3.10. Human health issues - European Environment Agency

263Human health issues

3.10. Human health issues

The environment in which people live, work and play is an important determinant ofhealth and well-being, but the extent of its importance in developed economies isdifficult to quantify.

The most common diseases in the EU – heart and circulatory diseases, cancer, respiratorydiseases, 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 impactof 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 biologicalmodels that connect them. Therefore considerable uncertainty surrounds many issues ofconcern, 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, particularlywhere the impacts may be serious, large-scale and irreversible – circumstances whichmerit the use of the precautionary principle. Preventive action on many of theenvironmental hazards covered in this chapter is being taken, but more integrated andeffective action is being proposed to reduce threats to health and well-being.

Main findings

1. Introduction

‘The environment is everything which isn’t me.’— Albert Einstein

People are at the centre of ‘their’ world, asEinstein observed, but they are also part ofthe environment, and play a significant rolein shaping it, as Chapter 2.1. and otherchapters have shown. But the relationship isnot just unidirectional: the environment‘shapes’ people by the impact it has on theirhealth.

This is not just in the obvious ways of sustain-ing life, through the provision of food, waterand shelter, but also through the less visibleimpact it has on genes, cells, organs andbiological systems which together can causedisease. In the more developed economies –such as the EU – where basic supplies ofclean water and sewage facilities are gener-ally available, environmental impacts onhealth are often less obvious – and moreinsidious – than in developing countries.However, people feel very concerned aboutthe links between their environment andtheir health, and more so now than in the

early 1990s when environmental issues weremuch higher on their and the media’sagenda (Figure 3.10.1). Politicians havereflected this concern and declared thathuman health is a key objective of environ-

Poland

Hungary

Spain

United

Kingdom

Fran

ce

Finlan

d

Germ

any

% o

f res

po

nden

ts

0

40

60

20

Greec

e

80

100

Italy

19981992

Source: EnvironicsInternational, 1998

Figure 3.10.1Opinions: Proportion of respondents who believe

environmental problems affect their health agreat deal/fair amount in 1992 and 1998

Environmental Issues264

mental policies (Box 3.10.1). However,unravelling the less obvious connectionsbetween the environment and health indeveloped economies is not easy.

Damage to health is the result of manyfactors acting in various combinations, overdifferent time periods, to a diverse range ofpeople, of varying sensitivities, and at differ-ent stages of their lives (Figure 3.10.2).Understanding the complexities of whatcauses ill health is clearly going to be diffi-cult – and, very often the more we know, themore we realise what we don’t know. It is notsurprising, therefore, that scientific andpublic controversies over environment andhealth have been or are currently commonwithin scientific and public circles (e.g.leaded petrol and brain damage in children,or antibiotic growth promoters in animalfeed and increased human resistance toantibiotics). Public policy decisions onenvironmental hazards (potential damage)and risks (probable damage) are difficult tomake and evaluate. However, understandingthe types of information needed for environ-mental health decision-making (as well as itsuse and limitations) will contribute to awider appreciation of the reasons for publicconcerns, differences in expert opinions andthe action (or inaction), of governments.

Environmental stresses for which there arereasonably good exposure and effect dataare estimated to be a major factor in anestimated 5% of disease, according topreliminary report prepared for the WHOon the basis of Dutch data (WHO, 1999a; De

The environment should be regarded as a resourcefor improving living conditions and increasing well-being (Frankfurt Conference, WHO 1989).

Human beings are at the centre of concern forsustainable development. They are entitled to ahealthy and productive life in harmony with nature(Earth Summit, Rio de Janeiro, UNCED 1993).

We have a shared goal before us: to improve theliving and health conditions of the presentgeneration, to ensure that the carrying capacityof nature is not exceeded and that the right ofthe future generations to a satisfying andproductive life is safeguarded (HelsinkiConference, WHO 1994).

Box 3.10.1. Health and the environment:key declarations

Hollander et al., in press). The main compo-nents of this environmental fraction are:external air pollution, which accounts formost of the total environment related healthloss in the Netherlands (in terms of reducedlife expectancy, the quality of life andnumber of people affected); environmentalnoise and indoor air pollution, includingradon, damp and environmental tobaccosmoke. Lead in drinking water is also signifi-cant. Traffic and domestic accidents, whichtogether would bring the total environmen-tal fraction of disease causation from 5% to12% are very important public healthhazards, but are not normally considered asenvironmental health issues.

2. Some dominant environmental healthissues in Europe

2.1. Air pollutionAtmospheric pollution is a major cause ofexposure to substances which are hazardousto health: the causes and effects of airpollution are discussed in chapters 3.3 and3.4.

2.1.1 Exposure of European population to ambient air pollutantsExposure data on suspended particulatematter is poor and is still measured bydifferent methods throughout Europe, andthe measurements of size-fractionatedparticulate matter of health relevance (PM10or PM2.5, i.e. particles up to 10 and 2.5microns in size respectively) has beenintroduced in only a few countries. Thisscarce data has to be extrapolated whichincreases the uncertainty of the analysis.Therefore the estimates presented belowprovide just an indication of the possiblemagnitude of the effects (Figure 3.10.3).

Environmental factors (e.g. overcrowding, diet, climate, stress) and exposures (e.g. from air,food, drink, surfaces) play a part in causing and/or aggravating disease and ill health, bothdirectly and via parents.

Source: EEA

Parents Mother

Indoorandoutdoorexposures

Evironmental

Adult

Ad

ult

Chi

ld

Factors and exposures

=

Child

HarmHostState

Foetus Infant

HostGenetics

Foetus

Figure 3.10.2Environment, people and health:some key relationships


Box 3.10.2. Scope of the chapter

The scope of this chapter, which summarisessome key environmental health impacts, islimited to a selection of those environmentalstresses to which people may be exposed athome or out of doors, and which illustrates arange of health impacts and knowledge abouttheir links to the environment. The selectedinformation presented is designed to illustratesome general points about the links betweenenvironment and health, rather than being acomprehensive review of the literature, which isbeyond the scope of this chapter. Where theissue is very well covered in other publications,such as climate change (WHO, 1999b), relativelylittle space is devoted to it.

The chapters on waste, hazardous substances,transboundary air pollution, climate change,stratospheric ozone, urban areas and water stressprovide background information on the drivingforces, pressures and associated exposures thatare linked to health problems.

This chapter does not cover occupationalimpacts on health in much detail, despite itssignificant influence on public health. Fully

integrated approaches to health need to includepotential stresses from all parts of the environment.This is not only because human lungs and livers donot discriminate between pollutants that comefrom the factory or the street. but also because thesum of the exposure to stresses from all sourcesmay be either additive, synergistic (more than thesum of the parts) or antagonistic (less than the sumof the parts), and therefore need to be included inany integrated assessment of environmental healthrisks (La Dou, 1998).

Knowledge of the distribution of environmentalhealth impacts between e.g. social groups,geographical areas and generations is critical forundertaking fully integrated assessments, but apartfrom a few references to geography, age, class andfuture generations, these equity issues are beyondthe scope of this chapter (Luhmann et al., 1998).

A more comprehensive view of this field is availablefrom the report ‘Overview of Environment andHealth in Europe in the 1990s’ prepared by WHOfor the 3rd European Conference on Environmentand Health held in London in June 1999 (WHO,1999a).

Over 24% of EU urban residents live in citieswhere the annual mean concentration ofparticulate matter (SPM) exceeds 30 µg/m3.In the eastern part of Europe for which thedata was available, close to 90% of the popula-tion live in cities with such relatively highconcentration of particles. Trends in SPMwere better in EU countries than in the rest ofEurope, with 35% of people in EU experienc-ing more than a 5% per year reduction inSPM levels (21% in central Europe) and only12% experiencing a more than 5% per yearincrease in SPM concentration (27% forcentral Europe) (for further information onurban air pollution, see Chapter 3.12).

Most of the population of Europe now livesin cities with low or medium concentrationsof SO2. In EU, 97% of urban residents haveenjoyed reductions in SO2 concentrations,whereas in the central part of Europe,almost of 20% of urban residents experi-enced increasing concentrations of SO2.

More people in the western cities wereexposed to medium and high levels of NO2

than in central Europe. However, the trendswere mostly stable (for 60% of urban resi-dents) or decreasing (15%) in the EUcountries, while NO2 concentration in-creased for 43% residents of cities in centralEurope.

Concentration of lead in ambient air hasbeen decreasing over the recent decade,mainly due to the phasing out of lead from

Low Medium High

West East West East West East

SPM SO2 NO2

0

10

20

30

40

50

60

70

80

90

100

% o

f urb

an p

op

ulat

ion

Figure 3.10.3Exposure to common air pollutants

Data on concentration of themost commonly-monitoredair pollutants (suspendedparticulate matter, SO

2 and

NO2) is shown for 1995 or

later.

In total, information on oneor more pollutants isavailable from 110 cities in24 countries, including 64cities in 13 EU countries withclose to 58 million residents.

Source: EEA-ETC AQ andWHO/ECEH

petrol. Several ‘hot spots’ were still observedin eastern Europe at the end of 1980s,mainly due to the poorly controlled emis-sions from industrial point sources. Monitor-ing data indicates that relatively high leadconcentrations were also measured in theproximity of busy roads in several large citiesin western Europe (Zaragosa, Toulouse,Lyon) in the early 1990s. More recent dataindicates that concentration of lead inambient air was decreasing even in thosehighly-polluted locations in the 1990s.


2.1.2. Estimates of health impacts of some ambient air pollution in the EUThe most common of the well-known airpollutants (suspended particulate matterand ozone) are associated with ill healtheven at relatively low concentrations of thepollutants frequently experienced by peoplein Europe. This observation comes from anumber of studies on the effects of dailychanges in pollution levels conducted inmany parts of the world, including Europe,as well as from a few studies on the healtheffects of longer term exposures, most ofwhich have been conducted in the UnitedStates. The results of these new studies havebeen used in the revision and update of theWHO Air Quality Guidelines, which, in turn,provide a basis for the work on the new so-called ‘Daughter’ Directives to the EU AirQuality Framework Directive (96/62/EC),which will set revised limit values for themain air pollutants.

The most important message from thesestudies is the health significance ofparticulate matter at low levels. The effectsinclude short-term impacts on pulmonaryfunction, increased incidence of respiratorysymptoms, and increased mortality implyingconsiderable reductions in life expectancy.However, there is still discussion on theapplicability of the results from long-termstudies conducted in the United States toEuropean conditions. One of the reasons fordoubts are the possible differences in thecomposition of the pollution mix in theEuropean and American cities.

In combining the information from epide-miological studies with the data on ambientconcentration of main air pollutants, it ispossible to calculate a proportion of healthproblems which can be associated with theexposure (Krzyzanowski, 1997).

The effects of long-term exposure to suspen-ded particulate matter are the most impor-tant health effect of ambient air pollution inEurope, and are involved in perhaps 41 000to 152 000 extra deaths of respiratory dis-eases per year in the EU cities. These effectsoccur at various concentration levels, includ-ing concentrations considered as ‘low’ andreduce life expectancy in middle age people(Brunekreef, 1997). The precise magnitudeof the effects of long-term exposure isuncertain, within a wide range of estimateswhich reflects the weakness of the scientificevidence available.

