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The potential adverse health effects of PM2.5 and vapor samples from three communities that neighbor railyards, Commerce (CM), Long Beach (LB), and San Bernardino (SB), were assessed by determination of chemical reactivities attributed to the induction of oxidative stress by air pollutants. The assays used were dithiothreitol (DTT) and dihydrobenzoic acid (DHBA) based procedures for prooxidant content and a glyceraldehyde-3-phosphate dehydrogenase (GAPDH) assay for electrophiles. Prooxidants and electrophiles have been proposed as the reactive chemical species responsible for the induction of oxidative stress by air pollution mixtures. The PM2.5 samples from CM and LB sites showed seasonal differences in reactivities with higher levels in the winter whereas the SB sample differences were reversed. The reactivities in the vapor samples were all very similar, except for the summer SB samples, which contained higher levels of both prooxidants and electrophiles. The results suggest the observed reactivities reflect general geographical differences rather than direct effects of the railyards. Distributional differences in reactivities were also observed with PM2.5 fractions containing most of the prooxidants (74–81%) and the vapor phase most of the electrophiles (82–96%). The high levels of the vapor phase electrophiles and their potential for adverse biological effects point out the importance of the vapor phase in assessing the potential health effects of ambient air.

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Background: Most studies on air pollution (AP) exposure have focused on adverse health effects of particulate matter (PM). Less well-studied are the actions of volatile organic compounds (VOCs) not retained in PM collections. These studies quantified chemical and biological properties of both PM2.5 and VOCs. Methods: Samples were collected near the Port of Los Angeles (Long Beach, LB), railroads (Commerce, CM), and a pollution-trapping topography-site (San Bernardino, SB). Quantitative assays were conducted: (1) chemical—prooxidant and electrophile content, (2) biological—tumor necrosis factor-α (TNF-α) and heme oxygenase-1 (HO-1) expression (3), VOC modulation of PM effects and (4), activation of the antioxidant response element (ARE) using murine RAW 264.7 macrophages. Results: SB site samples were the most potent in the chemical and biological assays, followed by a CM railroad site. Only PM2.5 exhibited significant proinflammatory responses. VOCs were more potent than PM2.5 in generating anti-inflammatory responses; further, VOC pretreatment reduced PM-associated TNF-α expression. VOCs significantly increased ARE activation compared to their corresponding PM2.5 which remained at background levels. Conclusion: Ambient VOCs are major contributors to adaptive responses that can modulate PM effects, in vitro, and, as such, need to be included in comprehensive assessments of AP.