THE BURDEN OF DISEASE
ATTRIBUTABLE TO ENVIRONMENTAL POLLUTION Professor Ian Mathews and Dr Sharon Parry
Department of Epidemiology, Statistics, Public Health
University of Wales College of Medicine
Cardiff University
Heath Park
Cardiff
CF14 4XN The views presented in this paper are those of the authors and do not necessarily
represent HPA views

July 2005 The burden of disease attributable to environmental pollution
1
Summary
This paper presents a summary of the information available in the literature aimed at
estimating the fraction of mortality and/or morbidity that can be attributed to

instance estimation has concentrated on health outcomes for which there is strong
evidence of an association with pollutants.

At a global level a summary of early estimates first appeared in the 1997 report ‘Health
and Environment in Sustainable Development’ by the World Health Organisation (WHO,
1997). In subsequent years further estimates have been made of the fraction of
mortality and morbidity that can be attributed to environmental factors (Smith KR et al,
1999; Ezzati M et al, 2002). Substantial proportions of global disease burden are
attributable to these major risks where developing countries bear the greatest burden,
unsafe water and indoor air pollution are the major sources of exposure and children
under five years of age seem to bear the largest environmental burden. Estimates vary
The burden of disease attributable to environmental pollution
2
but conservatively about 8-9% of the total disease burden may be attributed to pollution
(Briggs D, 2003).

In the framework of the European Environment and Health Strategy various
Technical Working Groups on priority diseases reviewed the evidence base in
support of the development of the Children’s Environment and Health Action Plan
for the European region (CEHAPE) expressed in the Budapest declaration (WHO
2004a). It was considered that one sixth of the total burden of disease from birth
to 18 years is accounted for by exposure to contaminated air, food, soil and water
causing respiratory
diseases, birth defects, neuro-developmental disorders and
gastrointestinal disorders. Waterborne gastrointestinal disorders are not a major public
health problem in the UK. The remaining priority diseases identified by CEHAPE are
considered below for children.

In Section 2 two different methodologies are outlined by which burden of disease
attributable to environment can be estimated. In the first the health loss due to

The burden of disease attributable to environmental pollution
3
series of distributions, rather than a single reference level such as the non-
exposed population.

• The health loss due to risk factor(s) is calculated as a time-indexed
“stream” of disease burden due to a time-indexed “stream” of exposure.

• The burden of disease and injury is converted into a summary measure of
population health, which allows comparing fatal and non-fatal outcomes,
also taking into account severity and duration
.

The CRA framework has been used to investigate the burden of disease associated with
exposure to a limited number of environmental risk factors. These are: unsafe water,
sanitation and hygiene, urban air pollution and indoor air pollution from household use of
solid fuels as well as lead exposure (WHO 2004c).

To provide the knowledge base for the development of the Children’s Environment and
Health Action Plan for the European region (CEHAPE), the burden of disease
attributable to environmental factors (BODAE) was assessed in terms of deaths and
disability-adjusted life years (DALYS) among children and adolescents. The
assessment was restricted to outdoor and indoor air pollution, inadequate water and
sanitation and lead (Valent F et al, 2004). The methodology employed is outlined in
Appendix 1 and used the distribution of risk-factor exposure within the study population
and the exposure-response relation for the risk factor to calculate the impact fraction for
the particular health outcome.

To date the estimates of burden of disease attributable to environmental factors
provided by the WHO are of limited value in a UK context with the exception of lead

variation that is found within Europe, and they obviously do not explain the time trends.

In children and young adults, asthma usually involves an allergic reaction to inhaled
allergens. The simplest explanation of variations in prevalence would be a
corresponding variation in exposure to the principal allergens. The house dust mite is
the source of the allergen to which asthmatic patients are most commonly sensitive. The
changes in asthma prevalence have therefore been ascribed to increased exposure to
house dust mites, consequent upon changes within houses such as more fitted carpets
and better insulation. But in fact there is little evidence that exposure to mites has risen,
apart from one study.

