
3:4:19 5-1 96.
Rees W, Wackengel M. (1992) Our Ecological Footprint: Reducing Human Input on the Earth.
Gabriola Island, B.C., Canada: New Society Publishers.
Rohock A. (1991) Nuclear winter: global horrendous death. In: Horrendous Death, Health,
and Well-Being. Leviton D (ed). New York: Hemisphere Publishing.
Royal Commission (on the Health and Safety of Workers in Mines). (1976) Report of the Royal
'ommission on the Health and Safety of Workers in Mines. Toronto: Government of Ontario.
Rundel RD, Nachtwey DS. (1983) Projections of increase non-melanoma skin cancer in-
cidence due to ozone depletion. Photochem Photobiol 38:577-591.
Rtitten AAJJ. (1997) Adverse Effects of Nutrients. In: deVries J (ed) Food Safety and Toxi-
city. Boca Raton, FL: CR Press, pp 163-171.
Rylander R. (1992) Eflects on humans of environmental noise particularly from road traf-
fic. In: Motor Vehicle Air Pollution: Public Health Impact and Control Measures. Mage DT,
Zali 0 (eds). Geneva: Ecotoxic logy Service and Canton of Geneva and World Health
Organization, pp. 63-83.
REFERENCES 417
Turco RP, et al. (1990) Climate and smoke: an appraisal of nuclear.
winter. Science 247:166-176.
Turkenburg W. (2000) Renewable energy technologies. In: World Energy Assessment. New
York: United Nations Development Program, Chapter 7.
UN. (1948) Universal Declaration of Human Riqhts. New York: United Nations.
UN. (1993) Agenda 21: The United Nations Programme of Action from Rio. New York: United
Nations.
UN. (1996). World Population Prospects 1950-2050 (The 1996 Revision). On diskette (U.N.
Population Division, New York).
UN. (1997) Population Division. (1997) World Urbanization Prospects: The 1996 Revision, An-
nex Tables New York: U.N. Population Division, pp. 66-71.
UNDP. (1995) Human Development Report. New York: Oxford University Press, United Na-
tions Development Program.
UNDP. (1997). Human Development Report 1997 New York: Oxford University Press, pp. 3-4.
United Nations Educational, Scientific and Cultural Organization (UNESCO). (1996). Sta-
tistical Yearbook 1996. Paris: UNESCO, pp. 2-9.
UNEP. (1992a) Saving Our Planet: The State of the Environment (1972-1992). Nairobi: United
Nations Environment Program.
UNEP. (1992b) Chemical Pollution: A Global Overview. Nairobi: United Nations Environment
Program.
UNEP. (1993) Enviromnnental Data Report. Nairobi: United Nations Environment Program.
UNEP/GEMS. (1992) Contamination of Food. Geneva: United Nations Environment Program
and Global Environmental Monitoring System.
UNEP/ILO/WHO. (1993) How to Use the IPCS Health and Safety Guides. Nairobi and Geneva:
United Nations Environment Program, International Labor Office, and the World
Health Organization.
UNEP/WHO. (1984) Urban Air Pollution 1973-1980. Nairobi and Geneva: United Nations
Environment Program and World Health Organization.
UNFP/ WHO. (1 987a) Improving Envi ronmental Health Conditions in Low-Income Settlements. Nairobi
and Geneva: United Nations Environment Program and the World Health Organization.
UNEP/WHO. (1 987b) Global Pollution and Health, Results of Health-Related Environmental Mon-
ito ring. London: United Nations Environment Program and World Health Organization.
UNEP/WHO. (1992a) Introductory Guide to Human Exposure Field Studies: Survey Methods and
Statistical Sampling. Nairobi and Geneva: United Nations Environment Program and the
World Health Organization.
UNEP/WHO. (1992b) Human Exposure to Pollutants. Nairobi and Geneva: United Nations
Environment Program and the World Health Organization.
UNEP/ WHO. (1 992c) Urban Air Pollution in Megacities of the World. Oxford: Blackwell, United
Nations Environment Program and the World Health Organization.
UNEP/WHO. (1993) Guidance on Survey Design for Human Exposure Assessment Locations
(HEAL) Studies. Nairobi: United Nations Environment Program and World Health Or-
ganization.
UNICEF. (1994) State of the World's Children. New York: Oxford University Press.
United Nations Environment Programme (UNEP). (2000) GEO-200 Global Environment
Outlook. (http://www-cger.nies.go.jp/geo2000lindex.htrn) )www.grida.no/geo2000) .
UNICEF. (1997) The Proqress of Nations 1997 New York: UNICEF.
USEPA. (1973) Public Health and Welfare Criteria for Noise. Washington, DC: U.S. Environ-
mental Protection Agency.
USEPA. (1997) 1997 Declaration of the Environment Leaders of the Fight on Children's Environ-
mental Health (Miami, Florida). Washington, DC: U.S. Environmental Protection Agency.
Utell MJ, Samet JM. (1993) Particulate air pollution and health. New evidence on an old
problem. Am Rev Respir Dis 147:1334-1335.
Van Wijnen JH. (1990) Health risk assessment of soil contamination. PhD Thesis, Uni-
versity of Amsterdam, Rodopi, Amsterdam, The Netherlands.
Vincent JFI. (1993) Perspectives on international standards for health related sampling of
airborne contaminants. AppI Occup Environ Hygiene 8:233-238.
REFERENCES 419
duction. WHO Regional Publications European Series #51. Geneva: World Health Or-
ganization.
WHO. (1995a) World Health Report 1995: Bridging the Gap. Geneva: World Health Organization.
WHO. (199 Sb) Twenty Steps for Developing a Health Cities Project. WHO Document ICP/HSC
644(2). Copenhagen: WHO Regional Office for Europe.
WHO. (1995c) Health consequences of the Chernobyl Accident. Geneva: World Health Organi-
zation.
WHO. (1996) Bovine Spongiform Encephalopathy (BSE) Fact Sheet NI 13. Geneva: World Health
Organization.
WHO. (1997) Health and Environment in Sustainable Development: Five Years After the Earth
Summit Geneva: WHO.
WHO. (1998a) The World Health Report. Life in the 21st Century. A Vision for All. Geneva:
World Health Organization.
WHO. (1998b) Problem-Based Training Exercises For Environmental Epidemiology. Document
WHO/EHGI98.2. Geneva: World Health Organization.
WHO. (1999) Air Quality Guidelines for Europe, World Health Organization, Regional Office for
Europe. Copenhagen. (www.who.intlpeh/airlAirqualitygd.htm).
%VHO /CEMP. (1992) Environmental Impact Assessment of Development Projects. A Handbook for
Practitioners. London: Elsevier Applied Science, World Health Organization and Center
for Environmental Management and Planning.
WHO/N1LU (1996) Quantification of Health Effects Related to SO 2, NO2, 03 and Particulate Mat-
ter Exposure. WHO Document EUR/ICP/EHAZ 94 04/DTOI. Copenhagen: WHO Re-
gional Office for Europe and Norwegian Institute for Air Research.
WHO /UNEP. (1 989) Global Freshwater Quality: A First Assessment. Geneva and Nairobi: World
Health Organization Global Environmental Monitoring Program.
WHO/UNEP. (1991) An Introductory Guide to Human Exposure Field Studies Survey Methods
and Statistical Sampling. Nairobi and Geneva: World Health Organization and United
Nations Environment Program.
Will RG, Ironside JW, Zeidler M, Cousens SN, Estibeiro K, Alperovitch A, Poser S, Poc-
chiari M, Hofman A, Smith PG. (1996) A new variant of Creutzfeldt-Jakob disease in
the UK. Lancet 347(9006):921-925.
Wilson R, Crouch EA. (1987) Risk assessment and comparisons: an introduction. Science
2 36(4799) :267-270.
World Bank. (1990) World Development Report. Washington, DC: World Bank.
World Bank. (1993) World Development Report. Washington, DC: World Bank.
WRI. (1992) World Resources (1 992-93). Washington, DC: World Resources Institute.
WRI. (1994) World Resources (1994-95). Washington, DC: World Resources Institute.
WRI. (1996) In collaboration with the United Nations Environment Programme, the
United Nations Development Programme, and the World Bank. World Resources Report
1996-97 New York: Oxford University Press.
WRI. (1998) in collaboration with the United Nations Environment Programme, the United
Nations Development Programme, and the World Bank. World Resources Report 1998-99
New York: Oxford University Press.
Yassi A. (1997) Repetitive strain injuries. Lancet 349:943-947.
Yassi A. (2000) Work-related musculoskeletal disorders. Curr Opin Rheumatol 12:124-130.
Yassi A, Cheang M, Tennebein M, Bawden G, Spiegel J, Redekop T. (1991) An analysis
of occupational blood lead trends in Manitoba, 1979 through 1987. Ani JPublic Health
81:736-740.
Yassi A, McLean D. (2001) Assault and abuse in healthcare facilities. C/in Occupational En-
viron Med. 1(2): in press.
Yassi A, Mas P. Bonet M, Tate RB, Fernandez N, Spiegel J, Perez M. (1999) Applying an
ecosystem approach to the determinants of health in centro Habana. Ecosystem Health
5(1):3-19.
Yassi A, Redekop T, Alberg N, Cheang M. (1996) Occupational blood lead trends in Man-
itoba, 1979-1994: assessing the effectiveness of regulation and surveillance. In: Lead
in the Americas: A Cal/for Action, Howson CP, Herrnandez-Avila M, Rail DP (eds).
