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A Single Transition Metal-Rich Particulate Inhalation Exposure Elicits Concentration-Dependent Cardiovascular Toxicity in Hypertensive Rats
Citation:
FARRAJ, A., D. W. WINSETT, N. HAYKAL-COATES, M. S. HAZARI, A. P. CARLL, A. D. LEDBETTER, AND D. L. COSTA. A Single Transition Metal-Rich Particulate Inhalation Exposure Elicits Concentration-Dependent Cardiovascular Toxicity in Hypertensive Rats. Presented at Annual Society of Toxicology meeting, Baltimore, MD, March 15 - 19, 2009.
Impact/Purpose:
We hypothesized that a single acute inhalation exposure to transition metal-rich particulate matter will cause concentration-dependent cardiovasular toxicity in Spontaneously Hypertensive (SH) rats. Metal particulate exposure increased circulatory markers of cardiac injury and disease in rats with hypertension suggesting that metal components of PM may be acutely toxic in individuals with preexisting cardiovascular disease.
Description:
Recently, investigators in the CALFINE study demonstrated an association between the fine particulate matter (PM)-associated metals, Ni and Fe, in ambient air in nine California counties and increased cardiovascular mortality (Ostro et al. 2007). 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 will cause concentration-dependent cardiovascular toxicity in Spontaneously Hypertensive (SH) rats. Rats were exposed once by nose-only inhalation for 4 hours to 3.5 mg/m3, 1.0 mg/m3 or 0.45 mg/m3 of a synthetic particulate matter (dried salt solution) consisting of Fe, Ni and V sulfates and that is similar in composition to a well-studied ROFA sample. Twenty-four hours after exposure, only the high dose caused an increase in plasma Angiotensin Converting Enzyme (ACE), an enzyme that stimulates vasoconstriction and increased blood pressure, and serum myoglobin, a muscle protein released by injured cardiac myocytes. Only rats exposed to 1.0 mg/m3 of ROFA had increased heart fatty acid binding protein (HFABP), a marker of myocardial infarction in humans. Thus, metal particulate exposure increased circulatory markers of cardiac injury and disease in rats with hypertension suggesting that metal components of PM may be acutely toxic in individuals with preexisting cardiovascular disease. Heart rate, core body temperature, activity, and electrocardiogram data are currently being analyzed to assess the physiological effects of metal sulfate particle exposure (This abstract does not reflect EPA policy).