National and regional story (Netherlands) - Environmental burden of disease in Europe: the EBoDE project
Introduction and main results
Negative impacts of environmental stressors on health can range from mild psychological effects (e.g. noise annoyance), to effects on morbidity such as asthma and increased mortality. Properly targeted and followed-up environmental health policies, such as the coal burning ban in Dublin (1990) and the smoking ban in public places in Rome (2005) have demonstrated significant and immediate population level reductions in death and diseases. The highest environment related health benefits are delivered by policies that target environmental stressors that greatly contribute to the burden of disease (BoD). The environmental burden of disease (EBD) can be expressed in Disability Adjusted Life Years (DALYs). DALYs standardise health effects by expressing the number of affected people, the duration and severity of the health effects in one number [1,2] (more information) (link to http://www.who.int/quantifying_ehimpacts/en/).
The Multinational European EBoDE project (Environmental Burden of Disease in the European region) has assessed the environmental burden of disease across six countries: Belgium, Finland, France, Germany, Italy and the Netherlands. The assessment implied nine environmental stressors: benzene, dioxins (including furans and dioxin-like PCBs), second-hand smoke, formaldehyde, lead, noise, ozone, particulate matter (PM) and radon. This selection was based on the public health relevance, potential for high individual risks, public concern and financial impacts of these environmental stressors. The objectives of the project are to update previous EBD assessments, to identify stressors relevant for the European region, to provide harmonised EBD assessments for the participating countries, and to develop and make available the methodology and databases for other countries.
Calculations were based on the most recent scientific evidence concerning population exposure and health effects, national exposure data, and WHO burden of disease data and methods for estimating disease burden where available [3-5]. Even though the most recent scientific knowledge and data were used, many uncertainties and controversies remain . Results give only a crude ranking of environmental health impacts and need to be interpreted with caution. The preliminary results suggest that 3-7 % of the burden of disease in the participating countries may be associated with the selected environmental stressors (see Figure 1). Relatively, Finland had the largest BoD and the smallest EBD, while for Italy this was vice versa. Particulate matter (PM) is estimated to be the leading factor associated with 6 000 to 10 000 DALYs per million people, followed by noise, radon and second-hand smoke (see Figure 2). Environmental health policies should focus increasingly on these exposures.
Figure 1: Relative public health impact of the selected environmental stressors in the participating countries. Numerical ranges reflect quantitative uncertainty in the average estimate. Variability between countries is in many cases much larger.
Figure 2: Relative contribution of the nine selected environmental stressors to the total environmental burden of disease attributable to these stressors (SHS = second-hand smoke).
The use of benzene as an additive in gasoline is now limited, but it is still used by industry in the production of, for example, drugs and plastics. In addition, cigarette smoke contains some benzene. Benzene is a known carcinogen for which no safe level of exposure can be recommended. The most significant adverse effects from prolonged exposure to benzene are haematotoxicity, genotoxicity and carcinogenicity (IARC group 1 carcinogen) . Increased mortality from leukaemia has been observed in workers occupationally exposed. Based on the available information about leukaemia , the total impact of benzene on public health is estimated to be low. Uncertainties relate mainly to the availability of exposure data, exclusion of health effects other than leukaemia, and the potential interaction of benzene with other components of tobacco smoke.
Dioxins (including furans and dioxin-like PCBs) are a group of chemicals which are considered to be highly toxic. They are by-products of various industrial processes and combustion activities. Long-term exposure to dioxins has been linked to effects on the immune system, the nervous system, the endocrine system and reproductive functions . In addition, chronic exposure may be related to several types of cancer . The relative burden of disease related to dioxins is estimated to be medium, however, uncertainties are large. Effects of dioxins cannot easily be distinguished from other occupational risk factors. Low-dose effects are very difficult to assess, thresholds for effects are mostly unknown, and exposure data are often only indirectly available. Our estimates only include effects of dioxins on total cancer incidence. It is as yet unclear whether our estimates over- or underestimate total health impacts.
Second-hand smoke (SHS; also called environmental tobacco smoke or passive smoking) is a known human carcinogen , causing lung cancer and a variety of other health effects . In our estimates, lower respiratory infections and acute otitis media in young children, child asthma, adult asthma, lung cancer and ischemic heart disease are included. Together, these health endpoints are estimated to lead to 600–1200 DALYs per million people (medium impact). Additional health effects supported by strong evidence, but for which disease statistics were not available, or which would overlap with the assessed outcomes, include sudden infant death syndrome, lower respiratory illness in young children, low birth weight, reduced pulmonary function among children and acute irritant symptoms and effects. In addition, uncertainties in our estimates relate to, for example, indirect exposure measurements and relative risks. Nonetheless, most evidence for SHS-related impacts is fairly consistent, and the estimates of the burden of disease are considered relatively stable.