The effects of air pollution on children’s health has been reviewed (WHO, 2005) and it is
considered that air pollution exacerbates symptoms of asthma and that the respiratory
health of children, especially those with asthma, will benefit substantially from a
reduction in air pollution especially that from motor vehicle exhausts. Some air
pollutants (diesel particulates) appear to potentiate the effects of airborne allergens.
There is little evidence for a causal association between prevalence/incidence of asthma
and air pollution. There is some (rather inconsistent) evidence that asthma prevalence
is related to the proximity of peoples’ residence to roads

(Maynard RL, 2001). Asthma
attacks can certainly be provoked by episodes of acute air pollution.

Most people spend most of their time indoors, so the quality of indoor air is probably
more important than that of outdoor air. Oxides of nitrogen are produced by gas cookers
and in some studies (though not in others) have been associated with respiratory
symptoms

(Hasselblad V et al, 1992). There is some evidence that asthma is
associated with formaldehyde and other volatile organic compounds in the home

later adult life. If asthma is defined more narrowly in some surveys than in others, large
differences in prevalence can be created quite artificially. Nevertheless, a useful body of
data has been produced by numerous surveys that have used similar methods, and
some fairly consistent patterns are now emerging.

The International Study of Asthma and Allergies in Childhood (ISAAC, 1998) was
conducted in 155 centres within 56 countries and the prevalence of wheeze in the last
12 months in 13-14 year olds was 29-32% in the UK. The European Community
Respiratory Health Survey (ECRHS) was conducted in 48 centres within 22 countries,
mostly in Western Europe

(Janson C et al, 2001). It showed a similar pattern to that
found by ISAAC. The prevalence of specific IgE, a marker of atopic sensitivity, which is
known to be associated with asthma was much higher in UK than in Iceland, Greece,
Norway, Italy and parts of Spain.

Wherever a survey has been repeated after an interval of 10 years or more, in the same
area using the same methods, the prevalence of asthma has been found to have risen.
Most of these surveys have used questionnaires enquiring about symptoms (particularly
wheeze) rather than asthma alone, so the increase is not merely attributable to a
change in diagnostic fashion.

One of these (in South Wales) used an exercise challenge test and from 1973 to 1988
asthma prevalence increased, as measured by symptoms and exercise challenge (Burr
ML et al, 1989).

A repeat survey in 2003 (unpublished) suggests that a further rise has
occurred in symptoms but not in the response to exercise. The consistency with which
increases have been reported from all parts of the world is remarkable. Some support
for a true increase is also provided by increases in related diseases such as allergic

years
25-34
years
35-44
years
45-54
years
55-64
years
65-74
years
75-84
years
85+
years
crude
rate (all
years)
age
standardised
rate (all
years)
rate per
1000 97 132.1 72.8 55.3 47.2 44.5 59.2 80.7 89.4 61.8 72.3 73.2
LCL 93.8 129.9 70.7 53.8 45.8 43.1 57.4 78.3 85.9 55.7 71.7 72.5
UCL 100.2 134.3 74.8 56.8 48.5 45.9 61.1 83.2 92.9 67.9 73 73.9
No. of
Cases
3182 11979 4571 5020 4274 3779 3745 3809 2303 373 43035 43035


years)
rate per
1000 62.5 104.1 85.2 65.3 62.4 64.8 79.9 88 80 52.2 76.2 76.5
LCL 59.8 102 83 63.6 60.8 63.1 77.8 85.6 77.4 48.7 75.6 75.8
UCL 65.2 106.1 87.5 66.9 64 66.5 82 90.4 82.7 55.6 76.9 77.2
No. of
Cases
1946 9014 5066 5818 5473 5369 4965 4694 3174 829 46348 46348LCL – Lower Confidence Level; UCL – Upper Confidence Level
The burden of disease attributable to environmental pollution
8
Some information is available as part of the Hospital Episode Statistics detailing
episodes of admitted patient treatment delivered by NHS hospitals in England. The
most recent data is available for the 2003/2004 financial year when 63,949 episodes of
unspecified asthma (ICD10: J45.9) and 9,228 episodes of status asthmaticus (ICD10:
J46.X), 60 episodes of nonallergenic asthma (ICD10: J45.1), 26 cases of mixed asthma
(ICD10: J45.8), were recorded.

