You are here:
Differential electrocardiogram efffects in normal and hypertensive rats after inhalation exposure to transition metal rich particulate matter
LAMB, C., A. P. Carll, N. HAYKAL-COATES, M. S. HAZARI, D. W. WINSETT, D. L. COSTA, AND A. FARRAJ. Differential electrocardiogram efffects in normal and hypertensive rats after inhalation exposure to transition metal rich particulate matter. Presented at Society of Toxicology 49th Annual meeting, Salt Lake City, UT, March 07 - 11, 2010.
This study demonstrates that hypertensive rats are more sensitive to the cardiotoxic effects of PM inhalation. this model may help elucidate the mechanisms by which PM exacerbates pre-existing cardiovascular disease.
Inhalation of particulate matter (PM) associated with air pollution causes adverse effects on cardiac function including heightened associations with ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. Some of these effects have been attributable to transition metal components of PM. Recent epidemiologic data (Bell et al, 2009) shows associations of cardiac hospitalization with fine PM-associated Ni and V. 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 a single acute inhalation exposure to transition metal-rich particulate matter designed to mimic ROFA will cause greater cardiopulmonary toxicity in Spontaneously Hypertensive (SH) rats than in similarly exposed Wistar Kyoto rats with normal blood pressure. Rats were exposed once by nose-only inhalation for 4 hours to approximately 500 µg/m3 of a synthetic particulate matter consisting of Fe, Ni and V sulfates that is similar in composition to a well-studied ROFA sample. PM exposure in SH rats caused an increase in T-wave area and amplitude (p<0.05) immediately after exposure (0 -6 h post exposure) but no ECG changes in the normotensive WKY rats. PM exposure did not significantly affect pulmonary inflammatory markers, antioxidant enzymes, or infiltrating inflammatory cells in either strain. PM caused electrocardiographic alterations only in SH rats, suggesting that metal components of PM may be acutely toxic in individuals with preexisting cardiovascular disease. Heart rate variability and ECG effects during exposure are currently being analyzed. (This abstract does not reflect EPA policy).