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Ischemic Heart Disease Mortality Associations with Long-Term Exposure to PM2.5 Components

Thurston, George*; Burnett, Richard; Krewski, Dan; Shi, Yuanli; Turner, Michelle; Ito, Kazuhiko*; Lall, Ramona*; Jerrett, Michael§; Calle, Eugenia; Tunne, Michael; Pope, C Arden**

doi: 10.1097/01.ede.0000362950.38471.a1
Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25–29, 2009: Poster Presentations

*New York University School of Medicine, New York, NY, United States; †Health Canada, Ottawa, Ontario, Canada; ‡University of Ottawa, Ottawa, Ontario, Canada; §University of California, Berkeley, CA, United States; ¶American Cancer Society, Atlanta, GA, United States; and **Brigham Young University, Provo, UT, United States.

Abstracts published in Epidemiology have been reviewed by the organizations of Epidemiology. Affliate Societies at whose meetings the abstracts have been accepted for presentation. These abstracts have not undergone review by the Editorial Board of Epidemiology.


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Background and Objective:

Numerous epidemiological studies have now documented that long-term exposure to fine particulate matter air pollution mass (PM2.5) is associated with an increased risk of mortality. In particular, Pope and collaborators have noted elevated risks in deaths, especially due to cardiac causes in the U.S. nationwide American Cancer Society (ACS) CP-II cohort (Pope et al., 2004). However, the types of particles that are most responsible for these associations are not yet known.

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Using the ACS cohort (extended through 2004), and the U.S. EPA PM2.5 speciation data, we evaluated associations between various composition and source components of PM2.5 in 80 U.S. metropolitan areas. Source apportionments were conducted using methods by Thurston and Spengler (1982). Individual elements were also considered as exposure indices. Mortality analyses employed Cox Proportional Hazards modeling. The focus of this new research was to determine which components of PM2.5 were most explanatory of the previously reported PM2.5 association with Ischemic Heart Disease (IHD) mortality.

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The major U.S. PM2.5 sources identified, their key tracer elements, and their mean nationwide PM2.5 impacts were: Soil (Ca, Si) 0.8 ug/m3; Metals (Pb, Zn) 0.2 ug/m3; Traffic (OC, EC, NO2) 4.6 ug/m3 ; Steel (Fe, Mn) < 0.1 ug/m3; Coal Combustion (As, Se) 1.1 ug/m3; Oil Combustion (V, Ni) 0.9 ug/m3; Salt (Na, Cl) 0.1 ug/m3; Biomass burning 1.3 ug/m3; Other Sulfates (S) 4.3 ug/m3; Other Nitrates (NO3 -) 0.6 ug/m3; and, Other Organic Carbon (OC) 0.5 ug/m3. While most industrial and fossil fuel combustion categories had relative risk (RR) estimates above 1.0 for IHD deaths, coal combustion and traffic emission-related particles were among the largest and strongest PM2.5-mortality associations.

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Particles resulting from industrial and fossil fuel combustion sources are most associated with increased risk of Ischemic Heart Disease mortality from long-term PM2.5 exposure.

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