The Effect of Air Pollution on Spatial Dispersion of Myocardial Repolarization in Healthy Human Volunteers

Objectives We tested the hypothesis that exposure to concentrated ambient particles (CAP) and/or ozone (O-3) would increase dispersion of ventricular repolarization. Background Elevated levels of air pollution are associated with cardiac arrhythmias through mechanisms yet to be elucidated. Methods Each of 25 volunteers (18 to 50 years of age) had four 2-h exposures to 150 mu g/m(3) CAP; 120 parts per billion O-3; CAP + O-3; and filtered air (FA). Exposure-induced changes (Delta = 5-min epochs at end-start) in spatial dispersion of repolarization were determined from continuous 12-lead electrocardiographic recording. Results Spatial dispersion of repolarization assessed by corrected Delta T-wave peak to T-wave end interval increased significantly for CAP + O-3 (0.17 +/- 0.03, p < 0.0001) exposure only, remaining significant when factoring FA (CAP + O-3 - FA) as control (0.11 +/- 0.04, p = 0.013). The influence on repolarization was further verified by a significant increase in Delta QT dispersion (for CAP + O-3 compared with FA (5.7 +/- 1.4, p = 0.0002). When the low-frequency to high-frequency ratio of heart rate variability (a conventional representation of sympathetic-parasympathetic balances) was included as a covariate, the effect estimate was positive for both corrected Delta T-wave peak to T-wave end interval (p = 0.002) and Delta QT dispersion (p = 0.038). When the high-frequency component (parasympathetic heart rate modulation) was included as a covariate with corrected Delta T-wave peak to T-wave end interval, the effect estimate for high frequency was inverse (p = 0.02). Conclusions CAP + O-3 exposure alters dispersion of ventricular repolarization in part by increasing sympathetic and decreasing parasympathetic heart rate modulation. Detection of changes in repolarization parameters, even in this small cohort of healthy individuals, suggests an underappreciated role for air pollutants in urban arrhythmogenesis. (J Am Coll Cardiol 2011;57:198-206) (C) 2011 by the American College of Cardiology Foundation