Short-term variation of population health

associated with the daily changes in airpollution levels is better documented. Airpollution with particulate matter is associ-ated with more deaths (22 000 to 47 000 ayear) or hospitalisation (4 000 to 8 000admissions) than exposures to SO2 andozone which together are responsible for3 000 to 6 000 deaths and 400 to 1 600hospital admissions a year in the EU. It canbe assumed that the health problems attrib-uted to the pollution and registered throughhospital admissions could have been avoidedin the absence of the pollution. However,this interpretation is not valid for mortality(McMichael et al., 1998). While there is anassociation between the daily number ofdeaths and air pollution level, it is notcertain to what extent the life of the affectedindividuals is shortened by the exposure.

In summary, the available data from the1990s indicates that a significant reductionin population exposure to sulphur dioxidehas occurred in the last decade, and that thisair pollutant remains a problem only in alimited number of cities in central Europe.However, the levels and trends of pollutionwith particulate matter are still of concern,and there is little improvement with respectto ambient levels of NO2 or ozone. Thesecomponents contribute to significant adverseimpacts on public health, including in-creased mortality and reductions in lifeexpectancy. The economic costs of these airpollution health impacts are considerable(WHO /EEA, 1997; Maddison, 1998).

2.1.3. Respiratory allergies and asthmaOutdoor air pollution also plays a role in theaggravation, and possibly the causation ofasthma and other allergic responses, whichare increasingly prevalent diseases, especiallyin children. Approximately 70% of outdoorair pollution penetrates indoors (WHO,1999a) so that an integrated approach toboth outdoor and indoor air pollution isneeded. Other key components of indoorpollution which have been associated withrespiratory and allergic responses are dustmites, spores from pets, damp, environmen-tal tobacco smoke and NOx from gas ovens.

The prevalence of asthma in children ofschool age varies from 4% to 27% in differ-ent parts of Europe. Wide geographicalvariation in asthma prevalence is also notedin adults. There is an indication that theprevalence rates have increased over the lastdecade. The frequency of asthma attacks,sometimes requiring medical assistance orhospitalisation, has been shown to be associ-


Box 3.10.3. Environment and immunity

There is increasing evidence that the fine ambientair particles involved in respiratory and cardio-vascular diseases impact on health via the immunesystem. Other examples of environmental stressesthat have a negative impact on the immune systemare:

• ultraviolet radiation, which is known to haveeffects on the immune system at doses that arecurrently encountered outdoors;

• natural and manmade chemicals, for which alarge data base on laboratory animals showseffects on the immune system, suggesting thatchronic exposures to even low concentrationsmay potentially have an impact on humans;and

• combinations of immunotoxic agents, such asin food, e.g. natural toxins, heavy metals etc.

However, except for allergies resulting fromsensitisation by pollutants directly, there is littleinformation or understanding about the linkbetween negative effects on the immune system

Source: EEA, based on European Commission, 1996

and adverse health effects in the individual. Thereare apparently large ‘reserve capacities’ in theimmune system that can absorb negative effectswithout adverse effects on health. However, forindividuals whose immune response system isalready adversely affected by others stresses (e.g.infections), and for populations that containsusceptible people (e.g. the sick and the elderly),the reserve capacity may not be sufficient toprevent adverse health effects, such as allergies(skin and respiratory), or cancers. Therefore ‘anydeviation from the normal situation is consideredundesirable: this ‘precautionary principle’ point ofview is aimed at the prevention of adverse effectsin the population’ (European Commission, 1996).Small increases in the incidence and duration offrequently occurring diseases may have large socialand economic impacts.

Further research is needed into identifying bio-markers that are relevant to adverse health effects,especially in sensitive groups such as children,pregnant women, the elderly and people withgenetic pre-dispositions to immune systemimpacts.

• Often limited to information on the coverage by services.

• Focused on operational control by water supply agencies and forcompliance assessment by regulatory agencies.

• Limited availability if collected by suppliers from private sector.

• Not suitable for statistical analysis and international comparisons.

• Different drinking water quality standards resulting in non-comparability ofpercentage compliance data.

• Different approaches to laboratory analysis and poor inter-laboratorycomparability.

Box 3.10.4. Problems with data for European assessment of health risksrelated to water quality

ated with air pollution levels. However, it isnot clear if environmental conditions cancause the onset of the disease or only makethe symptoms worse. Moreover, it is notknown to what extent the geographicalvariation in asthma levels and trends isrelated to environmental factors. Diet (e.g.less omega-3 fatty acids and antioxidants) orcompromised immune systems (Box 3.10.3)are also implicated in the development ofasthma. However, current data promptsmore questions than answers (Strachan,1995; UCB, 1997). Figure 3.10.10 in section4 below illustrates the multi-causal chain offactors implicated in childhood asthma.

Radon is another indoor air pollutant that isresponsible for several thousand lung cancerdeaths a year in the EU, confined to particu-lar localities where geological formationsgive off the radioactive gas into confinedspaces of houses (WHO, 1999a).

2.2. WaterWater quality is a significant factor in expo-sure to health risks. In general, water pollu-tion has declined in the EU, although con-cerns remain over localised quality problems,and particularly nitrate contamination ofgroundwater resources (see Chapter 3.5).

2.2.1. Quality of waterA Europe-wide assessment of drinking waterquality and estimation of related health risksfaces serious difficulties due to scarcity and

comparability of appropriate data (Box3.10.4). These problems are common toboth EU and Accession Countries.

2.2.2 Drinking water contamination and some health effectsThe detection systems across the EU forwater-borne disease are generally poor andonly the larger outbreaks are detected inpractice. Outbreaks affecting less than 10-20% of the supplied population are rarelydetected. Individual cases of gastrointestinaldisease, even if registered by medical caresystems, are impossible to link directly towater quality.

Inadequate microbiological water qualityand occasional outbreaks of water-bornediseases are reported across the EU, even


Box 3.10.5. Pharmaceutical substances in water, sewage etc.

Pharmaceutical substances, like pesticides, aredesigned to have a biological effect. As they arewidely used as medicines, (up to a tonne/day insome countries) and as growth promoters andveterinary medicines in animals, their presence inthe environment may be significant, followinghuman and animal excretion and other routes ofexposure. They have not received much attention,partly because exposure levels were thought to betoo low to be of concern. However, as the effects ofendocrine-disrupting substances can be observedat very low levels, similar levels of exposure topharmaceuticals in the environment may besignificant for human and ecological health.

About 70% of antibiotics used in fish farming arereleased into the environment (Schneider, 1994).Several studies have identified antibiotics insediment cores beneath fish farms (Samuelson,1992a; 1992b), in groundwater (Eckel et al., 1993;Hohm et al., 1995; Stan et al., 1994; Feuerpfeil etal., 1999), and in manure (Macri et al., 1998).

Modelling of exposure pathways and potentialdoses has indicated possible worst-case scenariosof 30 µg/kg for olaquindox and 70 µg/kg fortylosine, two pig-growth promoters (Jorgensen etal., 1998). Information about possible eco-toxiceffects is rare, though some rather potent effectshave been demonstrated for metronidazole andother antibiotics on green algae (Lanzky andHalling-Sørensen, 1997; Holten-Lutzhoft et al.,1999). There are few, if any, studies on possibleimpacts on endocrine or hormonal functions ineither humans or wildlife (Halling-Sørensen et al.,1997; Andersen et al., in press). However, there isincreasing evidence that the use of antibiotics as

growth promoters in cattle, pigs and poultry canlead to increasing antibiotic resistance in bothanimals and humans via the food chain (SwedishMinistry of Agriculture, 1997). For example,Denmark has a higher frequency of resistance toenterococci in pigs (55-84%) than does Sweden (14-15%) which banned antibiotics as growth promotersin 1986. The transfer of antibiotic resistance fromanimals to humans is possible but there is as yet littleor no data on the extent of the problem in humanscaused by antibiotics from growth promoters in thefood chain (Edqvist, 1997). However, vancomycin-resistant enterococci (VRE), which are associatedwith the use of avoparcin for growth promotion,have been identified in non-hospitalised humanswho eat meat, but not in vegetarians). There is also arisk of the development of cross resistance involvingseveral strains of bacteria. For example, Feuerpfeilfound cross resistance in 8 types of microbes. TheWHO recommends the reduction in the use ofantibiotics as growth promoters and the EU hasrecently (Dec. 1998) banned four antibiotics(virgianmycin, spiranycin, tysolin phosphate andbacitracin zinc) and is investigating four others.However, the evidence on animal growth promotersis not clear: the European Federation of FeedAdditives Manufacturers thinks there is insufficientscientific evidence for an EU ban (Swedish Ministryof Agriculture, 1997).

No new chemical class of antibiotics has beendeveloped in the past 20 years, despite extensiveresearch. This provides opportunities for increasedresistance. It takes at least 10-20 years to find andclinically test new antibiotics, a time lag within whichantibiotic resistance could increase withoutopposition from new drugs.

from countries with high standards of supply(and notwithstanding the often limitedsensitivity of surveillance systems). Forexample, 3 to 6 outbreaks of waterbornegastro-enteritis have been reported bySweden each year in the 1990s (WHO/EEA,1998). Contamination of drinking water byfaecal coliforms is detected in 1-4% ofsamples analysed in many European coun-tries. Microbiological pollution is especiallyprevalent in small supply systems, and insome countries private supplies are notsubject to such stringent standards as publicsupplies. In up to 33% of water samplestaken from small private water supply sys-tems in Ireland, faecal coliforms werepresent in amounts exceeding the standardlevel in 1995.

Increasing chemical water pollution fromagriculture is a significant problem inEurope. Nitrate concentrations ingroundwater are generally low in northernEurope, but high in several western andeastern countries.

Increased contents of nitrate pose a risk ofmethaemoglobinaemia to infants, a poten-

tially serious, life-threatening disease. How-ever, the total number of cases of methaemo-globinaemia reported are low and from onlya few countries, mainly in eastern Europe.

Old water distribution systems, using leadedpipes, may be a significant source of popula-tion exposure to lead, which, in turn, mayaffect neurobehavioural development ofchildren (see Section 3.6. below). Thisexposure can be markedly reduced byadequate treatment of water before itsdistribution, to reduce the solvency andbioavailability of lead. In Glasgow for exam-ple, effects of exposure-reduction measureshave been shown (Moore et al., 1998).Increasing water alkalinity and addingorganophosphate to the water supply re-duced the concentration of lead (Pb) indrinking water, which in turn lead to paralleldecreases in maternal-blood lead. Part of theobserved reduction of lead blood levels isattributed to a decrease of lead exposurefrom non-water sources, such as lead inpetrol, food cans etc.

