AAAR 36th Annual Conference October 16 - October 20, 2017 Raleigh Convention Center Raleigh, North Carolina, USA
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Cellular Neuroinflammatory Responses to Traffic Generated vs. Photochemically Aged Particulate Matter (PM2.5)
CHRISTOPHER LOVETT, Mafalda Cacciottolo, Farimah Shirmohammadi, Constantinos Sioutas, Caleb E. Finch, Todd E. Morgan, University of Southern California
Abstract Number: 581 Working Group: Linking Aerosol Oxidative Potential with Chemical Composition and Biological Endpoints
Abstract Primary (traffic derived) and secondary (photochemically aged) PM2.5 samples were obtained using a direct aerosol-into-liquid collection system located adjacent to a major freeway (I-110) near downtown Los Angeles, CA. The aqueous slurry samples were characterized by chemical analyses, and their effects on living neuronal cell cultures, including BV-2 (microglia) and N2a-APPswe (neuroblastoma) cell lines, were examined by performing in vitro neurobiological assays to quantify known biological endpoints associated with neuroinflammation and Alzheimer’s Disease, including Tumor Necrosis Factor α (TNF-α), Interleukins 6 and 1β (IL-6 & IL-1β), Interferon γ (IFN-γ), and the cellular signaling molecule nitric oxide (NO). A precise characterization of these two types of ambient PM2.5, using both chemical and neurobiological techniques of analysis, allows for increasingly finer distinctions to be made regarding individual particulate species and the associated neurobiological consequences of exposure.
Prior studies of primary vs. secondary particulates (e.g. Verma, et al., 2009) have found that products of photochemical oxidation (secondary PM) contain higher concentrations of oxygenated organic acids and water-soluble organic carbon (WSOC) species, and exhibit a greater intrinsic oxidative potential, as quantified by the dithiothreitol (DTT) assay. Other studies (e.g. Saffari, et al., 2015), have found a larger inflammatory response, as indexed by the macrophage ROS (reactive oxygen species) assay, to primary PM samples collected during morning hours as compared to secondary (afternoon) PM samples.
In the current study, neural cell lines were exposed to primary PM2.5, emitted by vehicles during morning rush hour (6-9am), and secondary PM2.5, dominated by photochemically oxidized products formed during afternoon hours (12-4pm). In vitro assays revealed a greater neuroinflammatory dose-dependent response, as indicated by the previously mentioned biological endpoints of interest, in response to primary, as compared to secondary, PM exposures. Additionally, ROS activity was found to be greater in response to the morning (primary) PM samples, and DTT activity was found to be greater in response to afternoon (secondary) PM exposure, duplicating the results of both previously mentioned studies.
This research will ultimately allow us to gain a more complete understanding of the complex, multi-component nature of particulate matter, as well as its health effects and possible role in the etiology, onset and development of Alzheimer’s Disease.