3.3 Burden of Asthma attributable to Environment

3.3.1 Asthma attributable to outdoor non-biologic pollution

The expert US panel on asthma considered only outdoor non-biologic pollutants from
sources potentially amenable to abatement such as vehicular exhausts and emissions
from stationary sources. Using this definition the panel estimated that 30% of acute
exacerbations of childhood asthma (range 10-35%) are environmentally related
(Landrigan PJ et al, 2002). Applying this EAF to national survey data, Primary Care
data and data on hospital inpatient episodes gives:

the same
(ii) Assuming the same prevalence in 0-10 year olds as in 12-13 year olds
The burden of disease attributable to environmental pollution
9
Environmentally attributable prevalence of treated asthma per 1,000 patients in Primary Care

Age Sex BODAE per 1000 patients
0 – 4 Male 97 x 30% = 29
5 – 15 Male 132.1 x 30% = 40
0 – 4 Female 62.5 x 30% = 19
5 – 15 Female 104.1 x 30% = 31
All ages Male 72.3 x 30% = 22
All ages Female 76.2 x 30% = 23

Inpatient episodes in NHS hospitals in England in 2003/2004 Unspecified asthma ICD10:J45.9 63949 x 30% = 19185

pollution. It is, therefore, likely that the EAF used to obtain the above estimates could be
doubled to give a more realistic estimate of the burden of asthma exacerbations attributable to
environmental factors.
The burden of disease attributable to environmental pollution
10

4. ALLERGY

4.1 Evidence of environmental aetiology
The term allergy describes those immune responses that are potentially harmful to the
host but which are directed against external agents that in themselves are not
particularly harmful to us. Many individuals synthesise specific IgE antibodies against
common environmental allergens, and they are termed atopic. For example, grass or
tree pollens or nickel jewellery are indeed foreign material but pose no threat to us when
we come into contact with them. However many individuals mount an immunological
reaction to such structures which results in inflammation at the site of contact with the
allergen and hence symptoms and disease.

The targets against which most allergic diseases are directed (i.e. the allergens
themselves – house dust mite, cat, grass pollens etc) are not becoming particularly
more prevalent but the level of sensitization to them in the general population is. The
change in the biologic response to them is thought to reflect the effects of unidentified
factors (possibly dietary fats and air pollutants) involved in the process of sensitization
which occur at the level of the antigen presenting cell – T cell interaction in each
individual.

There would appear to be an increase in the numbers of the general population exposed

similar to those involved in allergy, then the EAF for asthma (i.e. 30%), the percent of
children with skin complaints (11%) and of adults with allergic rhinitis (10%), may be
used to infer the BODAE for allergy.

Allergic rhinitis (Total population of Eng & Wales) 52,041,916 x 10% x 30% = 1,561,257
Skin complaints (Population of children) 10,488,736 x 11% x 30% = 346,128

4.4 Conclusion
Environmental factors may be responsible for one and a half million cases of allergic
rhinitis and one third of a million cases of skin complaints in children. 5 CANCER

5.1 Environmental aetiology

Monozygotic and dizygotic twins have been studied in an attempt to apportion the
relative importance of genes and environment in the aetiology of cancer (Ahlbom A, et al
1997, Verkasalo PK 1999, Lichtenstein P et al 2000). The largest dataset used for
family studies is the nationwide Swedish Family – Cancer Database with more than
700,000 cancers and a population of 9.6 million. Modelling of this data gave estimates
that environment has a principal causative role in cancer at all studied sites except for
thyroid (Czene K 2002).
5.2 Burden of disease and Burden of disease attributable to Environment

To assess the environmentally attributable fraction of childhood cancer an expert panel
was convened in the US in paediatric oncology, epidemiology and environmental
medicine. The panel considered that extra genetic factors, defined broadly, caused 80-
90% of cancers but noted that the specific causes of childhood cancer are largely
unknown. It concluded that insufficient evidence exists to assign a best estimate of the

persons 1243 5% 625.4 Conclusion

Currently the best available estimate is that between 5% and 90% of childhood cancers
may be attributable to toxic chemicals in the environment.

