3.10. Human Health Issues: The Environment Is Everything Which Isn't Me.' - Albert Einstein

Human health issues 263
3.10. Human health issues
The environment in which people live, work and play is an important determinant of Main findings
health and well-being, but the extent of its importance in developed economies is
difficult to quantify.
The most common diseases in the EU – heart and circulatory diseases, cancer, respiratory
diseases, stress and related symptoms – have many causes which are often interconnected;
including genetics, the condition people are in (via diet, exercise etc.), and the environmen-
tal circumstances to which they are exposed.
Identifying cause-and-effect relationships is therefore very difficult, especially if the impact

of the environment on health is delayed, or is the product of many, perhaps small,
environmental factors acting together.
There is a serious lack of data and information on exposures, effects and biological
models that connect them. Therefore considerable uncertainty surrounds many issues of
concern, such as air pollution, noise, water contamination, waste, climate change,
chemicals (including endocrine disruptors and antibiotics) and non-ionising radiation.
In many cases, however there is sufficient evidence to take preventive action, particularly
where the impacts may be serious, large-scale and irreversible – circumstances which
merit the use of the precautionary principle. Preventive action on many of the
environmental hazards covered in this chapter is being taken, but more integrated and
effective action is being proposed to reduce threats to health and well-being.
1. Introduction early 1990s when environmental issues were

much higher on their and the media’s
‘The environment is everything which isn’t me.’ agenda (Figure 3.10.1). Politicians have
— Albert Einstein reflected this concern and declared that
human health is a key objective of environ-
People are at the centre of ‘their’ world, as
Einstein observed, but they are also part of
the environment, and play a significant role Opinions: Proportion of respondents who believe
environmental problems affect their health a Figure 3.10.1
in shaping it, as Chapter 2.1. and other great deal/fair amount in 1992 and 1998
chapters have shown. But the relationship is
not just unidirectional: the environment Source: Environics
‘shapes’ people by the impact it has on their International, 1998
100
health. 1998
1992
This is not just in the obvious ways of sustain- 80
ing life, through the provision of food, water

% of respondents
and shelter, but also through the less visible 60

impact it has on genes, cells, organs and
biological systems which together can cause
40
disease. In the more developed economies –
such as the EU – where basic supplies of
clean water and sewage facilities are gener- 20
ally available, environmental impacts on
health are often less obvious – and more 0
insidious – than in developing countries.
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their health, and more so now than in the

264 Environmental Issues
mental policies (Box 3.10.1). However,

unravelling the less obvious connections Box 3.10.1. Health and the environment:
key declarations
between the environment and health in
developed economies is not easy. The environment should be regarded as a resource
for improving living conditions and increasing well-
being (Frankfurt Conference, WHO 1989).
Damage to health is the result of many
factors acting in various combinations, over Human beings are at the centre of concern for
different time periods, to a diverse range of sustainable development. They are entitled to a
healthy and productive life in harmony with nature
people, of varying sensitivities, and at differ- (Earth Summit, Rio de Janeiro, UNCED 1993).
ent stages of their lives (Figure 3.10.2).
Understanding the complexities of what We have a shared goal before us: to improve the
living and health conditions of the present
causes ill health is clearly going to be diffi- generation, to ensure that the carrying capacity
cult – and, very often the more we know, the of nature is not exceeded and that the right of
more we realise what we don’t know. It is not the future generations to a satisfying and
productive life is safeguarded (Helsinki
surprising, therefore, that scientific and Conference, WHO 1994).
public controversies over environment and
health have been or are currently common
within scientific and public circles (e.g.
leaded petrol and brain damage in children, Hollander et al., in press). The main compo-
or antibiotic growth promoters in animal nents of this environmental fraction are:
feed and increased human resistance to external air pollution, which accounts for
antibiotics). Public policy decisions on most of the total environment related health
environmental hazards (potential damage) loss in the Netherlands (in terms of reduced
and risks (probable damage) are difficult to life expectancy, the quality of life and
make and evaluate. However, understanding number of people affected); environmental
the types of information needed for environ- noise and indoor air pollution, including
mental health decision-making (as well as its radon, damp and environmental tobacco
use and limitations) will contribute to a smoke. Lead in drinking water is also signifi-
wider appreciation of the reasons for public cant. Traffic and domestic accidents, which
concerns, differences in expert opinions and together would bring the total environmen-
the action (or inaction), of governments. tal fraction of disease causation from 5% to
12% are very important public health
Environmental stresses for which there are hazards, but are not normally considered as
reasonably good exposure and effect data environmental health issues.
are estimated to be a major factor in an
estimated 5% of disease, according to
preliminary report prepared for the WHO 2. Some dominant environmental health
on the basis of Dutch data (WHO, 1999a; De issues in Europe
2.1. Air pollution

Atmospheric pollution is a major cause of
exposure to substances which are hazardous
Environment, people and health: to health: the causes and effects of air
Figure 3.10.2 some key relationships
pollution are discussed in chapters 3.3 and
3.4.
2.1.1 Exposure of European population to

Evironmental ambient air pollutants
Exposure data on suspended particulate
Parents Mother Child
matter is poor and is still measured by
Indoor
different methods throughout Europe, and
Adult
Child
Host Host and Harm

Genetics =
State outdoor
exposures the measurements of size-fractionated
Foetus Foetus Infant Adult particulate matter of health relevance (PM10
or PM2.5, i.e. particles up to 10 and 2.5
Factors and exposures
microns in size respectively) has been
introduced in only a few countries. This
scarce data has to be extrapolated which
Environmental factors (e.g. overcrowding, diet, climate, stress) and exposures (e.g. from air, increases the uncertainty of the analysis.
food, drink, surfaces) play a part in causing and/or aggravating disease and ill health, both Therefore the estimates presented below
directly and via parents.
provide just an indication of the possible
Source: EEA magnitude of the effects (Figure 3.10.3).
Box 3.10.2. Scope of the chapter
The scope of this chapter, which summarises integrated approaches to health need to include
some key environmental health impacts, is potential stresses from all parts of the environment.
limited to a selection of those environmental This is not only because human lungs and livers do
stresses to which people may be exposed at not discriminate between pollutants that come
home or out of doors, and which illustrates a from the factory or the street. but also because the
range of health impacts and knowledge about sum of the exposure to stresses from all sources
their links to the environment. The selected may be either additive, synergistic (more than the
information presented is designed to illustrate sum of the parts) or antagonistic (less than the sum
some general points about the links between of the parts), and therefore need to be included in
environment and health, rather than being a any integrated assessment of environmental health
comprehensive review of the literature, which is risks (La Dou, 1998).
beyond the scope of this chapter. Where the
issue is very well covered in other publications, Knowledge of the distribution of environmental
such as climate change (WHO, 1999b), relatively health impacts between e.g. social groups,
little space is devoted to it. geographical areas and generations is critical for
undertaking fully integrated assessments, but apart
The chapters on waste, hazardous substances, from a few references to geography, age, class and
transboundary air pollution, climate change, future generations, these equity issues are beyond
stratospheric ozone, urban areas and water stress the scope of this chapter (Luhmann et al., 1998).
provide background information on the driving
forces, pressures and associated exposures that A more comprehensive view of this field is available
are linked to health problems. from the report ‘Overview of Environment and
Health in Europe in the 1990s’ prepared by WHO
This chapter does not cover occupational for the 3 rd European Conference on Environment
impacts on health in much detail, despite its and Health held in London in June 1999 (WHO,
significant influence on public health. Fully 1999a).
Over 24% of EU urban residents live in cities petrol. Several ‘hot spots’ were still observed
where the annual mean concentration of in eastern Europe at the end of 1980s,
particulate matter (SPM) exceeds 30 µg/m3. mainly due to the poorly controlled emis-
In the eastern part of Europe for which the sions from industrial point sources. Monitor-
data was available, close to 90% of the popula- ing data indicates that relatively high lead
tion live in cities with such relatively high concentrations were also measured in the
concentration of particles. Trends in SPM proximity of busy roads in several large cities
were better in EU countries than in the rest of in western Europe (Zaragosa, Toulouse,
Europe, with 35% of people in EU experienc- Lyon) in the early 1990s. More recent data
ing more than a 5% per year reduction in indicates that concentration of lead in
SPM levels (21% in central Europe) and only ambient air was decreasing even in those
12% experiencing a more than 5% per year highly-polluted locations in the 1990s.
increase in SPM concentration (27% for
central Europe) (for further information on
urban air pollution, see Chapter 3.12).
Exposure to common air pollutants Figure 3.10.3
Most of the population of Europe now lives
in cities with low or medium concentrations Data on concentration of the
100 most commonly-monitored
of SO2. In EU, 97% of urban residents have SPM SO2 NO2 air pollutants (suspended
enjoyed reductions in SO2 concentrations, 90
particulate matter, SO2 and
whereas in the central part of Europe, 80 NO 2) is shown for 1995 or
almost of 20% of urban residents experi- later.
% of urban population
70
enced increasing concentrations of SO2. In total, information on one
60
or more pollutants is
50 available from 110 cities in
More people in the western cities were
24 countries, including 64
exposed to medium and high levels of NO2 40
cities in 13 EU countries with
than in central Europe. However, the trends 30 close to 58 million residents.
were mostly stable (for 60% of urban resi- 20 Source: EEA-ETC AQ and
dents) or decreasing (15%) in the EU 10 WHO/ECEH
countries, while NO2 concentration in-
0
creased for 43% residents of cities in central West East West East West East
Europe. Low Medium High
Concentration of lead in ambient air has