Pesticides and their degradation productsare, in some areas, found in drinking water


% of seawaterbathing pointscomplying withmandatoryvalues forfaecal andtotal coliforms

% of freshwaterbathing sitescomplying withmandatorylevels forfaecal andtotal coliforms

100

0

10

20

30

40

1992

50

60

70

80

90

1993 1994 1995 1996

Source: WHO

Figure 3.10.4Tests of recreational water qualityor in groundwater (see Chapter 3.7). Tri-azine herbicides are the pesticides mostfrequently detected in groundwaters andseveral countries have introduced bans orrestrictions on the use of products contain-ing the active ingredients. There has been asignificant overall downward trend in thecontamination of groundwater by triazineherbicides and their breakdown product inmost countries, although this is not the casewith all pesticides (see Chapter 3.5).

Data on microbiological quality of recrea-tional waters is collected in some countries,principally for compliance assessment byregulatory agencies. EU Member States co-operate to produce an annual assessment ofbathing water quality but despite manyattempts to collate and compare data fromdifferent locations (nationally or internation-ally), the quality of such data has severelimitations regarding its value in assessinghazards to human health, primarily due todifferent approaches to analysis and poorinter-laboratory comparability.

The quality of freshwater sites designated forbathing is considerably worse than those ofcoastal sites in the EU although the overallquality trend appears to be improving(Figure 3.10.4).

Other low-level contaminants of water maybe a threat to health in some areas (WHO/EEA, 1999).

A possibly emerging threat are trace residuesof pharmaceuticals, including antibiotics(Box 3.10.5), though there is little data andfew studies available.

2.3. NoiseNoise can have a variety of effects whichdepend on the type, duration and timing ofthe noise and the susceptibility of the recipi-ent (Box 3.10.6).

Reports from recent scientific research onthe precise health effects of nocturnal trafficnoise reveals that night-time traffic noise notonly disturbs sleep but also encouragespsychosomatic illnesses, shortens the periodof deep, dream-rich REM (rapid eye move-ment) sleep, lengthens the phase of lightslumber and may cause cardio-circulatoryproblems.

There may be some segments of the popula-tion at greater risk of adverse effects ofnoise. Young children, (especially duringlanguage acquisition), the blind, the hear-

ing-impaired and hospital patients areexamples of higher risk groups.

Noise affects more than our health andquality of life; it even influences socialbehaviour and cognitive development. In1997, studies carried out around Munichairport found that children exposed tofrequent aeroplane noise do not learn toread as well as other children. Excessivebackground noise caused the children totune out human voices and interfered withtheir language acquisition. The psychologistswho conducted the study speculated that as aresult of noise pollution, parents and teach-ers were also less willing to speak or readaloud.

Community noise needs to be assessed withrespect to risks for both human health andwell-being. Intensity, frequency, reversibilityand avoidability are pertinent criteria for theseverity of noise effects.

The knowledge about harmful impacts ofnoise exposure has to be transformed intoenvironmental standards. There is alsolimited evidence for noise impacts on birthweight, congenital effects, and the immunesystem (Ministère des affaires sociales, de lasanté et de la ville, 1995). However, esti-mated thresholds are available for only alimited range of noise impacts for whichthere is more substantial evidence of noisecausation (Table 3.10.1).

3. Other environmental hazards of concern

Besides the recognised and relatively well-understood issues described in the previous


Exposures

Noise remains a serious environmental problem: estimates of its costs rangefrom 0.2 to 2.0% of GDP (Quinet, 1993). It is estimated that about 32% of theEU population (approx. 120 million people) are exposed to road noise levelsover 55 Ldn dB(A) at house facades and that approx. 3 million people areexposed to aircraft noise (see Chapter 3.12). Perceptions of the various typesof transport noise differ between individuals and impacts can depend on thetype of noise, e.g. from rail or aircraft.

Effects: Public

• Annoyance;

• Interference with speech communication;

• Sleep disturbance effects (more than ‘awakenings’);

• Effects on performance and productivity (reading acquisition, learnedhelplessness, etc.);

• Effects on residential and social behaviour (opening windows, use ofdwelling area, etc.);

• Psychophysiological effects (the stress complex, hypertension, ischaemicheart disease, aggressiveness, etc.);

• Mental health effects (hospital admissions, etc.);

• Dose-effect for joint effects (e.g. annoyance + sleep disturbance +hypertension?);

• Vulnerable groups (children, hearing-impaired).

Effects: occupational

• Noise-induced hearing dysfunctions (e.g. tinnitus, temporal thresholdshifts, deafness, ‘impulse sounds’)

Source: EEA

Box 3.10.6. Noise: some exposure/effect relationships

Observationthreshold

Effect Situation Noise metric Level in dB (A) Inside/outside

Hearing work Laeq, 8hr 75 insidedamage

sport Laeq, 24hr 70 inside

Hypertension work Laeq, 8hr <85 inside

home LAeq, 6-22hr 70 outside

Ischaemic heart home LAeq, 6-22hr 70 outside

Annoyance home Ldn 42 outside

Awakening sleep SEL 55 inside

Sleep stages sleep SEL 35 inside

Self-reported sleep LAeq, night 40 outsidesleep quality

School school Laeq, day 70 outsideperformance

Source: Health Council of The Netherlands, 1994

Table 3.10.1. The long-term effects of noise exposure for whichthere is sufficient evidence

sections, a number of other environmentalfactors create potential risk for health andcause public concerns (Table 3.10.2). Inmost cases, the information and scientificbasis for assessment of the risk is not suffi-cient to confirm or deny the existence of therisk. The list of relevant issues is long, andthis section provides selected exampleswhich illustrate some general points aboutthe identification and management ofenvironmental health.

3.1. Chemicals and endocrine-disrupting chemicalsLow doses of some chemicals (EEA/UNEP,1998) are associated with cancer, cardiovas-cular disease, respiratory diseases, neurotox-icity, and chemical sensitivity, with varyingstrengths of evidence, but information aboutexposure /effect relationships is often pooror non-existent (Box 3.10.8).

A broad class of chemicals present in theenvironment, such as PCDDs, PCDFs, PCBs,persistent pesticides, some detergents andsome compounds used in the plastic indus-try, are known to have a capacity to interferewith hormonal regulation mechanisms(Toppari et al., 1996; EU Scientific Com-mittee, 1999). The Weybridge Report (EUR,1997) concluded that while there was in-creasing evidence about rising trends inreproductive ill health in wildlife and hu-mans, there were still great uncertaintiesabout the causes of the reproductive illhealth (Box 3.10.7). However, exposurereduction to endocrine disrupting chemicalswas recommended in line with the ‘precau-tionary principle’. Since then, reports by theEuropean Parliament and others haverepeated the call to reduce exposures.

3.2. Chemicals from waste disposal and treatmentPart of the still growing volume of wastegenerated and disposed in Europe is hazard-ous to health via exposure to hazardouschemicals or microbiological pollution.

Several epidemiological studies conducted inthe United States have suggested a smallincrease in risk of a range of health impactsassociated with the hazardous waste landfills,but a UK review concluded that ‘The epide-miological evidence that these substancesrepresent a cancer risk at much lowerenvironmental levels either does not exist oris equivocal. However, data on the effects ofbackground environmental exposures oncombinations of chemicals is absent, makingit difficult to assess any health impact result-ing from relatively small additional expo-sures from incinerators (MRC, 1997). A


Table 3.10.2.Major health impacts and someassociations with environmental exposures

Health impact

Infectious diseases

Cancer

Cardiovascular diseases

Respiratory diseases,including asthma

Skin diseases

Diabetes, obesity

Reproductivedysfunctions

Developmental (foetaland childhood) disorders

Nervous systemdisorders

Immune response

Chemical sensitivity?

Associations with some environmental exposures

• water, air and food contamination• climate change

• smoking and environmental tobacco smoke (ETS)• some pesticides e.g. phenoxy herbicides• asbestos• natural toxins• food, e.g. low fibre, high fat• polycyclic aromatic hydrocarbons, e.g. in

diesel fumes• some metals e.g. cadmium, chromium• radiation (incl. sunlight)• several hundred other animal carcinogens

• smoking and ETS• carbon monoxide (CO)• lead• inhalable particles• food, e.g. high cholesterol• stress

• smoking and ETS• sulphur dioxide• nitrogen dioxide• inhalable particles• fungal spores• dust mites• pollen• pet hair, skin and excreta• damp

• some metals, e.g. nickel• some pesticides, e.g. pentachlorophenol• some foods (allergies)

• food, e.g. high fat• poor exercise

• polychlorinated biphenyls (PCBs)• DDT• cadmium• pthalates and other plasticisers• endocrine disruptors

• lead• mercury• smoking and ETS• cadmium• some pesticides• endocrine disruptors

• lead• PCBs• methyl mercury• manganese• aluminium• some solvents• organophosphates

• UVB radiation• some pesticides

• trace amounts of many chemicals?

Note: Most diseases are the result of several causes. These include:

• inherited vulnerability,• factors which are related to poverty, e.g. diet, housing quality and location, stress,

alcohol and substances abuse, smoking, low birth weight etc.; work; unemployment;climate, and

• other environmental exposures arising from air, water, soil and surfaces.

The link between environmental exposures and health impacts varies from known causalrelationships such as inhalable particles and respiratory-system damage to suggestive butunproved associations, such as between some cancers and exposure to low levels of somepesticides. Poor diet plays a key role in the ‘diseases of affluence’, such as cancer, heart andcirculatory diseases.

Source: EEA

recently published European study adds tothe suspicion that the landfill operationsmay contribute to a small increase in risk ofcertain birth defects (Dolk et al., 1998).However, the present studies are not power-ful enough to indicate a particular character-istic of the landfill which may cause a risk,and a weakness of the exposure assessmentin those studies makes any causal relationbetween disease and landfills difficult toestablish.

An analysis of cancer incidence patternsaround municipal solid waste incinerators inthe UK revealed that the observed slightlyincreased overall incidence of cancers in theproximity of the incinerators is related to acombination of confounding factors, andnot to the waste treatment operations (Elliotet al., 1996). However, the need for a furtherstudy on a still unexplained incidence ofliver cancer in the vicinity of incinerators wasproposed.

Technical requirements of design and opera-tion of waste treatment at such facilities aim atthe elimination, or radical reduction, of therisk to population health. Whilst there is adecline in population exposure to hazardouschemicals which may be emitted from incin-erators such as dioxins, the average exposureof Europeans in industrialised countries todioxins is significant in relation to what is nowknown about their likely effects (see Chapter3.3) which include cancer, reproductivedisorders, neurotoxicity and heart disease(WHO, 1997d and 1998 a).

3.3. Climate change and ozone depletion-future burdens?The potential consequences of climatechange include increases in sea level, more

Breast cancer rates are rising in Europe. Somerisk factors are known (genetics and family histo-ry, use of the contraceptive pill etc.) and othersare suggested such as some occupational andenvironmental causes, such as pesticides, radia-tion and endocrine-disrupting chemicals but the-se account for only 30-40% of cases (Kristensen,1991; Davis, 1993; Woolff, 1993; Hulka, 1995;Cantor et al. 1995; Rachel’s Environment andHealth Weekly, 1997; Wallerson, 1995; McPherson,1994; Hoyer et al, 1998). However, the links withoccupational and environmental factors may besmall and the evidence for this is disputed. Dis-entangling the relative contributions of severalfactors in an inter-dependent causal chain isalways going to be difficult, and prevention callsfor an integrated, holistic approach, based on theprecautionary principle (Davis, 1997).

