Fine particles catalyze oxidative stress in the lungs

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“Based on our simulations, we believe that the overall concentrations of these reactive species in the lungs are large anyway and do not directly depend on air pollution levels,” says Dr. Thomas Berkemeier, head of the Mechanisms of Reaction and Chemical Kinetics at the MPIC. They use a computer model to understand the relevant physical, chemical, and biological processes and quantify the health effects of different types of air pollutants.

“Our new model simulates the chemical reactions that occur in the respiratory tract. For the first time, we included the production, diffusion, and removal of hydrogen peroxide from cells and the bloodstream in our computer model. This was quite a challenge, because en It is not so easy to put these processes in biological tissues into equations,” explains Thomas Berkemeier.

New research directions

“The findings of this study suggest that the current paradigms for evaluating the differential toxicity of individual PM2.5 components need to be critically re-evaluated,” says Prof. Dr. Ulrich Pöschl, Head of the Department of Multiphase Chemistry at MPIC. The study proposes that the chemical production of superoxide and H₂EITHER₂ in a cell-free assay may not be an adequate metric to assess the differential toxicity of individual PM2.5 components, and some cell-free oxidative potential assays may not capture the true deleterious effects of PM2.5.

Fine particles could act via Fenton chemistry

However, hydroxyl radical (OH) production was strongly correlated with the Fenton chemistry of PM2.5 in the model calculations. “Model simulations suggest that PM2.5 acts primarily by converting peroxides to highly reactive OH radicals. PM2.5 is therefore not so much the fuel, but rather the catalyst for chemical reactions that cause damage to cells and fabrics”. says Berkemeier explaining the role of inhaled particles in the model. Additionally, PM2.5 can stimulate the production of superoxide from endogenous sources, further contributing to the adverse health effects of air pollution.

The study underscores the importance of continuing research to better understand the chemical mechanisms underlying the health effects of air pollution and to develop effective strategies to mitigate these effects. The authors believe that this study will contribute significantly to this important research effort. Their findings are published in the scientific journal “Environmental Science: Atmospheres.”

Context information

Air pollution is a major health risk affecting millions of people around the world, but the underlying chemical mechanisms are still not fully understood. Fine particles (PM2.5) normally contain chemical components that can trigger oxidation reactions. When inhaled and deposited in the human respiratory tract, they can induce and maintain radical reaction cycles that produce reactive oxygen species (ROS) in the epithelial lining fluid (ELF) that lines the airways and alveoli in the human lungs. . Numerous studies have shown that excessive concentrations of ROS such as hydrogen peroxide (H₂EITHER₂) and hydroxyl (OH) radicals can cause oxidative stress and damage cells and tissues of the respiratory tract.