been decreasing over the recent decade,
mainly due to the phasing out of lead from
2.1.2. Estimates of health impacts of some ambient associated with the daily changes in air
air pollution in the EU pollution levels is better documented. Air
The most common of the well-known air pollution with particulate matter is associ-
pollutants (suspended particulate matter ated with more deaths (22 000 to 47 000 a
and ozone) are associated with ill health year) or hospitalisation (4 000 to 8 000
even at relatively low concentrations of the admissions) than exposures to SO2 and
pollutants frequently experienced by people ozone which together are responsible for
in Europe. This observation comes from a 3 000 to 6 000 deaths and 400 to 1 600
number of studies on the effects of daily hospital admissions a year in the EU. It can
changes in pollution levels conducted in be assumed that the health problems attrib-
many parts of the world, including Europe, uted to the pollution and registered through
as well as from a few studies on the health hospital admissions could have been avoided
effects of longer term exposures, most of in the absence of the pollution. However,
which have been conducted in the United this interpretation is not valid for mortality
States. The results of these new studies have (McMichael et al., 1998). While there is an
been used in the revision and update of the association between the daily number of
WHO Air Quality Guidelines, which, in turn, deaths and air pollution level, it is not
provide a basis for the work on the new so- certain to what extent the life of the affected
called ‘Daughter’ Directives to the EU Air individuals is shortened by the exposure.
Quality Framework Directive (96/62/EC),
which will set revised limit values for the In summary, the available data from the
main air pollutants. 1990s indicates that a significant reduction
in population exposure to sulphur dioxide
The most important message from these has occurred in the last decade, and that this
studies is the health significance of air pollutant remains a problem only in a
particulate matter at low levels. The effects limited number of cities in central Europe.
include short-term impacts on pulmonary However, the levels and trends of pollution
function, increased incidence of respiratory with particulate matter are still of concern,
symptoms, and increased mortality implying and there is little improvement with respect
considerable reductions in life expectancy. to ambient levels of NO2 or ozone. These
However, there is still discussion on the components contribute to significant adverse
applicability of the results from long-term impacts on public health, including in-
studies conducted in the United States to creased mortality and reductions in life
European conditions. One of the reasons for expectancy. The economic costs of these air
doubts are the possible differences in the pollution health impacts are considerable
composition of the pollution mix in the (WHO /EEA, 1997; Maddison, 1998).
European and American cities.
2.1.3. Respiratory allergies and asthma
In combining the information from epide- Outdoor air pollution also plays a role in the
miological studies with the data on ambient aggravation, and possibly the causation of
concentration of main air pollutants, it is asthma and other allergic responses, which
possible to calculate a proportion of health are increasingly prevalent diseases, especially
problems which can be associated with the in children. Approximately 70% of outdoor
exposure (Krzyzanowski, 1997). air pollution penetrates indoors (WHO,
1999a) so that an integrated approach to
The effects of long-term exposure to suspen- both outdoor and indoor air pollution is
ded particulate matter are the most impor- needed. Other key components of indoor
tant health effect of ambient air pollution in pollution which have been associated with
Europe, and are involved in perhaps 41 000 respiratory and allergic responses are dust
to 152 000 extra deaths of respiratory dis- mites, spores from pets, damp, environmen-
eases per year in the EU cities. These effects tal tobacco smoke and NOx from gas ovens.
occur at various concentration levels, includ-
ing concentrations considered as ‘low’ and The prevalence of asthma in children of
reduce life expectancy in middle age people school age varies from 4% to 27% in differ-
(Brunekreef, 1997). The precise magnitude ent parts of Europe. Wide geographical
of the effects of long-term exposure is variation in asthma prevalence is also noted
uncertain, within a wide range of estimates in adults. There is an indication that the
which reflects the weakness of the scientific prevalence rates have increased over the last
evidence available. decade. The frequency of asthma attacks,
sometimes requiring medical assistance or
Short-term variation of population health hospitalisation, has been shown to be associ-
Box 3.10.3. Environment and immunity
There is increasing evidence that the fine ambient and adverse health effects in the individual. There
air particles involved in respiratory and cardio- are apparently large ‘reserve capacities’ in the
vascular diseases impact on health via the immune immune system that can absorb negative effects
system. Other examples of environmental stresses without adverse effects on health. However, for
that have a negative impact on the immune system individuals whose immune response system is
are: already adversely affected by others stresses (e.g.
infections), and for populations that contain
• ultraviolet radiation, which is known to have susceptible people (e.g. the sick and the elderly),
effects on the immune system at doses that are the reserve capacity may not be sufficient to
currently encountered outdoors; prevent adverse health effects, such as allergies
(skin and respiratory), or cancers. Therefore ‘any
• natural and manmade chemicals, for which a deviation from the normal situation is considered
large data base on laboratory animals shows undesirable: this ‘precautionary principle’ point of
effects on the immune system, suggesting that view is aimed at the prevention of adverse effects
chronic exposures to even low concentrations in the population’ (European Commission, 1996).
may potentially have an impact on humans; Small increases in the incidence and duration of
and frequently occurring diseases may have large social
and economic impacts.
• combinations of immunotoxic agents, such as
in food, e.g. natural toxins, heavy metals etc. Further research is needed into identifying bio-
markers that are relevant to adverse health effects,
However, except for allergies resulting from especially in sensitive groups such as children,
sensitisation by pollutants directly, there is little pregnant women, the elderly and people with
information or understanding about the link genetic pre-dispositions to immune system
between negative effects on the immune system impacts.
Source: EEA, based on European Commission, 1996
ated with air pollution levels. However, it is comparability of appropriate data (Box
not clear if environmental conditions can 3.10.4). These problems are common to
cause the onset of the disease or only make both EU and Accession Countries.
the symptoms worse. Moreover, it is not
known to what extent the geographical 2.2.2 Drinking water contamination and some
variation in asthma levels and trends is health effects
related to environmental factors. Diet (e.g. The detection systems across the EU for
less omega-3 fatty acids and antioxidants) or water-borne disease are generally poor and
compromised immune systems (Box 3.10.3) only the larger outbreaks are detected in
are also implicated in the development of practice. Outbreaks affecting less than 10-
asthma. However, current data prompts 20% of the supplied population are rarely
more questions than answers (Strachan, detected. Individual cases of gastrointestinal
1995; UCB, 1997). Figure 3.10.10 in section disease, even if registered by medical care
4 below illustrates the multi-causal chain of systems, are impossible to link directly to
factors implicated in childhood asthma. water quality.
Radon is another indoor air pollutant that is Inadequate microbiological water quality
responsible for several thousand lung cancer and occasional outbreaks of water-borne
deaths a year in the EU, confined to particu- diseases are reported across the EU, even
lar localities where geological formations
give off the radioactive gas into confined
spaces of houses (WHO, 1999a). Box 3.10.4. Problems with data for European assessment of health risks
related to water quality
2.2. Water • Often limited to information on the coverage by services.
Water quality is a significant factor in expo-
sure to health risks. In general, water pollu- • Focused on operational control by water supply agencies and for
compliance assessment by regulatory agencies.
tion has declined in the EU, although con-
cerns remain over localised quality problems, • Limited availability if collected by suppliers from private sector.
and particularly nitrate contamination of
• Not suitable for statistical analysis and international comparisons.
groundwater resources (see Chapter 3.5).
• Different drinking water quality standards resulting in non-comparability of
2.2.1. Quality of water percentage compliance data.
A Europe-wide assessment of drinking water • Different approaches to laboratory analysis and poor inter-laboratory
quality and estimation of related health risks comparability.
