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      Air Pollution and Health: Bridging the Gap from Sources to Health Outcomes

      editorial
      Environmental Health Perspectives
      National Institute of Environmental Health Sciences

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          Abstract

          The U.S. Environmental Protection Agency (EPA) has established National Ambient Air Quality Standards (NAAQS) for six principal air pollutants (“criteria” pollutants): carbon monoxide (CO), lead (Pb), nitrogen dioxide (NO2), particulate matter (PM) in two size ranges [< 2.5 μm (PM2.5) and < 10 μm (PM10)], ozone (O3), and sulfur dioxide (SO2) (U.S. EPA 2010b). Although associations have been identified between these pollutants and adverse health effects, considerable uncertainty remains regarding a) methods and approaches to understanding relationships between air pollution and health effects; b) which components (gas and/or aerosol) and sources are most toxic; c) the mechanisms of actions of the pollutants and causal relationships; d) effect of confounding factors, and e) which populations are susceptible {U.S. EPA 2006a (Pb), 2006b (O3), 2008a [NOx Integrated Science Assessment (ISA)], 2008b (SOx ISA), 2009 (PM), 2010 (CO)}. This holds true especially for PM, because it is composed of many components with significant spatial and temporal variation (U.S. EPA 2009). Air pollution and health research continues to reduce these uncertainties across the source-to-health effects paradigm as described by the National Research Council (NRC) Research Priorities for Airborne Particulate Matter, volumes I–IV, (NRC 1998, 1999, 2001, 2004) and the U.S. EPA (2006a, 2006b, 2008a, 2008b, 2009b, 2010a). Linking air pollution and adverse health effects is complicated and requires expertise across a range of scientific disciplines—from atmospheric to exposure to health sciences, as well as inclusion of air quality managers and policy makers who implement and develop policy to reduce risk from air pollution. Interaction among these groups at different points in time helps to identify gaps in knowledge and suggest future research directions. One such opportunity was the international specialty conference “Air Pollution and Health: Bridging the Gap from Sources to Health Outcomes,” sponsored by the American Association for Aerosol Research (AAAR 2010). The conference, chaired by myself and Maria Costantini (Health Effects Institute), was designed to help disseminate and integrate results from scientific studies that cut across the range of air pollution– and health-related disciplines of the source-to-health effects continuum. The conference addressed the science of air pollution and health within a multipollutant framework, focusing on five key science areas—sources, atmospheric sciences, exposure, dose, and health effects—as identified by the NRC (1998). Eight key policy-relevant science questions that integrated across various parts of these science areas formed the basis of the meeting, and a ninth question addressed the policy implications of the findings (see Appendix). This was the AAAR’s third international specialty conference and extended the findings presented at the AAAR’s first specialty conference “Particulate Matter: Atmospheric Sciences, Exposure, and the Fourth Colloquium on PM and Human Health,” held in Pittsburgh, Pennsylvania, in 2003 (Davidson et al. 2005). Results from the 2010 AAAR Air Pollution and Health conference are being published in Environmental Health Perspectives (EHP); Air Quality, Atmosphere and Health; Aerosol Science and Technology; Atmospheric Environment; and Inhalation Toxicology (Solomon 2010). This issue of EHP includes conference papers on the importance of a multipollutant approach and of individual components of particulate matter to understanding linkages between sources and adverse health outcomes, including respiratory and/or cardiovascular diseases (Ito et al. 2011; Lall et al. 2011; Rohr et al. 2011; Spira-Cohen et al. 2011; Zhou et al. 2011), associated effects, such as inflammation (Alexeeff et al. 2011), and birth outcomes associated with exposures to traffic-related pollution during gestation (Malmqvist et al. 2011). Several air pollution components and sources were evaluated, including elemental carbon and secondary organic aerosol, traffic, local industrial sources, and residential oil and wood burning. Where studied, some effects varied by season and location over sufficient time (specifically, Detroit, MI; Seattle, WA; New York, NY), likely due to the influence of different source impacts. In addition, this issue includes a review of population characteristics related to susceptibility (Sacks et al. 2011), and an accountability study of the feasibility of hybrid regional–local modeling to assess health improvements in small communities (Lobdell et al. 2011).