Formaldehyde is widely present, both indoors and outdoors, but it reaches high levels mostly indoors. It is used in the production of several building materials and household products, and it can be a by-product of combustion. Exposure to formaldehyde may cause eye, nose, and throat irritation, may trigger asthma attacks and may cause cancer . The burden of disease related to formaldehyde, based on asthma incidence in children below three years is estimated to be relatively low. However, the consistency of the knowledge base is low, with uncertainties related to the difficulty of establishing a threshold for effects, a lack of epidemiological data and a large discrepancy in widely used models.
Exposure to lead may cause, amongst other things, kidney damage, miscarriages, effects on the nervous system, declined fertility, loss of IQ and behavioural disruptions [14,15]. Lead is present in the environment because of the former use of lead in gasoline, leaded drinking water pipes, and the use of lead in paints and other building materials. Exposure to lead has significantly decreased for many countries in the last two decades. Indeed, lead has been the success story in environmental policies, but the follow-up in exposure data in the general population is poor. Also, current studies suggest that there is no ’safe‘ level of lead exposure. IARC rated lead and inorganic lead compounds as probably carcinogenic to humans (Group 2A) in 2006 . Lead has been estimated to contribute to 100–500 DALYs per million people (medium impact). These preliminary estimates are based on a limited number of health endpoints, namely mild mental retardation (children zero to four years) and hypertensive disease (adults). Other uncertainties relate to the availability of dose-response functions over the complete exposure spectrum, and the aggregation of effects.
Exposure to transport noise from road, rail, and air traffic affects a great number of people, and may cause sleep disturbance as well as stress, leading e.g. to high blood pressure and increased incidence of myocardial infarction [5,17-19]. Noise exposure has also been linked to effects on cognition, but these are difficult to quantify and hence excluded from the assessment. Our estimates include severe sleep disturbance and myocardial infarction. Since so many people are exposed to noise, the total associated disease burden, despite the relatively small disability weights, is substantial. Important sources of uncertainties relate to incomplete exposure data from environmental noise directive reporting, unavailable exposure-response-functions for certain transport sources and health effects, and difficulty to establish thresholds for effects.
Exposure to ozone can lead to a variety of respiratory health effects, such as coughing, throat irritation and reduced lung function. In addition, it can worsen bronchitis, emphysema, and asthma . The relative impact of ozone on public health is medium, based on calculations which include total mortality, minor restricted activity days, coughing in children and lower respiratory symptoms in children. The selected morbidity health endpoints, which are based on the selection used by the CAFE (Clean Air For Europe) programme (link to: http://gains.iiasa.ac.at/index.php/policyapplications/cafe-clean-air-for-europe), are estimated to account for 90 % of the total morbidity effects. Uncertainties in the calculations relate, amongst other issues, to the estimated number of years of life lost for mortality.
Particulate matter (PM) is identified in our analysis as the biggest contributor to the total burden of disease. Exposure to PM has been associated with both respiratory and cardiovascular effects. The body of evidence is fairly consistent . The health endpoints and dose-response models have been selected based on the thorough review prepared for the CAFE programme (link to: http://gains.iiasa.ac.at/index.php/policyapplications/cafe-clean-air-for-europe). Exposure data were derived using a combination of models and measurements. Remaining uncertainties relate to the inclusion of PM from natural sources and sources outside Europe (which are included in this study), the exposure-response functions for e.g. chronic bronchitis, the estimated number of years of life lost for mortality, and the potential of double counting of morbidity effects by combining the restricted activity days and lower respiratory symptom days.
Radon is a short-lived radioactive gas that occurs naturally in soils and rocks because it is generated by the radioactive decay of uranium. Indoor radon concentrations differ based on the characteristics of the geological substrates beneath houses and the use of different building materials. Exposure to radon has been consistently linked to lung cancer . For our estimates, the results of the recent European EnVIE project (link to: http://paginas.fe.up.pt/~envie/), indoor air radon levels from the European Radon mapping project (link to: http://radonmapping.jrc.ec.europa.eu/) and risk estimates from the Darby et al. 2005 meta-analysis  were used. Radon is estimated to contribute 600–900 DALYs per million people in the participating countries.
1. Murray CJ, Lopez AD. The Global Burden of Disease. Cambridge, MA: Harvard University Press, 1996.
2. Prüss-Ustün, A and Corvalán, C. Preventing disease through healthy environments. Towards an estimate of the environmental burden of disease. 2006. WHO.