Page numbers followed by b, f and t indicate boxes, figures and tables, respectively
421
Air pollution (continued) Animal dung, combustion, indoor air
industrial, 198-201, 1991 l)011Ution from, 315
from accidents, 199-200, 200h Animal studies
control strategies, 204 limitations, 123, 125
public exposure, 333-35 toxicity testing, 75-79
types, 198-99, 1991 Antibiotics, biological hazards. 59-60
in workplace, 200-201 Aral Sea, 218-19
inhalation, 187-88 Area sampling, 130
during inversion, 182 Arm vibration, 85
liquid constituents, 185-86 Aromatic hydrocarbons, 65
magnitude, 201-2, 2021 from food preparation, 266
microbiological, 207 health effects and sources, 191t
monitoring, 204-6, 205b, 206f Arsenic
from motor vehicles, 204, 2050, 3011) in drinking water, 215
overview, 1 80-88 in general environment and workplace, 347
particulate constituents, 182-86, 183f, 1851 Asbestos, carcinogenicity, 76h
See also Aerosols Ashestosis, 356b
photochemical, 199, 1 99t Ascorbic acid, deficiency, 248
point-source emissions, 199, 1991 Ash, 182
from power stations, 321-22 4speigillus humus, 252
precipitation and, 186 Asperqillus parasiticus, 252
reduction, 198, 199t, 333-34 Asphyxianms
sources, 201-2, 202t chemical, 188
urban, 201, 202, 202t, 298-300, 299f, 300f, simple, 188
3010, 331 Asphyxiation, 188
Air quality Assault, 100
exceedance, 203 Association, in epid emiological field
guidelines, 40, 401, 202-4, 203t investigations, 116
indicators, 163t Asthma
nondegradation policy, 203-4 air pollution effects, 189, 1901
Airborne exposure, 55t occupational, 357b
biological hazards, 57, 58 rates, as health indicator, 160
inhalation estimation, 132-33, 1 331 Aswan dam, schistosomiasis and, 323
personal monitoring, 130-31 Atom
Airshed, 202 characteristics, 84h
Alcohols, 66 unstable, half-life of, 84h
Aldehydes, health effects and sources. 191t Attrihutable traction, 114, ml 5b
Alexandria, Egypt, water pollution, 2220 Australia, bicycle use, 301h
Algal blooms, 220, 382, 3830
Alicyclic hydrocarbons, 63, 65 Bacteria
Aliphatic hydrocarbons, 63 fecal, water monitoring for, 222-23, 223t
Alkali, in hazardous waste, 339 growth, 60
All-terrain vehicles, 99-100 lifecycle, 5 5-56
Allergic alveolitis toxin production, 57, 250
extrinsic, 357h-358h Bacterial disease
in farmers, 280 loodhorne, 250-51, 2510, 266, 267f
Allergies, occupational, 36 1-62 global warming and, 383h
Alpha radiation, 84b temperature control, 266, 267f
Altitude, health effects, 90 waterborne, 225t
Alvcolitis, allergic Barometric pressure, health effects, 89-90
extrinsic, 357b-3 580 Barotrauma, 90
in farmers, 280 Basel convention, 394t
Amazon rain forest, deforestation, 388-90 Batteries, manufacturing hazards, 343
American Congress of Governmental Becquerel )Bq), 84h
Industrial Hygienists (ACGIH), 366 Behavior
Ammonia, 63 change, health education and, 156-58,
Analytical epidemiology, 107-8, 108f 158h, 158f, 159h
Analytical errors, exposure assessment, determinants, 157-58, 1 58h, 1 58f
136-37 Benefit-cost analysis
Anemia, iron-deficiency, 247 issues, 175
422 Index
UI pollution prevention in Japan, Brazil
1 74b-1 75h air pollution, 202, 202t
of radon nhitigation in Canada, 176-79, deforestation, 389-90
1781 British Smoke, 185
SCOPC of study, 175 Bromine, 62-63
steps, 172-73, 1731, 177-79 Bronchitis
valuation methods, 173, 175 air pollution effects, 189, 190t
Benzene industrial, 358h
in hazardous waste, 337 Brownian movement, 183
metabolism, 69, 70h Brucellosis, 279, 361
toxicity, 65, 349 Bubble concept, industrial air pollution, 204
Berms, 336 Building nsaterials, manufacturing hazards,
Beta radiation, 84h 343
Bhopat incident, 200, 200h Building-related illness, 29 1-92, 2921
Bias, epidemiological studies, 1091, 110 Bulk materials, environmental hazards,
Bicycle use 349-50
injuries, 98 Bunds, 336
promotion, 301h Burden of disease, 25-27, 26h. 271
Bioaccumulation, 335, 335f global, 27, 28t, 35-37, 36t, 37t
Bioactivation, 69, 701) household environment and, 36, 37t
Bioconcentration, 335, 3351 Burns, 92, 98-99
Biodegradation, 335 Byssirtosis, 342, 355
Biodiversity. 390-92
biological significance, 390-91 Cadmium
defined, 390 exposure
economic aspects, 391-92 in air, 401
loss, 392 dose-response relationship, 120, 1221
Biological exposure indices, 366 in food, 257
Biological hazards, 55-61 from industrial pollution, 346-47
defense mechanisms, 59-60 provisional tolerable weekly intake,
distribution, 59 257
exposure assessment, 131-32, 1 311 poisoning, 347
exposure routes, 55t, 58-59 Calcium, deficiency, 248
foodhorne, 58-59, 250-54 Calcium hydroxide, 63
growth, 60 Calcium oxide, 63
health effects. 60 Canada
investigation methods, 60-61 bicycle use, 301 h
microbiological standards, 224-25, 225t chemical hazard classification system, 80t
occupational, 361-62, 361h infant mortality rates, 33, 33f, 34f
spread, 57-58 water quality guidelines, 236
types, 55-57 Cancer. See also Carcinogen(s)
Biological oxygen demand of water. 341 from air pollution. 189-90
Biological warfare, 373 developmental models, 73-74, 128
Biologically effective dose, 129 environmental influences, 35
Biomagnification, 335, 335f from radiation, 86-87, 326-27
I3iomass fuels rates, as health indicator, 160
action priorities, 331 Carhamale cholinesterase-inhihiting
alternative fuel sources, 317-18 insecticides, 276h
direct effects, 316-17, 3161, 3171 Carbohydrates, requirements and sources,
indirect effects, 317 2441
indoor air pollution from, 291, 315-18, Carbon cycle, 3861
31 5f Carbon dioxide
upgrading, 318 atmospheric concentration, 384, 385
Bioprospecting, 391 global sinks for, 385, 388-90
Biotransformation, 69, 70b Carbon monoxide
Blooms, algal, 220, 382, 383h health effects., 1911, 196-97, 1 97t
Blue baby syndrome, 279 oxygen uptake inhibition, 188
Bogota, Colombia, water pollution, 222b Carbon tetrachloride, 66
Bovine spongilorrn encephalopathy )BSE), Carhoxyhemoglohin levels., 196-97, 196t,
253-54 197t
INDEX 423
Carcinogen(s) classification, 80, 80t
categories. 75, 75t information on, 79-80, 80t, 811
dose-response relationships, 127-28 organ-specific, 70-71, 720
groups, 75, 76h reproductive and developmental, 71, 73f
inorganic. 760 risk versus. 62
waterhorne, guideline values, 227 systemic, 70, 72h
in workplace, 360t testing, 75-79, 77t
Carcinogenesis in water, 215-16, 2161, 237
initiation, 73-74 acceptable daily intake, 22 5-26
multihit model, 128 guideline values, 226-27
multistage model, 73-74 Chemical warfare, 371, 373
progression, 74 Chernohyl nuclear accident, 259, 325
promotion, 74 Child abuse, 100
Cardiovascular effects C hildrcn
of air pollution, 188-89 injuries, 94-99, 98-99
of noise, 302 inortality rate, female literacy and, 31, 31
Case -control studies, I 09t, 110 vulnerability to environniental hazards,
design, llOf 27-29
nested, 113 China 10, bicycle use, 301h
toxic oil syndrome in Spain example, 111 h Chlamydiosis, 280
Case definition, 19 Chloracne, 337
Cataracts, ultraviolet radiation-induced, 88-89 Chlorinated cyclic hydrocarbons, in hazardous
Causation, tests of, 116, 1 16t waste, 337, 339
Causes of death, 23, 24t Chlorination
Central nervous system effects, of air by-products, 229h
pollution, 190 process, 229h, 230
Centro Hahana, Cuba, ecosystem analysis, Chlorine, 62-63, 349
2850 Chlorolluorocarhons (CFCs)
Chagas' disease, 290 atmospheric concentration, 384
Chemical Abstracts Service (CAS), 79 ozone depletion and, 377
Chemical asphyxiants, 188 Chloroform, 66
Chemical hazards, 61-80 Chloromethane, 66
absorption, 68, 68f Choking, 99
in air, overview, 180-88. See also Air Cholera
pollution loodhorne transmission, 291
carcinogenicity. 71-79, 76b svaterborne transmission, 210, 213,
classification, 62. 80, 80t 214b-215b, 2141
distribution. 68-69, 681 Chromic acid, 63
dose-response relationship, 122-23, 1251 Ch romosomal alterations, 74h
excretion, 68f, 69, 71f Cigarette smoking, indoor air pollution from,
exposure routes, 5 5t, 67-68 207
in food, 254-57, 255f Climate
monitoring, 255 ch ange. See Global warming
provisional tolerable weekly intake, 257 natural disasters, 395-96
sources, 254-55, 2551 Cluster studies, 116-17
genotoxicity, 71-75, 74b Coal
global, 397-98 as energy source, 318, 31 8t, 319, 31 9t,
health effects, 70-71, 720 3200, 321-22, 3211
in home, 350 extraction, pollution and hazards related to.