Box 3.10.8. Breast cancer: an ‘integrated’disease?


Box 3.10.7. The ‘Weybridge Report’ on endocrine disruptors

Source: European Commission et al., 1997

There is increasing evidence and concern about rising trends of reproductiveill health in wildlife and humans, and some substances have been implicated,but there are great uncertainties about the causes of reproductive ill health.

Key conclusions are:

• Sufficient evidence exists that testicular cancer rates in humans areincreasing.

• The apparent decline in human sperm counts in some countries was likelyto be genuine.

• There is insufficient evidence to definitely establish a causal link betweenthe health effects seen in humans with exposure to chemicals.

• The major route of exposure to Endocrine Disrupting Substances (EDS) isusually by ingestion of food, and to a lesser extent water. It is valid forterrestrial animals, birds and mammals, including humans.

• Compared with the situation in the US, there are few cases ofreproductive ill-health in wildlife in the EU where the effects could bedefinitely associated with EDS.

• However, some cases exist within the EU area where adverse endocrineeffects, or reproductive toxicity, in birds and mammals coincide withhigh levels of anthropogenic substances shown to have endocrine-disrupting properties in some test systems.

• The considerable uncertainties and data gaps could be reduced byresearch and monitoring into exposure and effects in wildlife andhumans.

• Current eco-toxicological tests, studies and risk assessments are notdesigned to detect endocrine-disrupting activities.

• Meanwhile, consideration should be given to reducing the exposure ofhumans and wildlife to endocrine disrupters in line with the ‘precautio-nary principle’.

frequent and intensive storms, floods anddroughts, changes in biota and food produc-tivity. Changes in ecosystems may affect thegrowth, transmission and activity of vector-borne or infectious diseases, such as malariaand dengue fever. Human health is likely tobe adversely affected, either directly orindirectly, through complex interactions ofecological systems (McMichael, 1996a,WHO, 1999b). The direct effects may resultfrom changes in exposure to thermal ex-tremes, and be expressed by an increase inheat-related disease and death, but also by adecrease in cold-related disease. Otherextreme weather events can lead to psycho-logical disorders, disease or death, indirectlycausing an increase in morbidity. Althoughthere are some signs of these climate effectsalready beginning to happen, such as shift-ing geographical range and longer seasonsof some vector born diseases (WHO, 1999 b),much of the burden of ill health fromclimate change will be on our children andgrandchildren. However, climate changepolicies based on avoiding these health

impacts will have considerable secondarybenefits of avoiding shorter term healthimpacts from fossil fuel combustion (WRI1997).

Similarly, stratospheric ozone depletion isexpected to cause increased UV radiationand thereby increased skin cancer sometimein the next century (Figure 3.10.5). Therelation of UV radiation with some forms ofskin cancer is well-established, though notalways with respect to the specific wave-length, exposure-response or individualsusceptibilities. Though the current increasein skin cancer in Europe (3 to 5% per yearsince the 1960s, for malignant melanoma,WHO, 1999) seems mostly related to morefrequent sunbathing and other lifestylefactors, the depletion of the protective layerof ozone in the stratosphere will increase thelikelihood of increased skin cancer in thefuture, despite the reductions in the produc-tion of CFCs and other ozone-layer-depletingsubstances. However, the implementation ofthe Copenhagen amendments to the Mon-treal protocols (see Chapter 3.2) on thebanning and phased reduction of ozone-depleting substances has greatly reduced thefuture excess incidence of skin cancer.

Increased UV-radiation also reduces theresponse of the immune system (see Box3.10.3), and causes eye cataracts and otherimpacts. It can also be beneficial, by provid-ing extra vitamin D.

Environmental-health hazards that impact inthe future via long latent periods, such asasbestos and other carcinogens, presentdifficult issues of public health policy thatrequire considerations other than goodscience, such as appropriate levels of proof(see section 4). Decisions sometimes need tobe based on ‘early warnings’, which oftencome from the world of work, where expo-sures are usually higher and where themonitoring and the identification of impactsis often easier. Any integrated assessmenttherefore needs to embrace occupationalexposures, which in any case add to the sumof stresses on the body.

3.4. The occupational environment

’It is a sordid profit that is accompanied by thedestruction of health’ — Bernardino Ramazzini, ‘father’ of Occupa-tional Medicine, 1713

A full-time employee spends about one-halfof waking time in the workplace; the other


CFC’s production & consumption

1975 2000 2025 2050 2075 2100

Ozone depleting substancesin stratosphere

Estimated additional skin cancerfrom ozone layer depletion

Increased UV-radiationat the earth’s surface

Background skin cancer rate

Illus

trat

ive

rate

s o

f cha

nge

(no

t to

sca

le)

Average latentperiod forskin canceris 30–40 years

This graph illustrates the approximate time lags between CFC production, the resulting depletionof the stratospheric ozone layer and subsequent extra penetration of UV radiation and the impactthis will eventually have on increasing the background rate of skin cancer, given the 30-40 yearaverage latent period for such cancers. Reality is far more complex than this schematic illustration.For example, there are other ozone-depleting chemicals (HCFCs, HFCs and methyl bromide); theozone hole varies with latitude, time of the year and meteorological conditions; the increased UVradiation varies between different wavelengths and with latitude and cloud cover; and the skincancer excess comes on top of a rising background rate of skin cancer, with differential effects onthe 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 cataractsand immune response suppression. However, the figure illustrates the main relationships and timelags between CFC production and skin cancer, and the ‘success’ in stopping CFC production andaverting much more skin cancer from ozone depletion than what is now expected. (Slaper, et al.,1996).

Source: EEA

Figure 3.10.5CFCs, skin cancer and time lags

The World Health Organisation says:

• Some 50 physical factors, 200 biological factors and 20 adverseergonomic conditions, plus an innumerable number of psycho-socialfactors, have been identified as creating hazardous working conditions.These contribute to the risk of occupational injuries, diseases and stressreaction, as well as to job dissatisfaction and the absence of physical andmental well-being.

• The risk of cancer from work and workplace exposure is of particularconcern. Approximately 300-350 different chemical, physical andbiological factors have been identified as occupational carcinogens. Theyinclude benzene, chromium, nitrosamines, asbestos, ultraviolet radiation,ionizing radiation and aflatoxins. The most common cancers occurring asa result include lung, bladder, skin and bone cancer and sarcomas.

• Allergenic factors are also a growing cause of occupational illness. Anestimated 3 000 allergens have been catalogued which can causedermatoses and respiratory diseases (e.g. asthma).

• Approximately 30-50% of workers in industrialised countries complainabout psychological stress and overload. Such psychological factors havebeen associated with sleep disturbance and depression, as well as withelevated risks of cardiovascular diseases, particularly hypertension.

• Only 20-50% of workers in industrialised countries (with few exceptions)have access to adequate occupational health services.

Source: WHO, 1997a

Box 3.10.9. The dangerous world of work

half is spent on domestic or leisure activities,and one-third of the 24 hours is spentsleeping. It follows that many environmentalcontributions to all health will be found inand around the workplace. This is whyBernardino Ramazzini, the father of occupa-tional medicine, advised doctors to alwaysask their patients: ‘What work do you do?’(Ramazzini, 1713).

A European survey found that 23% of theEU workforce were absent from work duringthe previous 12 months due to work-relatedill health (European Foundation, 1996), andthe WHO has identified a range of occupa-tional stresses (Box 3.10.9).

The workplace is also an effective placethrough which to focus efforts on healthpromotion, embracing occupational,environmental and ‘lifestyle’ factors, suchas smoking, alcohol, diet and exercise. TheWHO considers that 30-40% of the totaldisease and ill-health burden in Europe canbe tackled effectively through workplaceactivity on either occupational factors, oron lifestyle/environmental factors that canbe addressed through employee or em-ployer activity (WHO, 1999a). Occupationalaccidents and ill health cost between 0.4and 4.0 % of GNP in the EU (EASHW,1998).

The monitoring, identification and ‘proof’of the occupational origins of disease are ascontroversial as identification of the environ-mental contributions to ill health. The‘occupational’ fraction of cancer has beenestimated at 4-5%, or up to 25% (WHIN,1998), but as with all diseases that have longtime lags (‘latent periods’) between expo-sure and harmful effect, the conditions ofexposure will always have changed by thetime ‘proof’ of causality can be provided,some 20-40 years after exposure first began.This then affords opportunities to argue thatcurrent conditions are now harmless, andthe point can only be ‘proven’ one way orthe other some 20-40 years later (Box3.10.10).

Both unemployment, via its link to poverty,alcohol, loss of self-esteem, etc. andoverwork can cause disease and ill health.

Many environmental diseases are firstidentified in the higher exposure, moreeasily monitored world of work, e.g. 95% ofthe 24 known lung carcinogens and over halfof all causes of cancer were identified inworkplace 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 in1898 concluded: ‘The evil effects of asbestos dusthave also attracted my attention. A microscopicinspection clearly revealed the sharp, glass-like,jagged nature of particles and … the effects havebeen found to be injurious, as might have beenexpected’ (ARCI, 1898).

Her fears were confirmed 30 years later. A govern-ment-funded study in 1929 found that one-third ofasbestos workers had asbestosis, a form of pneu-moconiosis. By 1955, a study of workers by SirRichard Doll showed that asbestos also caused lungcancer, and by 1964 other cancers, including themost deadly, mesothelioma, were added to the listof ‘evil effects of asbestos dust.’ Table 3.10.3 sum-marises the history of asbestos as it moved from theharmless substance of the 1880s to the recognisedkiller of the 1990s, now being responsible for about10 000 deaths a year in western Europe. Poorly-controlled asbestos use expanded right up until the1980s, by which time it had killed thousands ofpeople, and condemned thousands of others to diein the next 20-60 years as a result of their pastexposure. The costs of failing to control asbestosearly enough are not just health costs – dealing withcompensation and asbestos in buildings is costingbillions of pounds and was partly responsible for thebankruptcy of some Lloyds insurance underwriters inthe early 1990s.

Exposed group Asbestosis Lung cancer Mesotheliomacancer

Occupational

Workers (1898-1929) 1955 1960s

Mates 1964 1964 1964

Environmental

Relatives 1960s ? 1960s

Public ? ? 1980s

Note: Asbestos also causes other cancers, e.g. cancer of the larynx

Table 3.10.3.

The latest study on the extent of asbestos-induceddeaths ‘in the pipeline’ concludes that some250 000 men (mainly) will die of asbestos-relatedcancer in western Europe over the next 35 years,following a doubling of the current annual total ofdeaths from the main asbestos cancer, mesothelio-ma, from 5 000 a year in 1998 to 9 000 a year by2018 (Peto et al., 1999). The study was based onthe cancer registries of six European countries(France, Germany, Italy, the Netherlands, Switzer-land and the UK, which account for 72% of thepopulation of western Europe). Asbestos use inEurope remained high until about 1980, and asmesothelioma, a cancer of the lung or stomachlining, has a latent period of 30-60 years, deathswill peak around 2020 and decline slowly over thefollowing decades.

