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Airway inflammation and oxidative potential of air pollutant particles in a pediatric asthma panel

Abstract

Airborne particulate matter (PM) components from fossil fuel combustion can induce oxidative stress initiated by reactive oxygen species (ROS). Reported associations between worsening asthma and PM2.5 mass could be related to PM oxidative potential to induce airway oxidative stress and inflammation (hallmarks of asthma pathology). We followed 45 schoolchildren with persistent asthma in their southern California homes daily over 10 days with offline fractional exhaled nitric oxide (FENO), a biomarker of airway inflammation. Ambient exposures included daily average PM2.5, PM2.5 elemental and organic carbon (EC, OC), NO2, O3, and endotoxin. We assessed PM2.5 oxidative potential using both an abiotic and an in vitro bioassay on aqueous extracts of daily particle filters: (1) dithiothreitol (DTT) assay (abiotic), representing chemically produced ROS; and (2) ROS generated intracellularly in a rat alveolar macrophage model using the fluorescent probe 2′7′-dicholorohidroflourescin diacetate. We analyzed relations of FENO to air pollutants in mixed linear regression models. FENO was significantly positively associated with lag 1-day and 2-day averages of traffic-related markers (EC, OC, and NO2), DTT and macrophage ROS, but not PM2.5 mass. DTT associations were nearly twice as strong as other exposures per interquartile range: median FENO increased 8.7–9.9% per 0.43 nmole/min/m3 DTT. Findings suggest that future research in oxidative stress-related illnesses such as asthma and PM exposure would benefit from assessments of PM oxidative potential and composition.

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Acknowledgements

We thank staff in the Department of Epidemiology and the General Clinical Research Center, University of California Irvine. Funding Support: This study was supported by National Institute of Environmental Health Sciences, U.S. National Institutes of Health (R01 ES11615 and R21 ES019711), General Clinical Research Center University of California Irvine (National Institutes of Health grant MO1-RR00827), and South Coast Air Management District, through the University of California Los Angeles Asthma and Outdoor Air Quality Consortium (Contract No. UCLA-35692).

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Correspondence to Ralph J Delfino.

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Delfino, R., Staimer, N., Tjoa, T. et al. Airway inflammation and oxidative potential of air pollutant particles in a pediatric asthma panel. J Expo Sci Environ Epidemiol 23, 466–473 (2013). https://doi.org/10.1038/jes.2013.25

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