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 < or = 2.5 microm in aerodynamic diameter (PM(2.5)) 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 PM(2.5) monitor was used to measure individual-level real-time PM(2.5) exposures for 24 hr. We averaged these data and used 30-min time-specific average PM(2.5) 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 PM(2.5), the mean +/- SD was 14 +/- 22 microg/m3. We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (beta) between 30-min PM(2.5) and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM(2.5) exposure occurred within 3-4 hr. The multivariable adjusted beta (SE, p-value) due to a 10-microg/m3 increase in lag 7 PM(2.5) 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 PM(2.5) on ventricular repolarization. The time course of the effect is within 3-4 hr of elevated PM(2.5).