Oil fly ash-induced elevation of plasma fibrinogen levels in rats

Particulate matter air pollution (PM) has been associated with morbidity an d mortality from ischemic heart disease and stroke in humans. It has been h ypothesized that alveolar inflammation, resulting from exposure to PM, may induce a state of blood hypercoagulability, triggering cardiovascular event s in susceptible individuals. Previous studies in our laboratory have demon strated acute lung injury with alveolar inflammation in rats following expo sure to residual oil fly ash (ROFA), an emission source particulate. In add ition, increased mortality has been documented following exposure to ROFA i n rats with preexistent cardiopulmonary disease. ROFA's toxicity derives fr om its soluble metal content, which appears also to drive the toxicity of a mbient PM. The present study was conducted to test the hypothesis that expo sure of rats to a toxic PM, like ROFA, would adversely alter hemostatic par ameters and cardiovascular risk factors thought to be involved in human epi demiologic findings. Sixty-day-old male Sprague-Dawley rats were exposed by intratracheal instillation (IT) to varying doses (0.3, 1.7, or 8.3 mg/kg) of ROFA, 8.3 mg/kg Mt. Saint Helen's volcanic ash (MSH, control particle), or 0.3 mi saline (SAL, control). At 24 h post-IT, activated partial thrombo plastin time (APTT), prothrombin time (PT), plasma fibrinogen (PF), plasma viscosity (PV), and complete blood count (CBC) were performed on venous blo od samples. No differences from control were detected in APTT and PT in ROF A-exposed rats; however, ROFA exposure did result in elevated PF, at 8.3 mg /kg only. In addition, PV values were elevated in both ROFA and MSH-exposed rats relative to SAL-control rats, but not significantly. Although no chan ges were detected in APTT and PT, alteration of important hematologic param eters (notably fibrinogen) through PM induction of an inflammatory response may serve as biomarkers of cardiovascular risk in susceptible individuals.