Investigation of oxidative potential of fresh and O3-aging PM2.5 from various emission sources across urban and rural regions

Abstract

Inhalation of atmospheric PM2.5 can induce the generation of excessive reactive oxygen species (ROS) in human alveoli, triggering local and systemic inflammation, which can directly or indirectly result in respiratory and cardiovascular diseases. In this study, we assessed the oxidative potential (OP) of fresh and O3-aged PM2.5 particles from various urban and rural emission sources using the dithiothreitol (DTT) method. Our results revealed variations in the OP of fresh PM2.5 among different emission sources, with biomass burning sources exhibiting the highest OP, followed by industrial areas, vehicular emissions, cooking emissions, and suburban areas, respectively. Water-soluble organics and transition metals might potentially exert significant influence on particle OP. O3 aging notably decreased the OP of PM2.5 particles, possibly due to the oxidation of highly DTT-active components into low redox-active small molecules. Moreover, the evolution of OP in different PM2.5 components, including methanol-soluble and insoluble fractions, exhibited distinct responses to O3 aging for source-oriented PM2.5. Additionally, differences in chemical composition between fresh and aged PM2.5 were further elucidated through measurements of component-dependent hygroscopic behaviors and phase transitions. This study systematically delineates variances in the toxic potential of fresh and O3-aged PM2.5 from various anthropogenic sources. The findings highlight the intrinsic compositional dependence of particle OP and provide essential insights for assessing the health effects of source-oriented PM2.5, as well as for formulating human health protection policies.