Tài liệu THE BURDEN OF DISEASE ATTRIBUTABLE TO ENVIRONMENTAL POLLUTION pptx

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 environmental factors. It is a first step in the process of quantifying the possible burden of disease from environmental pollution. Current estimates are based on very uncertain data and limited datasets and therefore need to be interpreted with extreme caution. The extent to which environmental pollutants contribute to common diseases is not accurately resolved. However, global estimates conservatively attribute about 8-9% of the total burden of disease to pollution. Data is presented on the evidence available for diseases such as asthma, allergies, cancer, neuro-developmental disorders, congenital malformations, effects of ambient air pollution on birth weight, respiratory and cardiovascular diseases and mesothelioma. Health effects from environmental lead exposure and disruption of the endocrine function are also presented. 1. Background The need to estimate the burden of disease associated with pollutants is highlighted not only by the evidence base on associations but also by the scale of use of chemicals in our modern society. Fifteen thousand chemicals are produced in quantities in excess of 10,000 pounds annually and 2,800 are produced in annual quantities in excess of 1 million pounds. These high volume chemicals have the greatest potential to be dispersed in environmental media and less than half of these have been tested for human toxicity (US EPA, 1996; Goldman LR et al, 2000; NAS, 1984). There are approximately 30,000 chemicals in common use and less than 1% of these have been subject to assessment of toxicity and health risk (Royal Commission on Environmental Pollution, 2003). Environmental pollutants may be defined as chemical substances of human origin in air, water, soil, food or the home environment. The extent to which such pollutants may contribute to common diseases of multi-factorial aetiology is not accurately resolved. However in recent years attempts have been made to estimate the environmentally attributable burden of disease globally, in the USA and in regions of Europe. In the first 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 environmental risk factor(s) is calculated as a time-indexed “stream” of disease burden due to a time-indexed “stream” of exposure. Such a time-indexed “stream” of exposure data is only available for environmental lead and ambient urban outdoor air pollution. Therefore in Section 9 WHO estimates of the burden of disease attributable to environmental lead exposure are presented. Similarly in section 10 and 11 estimates are given of the burden of disease due to exposure to air pollution published by the Committee on the Medical Effects of Air Pollution of the Department of Health. Since population exposure data are lacking in connection with asthma, cancer and neurobehavioral disorders a second methodology is employed in Sections 3, 5 and 6. This was devised in the U.S. specifically for children and is outlined in Section 2. This method is also used to infer the burden of allergy attributable to environment in Section 4. Finally the primary research literature was assessed to estimate the burden of congenital malformations attributable to environment (Section 7) as well as effects of ambient air pollution on birth weight (Section 8) and on children’s lung function (Section 10). 2. Methodology The Global Burden of Disease (GBD) 1990 project stimulated debate about the crucial role of risk factor assessment as a cornerstone of the evidence base for public health action. It was affected by a lack of conceptual and methodological comparability across risk factors but the Comparative Risk Assessment (CRA) project co-ordinated by WHO was planned as one of the outputs of the GBD 2000 project to strengthen these aspects. (WHO 2004b). In particular in the CRA framework: • The burden of disease due to the observed exposure distribution in a population is compared with the burden from a hypothetical distribution or 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 exposure. Inadequate water and sanitation and indoor air pollution from household use of solid fuel for cooking and heating are not major issues in the UK. Further the population health effects arising from outdoor ambient air pollution have been estimated by the Committee on the Medical Effects of Air Pollution (COMEAP) of the Department of Health (COMEAP 1998). However, a different methodology has been developed and employed in the USA to estimate the morbidity and mortality for asthma, cancer and developmental disabilities in children. (Landrigan P.J. et al 2002) For each disease, expert panels were convened from prominent physicians and scientists with extensive research publication in the field. Each panel member was supplied with an extensive collection of reprints of published articles that discussed linkages between the disease in question and toxic environmental exposures. A formal decision-making process, the modified Delphi technique (Fink A. 1984), was then enacted by which the panel developed a best estimate from 0% to 100% of the Environmentally Attributable Fraction (EAF) for the disease in which they were expert. Panels chose deliberately not to consider outcomes related to tobacco or alcohol that are the consequence, at least in part, of personal or familial choice. It is these EAF’s which are used below in estimating the BODAE for the The burden of disease attributable to environmental pollution 4 population of children in England and Wales for asthma, cancer and developmental disabilities. 