Evaluation of PM2.5 Air Pollution Sources and Cardiovascular Health (Poster)
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Introduction: Air pollution exposure, notably fine particulate matter (diameter ≤ 2.5 μm, PM2.5), is a global contributor to morbidity and mortality and a known risk factor for myocardial infarctions (MI) and coronary artery disease (CAD). Novel modeling methods can provide source-apportionment, to estimate the source-specific impacts on cardiovascular health.
Methods: The Catheterization Genetics (CATHGEN) cohort consists of patients who underwent a cardiac catheterization at Duke University Medical Center (North Carolina, USA) from 2001-2010. History of MI was extracted from medical records. Severity of coronary blockage was determined by coronary angiography and converted into a binary indicator of clinical CAD. PM2.5 source-specific yearly averages were estimated using an improved gas-constrained source apportionment model for North Carolina from 2002 to 2010 at 12x12 kilometer resolution. We tested six PM2.5 source-specific mass estimates for associations with CAD and MI (per 1 µg/m3 increase) using multivariate logistic regression adjusted for age, race, sex, smoking history, home value, urbanity, and education.
Results: Of 5681 CATHGEN participants; 2497 (43.9%) had CAD, and 1652 (29.0%) had a history of MI. PM2.5 fractions of ammonium bisulfate and ammonium nitrate were associated with increased prevalence of CAD (odds ratio [OR] 1.52; 95%CI 1.24-1.86 and OR 1.62; 95%CI 1.28-2.05, respectively). PM2.5 from ammonium bisulfate and ammonium nitrate were also associated with increased prevalence of MI (OR 1.57; 95%CI 1.28-1.94 and OR 2.04; 95% CI 1.61-2.58, respectively). MI was associated with PM2.5 from ammonium sulfate (OR 1.44; 95%CI 1.15-1.82). Gasoline source-apportioned PM2.5 was inversely associated with CAD (OR 0.58; 95%CI 0.38-0.90). We did not observe association with diesel or secondary organic carbons PM2.5.
Conclusion: Greater PM2.5 fractions of ammonium bisulfate and ammonium nitrate are associated with greater MI and CAD prevalence. Our findings suggest analyses of source-specific PM2.5 mass may reveal novel associations. This abstract does not reflect EPA policy.