MSGID: 1:317/3 646c4169   
   PID: hpt/lnx 1.9.0-cur 2019-01-08   
   TID: hpt/lnx 1.9.0-cur 2019-01-08   
    Fine particulate matter catalyzes oxidative stress in the lungs    
      
     Date:   
         May 22, 2023   
     Source:   
         Max Planck Institute for Chemistry   
     Summary:   
         Study sheds new light on the adverse health effects of air   
         pollution: hydrogen peroxide production of fine particles may   
         not be as important as previously assumed. A new study reveals   
         that the adverse health effects of fine particulate matter   
         (PM2.5) are attributable to the conversion of peroxides into   
         more reactive species such as the hydroxyl radical (OH) rather   
         than the direct chemical production of hydrogen peroxide (H2O2)   
         as previously thought.   
      
      
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   FULL STORY   
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   In the scientific literature, the total production of reactive oxygen   
   species (ROS) such as H2O2 is commonly used as proxy for the toxicity   
   of air pollutants and their ability to induce oxidative stress and   
   inflammation. The research team led by Thomas Berkemeier from the MPIC in   
   Mainz found that ROS concentrations in the epithelial lining fluid (ELF)   
   of the human respiratory tract 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.   
      
   "Based on our simulations, we think that the overall concentrations of   
   these reactive species in the lungs are large anyway, and not directly   
   dependent on levels of air pollution," says Dr. Thomas Berkemeier, head   
   of the Chemical Kinetics & Reaction Mechanisms group 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 happen in the   
   respiratory tract. For the first time, we included production, diffusion,   
   and removal of hydrogen peroxide from cells and the blood stream into   
   our computer model. This was quite challenging, because 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 assessing the differential toxicity of individual   
   PM2.5 components need to be critically reassessed," says Prof. Dr. Ulrich   
   Po"schl, Head of the Multiphase Chemistry Department at the MPIC. The   
   study proposes that the chemical production of superoxide and H2O2   
   in a cell-free assay may not be a suitable metric for assessing the   
   differential toxicity of individual PM2.5 components, and some acellular   
   oxidative potential assays may not capture the actual deleterious effects   
   of PM2.5.   
      
   Fine particulates might act through Fenton chemistry However, the   
   production of hydroxyl radicals (OH) was strongly correlated with Fenton   
   chemistry of PM2.5 in the model calculations. "The model simulations   
   suggest that PM2.5 mostly acts by conversion of peroxides into highly   
   reactive OH radicals. Thus, PM2.5 is not so much the fuel, but rather   
   the catalyst of the chemical reactions that cause damage to cells and   
   tissues," says Berkemeier explaining the role of inhaled particles in   
   the model. Additionally, PM2.5 may stimulate the production of superoxide   
   from endogenous sources, which further contributes to the adverse health   
   effects of air pollution.   
      
   The study underscores the importance of continued 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."  Background   
   information Air pollution is a major health risk that affects millions   
   of people worldwide, but the underlying chemical mechanisms are not yet   
   fully understood. Fine particulate matter (PM2.5) typically contains   
   chemical components that can trigger oxidation reactions. When inhaled   
   and deposited in the human respiratory tract, they can induce and sustain   
   radical reaction cycles that produce reactive oxygen species (ROS) in   
   the epithelial lining fluid (ELF) that covers the airways and alveoli in   
   human lungs. Numerous studies have shown that excess concentrations of   
   ROS like hydrogen peroxide (H2O2) and hydroxyl radicals (OH) can cause   
   oxidative stress injuring cells and tissues in the respiratory tract.   
      
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   Story Source: Materials provided by   
   Max_Planck_Institute_for_Chemistry. Note: Content may be edited for   
   style and length.   
      
      
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   Journal Reference:   
      1. Eleni Dovrou, Steven Lelieveld, Ashmi Mishra, Ulrich Po"schl, Thomas   
         Berkemeier. Influence of ambient and endogenous H2O2 on reactive   
         oxygen species concentrations and OH radical production in the   
         respiratory tract. Environmental Science: Atmospheres, 2023; DOI:   
         10.1039/D2EA00179A   
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   Link to news story:   
   https://www.sciencedaily.com/releases/2023/05/230522131349.htm   
      
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