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Comparative Toxicity of Biodiesel Exhaust and Petroleum Diesel Exhaust Particulate Matter Using WKY Rat Alveolar Machrophages
Citation:
Bhavaraju, L., J. Shannahan, M. C. MADDEN, U. P. KODAVANTI, R. McCormick, AND A. Williams. Comparative Toxicity of Biodiesel Exhaust and Petroleum Diesel Exhaust Particulate Matter Using WKY Rat Alveolar Machrophages. Presented at Society of Toxicology (SOT) Annual meeting, Washington, DC, March 06 - 10, 2011.
Impact/Purpose:
In order to study the effects of BioDEP compared to PetDEP, we collected WKY alveolar macrophages (AM) via lavage and exposed the cells in vitro. We observed dose dependent cytotoxicty when exposed to B20 and DEP for 24 hours.
Description:
Exposure to fine ambient particulate matter <2.5um (PM2.5) can induce airway inflammation, cardiopulmonary morbidity and mortality. Combustion of petroleum diesel and biodiesel contributes to PM2.5. Possible toxicity caused by inhalation of biodiesel emission particles (BioDEP) have not been well studied compared to petroleum diesel emission (PetDEP). Biodiesel is an alternative fuel source for use in diesel engines that is commonly used as a 20% blend (B20) containing petroleum diesel in the US. In order to study the effects of BioDEP compared to PetDEP, we collected WKY alveolar macrophages (AM) via lavage and exposed the cells in vitro. We observed dose dependent cytotoxicty when exposed to B20 and DEP for 24 hours. Using non-cytotoxic exposures, AM exposed to concentrations as low as 1ug/mL. of B20, but not PetDEP, produced a statistically significant increase in the amount of the immune mediator Prostaglandin E2 when compared to untreated AM's after 24 hours of exposure. 100ug/mL PetDEP upregulated COX2 expression (involved in PGE2 production) relative to control AM. AM were incubated with endotoxin post PetDEP and B20 exposure, and the AM's showed a decreased production of PGE2, suggesting the macrophages have a diminished protective response to bacteria after exposure to PM. These data suggest that both diesel combustion particles can alter AM lipid metabolism and these responses may playa role in the health effects from exposure to ultrafine PM. [This is an abstract of a proposed presentation and may not necessarily reflect official US EPA Policy.]