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          Most cited references23

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          Fine Particulate Matter Constituents Associated with Cardiovascular Hospitalizations and Mortality in New York City

          Background Recent time-series studies have indicated that both cardiovascular disease (CVD)mortality and hospitalizations are associated with particulate matter (PM). However, seasonal patterns of PM associations with these outcomes are not consistent, and PM components responsible for these associations have not been determined. We investigated this issue in New York City (NYC), where PM originates from regional and local combustion sources. Objective In this study, we examined the role of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5) and its key chemical components on both CVD hospitalizations and on mortality in NYC. Methods We analyzed daily deaths and emergency hospitalizations for CVDs among persons ≥ 40 years of age for associations with PM2.5, its chemical components, nitrogen dioxide (NO2), carbon monoxide, and sulfur dioxide for the years 2000–2006 using a Poisson time-series model adjusting for temporal and seasonal trends, temperature effects, and day of the week. We estimated excess risks per interquartile-range increases at lags 0 through 3 days for warm (April through September) and cold (October through March) seasons. Results The CVD mortality series exhibit strong seasonal trends, whereas the CVD hospitalization series show a strong day-of-week pattern. These outcome series were not correlated with each other but were individually associated with a number of PM2.5 chemical components from regional and local sources, each with different seasonal patterns and lags. Coal-combustion–related components (e.g., selenium) were associated with CVD mortality in summer and CVD hospitalizations in winter, whereas elemental carbon and NO2 showed associations with these outcomes in both seasons. Conclusion Local combustion sources, including traffic and residual oil burning, may play a year-round role in the associations between air pollution and CVD outcomes, but transported aerosols may explain the seasonal variation in associations shown by PM2.5 mass.
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            Time-Series Analysis of Mortality Effects of Fine Particulate Matter Components in Detroit and Seattle

            Background Recent toxicological and epidemiological studies have shown associations between particulate matter (PM) and adverse health effects, but which PM components are most influential is less well known. Objectives In this study, we used time-series analyses to determine the associations between daily fine PM [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)] concentrations and daily mortality in two U.S. cities—Seattle, Washington, and Detroit, Michigan. Methods We obtained daily PM2.5 filters for the years of 2002–2004 and analyzed trace elements using X-ray fluorescence and black carbon using light reflectance as a surrogate measure of elemental carbon. We used Poisson regression and distributed lag models to estimate excess deaths for all causes and for cardiovascular and respiratory diseases adjusting for time-varying covariates. We computed the excess risks for interquartile range increases of each pollutant at lags of 0 through 3 days for both warm and cold seasons. Results The cardiovascular and respiratory mortality series exhibited different source and seasonal patterns in each city. The PM2.5 components and gaseous pollutants associated with mortality in Detroit were most associated with warm season secondary aerosols and traffic markers. In Seattle, the component species most closely associated with mortality included those for cold season traffic and other combustion sources, such as residual oil and wood burning. Conclusions The effects of PM2.5 on daily mortality vary with source, season, and locale, consistent with the hypothesis that PM composition has an appreciable influence on the health effects attributable to PM.
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              Personal Exposures to Traffic-Related Air Pollution and Acute Respiratory Health among Bronx Schoolchildren with Asthma

              Background Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level. Objective We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM2.5) air pollution versus the diesel-related carbonaceous fraction of PM2.5. Methods Daily 24-hr personal samples of PM2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays. Results We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants. Conclusion Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                April 2011
                : 119
                : 4
                : 156-157
                Affiliations
                U.S. Environmental Protection Agency, Office of Research and Development, Las Vegas, Nevada, E-mail: solomon.paul@ 123456epamail.epa.gov
                Author notes

                Paul A. Solomon, a senior environmental scientist with the National Exposure Research Laboratory, Office of Research and Development, at the U.S. EPA in Las Vegas, Nevada, organized and chaired the AAAR Air Pollution and Health International Specialty Conference. His research interests include developing and evaluating air quality measurement methods and conducting measurement projects in support of regulatory and research programs in the atmospheric sciences, and in air pollution exposure and health effects programs with an emphasis on particulate matter.

                The author declares he has no actual or potential competing financial interests.

                Article
                ehp-119-a156
                10.1289/ehp.1103660
                3080947
                21459697
                7725300e-d5b7-4e73-a903-182ca687adc3
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
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