Air pollution health impact assessment: PM 2.5 exposures, sources and components

Transcription

1 Assessing the Climate and Health Co-Benefits of Clean Cooking Global Alliance for Clean Cookstoves / Environmental Defense Fund July 16th 17th 2015 Washington D.C. Air pollution health impact assessment: PM 2.5 exposures, sources and components Michael Brauer

2 Source perspective What is air pollution? Petrochemical industry Residential cooking Metal industry Waste burning Biogenic Sources Processed emissions Agriculture Agricultural & forest fires Stationary power generation Residential heating Solvent and paint use Road transpor tation Off-road transpor tation Crustal material Fate and transport Natural processes Source: Draft IARC Air Pollution Monograph 2

3 Component perspective What is air pollution? VOCs Oxidants (O3, H2O2) Gaseous N- compounds gaseous S- compounds CO Gas-Phase SVOCs Other Gases EC and Organic Matter N Species Aerosol Metals S Species Crustal materials Salts & H2O Source: Draft IARC Air Pollution Monograph 3

4 Examples of Particle Types and Mixtures Present in Combustion Plumes USEPA, 2012

5 Health impacts of PM constituents Insufficient information to differentiate the health impacts of different PM constituents WHO, USEPA,IARC, GBD WHO REVIHAAP* Carbonaceous material from traffic traffic-generated dust including road, brake and tyre wear coal combustion (sulfate-contaminated particles) shipping (oil combustion) power generation (oil and coal combustion) metal industry (nickel) biomass combustion (residential wood combustion, landscape fires) desert dust episodes (CVD hospitalizations, mortality) *Review of EVIdence on Health Aspects of Air Pollution, 2013

6 EPA (2009) Insufficient basis for supplementing mass based, primary fine particle standards with standards using a separate indicator for ultrafine particles or a separate indicator for a specific PM 2.5 component or group of components associated with any source categories of fine particles many constituents of PM can be linked with differing health effects and the evidence is not yet sufficient to allow differentiation of those constituents or sources that are more closely related to specific health outcomes U.S. EPA Integrated Science Assessment for Particulate Matter, 2009

7 REVIHAAP (2013) Three important components or metrics black carbon, secondary organic aerosols, and secondary inorganic aerosols have substantial exposure and health research finding associations and effects. They each may provide valuable metrics for the effects of mixtures of pollutants from a variety of sources. Risk assessments based on PM 2.5 studies will be the most inclusive. Alternative metrics, such as black carbon, may be used in sensitivity analyses.

8 PM Size - Ultrafine particles HEI The current evidence does not support a conclusion that exposure to UFPs alone can account in substantial ways for the adverse effects of PM 2.5 WHO REVIHAAP increasing, though as yet limited, epidemiological evidence on the association between short-term exposures to ultrafine particles and cardiorespiratory health.clinical and toxicological studies have shown that ultrafine particles (in part) act through mechanisms not shared with larger particles that dominate mass-based metrics

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10 Coarse PM suggestive evidence of a causal relationship between short-term exposure to coarse PM and cardiovascular and respiratory health effects and mortality. not sufficient evidence to draw conclusions on the health effects of long-term exposure to coarse PM. (EPA ISA, 2009) short-term exposures to coarse particles (including crustal material) are associated with adverse respiratory and cardiovascular effects on health, including premature mortality hardly any long-term studies are available for coarse particles. toxicological studies report that coarse particles can be as toxic as PM 2.5 on a mass basis. The difference in risk between coarse and fine PM can, at least partially, be explained by differences in intake and different biological mechanisms. (REVIHAAP, 2013) Suggestive evidence of increased morbidity and mortality in relation to higher short-term PM concentrations, with stronger relationships for respiratory than cardiovascular endpoints. While suggestive evidence was found of increased mortality with long-term PM concentrations, these associations were not robust to control for PM 2.5. (Adar et al., 2014) dar SD, Filigrana PA, Clements N, Peel JL. Ambient Coarse Particulate Matter and Human Health: A Systematic Review and Meta-Analysis. urr Environ Health Rep Aug 8;1:

11 Global air pollution assessments Global coverage fine spatial resolution consistent temporal trends GBD estimates also used for World Bank, World Health Organization, EPA BenMAPs, OECD Source sector contributions Motor vehicles Solid fuel cooking, heating Coal

12 What is the Global Burden of Disease? Systematic quantification of magnitude of health loss due to diseases, injuries and risk factors Global disease, injury, & risk burden estimates for (5 yr intervals) using comparable methods for 188 countries (+ subcountry analyses) incidence and prevalence of 301 diseases and injuries and 2,337 relevant disabling sequelae, stratified by sex and 20 age groups Role of 76 modifiable risk factors in burden of disease Collaborative effort coordinated by (Gatesfunded) Institute for Health Metrics and Evaluation (UW), [WHO] + ~1000 volunteers. Annual updates beginning in

13 General approach Exposure to Outdoor Air Pollution Worldwide Health Evidence Country- Specific Mortality, Disease PM 2.5 Ozone Concentration Response Relationships Baseline Incidence Global Burden, DALYs, Mortality Population Attributable fraction X Deaths (cause-specific) Population Attributable fraction X DALYs (cause specific)

