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The Differential Oxidative Properties of Diesel Exhaust Particles
Citation:
MANZO, N., J. E. RICHARDS, R. SLADE, L. D. MARTIN, AND J. A. DYE. The Differential Oxidative Properties of Diesel Exhaust Particles. Presented at 2009 Annual Society of Toxicology Meeting, Baltimore, MD, March 15 - 19, 2009.
Impact/Purpose:
Information on the differential antioxidant responses elicited by exposure of lung epithelial cells to different compositions of DEP.
Description:
Diesel exhaust particles (DEP) accounts for a significant percentage of particulate matter (PM) released into the atmosphere and are associated with adverse pulmonary effects. Due to their extremely small size and high surface area, DEP can adsorb toxic substances, thus potentially influencing its effects. DEP compositions vary and are often characterized by their ratio of elemental to organic carbon (EC/OC). We hypothesized that lung epithelial cells exposed to DEP rich in adsorbed OC compounds would result in greater antioxidant responses, enhanced inflammatory chemokine release, or possibly cell injury. Three samples of varying EC/OC ratios were evaluated: OC deficient ultrafine carbon black (CB), OC poor NIST diesel standard reference material 2975 (SRM 2975), and OC rich diesel automobile (DEPA) particles. LA-4 epithelial cells were exposed (25ug/cm2) for 24hrs. Antioxidant responses of GSH vs. GSSG and heme oxygenase-1 (HO-1) were determined using HPLC and realtime RT-PCR, respectively. Inflammatory chemokine release and expression of RANTES and MIP-2 were evaluated by ELISA and realtime RT-PCR. Cell injury was inferred by the release of LDH. Exposure to DEPA resulted in significant increases in GSH, GSSG and HO-1 expression, but only minor increases in cell injury. Particle exposures had no effect on MIP-2 gene expression or release. While RANTES expression and release was not altered by CB, SRM 2975 reduced its release (most likely due to particle adsorption) without alterations in its expression, and DEPA not only reduced its release (again due to adsorption) but also decreased its gene expression. In conclusion, DEP can selectively bind mediators, thus interfering with their quantification which must be considered when interpreting their release. In addition, it appeared that epithelial exposure to simple elemental carbon particles was largely innocuous, while particles with increasing OC content (and related adsorbed material) were seemingly associated with cellular antioxidant responses. Funded by the EPA CT826512010 (Abstract does not represent USEPA policy)