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 PM 2.5 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 (FE NO), a biomarker of airway inflammation. Ambient exposures included daily average PM 2.5, PM 2.5 elemental and organic carbon (EC, OC), NO 2, O 3, and endotoxin. We assessed PM 2.5 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 FE NO to air pollutants in mixed linear regression models. FE NO was significantly positively associated with lag 1-day and 2-day averages of traffic-related markers (EC, OC, and NO 2), DTT and macrophage ROS, but not PM 2.5 mass. DTT associations were nearly twice as strong as other exposures per interquartile range: median FE NO increased 8.7-9.9% per 0.43 nmole/min/m 3 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. © 2013 Nature America, Inc.