Air pollution is a major risk factor for human health. Chemical reactions in the epithelial lining fluid (ELF) of the human respiratory tract result in the formation of reactive oxygen species (ROS), which can lead to oxidative stress and adverse health effects. We use kinetic modeling to quantify the effects of fine particulate matter (PM2.5), ozone (O₃), and nitrogen dioxide (NO₂) on ROS formation, interconversion, and reactivity, and discuss different chemical metrics for oxidative stress, such as cumulative production of ROS and hydrogen peroxide (H₂O₂) to hydroxyl radical (OH) conversion. All three air pollutants produce ROS that accumulate in the ELF as H₂O₂, which serves as reservoir for radical species. At low PM2.5 concentrations (<10 μg m^-3), we find that less than 4% of all produced H₂O₂ is converted into highly reactive OH, while the rest is intercepted by antioxidants and enzymes that serve as ROS buffering agents. At elevated PM2.5 concentrations (>10 μg m^-3), however, Fenton chemistry overwhelms the ROS buffering effect and leads to a tipping point in H₂O₂ fate, causing a strong nonlinear increase in OH production. This shift in ROS chemistry and the enhanced OH production provide a tentative mechanistic explanation for how the inhalation of PM2.5 induces oxidative stress and adverse health effects.