faces serious difficulties due to scarcity and
from countries with high standards of supply tially serious, life-threatening disease. How-
(and notwithstanding the often limited ever, the total number of cases of methaemo-
sensitivity of surveillance systems). For globinaemia reported are low and from only
example, 3 to 6 outbreaks of waterborne a few countries, mainly in eastern Europe.
gastro-enteritis have been reported by
Sweden each year in the 1990s (WHO/EEA, Old water distribution systems, using leaded
1998). Contamination of drinking water by pipes, may be a significant source of popula-
faecal coliforms is detected in 1-4% of tion exposure to lead, which, in turn, may
samples analysed in many European coun- affect neurobehavioural development of
tries. Microbiological pollution is especially children (see Section 3.6. below). This
prevalent in small supply systems, and in exposure can be markedly reduced by
some countries private supplies are not adequate treatment of water before its
subject to such stringent standards as public distribution, to reduce the solvency and
supplies. In up to 33% of water samples bioavailability of lead. In Glasgow for exam-
taken from small private water supply sys- ple, effects of exposure-reduction measures
tems in Ireland, faecal coliforms were have been shown (Moore et al., 1998).
present in amounts exceeding the standard Increasing water alkalinity and adding
level in 1995. organophosphate to the water supply re-
duced the concentration of lead (Pb) in
Increasing chemical water pollution from drinking water, which in turn lead to parallel
agriculture is a significant problem in decreases in maternal-blood lead. Part of the
Europe. Nitrate concentrations in observed reduction of lead blood levels is
groundwater are generally low in northern attributed to a decrease of lead exposure
Europe, but high in several western and from non-water sources, such as lead in
eastern countries. petrol, food cans etc.
Increased contents of nitrate pose a risk of Pesticides and their degradation products
methaemoglobinaemia to infants, a poten- are, in some areas, found in drinking water
Box 3.10.5. Pharmaceutical substances in water, sewage etc.
Pharmaceutical substances, like pesticides, are growth promoters in cattle, pigs and poultry can
designed to have a biological effect. As they are lead to increasing antibiotic resistance in both
widely used as medicines, (up to a tonne/day in animals and humans via the food chain (Swedish
some countries) and as growth promoters and Ministry of Agriculture, 1997). For example,
veterinary medicines in animals, their presence in Denmark has a higher frequency of resistance to
the environment may be significant, following enterococci in pigs (55-84%) than does Sweden (14-
human and animal excretion and other routes of 15%) which banned antibiotics as growth promoters
exposure. They have not received much attention, in 1986. The transfer of antibiotic resistance from
partly because exposure levels were thought to be animals to humans is possible but there is as yet little
too low to be of concern. However, as the effects of or no data on the extent of the problem in humans
endocrine-disrupting substances can be observed caused by antibiotics from growth promoters in the
at very low levels, similar levels of exposure to food chain (Edqvist, 1997). However, vancomycin-
pharmaceuticals in the environment may be resistant enterococci (VRE), which are associated
significant for human and ecological health. with the use of avoparcin for growth promotion,
have been identified in non-hospitalised humans
About 70% of antibiotics used in fish farming are who eat meat, but not in vegetarians). There is also a
released into the environment (Schneider, 1994). risk of the development of cross resistance involving
Several studies have identified antibiotics in several strains of bacteria. For example, Feuerpfeil
sediment cores beneath fish farms (Samuelson, found cross resistance in 8 types of microbes. The
1992a; 1992b), in groundwater (Eckel et al., 1993; WHO recommends the reduction in the use of
Hohm et al., 1995; Stan et al., 1994; Feuerpfeil et antibiotics as growth promoters and the EU has
al., 1999), and in manure (Macri et al., 1998). recently (Dec. 1998) banned four antibiotics
(virgianmycin, spiranycin, tysolin phosphate and
Modelling of exposure pathways and potential bacitracin zinc) and is investigating four others.
doses has indicated possible worst-case scenarios However, the evidence on animal growth promoters
of 30 µg/kg for olaquindox and 70 µg/kg for is not clear: the European Federation of Feed
tylosine, two pig-growth promoters (Jorgensen et Additives Manufacturers thinks there is insufficient
al., 1998). Information about possible eco-toxic scientific evidence for an EU ban (Swedish Ministry
effects is rare, though some rather potent effects of Agriculture, 1997).
have been demonstrated for metronidazole and
other antibiotics on green algae (Lanzky and No new chemical class of antibiotics has been
Halling-Sørensen, 1997; Holten-Lutzhoft et al., developed in the past 20 years, despite extensive
1999). There are few, if any, studies on possible research. This provides opportunities for increased
impacts on endocrine or hormonal functions in resistance. It takes at least 10-20 years to find and
either humans or wildlife (Halling-Sørensen et al., clinically test new antibiotics, a time lag within which
1997; Andersen et al., in press). However, there is antibiotic resistance could increase without
increasing evidence that the use of antibiotics as opposition from new drugs.
or in groundwater (see Chapter 3.7). Tri- Tests of recreational water quality Figure 3.10.4
azine herbicides are the pesticides most
frequently detected in groundwaters and
Source: WHO
several countries have introduced bans or % of seawater
100
restrictions on the use of products contain- bathing points 90
complying with
ing the active ingredients. There has been a mandatory 80
significant overall downward trend in the values for
faecal and 70
contamination of groundwater by triazine total coliforms
60
herbicides and their breakdown product in % of freshwater
most countries, although this is not the case bathing sites 50
complying with
with all pesticides (see Chapter 3.5). mandatory 40
levels for
faecal and 30
Data on microbiological quality of recrea- total coliforms
20
tional waters is collected in some countries,
10
principally for compliance assessment by
regulatory agencies. EU Member States co- 0
1992 1993 1994 1995 1996
operate to produce an annual assessment of
bathing water quality but despite many
attempts to collate and compare data from
different locations (nationally or internation-
ally), the quality of such data has severe ing-impaired and hospital patients are
limitations regarding its value in assessing examples of higher risk groups.
hazards to human health, primarily due to
different approaches to analysis and poor Noise affects more than our health and
inter-laboratory comparability. quality of life; it even influences social
behaviour and cognitive development. In
The quality of freshwater sites designated for 1997, studies carried out around Munich
bathing is considerably worse than those of airport found that children exposed to
coastal sites in the EU although the overall frequent aeroplane noise do not learn to
quality trend appears to be improving read as well as other children. Excessive
(Figure 3.10.4). background noise caused the children to
tune out human voices and interfered with
Other low-level contaminants of water may their language acquisition. The psychologists
be a threat to health in some areas (WHO/ who conducted the study speculated that as a
EEA, 1999). result of noise pollution, parents and teach-
ers were also less willing to speak or read
A possibly emerging threat are trace residues aloud.
of pharmaceuticals, including antibiotics
(Box 3.10.5), though there is little data and Community noise needs to be assessed with
few studies available. respect to risks for both human health and
well-being. Intensity, frequency, reversibility
2.3. Noise and avoidability are pertinent criteria for the
Noise can have a variety of effects which severity of noise effects.
depend on the type, duration and timing of
the noise and the susceptibility of the recipi- The knowledge about harmful impacts of
ent (Box 3.10.6). noise exposure has to be transformed into
environmental standards. There is also
Reports from recent scientific research on limited evidence for noise impacts on birth
the precise health effects of nocturnal traffic weight, congenital effects, and the immune
noise reveals that night-time traffic noise not system (Ministère des affaires sociales, de la
only disturbs sleep but also encourages santé et de la ville, 1995). However, esti-
psychosomatic illnesses, shortens the period mated thresholds are available for only a
of deep, dream-rich REM (rapid eye move- limited range of noise impacts for which
ment) sleep, lengthens the phase of light there is more substantial evidence of noise
slumber and may cause cardio-circulatory causation (Table 3.10.1).
problems.
There may be some segments of the popula- 3. Other environmental hazards of concern
tion at greater risk of adverse effects of
noise. Young children, (especially during Besides the recognised and relatively well-
language acquisition), the blind, the hear- understood issues described in the previous
sections, a number of other environmental

