Comment on egusphere-2026-566

<strong class="journal-contentHeaderColor">Abstract.</strong> Exposure to ambient air pollution is a major risk factor for human health yet, the physiological effects of particulate matter (PM) remain poorly understood. Oxidative stress due to excess formation of reactive oxygen species (ROS) is a leading hypothesis for the molecular mechanism behind the adverse health effects of PM. Thus, measurements of ROS production and antioxidant depletion are widely used to assess the oxidative potential (OP) of PM. Here we introduce a chemical kinetic model of oxidative potential (KM-OP) to elucidate and quantify the effects of PM on the production of ROS and consumption of antioxidants, such as ascorbic acid (AA) and dithiothreitol (DTT). The chemical mechanism of the model is based on literature rate coefficients and a large compilation of laboratory data on the effects of transition metal ions, quinones, and secondary organic aerosol (SOA). We apply the model to field measurement data of PM composition and OP, obtaining good agreement for three different locations in Europe. Previous studies found that PM may inflict damage to biomolecules in the lungs mainly via the production of hydroxyl (OH) radicals. The antioxidant-based OP assays investigated in this study show a good correlation with modeled OH production. We identify SOA as the strongest contributor to antioxidant-based OP assays, with minor contributions from Cu and Fe ions. Cu dominates the production of H₂O₂, but does not substantially affect OH production. Our model and results provide a basis for further investigation and comparison of different metrics of the potential toxicity of PM.