Hydroxyl Radical Production by Air Pollutants in Epithelial Lining Fluid Governed by Interconversion and Scavenging of Reactive Oxygen Species

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), 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.