气候变化领域集成服务门户

Background: Air pollution-induced changes in cardiac electrophysiological properties could be a pathway linking air pollution and cardiovascular events. The evidence of air pollution effects on the cardiac conduction system is incomplete yet. We investigated short-term effects of particulate matter <= 2.5 mu m in aerodynamic diameter (PM2.5) and ozone (O-3) on cardiac electrical impulse propagation and repolarization as recorded in surface electrocardiograms (ECG).

Methods: We analyzed repeated 12-lead ECG measurements performed on 5,332 patients between 2001 and 2012. The participants came from the Duke CATHGEN Study who underwent cardiac catheterization and resided in North Carolina, United States (NC, U.S.). Daily concentrations of PM2.5 and O-3 at each participant's home address were predicted with a hybrid air quality exposure model. We used generalized additive mixed models to investigate the associations of PM2.5 and O-3 with the PR interval, QRS interval, heart rate-corrected QT interval (QTc), and heart rate (HR). The temporal lag structures of the associations were examined using distributed-lag models.

Results: Elevated PM2.5 and O-3 were associated with four-day lagged lengthening of the PR and QRS intervals, and with one-day lagged increases in HR. We observed immediate effects on the lengthening of the QTc interval for both PM2.5 and O-3, as well as delayed effects for PM2.5 (lagged by 3 - 4 days). The associations of PM2.5 and O-3 with the PR interval and the association of O-3 with the QRS interval persisted until up to seven days after exposure.

Conclusions: In patients undergoing cardiac catheterization, short-term exposure to air pollution was associated with increased HR and delays in atrioventricular conduction, ventricular depolarization and repolarization.