Acute effects of fine particulate air pollution on cardiac arrhythmia: the APACR study

The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood.

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.

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.

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.

PM(2.5) exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.