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HEMATOLOGICAL AND MOLECULAR CARDIAC EFFECTS FOLLOWING PULMONARY EXPOSURE TO OIL COMBUSTION PARTICLES
Citation:
Akland, G G. HEMATOLOGICAL AND MOLECULAR CARDIAC EFFECTS FOLLOWING PULMONARY EXPOSURE TO OIL COMBUSTION PARTICLES. Presented at Orlando, Florida, March 31-April 4, 2001.
Description:
Hematological and Molecular Cardiac Effects Following Pulmonary Exposure to Oil Combustion Particles
K. Dreher, R. Jaskot, and J. Richards. USEPA, Research Triangle Park, NC
Systemic health effects induced following pulmonary exposure to various combustion particles are not known. This information will provide important insight into the adverse health effects associated with exposure to air particulate pollution. This study examined the hematological and molecular cardiac effects following pulmonary exposure to residual oil fly ash (ROFA). Rats were exposed to saline or ROFA (8.3 mg/kg) by intratracheal ? instillation and examined at various times up to 48h post-exposure. Plasma recovered from experimental animals was analyzed for vanadium and beta-fibrinogen content. Gene expression profiling was performed on RNA extracted from lung, heart, and liver recovered from experimental animals by RT-PCR. Plasma vanadium concentration peaked at 15min post-ROFA exposure and decreased toward control levels over the next 48h. ROFA induced an increase in plasma beta-fibrinogen concentration that was initially detected at 12h post-exposure, reached maximal levels (51% increase over controls) at 24h post-exposure and returned to control levels by 48h post-exposure. Elevated lung beta-fibrinogen mRNA content was detected at 3h (2.8-fold increase), 6h (4-fold increase) and 12h (7-fold increase) post-ROFA exposure. No increase in liver beta-fibrinogen mRNA content was detected by 24h post-exposure suggesting a pulmonary origin for ROFA-induced elevation of plasma beta-fibrinogen. A transient increase in cardiac mRNA levels encoding TNF alpha (4.5-fold increase) and matrix metalloproteinases [MMP-2, 3.5-fold increase; and MMP-11, 3-fold increase] were detected at 1h post-ROFA exposure. Alterations in cardiac gene expression occurred immediately following peak plasma vanadium levels suggesting that bioavailable metals were responsible for this effect. These findings demonstrate the ability of ROFA, a component of air particulate pollution, to induce extra-pulmonary effects that could initiate and exacerbate cardiovascular disease. (This abstract does reflect USEPA policy)