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Variability in onset of ECG changes indicative of ischemia after exposure to whole vs filtered diesel exhaust in hypertensive rats. Insight on mechanism?
Citation:
LAMB, C., N. HAYKAL-COATES, A. P. Carll, M. S. HAZARI, D. W. WINSETT, D. L. COSTA, AND A. FARRAJ. Variability in onset of ECG changes indicative of ischemia after exposure to whole vs filtered diesel exhaust in hypertensive rats. Insight on mechanism? Presented at Society of Toxicology (SOT) Annual Meeting, Washington, DC, March 06 - 10, 2011.
Impact/Purpose:
The data from this study strongly suggest that hypertension may predispose to the potential ischemic effects of DE and that the components of DE may have digergent effects with some elicting immmediate irritant effects (e.g., gases) while others (e.g., PM) triggering persistent effects potentially via separate mechanisms.
Description:
Diesel exhaust (DE) is a complex mixture of gases including C02, O2, N02, CO, aldehydes, benzene, and polycyclic aromatic hydrocarbons (PAHs) as well as highly respirable particulate matter. DE is a significant component of fine particulate matter (PM2.5) air pollution, which itself has been positively associated with hospital admissions and cardiovascular morbidity and mortality, especially in individuals with pre-existing cardiovascular diseases . including hypertension. We hypothesized that exhausted exposure will result in concentration dependent cardiac dysfunction in hypertensive but not normal rats. Spontaneously hypertensive (SH) and Wistar Kyoto (WKY; rats with normal blood pressure) rats, were implanted with biopotential radiotelemetry transmitters to monitor electrocardiogram (ECG) and heart rate, and exposed once for 4 hours to 150ug/m3 or 500ug/m3 of whole (WDE; gases + PM) or filtered (FDE; gases alone) diesel exhaust, or filtered air (control) in whole body exposure chambers. Only the FDE, but not the WDE, caused decreases in HR during exposure at both concentrations in SH rats. In addition, only the low concentration of FDE caused ST depression (a change in the ECG often associated with myocardial ischemia) during exposure in SH rats, and this change persisted 18 hours after exposure. DE exposure also caused a decrease in HR in normal rats but did not affect ST amplitude. Taken together, the data suggest that hypertension may predispose to the potential ischemic effects of DE and that the components of DE may have divergent effects with some eliciting immediate irritant effects (e.g., gases) while others (e.g., PM) triggering persistent effects potentially via separate mechanisms. (This abstract does not reflect EPA policy