identification, 62, 118-19 340
from industrial pollution, 336-40 Coal workers pneomoconiosis, 3570
inorganic, 62-63 Cochlea, hair cells, 82
in manufacturing, 342-43 Codex Alimentarius Commission, 262, 263h
metabolism, 69, 70f, 71f Cold stress, 91
occupational exposure, 118-19, 355-98, Communicable disease. See Infectious disease
356b-358h Communicat ion
organic, 63, 65-67 with news media, 151 b
public exposure. 3 36-40 risk, 147-50, 1 50t, 1510
in recreational water, 237 Cornniunity. See also Human settlements
sensiovity to, 337, 338h-339b air pollution and, 201-7
toxicity, 61-62 chemical poisoning in, 350
424 Index
injury prevention, 95-96 Developing countries
networks, 408 industrial pollution, 13-14
presentations to, 405 malnutrition, 270t
rural. See Rural communities poverty, 43, 43t, 44
urban. See Urban areas sanitation, 2371, 239
Computer chips, manufacturing hazards, 343 water pollution, 220, 222h
Confidence interval, 114-15 water-related diseases, 211
Confounders, epidemiological studies, 1 09t, water supply, 2371, 239
110 Development
Conservation movement, 12 economic, environmental health and,
Consumer products, safety, 343 10-11
Consumption patterns, environmental health international, impact on water resources,
problems and, 44-45 219
Coping strategies, 146-47 sustainable, 7, 8, 14
Corrosive materials, 63 water pollution related to, 220, 221b
Cost-effectiveness analysis Developmental hazards, chemical, 71, 73f
issues, 175 Developmental toxicology, 27
of pollution prevention in Japan, Diagnosis of occupational or environmental
I 74h-1 75h disorders, 166
of radon mitigation in Canada, 176-79, Diagnostic tests, biological hazards, 60-61
I 78t Diarrheal disease
scope of study. 175 associated with water, 210, 212h
steps, 172-73, 1731, 177-79 from biological hazards, 57, 60
valuation methods, 173, 175 deaths from, 211
Creutzfeldt-Jakoh disease, 254 as health indicator, 160
Critical incident debriefing, 397 Dichlorodiphenyl-trichloroethane (DDT), 64f,
Crop rotation, 279 274, 275b, 398
Cross-sectional studies, 108, 1 09t Dichloromethane, 66
Cryptosporidiosis, waterborne transmission, Dietary preferences, disease and, 272-73
212h Diethyistilbestrol, structure, 641
Cuba Dioxin, in hazardous waste, 337, 339
bicycle use, 301b Direct casualties, 370
ecosystem analysis, 285b Disability-adjusted life years (DALY5), 25, 26h
Cumulative trauma disorder (CTD), 344, 361 global, 37, 38t
Cyanide, 188, 339.349-50 Disabled people, vulnerability to
environmental hazards, 32
Dams. See Hydroelectric power Disadvantaged groups, injuries, 95
Data preparation errors, exposure assessment Disasters, 394-97, 3951
137 drought as, 396-97
DDT (dichlorodiphenyl-trichloroethane), 64f, emergency actions, 394-95
274, 275b, 398 natural versus technological. 395-97,
Death, causes, 23, 24t 395t
Debt-for-equity swap, 390 psychological effects, 397
Decibel (dB), 82 Disease
Decompression eflects, 90 burden of, 2 5-27, 26h, 27f, 28t, 3 5-37, 361,
Deforestation, 387-90, 3891) 371
biomass fuel consumption and, 317 communicable. See Infectious disease
desertilication and, 387-88 demographic transition, 21-22, 22f
land degradation from, 272h dietary preferences and, 272-73
Demographic transition, 2 1-22, 221 environmental
Denmark diagnosis, 166
bicycle use, 3011) outbreaks, 362-63, 3621
healthy city program, 309 rehabilitation, 167
Desalination, 228 environmental influences, 35-37, 361-391
Descriptive epidemiology, 107, 108, 108f epidemiologic transition, 22, 231, 24-2 5,
Desertification, 272b, 387-88 24f
Deterministic effects global patterns, 2 1-35
dose-response relationship, 120-27, rate of, 113, 1131
121f-124f, 1271 vulnerable groups, 27-3 5
radiation, 86, 327 Disinfection of water, 230
Detoxification, 69 Displaced persons camps, 371, 372b
INDEX 425
Dose Electrical transformers, manufacturing
biologically effective, 129 hazards, 343
effective, 76 Electricity
infectious, 58-59 from alternative energy sources, 328-30,
internal, 129 328b, 329f, 329t
lethal, 76 versus biomass fuel consumption, 317-18
risk-specific, 128, 144-45 hazards, 324
total, 138 Electrolytes, requirements and sources, 244t
Dose-effect relationship, 119-20, 11 9f Electromagnetic fields, 87, 89
Dose-response relationship, 105, 119-28, Electromagnetic radiation, 87, 343
1 19f, 121t Electromagnetic spectrum, 87, 88f
for cadmium, 120, 122f Electronic products, manufacturing hazards,
chemical hazards, 122-23, 1251 343
high-risk groups, 127 Emission standards
for injuries, 121, 123f control at source by, 153
for lead, 120, 121f exceedance, 203
at lower levels, extrapolation, 125-27, 127f monitoring, 204
between noise level and annoyance, 121, 124f nondegradation policy, 203-4
for non-threshold effects, 127-28 for United States, 202, 202t
for physical hazards, 120, 122f Emotion-focused coping, 146
for threshold effects, 120-27, 121f-124f, Energy
1 27f hiomass fuel. See Biomass fuels
uncertainty factors, 123, 125-27, 125t, 127f consumption
Dose-response relationship, for ionizing cycle, 312
radiation, 86-87 trends, 312-15, 312f
DPSEEA framework fossil fuel. See Fossil fuels
for ecosystem health, 282, 283b-285b geothermal, 329, 329t
for environmental health indicators, 164, hydroelectric, 322-25, 329t
165h needs
for housing quality assessment, 286b-288h for agriculture, 314
relationship to PRECEDE-PROCEED model for basic human needs, 314
of health promotion, 158, 1 59h caloric requirements, 243
Draize test, 78 for health and sustainability, 3 11-12, 312t
Droplets, 185-86 for industrial production, 314-15
Drought, 396-97 for transportation, 314
Drownings, 98 in urban areas, 314
Dung, combustion, indoor air pollution from. nuclear. See Nuclear power
315 solar, 328, 328b, 3291
Dust SOU rces
defined, 182 action triorities, 330-31
deposition, 184-85, 185f alternative, 328-30, 328b, 329f, 329t
consumption by. 313-14, 313f
Ecological footprint, 44 risk comparison, 330
Ecological studies, 117-18, 1181 wind, 328b, 3291, 329t
Ecological vandalism, 375 Environment
Ecology movement, history, 12-I 3 defined, 5
Economic analyses of interventions, 172-79, deliberate destruction, 375
1731, 174b-175b, 1781 food security and, 271, 272h
Economic development, environmental health global degradation, 370
and, 10-11 global stability, 17-18
Ecosystem, defined, 3 human health and, 3-9
Ecosystem health, human health and, 3-4, human interaction with, health and, 6-8, 6f
17-18, 282-86, 283h-285b influences
Education on cancer, 35
health, 156-58, 1 58b, 1581, 1 59b on infectious disease, 35
public, 404-6, 405t on life expectancy, 2-3, 31
for women, 3 1-32 supportive, for health, 9, 9b
Effective dose at 50% (ED50), 76 Environmental disease
Elderly people diagnosis, 166
injuries, 95 outbreaks, 362-63, 362t
vulnerability to environmental hazards, 32 rehabilitation, 167
426 Index
Environmental epidemiology, 47-48, 402t. See Environmental justke, 300
also Epidemiology Environmental management
Environmental friendliness, of consumer hydroelectric dams, 324-2 5
products, 343 vector-borne disease, 324
Environmental health Environmental medicine, risk management
basic requirrments, 14-18 approach in, 164, 166-67, 168h
Consumption patterns and, 44-45 Environmental movement, history, 12-13
defined, 7 Environtuental noise, 300-304
demographic issues, 41-42, 42f Environmental Protection Agency (EPA), risk
economic development and, 10-11 communication rules, 1 Sot
emergency problems, 167, 169-72 Epidemiologic transition, 22, 231, 24-2 5, 24f
global concerns. See Global health concerns Epidemiology, 107-18
hazards. See Hazards analytical, 107-8, 108f
historical perspective, 10-14, 1 3h case-control studies, 1 09t, 110
impact, 5 design, 1 lOf
indicators. See also Environmental nested, 113
indicators; Health indicators toxic oil syndronie in Spain example, 1111)
guidelines for use, 21 causation, 116, 1 16t
macroeconomic policies and, 45 clttster studies, 116-17
monitormg, 18, 20-2 1, 20t, 130. See also cohort studies, 109t, 110-13
Exposure assessment design, 1 lOf
occupational health and, links between, historical, 113
38-41 prospective, 111, 113
poverty and, 43-44, 43t vinyl chloride and cancer example, I 12h
problents conlounding bias, 109t, 110
action on, 399-409 cross-sectional studies, 108, 109t
ethical guidelines, 401, 402t, 403t defined, 19
history, 11-14, 13b descriptive, 107, 108, 109t
mininial components, 400, 400t ecological studies, 117-18, 1 18f
role of environmental health environmental, 47-48, 402t
