ABSTRACT
Epidemiological studies show correlations between air pollution and adverse health effects like cardiovascular and respiratory diseases, but the causative relations and mechanisms of interaction on the molecular level are still not fully elucidated. Chemical reactions of air pollutants 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 related health effects. Mathematical models can be utilized to determine chemical exposure-response relations between ambient concentrations of air pollutants and the production rates and concentrations of ROS in the ELF and provide chemical metrics for oxidative stress. Fine particulate matter (PM2.5) can contain redox-active substances like transition metals, quinones, and secondary organic aerosols, which can promote the formation and interconversion of ROS. The most abundant ROS in the ELF is hydrogen peroxide (H2O2), which serves as a reservoir for the generation of radical species, while antioxidants and enzymes serve as ROS buffering agents. The reactive gases ozone (O3) and nitrogen dioxide (•NO2) deplete antioxidants in the ELF and contribute to ROS formation. Transition metal ions induce Fenton-like reactions, converting H2O2 into highly reactive •OH radicals, which can react with all kinds of organic matter and damage biological tissues and cellular components such as lipid membranes, proteins, and DNA.
