title: Oil fly ash-induced elevation of plasma fibrinogen levels in rats.
abstract: Particulate matter air pollution (PM) has been associated with morbidity and mortality from ischemic heart disease and stroke in humans. It has been hypothesized that alveolar inflammation, resulting from exposure to PM, may induce a state of blood hypercoagulability, triggering cardiovascular events in susceptible individuals. Previous studies in our laboratory have demonstrated acute lung injury with alveolar inflammation in rats following exposure to residual oil fly ash (ROFA), an emission source particulate. In addition, increased mortality has been documented following exposure to ROFA in rats with preexistent cardiopulmonary disease. ROFA's toxicity derives from its soluble metal content, which appears also to drive the toxicity of ambient PM. The present study was conducted to test the hypothesis that exposure of rats to a toxic PM, like ROFA, would adversely alter hemostatic parameters and cardiovascular risk factors thought to be involved in human epidemiologic 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 ml saline (SAL, control). At 24 h post-IT, activated partial thromboplastin time (APTT), prothrombin time (PT), plasma fibrinogen (PF), plasma viscosity (PV), and complete blood count (CBC) were performed on venous blood samples. No differences from control were detected in APTT and PT in ROFA-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 changes were detected in APTT and PT, alteration of important hematologic parameters (notably fibrinogen) through PM induction of an inflammatory response may serve as biomarkers of cardiovascular risk in susceptible individuals.
authors.affiliation: Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina 27711, USA. sarah_gardner@ncsu.edu
authors.forename: S Y
authors.initials: SY
authors.lastname: Gardner
authors.forename: J R
authors.initials: JR
authors.lastname: Lehmann
authors.forename: D L
authors.initials: DL
authors.lastname: Costa
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001772:Blood Cell Count; D001780:Blood Coagulation Tests; D001809:Blood Viscosity; D002244:Carbon / Q000008:administration & dosage / Q000633:toxicity*; D060729:Coal Ash; D004195:Disease Models, Animal; D005340:Fibrinogen / Q000378:metabolism*; D007442:Intubation, Intratracheal; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D052638:Particulate Matter; D011658:Pulmonary Fibrosis / Q000097:blood / Q000139:chemically induced*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018707:Volcanic Eruptions
chemical_list: D000393:Air Pollutants; D060729:Coal Ash; D052638:Particulate Matter; D002244:Carbon; D005340:Fibrinogen