Box 3.10.6. Noise: some exposure/effect relationships factors create potential risk for health and
Exposures cause public concerns (Table 3.10.2). In
most cases, the information and scientific
Noise remains a serious environmental problem: estimates of its costs range basis for assessment of the risk is not suffi-
from 0.2 to 2.0% of GDP (Quinet, 1993). It is estimated that about 32% of the
EU population (approx. 120 million people) are exposed to road noise levels cient to confirm or deny the existence of the
over 55 Ldn dB(A) at house facades and that approx. 3 million people are risk. The list of relevant issues is long, and
exposed to aircraft noise (see Chapter 3.12). Perceptions of the various types this section provides selected examples
of transport noise differ between individuals and impacts can depend on the
type of noise, e.g. from rail or aircraft. which illustrate some general points about
the identification and management of
Effects: Public environmental health.
• Annoyance;
3.1. Chemicals and endocrine-disrupting chemicals
• Interference with speech communication; Low doses of some chemicals (EEA/UNEP,
• Sleep disturbance effects (more than ‘awakenings’); 1998) are associated with cancer, cardiovas-
cular disease, respiratory diseases, neurotox-
• Effects on performance and productivity (reading acquisition, learned icity, and chemical sensitivity, with varying
helplessness, etc.);
strengths of evidence, but information about
• Effects on residential and social behaviour (opening windows, use of exposure /effect relationships is often poor
dwelling area, etc.); or non-existent (Box 3.10.8).
• Psychophysiological effects (the stress complex, hypertension, ischaemic
heart disease, aggressiveness, etc.); A broad class of chemicals present in the
environment, such as PCDDs, PCDFs, PCBs,
• Mental health effects (hospital admissions, etc.);
persistent pesticides, some detergents and
• Dose-effect for joint effects (e.g. annoyance + sleep disturbance + some compounds used in the plastic indus-
hypertension?); try, are known to have a capacity to interfere
• Vulnerable groups (children, hearing-impaired). with hormonal regulation mechanisms
(Toppari et al., 1996; EU Scientific Com-
Effects: occupational mittee, 1999). The Weybridge Report (EUR,
• Noise-induced hearing dysfunctions (e.g. tinnitus, temporal threshold 1997) concluded that while there was in-
shifts, deafness, ‘impulse sounds’) creasing evidence about rising trends in
reproductive ill health in wildlife and hu-
Source: EEA
mans, there were still great uncertainties
about the causes of the reproductive ill
health (Box 3.10.7). However, exposure
reduction to endocrine disrupting chemicals
was recommended in line with the ‘precau-
The long-term effects of noise exposure for which
Table 3.10.1. there is sufficient evidence tionary principle’. Since then, reports by the
European Parliament and others have
Observation repeated the call to reduce exposures.
threshold
Effect Situation Noise metric Level in dB (A) Inside/outside 3.2. Chemicals from waste disposal and treatment
Part of the still growing volume of waste
Hearing work Laeq, 8hr 75 inside generated and disposed in Europe is hazard-
damage
ous to health via exposure to hazardous
sport Laeq, 24hr 70 inside chemicals or microbiological pollution.
Hypertension work Laeq, 8hr <85 inside
Several epidemiological studies conducted in
home LAeq, 6-22hr 70 outside the United States have suggested a small
increase in risk of a range of health impacts
Ischaemic heart home LAeq, 6-22hr 70 outside
associated with the hazardous waste landfills,
Annoyance home Ldn 42 outside but a UK review concluded that ‘The epide-
miological evidence that these substances
Awakening sleep SEL 55 inside
represent a cancer risk at much lower
Sleep stages sleep SEL 35 inside environmental levels either does not exist or
is equivocal. However, data on the effects of
Self-reported sleep LAeq, night 40 outside
sleep quality background environmental exposures on
combinations of chemicals is absent, making
School school Laeq, day 70 outside it difficult to assess any health impact result-
performance
ing from relatively small additional expo-
Source: Health Council of The Netherlands, 1994 sures from incinerators (MRC, 1997). A
recently published European study adds to Major health impacts and some
the suspicion that the landfill operations associations with environmental exposures Table 3.10.2.
may contribute to a small increase in risk of
Health impact Associations with some environmental exposures
certain birth defects (Dolk et al., 1998).
However, the present studies are not power- Infectious diseases • water, air and food contamination
• climate change
ful enough to indicate a particular character-
istic of the landfill which may cause a risk, Cancer • smoking and environmental tobacco smoke (ETS)
and a weakness of the exposure assessment • some pesticides e.g. phenoxy herbicides
• asbestos
in those studies makes any causal relation • natural toxins
between disease and landfills difficult to • food, e.g. low fibre, high fat
establish. • polycyclic aromatic hydrocarbons, e.g. in
diesel fumes
• some metals e.g. cadmium, chromium
An analysis of cancer incidence patterns • radiation (incl. sunlight)
around municipal solid waste incinerators in • several hundred other animal carcinogens
the UK revealed that the observed slightly Cardiovascular diseases • smoking and ETS
increased overall incidence of cancers in the • carbon monoxide (CO)
• lead
proximity of the incinerators is related to a • inhalable particles
combination of confounding factors, and • food, e.g. high cholesterol
not to the waste treatment operations (Elliot • stress
et al., 1996). However, the need for a further Respiratory diseases, • smoking and ETS
study on a still unexplained incidence of including asthma • sulphur dioxide
liver cancer in the vicinity of incinerators was • nitrogen dioxide
• inhalable particles
proposed. • fungal spores
• dust mites
Technical requirements of design and opera- • pollen
• pet hair, skin and excreta
tion of waste treatment at such facilities aim at • damp
the elimination, or radical reduction, of the
Skin diseases • some metals, e.g. nickel
risk to population health. Whilst there is a • some pesticides, e.g. pentachlorophenol
decline in population exposure to hazardous • some foods (allergies)
chemicals which may be emitted from incin-
Diabetes, obesity • food, e.g. high fat
erators such as dioxins, the average exposure • poor exercise
of Europeans in industrialised countries to
Reproductive • polychlorinated biphenyls (PCBs)
dioxins is significant in relation to what is now • DDT
dysfunctions
known about their likely effects (see Chapter • cadmium
3.3) which include cancer, reproductive • pthalates and other plasticisers
• endocrine disruptors
disorders, neurotoxicity and heart disease
(WHO, 1997d and 1998 a). Developmental (foetal • lead
and childhood) disorders • mercury
• smoking and ETS
3.3. Climate change and ozone depletion-future • cadmium
burdens? • some pesticides
The potential consequences of climate • endocrine disruptors
change include increases in sea level, more Nervous system • lead
disorders • PCBs
• methyl mercury
• manganese
Box 3.10.8. Breast cancer: an ‘integrated’ • aluminium
disease? • some solvents
• organophosphates
Breast cancer rates are rising in Europe. Some
risk factors are known (genetics and family histo- Immune response • UVB radiation
ry, use of the contraceptive pill etc.) and others • some pesticides
are suggested such as some occupational and
environmental causes, such as pesticides, radia- Chemical sensitivity? • trace amounts of many chemicals?
tion and endocrine-disrupting chemicals but the-
se account for only 30-40% of cases (Kristensen, Note: Most diseases are the result of several causes. These include:
1991; Davis, 1993; Woolff, 1993; Hulka, 1995;
• inherited vulnerability,
Cantor et al. 1995; Rachel’s Environment and
• factors which are related to poverty, e.g. diet, housing quality and location, stress,
Health Weekly, 1997; Wallerson, 1995; McPherson,
alcohol and substances abuse, smoking, low birth weight etc.; work; unemployment;
1994; Hoyer et al, 1998). However, the links with
climate, and
occupational and environmental factors may be
• other environmental exposures arising from air, water, soil and surfaces.
small and the evidence for this is disputed. Dis-
entangling the relative contributions of several The link between environmental exposures and health impacts varies from known causal
factors in an inter-dependent causal chain is relationships such as inhalable particles and respiratory-system damage to suggestive but
always going to be difficult, and prevention calls unproved associations, such as between some cancers and exposure to low levels of some
for an integrated, holistic approach, based on the pesticides. Poor diet plays a key role in the ‘diseases of affluence’, such as cancer, heart and
precautionary principle (Davis, 1997). circulatory diseases.
Source: EEA
impacts will have considerable secondary