Workers not directly employed with asbestos, suchas electricians, carpenters, plumbers and main-tenance men, are also at risk. Although the non-occupational risk from asbestos is very muchsmaller, the possibility of 24-hour exposure, and ofchildren’s exposure, contributes to a significant riskfor some ‘public’ groups, e.g. those living in thehouses of asbestos workers, where contaminatedclothing has caused mesothelioma in wives, sistersand children and those living and playing in thestreets near asbestos plants (Camus et al., 1998).

Although there have been ‘early warnings’ aboutasbestos for 100 years, effective preventativemeasures were not taken until it was too late tostop deaths ‘in the pipeline’ of the latent period.And even accurate monitoring of mesothelioma,lung cancer and of their relationship (which may be1:1 or 1:3 or 4) is still poor. ‘It is unfortunate thatthe evolution of the epidemic of asbestos-inducedmesothelioma, which far exceeds the combinedeffects of all other known occupational industrialcarcinogens, cannot be adequately monitored.’(Peto, 1999).

Smoking and asbestos together have a strongsynergistic effect causing a 50 fold excess of lungcancer while their separate effects are ‘only’ a 10and five-fold excess for smoking and asbestosrespectively (Hammond, 1979).

Synergy from smoking and other pollution is notconfined to asbestos. The WHO (1998b) hasconcluded that smoking and other workplacecontaminants can also act together to ‘amplify theseverity of adverse effects beyond what could beexpected from smoking or the toxic hazard alone’.

Source: EEA based on Gee, 1995

International Agency for Research onCancer. Many ‘early warnings’ of environ-mental health hazards will therefore con-tinue to come from workplace studies(Wegman, 1996). For example, the potentialhuman health effects of non-ionising radia-tion were first identified in occupationalstudies (Box 3.1.11).

3.5. DietHealthy eating plays a crucial role in diseaseprevention. For example, in addition togenetics, occupational and environmentalfactors, diet plays a key role in cancer causa-tion, perhaps 30-40% of all cancers.

Recommendations on balanced diets havebeen available for many years (Figure 3.10.6).However, advice can vary, depending onscientific knowledge. Poor consumer labellingcan make it difficult to make the right choice,assuming the consumer already has physicaland financial access to healthy food. Contami-nation with chemicals, such as antibiotics andpesticides (Box 3.10.12) can diminish some ofthe value of healthy eating, but, as with breastfeeding when the milk may be contaminatedwith very low levels of dioxins or PCBs, theother benefits of a healthy diet usually over-whelm the costs from micro-contaminants.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 thatresearch into possible adverse health effects ofelectromagnetic fields (EMF) should be a priorityfor the next four years.

The WHO’s EMF project will be co-ordinating andencouraging research into the possible associationsbetween low-frequency EMF (less than 300 Hz) andchildhood leukaemia, breast cancer and diseases ofthe central nervous system.

WHO also recommended further research intopossible associations between exposure to radiofrequency fields (300 Hz – 300Ghz) and leukaemia/lymphoma and brain and cancers.

Dr Paul Kleihues, Director of WHO’s InternationalAgency for Research on Cancer, has observed that,‘with an estimated 15 million new cancer caseseach year by the year 2020, we must know ifexposure to EMF is contributing to any significantextent to the incidence of disease’.

The controversial theory that electric fields likethose around power lines can cause cancer hasreceived some support from a National Institute ofHealth scientific panel in the US. ‘This report doesnot suggest the risk is high’, and ‘The risk isprobably quite small compared to many otherpublic health risks’, said Michael Gallo, chairman ofthe group and a professor at the university ofMedicine and Dentistry of New Jersey-RobertWood Medical School, Pistacaway.

The report comes from a National Institutes ofEnvironmental Health Sciences panel convened toreview scientific research on electromagnetic fields.

The group voted 19-9 in June 1998 thatelectromagnetic fields should be regarded apotential cause of cancer, using the InternationalAgency for Research on Cancer criteria forcancirogenicity.

Eight members said that, because of conflictingstudies, they could not decide whether electricalfields were potential cancer causes. One said theyprobably were not.

The new finding is at odds with a 1996 report by aNational Research Council panel of scientists whoevaluated about 500 studies on the health effectsof high voltage power lines and found ‘noconclusive and consistent evidence’ that electricand magnetic fields cause any human disease.Studies of the incidence of disease analysed by thenew NIH group found a slight increase in childhoodleukaemia risk for children whose homes are nearpower lines and an increase in chronic leukaemia inadults working in industries where they areexposed to intensive electric fields.

The group said that there wasn’t enough evidenceto link household exposure to power lines to cancerin adults, or to associate electromagnetic fields tosuch diseases as Alzheimer’s, depression and birthdefects.

They found no evidence of abortion from videodisplay terminals and no evidence of illness otherthan leukaemia in children (WHIN, 1998).

A re-assessment of the organochlorineinsecticide lindane has concluded that consumersafety limits can be exceeded by over 12 times.

The joint FAO/WHO Food Standards ProgrammeCodex Committee on Pesticide Residues has seta more stringent acceptable daily intake (ADI) forthe insecticide lindane of 0.001mg/kg bodyweight.

For a 60 kg adult, therefore, the maximum dailydose should not exceed 0.06 mg in total. TheADI is the amount of pesticide that can beconsumed every day for a lifetime without harm.

Codex data discussed at a recent meeting showsthat any person consuming an average local dietin any region of the world could theoreticallyexceed the ADI for lindane by between 3.8 and12 times if foods containing the maximumlindane residues were consumed.

Source: FAO/WHO, IN WHIN 1998

Box 3.10.12. Lindane safety re-assessed

Bread, cereal, rice and pasta group: 300-500g

Fats, oilsand sweets:

25g

Meat, poultry,fish, dry beans,

eggs andnuts group:

150-250g

Milk, yougurtand cheesegroup:100g

Vegetablegroup:400-500g

Fruitgroup:

100-200g

Figure 3.10.6Healthy eating

Source: CECHE, 1998

free food and drink may be possible if bothsustainable agriculture and the reduced useand exposure to hazardous chemicals arepursued in an integrated approach to ecologi-cal and human health.


Box 3.10.13 Children and lead

‘Lead makes the mind give way.’— Greek physician, 2000 BC

• Lead is brought into the environment throughhuman activities in 300 times greater amountsthan through natural processes (Unicef, 1992).

• People, particularly children, may be exposedto lead from car emissions through leadedpetrol, water contaminated by lead pipes,some factories (e.g. metal polishing and smel-ters; old paintwork in houses), contaminatedsoil (e.g. nurseries built on old petrol stationsites), certain cultural practices (e.g. use of folkmedicines containing lead), use of improperlyglazed lead ceramic ware for cooking and foodstorage, and use of lead-contaminatedcosmetics such as surma and kohl.

• Children absorb up to 50% of lead taken intotheir bodies, compared to 10-15% in adults.Children may receive three times the dose ofadults because they have a larger surface-to-volume ratio.

• Lead in dust and dirt can be ingested viachildren’s hands and toys, for example bythumb-sucking or by putting objects in theirmouths.

• Even in the world’s most developed countries,it is estimated that a large proportion ofchildren suffer from lead poisoning. It is themost common, chemical-related, environmen-tal child health problem. It is especiallypronounced in economically-disadvantagedsections of the population. Poverty can causemalnourishment or physical stress, whichintensifies disabilities caused by leadabsorption.

Source: UNEP and UNICEF, 1997

• At low levels, i.e. 10-25 µg/dl (indicating theamount of lead in a tenth of a litre of blood)lead poisoning in children causes:

- reduction in IQ and attention span;

- reading and learning disabilities;

- hyperactivity and behavioural problems;

- impaired growth and visual and motorfunctioning; and

- hearing loss.

• Exposure to these levels in maternal andumbilical-cord blood is associated with lowbirth weight and prematurity. The body canstore lead for more than 20 years and thenrelease it during pregnancy, harming thefoetus (lead can move across the placenta withease).

• At higher levels, i.e. 60-100 µg/dl, leadpoisoning in children causes:

- anaemia; and

- brain, liver, kidney, nerve and stomachdamage.

• According to the World Bank, countries cansave five to ten times the cost of converting tounleaded petrol in health and economicsavings due to reduced health costs, savingson engine maintenance and improved fuelefficiency.

3.6. ChildrenAs has been seen with several health hazards(air pollution, noise, skin cancer, allergiesetc.) children can be particularly sensitive toenvironmental stresses. They are a‘biomarker’ for environmental threats thatrequire special protection, not only becausethey are more at risk but because they canalso provide early warnings of hazards toothers, as well as being effective points ofintervention for the prevention of disease intheir later lives.

Chemical pollutants that may affect reproduc-tive health and new-born children includecertain metals (e.g. lead and methyl mercury;Box 3.10.13), pesticides (e.g. DDT), industrialchemicals (e.g. PCBs), solvents and othersubstances (Foster and Rousseaux, 1995;CJPH, 1998). Exposures can occur throughplacenta and breast milk (Jensen, 1996;Rogan, 1996), and some may cause smallabnormalities of the immune responsesystem. However, WHO and others conclude

that the benefits for breast-feeding outweighthe risks of pollutants in breast milk(Weisglas-Kuperus et al., 1996; WHO, 1996b).

Children may be particularly at risk fromchemicals because of their greater biologicalsensitivity and greater exposure to environ-mental pollution relative to body weight(NRC, 1993; McConnell, 1992; Bearer, 1995).Their physiological and intellectual develop-ment may be impaired by exposure to chemi-cals (Rodier, 1995; Rylander et al., 1995;Jacobson 1996; Grand Jean et al., 1997). Low-level pesticide contamination of food (infantsconsume eight times more food per kilogramof body weight than adults, making this amore significant exposure pathway; CICH,1997), and of residential surfaces and toys inthe UK and US, is being reported (PesticidesTrust, 1998; Gurunathan et al., 1998). Someregulatory authorities are giving specialattention to the higher levels of risk to chil-dren from pollution (USEPA, 1996). Forexample, the Food Quality Protection Act in


Hostgenetics

Hoststate

Exposures/ Doses Effects Harm

- infections. - cancers - CNS damage - respiratory. - circulatory.- reproductive. - developmental - other adverse

health impacts

- genotypesandphenotypes

- nutritional status (diet)

- immune status (infections)

- health status(lifestyle)

- age

- multiple Exposures/Doses

- via several exposure routes (skin, inhalation, ingestion)

- environmental - indoor- environmental - outdoor- occupational- low and/or peaks- can be 24 hours

continuous- or single dose at critical

time- pre- and post-natal - lifetime and cumulative

"target" organ dose - biologically effective

dose- often unknown

etc…

- initiating- promoting- retarding- suppressing- causing:- changes in:cells, tissues,organs,

- functions; - shifts in

"normal" distributions of bio-functions, etc

+ + = =>

Figure 3.10.7Multifactoral disease causation

Source EEA:

the US requires the government to add anextra margin of safety to the risk assessmentof chemicals that children may be exposed to.