3 Asthma 3.1 Evidence of environmental aetiology It is reasonable to assume that the variations in asthma prevalence are largely attributable to environmental factors. Although genetic differences could contribute to the geographical pattern, it seems very unlikely that they could account for the great 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 (Krzyzanowski M et al, 1990; Hosein HR et al, 1989) or school (Smedie G et al, 1997) environment. These compounds are emitted by various sources used in furniture, hobbies and other indoor activities; they may act as respiratory irritants or increase the risk of allergy as represented by serum IgE levels. In numerous surveys, indoor mould growth and dampness have been associated with respiratory symptoms (Burr ML, 2001). Environmental tobacco smoke (passive smoking) increases a child’s risk of respiratory illness, and smoking during pregnancy has adverse effects on the lungs of the unborn child. There is some uncertainty as to whether smoking (active or passive) actually causes asthma, partly depending on how the disease is defined. It may be the case that it aggravates rather than causes it (Strachan DP et al, 1998). The burden of disease attributable to environmental pollution 5 3.2 Burden of disease Asthma is a common disease. Although its mortality is fairly low, it gives rise to a great deal of anxiety, particularly in childhood, when it is a major cause of hospital admission and morbidity. The peak incidence is in the first five years of life, though the disease can start at any age. The prevalence declines at adolescence, when remissions tend to exceed incidence, but relapse often occurs during adult life after a symptom-free interval. It is sometimes difficult to distinguish asthma from other common conditions, such as respiratory infections in infants and chronic obstructive pulmonary disease in 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 rhinitis and eczema (although the data are largely derived from questionnaires); successive surveys in Japan have shown a rise in the prevalence of specific IgE in serum (Nakagomi T et al, 1994). The Welsh Health Survey recorded that in 2003/2004 10% of adults (aged over 16 years) and 12% of children reported that they were currently being treated for asthma and 1% of children reported that they were currently being treated for other respiratory conditions (Welsh Health Survey, 2003). The Health Survey for England (2002) reported rates of doctor diagnosed asthma of 20.5% in 0-15 year olds and 14.5% for all ages. The burden of disease attributable to environmental pollution 6 The burden of disease registered in Primary Care is recorded by 371 practices across the UK submitting data to the General Practice Research database. The prevalence of asthma in different age groups is shown below. The burden of disease attributable to environmental pollution 7 Prevalence of treated asthma per 1000 patients For Males (1998) 0-4 years 5-15 years 16-24 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 Prevalence of treated asthma per 1000 patients For Females (1998) 0-4 years 5-15 years 16-24 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 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 46348 LCL – 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: Total Population ▲ Prevalence rate EAF BODAE Number of children in England and Wales aged 10-14 years with wheeze in last 12 months 3425023 29.0% 30% 297977 Number of children in England and Wales aged 0-9 years with wheeze in last 12 months 6401995 29.0% 30% 556974 Number of children in England and Wales aged 0-15 years currently being treated for asthma 10488736 12.0% 30% 377594 Number of children in England and Wales aged 0-15 years with doctor diagnosed asthma 10488736 20.5% 30% 645057 Number of adults in England and Wales aged 16 and over currently being treated for asthma 41553180 10.0% 30% 1246595 Number of adults in England and Wales aged 16 and over with doctor diagnosed asthma 41553180 14.5% 30% 1807563 ▲ Source: Census 2001 data. (i) ISAAC survey data was for 13 to 14 year olds so it is assumed that the prevalence of wheeze in 10-12 year olds is 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 Status asthmaticus ICD10:J46.X 9228 x 30% = 2768 Nonallergenic asthma ICD10:J45.1 60 x 30% = 18 Mixed asthma ICD10:J45.8 26 x 30% = 8 3.2.2 Proportion of asthma attributable to indoor biologic pollution. There is strong evidence linking asthma exacerbations to derp 1 allergen indoors and relatively strong evidence linking asthma exacerbations to contamination of the indoor environment with moulds. Survey data demonstrates that 95% of asthmatics have derp 1 concentrations in their mattress dust in excess of WHO guideline value of 2 µg/g -1 . Survey data also demonstrates that approximately 17% of homes are contaminated with mould. Since most people spend more than 90% of their time indoors there is significant exposure of the asthmatic population to these allergens. Although no estimates of EAF from these sources are available it is likely to be of similar magnitude to that due to outdoor non biologic sources. 