Box 3.10.7. The ‘Weybridge Report’ on endocrine disruptors benefits of avoiding shorter term health
There is increasing evidence and concern about rising trends of reproductive impacts from fossil fuel combustion (WRI
ill health in wildlife and humans, and some substances have been implicated, 1997).
but there are great uncertainties about the causes of reproductive ill health.
Key conclusions are: Similarly, stratospheric ozone depletion is

expected to cause increased UV radiation
• Sufficient evidence exists that testicular cancer rates in humans are and thereby increased skin cancer sometime
increasing.
in the next century (Figure 3.10.5). The
• The apparent decline in human sperm counts in some countries was likely relation of UV radiation with some forms of
to be genuine. skin cancer is well-established, though not
• There is insufficient evidence to definitely establish a causal link between always with respect to the specific wave-
the health effects seen in humans with exposure to chemicals. length, exposure-response or individual
susceptibilities. Though the current increase
• The major route of exposure to Endocrine Disrupting Substances (EDS) is
usually by ingestion of food, and to a lesser extent water. It is valid for in skin cancer in Europe (3 to 5% per year
terrestrial animals, birds and mammals, including humans. since the 1960s, for malignant melanoma,
WHO, 1999) seems mostly related to more
• Compared with the situation in the US, there are few cases of
reproductive ill-health in wildlife in the EU where the effects could be frequent sunbathing and other lifestyle
definitely associated with EDS. factors, the depletion of the protective layer
of ozone in the stratosphere will increase the
• However, some cases exist within the EU area where adverse endocrine
effects, or reproductive toxicity, in birds and mammals coincide with likelihood of increased skin cancer in the
high levels of anthropogenic substances shown to have endocrine- future, despite the reductions in the produc-
disrupting properties in some test systems. tion of CFCs and other ozone-layer-depleting
• The considerable uncertainties and data gaps could be reduced by substances. However, the implementation of
research and monitoring into exposure and effects in wildlife and the Copenhagen amendments to the Mon-
humans. treal protocols (see Chapter 3.2) on the
• Current eco-toxicological tests, studies and risk assessments are not banning and phased reduction of ozone-
designed to detect endocrine-disrupting activities. depleting substances has greatly reduced the
future excess incidence of skin cancer.
• Meanwhile, consideration should be given to reducing the exposure of
humans and wildlife to endocrine disrupters in line with the ‘precautio-
nary principle’. Increased UV-radiation also reduces the
Source: European Commission et al. , 1997 response of the immune system (see Box
3.10.3), and causes eye cataracts and other
impacts. It can also be beneficial, by provid-
ing extra vitamin D.
frequent and intensive storms, floods and Environmental-health hazards that impact in
droughts, changes in biota and food produc- the future via long latent periods, such as
tivity. Changes in ecosystems may affect the asbestos and other carcinogens, present
growth, transmission and activity of vector- difficult issues of public health policy that
borne or infectious diseases, such as malaria require considerations other than good
and dengue fever. Human health is likely to science, such as appropriate levels of proof
be adversely affected, either directly or (see section 4). Decisions sometimes need to
indirectly, through complex interactions of be based on ‘early warnings’, which often
ecological systems (McMichael, 1996a, come from the world of work, where expo-
WHO, 1999b). The direct effects may result sures are usually higher and where the
from changes in exposure to thermal ex- monitoring and the identification of impacts
tremes, and be expressed by an increase in is often easier. Any integrated assessment
heat-related disease and death, but also by a therefore needs to embrace occupational
decrease in cold-related disease. Other exposures, which in any case add to the sum
extreme weather events can lead to psycho- of stresses on the body.
logical disorders, disease or death, indirectly
causing an increase in morbidity. Although 3.4. The occupational environment
there are some signs of these climate effects
already beginning to happen, such as shift- ’It is a sordid profit that is accompanied by the
ing geographical range and longer seasons destruction of health’
of some vector born diseases (WHO, 1999 b), — Bernardino Ramazzini, ‘father’ of Occupa-
much of the burden of ill health from tional Medicine, 1713
climate change will be on our children and
grandchildren. However, climate change A full-time employee spends about one-half
policies based on avoiding these health of waking time in the workplace; the other
half is spent on domestic or leisure activities, CFCs, skin cancer and time lags Figure 3.10.5
and one-third of the 24 hours is spent
sleeping. It follows that many environmental
contributions to all health will be found in
and around the workplace. This is why
Bernardino Ramazzini, the father of occupa-
tional medicine, advised doctors to always Average latent
period for
ask their patients: ‘What work do you do?’ skin cancer
Illustrative rates of change (not to scale)

(Ramazzini, 1713). is 30–40 years
A European survey found that 23% of the

EU workforce were absent from work during
the previous 12 months due to work-related
ill health (European Foundation, 1996), and
the WHO has identified a range of occupa-
tional stresses (Box 3.10.9).
The workplace is also an effective place

through which to focus efforts on health
promotion, embracing occupational, 1975 2000 2025 2050 2075 2100
environmental and ‘lifestyle’ factors, such CFC’s production & consumption Increased UV-radiation
at the earth’s surface
Background skin cancer rate
as smoking, alcohol, diet and exercise. The
Ozone depleting substances Estimated additional skin cancer
WHO considers that 30-40% of the total in stratosphere from ozone layer depletion
disease and ill-health burden in Europe can
be tackled effectively through workplace This graph illustrates the approximate time lags between CFC production, the resulting depletion
of the stratospheric ozone layer and subsequent extra penetration of UV radiation and the impact
activity on either occupational factors, or this will eventually have on increasing the background rate of skin cancer, given the 30-40 year
on lifestyle/environmental factors that can average latent period for such cancers. Reality is far more complex than this schematic illustration.
be addressed through employee or em- For example, there are other ozone-depleting chemicals (HCFCs, HFCs and methyl bromide); the
ozone hole varies with latitude, time of the year and meteorological conditions; the increased UV
ployer activity (WHO, 1999a). Occupational radiation varies between different wavelengths and with latitude and cloud cover; and the skin
accidents and ill health cost between 0.4 cancer excess comes on top of a rising background rate of skin cancer, with differential effects on
and 4.0 % of GNP in the EU (EASHW, the different types of skin cancer, such as malignant melanoma and non-malignant skin cancers.
Human behaviour is also a determining effect in skin cancer. Health effects also include cataracts
1998). and immune response suppression. However, the figure illustrates the main relationships and time
lags between CFC production and skin cancer, and the ‘success’ in stopping CFC production and
The monitoring, identification and ‘proof’ averting much more skin cancer from ozone depletion than what is now expected. (Slaper, et al.,
1996).
of the occupational origins of disease are as Source: EEA
controversial as identification of the environ-
mental contributions to ill health. The
Box 3.10.9. The dangerous world of work
‘occupational’ fraction of cancer has been
estimated at 4-5%, or up to 25% (WHIN, The World Health Organisation says:
1998), but as with all diseases that have long
• Some 50 physical factors, 200 biological factors and 20 adverse
time lags (‘latent periods’) between expo- ergonomic conditions, plus an innumerable number of psycho-social
sure and harmful effect, the conditions of factors, have been identified as creating hazardous working conditions.
exposure will always have changed by the These contribute to the risk of occupational injuries, diseases and stress
reaction, as well as to job dissatisfaction and the absence of physical and
time ‘proof’ of causality can be provided, mental well-being.
some 20-40 years after exposure first began.
This then affords opportunities to argue that • The risk of cancer from work and workplace exposure is of particular
concern. Approximately 300-350 different chemical, physical and
current conditions are now harmless, and biological factors have been identified as occupational carcinogens. They
the point can only be ‘proven’ one way or include benzene, chromium, nitrosamines, asbestos, ultraviolet radiation,
the other some 20-40 years later (Box ionizing radiation and aflatoxins. The most common cancers occurring as
a result include lung, bladder, skin and bone cancer and sarcomas.
3.10.10).
• Allergenic factors are also a growing cause of occupational illness. An
Both unemployment, via its link to poverty, estimated 3 000 allergens have been catalogued which can cause
dermatoses and respiratory diseases (e.g. asthma).
alcohol, loss of self-esteem, etc. and
overwork can cause disease and ill health. • Approximately 30-50% of workers in industrialised countries complain
about psychological stress and overload. Such psychological factors have
been associated with sleep disturbance and depression, as well as with
Many environmental diseases are first elevated risks of cardiovascular diseases, particularly hypertension.
identified in the higher exposure, more
easily monitored world of work, e.g. 95% of • Only 20-50% of workers in industrialised countries (with few exceptions)
have access to adequate occupational health services.
the 24 known lung carcinogens and over half
of all causes of cancer were identified in Source: WHO, 1997a
workplace studies, according to the WHO’s
Box 3.10.10. Asbestos and disease 1898-1998: A 100 years of ‘early’ warnings…
An astute observation by a lady factory inspector in The latest study on the extent of asbestos-induced
1898 concluded: ‘The evil effects of asbestos dust deaths ‘in the pipeline’ concludes that some
have also attracted my attention. A microscopic 250 000 men (mainly) will die of asbestos-related
inspection clearly revealed the sharp, glass-like, cancer in western Europe over the next 35 years,
jagged nature of particles and … the effects have following a doubling of the current annual total of
been found to be injurious, as might have been deaths from the main asbestos cancer, mesothelio-
expected’ (ARCI, 1898). ma, from 5 000 a year in 1998 to 9 000 a year by
2018 (Peto et al., 1999). The study was based on
Her fears were confirmed 30 years later. A govern- the cancer registries of six European countries
ment-funded study in 1929 found that one-third of (France, Germany, Italy, the Netherlands, Switzer-
asbestos workers had asbestosis, a form of pneu- land and the UK, which account for 72% of the
moconiosis. By 1955, a study of workers by Sir population of western Europe). Asbestos use in
Richard Doll showed that asbestos also caused lung Europe remained high until about 1980, and as
cancer, and by 1964 other cancers, including the mesothelioma, a cancer of the lung or stomach
most deadly, mesothelioma, were added to the list lining, has a latent period of 30-60 years, deaths
of ‘evil effects of asbestos dust.’ Table 3.10.3 sum- will peak around 2020 and decline slowly over the
marises the history of asbestos as it moved from the following decades.
harmless substance of the 1880s to the recognised
killer of the 1990s, now being responsible for about Workers not directly employed with asbestos, such
10 000 deaths a year in western Europe. Poorly- as electricians, carpenters, plumbers and main-
controlled asbestos use expanded right up until the tenance men, are also at risk. Although the non-
1980s, by which time it had killed thousands of occupational risk from asbestos is very much
people, and condemned thousands of others to die smaller, the possibility of 24-hour exposure, and of
in the next 20-60 years as a result of their past children’s exposure, contributes to a significant risk
exposure. The costs of failing to control asbestos for some ‘public’ groups, e.g. those living in the
early enough are not just health costs – dealing with houses of asbestos workers, where contaminated
compensation and asbestos in buildings is costing clothing has caused mesothelioma in wives, sisters
billions of pounds and was partly responsible for the and children and those living and playing in the
bankruptcy of some Lloyds insurance underwriters in streets near asbestos plants (Camus et al ., 1998).
the early 1990s.
Although there have been ‘early warnings’ about
asbestos for 100 years, effective preventative
measures were not taken until it was too late to
Table 3.10.3. stop deaths ‘in the pipeline’ of the latent period.
And even accurate monitoring of mesothelioma,
Exposed group Asbestosis Lung cancer Mesothelioma lung cancer and of their relationship (which may be
cancer 1:1 or 1:3 or 4) is still poor. ‘It is unfortunate that
the evolution of the epidemic of asbestos-induced
Occupational mesothelioma, which far exceeds the combined
effects of all other known occupational industrial
Workers (1898-1929) 1955 1960s carcinogens, cannot be adequately monitored.’
(Peto, 1999).
Mates 1964 1964 1964
Smoking and asbestos together have a strong
Environmental synergistic effect causing a 50 fold excess of lung
cancer while their separate effects are ‘only’ a 10
Relatives 1960s ? 1960s and five-fold excess for smoking and asbestos
respectively (Hammond, 1979).
Public ? ? 1980s
Synergy from smoking and other pollution is not
Note: Asbestos also causes other cancers, e.g. cancer of the larynx confined to asbestos. The WHO (1998b) has
concluded that smoking and other workplace
contaminants can also act together to ‘amplify the
Source: EEA based on Gee, 1995 severity of adverse effects beyond what could be
expected from smoking or the toxic hazard alone’.
International Agency for Research on Recommendations on balanced diets have

