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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 (PM(2.5)) 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 PM(2.5) nephelometer was used to measure individual-level real-time PM(2.5) exposures for 24 hr. We averaged these data to obtain 30-min average time-specific PM(2.5) 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 PM(2.5) 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 PM(2.5) 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 PM(2.5) concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM(2.5) was not significantly associated with PAC count. CONCLUSION: PM(2.5) exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.
He et al. (Fri,) studied this question.
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