3.4 Conclusion The burden of asthma exacerbations attributable to non-biologic air pollution is considerable. Asthma exacerbations can be measured by the prevalence of wheeze in the last 12 months and prevalence of current treatment for asthma. Using UK data on such prevalence and the EAF cited above the burden of asthma exacerbations attributable to non-biologic pollution can be estimated. This is 855,000 of those children reporting wheeze in the last twelve months and 378,000 of those children currently being treated for asthma as well as approximately one and a quarter million of those adults currently reporting being treated for asthma and 22,000 of inpatient episodes per annum. The epidemiological evidence base linking asthma exacerbations to indoor allergens such as der p1 and moulds is no less strong than that relating asthma to non-biologic outdoor air 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. [...]... (www.statistics.gov.uk) Burden of respiratory disease attributable to Environment 10.3.1 COMEAP statement on the short-term effects of air pollution on mortality and hospital admissions The Department of Health (DH) asked COMEAP to advise on the extent of effects of air pollutants on health in the UK including an estimate of the number of people affected 25 The burden of disease attributable to environmental pollution The. .. been reviewed by the Committee on the Medical Effects or Air Pollution (COMEAP) of the Department of Health who have published risk estimates (see section 10.3) 24 The burden of disease attributable to environmental pollution 10.2 Burden of respiratory disease The percentage of adults reporting respiratory disease is available from the Welsh Health Survey (2003) Per cent of adults reporting being treated... ages in 2001: 10 The burden of disease attributable to environmental pollution 4.3 Burden of allergic disease attributable to environment There is no evidence on the EAF for allergic disease If it is assumed that the exposures and mechanisms involved in the aetiology and exacerbation of asthma are similar to those involved in allergy, then the EAF for asthma (i.e 30%), the percent of children with skin... Milder disease outcomes, in particular hypertension in adults and the loss of IQ points and the resultant increase in mild mental retardation (MMR) in children are of increasing concern at levels of exposure that were previously considered safe (ATSDR 1999) 22 The burden of disease attributable to environmental pollution 9.4 Burden of disease The World Health Organisation has assessed the disease burden. .. 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... individual There would appear to be an increase in the numbers of the general population exposed to some allergens, and possibly in their levels of exposures to some of these materials 1 As consumers: toothpastes, household sprays, cleaning materials, perfumes 2 Indoor environmental agents: e.g volatile organic compounds 3 Outdoor pollutants: diesel exhaust fumes 4.2 Burden of allergic disease Up to 35% of the. .. year) and the population in the grid square Satisfactory data on the concentrations of these pollutants were available for urban areas of Great Britain and thus estimates of effects of these pollutants were limited to these areas The urban population of England and Wales is 46,794,939i : The committee stressed that the affects are likely to occur in those with severe preexisting disease Numbers of deaths... BODAE 6.3% = 594,182 The burden of disease attributable to environmental pollution The infant respiratory system may be particularly susceptible to air pollution (Teague WG et al, 2001; Bates DV, 1995; American Academy of Pediatrics Committee on Environmental Health, 2003) There are few studies which have focused upon the effects of air pollution on infants Infant mortality studies in the Czech Republic... respect of long term effects on children’s lung function The limited amount of evidence reviewed above indicates that the burden attributable to air pollution may be considerable There is evidence of an effect of air pollution on respiratory deaths in the post-neonatal period which it appears may be due mainly to particulate air pollution (WHO, 2005) 11 CARDIO-VASCULAR DISEASE 11.1 Evidence of environmental. .. 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 17 The burden of disease attributable to environmental pollution They suggested that . estimate of the burden of asthma exacerbations attributable to environmental factors. The burden of disease attributable to environmental pollution. given of the burden of disease due to exposure to air pollution published by the Committee on the Medical Effects of Air Pollution of the Department of Health.