professionals, 401-9 ethical guidelines, 402t
emergency, 167, 169-72 historical, 108
of individuals, risk management interventional, 109t
approach, 164, 166-67, 168h limitations, 116
Envjronntental Healtit Criteria (IPCS), 62 molecular. 132
Environtnental health officer, 47 proportional morbidity studies, 113
Environmental health physician, 49-50 risk measures, 113-15, 11 3f, 11 Sb
Environmental health professionals statistical power, 116, 11 7t
advocacy, 407-8 steps, 19-20, 107-8, 108f
ethical guidelines, 401, 402t, 403t study designs, 108-1 3, 109t
networking, 408 Epoxides, formation, 70h
personal example, 401, 403t, 406-7 Epoxy compounds, 66
prolessional practice, 403-4 Ergonomic hazards, 97, 344, 360, 361
public education and capacity building, Ergonomist, 48
404-6, 405t Erosion, land degradation from, 272h
research and documentation, 408-9 Escherichia coli
roles, 46-50, 40 1-9 water grtidelines, 222-2 3, 223t
technical expertise, 401-3 water monitoring for, 61
training, 403 Estimated daily intake (EDT), via ingestion
transdisciplinary approach, 46-47 and skin absorption, 133-34, 13 Sb
Environmental health technician, 47 Estimation approach, time-activity
Environmental hypersensitivity disorder, 3 38h information, 132
Environmental inipact assessment (EfA), Estrogen, 64
139-42, 141b mimics, 64b-65b, 64f, 65-66
hydroelectric dams, 325 structure, 64f
public involvement, 142 Ethanol, 66
Environmental indicators Ethers, 66
and health indicators, linkage between, Ethical guidelines, environmental health
164, l65h professionals, 401, 402t, 403t
for health risk assessment, 21, 161, 1 63t- 1 64t Ethnic cleansing, 371
Environmental inspector, 47 Ethylene glycol, 66
INDEX 427
Europe Fishing, occupational hazards, 273
air quality guidelines, 202, 203t Fission, nuclear, 325
cheniical hazard classification system, 80t Flammable gases, 349
food standards, 262 Flocculation, 229-30
Event tree, 145 Fluoride
Excreta disposal systems, 231, 232, 232h deficiency, 248
Exposure in drinking water, 21 5-16, 230
airborne. See Airborne exposure Fluorine, 62-63
biological markers, 131-32, 13 It Food
foodborne. See Foodhorne exposure additives, 249-50, 261
human, defined, 128 and culture, 243, 245, 246h
public, to industrial pollution, 333-40, 335f flow scheme, 262-63, 264f
skin, 131, 134, 135b genetically engineered, 263-64
soilborne, 59, 133, 1 33t groups, 243, 245
total, 40, 128, 137-38 intake
waterborne. See Waterhorne exposure dietary standards and guidelines, 260
Exposure assessment, 18-19, 105-6, 128-37, inadequate, health effects, 16-17
129f irradiation, 264, 26 5-66
area sampling, 130 manufacturing hazards, 343
biological monitoring, 131-32. 13 it natural toxins, 249, 260-6 1
direct, 19, 130-32 new components, safety assessment, 261
environmental monitoring, 130 nutritional value, 260
errors, 136-37 poisoning, 249, 250, 2511)
indirect, 19, 132 preparation
personal monitoring, 130-31 in food services industry, 267-68, 268b
population sampling, 134-35, 1 36f in home, 266-67, 2671
quality assurance, 137 preservation, 265-66
sample size, 137 processing, 254-55, 264-65, 265t, 342
surveys, 132 production
time-activity information, 132 crucial conditions for, 269-70, 271f
Exposure control, 150, 157-58 occupational hazards. See Agricultural
along the path, 154, 1 55f hazards
framework for, 150, 152-53, 1 52f, 1 52t safety, 26 3-64
health education in, 156-58, 1 58h, 1 58f, I 59h trends., 16, 1 6f
at source, 153-54 world food situation, 268-69
at target/person level, 154-56, 1 56t, 1571 quality
Exposure routes. 54 assurance, 262-68, 264f, 265t, 268b
biological hazards, 55t, 58-59 criteria, 259-62
chemical hazards, 55t, 67-68 1)roperties, 259
physical hazards, 55t regulatory authorities and standard
Eye disease, occupational, 356 setting, 261-62, 263b
Eye irritation, from air pollution, 189, 1 90t safety, 261, 268b
standards, 260-62
Falls, 99 security
Famine, 396-97 environment and, 271, 272b
Farmer's lung, 280, 357h global trends, 271-73
Farming. See Agriculture storage, 254, 265-66
Fecal coliforms, recreational water guidelines, street-vended, 268h
236 Foodhorne disease, 248-59
Fecal-oral patliogens bacterial, 250-51, 2511), 266, 2671
foodhorne, 224-2 5 bovine spongiform encephalopathy as,
waterhorne, 224-25, 2251 2 5 3-54
Fecal pollution, indicator organisms, 222-23, fecal-oral pathogens, 224-25
223t fungal, 252-53
Fecal streptococci, recreational water parasitic, 251-52, 252b, 2531
guidelines, 236-37 prevention, 262-68, 2641, 2651, 268h
Fertility rates, 30t, 31 viral, 251
Fertilizers, 279 Foodborne exposure
Fetal development, critical periods, 731 biological hazards, 58-59, 249, 250-54
Fibers, 185 chemical hazards, 254-57, 255f
Fires, industrial, 349, 363 ingestion estimation, 133-34
428 Index
radioactive hazards, 257-59 Global Environment and Health Libraries
safety standards, 260-6 1 Network (GELNET), 408
Forest ecosystems Global Environment Monitoring System
hmmass fuel consumption and, 317 GEMS). 228h
changes, 272b, 387-88 air pollution program. 298, 2991, 3001
and global change, 388-90, 389h classification of chemicals in drinking
Forestry water. 215
occupational hazards, 273 food contamination program. 255
pollution and hazards related to, 341 Global Environmental Epidemiology Network
processing hazards, 341-42 )GEENET), 408
Formaldehyde Global Environmental Project, 18
in air, WHO guidelines, 40t Global Estintates for Health Situation Assessntents
health effects and sources, 191 and Projectio;ts, 354
Fossil fuels Global health concerns, 53, 368-98
atmospheric pollution from, 319 acid precipitation, 392-93
direct effects, 300b, 301f, 318t, 319-22, 319t hiodiversity, 390-92
extraction and processing hazards, 3181, chemical contamination, 397-98
319, 320h, 321, 321f climate change and greenhouse effect,
indirect clfects, 322 378-87, 379f-381f, 383b-385h, 3861
indoor air pollution from, 291, 318, 319 deforestation and desertification, 387-90,
pollution prevention strategies, 322 389b
use, 318 disasters, 394-97, 3951
Free erythrocyte protoporphyrin (FEP), 131 hazardous waste lransbouncfary movement,
Frostbite, 91 393-94, 394t
Fume fever, 3581) ozone depletion and UV radiation, 37 5-77,
Fumes, 183 376f, 378f
Fumigants, 274t warfare, 370-75, 370t, 372b
Fungal disease, foodhorne, 252-53 Global sinks, 385, 388-90
Fungicides, 2741 Global trends
Furniture, manufacturing hazards, 343 food security. 271-73
Fusion, nuclear, 326 water supply, 2 18-19
Global warming
Gaia Hypothesis, 4h biomass fuel consumption and, 317
Gannna radiation, 84h-85h cattses, 383-85
Gas(es) effects, 380-83, 381f
adsorption, 187 fossil fuel consumption and, 322
flammable, 349 greenhouse effect, 378-80, 379f, 383-85
natural malaria and, 382, 384h
as energy source, 318, 318t, 3 19-20, marine environment citanges associated
319t, 321-22 svith. 382, 383b
leaks, 321 solutions to problelTi, 385-87, 386t
solubility. 186-87 temperature changes associated with. 380,
sour, 321 380f
toxic tickhorne disease and, 382-83. 385h
health effects, 187 Glycols, 66, 348
inhalation, 357h Goitrogens, 246
Gene mutation, 74b Gray (Gy), 84h
Gene rearrangements, 74h Green labeling, 343
Genetic engineering, 263-64, 278 Green teams, 407
Geneva Protocol, 373 Greenhouse effect
Genotoxicity hiotnass fuel consumption and, 317
chemical hazards, 7 1-75, 741) description, 378-80, 3791
types, 74h fossil fuel consumption and, 322
Geological activity, natural disasters, 396 global warming and, 378-87, 379f-381f,
Geothermal energy, 329. 329t 383b-385h, 386f
Giardiasis Guerrilla warfare, 374
foodhorne transmission, 2 52b, 25 3f
waterborne transmission, 21 2b 1-laddon's injury reduction strategies, 101, 101
Global burden of disease, 27, 281, 3 5-37, 36t, Halogenated hydrocarbons, 66, 67b
37t Halogens, 62-63
Global ecological changes. 369 Hand vibration, 85
INDEX 429
Hazard Analysis and Critical Control Point Health hazard transition, 25
)HACCP) system, 265, 2651 Health indicators, 21, 21 t, 160, 161, 1 65t
Hazard audits, 118 and envirotimetital indical ors, linkage
Hazardous wastes between, 164, 165h
disposal, 339-40 Heallh physicist. 48
incidents involving, 337 Health policy analyst, 48
public exposure, 336-40 Health promotion
storage, 336 conceptttal models, 158, 1 59h
transboundary movement, 393-94, 394t defined, 9
Hazards, 52-103 responsibility for, 6
biological, 55-61. See also Biological hazards "Healthy Cities" program, 306-10, 307b
chemical, 61-80. See also Chemical hazards actions taken, 309-10