The burden of disease attributable to environmental pollution
13
6. Neuro-developmental disorders

6A Attention Deficit Hyperactivity Disorder (ADHD)

6A.1 Evidence of environmental aetiology

For all complex diseases, there is increasing evidence that genes may operate by
influencing sensitivity to environmental risk factors. There have been more than 14 twin
studies across the world that have shown that ADHD is highly heritable with reported
heritability estimates of between 60% and 91% (Thapar et al, 1999; Thapar 2002).
Finally adoption studies have also shown increased rates of ADHD amongst biological
but not adopted relatives of individuals affected by ADHD (Thapar, 2002). Most interest
to date has focussed on examining variants within genes coding for enzymes and
proteins in the dopamine neurotransmitter system. Association of a variant in the
dopamine D4 receptor gene (the 7 repeat allele of a 48 bp VNTR) with ADHD has been
widely replicated and shown to be significantly in a meta analysis of 14 studies (Faraone
et al, 2001).

There has been increased interest in gene-environment interaction effects in childhood
psychopathology. To date there have been virtually no published studies examining the

only diagnosed if the child meets stringent diagnostic criteria. Two main diagnostic
schemes are used in psychiatry, the International Classification of Diseases (ICD; WHO,
1993), more often used in Europe and the DSM (American Psychiatric Press, 1994)
from the United States. The diagnostic criteria in the current versions of the
classification systems are similar although DSM-IV ADHD remains a more broadly
defined category than ICD-10 Hyperkinetic disorder.

The key features of ADHD are early onset, significant symptoms of inattention,
impulsiveness and over activity. These symptoms need to be developmentally
inappropriate and associated with functional impairment (for example educational
failure, peer difficulties). Both ICD-10 and DSM-IV also require that the symptoms (or
impairment) are pervasive, that is occur in different settings (typically home and school).

Evidence of brain dysfunction in individuals with ADHD has been found in cerebral
imaging studies including functional MRI (Magnetic Resonance Imaging), PET (Positron
Emission Tomography) and SPECT (single photon computed emission tomography)
studies (Overmeyer et al, 2000, Volkow et al, 2001). A recent well designed controlled
study published in the Journal of the American Medical Association reported clear
evidence that drug naive children with ADHD had decreased grey and white matter
volume and significantly smaller cerebellar volume compared to control children
(Castellanos et al, 2002). Many of these neurobiological studies have suggested
involvement of the prefrontal cortex and basal ganglia and there has been considerable
interest in dopaminergic neurotransmitter system (Zametkin & Liotto 1998) but it is clear
that the neurobiological basis of ADHD is complex with involvement of many pathways.
The prevalence of ADHD has been estimated at between 2 % and 5% (Faraone &
Wilens, 2003) although prevalence figures vary according to the diagnostic criteria used
(Costello et al 1996; Barkley, 1998). For Hyperkinetic Disorder, prevalence rates in the
UK have varied between 0.5% (for boys only) (Taylor et. al, 1991) to 1.4% in the most
recent UK survey (Meltzer et al, 2000). ADHD is much commoner in boys with a 3:1 sex
ratio found in epidemiological studies and an even higher sex ratio in referred samples

England and Wales can be estimated as follows:

Disease No. of children
(0-14)*
Prevalence rate No. of
cases**
EAF BODAE
ADHD 9,827,018 1.40% 137578 10% 13757

* in England and Wales (Census 2001)
** in England and Wales

6B Autism
Autism is now commonly regarded as belonging to a group of neurodevelopmental
disorders that are sometimes called pervasive developmental disorders. These are
childhood onset conditions but problems nearly always persist into adulthood. The key
clinical features of autism include:
• onset in early childhood (some type of abnormality by 36 months of age)
• communication problems (both comprehension and expression and gesture as well
as spoken language)
• social interaction (reciprocal -includes features like poor eye contact, lack of interest
in people)
• restrictive, repetitive patterns of behaviour (includes routines and rituals and
preoccupations with restricted subjects).

Other autistic spectrum disorders, notably Asperger’s syndrome, have similar
manifestations to autism but are generally less severe and meet some but not all of the
diagnostic criteria for childhood autism. The majority of children with autism (around 2/3)
have learning disability (mental retardation) and many develop epilepsy in adolescence
.

not known why this is the case (Rutter et al, 2003).

An increased prevalence rate over time has been reported with studies between 1966
and 1991 reporting an average prevalence of 0.044% and studies between 1992 and
2001 reporting an average prevalence of 0.127% (Volkmar et al, 2004).

In the only instance where prevalence rates were derived from successive birth cohorts
no statistically significant changes in prevalence rates of the disorder were found
(although the relatively low prevalence rates found in these 2 studies have raised some
concern that cases may have been missed (Volkmar et al., 2004).

