摘要：Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood. Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania. Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM2.5 nephelometer was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data to obtain 30-min average time–specific PM2.5 exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10-μg/m3 increases in average PM2.5 over 30-min intervals and ectopy counts. Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM2.5 exposure was 13 ± 22 μg/m3, and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m3 in average PM2.5 concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM2.5 was not significantly associated with PAC count. Conclusion: PM2.5 exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.
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