Evaluation of PM2.5 Air Pollution Sources and Cardiovascular Health
Citation:
Slawsky, E., A. Weaver, C. Ward-Caviness, L. Neas, R. Devlin, W. Cascio, A. Russell, R. Huang, W. Kraus, E. Hauser, AND D. Diaz-Sanchez. Evaluation of PM2.5 Air Pollution Sources and Cardiovascular Health. ENVIRONMENTAL HEALTH PERSPECTIVES. National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC, 2020:1, (2020). https://doi.org/10.1289/isee.2020.virtual.P-0895
Impact/Purpose:
Fine particulate matter air pollution (PM2.5) is well-known to be associated with health outcomes, including heart disease. However, PM2.5 can come from many different sources and have different chemical compositions. Whether heart disease outcomes are affected differently by different sources of PM2.5 is not well understood. In this study, we examined effects of PM2.5 from various sources on coronary artery disease (CAD) or myocardial infarction (MI) among a group of 5681 patients at Duke University Medical Center who received cardiac catheterization between 2002 and 2010. We estimated sources of PM2.5 using a gas-constrained source apportionment model. We observed that those with higher exposures to PM2.5 from ammonium bisulfate and ammonium nitrate were more likely to have CAD and MI. Those with higher exposures to PM2.5 from ammonium sulfate were also more likely to have MI. However, those with higher exposures to PM2.5 from gasoline were less likely to have CAD. This research is a starting point for similar research in other areas, especially those with different sources of PM2.5.
Description:
Introduction: Long-term 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 coronary artery disease (CAD) and myocardial infarctions (MI). Knowledge of impacts related to source-appointed PM2.5 is limited and new modeling methods allow researchers to estimate the source-specific long-term impacts on the prevalence of CAD and MI. Methods: The Catheterization Genetics (CATHGEN) cohort consists of patients who underwent a cardiac catheterization at Duke University Medical Center (North Carolina, USA) between 2002-2010. Severity of coronary blockage was determined by coronary angiography and converted into a binary indicator of clinical CAD. History of MI was extracted from medical records. Annual averages of source specific PM2.5 were estimated using an improved gas-constrained source apportionment model for North Carolina from 2002 to 2010 at 12x12 km resolution. We tested six sources of PM2.5 mass estimates (ammonium bisulfate, ammonium nitrate, ammonium sulfate, gasoline, diesel, and secondary organic carbon) for associations with CAD and MI (per IQR increase) using mixed effects multivariate logistic regression with a random intercept for county and adjustments for age, race, sex, smoking history, home value, urbanicity, 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] 1.20; 95%CI 1.11-1.22 and OR 1.18; 95%CI 1.05-1.32, respectively). PM2.5 from ammonium bisulfate and ammonium nitrate were also associated with increased prevalence of MI (OR 1.20; 95%CI 1.10-1.29 and OR 1.35; 95% CI 1.20-1.53, respectively). We did not observe associations with ammonium sulfate, diesel, gasoline, or secondary organic carbon PM2.5. Conclusion: Greater PM2.5 concentrations of ammonium bisulfate and ammonium nitrate are associated with greater MI and CAD prevalence. The association with bisulfate suggests aerosol acidity may play a role. Our findings suggest analyses of source specific PM2.5 mass can reveal novel associations.