classification, 54 characteristics, 307-8
defined. 53 regional influence, 308-9
ergonomic, 97, 344, 360, 361 Hearing
global, 53, 368-98. See also Global health conservation programs, 83, 85
concerns loss
hierarchy of controls, 150, 152-53, 1521, 1 521 noise-induced, 83
identification, 105 incidence, 355
epidemiologic investigations, 107-18 surveillance programs, 167, 1 68h
field investigations, 118-19 sound intensity and, 83
measurement of health effects, 19-20 Heal loss, mechanisms, 91
mechatsical, 92-1 02. See also Injuries Heat stress, 91-92
physical. 80-92. See also Physical hazards Heat stroke, 91-92
psychosocial, 102-3, 344, 350, 362 Helmet use, 98
routes of exposure, 54, 551 Helnunth, 59, 225t
traditional versus modern, 2, 24-25, 541 Hepatitis A virus, foodhorne transmission, 251
types, 25, 53-54 Herbicides, 274t
vulnerability to, 27-35 Historical descriptive smtidies, 108
in children, 27-29 HIV (hutnan immunodeficiency virus), spread
in disabled people, 32 of disease and, 60
in elderly people, 32 Home
in indigenous peoples, 3 3-35. 331' 341 chemical poisoning in, 350
in women, 29-32 environment, burden of disease and, 36,
Headache, from air pollution, 190t 371
Health (human). See also Environmental health; lood preparation in, 266-67, 267f
Occupational health and safely injuries, 98-99, 290
defined, 4 Host-agent-environment triangle. 96-97
ecosystem health and, 3-4, 17-18, 282-86, Housing. See also Human seltlements
283b-285h communicable diseases and, 289-90
energy needs for, 311-12, 3121 health and, 286h-288h, 288-92, 2881
environmental influences, 35-37, 36t-39t physical hazards, 290-92
housing and, 286h-288h, 288-92, 288t psychosocial problems and, 292, 2921
human adaptability and, 8-9 toxic exposures, 29 1-92, 292t
human interaction with environment and, Human health See Health (human)
6-8, 61 Human imniunodeficiency virus (HIV), spread
nutrition and, 243-48. See also Nutrient(s) of disease and, 60
poor. See Disease among hospital workers, 361
poverty and, 43-44, 43t Human settlements, 281-310. See also
supportive environments for, 9, 9b Community
urbanization and, 297-306. See also basic health reqrtirenlents, 17, 282, 285-86
Urbanization as ecosystems, 282, 283h-285b
vitamins and, 2471) housing qualily assessment, 286h-288h
Health and Geographic Infortnation System Humidity, air pollution and, 186
(HEGIS), environmental indicators Hunting, occupational hazards, 273
in, 161, 163t-164t Hydrocarbons, 63
Health and safety consnsittee, 352 alicychic, 63. 65
Health education, as risk managemenl tool, aliphatic, 63
156-58, 158b, 158f, 159h aromatic, 65
Health effect, defined, 19 frons food preparation, 266
Health hazard evaluations, 118 health effects and sources, 1911
430 Index
chlorinated cyclic, in hazardous waste, 337 noise-related, 83-84
339 processing industries, 341-42
halogenated, 66, 67h public exposure, 333-40, 335f
polychiorinated, 66, 67h service industries, 343-44
Hydroelectric power, 322-25 solvents, 347-49
electricity hazards, 324 water
environmental management, 324-25 control. 2 34-35
health effects, 323-24, 3291 public expostire, 335, 3351
use, 322-23 tndustrial production, energy needs, 3 14-15
Hydrofluoric acid, in hazardous waste, 339 Infections, 561
Hydrogen cyanide, 188, 339, 349-50 housing and, 288-89
Hygiene, infections and, 288-89 respiratory
Hypersensitivity pneumoriitis, 3 57h- 3 58h from air pollution, 189, 1 90t
Hypothermia, 91 from biological hazards, 60
from indoor air pollution, 207
Illness. Set' Disease toxic reaction versus, 57
Immune defenses water-dispersed, 213
abnormalities, ultraviolet radiation-induced, Infectious disease
89 from agricultural hazards, 273, 279-80
biological hazards, 59-60 from biological hazards, 60
lot inunization, control at target/person level deaths from, 56t
by, 155-56 environmental influences, 35, 57-58
Inimunotoxicity, chemical hazards, 72h toodborne, 249, 250-51
Impairment assessment, 167 bacteria causing. 250, 251h
Incidence of disease, 19, 113, 11 3f parasitic, 251-52, 252b, 253f
Income, dietary preference and, 272-73 historical concern with, It
Indigenous peoples, vulnerability to housing and, 289-90, 2891
environmental hazards, 33-35, 33f, 34f immunization against. 155-56
Indoor air pollution occupational, 361, 361 b
front hiornass luels, 291, 315-18, 31 5f spread, 56-57, 38
from fossil fuels, 291, 318 water-associated, 210-13, 212h
from sick htulding syndrome, 291-92, 2921 Inlectious dose, 58-59
sources, 206-7, 291 Ingestion estimation, 133-34, 1 33t, I 35h
Industrial accidents, 199-200, 200b, 362-6 3, tnhalable traction, 184
362t Inhalation of toxicanls, 187-88, 357h
Industrial controls, hierarchy of, 150, 152-53, exposure esti nation, 132-33, 13 3t
152f, 1521 oxygen deprivation from, 187-88
Industrial cleveIoptnent, environmental health smoke-related, 316, 317t
and, 10-11 inhalation studies, toxicity testing, 78
Industrial lires, 349, 363 Injuries, 92-102
Industrial pollution agriculture-related, 273
air, 198-201, 199t in children, 94-95, 98-99
from accidents, 199-200, 200b cost, 94
control strategies, 204 cultural attitudes toward, 93
pit blic exposure, 333-35 in disadvantaged groups, 95
types, 198-99, 199t dose-response relationship, 121, 1 23f
in workplace, 200-20 1 in elderly persons, 95
arsenic exposure, 347 home-related, 98-99, 290
hulk rosy materials, 349-50 impact, 93-94
cadmium exposure. 346-47 intentional. 100
chemical contamination, 336-40 motor vehicle, 97-98, 101, 101t, 121, 123f,
in developing countries, 13-14 305-6
extent. 333, 334h occupational, 95, 96-97, 360-61
hazardous waste, 3 36-40 prevention
historical concern with, 12-13, 14 active versus passive, 100-101
by industry, 340-44. See also Occupational community, 95-96
hazards Haddon countermeasure strategies, 101,
lead exposure, 344-45 1 0 It
manufacturing, 342-43 phases, 101. IOU
materials extraction, 340-41 workplace, 95, 96-97
mercury exposure, 345-46 recreation-related, 98-100
INDEX 431
Injuries (continued) Kidney toxicity, chemical hazards, 721)
repetitive strain, 344, 361 Kuru, 254
settings, 95-96
SOClOCCOflOfliic factors, 93 Laboratory analytical scientist, 48-49
surveillance systems, 93-94 Lagoons, aerated, 235
traffic-related, 97-98 Land
Insect vectors, global warming and, 382, 384h degradation, environmental stresses leading
Insecticides, 274t, 276h to, 271, 272h
Internal dose, 129 development and ownership, rural
international Agency for Research on Cancer communities, 296
(IARC), 24, 75, 75t environmental health hazards, 54, 5 5t
International Chemical Safety Card, 80, 811 Land mines, 374
International development, impact on water Laser light, health effects, 89
resources, 219 Latin America, cholera epidemic, 213.
International Drinking Water Supply and 214h-2151), 214f
Sanitation Decade, 237, 239-40 Lead
International Monetary Fund (IMF), 45 exposure
International networks, 408 in air, WHO guidelines, 40t, 198
International Program on Chemical Salety dose—response relationship, 120, 121
(IPCS) in food, 256-57
food standards, 261-62 health effects, 1911, 198
personal protective equipment guidelines, industrial pollution, 344-45
155 learning disabilities from. 190
publications, 62 provisional tolerable weekly intake, 257
reference materials on environmental poisoning. 345
hazards. 170, 1 70h incidence, 355
International Register of Potentially Toxic surveillance system, 160-61. 1621)
Chemicals (IRPTC), 61-62 Leptospirosis, 273, 279, 361
Interventional epidemiology, 1091 Lethal concenlration at 50% (LCSO), 76
Interventions, economic analyses, 172-79, Lethal dose at 50% (LD50), 76
1731, 174b-175h, 178t Leukemia, from radiation, 326
mutt diet, 246h Liige, healthy city program, 309
Inversion, air pollution during. 182 Life expectancy. 23
Iodine, 62-63 environmental influences, 2-3, 3f
deficiency, 246 Lifetime individual risk, 138
in drinking water. 216 Light, laser, health effects. 89
tod ne - 1 3 1, afte r nuclear reactor mat in oct ion, Lighting, poor. 89
2 58-59 linkage Methods for Environmental Health
Ionizing radiation Analysis, 21
carcinogenicity, 76h Lipids, requirements and sources, 2441
defined, 85 Liver toxicity, chemical hazards, 72h
dose—response relationship. 86-87 Liverpool, healthy City program, 309
health effects, 8 5-87 Logging wastes, combustion, indoor air
nonthreshold effects, 86 poll ciii (in from, 3 1 5
sources, 86 London Fog, 193, I93b, 194f
threshold effects, 86 Lower Seyhan Irrigation Project,
Iron environmental impact assessment.