Cancer in children in the US appears to beincreasing (Pogoda, 1997; EHP, 1998;Rachel’s EHW, 1998), and a large-scale studyof childhood leukaemia and other cancers inthe UK has found them to be associated withliving close to industrial plants, particularlywhere fossil fuels were being used or proc-essed (Knox and Gilman, 1997).

4. Approaches to environment and health

4.1. Multifactoral causes of diseaseAs has been seen in earlier sections much illhealth and many diseases are multifactoral(Figure 3.10.7). Identifying the causes of illhealth in populations is therefore very diffi-cult and quantifying the contributions ofenvironmental exposures to adverse healthimpacts is even more so, particularly at thelevel of the individual. Adverse health impactsare the results of varying combinations of hostgenetics, host state (including ‘lifestyle’factors such as smoking, alcohol, diet parentsetc.) and exposures to other environmentalstresses, both indoors and outdoors. All thesefactors can operate at different times, influ-encing each other in various ways, andcausing changes in cells, tissues and functionsthat may or may not lead to adverse healthimpacts. The same ‘dose’ of air pollution forexample does not have the same impactbecause of differences between people, withsensitive groups, such as the elderly, the sickchildren, and pregnant women respondingmore than less sensitive groups. The same‘exposure’ may not lead to the same ‘dose’because of biological and activity differences,e.g. children and joggers who have higherbreathing rates.

Several key questions need to be addressedin dealing with environmental health issues:

• what is the nature and strength of theevidence for an adverse impact and forthe role of the environment in thatimpact,

• what is the nature of the impact (trivialor serious, reversible or irreversible,immediate or long term, large or smallnumbers affected etc.),

• what level of proof is to be used inmaking a decision, particularly aboutwhether an association between anenvironmental stressor and an adverseimpact is actually causation (Box 3.10.14),

• are exposure or effects avoidance meas-ures available, and actors identifiableand willing to take action,

• the cost and benefits of action andinaction, and their distribution betweenclasses, races, sexes, the regions andgenerations,

• how uncertainties are to be handled ,• how informed consent and public

involvement in ‘acceptable risks’ can tobe achieved,

• and how the consequences of action/inaction are to be evaluated?

The answers to these questions require goodinformation for effective decision-making,but in practice, a lack of data, information orunderstanding, or disagreements about theinterpretation of the information can lead todelays in preventing public ill health. Forexample, one of the main weaknesses ofanimal evidence is the difference betweenthe healthy young rats used in experiments(which breathe through the nose) and apopulation of mixed age and health statushumans, who partly breathe through theirmouths. These three differences (age, healthstatus and mouth-breathing) are the mainreasons why experts ‘dramatically’ under-estimated the health impacts on humans offine particles in air pollution in 1987 com-pared to 1997 (WHO, 1997b).

The level of proof used in decision-making iscrucial, and it can vary from very high to low,depending on the issue being addressed. For‘sound science’, a high level is required,


It is often fairly easy to show that a measure of ill-health, e.g. the number ofadmissions to hospital per day, is associated with a possible cause, such asthe day-to-day variation in levels of air pollutants. To show that a causalrelationship exists, a number of guidelines or tests have been developed.These include the consistency of results between different studies, the way inwhich the results of different studies fit together (coherence); whether there isa ‘dose-response relationship’ between the proposed causal factor and theeffect; and whether the sequence of events makes sense, i.e. the cause alwayspreceding the effect.

Proof of causality is often very difficult, but by the application of these andother criteria, an expert judgement as to whether an association is likely to becausal can often be made. Where effects are likely to be serious and/orirreversible, then a low level of proof, as in the ‘precautionary principle’, maybe sufficient to justify action to remove or reduce the probable causes (EEA/WHO, 1997).

Box 3.10.14. Association and causality

This principle featured in the 1992 RioDeclaration on Environment and Development(as Principle 15):

‘In order to protect the environment, theprecautionary approach shall be widely appliedby States according to their capabilities. Wherethere are threats of serious or irreversibledamage, lack of full scientific certainty shall notbe used as a reason for postponing cost-effectivemeasures to prevent environmental degradation.’

The precautionary principle permits a lower levelof proof of harm to be used in policy-makingwhenever the consequences of waiting for higherlevels of proof may be very costly and/orirreversible; the UN Intergovernmental Panel onClimate Change recently used the precautionaryprinciple in concluding that ‘the balance ofevidence … suggests a discernible humaninfluence on global climate’ (IPCC, 1995).

Box 3.10.15 Precaution

such as ‘beyond all reasonable doubt’. Thismeans that the costs of being ‘wrong’ infailing to reach the high level of proof (suchas new and correct, scientific hypothesesbeing initially dismissed, called ‘false nega-tives’), is considered by society to be lesscostly than being ‘wrong’ in the otherdirection when using a lower level of proofi.e. the ‘false positive’ of incorrect scientifichypotheses being accepted as correct.Similarly, in criminal trials, where the ‘cost’of being wrong in one direction i.e. innocentpeople being jailed (or sometimes ex-ecuted), is regarded as being worse thanbeing wrong in the other direction (i.e.guilty people going free), a high level ofproof is also used.

For other purposes in society, such as com-pensating injured people through thecourts, a lower level of proof, such as ‘thebalance of probabilities’, is generally used.In this case society considers that the costs ofbeing ‘wrong’ in reaching the lower level ofproof, i.e. the ‘false positive’ of compensat-ing injured people for injuries that were notcaused by the negligence of others, is lesscostly than being ‘wrong’ in the otherdirection, i.e. the ‘false negative’ of notcompensating people for the injuries thatwere caused by the negligence of others.Another example of the use of a low level ofproof, or probability, is disaster insurancewhere the cost of being wrong when nodisaster happens is generally consideredmore acceptable than the cost of beingwrong in the other direction, i.e. where noinsurance premiums are paid and disasterstrikes. ‘It is better to be safe than sorry ‘ isthe popular expression of this sentiment.

For public health policy-making, where theremay be serious and irreversible healthimpacts, the use of a lower level of proofthan used in good science is recommendedin various international agreements, via the‘precautionary principle’ (Box 3.10.15).

4.2. Integrated approaches to preventionThe multi-causal disease process also offersseveral points at which strategies for avoidingreducing or compensating harm can befocused (Figure. 3.10.8). However, identify-ing and implementing the most effectivestrategy is difficult, and involves questions offeasibility (technical, economic and practi-cal), cost-effectiveness and ethics. Responsescan also be focused on the individual (behav-iour change or medical intervention), or atthe community and its environmentalexposures. When the response strategy is

Hostgenetics

Geneticengineering?

Remove’sensitive‘groups fromexposure?

Hoststate

Improvenutrition?

Promotegood health?

Vaccinate?

Exposures

Reduce?

Eliminate?

Effects

Predict?

Identifyearlier?

Stop/slowprogressionto harm?

Harm

Cure?

Compensate?

Clean up?

Learn from’mistakes‘?

Warn?

Possible strategies for avoiding, reducing and compensating harm...

...but which strategies would be most effective?

Source: EEA

Figure 3.10.8 Strategies: points of intervention


Box 3.10.17. Traffic accidents

Road traffic accidents are 1.4% of all deaths (some45 000 deaths in 1994 in the EU) and 20% of allaccidental deaths in the European Region of WHO.About 1 in every 3 deaths involves people youngerthan 25 years. Due to the high proportion of youngvictims, it is estimated that on average peoplekilled in traffic accidents die about 40 years earlierthan their life expectancy.

From 1993, it appears that the decreasing trend islevelling-off, especially in western countries, wherethere has been little progress in achieving a furtherreduction in mortality over the past few years.

The reduction in the number of fatalities has notbeen paralleled by a proportional reduction in thenumber of traffic accidents with injuries, whichsince 1993 have increased slightly.

More pedestrians are killed per 1 000 accidentswith injury than other road user categories.

Pedestrians account for around 13% of casualties(dead and injured) and 22.5% of deaths by roadtraffic accidents in the 26 countries of the ECMT.Pedestrians report the second highest number offatalities among road users in all OECD countries,with the exception of the Netherlands, wherecyclists account for more fatal accidents thanpedestrians (OECD, 1998).

Cyclists are more likely to have an accident thanother road users and they will sustain a greaterproportion of head injuries than other road users(OECD, 1998). At least two-thirds of the cyclistskilled in accidents had head injuries whichcontributed to or resulted in death. However, bothcycling and walking have very beneficial healtheffects. WHO estimates that half an hour’s walkingand cycling a day could reduce the prevalence ofheart disease, obesity and diabetes by 50% (WHO,March 1999, press release).

x

Drivingforce

Pressure

State

Exposure

Effect

Act

ion

Increasing cardensity

Conflictsbetween carsand pedestriansRoad quality

Time spentin hazardoussituationsparticles,irritants

Motor vehicleaccidentsand injuries

Transport policyrelying on cartransport

Emmisions of airpollutants

Air concentrationof lead NO etc.

Personalexposure, e.g.Blood lead

Effects onrespiratorysystems;lead poisoning

Noise emissionsfrom roads

Noise levelsin community

Time spentin noisyenvironment

Noisedisturbance

Figure 3.10.9Transport: multi-causality in transport hazards

Source: WHO

focused on reducing exposures, say to trafficfumes, there are many points of policyintervention, involving both ‘upstream’, e.g.the ‘driving forces’ of transport policy, and‘downstream’, e.g. noise barriers (Figure3.10.9). In general, strategies-focused ‘up-stream’ will be more effective than thosefocused ‘downstream’, partly because of theneed to take an integrated approach thatembraces the linkages between differentparts of transport policy. An integratedapproach will also take into account the fullrange of benefits and costs of policy re-sponses, and allow for adaptation to amodified transport system. For example,policies designed to reduce air pollutionfrom traffic by reducing traffic volumes willalso yield substantial benefits from reducednoise, accidents (Box 3.10.17), congestion,less divided communities and increasedfreedoms to play, walk and cycle in safety.Such holistic approaches can help counterthe common ‘tendency to over-estimate thecosts and under-estimate the benefits’ ofpolicy action (WHO, 1997c).

There may also be differences betweencauses of ill health that are most importantfrom a scientific point of view, and causesthat may be most important from a policyresponse point of view. Figure 3.10.10illustrates the differences between ‘scientific’and ‘social intervention’ causes in multi-factoral disease processes, such as asthma inchildren. Whilst genetic pre-disposition,respiratory hyper-sensitivity from pre-natalexposures, diet or indoor air pollution fromdamp or mites, may be the most importantscientific causes of asthma in children, therelatively minor role of traffic pollution may

be the most important ‘social intervention’cause, given the secondary benefits of areduction in traffic growth, and the impactof removing one link in a multi-causal chain.

In practice, given the multi-causal nature ofdiseases like asthma, policy responses areneeded in several areas: single cause ap-proaches can not reduce more than aproportion of disease. Integrated ap-proaches to prevention (BMA, 1998) andhazard exposure reductions, as well as moreresearch on the links between environmentand health (ESF, 1998) are needed toachieve improved health and wellbeing.


