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Exposures to Emissions from Combustion of Biodiesel Fuels (B100/B20) Elicit Differential Responses in Redox-Sensitive Pathways
Citation:
Palmer, B, S. H. GAVETT, M. Li, E. H. Boykin, M. J. DANIELS, R. H. JASKOT, Q. T. KRANTZ, C. KING, M. I. GILMOUR, B. Holmen, AND N. K. Fukagawa. Exposures to Emissions from Combustion of Biodiesel Fuels (B100/B20) Elicit Differential Responses in Redox-Sensitive Pathways. Presented at Society of Toxicology (SOT) Annual Meeting, San Francisco, CA, March 11 - 15, 2012.
Impact/Purpose:
This study shows that in a mouse model of atlteroscIcrosis (ApoE knockout mice), short-term (3-day) exposure to pure soy biodiesel exhaust was associated with Oxidative stress and consequent activation of redox-sensitive pathways (Nrf2and GCLC) and that PAI-1 rnay contribute to lung injury and risk for thrombisis
Description:
Exposure to airborne particulate matter (PM) is associated with higher risk for cardiopulmonary diseases but mechanisms for the effects remain unknown. Combustion of biodiesel fuels (BD) is associated with lower emission of PM but the health consequences of exposure to exhaust from combustion of pure soy BD (B100) or a 20% (w/w) blend (B20) is unclear. To examine the in vivo responses to inhalation of exhaust generated by Bl00 and B20 combustion, ApoE-deficient mice were exposed by inhalation to B100 or B20 PM at 0, 50 or 150 ug/m3 (n =8-10/group), 4 h/day for 3-days. Mice were sacrificed ~24 h after the last exposure and blood, tissue, and bronchoalveolar lavage fluid (BAL) were obtained. Total cell and differential counts as well as protein and LDH concentrations in blood and BAL were not affected by exposure to either exhaust. However, Western blots of lung homogenates revealed higher plasminogen activator inhibitor-1 (PAI-1), catalytic subunit of glutamatecysteine ligase (GCLC), the transcription factor, NF-E2-related factor 2 (Nrf2) and protein carbonyls in mice exposed to 50 ug/m3 B100 in comparison with mice exposed to filtered air or 150 ug/m3, No significant differences were found in any of these parameters in the B20-exposed mice. These data suggest that short-term exposure to the lower dose of Bl00 exhaust was associated with oxidative stress (protein carbonyls) and consequent activation of redox-sensitive pathways (Nrf2 and GClC) and that PAI-1 may contribute to lung injury and risk for thrombosis. It would be important to determine the relative contribution of pure BD versus the presence of petrodiesel in the B20 blend in producing the differential responses, both of which would affect particle size and composition. (This abstract does not reflect U.S. EPA policy).