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Oxidative Responses to Extracted Cookstove Emissions in Lung Epithelial Cells
Citation:
Gibbs-Flournoy, E., Jim Jetter, E. Boykin, Steve Simmons, M. Higuchi, AND J. Dye. Oxidative Responses to Extracted Cookstove Emissions in Lung Epithelial Cells. Society of Toxicology (SOT) Meeting, San Diego, CA, March 22 - 26, 2015.
Impact/Purpose:
The current study examines the direct impact of different cookstove emissions (CE) on cellular antioxidant balance. This end point was examined because CE contain numerous redox-active components including VOCs, PAHs, metals, particulates, and radicals -- and thus, oxidative stress is likely a key mechanistic feature of CE toxicity. Using this text system, the ranking of oxidative responses was determined for cookstoves of different efficiency.
Description:
Exposure to cookstove emissions (CE) has been linked to significant increases in morbidity and mortality, with current estimates attributing CE exposure to over 4 million deaths annually. The development of several new cookstove (CS) designs has led efforts to reduce CE with relative success, yet data supporting potential health benefits from the implementation of such devices remain limited. Since CE contain numerous redox-active components including VOCs, PAHs, metals, particulates, and radicals, oxidative stress is likely a key mechanistic feature of CE toxicity. Emissions from four CS; 3-Stone (3S), Natural Draft (ND), Forced Draft (FD), and Propane (PR); were previously determined to have substantial influence on the alteration of the lung redox balance in female CD-1 mice. As an extension, the current study examines the impact of CE on the intracellular oxidation of glutathione using fluorescent reporters expressed in both murine and human-derived lung epithelial cell-lines. In brief, roGFP2, a reporter of intracellular glutathione redox potential (EGSH) was stably transduced into LA-4 (murine) or BEAS-2B (human) cells. Cells were exposed to methanol-derived extracts obtained from filters collected during the original in-vivo study. Using live-cell imaging, intracellular responses to each CE extract were observed in real-time. The CE extracts caused potent increases in the EGSH in both cell lines across equal- and compensated-dosing schemes, yielding the following relative potencies: 3S>ND≈FD>PR. Importantly, validation experiments confirmed the response of roGFP2 to be indicative of the oxidation status of glutathione. Together, these data indicate that exposure to various CE induces a substantial increase in intracellular EGSH in both human and murine epithelial cells, which is indicative of an oxidant-dependent impairment of redox homeostasis. Moreover, the use of cleaner CS appears to attenuate the oxidative changes observed. (Does not necessarily reflect USEPA policy)