deficiency. 247-48 141 h
exposure, health effects, 198 Lowest observed adverse effect level (LOAEL),
processing hazards, 341 121-22, 124f
Irrigation, waslewaler for, 235-36 Lung .3'i' also R espiratory
Isocyanates, asthma from, 357h black, 357h
Itai-itai disease, 347 cancer, from uranium nsining, 326
disease
Japan in larmers, 280
mercury poisoning in. 258h, 346 occupational, 355, 356b-3581)
pollution in, economic analysis, 1 74b—I 75h from smoke inhalation, 316, 3171
Joint health and salety committee. 352 dust particles in, 184-85, 1851
larmer's, 280. 357b
Karachi, Pakistan, water pollution in, 222h white, 356h
Karasek model, 102 Lynle disease, 382
432 Index
Macroeconomic policies, environmental Microorganisms, health effects and sources, 191
health problems and, 45 Milan, Italy, healthy city program, 309
Mad-cow disease. 253-54 Mivamata, Japan, mercury poisoning, 25$b,
Malaria 346
and climate change. 384 Mineral fibers, synthetic, carcinogenicity, 761)
Maillard reaction, 266 Minerals
Malnutrition mining hazards, 340
health effects, 245-48, 269b requirements and sources, 245t
world situatiOn, 268-69, 269h, 270t Minimal infectious dose, 58-59
Manganese exposure, in air, WHO guidelines, Mining industry, pollution and hazards
401 related to, 340
Manufacturing, pollution and hazards related Mist, 186
to, 342-43 Molecular epidemiology, 132
Mar del Plata Action Plan, 237 Molluscicides, 2741
Marine environment, global warming and, Monocu Iture, 391
382, 383h Montreal Protocol, 377
Marker of effect, 131-32, 1 311 Mortality rate
Material Safety Data Sheet (MSDS), 169 for children, female literacy and, 31, 311
Ma lena Is infant, 33, 331, 341
building, manufacturing hazards, 343 injury-related, 93
bulk, environmental hazards, 349-50 trends, 23-25, 243
exnaction, industrial pollution fron, 34011 Mortality ratio, standardized, 114
Maximum allowable concentrations, 365 Mosqu i los
Mechanical hazards, 92-102. Sec also Injuries anophelene and colicine, 382
Media Motor vehicles
Communication guidelines, 151 h air pollution control strategies, 204, 205b,
education through, 406 301 h
Medical waste hazards, 343 injuries, 97-98, 305-6
Megacities, 293, 294t dose-response relationship, 121, 1231
air pollution, 201, 202, 2021 Haddon matrix analysis, 101, 10 It
Megamouse toxicity studies, 78 off-road, 99-100
Melanoma usage, 304-5, 305f
malignant, 377 Mucosal irritation, from air polltttion, 189
non-malignant, 377 Multidisciplinary team, 46-47
Meningitis, housing conditions and, 290 Multiple chemical sensitivity, 337, 3381)-339h
Mercury Mutation fixation, 73-74
exposure Mvula Trust, South America, 238h-239b, 240
in air, WHO guidelines, 40t Mycotoxins, 252-53
in food, 257, 258h
health effects, 198 National Institute for Occupational Safety and
industrial pollu I ion, 345-46 Health (NIOSH), 79
provisional tolerable weekly intake, 257 Natural disasters, 395-96, 3951, 397
poisoning, 258b, 346 Natural gas
Metals. See also .sj'eo fic iiietal as energy source, 318, 3181, 31 9-20, 31 9t,
fume fever, 358b 321-22
in hazardous waste, 337 leaks, 321
mining hazards, 340 Natural resource conservation, historical
processing hazards, 341 movement, 12
tOxic, 63, 344-47 Nephelometric turbidity units, 237
trace, health effects, 191 t, 198 Netherlands, bicycle usc', 301b
Metastases, 74 Networking, 408
Methane, atmospheric concentration, 384, Nectrotoxicity, chemical hazards, 721)
385 Neutron radiation, 85b
Methanol, 66 News media
Met hylne rcu ry contmtmnication gctidelines, 151 h
in food, 257 education through, 406
health effects, 546 Nile Waters Agreement, 219
Microbiological air pollution, in door, 207 Nitrates
Microbiological standards, biological hazards, in drinking water, 216
274-25, 225t health effects, 279
Microclectronks, manuiarturing hazards, 343 in selected river systetils, 216, 2161
INDEX 433
Nitric acid, in hazardous waste, 339 agricultural sector. See Agricultural hazards
Nilrogcn dioxide airborne, 200-201
in air, WHO guidelines, 40t biological, 361-62, 36 lb
health effects, 194-95, 195t carcinogenic, 360t
Nitrogen-fixing plants, 279 chemical, 118-19, 355-58, 3561)-358h
Nitrogen oxide dimensions of health problems, 354-55
atmospheric concentration, 384 distribution, 355
corrosive effects. 63 environmental health hazards and, links
health effects, 191t, 194-95, 1951 between, 38-39
No observed adverse effect level (NOAEL), ergonomic, 97, 344, 360, 361
121, 124! exposure standards, 364, 365-66
No observed effect level (NOEL), 122 fossil fuel extraction and processing. 3 18t,
Noise 319, 320h, 321, 321f
annoyance with, 121, 124f, 302-3, 303h identification, 118-19
cardiovascular effects, 302 manufacturing, 342-43
control, 83, 303-4 materials extraction, 340-41
defined, 82 mechanical, 360-61
direct effect, 301 monitoring, 364-65. 365t
environmental (community), 300-304 physical, 358-59
guidelines and standards, 302, 303, 3041 prevention approaches, 363-66
health effects, 83 processing industries. 341-42
hearing loss from, 83 protective equipment, 364
incidence, 355 psychosocial, 102, 350, 362
surveillance program, 167, 168h service industries, 343-44
indirect effects, 301 types, 3 54-62
industrial, control, 83-84 uranium mining. 326
level, of familiar sounds, 83t worker training and, 364
pollution, service industries. 343-44 Occupational health and safety
sleep disturbance from. 302 air quality guidelines, 40, 40t
sound intensity measurement. 82-83 environmental health and, links between.
Nuclear accidents. 2 58-59, 325 38-41
Nuclear fission, 325 internal responsibility for, 351-52
Nuclear fusion, 326 prevention framework, 363-65
Nuclear power, 32 5-28 for small enterprises, 351
deterministic effects, 327 social context, 3 50-54
fusion-based, 326 surveillance programs. 364-65. 365t
safety approaches. 327 UI mvontcn, 352-54
stochastic effects, 326-27 ivorkers' compensation and, 352
use, 32 5-26 Occtipational health and safety inspector.
waste disposal, 327-28 50
Nuclear reactor malfunction, 2 58-59 Occupational health nurse, 49
Nuclear warfare, 373-74 Occupational hygienist, 49
Nuclear weapons plants, contamination, 373-74 Occupational injury, 360-61
Nuclear winter, 373 ergonomics and, 97
Nutrient(s) prcvetltion, 95. 96-97
deficiencies, 24 5-48 Occupational overuse syndronie, 344. 361
world situation, 268-69, 2691), 270t Ocean currents, global warming and, 38 1-82
recommended intake, 260 Odds ratio, t I 3f, 114
requirements, 213, 244t-245t Odor pollution, processing industries, 341,
342
Obesity, health effects, 243 Oft-road vehicles, 99-100
Observational approach, time -activity Oil
information. 132 as energy source .318, 31 8t, 319, 31 9t,
Occupational and environmental health 321-22
physician, 49-50 extraction, pollution and hazards related to,
Occupational and environmental medicine, 340
risk management approach in, 164, Olefins, 63
166-67, l68h Operatimig practices, control at source by,
Occupational exposure levels (OELs). 365 153-54
Occupational hazards. See also Industrial Organic polltitamits, persistent, 67b
pollution Organic solvents, 66-67
434 Index
Organization for Economic Cooperation and Photochemical air pollution. 199, 1991
Development (OECD) countries Physical hazards. 80-92. See also specific type
anthropogenic air pollution in, 181, 181f dose-response relationship, 120, 122f
energy consumption in, 312 housing-related, 290-92
Organophospliates, 276h, 339 occupational, 358-59
Our Common Future (WCED), 7 recreational water, 237
Our Planet, Our Health (WHO), 6, 239-40 routes of exposure, 551
Outbreaks, environmental disease, 362-63. types, 80. 82
362t Plant fibers, processing hazards, 342
Overcrowding, communicable disease and, Playground equipment, 99
289-90 Pneumoconiosis, 185, 356h-357b
Oxygen uptake, inhibition, 188 Pneumonitis, hypersensitivity, 357h-3581)
Ozone Poisonirtg
atmospheric concentration, 384 cadmium, 347
corrosive effects, 63 chemical, in home, 350
depletion food, 249, 250. 251h
health effects, 377, 378f inadvertent, 99
stratospheric, 375-77 lead. See Lead, poisoning
tropospheric accumulation, 375 mercury, 258h, 346
and UV radiation, 375-77, 3761, 378f Political violence, too
health effects, 190, 19 It, 192, 192f, 196 Polluter-pays principle, 240
Polybrominated biphenyls (PB Es), in food, 256
Painter's syndrome, 348 Polychlorinated hiphenyls (PCB5)
Paper industry, hazards. 341-42 average daily intake, 256f
Para-dichlorohenzene, acceptable daily intake, bioaccumulation and hiomagnification, 335,
1261) 335f
Parasitic disease in food, 254, 255-56, 256f
foodborne, 251-52, 2 52h, 253f in hazardous waste, 337, 339
tropical, 57 Polychlorinated hydrocarbons, 66. 671)
Parental leave, 354 Polycyclic aromatic hydrocarbons
Particles from food preparation. 266
in air. Ses' Aerosols health effects and sources, 191
dust, deposition, 184-85, 185f Polycyclic henzene rings., 65
PCBs. See Polychlorinated hiphenyls (PCB5) Polymer fume fever, 358h
Pentachlorophenol, in hazardous waste, 337, Polyphenyl, 65
339 Poor health .9cc Disease
Peripheral neuropathy, from solvents, 348 Population at risk, definitions, 19-20
Persistent organic pollutants, 67h, 398 Population displacement, hydroelcctric dams
Personal tisonitoring, exposure assessment, and, 323
130-31 Population growth, environmental health
Personal protective equipment (PPE) problems and, 41-42, 421
control at target/person level by. 154-55, Population sampling, 134-35. 1361
1571 Post-traumatic stress syndrome, disaster-
for farmeim, 280 related, 397
guidelines, 155 Potassium hydrcxide, 63
against occupational hazards, 364 Potential years of life lost (PYLL)
program checklist, 1561 injury-related. 94
Personality, stress response and, 147 stticide -related, 100
Pest management, integrated, 278 Poverty
Pesticides environnsental health problems and, 43-44,
categories. 274t 43t
defined, 274 urban areas, 297, 2981
exposure, populations at risk, 275-77. 277f Posve r
in hazardous waste, 339 energy. See Energy
