Triggering of ST-elevation myocardial infarction by ambient wood smoke and other particulate and gaseous pollutants
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Updated: Mar 22, 2026

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
Kristin A Evans1, Philip K Hopke2, Mark J Utell3
1Department of Public Health Sciences, University of Rochester, School of Medical Center, Rochester, New York, USA.
Abstract:
We previously observed increased odds of ST-elevation myocardial infarctions (STEMIs) associated with increased ambient fine particulate matter (PM2.5) in the previous hour. However, data are lacking on the effects of specific PM sources. Using data from 362 patients, a case-crossover design, and conditional logistic regression, we estimated the relative odds of STEMI associated with increased Delta-C (wood smoke), black carbon (BC; traffic), PM2.5, and gaseous pollutants in the previous 1-72 h. We did not observe increased odds of STEMIs associated with increased Delta-C or BC. We did observe increased odds associated with each 7.1 μg/m3 increase in PM2.5 (OR (95% CI): 1.17 (0.99, 1.39)) and each 19.9 p.p.b. increase in ozone (O3; 1.27 (1.00, 1.63)) in the previous hour, and each 0.22 p.p.m. increase in 48-h carbon monoxide (CO) concentrations (1.32 (1.00, 1.73]). Larger relative odds were associated with PM2.5 in May-October, and O3 and CO in November-April. Increased PM2.5, O3, and CO, but not wood smoke or BC, were associated with increased odds of STEMI, and effects may differ by season. Studies using spatially adjusted pollution estimates are needed, as well as studies further examining O3 and CO effects on the risk of STEMI.
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