Short-term exposure to ambient ozone associated with cardiac arrhythmias in healthy adults

Objective

The exact biological mechanism whereby exposure to ambient ozone (O₃) may contribute to clinical onset of cardiovascular events remains unclear. In this study, we aim to examine the impacts of O₃ exposure on cardiac arrhythmias and potential pathways involved through autonomic dysfunction and myocardial injury.

Methods

Seventy-three non-smoking healthy adults were followed with 4 repeated measurements of 24-hour ambulatory arrhythmias, heart rate variability, ST-segment deviation, and blood pressure (BP) in Beijing, China, 2014‒2016. Generalized additive mixed models coupled with distributed lag nonlinear models were constructed to evaluate the associations and potential interlinks between O₃ exposure and outcome measurements.

Results

During the study period, 24-hour average concentrations of ambient O₃ were 47.4 µg/m³ (ranging from 1.0 to 165.9 µg/m³). Increased risks of premature ventricular contraction and ventricular tachycardia were associated with interquartile range increases in O₃ exposure during the last 5 days before each participant's clinic visit, with relative risks of 2.14 (95% confidence interval [CI]: 1.95 to 2.32) and 5.47 (95% CI: 3.51 to 7.43), respectively. Mediation analyses further showed that sympathetic activation, parasympathetic inhibition, and elevated BP levels, as well as heightened risks of ST-segment depression could mediate up to 47.74% of the risks of arrhythmias attributable to O₃ exposure.

Conclusion

Our results suggest that short-term exposure to ambient O₃ could prompt the genesis of arrhythmias partially through worsening autonomic function and myocardial burden.