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Hypotension and AV block after diesel exhaust exposure in heart failure-prone rats: role of gaseous and particulate components
Citation:
Carll, A. P., C. Lamb, M. S. HAZARI, N. HAYKAL-COATES, D. W. WINSETT, Q. T. KRANTZ, D. L. COSTA, AND A. FARRAJ. Hypotension and AV block after diesel exhaust exposure in heart failure-prone rats: role of gaseous and particulate components. Presented at Society of Toxicology (SOT) Annual Meeting, Washington, DC, March 06 - 10, 2011.
Impact/Purpose:
We used the young SHHF rat, a heart-failure prone strain, to compare the effects of inhalation exposure to whole and filtered diesel exhaust, relative to clean air. Exposure to SHHF rats to diesel exhaust, either filtered or whole, decreased blood pressure. Only exposure to gaseous components of particle-free diesel exhaust increasedd atrioventricular blook arrhythmias.
Description:
Acute inhalations ofdiesel engine exhaust (DE) and fine particulate matter (PM2.5) have been demonstrated to provoke adverse cardiac events in humans with preexisting heart disease. Electrophysiologic dysfunction and autonomic imbalance are among the mechanisms widely held to underlie the cardiac effects of DE and PM2.5. We previously demonstrated that acute PM2.5 inhalation (580 ug/m3 metal sulfate, 4 hours) provoked cardiac arrhythmias, vagal dominance, delayed atrioventricular (AV) conduction, and systolic hypotension in young heart failure-prone hypertensive rats (SHHF strain) with cardiomyopathy. We hypothesized that inhalation of either whole (WDE: gases + PM) or filtered DE (FDE: gases alone), would similarly elicit cardiac dysfunction in naive SHHFs. Unrestrained 10-week-old SHHFs were exposed once for 4 hours by inhalation to WDE (500 ug/m3 PM2.5), FDE, or filtered air (n=67/group). Both WDE and FDE decreased mean arterial pressure during exposure. Over the 8 hours following inhalation exposure, WDE-and FDE-exposed rats remained hypotensive, with effects more pronounced in the WDE group. WDE and FDE had minimal effects on heart rate variability, and pulmonary, cardiovascular, and systemic markers ofinflammation, injury, and oxidative stress. FDE, but not WDE, significantly increased AV block Mobitz II arrhythmias after exposure relative to pre-exposure. Similar exposures in normal rats (Wistar Kyoto) failed to elicit bradyarrhythmias. Thus, predisposition to heart failure may confer susceptibility to the adverse effects of DE inhalation on cardiac function. This study demonstrates that gaseous and particulate components of air pollution may have divergent effects that are triggered. by disparate mechanisms. (Abstract does not reflect EPA policy; Supported by UNC/EPA CR83323601.)