Health effects of particulate matter in Europe: Difference between revisions
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[[Category: | [[Category:EBoDE]] | ||
[[File:PM2.5daily.png|thumb|400px|]] | |||
==About particulate matter== | |||
Exposure to Particulate matter (PM) has been associated with both respiratory and cardiovascular effects and total non-violent mortality (Pope and Dockery, 2006, WHO, 2006a,b) and it is the most thoroughly internationally reviewed environmental pollutant during the last decade. PM was selected in EBoDE due to its high public health impact, economic significance (industry, transport) and political concern. Particulate matter is a complex mixture of components from natural and anthropogenic sources and is partly created in chemical and physical processes in the atmosphere from gaseous primary components like sulphur dioxide, nitrogen oxides, ammonia, and volatile organic compounds. The health implications of the particulate matter components have been extensively studied, but still the most convincing epidemiological evidence associates PM2.5 mass concentrations with the health impacts (Pope & Dockery, 2006). | |||
<ref name="EBoDe"></ref> | |||
==Selected health endpoints and exposure-response functions== | |||
For PM (and ozone) we followed the health impact assessment approach as laid out in the Clean Air For Europe (CAFE) project and based on WHO European Centre for Environment and Health and CLTRAP Task Force on Health consultations (Hurley et al. 2005, WHO, 2006a, b). PM2.5 and PM10 both serve as indicators of a complex mixture of physically and chemically heterogeneous composition. In the EBoDE calculations, we calculated burden of disease related both to PM10 and to PM2.5 exposure. Due to the overlap between these two indicators, in the aggregate results only the results for PM2.5 are included. For PM2.5, we calculated the burden of disease for cardiopulmonary mortality, lung cancer mortality, total non-violent mortality, chronic bronchitis and restricted activity days (RAD; defined by Hurley et al., 2005). Due to the overlap between the different mortality endpoints, we included only cause specific mortality in the aggregate results. For PM10, lower respiratory symptoms (LRS) and new cases of chronic bronchitis were included. | |||
For mortality, we used the relative risks as provided by Pope (Pope et al., 2002; WHO, 2006a,b). For morbidity, relative risks are based on the thorough review made for the CAFE estimates by Hurley et al. (2005) and WHO (2006b). The health endpoints and corresponding exposure-response functions are summarized in Table 3-19 in section 3.12. | |||
<ref name="EBoDe"></ref> | |||
==Exposure data== | |||
Annual population weighed mean ambient concentrations of PM2.5 and PM10 were estimated, similarly to the values for ozone, by the European Topic Centre on Air and Climate Change (ETC/ACC) using geographical modelling. Population density data were based on JRC data. For further details, see the ozone section. Exposure values are presented in Table 3-13 and summarized in Table 3-21 in section 3.12. | |||
The calculations involve no reference concentration for estimating the PM effects, so all PM-related morbidity and mortality are included in the burden of disease estimates. This is in contrast to, for example, the CAFE calculations, in which only the impacts of European anthropogenic emissions were estimated. The EBoDE calculations include the contribution to PM from natural sources and sources outside Europe. | |||
<ref name="EBoDe">Otto Hänninen, Anne Knol: European Perspectives on Environmental Burden of Disease: Esimates for Nine Stressors in Six European Countries, | |||
Authors and National Institute for Health and Welfare (THL), Report 1/2011 [http://www.thl.fi/thl-client/pdfs/b75f6999-e7c4-4550-a939-3bccb19e41c1]</ref> | |||
{|{{prettytable}} | |||
|+ TABLE 3-13. National population weighted averages of ambient PM levels in 2005 for the target countries (de Leeuw and Horalek, 2009). | |||
! rowspan="2" scope="col" width="100" | Country | |||
! colspan="2" scope="col" width="200" | Concentrations | |||
|----- | |||
| PM<sub>10</sub> | |||
(μg m<sup>-3</sup>) | |||
| PM<sub>2.5</sub> | |||
(μg m<sup>-3</sup>) | |||
|----- | |||
| Belgium | |||
| 28.9 | |||
| 18.7 | |||
|----- | |||
| Finland | |||
| 13.3 | |||
| 9.1 | |||
|----- | |||
| France | |||
| 19.1 | |||
| 12.3 | |||
|----- | |||
| Germany | |||
| 22.1 | |||
| 16.0 | |||
|----- | |||
| Italy | |||
| 32.7 | |||
| 19.6 | |||
|----- | |||
| Netherlands | |||
| 29.1 | |||
| 18.7 | |||
|} | |||
==Uncertainties per stressor and comparison with other studies== | |||
