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Environ Health Perspect; DOI:10.1289/ehp.1509777

Ischemic Heart Disease Mortality and Long-Term Exposure to Source-Related Components of U.S. Fine Particle Air Pollution

George D. Thurston1, Richard T. Burnett2,3, Michelle C. Turner3, Yuanli Shi3, Daniel Krewski3, Ramona Lall1, Kazuhiko Ito1, Michael Jerrett4, Susan M. Gapstur5, W. Ryan Diver5, and C. Arden Pope III6
Author Affiliations open
1New York University School of Medicine, Departments of Environmental Medicine and Population Health, Tuxedo, New York, USA; 2Healthy Environments and Consumer Safety Branch, Health Canada, Ottawa, Canada; 3McLaughlin Centre for Population Health Risk Assessment, University of Ottawa, Ottawa, Canada; 4Department of Environmental Health Sciences, University of California, Berkeley, Berkeley, California, USA; 5Epidemiology Research Program, American Cancer Society, Atlanta, Georgia, USA; 6Economics Department, Brigham Young University, Provo, Utah, USA

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  • Background: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. In this work, we sought to identify the causal characteristics and sources of air pollution underlying past published associations in the American Cancer Society’s Cancer Prevention Study-II cohort between long-term PM2.5 exposure and Ischemic Heart Disease (IHD) mortality.

    Methods: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 to 2004 for vital status and cause of death. Using Cox proportional hazard models, IHD mortality hazard ratios (HRs) were derived for PM2.5, trace constituents, and pollution source-associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000-2005.

    Results: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI=1.02, 1.08) per µg/m3, versus an IHD HR = 1.01 (95% CI=1.00, 1.02) per µg/m3 PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per µg/m3 PM2.5 basis. Diesel traffic-related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26 μg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion were not associated with IHD mortality.

    Conclusions: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning, but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5 – mortality associations can vary greatly by source, and that the largest IHD health benefits per µg/m3 from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources.

  • This EHP Advance Publication article has been peer-reviewed, revised, and accepted for publication. EHP Advance Publication articles are completely citable using the DOI number assigned to the article. This document will be replaced with the copyedited and formatted version as soon as it is available. Through the DOI number used in the citation, you will be able to access this document at each stage of the publication process.

    Citation: Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. Ischemic Heart Disease Mortality and Long-Term Exposure to Source-Related Components of U.S. Fine Particle Air Pollution. Environ Health Perspect;

    Received: 2 February 2015
    Accepted: 17 November 2015
    Advance Publication: 2 December 2015

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