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A single exposure to particulate or gaseous air pollution increases the risk of aconitine-induced cardiac arrythmia in hypertensive rats
Citation:
HAZARI, M. S., N. HAYKAL-COATES, D. W. WINSETT, D. L. COSTA, AND A. FARRAJ. A single exposure to particulate or gaseous air pollution increases the risk of aconitine-induced cardiac arrythmia in hypertensive rats. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 112(2):532-542, (2009).
Impact/Purpose:
This study describes the effects of a single exposure to residual oil fly ash (ROFA)-like particles on arrhythmogenicity in spontaneously hypertensive (SH) rats. ROFA is an emission source particle which is produced by the combustion of fossil fuels. Rats were intravenously challenged with the arrhythmogenic drug aconitine to assess the dose required to trigger arrhythmias. The cumulative dose of aconitine necessary to elicit ventricular premature beats (VPB), ventricular tachycardia (VT), and ventricular fibrillation (VF) was significantly lower in rats exposed to ROFA-like particles when compared to air-exposed rats. Thus, a single exposure produces significant risk of arrhythmia in hypertensive animals. Over one million Americans suffer from arrhythmias, and although arrhythmias occur in healthy individuals with minimal consequence, some arrhythmias represent serious underlying conditions and risk of heart disease or sudden cardiac death. Several epidemiological studies have shown a significant association between cardiac arrhythmias and air pollution (Poloniecki et al. 1997). This study demonstrates that a single exposure to ROFA, a fugitive emission source particle which is produced by the combustion of fossil fuels and contributes heavily to the environmental PM mass concentrations in the United States, produces significant risk of arrhythmia in hypertensive animals. These results are important because of the known hazardous health effects of particulate air pollution, particularly in a susceptible population (i.e. those with hypertension and underlying cardiovascular disease). Since USEPA has identified particulate matter as a major respiratory irritant, these results shed light on how this toxicant produces its effects and provides a model for studying other common air pollutants. This work also fulfills air research program goals.
Description:
Epidemiological studies demonstrate a significant association between arrhythmias and air pollution exposure. Sensitivity to aconitine-induced arrhythmia has been used repeatedly to examine the factors that increase the risk of such cardiac electrical dysfunction. In this study, we are the first to use a technique known to elicit arrhythmia to "challenge" rats acutely exposed to inhaled air pollutants in order to examine the adverse cardiac effects of a single exposure and the stress it places on the heart. Aconitine-induced arrhythmogenesis was assessed twenty-four hours following a single inhalation exposure to either a particulate air pollutant or a gaseous irritant. Pollutant-exposed hypertensive rats developed ventricular premature beats, tachycardia, and fibrillation at significantly lower doses of aconitine than air-exposed animals. These findings suggest that a single exposure to a toxic air pollutant can increase the sensitivity of the cardiac electrical conduction system and trigger arrhythmia; which poses a particular health risk to individuals with cardiovascular disease.
