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Electrocardiographic and autonomic effects of acute particulate matter (PM) exposure in a rat model of cardiomyopathy
Citation:
Carll, A. P., N. HAYKAL-COATES, D. W. WINSETT, W. Darrell, M. S. HAZARI, A. D. LEDBETTER, J. Callaway, J. H. Richards, D. L. COSTA, AND A. FARRAJ. Electrocardiographic and autonomic effects of acute particulate matter (PM) exposure in a rat model of cardiomyopathy. Presented at Society of Toxicology 49th Annual meeting, Salt Lake City, UT, March 07 - 11, 2010.
Impact/Purpose:
This study demonstrates that PM exposure in an animal model of cardiomyopathy results in cardiopulmonary injury. This model may help elucidate the mechanisms by which PM exacerbates heart failure.
Description:
Human exposure to ambient PM from fossil-fuel emissions is linked to cardiovascular disease and death. This association strengthens in people with preexisting cardiac disease--especially heart failure (HF). Cardiomyopathy is the most common cause of heart failure. The mechanisms explaining PM-induced exacerbation of HF are unclear. Some of the effects of PM have been attributable to transition metal components. Residual oil fly ash (ROFA), a waste product of fossil fuel combustion from boilers, is rich in the transition metals Fe, Ni, and V, and when released as a fugitive particle, is an important contributor to ambient fine particulate air pollution. We hypothesized that PM exposure would exacerbate cardiopulmonary responses in a rat model of cardiomyopathy. Cardiomyopathy was induced in Spontaneously Hypertensive Heart Failure (SHHF) rats via continuous infusion with isoproterenol. Five days later, the rats were exposed by nose-only inhalation for 4 h to either filtered air or 580 µg/m3 of the PM2.5 fraction of a synthetic PM (dried salt solution) consisting of Fe, Ni and V sulfates and that is similar in composition to ROFA. PM exposure increased pulmonary inflammatory influx, decreased systolic blood pressure and Q-wave amplitude, and increased PR interval in rats with cardiomyopathy during exposure. Thus, PM exposure exacerbated cardiopulmonary injury in rats with cardiomyopathy suggesting that this model may help elucidate the mechanisms by which PM exposure exacerbates HF exacerbation. ECG data is currently being analyzed for mid-and post-inhalation effects on heart rate variability, cardiac arrhythmias, and ECG morphology. (Abstract does not reflect EPA policy; Supported by UNCIEPA CR8332360l.)