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Cellular oxidative response from exposure to size-resolved ambient particulate matter
Citation:
Peltier, R., L. Chen, R. Lall, R. B. DEVLIN, AND T. Gordon. Cellular oxidative response from exposure to size-resolved ambient particulate matter. Presented at American Association for Aerosol Research , San Diego, CA, March 22 - 26, 2010.
Impact/Purpose:
The goal of this study was to characterize the in vitro effects of ambient PM and PM components from eight different locations in the U.S. and to investigate the effects of chemical composition on markers of oxidative stress
Description:
Recent studies suggest that particulate matter (PM) derived from different sources may differ in toxicity. The goal of this study was to characterize the in vitro effects of ambient PM and PM components from eight different locations in the U.S. and to investigate the effects of chemical composition on markers of oxidative stress. Airborne particles in the ultrafine, fine, and coarse thoracic size ranges were collected in Manhattan and South Bronx, in New York City, Tuxedo, NY, Seattle, WA, Phoenix, AZ, and Provo, UT, for a period of one month in 2003 and 2004 using high-volume particle samplers. Chemical composition of these PM samples was determined using ICP-MS and the composition data were modeled using factor analysis with varimax orthogonal rotation to determine particle source categories contributing to ambient PM size ranges at these locations. Chemical composition of sampled aerosol was highly variable depending on location and size fraction and was consistent with different sources of aerosol at each location. A respiratory epithelial cell line (BEAS-2B) stably transfected with a NF-kB-luciferase reporter plasmid was used to report NF-kB and reactive oxygen intermediate formation upon exposure to extracted, size-specific particles from each location. Intracellular pH was also evaluated for each size fraction from each location sampled. In-vivo results also showed that the stress response was both size and location dependent. The coarse particle fraction produced the greatest oxidative stress (by RaI production and NF-kB activation) at all locations, and in general, oxidative stress was driven by oil combustion and traffic sources, but not a soil source, for all size categories. The RaI and NF-kB changes produced by ultrafine particles appeared to be driven by different mechanisms, possibly linked to elemental composition ofthe sample. It is interesting to note that responses were not always consistent with dose, particle size, or sampling location of particles which suggests that toxicological responses are likely to depend on other physicochemical factors. From the sampled locations, NF-kB and RaI were inversely correlated for fine and coarse fractions, but no association was observed for the extracted ultrafine fraction. Thus, our results call into question whether NF-kB and Ral are equivalent measurements of cellular oxidative stress. This paper will discuss the biomarker endpoints and the observed chemical composition for each size range at each site. This abstract of a proposed presentation does not necessarily reflect EPA policy.