Reactive oxygen species induced by personal exposure to
fine particulate matteremitted from solid fuel combustion
in rural Guanzhong Basin, northwestern China
Fine particulate matter (PM2.5) released by the burning of domestic solid fuels is an important air pollutant in the rural indoor environment in China. Here, personal exposure to PM2.5-induced oxidative damage resulting from household solid fuel combustion was examined in winter in rural areas of Guanzhong Basin, northwestern China. The volume-based average exogenous reactive oxygen species (exo-ROS) activities were 1943.7 ± 3668.0 and 1628.5 ± 2618.7 μM H2O2/min/m3 for 50 and 100 μL of PM2.5 extracts, respectively. While the different patterns were found for endogenous reactive oxygen species (endo-ROS), 465.8 ± 2427.4 and 1740.4 ± 2643.2 μM H2O2/min/m3 for 4 h exposed to 50 and 100 μL of PM2.5 extract. When the exposure time was extended to 24 h, endo-ROS activities were 3789.5 ± 4582.0 and 3534.8 ± 4595.6 μM H2O2/min/m3 for 50 and 100 μL of PM2.5 extracts, respectively. Among four common dwelling heating ways used in northwestern China, the highest ROS activity (160.4 μM H2O2/min/m3 for 4-h endo-ROS at 50 μL of PM2.5 extracts) was found for households using indoor coal chunks stove. The ROS activity in households using electric power heating was 2.9–15.9-fold lower than that in households using indoor coal chunks stove; thus, electric power heating was found to be the cleanest method for rural household heating. PM2.5-bound K+ , organic carbon 1 (OC1), elemental carbon 1 (EC1), several polycyclic aromatic hydrocarbons (PAHs), and two hopanes species were observed to be significantly correlated with exo-ROS and 4-h endo-ROS, indicating that these chemical compounds and the sources in PM2.5 exposure samples may induce more ROS and affect human health strongly. The results indicate that heating methods used in rural households in winter can greatly impact the health of residents living in rural areas of northwestern China through personal exposure PM2.5-induced oxidative damage.