Abstract 3471: Ambient particulate air pollution and ectopy - The Environmental Epidemiology of Arrhythmogenesis in WHI (EEAWHI), 1999–2004
We investigated relationships between exposures to ambient particles (PM) < 2.5 μm (PM2.5) or <10 μm (PM10) in diameter and ventricular or supraventricular ectopy as detected by a resting, standard 12-lead ECG. We also investigated effect modification of the acute PM-ectopy association by cigarette smoking, chronic PM exposure, and individual or neighborhood socioeconomic status. This study is part of an ancillary study of Women’s Health Initiative clinical trial participants. We used data from EPA air quality monitors and an established national-scale, log-normal kriging to spatially estimate daily mean concentrations of PM at geocoded addresses of 57,913 participants in 1999–2004. We estimated acute and chronic exposures as mean residential-level PM concentrations on the day of, 0–2 days before, and averaged over 30 and 365 days prior to the ECG (Lag0; Lag1; Lag2; Lag1–30; Lag1–365). At the time of the ECG, the mean age (SD) of participants was 68 (6.9) years (84% non-Hispanic White; 6% current smoker; 15% with CHD or congestive heart failure; 5% with ectopy). We estimated center-specific logistic regression coefficients and SEs first, and then combined them at the second stage using random-effects meta-regression. We express the pooled coefficients as odds ratios, 95% confidence intervals (OR, 95% CI) for 10 μg/m3 increases in PM concentrations. Among current smokers, Lag1 concentrations were significantly associated ventricular ectopy: OR (95% CI) = 1.73 (1.20–2.49) for PM2.5 and 1.28 (1.03–1.59) for PM10, in contrast to that of 1.01 (0.92–1.11) and 1.00 (0.94–1.07), respectively for non-current smokers. Lag0 and Lag2 concentrations were also associated with ventricular ectopy, but the associations did not reach statistical significance (p< 0.05). The interactions between smoking and acute exposures were significant (p < 0.05) in relationship to ventricular ectopy.Acute exposures were not significantly associated with supraventricular ectopy. Chronic exposures were not significantly associated ventricular or supraventricular ectopy.
Conclusion: Acute exposure to ambient PM2.5 and PM10 is directly associated with the odds of ventricular ectopy among smokers, suggesting smokers are more vulnerable to the arrhythmogenic effects of PM.