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Extracted Cookstove Emissions Differentially Alter Pro-inflammatory and Adaptive Gene Expression in Lung Epithelial Cells
Citation:
Gibbs-Flournoy, E., B. Preston, M. Hays, J. Mcgee, L. Copeland, AND J. Dye. Extracted Cookstove Emissions Differentially Alter Pro-inflammatory and Adaptive Gene Expression in Lung Epithelial Cells. Society of Toxicology Annual Meeting, New Orleans, LA, March 13 - 17, 2016.
Impact/Purpose:
Several new cookstove (CS) designs has led efforts to reduce cookstove emissions with relative success, however the data supporting potential health benefits from the use of new CS remain limited. Therefore the current study examined the impact of CE exposure on redox-sensitive inflammatory and adaptive gene expression of both murine and human-derived lung epithelial cell-lines and demonstrated that cleaner cooking technologies appear to attenuate the pulmonary epithelial cell toxicity of methanol-extractable emissions.
Description:
Current estimates attribute exposure to cookstove emissions (CE) to over 4 million deaths annually. While the development of several new cookstove (CS) designs has led efforts to reduce CE with relative success, the data supporting potential health benefits from the use of new CS remain limited. We previously demonstrated that direct exposure of extracted emissions from three CS: 3-Stone (3S), Natural Draft (ND), and Forced Draft (FD); adversely altered the oxidative status of human (Beas-2B) and murine (LA-4) lung epithelial cells. Furthermore, in-vivo exposure of female CD-1 mice substantially influenced lung redox balance. Since CE contain numerous redox-active components including VOCs, PAHs, metals, particulates, and radicals, we hypothesize that oxidative stress is a key mechanistic feature of CE toxicity. As an extension, the current study examined the impact of CE exposure on redox-sensitive inflammatory and adaptive gene expression of both murine and human-derived lung epithelial cell-lines. In brief, LA-4 or BEAS-2B cells were exposed to methanol-derived extracts obtained from filters collected during the aforementioned in-vivo study. Using real-time quantitative PCR, intracellular responses to each CE extract were examined. The three CE extracts were observed to differentially cause increases in the expression of adaptive, antioxidant, and pro-inflammatory genes including HO-1, GCLC, and IL-8 / MIP-2. Like the oxidative stress assessments, gene expression alterations corresponded to the relative emissions of each stove, with the rudimentary 3S stove most often inducing the greatest effect. Together, these data indicate that exposure to various CE has a profound effect on the pro-inflammatory and adaptive gene expression of both human and murine lung epithelial cells. Moreover, the cleaner cooking technologies appear to attenuate the pulmonary epithelial cell toxicity of methanol-extractable emissions. (Does not necessarily reflect USEPA policy.)