+ + =

+ + =

Hostgenetics

e.g.

Allergicsensitivity

25%

Hoststate

e.g.

Nutritionalandimmunestatus

25%

Exposures

e.g.

• Mites 10%

• Pets 5%

• Passivesmoking 5%

• NO 5%

• Damp 5%

e.g.

• Pollen 10%

• Industrialpollution 5%

• Trafficpollution 5%

50%

30% indoor

20% outdoor

Harm

100%

e.g.

Asthmain somechildren

Illustrative* toxicological ’causes‘ of childhood asthma in anaverage population

‘Allergic sensitivity may be the most important single ‘scientific cause in the multi-factoral chain of causation but ...

Percentages are only illustrative contributions to the casual chain: but researchsupports the broad percentage contributions (Swedish EPA, 1996). Particularcombinations of causes e.g. Pets and damp/passive smoking can produce greatercontributions than others such as pets and air pollution.

*

X

+ = HarmHoststate

e.g.

• Nutritionadviceandsupple-ments?

• Avoidimmunesup-pressants

Exposures

Indoor

Outdoor

e.g.

• Miteelimination?

• Eliminatedamp?

• Stopsmoking?

• Switch fuels?

• Ban pets?

e.g.

• Avoid/reducepollen?

• Avoid/reducetrafficpollution?

• Avoid/reduceindustrialpollution?

Illustrative ’social intervention‘ causes and related actions

… ’Reducing traffic pollution‘ may be the most effectivesocial intervention cause/action given:

• Less dependence on individual behaviour change

• Cost effectiveness

• More equitable cost sharing

• Largest supplementary gains e.g. reduced trafficcongestion and accidents

Figure 3.10.10Scientific causes and socialintervention causes for childhood asthma

Source: EEA

ReferencesAndersen, H.R., Halling-Sørensen, B. and Kusk, K.O.(in press). ‘A parameter for detecting oestrogenicexposure in the copepod Acartia tonsa.’ Ecotoxico-logy and Environmental Safety.

ARCI, 1898. Annual Reports of the Chief Inspector ofFactories and Workshop, London.

Bearer, C.F., 1995. ‘How are Children Different FromAdults?’ Environmental Health Perspectives, Vol. 103,Supp. 6.

BMA, 1998, Health and Environmental ImpactAssessment: An Integrated Approach, British MedicalAssociation, London.

Brunekreef B., 1997. ‘Air pollution and life expectan-cy: is there a relation?’ Occup. Environ. Med. 1997;54: 781-84

Camus M., et al., 1998. ‘Non-occupational exposure tochrysotile asbestos and the risk of lung cancer’. NewEngland Journal of Medicine, 338, 1565-1571, 1998.

Cantor, K.P., Stewart, P.A., Brinton, L.A. andDosemeci, M., 1995. ‘Occupational exposures andFemale Breast Cancer Mortality in the USA.’ ACOEM,37: 336-348.

CECHE, 1998. Global Health and EnvironmentMonitor Vol 6, Issue 2. Centre for Communications,Health and the Environment, Washington.

CICH, 1997. ‘Children Need Special Protection’, CICHNewsletter Vol. 19, No 1, p. 6. Canadian Institute ofChild Health, Ottawa.

CJPH, 1998 in press. Proceedings from the CICH Con-ference on Children and Environmental Health, May1997, Canadian Journal of Public Health, details avail-able from Canadian Institute of Child Health, Ottawa.

Davis, D.L., Axelrod, D., Bailey, L., Gaynor, M., Sasco,A.J., 1997. Rethinking breast cancer risk and theenvironment: The case for the precautionary principle.World Resources Institute, Washington DC.

Davis, D.L., Bradlow, H.L., Wolff, M., Woodruff, T.,Hoel, D.G. and Anotn-Culver, H., 1993. ‘MedicalHypothesis: Xeno-oestrogens as Preventable Causesof Cancer’. Environmental Health Perspectives 101:372-377.

de Hollander, A., Melse, J.M., Lebret, E., Kramers, P.(in press). An aggregate public health indicator torepresent the impact of multiple environmentalexposures. National Institute of Public Health and theEnvironment, Bilthoven.

Dolk, H., et al., 1998. ‘Risk of congenital anomaliesnear hazardous-waste landfill sites in Europe: theEUROHAZCON study’. Lancet 1998; 352: 423-27.

EASHW, 1998, ‘Economic Impact of OccupationalSafety and Health in the Member States of the EU’,European Agency for Safety and Health at Work,Bilbao.

Eckel, W.P., Ross, B. and Isensee, R., 1993. Pento-barbital Found in Ground Water’. Ground Water Vol.31, No 5, pp. 801-4.

ECMT, Statistical report on road accidents in 1992,1997. European Conference of Ministers of Transport,OECD, Paris.


Edqvist, Prof. L.E., 1997. Swedish National VeterinaryInstitute. ‘Introduction to the Scientific Report onAntrimocrobial Feed Additives.’ Swedish Ministry ofAgriculture, 1997. Today we defeat bacteria. Whatabout tomorrow? Documentation from a conferencein Brussels, 13 Nov. 1997. Regeringskansliet,Stockholm.

EEA, 1998. Europe’s Environment: The SecondAssessment. European Environment Agency,Copenhagen. Office for Official Publications of theEuropean Communities, Luxembourg, and ElsevierScience Ltd., Oxford, UK.

EEA/UNEP 1998, Chemicals in Europe: Low Doses,High Stakes? European Environment Agency,Copenhagen

EHP, 1998. ‘Childhood Cancer: A Growing Problem’.Environmental Health Perspectives, Vol. 106, No 1,January.

Elliot, P., et al., 1996. Cancer incidence near municipalsolid waste incinerators in Great Britain. Brit J Cancer1996; 73: 702-10

Environics International, 1998. InternationalEnvironmental Monitor, Toronto.

Environment and Health News, UK Vol 3 Edition 2,May 1998. Reported in Workers’ Health InternationalNewsletter July- December 1998, Sheffield, UK.

ESF, 1998. An Environment for Better Health.Integrated report of the ESF Environment and HealthProgramme, ed. Prof R Kroes. European ScienceFoundation. Strasbourg 1998.

EU Scientific Committee on Toxicity, Exotoxicity andthe Environment. Opinion on Human and WildlifeHealth. Effects of Endocrine Disrupting Chemicalswith Emphasis on Wildlife and on Exotoxicity TestMethods, 1999. Http://www.europe.eu.int/comm/dg24/health/sc/sct/outcome/en.htm

European Commission, 1996, Environment andImmunity, Air Pollution Epidemiology Reports Series,Nr. 11, EUR 17 475 EN., Luxembourg

European Commission et al., 1997. EC, EEA, OECD,WHO, ECEH, KEMI, IEH, BUM, CEFIC, 1997,European Workshop on the impact of endocrine-disrupters on human health and wild-life, Weybridge,UK 2-4 December, 1996, Cat. No EUR 17549,available from DG XII, Brussels.

European Foundation, 1996. Second European Surveyon Working Conditions, 1996. From: EuropeanFoundation, Dublin, Ireland.

Eurostat. EU Transport in figures – Statisticalpocketbook. Luxembourg: Office for OfficialPublications of the European Communities; 1997;ISBN: 92-827-9693-0.

FAO/WHO, 1998. Joint Food Standards Programme.Codex Committee on Pesticide Residues. 13th

Session. The Hague, the Netherlands. 20-25 April1998 in Pesticide News, UK. No. 40, June 1998.

Feurpfeil, I:, Lopez-Pila, J., Schmidt, R., Schneider, E.,Szewzyk, R., 1999. Bundesgesundheitsbl-Gesundheitsforsch-Gesundheitschutz, 42, 37-50,Springer-Verlag.

Foster, W.G. and Rousseaux, C.G,. 1995. ‘TheReproductive Toxicology of Great LakesContaminants’, Environmental Health Perspectives,Vol. 103, Supp. No 9.

Gee, D., 1995. ‘Approaches to Scientific Uncertainty’.

In Transport and Health 1995 by Fletcher andMcMichael, London.

Grandjean P. et al., 1997. ‘Cognitive deficit in seven-year-old children with prenatal exposure tomethylmercury’, Neurotoxicology and Teratology, Vol.19, no 6, pp. 417-428.

Gurunathan S., et al., 1998. ‘Accumulation ofchlorpyrifos on residential surfaces and toysaccessible to children’, Environmental HealthPerspectives Vol. 106, No 1, January.

Halling-Sørensen, B., Nors Nielsen, S., Lanzky, P.F.,Ingerslev, F., Holten-Lützhoft, H.-C. and Jørgensen,S.E., 1998. ‘Occurrence, Fate and Effects ofPharmaceutical Substances in the Environment – Areview. Chemosphere Vol. 36, No 2, pp. 357-393.Elsevier Science Ltd, UK, 1997.

Hammond EC, Selikoff IJ, Seidman H, 1979. Asbestosexposure, cigarette smoking and death rates. Annalsof New York Academy of Sciences, pp. 330, 473-490.

Health Council of the Netherlands, 1994. Noise andHealth, September 1994. Amsterdam.

Holm, J.V., Rugge, K., Bjerg, P.L. and Christensen,T.H., 1995. ‘Effects of ivermectin treatment on theattention of dung beetles to cow pats.’ Bull Entomol.Research.

Holten-Lutzhoft, H.-C., Halling-Sørensen, B. andJørgensen, S.E., 1999. ‘Algal Toxicity of AntibacterialAgents Applied in Danish Fish Farming.’ Archives ofEnvironmental Contamination and Toxicology,Springer-Verlag New York Inc., 1999

Hoyer, A.P., et al., 1998. ‘Organochlorine exposureand risk of breast cancer’, Lancet Vol 352, 1816-1820,December, London.

Hulka, B.S. and Stark, A.T., 1995. ‘Breast Cancer:cause and prevention.’ Lancet 346: 883-887.

IPCC, 1995. Climate Change: Second Assessment,Intergovernmental Panel on Climate Change, UNEP,Geneva

Jacobson, J.H. & Jacobson, S.W., 1996. ‘IntellectualImpairment in Children exposed to polychlorinatedbyphenols in utero’, N. Engl. J. Med. Vol. 335, Boston.

Jensen, A. A., 1996. Environmental and OccupationalChemicals, in Drugs and Human Lactation, Ed.Bennett P.N., Elsevier, Amsterdam.

Jørgensen, S.E., Lützhøft, H.C. and Sørensen, B.H.,1998. ‘Development of a model for environmental riskassessment of growth promoters.’ EcologicalModelling 107, 63-72, Elsevier Science B.V.

Knox, E.G. & Gilman, E.A., 1997. ‘Hazard Proximitiesof Childhood Cancers in Great Britain, 1953-80’. J. ofEpidemiology and Community Health, Vol. 51.

Kristensen, T.S., Olsen, O, 1991. ‘Impact of the workenvironment on cardiovascular disease.’ J Epidemio-logy Community Health, 1991; vol. 45, pp. 4-7.

