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Overt and Latent Cardiac Effects of Ozone Inhalation in Rats: Evidence for Autonomic Modulation and Increased Myocardial Vulnerability*
Citation:
FARRAJ, A., M. S. HAZARI, D. W. WINSETT, A. Kulukulalani, A. P. Carll, C. Najwa Haykai, C. Lamb, E. LAPPI, D. TERRELL, W. CASCIO, AND D. L. Costa. Overt and Latent Cardiac Effects of Ozone Inhalation in Rats: Evidence for Autonomic Modulation and Increased Myocardial Vulnerability*. Presented at Society of Toxicology (SOT) Annual Meeting, San Francisco, CA, March 11 - 15, 2012.
Impact/Purpose:
03 exposure caused several changes in cardiac electrophysiology that are likely mediated by modulation of autonomic input to the heart. Moreover, exposure to low 03 concentrations may cause subclinical effects that are only manifested when triggered by a stressor, suggesting that the health effects of ambient levels of air pollutants may be insidious and potentially underestimated.
Description:
Ozone (O3) is a well-documented respiratory oxidant, but increasing epidemiologic evidence points to extra-pulmonary effects including positive associations between ambient O3 concentrations and cardiovascular morbidity/mortality. With preliminary reports linking O3 exposure with changes in heart rate (HR), we hypothesized that a single inhalation exposure to O3 will cause concentration-dependent autonomic modulation of cardiac function in rats. Rats implanted with telemeters to monitor HR and the electrocardiogram (ECG) were exposed once by whole-body inhalation for 4 hr to 0.2 or 0.8 parts per million (ppm) O3 or filtered air. A separate cohort was tested for vulnerability to aconitine-induced arrhythmia 24 hr after exposure. Low O3 exposure failed to elicit any overt changes in autonomic tone, heart rhythm or the ECG. Exposure to 0.8 ppm O3, however, caused bradycardia, PR prolongation, ST depression, and substantial increases in atrial premature beats (APB), sinoatrial block (SAB) and atrioventricular block (AVB) that were accompanied by concurrent increases in several heart rate variability (HRV) parameters suggesting increased parasympathetic tone. Despite not eliciting overt effects, exposure to 0.2 ppm O3 increased sensitivity to aconitine-induced arrhythmia formation in a manner similar to 0.8 ppm O3, suggesting a latent O3-induced alteration in myocardial excitability. Thus, O3 exposure causes several changes in cardiac electrophysiology that are likely mediated by modulation of autonomic input to the heart. Moreover, exposure to low O3 concentrations may cause subclinical effects that are only manifested when triggered by a stressor, suggesting that the health effects of ambient levels of air pollutants may be insidious and potentially underestimated (This abstract does not reflect EPA policy).