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Subclinical and Overt Adverse Cardiac Effects with Ozone Inhalation in Rats: Potentially Dire Implications of Low Exposures
Citation:
FARRAJ, A., M. S. HAZARI, D. W. WINSETT, A. Kulukulualani, A. P. Carll, N. HAYKAL-COATES, C. Lamb, E. LAPPI, D. TERRELL, AND D. L. Costa. Subclinical and Overt Adverse Cardiac Effects with Ozone Inhalation in Rats: Potentially Dire Implications of Low Exposures. Presented at 2011 American Heart Association Scientific Session Meeting, Orlando, FL, November 12 - 16, 2011.
Impact/Purpose:
This study demonstrates that ozone inhalatioon causes several adverse effects on cardiac electrophysiology that are perhaps mediated by autonomic dysfunction. Additionally, exposure to low ozone concentrations may cause subclinical effects that are only manifested when triggered by a stressor, suggesting that health effects of ambient levels of air pollutants may be insidious and potentially underestimated
Description:
Ozone is a ubiquitous smog-associated photochemical oxidant with deleterious health effects. While most of the adverse effects described to date involve the respiratory system (i.e, decrements in lung function, airway injury and inflammation, exacerbation of asthma, and compromised host defense), there is increasing epidemiological evidence pointing to the cardiovascular system as a target. Despite this new evidence, much work remains to further substantiate the linkage between ambient ozone exposure and adverse cardiovascular effects. One of the most conspicuous data gaps is the impact of ozone exposure on normal cardiac electrophysiology and heart rate. We hypothesized that a single inhalation exposure to ozone will cause concentration-dependent cardiac dysfunction in rhythm and impulse propagation. Rats implanted with telemeters to monitor heart rate and the electrocardiogram were exposed once by whole body inhalation for 4 h to 0.8 or 0.2 parts per million (ppm) O3 or filtered air. A separate cohort was tested for increased arrhythmia sensitivity using the arrhythmogenic agent aconitine 24 h after exposure. Exposure to 0.8 ppm O3 caused bradycardia, PR prolongation, ST depression, and substantial increases in episodes of sinoatrial block and second degree Mobitz Type II atrioventricular block. These effects were accompanied by concurrent increases in several heart rate variability parameters that were suggestive of increased parasympathetic tone to the heart. Low ozone exposure failed to elicit any overt indicators of cardiac toxicity. Both 0.8 ppm and 0.2 ppm O3, however, caused an increase in the sensitivity to triggered cardiac arrhythmia, suggesting an alteration in the myocardial conduction apparatus. Thus, ozone exposure causes several adverse effects on cardiac electrophysiology that are perhaps mediated by autonomic dysfunction. Additionally, exposure to low ozone concentrations may cause subclinical effects that are only manifested when triggered by a stressor, suggesting that health effects of ambient levels of air pollutants may be insidious and potentially underestimated (This abstract does not reflect EPA policy).