6B.3 Burden of Autism attributable to Environment

Disease
No of children
(0-14)*
Prevalence rate
No of
cases**
EAF BODAE
Autism 9,827,018 0.10% 9827 10% 982

* in England and Wales (Census 2001)
** in England and Wales

6C Learning disability

Definitions
The formal definition of ‘learning disabilities’ or ‘intellectual disabilities’ includes the
presence of:

difficulties.

Studies of mild learning disabilities have reported between less than 10 and 25-30
people per 1,000 population which suggests that between 580,000 and 1,750,000
people in the UK have a mild learning disability.

The latest figures (2002/2003) for children on the social services register of children with
learning disabilities in Wales are 2805.

The Welsh Assembly Government collates information on children in education with
special educational needs including those with a formal statement of special need. See
table below for numbers.

The UK education system uses the term ‘learning difficulties’, rather than ‘learning
disabilities’. The Warnock Committee proposed that the term ‘learning difficulties’ be
defined as:
• A greater difficulty in learning than the majority of children of the same age
• A disability which prevents or hinders the child from making use of ordinary
educational facilities.

The burden of disease attributable to environmental pollution
18
They suggested that about one in five children would have a learning difficulty at some
time in their lives, arising, for example, from medical problems, sensory impairments,
physical disabilities, emotional and behavioural difficulties, language impairments,
specific learning problems (such as dyslexia), autism or pervasive learning difficulties.

Pupils (of any age) with statements in schools, by type of school and need (Source
Statistical Directorate, 2004)


8 .
27
Speech, language & communication 4,017
521 .
4,538
Emotional & behavioral difficulties 3,437
4,010
.
7,447
Medical difficulties 384
158 .
542
Other 11,045
5,088
.
16,133
Not stated 4,312 2,701
.
7,013
Pupils with a statement of special need: 5,817 6,350 3,752 15,919
Moderate learning difficulties 1,464
2,124
680 4,268
Severe learning difficulties 427
280
1,239 1,946
Profound & multiple learning difficulties 152
38
519 709
Specific learning difficulties 485


Disease No children/
adults
Prevalence
rate
No. of cases
**
EAF BODAE
Learning difficulties
(children 0-14)
9,827,018 13.50% 1326647 10% 132664
Learning difficulties
(adults)
41553180 0.3% 124659.5 10% 12466

* in England and Wales (Census 2001); ** in England and Wales
The burden of disease attributable to environmental pollution
19

6.4 Conclusion
In children, approximately 133,000 cases of learning difficulty, 14,000 cases of ADHD
and 1000 cases of Autism may be attributable to environmental factors. However, these
estimates are very rough and should be treated with caution
.

7 CONGENITAL ABNORMALITIES

7.1 Evidence for environmental aetiology

A large study in the UK revealed that 80% of the UK population reside within 2 Km of a

Cleft Lip and Cleft Palate 133 7
Cleft Lip 66 3
Cleft Palate 187 10
Upper Limb reduction defects 147 8
Lower Limb reduction defects 76 4
Anencephalus 143 8
Spina bifida 155 8
Encephalocele 39 2
Complex Cyanotic Disease (CHD) 134 7
Transpositional great vessels 79 4
Fallots 55 3
Ventricual septal defects (VSD) 945 50
Atrioventicual septal defects (AVSD) 113 6
Hypospadias 356 19
Chromosomal 908 48
trisomy 21 - Down syndrome 377 20
trisomy 18 - Edwards syndrome 89 5
trisomy 13 - Patau syndrome 53 3
triploidy / polyploidy 44 2
Turner's syndrome 83 4
Klinefelter's syndrome 19 1
other anomalies sex chromosomes 36 2
deletions 57 3
other chromosome anomalies 157 8 7.3 Burden of congenital malformations attributable to environment