production and use, 274-75, 275h, 276h statistical, 116, 1171
toxic effects, 277-78, 2781 Power stations, air pollution from, 321 -22
Petrochemical industries, processing PRECEDE-PROCEED model of health
hazards, 341 promotion, 158, 1 59b
Petroleum gas, liquid, versus hiomass fuel Precipitation
consumption, 317-18 air pollution and, 186
Phenols, health effects and sources, 191 global warming and, 38 1-82
INDEX 435
Pregnancy leave, 354 nonstochastjc effects, 86, 327
Press conferences, 406 stochastic effects, 86, 326-27
Pressure, health effects, 89-90 ultraviolet See Ultraviolet radiation (UVR)
Prevalence of disease, 19, 113, 1131 Radioactive contaminants, food, 257-59
Prion, 55, 254 Radioactivity u iii 1, 84h
Prion disease, 253-54 Radionuclides, internal emitters, 258
Problem-focused coping, 146-47 Radon, 87
Process standards, control at source by, 153 health effets and sources, 1911
Processing industries, pollution and hazi rds mitigation, economic analysis, 176-79, 1781
related to, 341-42 Random sampling, stratified, 135
Product standards, control at source by. 153 Rate of disease, 113, 1131
Professional associations, 407-8, 409 Recommended dietary allowances, 260
Professional practice in environmental health, Recreational injuries, 98-100
403-4. See also Environmental health Recreational water, physical and chemical
professionals characteristics, 237
Promoter, 74 Relorestation, 388, 390
Propanol, 66 Refugee camps, 371, 372h
Proportional morbidity studies. 113 Refugees, 371
Protective equipment Registry of Toxic Effects of Chemical
control at target/person level by, 154-55, 157f Substances (RTEC), 79
for farmers, 280 Rehabilitation of occupational or
guidelines, 155 environmental disorders, 167
against occupational hazards, 364 Repetilive strain injuries, 344, 361
program checklist, 1 56t Representative errors, exposure assessment, 136
Proteins, requirements and sources, 244t Reproductive hazards. occupational, 354, 359t
Protozoa Research, by environmental health
lifecycle, 55-56 professionals, 408-9
waterborne, 225t Respiratory effects
Psychological effects, disasters, 397 of air pollution, 188-89
Psychosocial hazards, 102-3 of ozone, 192, 1 92f
occupational, 102, 350, 362 Respiratory infections
service industries, 344 from dir pollution. 189, 190t
tirban areas, 102-3 from biological hazards, 60
Psychosocial problems, housing and, 292, 292t from indoor air pollution, 207
Public education, 404-6, 4051 Risk
Public exposure, to industrial pollution, acreptable level of, 128
333-40, 3351 acceptance, 146-50, I 48t- t49t, 1 501, 1511)
Public Health Act, 11 assessment, 104-2 See also Risk assessment
Public health inspector, 47 characterization, 106, 1 57-39, 1 38t
Public health laws, 1] communication, 147-50, 1 501, 1 Sib
Pulp and paper industry, processing hazards, comparison, for energy sources, 330
341-42 defined, 53
diniensions, 1 48t- 1491
Quality-adjusted life years (QALYs), 25 evaluation, 144-46
Quality assurance with no historical data, 145-46
exposure assessment, 137 versus standards or guidelines, 144-45
food, 262-68, 264f, 265t, 268h incremental, 114, 11 Sb
lifetime individual, 138
Radiation management, 143-79. 5cc' also Risk
alpha, 84h ma nageni cut
basics of, 84h-85b measures, 113-15, 1131, 115h
beta, 84h ilionitoring, 160-64
cancer from, 86-87, 326-27 health surveillance systems, 160-61,
electromagnetic, 87, 343 161h, 1621)
gamma, 84h-85h indicators in, 161, 1631-165t, 164, 1 65h
hazards, 85-89 perception, 146-50, 148t- 149t, 1 50t, 151 b
ionizing, 76h, 85-87 pol)tilatfoii at, 19-20
leukemia from, 326 toxicity versus, 62
neutron, 85b Risk assessment, 104-42
non ionizing, 87-89 dose-response assessment, 105, 119-28, 1211
436 Index
environmental impact assessment and, Sanitation, 231-33
1 39-42 Costs, 233, 234t
exposure assessment, 105-6, 128-37, 1291 in developing countries, 2371, 239
in field situations, 139 excreta disposal systems, 231, 232, 232h
generic versus specific, 106 poptilation coverage, urban areas, 231, 233,
hazard identification, 105, 107-19 233t
health, environmental indicators for, 21 Sao Paulo. Brazil, air pollution, 202, 202t
161, 163t-1641 Saturated aliphatic hydrocarbons, 63
for nonthreshold effects, 127-28 Sawdust, combustion, indoor air pollution
qualitative, 106-7 from, 315
risk characterization, 106, 137-39, 1381 Schistosomiasis
sources of uncertainty, 106, 1071 Aswan dam and, 323
steps, 105-6, 106f waterborne transmission, 210, 21 2b, 382
for threshold effects, 120-27, 1211-1241, Scorched-earth strategies. 371
1271 Screening tests, for surveillance programs,
Risk difference, 114, 11 5h 160, 161h
Risk management, 143-79 Sea level, global warming and. 382
approach, 144, 144f Seattle, Washington
to environmental health concerns of bicycle use, 301 h
individuals, 164, 166-67, 168b healthy city program, 309
to environmental health emergency, 167, Sensitivity analysis, 106
16 9-7 2 Service industries
communication of risk, 147-50, 150t, 15 lb pollution and hazards related to, 343-44
control of exposure, 150, 152-58 psychosocial hazards, 344
along the path, 154. 1551 Sexual abuse, 100
framework for, 150, 152-5 , 1521, 1 52t Shanghai, China, water pollution, 222b
at source, 153-54 Shanty-towns, 286
at target/person level, 1 54-56. 1 561, 1 571 Shellfish poisoning. 382
delined, 105 Shigellosis, foodhorne transmission, 251
evaluation of risk, 144-46 Short-term exposure levels, 366
health education in, 156-58, 1 58b, t 581, 1 59b Sick building syndronie, 29 1-92, 292t
monitoring of risk, 160-64, 161 b, 1621), Sievert (5v), 84h, 86
163t-165t, 165b Silent Sprinq (Carson), 12
perception and acceptance of risk, 146-50, Silicosis, 356b-357h
148t-149t, 1501, 1511) incidence, 355
Risk ratio, 113-14, 1131 from uranium nlinirlg, 326
Risk-specific dose (RsD), 128, 144-45 Silo eniptier's disease, 280
Rodenticides, 2741 Silo filler's disease, 280
Rtimor control, 171 Skin
Rural comni.unities absorption, factors affecting, 134
economy, 295-96 cancer
environmental protection implications, 297 ozone depletion and, 377, 3781
land development and ownership, 296 ultraviolet radiation-induced, 76b, 88
time and space differences, 295 chemical hazards, 72h
values, 296 disease, occupational, 355, 356
cxpos tire
Safe Community Network, 96 estimation, 134, 1 35b
Safety factors, dose-response relationship personal monitoring, 131
123, 125-27, 125t, 1271 Sludge, activated, 235
Salety prolessional, 50 Sludge blanket reactors, upilow anaerobic,
Salmonellae, foodhorne transmission, 251 235
Sample collection errors, exposure Sniog, 199
assessment, 136 Smoke, 182
Sample size, 116, 11 7t, 137 detectors, 99
Sampling inhalation, adverse effects, 316, 31 7t
multistage, 135, 1361 Smoking, indoor air polltition Irom, 207
stratified random, 135 Social support, stress response and, 147
Sampling frame, 134 Soditim carbonate, 63
Sanitarian, 47 Sodiuni hydroxide. 63
Sanitary engineer, 50 Sotia, healthy city program, 309, 310
INDEX 437
Soilborne exposure, 59, 133, 1 33t Surveys, exposure assessment, 132
helminths and, 59 Survival curves, 2-3, 31
ingestion estimation, 133, 1 33t Susceptibility markers, 131-32, 131
Solar energy, 328, 328h, 3291 Suspended particulate matter, 182, 185
Solvents annual levels, 298, 3001
in general environment and workplace, Sustainability, energy needs for, 311-12, 3121
347-49 Sustainable developnsent
in hazardous waste, 337 current focus on, 14
Sound intensity defined, 7
dose-response relationship, 120, 1 22f implications of, 8
of familiar sounds, 83t Sustainable urban ecosystem, 282
hearing loss and, 83 Sweden, coal use, 320h, 3211
measurement, 82-83
Sound level (dB(A)), 82-83, 83t Teaching methods, 404-6, 4051
Sour gas, 321 Technical expertise, environmental health
Spain, toxic oil syndrome, 111 h professionals, 401-3
Stabilization ponds, 235 Technological disasters, 395, 395t, 396, 397
Standard operating practices, control at source Temperature (ambient)
by, 153-54 extremes, health effects, 90-92
Standardized mortality ratio (SMR), 114 global, increased, 380, 380f. See also Global
Staphylococci, loodborne transmission, 251 warming
Statistical power. 116, 1171 Temperature (body), regulation. 90-91
Statistician, 50 Terrorism, 374-75
Steel processing hazards, 341 Testosterone, 64f
Stochastic effects Textiles, manufacturing hazards, 342
dose-response relationship. 127-28 Thailand, food standards and export, 263h
radiation, 86, 326-27 Three-Mile Island accident, 258, 259, 325
Stoves Threshold dose
biomass fuel, teclitiological improvements, high-risk groups, 127
317 uncertainty factors, 123, 125-27, 1251, 127f
kerosene, air pollution from, 317 Threshold effects
Strangulation, 99 dose-response relationship, 120-27,
Street foods, safety, 268h 121f-124f, 1271
Stress radiation, 86. 327
defined, 102 Threshold limit values. 366
health effects, 103 Tickhorne disease, global warming and,
occupational, 344, 362 382-83, 385h
physiological response, 103 Time-weighted average, 365
post-traumatic, 397 Time-activity diaries, 132
psychosocial, 102-3, 344 Tobacco smoke, indoor air pollution from,
response, factors affecting, 147 207
Structural adjustment programs, 45 Tolerable daily intake (TOt), 122-23, 1251
Study designs, epidemiological, 108-13, 1 09t Tolucne
Suffocation, 99 asthma from, 357b
Suicide, 100 in hazardous svaste, 337
Sulfate, health effects, 194, 196 Total dose, 138
Sulfur dioxide, 298, 299f Total exposure, 40, 128, 137-38
in air, WHO guidelines, 40t Total suspended particles, 185
concentration, trends, 206, 206f Toxic oil syndrome, 1 lib
health effects, 191t, 193-94, 193h, 1941 Toxic stibstances
Sulfuric acid, 63, 1911 bacteria-produced, 57, 250
Supportive environments for health, 9, 9h classification, 80, SOt
Surveillance systems collection from consumers, 350
health, 160-61, bIb, 162h health effects, 72h
for injtiries, 93-94 inhalation, 187, 357h
for lead poisoning. 160-61, 162h expoire estimation, 132-33, 1331
