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Differential Responses upon Inhalation Exposure to Biodiesel versus Diesel Exhaust on Oxidative Stress, Inflammatory and Immune Outcomes
Citation:
Shvedova, A., N. Yanamala, A. Tkach, E. Kisin, A. Murray, T. Khaliullin, M. Hatfield, S. Gavett, AND Ian Gilmour. Differential Responses upon Inhalation Exposure to Biodiesel versus Diesel Exhaust on Oxidative Stress, Inflammatory and Immune Outcomes. Presented at Society of Toxicology, March 10 - 14, 2013.
Impact/Purpose:
Distinctive compounds formed from biodiesel exposure are capable of targeting biological pathways distinct from diesel exposure in normal mice.
Description:
Biodiesel (BD) exhaust may have reduced adverse health effects due to lower mass emissions and reduced production of hazardous compounds compared to diesel exhaust. To investigate this possibility, we compared adverse effects in lungs and liver of BALB/cJ mice after inhalation exposure (0, 50, 150 and 500 g/m3; 4 hr/day, 5 d/wk, for 4 wk) to combustion exhaust from 100% biodiesel (B100) and diesel (D100). Compared to D100, B100 exhaust caused a significant accumulation of oxidatively modified proteins (carbonyls), increase in 4-hydroxynonenal (4-HNE), reduction of protein thiols, depletion of antioxidant - gluthatione (GSH), a dose-dependent increase in the levels of biomarkers of tissue damage (LDH) in lungs, and inflammation (myeloperoxidase, MPO) in both lungs and liver. B100 exposure also significantly enhanced expression of cytokines IL-6, and IL-12p70 (in a dose-dependent manner), along with IL-10, TNF- and MCP-1 (increased compared to control) in both lung and liver tissues. Overall, the cytokine profiles in the lung and liver suggest that B100 and D100 exhaust elicit similar innate immune responses, predominantly involving T-cell independent pathways; however, the magnitude of inflammation was greater following B100 exhaust exposure. Interestingly, exposure to D100, but not B100 exhaust, induced a significant increase in the levels of IFN- in the lungs, suggesting a broader engagement of Th1 component by D100 exhaust. Based on this, we hypothesize that the distinctive organic compounds and/or oxidative products formed as a result of increased oxidative stress upon B100 exposure, are capable of targeting biological/molecular pathways that are distinct from D100 exposure. (This abstract does not represent US EPA policy).