Cancer. Many ‘early warnings’ of environ- been available for many years (Figure 3.10.6).
mental health hazards will therefore con- However, advice can vary, depending on
tinue to come from workplace studies scientific knowledge. Poor consumer labelling
(Wegman, 1996). For example, the potential can make it difficult to make the right choice,
human health effects of non-ionising radia- assuming the consumer already has physical
tion were first identified in occupational and financial access to healthy food. Contami-
studies (Box 3.1.11). nation with chemicals, such as antibiotics and
pesticides (Box 3.10.12) can diminish some of
3.5. Diet the value of healthy eating, but, as with breast
Healthy eating plays a crucial role in disease feeding when the milk may be contaminated
prevention. For example, in addition to with very low levels of dioxins or PCBs, the
genetics, occupational and environmental other benefits of a healthy diet usually over-
factors, diet plays a key role in cancer causa- whelm the costs from micro-contaminants.
tion, perhaps 30-40% of all cancers. Achieving a healthy diet and contaminant-
Box 3.10.11. Electromagnetic fields: an emerging occupational, environmental and consumer hazard?
The World Health Organisation (WHO) has said that The group voted 19-9 in June 1998 that
research into possible adverse health effects of electromagnetic fields should be regarded a
electromagnetic fields (EMF) should be a priority potential cause of cancer, using the International
for the next four years. Agency for Research on Cancer criteria for
cancirogenicity.
The WHO’s EMF project will be co-ordinating and
encouraging research into the possible associations Eight members said that, because of conflicting
between low-frequency EMF (less than 300 Hz) and studies, they could not decide whether electrical
childhood leukaemia, breast cancer and diseases of fields were potential cancer causes. One said they
the central nervous system. probably were not.
WHO also recommended further research into The new finding is at odds with a 1996 report by a
possible associations between exposure to radio National Research Council panel of scientists who
frequency fields (300 Hz – 300Ghz) and leukaemia/ evaluated about 500 studies on the health effects
lymphoma and brain and cancers. of high voltage power lines and found ‘no
conclusive and consistent evidence’ that electric
Dr Paul Kleihues, Director of WHO’s International and magnetic fields cause any human disease.
Agency for Research on Cancer, has observed that, Studies of the incidence of disease analysed by the
‘with an estimated 15 million new cancer cases new NIH group found a slight increase in childhood
each year by the year 2020, we must know if leukaemia risk for children whose homes are near
exposure to EMF is contributing to any significant power lines and an increase in chronic leukaemia in
extent to the incidence of disease’. adults working in industries where they are
exposed to intensive electric fields.
The controversial theory that electric fields like
those around power lines can cause cancer has The group said that there wasn’t enough evidence
received some support from a National Institute of to link household exposure to power lines to cancer
Health scientific panel in the US. ‘This report does in adults, or to associate electromagnetic fields to
not suggest the risk is high’, and ‘The risk is such diseases as Alzheimer’s, depression and birth
probably quite small compared to many other defects.
public health risks’, said Michael Gallo, chairman of
the group and a professor at the university of They found no evidence of abortion from video
Medicine and Dentistry of New Jersey-Robert display terminals and no evidence of illness other
Wood Medical School, Pistacaway. than leukaemia in children (WHIN, 1998).
The report comes from a National Institutes of

Environmental Health Sciences panel convened to
review scientific research on electromagnetic fields.
free food and drink may be possible if both Healthy eating Figure 3.10.6
sustainable agriculture and the reduced use
and exposure to hazardous chemicals are
Source: CECHE, 1998
pursued in an integrated approach to ecologi-
cal and human health. Fats, oils
and sweets:
25g
Milk, yougurt Meat, poultry,

and cheese fish, dry beans,
Box 3.10.12. Lindane safety re-assessed group: eggs and
100g nuts group:
A re-assessment of the organochlorine 150-250g
insecticide lindane has concluded that consumer
safety limits can be exceeded by over 12 times. Vegetable Fruit
group: group:
The joint FAO/WHO Food Standards Programme 400- 100-200g
500g
Codex Committee on Pesticide Residues has set
a more stringent acceptable daily intake (ADI) for
the insecticide lindane of 0.001mg/kg body
weight.
For a 60 kg adult, therefore, the maximum daily

dose should not exceed 0.06 mg in total. The
ADI is the amount of pesticide that can be
consumed every day for a lifetime without harm. Bread, cereal, rice and pasta group: 300-500g
Codex data discussed at a recent meeting shows

that any person consuming an average local diet
in any region of the world could theoretically
exceed the ADI for lindane by between 3.8 and
12 times if foods containing the maximum
lindane residues were consumed.
Source: FAO/WHO, IN WHIN 1998