for noise-induced hearing loss, 167, 1 oSh oxygen deprivation from, 187-88
occupational health and safety, 364-65, Toxic wastes. See Hazardous wastes
3651 Toxicity testing
screening tests for, 160, 361 b acute, 75-78, 77t
438 Index
chemical hazards, 75-79, 77t Liraniu in
chronic, 77t, 78 mining, health hazards, 326
in experimental animals, 75-79 for nuclear energy, 325, 326
genotoxic short-term, 79 Urban areas
in humans, 79 air pollution, 201. 202, 202t, 298-300,
reproductive studies, 77t, 78 299f, 300f, 301h, 331
specialized studies, 771, 78-79 energy needs, 314
structure-activity relationships, 79 "Healthy Cities" approach, 306-10, 307h
suhchronic, 77t, 78 pos'erty, 297, 2981
Toxicologist, 50 psychosocial hazards, 102-3
Toxicology, developmental, 27 sanitation, 231, 233, 2331
Toxins, natural, in food, 249, 260-61 water supply, 233t
Trace elements, health effects, 1911, 198 Urban ecosystem
Transportation, energy needs, 314 basic health requirements, 282. 285-86
Trichinellosis,foodborn e transmission, 2 52b, DPSEEA framework, 282, 283h-285h
2531 sustainable, 282
Trickling filters and towers, 235 Urbanization, 297-306
Trihalomethanes, cancer and, 229h factors affecting, 294-95, 2941
Tropical parasitic disease, 57 infrastructural requirements. 297-98
Tuberculosis trends, 293, 293f, 294t
among hospital workers, 361 UVR See Ultraviolet radiation (UVR)
hottsing conditions and, 289-90
resurgence, HIVIAIDS and, 60 Valttation methods
Tumor, primary, 74 contingent, 173, 175
Turkey, Lower Seyhan Irrigation Project cost -of- illness approach, 175
environmental impact assessment, 141 h Vanadium exposure, health eflects. 198
ntalaria and, 323-24 Vapor, 186
Typhoid, transmission, 212-13, 251 Vasculitis, vibration, 85
Vector-borne disease
Ultraviolet radiation )UVR), 87-89 environmental management, 324
carcinogenicity, 769, 88 global warnting and, 382, 384h
health etfects, 88-89, 377, 3781 spread, 57, 59
ozone depletion and, 375-77, 378f Vegetable matter, combustion, mndoot air
protection against, 377 pollution from, 515
sources, 88 Vehicles
types, 375, 376f motor. See Motor vehicles
Uncertainty, sources of, 106, 1 07t nonmotorized, 301 b
Uncertainty lactors, dose-response Ventilated improved pituitary latrine, 231,
relationship, 123, 125-27, 125t, 232, 232h
1271 Ventilation
United Kingdom, industrial development, general (dilution), control at source by,
11-12 l52b, 153
United Nations local cx ha 0 st, u nit rol a long the path by,
Agenda 21, 7 154, t551
Universal Declaration of Human Rights, 8 Vibration
United Nations Conference on Human arnt and hand, 85
Settlements, 237 health eflecis, 82-8, 85
United Nations Environmental Program V/brie c/wlercme outbreaks, 382, 38 Sb
(UNEP) Vinyl chloride
Global Env i ro nnten ta I Pu j ccl, 18 and cancer, 1129
International Register of Potentially Toxic metabolistn, 709
Chenticals, 61-62 Violence
United States, air quality standards, 202, 203t intentional, 100
United States Environmental Protection political, 100
Agency (EPA), risk communication Viral disease
rules, 1 50t loodborne, 251
Universal Declaration of Huotan Rights, 8 global warming and, 383b
Unsaturated aliphatie hydrocarbons, 63 waterhorne. 225t
Upllosv anaerobic sludge blanket reactors, Viruses
235 carcinogenicity, 76h
INDEX 439
lifecycle. 56 recreational, 236-37
Vitamin A requirements, 15
deficiency, 246, 2471 water uses and, 210, 21 lb
toxicity, 247h, 247f recreational
Vitamin E, deficiency, 248 physical and chemical characteristics,
Vitamin D deficiency, 248 237
Vitamins quality guidelines, 2 36-37
and health, 247b salety, 15
requirements and sources, 244t-245t 55' 1P1Y
Volatile organic compounds, health effects, adequacy, 2 17-18, 218f
191t, 197-98 in developing countries, 2371, 239
ensuring, 2 37-41
War global trends, 218-19
health consequences, 370-75, 3701, 372b management, 240-41
military deaths, 370t protection, 227-28, 228h
refugee issues, 371, 3721) urban areas, 2331
War and Public Health, 370 taste, 217
Warfare temperature, 217, 237
biological, 373 turbidity, 217, 237
chemical, 371, 373 uses, 209-10, 211h
conventional, modern, 370-71 wastewater reuse, 235-36
guerrilla, 374 withdrawal, 217, 2181
nuclear, 373-74 Water-dispersed infections, 213
Wastewater Water pollution, 219-20
reuse, 235-36 from air, 194, 220, 2211), 322, 392-93
safeguard measures, 236 control, 2 34-36
treatment, 235 in developing countries, 220, 222h
Water. See also Sanitation development-related. 220, 221h
acidification, 194. 220, 22 lb. 322, 392-9 from direct discharge. 22 lb
algal blooms, 220, 382, 383b historical concern with, 11
biological oxygen demand, 341 industrial
chemical constituents, 215-16, 21 6f control, 234-35
acceptable daily intake, 22 5-26 public exposure, 335. 3351
guideline values, 226-27 sources. 220
color, 2 16-17 Water-privation disease, 210, 213
Water. (continued) Water-related disease, 211, 213
communicable disease associated with, Waterhorne disease, 213. 21 4h-2 I Sb, 21 4f
210-13, 212b viral, 2251
desalination, 228 Waterhorne exposure, 55t
disinfection, 230 biological hazards, 57, 58
drinking ingestion estimation, 133, 1 33t
distribution, 230-31 personal monitoring, 130-31
fluoridation, 215-16, 230 Wal erhorne pathogens, microbiological
place of use, 231 standards, 224-2 5, 225t
quality criteria, 220-27, 2231, 225t While finger disease, 85
sources. 227-28 Wind energy. 328h, 329f, 329t
storage, 230-31 Windseale accident, 2 58-59
treatment, 228-30, 229b, 230f Women
eutrophication, 220, 221 h education and training progrants, 31-32
monitoring, 61 literacy, 31
for contaminants, 22 3-24 fertility rate by, 30t
for fecal bacteria. 222-23, 2231 mortality rate for children by. 31
GEMS project, 228b occupational health and safety, 352-54
microbiological standards, 224-2 5, 2251 smoke inhalation, 316, 31 7t
odor, 217 vulnerability to environmental hazards,
pH levels, 237 29-32
quality VVoozcu, Health and the Eni'ironmnenl ( Sims),
guidelines and standards, 220-27, 223t, 30
2251, 236-37 ,Vood, conshustion, indoor air pollution front,
indicators, 163t, 341 315
pollution and, 219-20, 2211), 222h Workers' compenSation, 352
440 Index
Workers' Compensation Board, 352 Health for All policy, 5
Workiorce, importance of. 38 network initiatives, 408
Workplace, as sentinel for environmental noise guidelines, 302
hazards, 39 water quality guidelines, 220-27, 223t
Workplace Hazardous Materials Information World Resources 1998-1999: A Guide to the Global
System (WHMIS), 80 Environment, 21
World Commission on Environment and
Development (WCED), 7 Xenobiotics, metabolism and excretion, 71
World Health Organization (WHO Xenoestrogens, 64h-65h, 64f, 65-66
air quality guidelines, 40t, 202, 203t
energy priorities, 330-31 Zoonoses, 57, 273, 279
INDEX 441
text for courses h'i m1t health fri medtiisihii
students who require a comprehensive introduction to the subject. I recommend it unreservedly.
—John Last, MD, FRACP, FRCPC, .Universijy of Ottawa,
Annals of the Royal College of Physicians and Surgeons of Canada
This comprehensive interdisciplinary text draws frqm the social sciences, the natural sciences and the
health sciences to introduce students to the principles and methods of environmental health. It offers an
overview of the basic sciences needed to understand environmental health hazards, including toxicology,
microbiology, health physics, injury analysis and relevant psychosocial conCepts. It also presents a basic ,
approach to risk assessment and risk management. The first part of the hook concentrates on broad issues,
providing frameworks for the investigation and management of environmental health problems. The middle
section deepens the discussion of routes of e*posure (air quality ; water and sanitation, food and agricul-
tural issues). The final section addresses environmental health in terms of sustainable development themes
(settlements and urbanization, energy, industry, and global concerns). The final chapter focuses on ethical ,
issues and action planning. Thus, the text alms to enhanqknowledge, skills and attitudes in environmen-
tal health.
Tord Kjellström, Med Dr, MMEng, is Professor of Environmental. Health at the University of Auckland,
New Zealand and Director, New Zealand Environmental and Occupational Health Research Centre. He has
20 years experience as an environmental and occupational health researcberçi teacher, in Sweden,
Australia, and New Zealand and worked from 1985 to 1997 at the World Healtlirganization, Geneva, as
envirQnmental epidemiologist and Director, Office of Global and Integrated Environmental Health. In this
position he developed teaching materials and teachersI guidelines for environmental health, and this text
is a product of these activities.
Theo de Kok, PhD, is coordinator of the Environmental Health Sciences program at Maastricht University,
The Netherlands. He is .a member of the Department of Heath Risk Analysis and Toxicology, and of the
Nutrjtkui and Toxicology'Research Institute, where his research activities focus on the assessment of envi-
ronmental and occupational health risks, biomonitoring of genotoxic effects, and colorecuil carcinogene-
sis. At the Open University of The Netherlands he developed distance teaching materials in the fields of
environmental and occupational health, nutrition, and toxicology.
Tee L. Guidotti, MD, MPH, is Professor of Occupational and Environmental Medicine, Epidemiology, and
Pulnonary Medicine at Gerge Washington University Medical Center, Washington DC, where he serves
as Chair of the Department of Environmental and Occupational Health in the School of Public Health and
Health Services, and Director of the Division of Occupational Medicine and Toxicology, Department of
Medicine in the School of Medicine and Health Sciences. He continues to serve on the adjunct faculty of
the University of Alberta, where he was Killam Annual Professor.
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