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Divergent Electrocardiographic Responses to Whole and Particle-Free Diesel Exhaust Inhalation in Spontaneously Hypertensive Rats
Citation:
Lamb, C. M., M. S. HAZARI, N. Haykal-Coates, A. P. Carll, T. Krantz, C. King, D. W. Winsett, W. CASCIO, D. L. Costa, AND A. FARRAJ. Divergent Electrocardiographic Responses to Whole and Particle-Free Diesel Exhaust Inhalation in Spontaneously Hypertensive Rats. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 125(2):558-68, (2012).
Impact/Purpose:
We demonstrate that exposure to filtered and whole diesel exhaust (DE) results in altered electrocardiographic effects in hypertensive but not normaI rats, corroboratmg studies that demonstrate exaggerated sensitivity to air pollution in susceptible subgroups. In addition, whole and particle-free DE elicited divergent electrocardiographic responses suggesting that the gaseous components of DE may activate separate pathways than the gas/particle mixture of whoe DE.
Description:
Diesel exhaust (DE) is a major contributor to traffic-related fine PM2.5. While inroads have been made in understanding the mechanisms of PM related health effects, DE’s complex mixture of PM, gases and volatile organics makes it difficult to determine how the constituents contribute to DE’s effects. We hypothesized that exposure to particle-filtered DE (gases alone) will elicit less cardiac effects than whole DE (particles plus gases). In addition, we hypothesized that Spontaneously Hypertensive (SH) rats will be more sensitive to the electrocardiographic effects of DE exposure than Wistar Kyoto rats (WKY; background strain with normal blood pressure). SH and WKY rats, implanted with telemeters to monitor electrocardiogram (ECG) and heart rate (HR), were exposed once for 4 hrs to 150ug/m3 or 500ug/m3 of whole (wDE; gases plus PM) or filtered (fDE; gases alone) DE, or filtered air. Exposure to fDE, but not wDE, caused immediate electrocardiographic alterations in cardiac repolarization (ST depression) and atrioventricular conduction block (PR prolongation) as well as bradycardia in SH rats. Exposure to wDE, but not fDE, caused post-exposure ST depression and increased sensitivity to the pulmonary C fiber agonist capsaicin in SH rats. The only notable effect of DE exposure in WKY rats was a decrease in heart rate. Taken together, hypertension may predispose to the potential cardiac effects of DE and components of DE may have divergent effects with some eliciting immediate irritant effects (e.g., gases) while others (e.g., PM) trigger delayed effects potentially via separate mechanisms. (This abstract does not reflect EPA policy).
