Abstract
BackgroundThe mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood. Air pollution-induced myocardial ischemia is one of the potentially important mechanisms.MethodsWe investigate the acute effects and the time course of fine particulate pollution (PM2.5) on myocardium ischemic injury as assessed by ST-segment height in a community-based sample of 106 healthy non-smokers. Twenty-four hour beat-to-beat electrocardiogram (ECG) data were obtained using a high resolution 12-lead Holter ECG system. After visually identifying and removing all the artifacts and arrhythmic beats, we calculated beat-to-beat ST-height from ten leads (inferior leads II, III, and aVF; anterior leads V3 and V4; septal leads V1 and V2; lateral leads I, V5, and V6,). Individual-level 24-hour real-time PM2.5 concentration was obtained by a continuous personal PM2.5 monitor. We then calculated, on a 30-minute basis, the corresponding time-of-the-day specific average exposure to PM2.5 for each participant. Distributed lag models under a linear mixed-effects models framework were used to assess the regression coefficients between 30-minute PM2.5 and ST-height measures from each lead; i.e., one lag indicates a 30-minute separation between the exposure and outcome.ResultsThe mean (SD) age was 56 (7.6) years, with 41% male and 74% white. The mean (SD) PM2.5 exposure was 14 (22) μg/m3. All inferior leads (II, III, and aVF) and two out of three lateral leads (I and V6), showed a significant association between higher PM2.5 levels and higher ST-height. Most of the adverse effects occurred within two hours after PM2.5 exposure. The multivariable adjusted regression coefficients β (95% CI) of the cumulative effect due to a 10 μg/m3 increase in Lag 0-4 PM2.5 on ST-I, II, III, aVF and ST-V6 were 0.29 (0.01-0.56) μV, 0.79 (0.20-1.39) μV, 0.52 (0.01-1.05) μV, 0.65 (0.11-1.19) μV, and 0.58 (0.07-1.09) μV, respectively, with all p < 0.05.ConclusionsIncreased PM2.5 concentration is associated with immediate increase in ST-segment height in inferior and lateral leads, generally within two hours. Such an acute effect of PM2.5 may contribute to increased potential for regional myocardial ischemic injury among healthy individuals.
Highlights
The mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood
Numerous studies have consistently found a significant association between exposures to fine particulate matter, defined as fine particles with aerodynamic diameter less or equal to 2.5 micrometers (PM2.5), and the risk of clinical cardiovascular disease (CVD) [1,2,3,4]
No studies to date have investigated whether the Particulate Matter (PM) and myocardial ischemia association is mediated through its adverse effects on other ECG parameters, such as cardiac autonomic modulation (CAM)
Summary
The mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood. Air pollution-induced myocardial ischemia is one of the potentially important mechanisms. Numerous studies have consistently found a significant association between exposures to fine particulate matter, defined as fine particles with aerodynamic diameter less or equal to 2.5 micrometers (PM2.5), and the risk of clinical cardiovascular disease (CVD) [1,2,3,4]. The mechanisms responsible for such an association have been the focus of recent environmental health studies. Several studies [5,6,7,8,9,10] have suggested that electrocardiographic (ECG) morphologies indicative of myocardial
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