Influence of ambient and endogenous H2O2 on reactive oxygen species concentrations and OH radical production in the respiratory tract

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) in the epithelial lining fluid (ELF), and hydrogen peroxide (H2O2) is the most abundant ROS in the human body. Here, we show that H2O2 concentrations in the ELF may be primarily determined by the release of endogenous H2O2 and the inhalation of ambient gas-phase H2O2, while the chemical production of H2O2 through inhaled PM2.5 is less important. The production of hydroxyl radicals (OH), however, was strongly correlated with Fenton chemistry of PM2.5 in the model calculations. Hence, our findings suggest that the adverse health effects of PM2.5 may not be primarily related to direct chemical production of H2O2, but rather to the conversion of peroxides into more reactive species such as the OH radical, or the stimulation of biological ROS production. The analysis highlights remaining uncertainties in the relevant physical, chemical and biological parameters, suggesting a critical reassessment of current paradigms in elucidating and mitigating the health effects of different types of air pollutants.

Automated summary

Air pollution, particularly PM2.5 and gaseous pollutants, can generate ROS in the ELF. H2O2 concentrations in the ELF are primarily determined by endogenous release and inhalation of ambient gas-phase H2O2, rather than the chemical production of H2O2 through inhaled PM2.5. The production of OH radicals was strongly correlated with Fenton chemistry of PM2.5, indicating the potential health effects of air pollutants may be due to the conversion of peroxides into more reactive species.