Assessing oxidative stress induction ability and oxidative potential of PM2.5 in cities in eastern and western Japan

Abstract

Oxidative stress is an important cause of respiratory diseases associated with exposure to PM2.5. Accordingly, acellular methods for assessing the oxidative potential (OP) of PM2.5 have been evaluated extensively for use as indicators of oxidative stress in living organisms. However, OP-based assessments only reflect the physicochemical properties of particles and do not consider particle-cell interactions. Therefore, to determine the potency of OP under various PM2.5 scenarios, oxidative stress induction ability (OSIA) assessments were performed using a cell-based method, the heme oxygenase-1 (HO-1) assay, and the findings were compared with OP measurements obtained using an acellular method, the dithiothreitol assay. For these assays, PM2.5 filter samples were collected in two cities in Japan. To quantitatively determine the relative contribution of the quantity of metals and subtypes of organic aerosols (OA) in PM2.5 to the OSIA and the OP, online measurements and offline chemical analysis were also performed. The findings showed a positive relationship between the OSIA and OP for water-extracted samples, confirming that the OP is generally well suited for use as an indicator of the OSIA. However, the correspondence between the two assays differed for samples with a high water-soluble (WS)–Pb content, which had a higher OSIA than would be expected from the OP of other samples. The results of reagent-solution experiments showed that the WS-Pb induced the OSIA, but not the OP, in 15-min reactions, suggesting a reason for the inconsistent relationship between the two assays across samples. Multiple linear regression analyses and reagent-solution experiments showed that WS transition metals and biomass burning OA accounted for approximately 30–40% and 50% of the total OSIA or the total OP of water-extracted PM2.5 samples, respectively. This is the first study to evaluate the association between cellular oxidative stress assessed by the HO-1 assay and the different subtypes of OA.