''A list of the most important sources of uncertainty for each stressor in the EBoDE calculations is provided in Table 5-1. Some of these are further explained below. In addition, we will compare our estimates to results of a selection of similar studies. Comparison of different studies on environmental burden of disease helps to understand the role of various methodological and strategic selections made in each study, like the selection of stressors or health endpoints.'' | |||
'''PM and ozone''' | |||
The methodology developed in Clean Air for Europe -project (CAFE) (Hurley et al., 2005) was applied using updated exposure estimates. The updated exposures are based on ambient air quality monitoring data that contain, besides the anthropogenic components that CAFE focused on, also natural sources of PM<sub>2.5</sub>. The spatial resolution of the updated model is 25 times higher (grid size 10x 10 km² instead of 50x50 km²). Compared to the CAFE estimates the current work adds estimation of the impacts in DALYs. The WHO Environmental Burden of Disease programme uses a non-linear exposure-response function (Ostro, 2004) that at higher exposures yields lower impacts than the linear CAFE model. WHO also sets a threshold level at 7.5 μg m<sup>-3</sup>.<ref name="EBoDe"></ref> | |||
{| {{prettytable}} | |||
| | |||
| Excluded health endpoints and related assumptions | |||
| Exposure data | |||
| Exposure response function | |||
| Calculation method | |||
| Level of overall uncertainty a) | |||
| Likely over- or underestimation b) | |||
|---- | |||
| Particulate matter | |||
| Morbidity outcomes evaluated using the CAFE simplifications | |||
| Total PM (not just anthropogenic emissions) | |||
| Potential threshold level | |||
| Unit risk simplifications for morbidity outcomes | |||
| * | |||
| No substantial error expected or overestimation due to inclusion of natural background | |||
|---- | |||
|} | |||
==References== | |||
<references/> |
Latest revision as of 14:11, 19 November 2012
This page is a product of the EBoDE project. The final report of the EBoDE project has been published as a report in 2011[1] and also as web pages in Opasnet. These links lead to parts of the report.
EBoDE project: main page | overview | contributors | data overview | Parma meeting | abbreviations | all pages Methods: environmental burden of disease calculation | selection of exposures and health effects | data needed | impact calculation tool Health effects in Europe: benzene | dioxins | formaldehyde | lead | ozone | particulate matter | radon | second-hand smoke | transport noise | environmental burden of disease | results by country |
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The page identifier is Op_en5223 |
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About particulate matter
Exposure to Particulate matter (PM) has been associated with both respiratory and cardiovascular effects and total non-violent mortality (Pope and Dockery, 2006, WHO, 2006a,b) and it is the most thoroughly internationally reviewed environmental pollutant during the last decade. PM was selected in EBoDE due to its high public health impact, economic significance (industry, transport) and political concern. Particulate matter is a complex mixture of components from natural and anthropogenic sources and is partly created in chemical and physical processes in the atmosphere from gaseous primary components like sulphur dioxide, nitrogen oxides, ammonia, and volatile organic compounds. The health implications of the particulate matter components have been extensively studied, but still the most convincing epidemiological evidence associates PM2.5 mass concentrations with the health impacts (Pope & Dockery, 2006). [1]
Selected health endpoints and exposure-response functions
For PM (and ozone) we followed the health impact assessment approach as laid out in the Clean Air For Europe (CAFE) project and based on WHO European Centre for Environment and Health and CLTRAP Task Force on Health consultations (Hurley et al. 2005, WHO, 2006a, b). PM2.5 and PM10 both serve as indicators of a complex mixture of physically and chemically heterogeneous composition. In the EBoDE calculations, we calculated burden of disease related both to PM10 and to PM2.5 exposure. Due to the overlap between these two indicators, in the aggregate results only the results for PM2.5 are included. For PM2.5, we calculated the burden of disease for cardiopulmonary mortality, lung cancer mortality, total non-violent mortality, chronic bronchitis and restricted activity days (RAD; defined by Hurley et al., 2005). Due to the overlap between the different mortality endpoints, we included only cause specific mortality in the aggregate results. For PM10, lower respiratory symptoms (LRS) and new cases of chronic bronchitis were included.