14 Risk factor definition: Outdoor air pollution Air pollution exposures are mixtures Relative contribution of different pollutants a function of location-specific Economic/development, social, technological factors meteorology, topography, geography (transport) Literature (measurements) for small number of selected pollutants PM (TSP, PM 10, PM 2.5 ), O 3, NO x, SO 2, CO 14

15 Air pollution metrics PM 2.5 (ambient particulate matter) Most robust indicator in epidemiologic studies Biological plausibility supported by toxicology, dosimetry, studies of acute exposures, controlled exposures General indicator of combustion source air pollution Also incorporates respirable fraction of crustal PM ( dust ) Evidence does not support differential risk based on PM 2.5 mixture composition 15

16 Brauer et al., Submitted SAT TM5 Final estimates based on average of (1.4 million) grid cell values (SAT, TM5) and calibrated (regression model) with measurements 0.1 x 0.1 resolution extrapolated to 2013 using trend in SAT Incorporate variance between two estimates and measurements in uncertainty assessment Unique contributions from each approach Adjusted R 2 : 0.64 N = 4,073 PM 2.5 = exp[ ( *ln(avg))] approximate location PM 2.5 calculated (from PM 10 ) unspecified monitor type

17 2013 Annual Average PM 2.5 Brauer et al., Submitted. 2015

18 Change in Annual Average PM 2.5 Brauer et al., Submitted. 2015

19 Brauer et al., Submitted. 2015

20 Integrating risk from multiple sources to estimate risk due to ambient PM 2.5 Key assumption Risk is function of PM 2.5 inhaled dose regardless of source Integrated Exposure-Response functions (IER) Extrapolation model reflect change in risk observed in cohort studies at low concentrations near-linear at low concentrations predict risk for highest PM 2.5 consistent with risks from smoking (Pope et al.2011) Burnett et al. 2014

21 Household air pollution Total population using solid fuels (%), 2010

22 *PRELIMINARY ESTIMATES SUBJECT TO CHANGE* GBD 2013

23 *PRELIMINARY ESTIMATES SUBJECT TO CHANGE* GBD 2013

24 *PRELIMINARY ESTIMATES SUBJECT TO CHANGE* GBD 2013

25 Smith KR et al. Millions Dead: How Do We Know and What Does It Mean? Methods Used in the Comparative Risk Assessment of Household Air Pollution. Annu. Rev. Public Health :

26 Smith KR et al. Millions Dead: How Do We Know and What Does It Mean? Methods Used in the Comparative Risk Assessment of Household Air Pollution. Annu. Rev. Public Health :

27 No PM - HAP studies for IHD, stroke, LC Integrating risk from multiple sources to estimate risk due to household PM 2.5 Integrated Exposure-Response functions (IER) Burnett et al. 2014

28 Smith KR et al. Annu. Rev. Public Health : Balakrishnan K et al. Environ Health (1):77 GBD 2013: PM 2.5 exposures estimated (country, year) with meta-analysis of measured PM 2.5 levels associated with household solid fuel use.

29 Sector contributions PM 2.5, Sector x Burden PM2.5 = sector burden attribution Global motor vehicle air pollution: 184,000* deaths/yr

30 Estimating household cooking contribution % ambient PM 2.5 from cooking Concentrations of PM 2.5 Deaths from AAP DALYs from AAP % residential PM 2.5 from cooking PM 2.5 cooking (open pit + cookstoves) emissions PM 2.5 household emissions % ambient PM 2.5 from household sources PM 2.5 household Ambient PM 2.5 Ambient PM 2.5 Burden of Disease GAINS TM5-FASST, MESSAGE GBD (TM5, SAT, MEASUREMENTS) Chafe et al., 2014

31 Global Pop-weighted contribution: 12% (4 µg/m 3 ) 0% 26% 10% 11% 15% 37% 0 µg/m µg/m µg/m µg/m 3 1 µg/m µg/m 3 Chafe et al., 2014

32 GBD MAPS Assess contribution to disease burden from Major Air Pollution Source sectors (emphasis on coal) o China o India o Eastern Europe

33 Population-weighted annual average PM 2.5 (2013). PM 2.5 % contribution from domestic coal use (GEOS Chem) Bars: Magnitude of PM 2.5 from: all sources all coal sources industrial coal power plant coal domestic coal Deaths attributable to PM 2.5 from domestic coal use

34 Absolute (1 kg/km 2 yr) reduction Relative (10%) reduction

35 PURE-AIR N~220,000 (35-70 yrs) ~800 urban/rural communities in 26 countries

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37 PURE-AIR Outdoor Air Pollution 3 sites initiated in Summer 2015 (N. India, S. India, Bangladesh) Co-locate with inexpensive photometer(s) Co-locate with inexpensive filter sampler MET ONE Neighborhood Monitor

38 Ambient PM measurements Restrict to PURE communities (N~800) Distance to nearest monitor Large (satellite ground) Δ Establish 3 additional sites in Fall 2015 ~ 6-12 months: rotate (target of ~ 30 over 4 years) Use directly and as external evaluation of satellite based estimates Analyze for mass, BC (other components? $$) SPARTAN Network (mass, BC, ions, metals, OC)

39 PURE-AIR Household 2 pilot sites studies in Summer 2015 (N. India, S. India) Evaluate devices Establish protocol to implement remotely Device selection Sampling duration Personal vs household Expand to communities w/hhsfu (~230) Model distribution of community level exposures Sample community exposures ($) AST UPAS PUWP TZOA