It has been widely accepted that the induction of reactive oxygen species (ROS) is an important pathophysiologic pathway linking particulate matter (PM) exposure and adverse health effects. ROS can be either present on and/or within PM or generated in vivo by the interactions between PM and biological systems. Within the context of toxicology, PM oxidative potential (OP) is the capacity of PM to oxidize molecules in biological tissues or cells directly by oxidants that are present on and/or within PM and indirectly by the ROS generated via PM interactions with the biological system (e.g., fluids, cells, and tissues). In this review, we summarized the current PM OP measurement methods, current understanding of how PM physical characteristics and chemical compositions affect OP, and the epidemiological and toxicological evidence on whether PM OP is a better indicator than PM mass concentration for health effects. Among the two major types of OP measurement methods, cellular assays have been regarded to better reflect the actions of PM in a biological system than acellular assays. Recent epidemiological studies have associated short-term PM OP exposure with adverse cardiorespiratory health outcomes. Little is known about the health effects of long-term PM OP exposure and on the effect beyond the cardiovascular and respiratory systems. The existing evidence may be sufficient to suggest the use of PM OP as a more health-relevant exposure metric than conventional PM mass concentration, but critical methodologic issues must be resolved before this metric can be widely and accurately used. Graphical Abstract

The molecular mechanisms underlying the associations between air pollution exposure and adverse cardiopulmonary effects remain to be better understood. Altered amino acid metabolism may plays an important role in the development of cardiopulmonary diseases and may be perturbed by air pollution exposure. To test this hypothesized molecular mechanism, we conducted an association analysis from an existing intervention study to examine the relations of air pollution exposures with amino acids in 43 Chinese healthy adults. Plasma levels of amino acids were measured using a UPLC-QqQ-MS system. Time-weighted personal exposure to O₃, PM_2.5, NO₂, and SO₂ over four time windows, i.e., 12 h, 24 h, 1 week, and 2 weeks, were calculated using the measured indoor and outdoor concentrations coupled with the time-activity data for each participant. Linear mixed-effects models were used to estimate the associations between air pollutants at each exposure window and amino acids by controlling for potential confounders. We observed significant associations between exposures and plasma concentrations of amino acids, with the direction of associations varying by amino acid and air pollutant. While there is little evidence of associations for NO₂ and SO₂, the associations with amino acids were fairly pronounced for exposure to PM_2.5 and O₃. In particular, independent O₃ (12- and 24-hour) associations were observed with changes in the amino acids that were related to the urea cycle, including aspartate, asparagine, glutamate, arginine, citrulline, and ornithine. Our findings indicated that air pollution may cause acute perturbation of amino acid metabolism, and that O₃ and PM_2.5 may affect the metabolism of amino acids in different pathways. Main finding: Acute air pollution exposure might affect the perturbation of amino acid metabolism, and in particular, was associated with amino acids in relation to the urea cycle.