For mortality, we used the relative risks as provided by Pope (Pope et al., 2002; WHO, 2006a,b). For morbidity, relative risks are based on the thorough review made for the CAFE estimates by Hurley et al. (2005) and WHO (2006b). The health endpoints and corresponding exposure-response functions are summarized in Table 3-19 in section 3.12. [1]
Exposure data
Annual population weighed mean ambient concentrations of PM2.5 and PM10 were estimated, similarly to the values for ozone, by the European Topic Centre on Air and Climate Change (ETC/ACC) using geographical modelling. Population density data were based on JRC data. For further details, see the ozone section. Exposure values are presented in Table 3-13 and summarized in Table 3-21 in section 3.12.
The calculations involve no reference concentration for estimating the PM effects, so all PM-related morbidity and mortality are included in the burden of disease estimates. This is in contrast to, for example, the CAFE calculations, in which only the impacts of European anthropogenic emissions were estimated. The EBoDE calculations include the contribution to PM from natural sources and sources outside Europe. [1]
Country | Concentrations | |
---|---|---|
PM10
(μg m-3) |
PM2.5
(μg m-3) | |
Belgium | 28.9 | 18.7 |
Finland | 13.3 | 9.1 |
France | 19.1 | 12.3 |
Germany | 22.1 | 16.0 |
Italy | 32.7 | 19.6 |
Netherlands | 29.1 | 18.7 |
Uncertainties per stressor and comparison with other studies
A list of the most important sources of uncertainty for each stressor in the EBoDE calculations is provided in Table 5-1. Some of these are further explained below. In addition, we will compare our estimates to results of a selection of similar studies. Comparison of different studies on environmental burden of disease helps to understand the role of various methodological and strategic selections made in each study, like the selection of stressors or health endpoints.
PM and ozone
The methodology developed in Clean Air for Europe -project (CAFE) (Hurley et al., 2005) was applied using updated exposure estimates. The updated exposures are based on ambient air quality monitoring data that contain, besides the anthropogenic components that CAFE focused on, also natural sources of PM2.5. The spatial resolution of the updated model is 25 times higher (grid size 10x 10 km² instead of 50x50 km²). Compared to the CAFE estimates the current work adds estimation of the impacts in DALYs. The WHO Environmental Burden of Disease programme uses a non-linear exposure-response function (Ostro, 2004) that at higher exposures yields lower impacts than the linear CAFE model. WHO also sets a threshold level at 7.5 μg m-3.[1]
Excluded health endpoints and related assumptions | Exposure data | Exposure response function | Calculation method | Level of overall uncertainty a) | Likely over- or underestimation b) | |
Particulate matter | Morbidity outcomes evaluated using the CAFE simplifications | Total PM (not just anthropogenic emissions) | Potential threshold level | Unit risk simplifications for morbidity outcomes | * | No substantial error expected or overestimation due to inclusion of natural background |
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Otto Hänninen, Anne Knol: European Perspectives on Environmental Burden of Disease: Esimates for Nine Stressors in Six European Countries,
Authors and National Institute for Health and Welfare (THL), Report 1/2011 [1] [2] Cite error: Invalid
<ref>
tag; name "EBoDe" defined multiple times with different content