High level of source-specific particulate matter air pollution associated with cardiac arrhythmias

Abstract

Epidemiological evidence linking source-specific ambient particulate matter with aerodynamic diameter <2.5 μm (PM2.5) and cardiac arrhythmias is limited. In this study, we investigated the impact of source-specific PM2.5 on cardiac arrhythmias in a panel of forty-five healthy adults living in Beijing, China, between 2015 and 2016. Repeated measures of 24-hour electrocardiograms were conducted during clinical visits, and daily counts of four arrhythmia events including supraventricular premature beat (SVPB), atrial tachycardia (AT), premature ventricular contraction (PVC) and ventricular tachycardia (VT) were recorded. One hundred forty-seven constituents in PM2.5 were analyzed for collected particulate samples, in which fifty-six of them above laboratory detection limits were selected for source apportionment analysis using positive matrix factorization. The average contributions of identified five major sources to PM2.5 were 45.9% from secondary nitrate/sulfate, 18.0% from coal combustion, 16.9% from crustal soil, 13.8% from biomass burning, and 5.4% from cooking. Generalized estimating equation models were used to estimate relative risks (RR) of arrhythmias in association with interquartile-range (IQR) increases in PM2.5 constituents and specific sources. Total PM2.5 mass as well as several combustion related constituents were found of significant impacts on increased risks of arrhythmia events. Among the identified sources of PM2.5, coal burning has been found the major source that associated with increased risks of SVPB, PVC and VT with RR of 1.19 [95% confidence intervals (CI): 1.04, 1.36] to 1.64 (95% CI: 1.35, 2.00). PM2.5 from combustion related secondary nitrate/sulfate was also found of significant impact on SVPB and AT, followed by PM2.5 from biomass burning and crustal soil. Our results indicated that PM2.5 from anthropogenic activity related sources were most responsible for increased risks of arrhythmia events. Our findings enhance the understanding of increased risks of arrhythmias from exposure to PM2.5, and provide evidence on source-specific PM control priorities.