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CARDIAC INJURY FROM LONG TERM EPISODIC EXPOSURE TO PARTICULATE MATTER (PM): SOLUBLE COMPONENTS OR SOLID PARTICLES?
Kodavanti, U P., M. Schladweiler, P. S. Gilmour, J K. McGee, W P. Watkinson, R. H. Jaskot, J H. Richards, A. D. Ledbetter, D. C. Christiani, D L. Costa, AND A. Nyska. CARDIAC INJURY FROM LONG TERM EPISODIC EXPOSURE TO PARTICULATE MATTER (PM): SOLUBLE COMPONENTS OR SOLID PARTICLES? Presented at Society of Toxicology Annual Meeting, New Orleans, LA, March 06 - 10, 2005.
Long-term exposure to PM has been associated with cardiac injury in rats. The purpose of this study was to investigate if cardiac injury was due to soluble metals (i.e., zinc), insoluble PM, or pulmonary injury/inflammation. Male Wistar Kyoto rats (n=8) were exposed intratracheally (IT), once/wk x 8 wks to either saline, Mount St. Helen's ash (MSH, no soluble metals) - 2.3 mg/kg/wk, environmental combustion particles (PM, zinc as soluble metal) - 1.15 or 2.3 mg/kg/wk, the saline-leachable fraction of PM (PM/L) - 2.3 mg/kg/wk or ZnSO4 (Zn) - 33.4 g/kg/wk (equivalent soluble zinc in PM). Another group of rats was exposed to half the concentration of all components above but for 16 wks. All IT exposures, except saline, caused marked lung inflammation including MSH. Lavage fluid protein, albumin, and LDH activity also increased in all groups relative to saline. PM high dose demonstrated the greatest pulmonary effects. No changes were apparent among the hematological parameters. Four sections of each cardiac tissue were examined microscopically. Lesions were scored in a blinded manner for extension (e.g., focal or multifocal) of inflammation, fibrosis and myofiber degeneration. Minimal to no lesions were noted in controls. Mild to moderate myocardial lesions were noted in all other groups including MSH, however, the mean severity was highest in PM high dose group. Subepicardial and random myocardial lesions were characterized by inflammation with fibrotic degeneration. Gene expression arrays are being evaluated to understand potential differential roles of the PM components associated with these exposures. In summary, long-term episodic IT exposure to insoluble PM or soluble zinc causes persistent pulmonary inflammation/injury as well as varying degrees of cardiac lesions. These findings support the hypothesis that both soluble and insoluble components may cause cardiac injury. (Does not reflect US EPA policy. Supported in part by #CR829522 between EPA and UNC).
Record Details:Record Type: DOCUMENT (PRESENTATION/ABSTRACT)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LAB
EXPERIMENTAL TOXICOLOGY DIVISION
PULMONARY TOXICOLOGY BRANCH