AAAR 34th Annual Conference
October 12 - October 16, 2015
Hyatt Regency
Minneapolis, Minnesota, USA
Abstract View
Isoprene-derived Secondary Organic Aerosol Induces Expression of Nuclear Factor Erythroid 2-like 2 (NRF2)-mediated Oxidative Stress Response Genes in Human Lung Cells
Ying-Hsuan Lin, Amanda Kramer, Maiko Arashiro, Weruka Rattanavaraha, Elizabeth Martin, Zhenfa Zhang, Kenneth Sexton, Avram Gold, Ilona Jaspers, Rebecca Fry, JASON SURRATT, University of North Carolina at Chapel Hill
Abstract Number: 256 Working Group: Health Related Aerosols
Abstract Isoprene-derived secondary organic aerosol (SOA) has been estimated to contribute to a significant mass fraction of tropospheric fine particulate matter (PM2.5). In particular, the isoprene-derived epoxides, isoprene epoxydiols (IEPOX) and methacrylic acid epoxide (MAE), have been recently identified as the key gaseous intermediates leading to isoprene SOA formation through heterogeneous reactions under low-NOx and high-NOx pathways, respectively. To date, there is scant information about the potential toxicity and impact of isoprene-derived SOA on human health. This study seeks to characterize the potential toxicogenomic effects of isoprene-derived SOA in an in vitro model of human airway epithelial cells (BEAS-2B). Pathway-focused oxidative stress-associated gene expression assays were performed. Oxidative potential of isoprene-derived SOA generated in smog chamber experiments were also assessed by the rate of dithiothreitol (DTT) consumption. We found that the resultant SOA constituents enrich for the expression of nuclear factor erythroid 2-like 2 (NRF2)-mediated oxidative stress response genes in human lung cells under non-cytotoxic conditions, with MAE-derived SOA showing greater potency than IEPOX-derived SOA. The relative oxidative potential assessed by the dithiothreitol (DTT) assay indicates MAE-derived SOA has greater oxidizing potential relative to IEPOX-derived SOA. These results suggest chemical composition and reactivity of the stressors play a key role in the observed differential toxicogenomic responses.