Krzyzanowski M., 1997. ‘Methods for assessing theextent of exposure and effects of air pollution’.Occup Environ Med 1997; 54: 145-51

La Dou, J. (ed), 1998. Occupational and EnvironmentalMedicine. Second edition. USA, Appleton Lange.

Lanzky, P.F. and Halling-Sørensen, B, 1997. ‘The toxiceffect of the antibiotic metronidazole on aquaticorganisms.’ Chemosphere Vol 35, No 11, pp. 2553-2561, 1997, Elsevier Science Ltd., UK.


Luhmann, HJ, Renate E, Roemer M, 1998. Unevenlydistributed benefits from reducing pollutants,especially road traffic emissions, via reducing roadtransport. Wuppertal Institute for Climate,Enviornment and Energy. Environmental Fiscal ReformWorking Paper no. 6. Wuppertal.

Macri, A., Staza, A.V. and Dojmi di Delupis, G., 1998.‘Acute Toxicity of Furazolidone on Artemia salina,Daphnia magna and Culex pipiens molestus Larvae.’Ecotoxicol. Environ. Safety Vol. 16, p. 90-94.

Maddison, D, 1998. ‘Valuing changes in life expectan-cy in England and Wales caused by ambient concen-trations of particulate matter’. CSERGE workingpaper, GEC 98-06, Norwich.

McConnell, E.E., 1992. ‘Comparative Responses inCarcinogenesis bioassays as a function of age at firstexposure’, in Similarities and Differences betweenChildren and Adults: Implications for Risk Assess-ment, Guzelian P.S., Henry C.J. & Olin S.S. Eds. ILSIPress, Washington.

McMichael, M., et al., 1996. Climate change andhuman health. World Health Organization, 1996.Geneva.

McMichael, AJ, Anderson HR, Brunekreef B, CohenAJ, 1998. ‘Inappropriate use of daily mortalityanalyses to estimate longer-term mortality effects ofair pollution’. Int J Epidemiol 1998; 27: 450-53

McPherson, K., Steel, C.M.J. and Dixon, J.M., 1994.‘Breast Cancer Epidemiology, Risk Factors, andGenetics.’ BJM 309: 1003-1006.

Ministere des affaires sociales de sante et de la ville,Lyon 1995, REF ‘Les effets du bruit sur la sante’,

Moore, M.R., et al., 1998.. ‘Decline in maternal bloodlead concentrations in Glasgow’. J EpidemiolCommunity Health 1998; 52: 672-3.

MRC, 1997. IEH report on Health Effects of WasteCombustion Products, Medical Research Council,Institute for Environment and Health, University ofLeicester. Report R7, 1997

NRC, 1993. Pesticides in the diets of infants andchildren, National Research Council, NationalAcademy Press, Washington DC.

OECD, 1998. Safety of vulnerable road users. http://www.oecd.org/dsti/sti/transpor/road/index.htm; 1998.

Pesticides Trust, 1998. Children at Risk: MoreEvidence Against OPs, Pesticides News, No. 34,March. London.

Peto et al., 1999. ‘The European MesotheliomaEpidemic’, British Journal of Cancer Vol 79, 314, pp.666-672, Cancer Research Campaign, London.

Pogoda, J.M., & Preston-Martin, S., 1997. ‘Householdpesticides and rsk of pediatric brain tumours’, En-vironmental Health Perspectives, Vol. 105, No 11,Nov., N. Carolina.

Quinet, E., 1993. The Social costs of transport:evaluation and links with internalisation policies in :Internalising the Social Costs of Transport. ECMT/OECD, Paris 1993.

Rachel’s EHW, 1997. ‘The truth about breast cancer’,Rachel’s Environment & Health Weekly Nos 571-575,6 November 1997 – 4 December 1997. EnvironmentalResearch Foundation, Annapolis, Maryland.

Rachel’s EHW, 1998. ‘Children’s Cancer andPesticides’, Rachel’s Environment & Health Weekly,

March 5, Environmental Research Foundation,Annapolis, Maryland

Ramazzini, B., PhD., 1713. The Diseases of Artisans.For further details about Collegian Romazzini, Carpi,Italy.

Peto J et al., 1999. The European mesotheliomaepidemic. British Journal of Cancer, 1999, vol. 79 ¾,Cancer Research Campaign, London.

Rodier P.M., 1995. ‘Developing Brain as a Target ofToxicity’, Environmental Health Perspectives.

Rogan W., 1996. ‘Pollutants in Breast Milk’, Arch. ofPediatr. Adolesc. Med., Vol. 150.

Rylander L., Stromberg U. & Hagmar L., 1995. Vol. 21‘Decreased birth weight among infants born to womenwith a high dietary intake of fish contaminated withpersistent organochlorine compounds’, Scand. J. Work,Envir. & Health, Stockholm.

Samuelson, O.B., Torsvik, V. and Ervik, A.,1992a.‘Long-range changes in oxytetracycline concentrationand bacterial resistance towards oxytetracycline in afish farm sediment after medication.’ Sci. Tot. Environ.Vol 114, pp. 25-36.

Samuelson, O.B., Lunestad, B.T., Husevåg, B.,Hølleland, T. and Ervik, A., 1992b. ‘Residues ofoxolinic acid in wild fauna following medication in fishfarms.’ Dis. aquat. Org. Vol 12, pp. 111/19.

Schneider, J., 1994. Problems related to the usage ofveterinary drugs in aquaculture – a review’. QuimicaAnalitica Vol 13 (supp. 1) pp. S34-S42.

Slaper, H., et al., 1996. Estimates of ozone depletionand skin cancer incidence to examine the ViennaConvention achievements. Nature 384; 256-258.

Stan, H-J., Heberer, T. and Linkerhägner, M., 1994.‘Occurrence of clofibric acid in the aquatic system – isthe use in human medical care the source of thecontamination of surface, ground and drinkingwater?’ Vom Wasser Vol. 83, pp.57-68.

Strachan, D.P, 1995. Editorial: Time trends in asthmaand allergy: ten questions, fewer answers. Clin ExperAllergy 1995; 25: 791-94

Swedish EPA, 1996. Risk assessment, health,environment, Swedish Environmental ProtectionAgency, Stockholm.

Swedish Ministry of Agriculture, 1997. Today wedefeat bacteria. What about tomorrow? Documen-tation from a conference in Brussels, 13 Nov. 1997.Regeringskansliet, Stockholm.

Toppari, J., et al., 1996, ‘Male Reproductive Healthand Environmental Xenoestrogens’, EnvironmentalHealth Perspectives Vol 104 Supplement 4 August.

UCB, 1997. European Allergy White Paper, UCBInstitute of Allergy, Brussels

UNEP and UNICEF, 1997. Childhood lead poisoning,Information for Advocacy and Action. ISBN 92-807-1658-0

UNICEF, 1992. Impact of Lead and Agrochemicals onChildren, a report to UNICEF by EnvironmentalProtection Encouragement Agency, Hamburg, 1992.Total amount of lead released into the environment isestimated at approximately 860 000 to 1 670 000metric tons per year.

USEPA, 1996. Environmental Threats to Children, USEnvironmental Protection Agency, Washington.


Watterson, A., 1995. ‘Occupational andenvironmental factors linked to breast cancer.’ Centrefor Occupational and Environmental Health. DeMontfort University, Scraptoft Campus, Leicester, UK.A revised 1998 version of this publication is nowavailable, e-mail: [email protected]

Wegman, D. and Fine, L., 1996. ‘Occupational andEnvironmental Medicine.’ J: Am Med Ass, 1996, Vol.275, pp. 1831-4.

Weisglas-Kuperus, et al., 1996. ‘Immunological effectsof background perinatal and post natal exposure todioxins and polychlorinated biphenyls in Dutchinfants’. Pediatr Res 1996.

WHIN, 1998. Workers’ Health InternationalNewsletter (WHIN), July-December 1998, p. 30. Webinfo: http://www.niehs.nih.gov/emfrapid/home.htmand http://www.nytimes.com/aponline/w/AP.Electric-Fields-Cancer.html; WHO, home page: http//www.who.ch/, reproduced in Workers’ HealthInternational Newsletter (WHIN), January-June 1998,p. 3 and p. 5.

WHO, 1993. The Environmental Health CriteriaDocument on Community Noise. Report on the TaskForce Meeting, Düsseldorf, Germany, 24-28November, 1992. World Health Organization, WHORegional Office for Europe, Copenhagen. [ReportEUR/HFA Target 24].

WHO, 1994. Joint WHO/German Regional seminar onDrinking Water Quality. Report on a WHO seminar,Bad Elster, Germany 10-14 October 1994. EUR/ICP/EHAZ 94 11/WS03. 25pp.

WHO, 1996a. Mc Michael, A.J., Haines, A., Sloof, R.,Kovats, S. Climate change and human health. Anassessment prepared by a task group. WHO/EHG/96.7.

WHO, 1996b. ‘Levels of PCBs, PCDDs and PCDFs inHuman milk’, Environmental Health in Europe, No 3,World Health Organization, Regional Office forEurope, Copenhagen.

WHO, 1997a. Occupational Health. WHO Fact Sheet,no 84. Revised December 1997. Web: http://www.who.ch/

WHO, 1997b. Update and Revision of the WHO AirQuality Guidelines for Europe, Particulate Matter (inpress), World Health Organization, Regional Ofrice forEurope, Copenhagen.

WHO, 1997c, Guidance For Setting Air QualityStandards, May, World Health Organization, RegionalOffice for Europe, Copenhagen.

WHO, 1997d. Health and environment in sustainabledevelopment. Five years after the Earth Summit.WHO/EHG/97.8. World Health Organization, Geneva,242 pages.

WHO, 1998a. ‘Assessment of the health risk ofdioxins: Re-evaluation of the tolerable daily intake(TDI)’, Final note on consultation, December, WorldHealth Organization, Geneva.

WHO, 1998b, ‘When the smoke gets thicker: Smokingwhile being exposed to chemical or physical agents orbiological dust is extremely dangerous’ World HealthOrganization Factsheet No 158 (rev), Geneva.

WHO, 1999a. An overview of Environment and Healthin Europe in the 1990s. Background paper for 1999London conference. World Health Organization,Regional Office for Europe, Copenhagen.

WHO, 1999b. Early human health effects of climatechange. Background document for 1999 Londonconference. World Health Organization, RegionalOffice for Europe, Copenhagen.

WHO/EEA, 1997. Air and Health. World HealthOrganization/European Environment Agency.Copenhagen.

WHO/EEA, 1999. Monograph on Water Resourcesand Human Health in Europe. Draft Report. InPreparation.

WHO/EURO, 1998. Health in Europe 1997. WHORegional Publications, European Series No. 83.Woolff, M:S:, Tomiolo, P:G:, Lee, E:W:, Rivera, M. andDubin, N, 1993. ‘Blood Levels of OrganochlorineResidues and Risk of Breast Cancer.’ JNCI 85: 648-652.

WRI, 1997. Working Group on Public Health andFossil Fuel Combustion. Short-term improvements inpublic health from global-climate policies on fossil-fuel combustion: an interim report. Lancet 1997; 350:1341-49.


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3.10. Human health issues - European Environment Agency