(302a) Oxidative Stress Induced By Secondary Organic Aerosols (SOA) Generated from Biogenic and Anthropogenic Precursors

Secondary organic aerosols (SOA), formed from oxidation of hydrocarbons followed by gas-particle partitioning, constitute a substantial fraction of ambient fine particulate matter (PM). The health implications resulting from exposure to SOA is unclear. In this work, we investigate reactive oxygen and nitrogen species (ROS/RNS) and inflammatory responses to SOA generated from biogenic and anthropogenic precursors. Experiments are performed in the Georgia Tech Environmental Chamber (GTEC) facility, which consisted of two 13m³ Teflon reactors surrounded by UV and fluorescent sunlights. Hydrocarbons studied include biogenic (isoprene, α-pinene, β-caryophyllene) and anthropogenic (pentadecane, m-xylene, and naphthalene) sources. A series of chamber experiments is designed to probe the 1) effect of NO_x (RO₂+HO₂ vs. RO₂+NO reactions), 2) effect of relative humidity, and 3) presence of transition metals, on the ROS/RNS and inflammatory responses of different SOA generated. Murine alveolar macrophages were used to measure intracellular ROS/RNS production. The secreted levels of cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) are also measured. We find that SOA precursor identity, reaction condition, and chemical composition affect all measured responses in a hydrocarbon-specific manner. TNF-α levels reach a plateau with increasing IL-6 levels; naphthalene SOA is an exception to this trend and it induces higher levels of TNF-α and ROS/RNS than other SOA. The correlations between SOA chemical composition (bulk elemental ratios) and cellular response will be discussed. Overall, results from this study suggest that the health effects of SOA are important when considering the health impacts of ambient PM.