Abstract
The relationships between ambient PM(2.5) and PM(10) and arrhythmia and the effect modification by cigarette smoking were investigated. Data from U.S. Environmental Protection Agency (EPA) air quality monitors and an established national-scale, log-normal kriging method were used to spatially estimate daily mean concentrations of PM at addresses of 57,422 individuals from 59 examination sites in 24 U.S. states in 1999-2004. The acute and subacute exposures were estimated as mean, geocoded address-specific PM concentrations on the day of, 0-2 d before, and averaged over 30 d before the electrocardiogram (ECG) (Lag(0); Lag(1); Lag(2); Lag(1-30)). At the time of standard 12-lead resting ECG, the mean age (SD) of participants was 67.5 (6.9) yr (84% non-Hispanic White; 6% current smoker; 15% with coronary heart disease; 5% with ectopy). After the identification of significant effect modifiers, two-stage random-effects models were used to calculate center-pooled odds ratios and 95% confidence intervals (OR, 95% CI) of arrhythmia per 10 mug/m(3) increase in PM concentrations. Among current smokers, Lag(0) and Lag(1) PM concentrations were significantly associated ventricular ectopy (VE)-the OR (95% CI) for VE among current smokers was 2 (1.32-3.3) and 1.32 (1.07-1.65) at Lag(1) PM(2.5) and PM(10), respectively. The interactions between current smoking and acute exposures (Lag(0); Lag(1); Lag(2)) were significant in relationship to VE. Acute exposures were not significantly associated with supraventricular ectopy (SVE), or with VE among nonsmokers. Subacute (Lag(1-30)) exposures were not significantly associated with arrhythmia. Acute PM(2.5) and PM(10) exposure is directly associated with the odds of VE among smokers, suggesting that they are more vulnerable to the arrhythmogenic effects of PM.