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

被引:357
作者
Thurston, George D. [1 ,2 ]
Burnett, Richard T. [3 ,4 ]
Turner, Michelle C. [4 ]
Shi, Yuanli [4 ]
Krewski, Daniel [4 ]
Lall, Ramona [1 ]
Ito, Kazuhiko [1 ]
Jerrett, Michael [5 ]
Gapstur, Susan M. [6 ]
Diver, W. Ryan [6 ]
Pope, C. Arden, III [7 ]
机构
[1] NYU, Sch Med, Dept Environm Med, 57 Old Forge Rd, Tuxedo Pk, NY 10987 USA
[2] NYU, Sch Med, Dept Populat Hlth, 57 Old Forge Rd, Tuxedo Pk, NY 10987 USA
[3] Hlth Canada, Hlth Environm & Consumer Safety Branch, Ottawa, ON K1A 0L2, Canada
[4] Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON, Canada
[5] Univ Calif Berkeley, Dept Environm Hlth Sci, Berkeley, CA 94720 USA
[6] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA
[7] Brigham Young Univ, Dept Econ, Provo, UT 84602 USA
关键词
19 EUROPEAN COHORTS; PARTICULATE MATTER; UNITED-STATES; SOURCE APPORTIONMENT; CARDIOPULMONARY MORTALITY; CARDIOVASCULAR MORTALITY; HEALTH-BENEFITS; ASSOCIATIONS; PM2.5; CANCER;
D O I
10.1289/ehp.1509777
中图分类号
X [环境科学、安全科学];
学科分类号
083001 [环境科学];
摘要
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. OBJECTIVES: We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society's Cancer Prevention Study-II cohort. METHODS: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) 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 microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter 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 microgram/cubic meter 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-mu g/m(3) EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was 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 microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources.
引用
收藏
页码:785 / 794
页数:10
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