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 (O 3 ), and nitrogen dioxide (NO 2 ) on ROS formation, interconversion, and reactivity, and discuss different chemical metrics for oxidative stress, such as cumulative production of ROS and hydrogen peroxide (H 2 O 2 ) to hydroxyl radical (OH) conversion. All three air pollutants produce ROS that accumulate in the ELF as H 2 O 2 , 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 H 2 O 2 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 H 2 O 2 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.

Cerium dioxide nanoparticles and nanorods were found to exhibit much stronger scavenging activity than ·OH generation in quasi-physiological conditions.

Air pollution is a major health risk, but the underlying chemical mechanisms are not yet well understood. Fine particulate matter (PM2.5) and gaseous pollutants can generate reactive oxygen species (ROS)...

Abstract. Oxidative potential is a measure of redox activity of airborne particulate matter (PM) and is often used as a surrogate to estimate one form of PM toxicity. The evaluation of oxidative potential in a physiologically relevant environment is always challenging. In this work, we developed a chromatographic method, employing an ultra-high-performance liquid chromatograph coupled to a triple–quadruple mass spectrometer, to determine the oxidative potential of PM from different sources. To this purpose, we measured the PM-induced oxidation of glutathione, cysteine, and ascorbic acid, and formation of glutathione disulfide and cystine, following PM addition to simulated epithelial lining fluids, which, in addition to the antioxidants, contained inorganic salts, a phospholipid, and proteins. The new method showed high precision and, when applied to standard reference PM, the oxidative potential was found to increase with the reaction time and PM concentration in the lung fluid. The antioxidant depletion rates were considerably higher than the rates found with the conventional dithiothreitol assay, indicating the higher sensitivity of the new method. The presence of the lung fluid inorganic species increased the oxidative potential determined through glutathione and cysteine, but showed an opposite effect with ascorbic acid, whereas the presence of proteins resulted in a moderate decrease in the oxidative potential. In the presence of PM2.5, glutathione and cysteine demonstrated similar depletion patterns, which were noticeably different from that of ascorbic acid, suggesting that cysteine could be used as an alternative to glutathione for probing oxidative potential.