3.6. Children that the benefits for breast-feeding outweigh

As has been seen with several health hazards the risks of pollutants in breast milk
(air pollution, noise, skin cancer, allergies (Weisglas-Kuperus et al., 1996; WHO, 1996b).
etc.) children can be particularly sensitive to
environmental stresses. They are a Children may be particularly at risk from
‘biomarker’ for environmental threats that chemicals because of their greater biological
require special protection, not only because sensitivity and greater exposure to environ-
they are more at risk but because they can mental pollution relative to body weight
also provide early warnings of hazards to (NRC, 1993; McConnell, 1992; Bearer, 1995).
others, as well as being effective points of Their physiological and intellectual develop-
intervention for the prevention of disease in ment may be impaired by exposure to chemi-
their later lives. cals (Rodier, 1995; Rylander et al., 1995;
Jacobson 1996; Grand Jean et al., 1997). Low-
Chemical pollutants that may affect reproduc- level pesticide contamination of food (infants
tive health and new-born children include consume eight times more food per kilogram
certain metals (e.g. lead and methyl mercury; of body weight than adults, making this a
Box 3.10.13), pesticides (e.g. DDT), industrial more significant exposure pathway; CICH,
chemicals (e.g. PCBs), solvents and other 1997), and of residential surfaces and toys in
substances (Foster and Rousseaux, 1995; the UK and US, is being reported (Pesticides
CJPH, 1998). Exposures can occur through Trust, 1998; Gurunathan et al., 1998). Some
placenta and breast milk (Jensen, 1996; regulatory authorities are giving special
Rogan, 1996), and some may cause small attention to the higher levels of risk to chil-
abnormalities of the immune response dren from pollution (USEPA, 1996). For
system. However, WHO and others conclude example, the Food Quality Protection Act in
Box 3.10.13 Children and lead
‘Lead makes the mind give way.’ • At low levels, i.e. 10-25 µg/dl (indicating the
— Greek physician, 2000 BC amount of lead in a tenth of a litre of blood)
lead poisoning in children causes:
• Lead is brought into the environment through
human activities in 300 times greater amounts - reduction in IQ and attention span;
than through natural processes (Unicef, 1992).
- reading and learning disabilities;
• People, particularly children, may be exposed
to lead from car emissions through leaded - hyperactivity and behavioural problems;
petrol, water contaminated by lead pipes,
some factories (e.g. metal polishing and smel- - impaired growth and visual and motor
ters; old paintwork in houses), contaminated functioning; and
soil (e.g. nurseries built on old petrol station
sites), certain cultural practices (e.g. use of folk - hearing loss.
medicines containing lead), use of improperly
glazed lead ceramic ware for cooking and food • Exposure to these levels in maternal and
storage, and use of lead-contaminated umbilical-cord blood is associated with low
cosmetics such as surma and kohl. birth weight and prematurity. The body can
store lead for more than 20 years and then
• Children absorb up to 50% of lead taken into release it during pregnancy, harming the
their bodies, compared to 10-15% in adults. foetus (lead can move across the placenta with
Children may receive three times the dose of ease).
adults because they have a larger surface-to-
volume ratio. • At higher levels, i.e. 60-100 µg/dl, lead
poisoning in children causes:
• Lead in dust and dirt can be ingested via
children’s hands and toys, for example by - anaemia; and
thumb-sucking or by putting objects in their
mouths. - brain, liver, kidney, nerve and stomach
damage.
• Even in the world’s most developed countries,
it is estimated that a large proportion of • According to the World Bank, countries can
children suffer from lead poisoning. It is the save five to ten times the cost of converting to
most common, chemical-related, environmen- unleaded petrol in health and economic
tal child health problem. It is especially savings due to reduced health costs, savings
pronounced in economically-disadvantaged on engine maintenance and improved fuel
sections of the population. Poverty can cause efficiency.
malnourishment or physical stress, which
intensifies disabilities caused by lead
absorption.
Source: UNEP and UNICEF, 1997

the US requires the government to add an • are exposure or effects avoidance meas-
extra margin of safety to the risk assessment ures available, and actors identifiable
of chemicals that children may be exposed to. and willing to take action,
• the cost and benefits of action and
Cancer in children in the US appears to be inaction, and their distribution between
increasing (Pogoda, 1997; EHP, 1998; classes, races, sexes, the regions and
Rachel’s EHW, 1998), and a large-scale study generations,
of childhood leukaemia and other cancers in • how uncertainties are to be handled ,
the UK has found them to be associated with • how informed consent and public
living close to industrial plants, particularly involvement in ‘acceptable risks’ can to
where fossil fuels were being used or proc- be achieved,
essed (Knox and Gilman, 1997). • and how the consequences of action/
inaction are to be evaluated?
4. Approaches to environment and health The answers to these questions require good
information for effective decision-making,
4.1. Multifactoral causes of disease but in practice, a lack of data, information or
As has been seen in earlier sections much ill understanding, or disagreements about the
health and many diseases are multifactoral interpretation of the information can lead to
(Figure 3.10.7). Identifying the causes of ill delays in preventing public ill health. For
health in populations is therefore very diffi- example, one of the main weaknesses of
cult and quantifying the contributions of animal evidence is the difference between
environmental exposures to adverse health the healthy young rats used in experiments
impacts is even more so, particularly at the (which breathe through the nose) and a
level of the individual. Adverse health impacts population of mixed age and health status
are the results of varying combinations of host humans, who partly breathe through their
genetics, host state (including ‘lifestyle’ mouths. These three differences (age, health
factors such as smoking, alcohol, diet parents status and mouth-breathing) are the main
etc.) and exposures to other environmental reasons why experts ‘dramatically’ under-
stresses, both indoors and outdoors. All these estimated the health impacts on humans of
factors can operate at different times, influ- fine particles in air pollution in 1987 com-
encing each other in various ways, and pared to 1997 (WHO, 1997b).
causing changes in cells, tissues and functions
that may or may not lead to adverse health The level of proof used in decision-making is
impacts. The same ‘dose’ of air pollution for crucial, and it can vary from very high to low,
example does not have the same impact depending on the issue being addressed. For
because of differences between people, with ‘sound science’, a high level is required,
sensitive groups, such as the elderly, the sick
children, and pregnant women responding
more than less sensitive groups. The same
‘exposure’ may not lead to the same ‘dose’ Multifactoral disease causation Figure 3.10.7
because of biological and activity differences,
e.g. children and joggers who have higher
breathing rates. Host Host Exposures/ Doses Effects Harm
+ state + = =>
genetics
Several key questions need to be addressed
- genotypes - nutritional - multiple Exposures/ - initiating - infections.
in dealing with environmental health issues: and status Doses - promoting - cancers
phenotypes (diet) - via several exposure - retarding - CNS damage
- immune routes (skin, inhalation, - suppressing - respiratory.
• what is the nature and strength of the status ingestion) - causing: - circulatory.
(infections) - environmental - indoor - changes in: - reproductive.
evidence for an adverse impact and for - health - environmental - outdoor cells, tissues, - developmental
- occupational organs, - other adverse
the role of the environment in that status
(lifestyle) - low and/or peaks - functions; health impacts
impact, - age - can be 24 hours - shifts in
continuous "normal"
• what is the nature of the impact (trivial - or single dose at critical distributions
time of bio-
or serious, reversible or irreversible, - pre- and post-natal functions,
immediate or long term, large or small - lifetime and cumulative etc
"target" organ dose
numbers affected etc.), - biologically effective
dose
• what level of proof is to be used in - often unknown
making a decision, particularly about etc…
whether an association between an

environmental stressor and an adverse
impact is actually causation (Box 3.10.14), Source EEA:
such as ‘beyond all reasonable doubt’. This

Box 3.10.14. Association and causality means that the costs of being ‘wrong’ in
It is often fairly easy to show that a measure of ill-health, e.g. the number of failing to reach the high level of proof (such
admissions to hospital per day, is associated with a possible cause, such as as new and correct, scientific hypotheses
the day-to-day variation in levels of air pollutants. To show that a causal being initially dismissed, called ‘false nega-
relationship exists, a number of guidelines or tests have been developed.
These include the consistency of results between different studies, the way in tives’), is considered by society to be less
which the results of different studies fit together (coherence); whether there is costly than being ‘wrong’ in the other
a ‘dose-response relationship’ between the proposed causal factor and the direction when using a lower level of proof
effect; and whether the sequence of events makes sense, i.e. the cause always
preceding the effect. i.e. the ‘false positive’ of incorrect scientific
hypotheses being accepted as correct.
Proof of causality is often very difficult, but by the application of these and Similarly, in criminal trials, where the ‘cost’
other criteria, an expert judgement as to whether an association is likely to be
causal can often be made. Where effects are likely to be serious and/or of being wrong in one direction i.e. innocent
irreversible, then a low level of proof, as in the ‘precautionary principle’, may people being jailed (or sometimes ex-
be sufficient to justify action to remove or reduce the probable causes (EEA/ ecuted), is regarded as being worse than
WHO, 1997).
being wrong in the other direction (i.e.
guilty people going free), a high level of
proof is also used.
For other purposes in society, such as com-

pensating injured people through the
Box 3.10.15 Precaution courts, a lower level of proof, such as ‘the
balance of probabilities’, is generally used.
This principle featured in the 1992 Rio In this case society considers that the costs of
Declaration on Environment and Development
(as Principle 15): being ‘wrong’ in reaching the lower level of
proof, i.e. the ‘false positive’ of compensat-
‘In order to protect the environment, the ing injured people for injuries that were not
precautionary approach shall be widely applied
by States according to their capabilities. Where caused by the negligence of others, is less
there are threats of serious or irreversible costly than being ‘wrong’ in the other
damage, lack of full scientific certainty shall not direction, i.e. the ‘false negative’ of not
be used as a reason for postponing cost-effective
measures to prevent environmental degradation.’ compensating people for the injuries that
were caused by the negligence of others.
The precautionary principle permits a lower level Another example of the use of a low level of
of proof of harm to be used in policy-making
whenever the consequences of waiting for higher proof, or probability, is disaster insurance
levels of proof may be very costly and/or where the cost of being wrong when no
irreversible; the UN Intergovernmental Panel on disaster happens is generally considered
Climate Change recently used the precautionary
principle in concluding that ‘the balance of more acceptable than the cost of being
evidence … suggests a discernible human wrong in the other direction, i.e. where no
influence on global climate’ (IPCC, 1995). insurance premiums are paid and disaster
strikes. ‘It is better to be safe than sorry ‘ is
the popular expression of this sentiment.
For public health policy-making, where there

may be serious and irreversible health
impacts, the use of a lower level of proof
Figure 3.10.8 Strategies: points of intervention than used in good science is recommended
in various international agreements, via the
‘precautionary principle’ (Box 3.10.15).
Possible strategies for avoiding, reducing and compensating harm...
4.2. Integrated approaches to prevention

