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The triggering of myocardial infarction by fine particles is enhanced when particles are enriched in secondary species
Rich, D., H. Ozkaynak, J. Crooks, L. Baxter, J. Burke, P. Ohman-Strickland, K. Thevenet-Morrison, H. Kipen, J. Zhang, J. Kostis, M. Lunden, N. Hodas, AND B. Turpin. The triggering of myocardial infarction by fine particles is enhanced when particles are enriched in secondary species. ENVIRONMENTAL SCIENCE AND TECHNOLOGY. John Wiley & Sons, Ltd., Indianapolis, IN, 47(16):9414-9423, (2013).
Previous studies have reported an increased risk of myocardial infarction (MI) associated with acute increases in PM concentration. Recently, we reported that MI/fine particle (PM2.5) associations may be limited to transmural infarctions. We used PM2.5 species concentrations, predicted by the Community Multiscale Air Quality chemical transport model, ambient PM2.5 concentrations, and the same MI dataset and case-crossover methods to estimate the relative odds of transmural MI associated with increased PM2.5 concentration on days with varying mass fractions of sulfate, nitrate, elemental carbon, organic carbon, and ammonium. We found the largest relative odds estimates on the days with the highest tertile of sulfate (OR=1.13; 95% CI = 1.00, 1.27), nitrate (OR=1.18; 95% CI = 0.98, 1.35), and ammonium (OR=1.13; 95% CI = 1.00 1.28), and the lowest tertile of EC (OR=1.17; 95% CI = 1.03, 1.34). Air pollution mixtures on these days were enhanced in pollutants formed through atmospheric chemistry (i.e., secondary PM2.5) and depleted in primary pollutants (e.g., EC). Mixtures laden with secondary PM species (sulfate, nitrate, and/or organics) appear to be associated with increased incidence of myocardial infarctions. Further work is needed to confirm these findings and to examine which PM2.5 component(s) is responsible for any acute MI response.
The National Exposure Research Laboratory′s (NERL′s) Human Exposure and Atmospheric Sciences Division (HEASD) conducts research in support of EPA′s mission to protect human health and the environment. HEASD′s research program supports Goal 1 (Clean Air) and Goal 4 (Healthy People) of EPA′s strategic plan. More specifically, our division conducts research to characterize the movement of pollutants from the source to contact with humans. Our multidisciplinary research program produces Methods, Measurements, and Models to identify relationships between and characterize processes that link source emissions, environmental concentrations, human exposures, and target-tissue dose. The impact of these tools is improved regulatory programs and policies for EPA.
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CMAQ_PAPER FINAL REVISED CLEAN 3.PDF (PDF,NA pp, 268.073 KB, about PDF)
Record Details:Record Type: DOCUMENT (JOURNAL/PEER REVIEWED JOURNAL)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL EXPOSURE RESEARCH LAB
HUMAN EXPOSURE AND ATMOSPHERIC SCIENCES DIVISION
EXPOSURE MODELING RESEARCH BRANCH