Assuming that the observed increased risk in proximity to landfill sites is due to
environmental factors and using an EAF of 0.2 then the burden attributable to


increase in mean PM
10
concentrations during the third trimester of pregnancy was
associated with a reduction in birth weight of 11g (95% CI 2.3-19.8) [Chen et al 2002]. A
European study carried out in the Czech Republic examined the relationship between
low birth weight, premature birth, and ambient TSP during each trimester in 108,000
singleton live births [Bobak 2000]. The effects of these adverse birth outcomes were
marginally stronger for exposures during the first trimester. Adjusted odds ratios of low
birth rate and prematurity were 1.15 (95% CI 1.07-1.24) and 1.18 (95% CI 1.05-1.31) for
a 50µg/m
3
increase in TSP respectively. In contrast, Landgren who studied the effects of
air pollution on delivery of 38,000 Swedish women in 1985-1990 [Landgren 1996], and
Maisonet et al who studied the effects of PM
10
in live births born in six northeastern
cities of the United States [Maisonet et al 2001], both showed results with no indication
of a positive association between prenatal exposure to particulate air pollution and low
birth weight.

8.1 Conclusion

To date, only a limited amount of epidemiological evidence has been collected and the
results are equivocal.

9. Environmental lead exposure9.1 Exposure to environmental lead.

representative data. For subjects aged over 11 years, a geometric mean blood lead
level of 2.0 µg/dl was recorded. Blood lead levels were higher in males than females,
increased with age and were highest in adults having higher consumptions of cigarettes
and alcohol. No differences between urban and non-urban populations were identified.
(Institute for Environment and Health, 1998)

Despite differences in methodology between this and previous UK surveys, blood lead
levels appeared to have fallen since the 1984-1987 period (Delves et al. 1996) with a
long term downward trend of around 4% per year (DoE, 1988).

The Avon Longitudinal Study of Pregnancy and Childhood (ALSPAC) included a
measurement of blood lead levels in 584 two year old children in 1994 so that future
follow up could assess the impact of lead exposure on their IQ. Levels ranged from 0.8
to 27.6 µg/dl with a geometric mean of 3.44 µg/dl. Children of younger mothers, children
exposed to environmental tobacco smoke, children with pets in the home, children living
close to higher levels of traffic and children who were not breast fed had statistically
significantly higher blood lead levels. Furthermore, children living in inner city areas had
the highest levels whilst those living in outer areas had the lowest levels. (Golding et al.,
1996; Institute for Environment and Health, 1998).

9.3 Health effects

At high levels of exposure (blood lead level > 60µg/dl) acute effects are recorded
ranging from gastrointestinal problems, lethargy and irritability, encephalopathy and
death. Chronic low level toxicity can remain asymptomatic. However, in infants and
young children the developing brain is particularly vulnerable and blood lead levels as
low as 10 µg/dl or less can cause neurological deficits (Needleman and Gastonis, 1990;
Canfield et al. 2003).

Milder disease outcomes, in particular hypertension in adults and the loss of IQ points

between 50 and 69 and estimates were calculated using the ratio of those who already
had a low IQ score and for whom a loss of a few points would result in them being
categorised as having MMR.

Using studies from 6 European Region A countries (which did not include any studies
from the UK) the mean blood level for urban children was 3.5 µg/dl and the mean blood
level for urban adults was 3.7 µg/dl. It was calculated that for Region A, 227 people per
1000 population had a loss of 0.65 IQ points as a result of lead exposure. Higher IQ
losses affected smaller proportions of the population i.e 41/1000 population had losses
of 1.95 IQ points, 10/1000 population had losses of 3.25 IQ points and 5/1000
population had losses of 3.5 IQ points.

It was estimated that 1.1 persons per 1000 population were affected by MMR and that
55,000 DALYS were lost as result of lead exposure.

Using a similar calculation, the burden of disease in children expressed as the presence
of MMR in the age group 0-4 years, attributable to lead exposure was calculated.
(Valent et al. 2004). Using studies from 11 European Region A countries including one
from the UK (O’Donohoe et al. 1998), the best estimate blood lead level in children aged
0-4 years was 2.9 µg/dl. It was calculated that, 93 children per 1000 population had a
loss of 0.65 IQ points as a result of lead exposure. Higher IQ losses affected smaller
The burden of disease attributable to environmental pollution
24
proportions of the child population i.e 1/1000 population had losses of 1.95 IQ points,
none had losses of 3.25 IQ points or above. It was estimated that 0.5 children per 1000
population were affected by MMR and that 14,000 DALYS were lost as result of lead
exposure. (Valent et al. 2004).

9.4.2 Cardiovascular disease


estimates (see section 10.3).