3. Fewtrell, L., Kaufman, R, and Prüss-Ustün, A. Lead: Assessing the environmental burden of disease. Environmental burden of disease series No. 2. 2003. WHO.
4. Oberg, M, Jaakkola, M, Prüss-Ustün, A, and Woodward, A. Second-hand smoke: Assessing the burden of disease at national and local levels. 2010. Geneva, World Health Organization.
5. WHO. Guidance for health risk assessment of environmental noise. 2010. Bonn, World Health Organization.
6. Knol AB, Petersen AC, van der Sluijs JP, Lebret E. Dealing with uncertainties in environmental burden of disease assessment. Environ Health 2009;8:21.
7. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Industrial Chemicals and Dyestuffs. 29. 1982. International Agency for Research on Cancer.
8. WHO. Air quality guidelines for Europe; Second edition. 2000. Copenhagen, World Health Organization, Regional Office for Europe. 91.
9. EPA (U.S.Environmental Protection Agency). Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds Part II: Health Assessment for 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds. 200. Environmental Protection Agency.
10. NAS. Dioxin Reassessment. National Academy of Sciences (NAS) Review, draft. 2004. National Academy of Sciences.
11. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Tobacco Smoke and Involuntary Smoking. 83. 2002. Lyon, International Agency for Research on Cancer.
12. U.S.Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke. A report of the Surgeon General. 2006. Rockville (MD), USA, U. S. Department of Health and Human Services.
13. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. 88, 39-325. 2006. Lyon, International Agency for Research on Cancer.
14. Khoury J YKBPBDCRDKBRGTRSNHSLWGGJRR. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. . 2005 Jul;113(7):894-9. Environmental Health Perspectives 2005;113:894-899.
15. WHO. Health risks of heavy metals from long-range transboundary air pollution. 2007. Copenhagen, WHO Regional Office for Europe.
16. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Inorganic and organic lead compounds. 87. 2006. Lyon, International Agency for Research on Cancer.
17. WHO. Transport-related Health Effects with a Particular Focus on Children. Topic report: noise. CONTRIBUTION TO THE UNECE - WHO TRANSPORT, HEALTH AND ENVIRONMENT PAN-EUROPEAN PROGRAMME - THE PEP. Available at: http://www.euro.who.int/Document/trt/PEPNoise.pdf. 2000.
18. Babisch, W. Transportation Noise and Cardiovascular Risk: Review and Synthesis of Epidemiological Studies, Dose-effect Curve and Risk Estimation. 2006. Berlin, UBA.
19. Miedema H, Vos H. Associations between self-reported sleep disturbance and environmental noise based on reanalyses of pooled data from 24 studies. Behavioural Sleep Medicine 2007;5:1-20.
20. WHO. Air quality guidelines, Global update 2005. 2006. Copenhagen, WHO Regional Office for Europe.
21. WHO. WHO handbook on indoor radon: A public health perspective. 2009. Geneva, World Health Organization.
22. Darby S, Hill D, Auvinen A, Barros-Dios J, Baysson H, Bochicchio F, Deo H, Falk R, Forastiere F, Hakama M, Heid I, Kreienbrock L, Kreutzer M, Lagarde F, Mäkeläinen I, Muirhead C, Obereigner W, Pershagen G, Ruano-Ravina A, Ruosteenoja E, Schaffrath-Rosario A, Tirmarche M, Tomasek L, Whitley E, Wichmann HE, Doll R. Radon in homes and lung cancer risk: collaborative analysis of individual data from 13 European case-control studies. British Medical Journal 2005;330:223-226.
o Flemish Institute for Technological Research (VITO), Belgium
o National Institute for Health and Welfare (THL), Department of Environmental Health, Kuopio, Finland
o French Institute for Public Health Surveillance (InVS) , Paris, France
o University of Bielefeld, School of Public Health, Department ‘Environment & Health’, Germany
o NRW Institute of Health and Work, WHO Collaborating Center for Regional Health Policy and Public Health, Bielefeld, Germany
o Federal Environment Agency (Umweltbundesamt), Berlin/Dessau-Roßlau, Germany
o Department of Occupational and Environmental Health, University of Milan, Italy
o Italian National Health Institute, Rome, Italy
o National Institute of Public Health and the Environment (RIVM), Bilthoven, Netherlands
o WHO, European Centre for Environment and Health, Bonn, Germany
o WHO, Geneva, Switzerland
For references, please go to http://www.eea.europa.eu/soer/countries/nl/national-and-regional-story-netherlands-1 or scan the QR code.
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