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INHALED ENVIRONMENTAL COMBUSTION PARTICLES CAUISE MYOCARDIAL INJURY IN THE WISTAR KYOTO RAT
Citation:
Kodavanti, U P., C. F. Moyer, A. D. Ledbetter, M. Schladweiler, D L. Costa, R. Hauser, D. C. Christiani, AND A. Nyska. INHALED ENVIRONMENTAL COMBUSTION PARTICLES CAUISE MYOCARDIAL INJURY IN THE WISTAR KYOTO RAT. TOXICOLOGICAL SCIENCES 71(2):237-245, (2003).
Description:
Abstract Epidemiologists have associated particulate matter (PM) air pollution with cardiovascular morbidity and premature mortality worldwide. However, direct experimental evidence showing causality and pathogenesis of PM-induced cardiovascular damage has been insufficient. We hypothesized that protracted, repeated inhalation by rats of oil combustion-derived, fugitive emission PM (EPM), compositionally related to air, or ambient PM, would cause myocardial injury. Male Sprague Dawley, Wistar Kyoto, and Spontaneously Hypertensive rats were exposed nose-only to EPM 10 mg/m3, 6 h/d, 1d/wk for 16 consecutive wk. Histopathological and histochemical techniques were used to determine myocardial degeneration, inflammation, fibrosis, calcium deposits, apoptosis, and the presence of mast cells. Decreased numbers of granulated mast cells, suggesting increased degranulation, and multifocal lesions consisting of myocardial degeneration, inflammation, and fibrosis were present in 5 of 6 Wistar Kyoto rats exposed to EPM, but none of these lesions was observed in any Wistar Kyoto exposed to clean air. No cardiac EPM-related lesions were seen in the exposed Sprague Dawley and Spontaneously Hypertensive rats. The only prominent lung effect of EPM exposure was accumulation of particle-laden macrophages in all three rat strains. This study demonstrates that inhalation exposures to environmentally relevant PM can cause myocardial injury in rats, thereby providing a coherence to the epidemiological associations of cardiovascular morbidity and ambient PM.
Key Words: inhaled particulate matter myocardial injury Wistar Kyoto rats bioavailable zinc