Acute Adverse Effects of Fine Particulate Air Pollution on Ventricular Repolarization

BACKGROUND: The mechanisms for the relationship between particulate pollution and cardiac disease are not fully understood. OBJECTIVE: We examined the effects and time course of exposure to fine particulate matter = 2.5 mu m in aerodynamic diameter (PM2.5) on ventricular repolarization of 106 nonsmoking adults who were living in communities in central Pennsylvania. METHODS: The 24-hr beat-to-beat electrocardiogram (ECG) data were obtained using a high-resolution 12-lead Holter system. After visually identifying and removing artifacts and arrhythmic beats, we summarized normal beat-to-beat QTs from each 30-min segment as heart rate (HR)corrected QT measures: QT prolongation index (QTI), Bazett's HR-corrected QT (QTcB), and Fridericia's HR-corrected QT (QTcF). A personal PM2.5 monitor was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data and used 30-min time-specific average PM2.5 exposures. RESULTS: The mean age of the participants was 56 +/- 8 years, with 41% male and 74% white. The means +/- SDs for QTI, QTcB, and QTcF were 111 +/- 6.6, 438 +/- 23 msec, and 422 +/- 22 msec, respectively; and for PM2.5, the mean +/- SD was 14 +/- 22 mu g/m(3). We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (beta) between 30-min PM2.5 and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM2.5 exposure occurred within 3-4 hr. The multivariable adjusted beta (SE, p-value) due to a 10-mu g/m(3) increase in lag 7 PM2.5 on QTI, QTcB, and QTcF were 0.08 (0.04, p < 0.05), 0.22 (0.08, p < 0.01), and 0.09 (0.05, p < 0.05), respectively. CONCLUSIONS: Our results suggest a significant adverse effect of PM2.5 on ventricular repolarization. The time course of the effect is within 3-4 hr of elevated PM2.5.