Host Host Exposures Effects Harm
genetics state The multi-causal disease process also offers
several points at which strategies for avoiding
Genetic Improve Reduce? Predict? Cure? reducing or compensating harm can be
engineering? nutrition?
Eliminate? Identify Compensate? focused (Figure. 3.10.8). However, identify-
Remove Promote earlier?
’sensitive‘ good health? Clean up? ing and implementing the most effective
groups from Stop/slow
exposure? Vaccinate? progression Learn from strategy is difficult, and involves questions of
to harm? ’mistakes‘?
feasibility (technical, economic and practi-
Warn?
cal), cost-effectiveness and ethics. Responses
can also be focused on the individual (behav-
...but which strategies would be most effective?
iour change or medical intervention), or at
the community and its environmental
Source: EEA exposures. When the response strategy is
focused on reducing exposures, say to traffic Transport: multi-causality in transport hazards Figure 3.10.9
fumes, there are many points of policy
intervention, involving both ‘upstream’, e.g.
the ‘driving forces’ of transport policy, and Driving Transport policy
force relying on car
‘downstream’, e.g. noise barriers (Figure transport
3.10.9). In general, strategies-focused ‘up-
stream’ will be more effective than those
focused ‘downstream’, partly because of the Pressure Increasing car Emmisions of air Noise emissions
density pollutants from roads
need to take an integrated approach that
embraces the linkages between different
parts of transport policy. An integrated
approach will also take into account the full State Conflicts Air concentration Noise levels
Action
between cars of lead NOx etc. in community
range of benefits and costs of policy re- and pedestrians
Road quality
sponses, and allow for adaptation to a
modified transport system. For example,
policies designed to reduce air pollution Exposure Time spent Personal Time spent
in hazardous exposure, e.g. in noisy
from traffic by reducing traffic volumes will situations Blood lead environment
particles,irritants
also yield substantial benefits from reduced
noise, accidents (Box 3.10.17), congestion,
less divided communities and increased Effect Motor vehicle Effects on Noise
accidents respiratory disturbance
freedoms to play, walk and cycle in safety. and injuries systems;
lead poisoning
Such holistic approaches can help counter
the common ‘tendency to over-estimate the
costs and under-estimate the benefits’ of Source: WHO
policy action (WHO, 1997c).
be the most important ‘social intervention’
There may also be differences between cause, given the secondary benefits of a
causes of ill health that are most important reduction in traffic growth, and the impact
from a scientific point of view, and causes of removing one link in a multi-causal chain.
that may be most important from a policy
response point of view. Figure 3.10.10 In practice, given the multi-causal nature of
illustrates the differences between ‘scientific’ diseases like asthma, policy responses are
and ‘social intervention’ causes in multi- needed in several areas: single cause ap-
factoral disease processes, such as asthma in proaches can not reduce more than a
children. Whilst genetic pre-disposition, proportion of disease. Integrated ap-
respiratory hyper-sensitivity from pre-natal proaches to prevention (BMA, 1998) and
exposures, diet or indoor air pollution from hazard exposure reductions, as well as more
damp or mites, may be the most important research on the links between environment
scientific causes of asthma in children, the and health (ESF, 1998) are needed to
relatively minor role of traffic pollution may achieve improved health and wellbeing.
Box 3.10.17. Traffic accidents
Road traffic accidents are 1.4% of all deaths (some Pedestrians account for around 13% of casualties
45 000 deaths in 1994 in the EU) and 20% of all (dead and injured) and 22.5% of deaths by road
accidental deaths in the European Region of WHO. traffic accidents in the 26 countries of the ECMT.
About 1 in every 3 deaths involves people younger Pedestrians report the second highest number of
than 25 years. Due to the high proportion of young fatalities among road users in all OECD countries,
victims, it is estimated that on average people with the exception of the Netherlands, where
killed in traffic accidents die about 40 years earlier cyclists account for more fatal accidents than
than their life expectancy. pedestrians (OECD, 1998).
From 1993, it appears that the decreasing trend is Cyclists are more likely to have an accident than
levelling-off, especially in western countries, where other road users and they will sustain a greater
there has been little progress in achieving a further proportion of head injuries than other road users
reduction in mortality over the past few years. (OECD, 1998). At least two-thirds of the cyclists
killed in accidents had head injuries which
The reduction in the number of fatalities has not contributed to or resulted in death. However, both
been paralleled by a proportional reduction in the cycling and walking have very beneficial health
number of traffic accidents with injuries, which effects. WHO estimates that half an hour’s walking
since 1993 have increased slightly. and cycling a day could reduce the prevalence of
heart disease, obesity and diabetes by 50% (WHO,
More pedestrians are killed per 1 000 accidents March 1999, press release).
with injury than other road user categories.
Scientific causes and social

Figure 3.10.10 intervention causes for childhood asthma
Source: EEA
Illustrative* toxicological ’causes‘ of childhood asthma in an Illustrative ’social intervention‘ causes and related actions
average population
Host Exposures Harm
Host Host Exposures Harm state + =
genetics + state + =
25% + 25% + 50% = 100% e.g. Indoor

• Nutrition e.g.
e.g. e.g. 30% indoor e.g. advice
and • Mite
Allergic Nutritional e.g. Asthma supple- elimination?
sensitivity and in some ments?
immune • Mites 10% children • Eliminate
status • Avoid damp?
• Pets 5% immune
sup- • Stop
• Passive pressants smoking?
smoking 5%
• Switch fuels?
• NOX 5%
• Ban pets?
• Damp 5%
Outdoor
20% outdoor
e.g.
e.g.
• Avoid/reduce
• Pollen 10% pollen?
• Industrial • Avoid/reduce
pollution 5% traffic
pollution?
• Traffic
pollution 5% • Avoid/reduce
industrial
pollution?
* Percentages are only illustrative contributions to the casual chain: but research
supports the broad percentage contributions (Swedish EPA, 1996). Particular
combinations of causes e.g. Pets and damp/passive smoking can produce greater
contributions than others such as pets and air pollution.
… ’Reducing traffic pollution‘ may be the most effective
social intervention cause/action given:
‘Allergic sensitivity may be the most important single
scientific cause in the multi-factoral chain of causation but ‘... • Less dependence on individual behaviour change
• Cost effectiveness
• More equitable cost sharing
• Largest supplementary gains e.g. reduced traffic
congestion and accidents
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press), World Health Organization, Regional Ofrice for
Europe, Copenhagen.

3.10. Human Health Issues: The Environment Is Everything Which Isn't Me.' - Albert Einstein

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Human health issues 263

3.10. Human health issues

Identifying cause-and-effect relationships is therefore very difficult, especially if the impact

1. Introduction early 1990s when environmental issues were

ing life, through the provision of food, water

and shelter, but also through the less visible 60

However, people feel very concerned about

the links between their environment and

their health, and more so now than in the

mental policies (Box 3.10.1). However,

2.1. Air pollution

2.1.1 Exposure of European population to

Host Host and Harm

Box 3.10.2. Scope of the chapter

Concentration of lead in ambient air has

Box 3.10.3. Environment and immunity

Source: EEA, based on European Commission, 1996

Box 3.10.5. Pharmaceutical substances in water, sewage etc.

sections, a number of other environmental

impacts will have considerable secondary

Key conclusions are: Similarly, stratospheric ozone depletion is

Illustrative rates of change (not to scale)

A European survey found that 23% of the

The workplace is also an effective place

International Agency for Research on Recommendations on balanced diets have

The report comes from a National Institutes of

Milk, yougurt Meat, poultry,

For a 60 kg adult, therefore, the maximum daily

Codex data discussed at a recent meeting shows

Source: FAO/WHO, IN WHIN 1998

3.6. Children that the benefits for breast-feeding outweigh

Box 3.10.13 Children and lead

Source: UNEP and UNICEF, 1997

whether an association between an

such as ‘beyond all reasonable doubt’. This

For other purposes in society, such as com-

For public health policy-making, where there

4.2. Integrated approaches to prevention

Box 3.10.17. Traffic accidents

Scientific causes and social

25% + 25% + 50% = 100% e.g. Indoor

References CJPH, 1998 in press. Proceedings from the CICH Con-

WHO, 1997b. Update and Revision of the WHO Air

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