New computer model provides exposure-response relationship between air pollutants and reactive oxygen species in the epithelial lining fluid of the human respiratory tract
Air pollution can cause oxidative stress and adverse health effects such as asthma and other respiratory diseases. The underlying chemical processes, however, are not well characterized. Scientists from the Max Planck Institute for Chemistry in Mainz, Germany, and the University of California Irvine, USA, have now obtained chemical exposure-response relations between ambient concentrations of air pollutants and the production rates and concentrations of reactive oxygen species (ROS) in the epithelial lining fluid (ELF) of the human respiratory tract.
They found that in highly polluted environments, ozone and fine particulate matter containing metal ions and organic aerosols can increase ROS concentrations in the ELF to levels characteristic for respiratory diseases. The new chemical exposure-response relations provide a quantitative basis for assessing the importance of specific air pollutants in different regions of the world.
Anthropogenic pollution leads to a massive increase of atmospheric aerosol particles and trace gases on local, regional, and global scales. For example, the concentration of fine particulate matter with particle diameters smaller than 2.5 µm (PM2.5) in polluted megacity air can get as high as several hundred micrograms per cubic meter, which is tens to hundreds of times higher than in pristine rainforest air.
Fine particulate matter typically contains chemical components that can trigger oxidation reactions. Such components are metals like copper, iron and organic compounds originating from traffic emissions, cigarette smoke, and other sources. 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 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. Thus, characterizing the formation of ROS is crucial for understanding how air pollution leads to adverse health effects such as asthma, allergies and other respiratory diseases. The production rates and concentrations of ROS induced by air pollutants in the epithelial lining fluid (ELF), however, have hardly been quantified so far.
Scientists from the Max Planck Institute for Chemistry in Mainz, Germany, and the University of California Irvine, USA, have now bridged this gap with a study published in the new issue of the research magazine “Science Reports”.
Formation of reactive oxygen species (ROS) is crucial for understanding how air pollution leads to adverse health effects.
“With a new detailed computer model of the relevant chemical reactions we can now calculate the previously unknown production rates and characteristic concentrations of ROS produced by air pollutants in the ELF,” explains Pascale Lakey, postdoctoral researcher at the Max Planck Institute for Chemistry in Mainz.
Under very clean conditions like in pristine rainforest air with PM2.5 concentrations smaller than 10 microgram per cubic meter (µg m-3), the amount of ROS chemically produced by inhaled particulate matter does not generate any oxidative stress. It is smaller than the natural physiological background level of ROS in the ELF, which is around 100 nanomole per liter. In moderately polluted air with PM2.5 levels between 10 and 50 micrograms per cubic meter, the particle-generated amount of ROS is similar or larger than the physiological background level and can cause oxidative stress depending on aerosol concentration and chemical composition. In heavily polluted air with PM2.5 levels above 50 micrograms per cubic meter, particle-generated ROS concentrations are as high as the ROS concentrations observed in the ELF or bronchoalveolar lavage of patients with acute inflammatory diseases in the respiratory tract (up to 250 nanomole per liter). In addition, ozone inhaled with ambient air can further enhance the oxidative stress by depleting physiological antioxidants like ascorbic acid in the ELF.
The pathologically high ROS concentrations calculated for the ELF in airways exposed to high ambient aerosol concentrations are consistent with epidemiology-based air quality standards and regulations of the World Health Organization (WHO) and various national environmental protection agencies. They aim at PM2.5 concentrations less than 20 to 40 micrograms per cubic meter averaged over one day and less than 10 to 20 micrograms per cubic meter averaged over one year.
“Our study provides the first quantitative approach for assessing the chemical effects and importance of specific air pollutants and individual components of fine particulate matter like copper, iron, organic aerosols, and ozone,“ says Manabu Shiraiwa, Assistant Professor at the University of California Irvine.
Copper and iron ions are among the most hazardous components of PM2.5.
In accordance with toxicological investigations, the model calculations indicate that copper and iron ions are among the most hazardous components of PM2.5. They originate largely from traffic-related emissions like brake and tire wear, which are particularly relevant targets for air pollution control. The presented exposure-response relations and additional model calculations can help to identify the most promising and efficient air pollution control strategies. They enable quantitative estimations of how much a reduction in the emission and ambient concentration of specific air pollutants like copper, iron, organic compounds or ozone may contribute to the reduction of pollution-generated ROS in the human respiratory tract. In particular, the detailed chemical model can resolve non-linear interactions and concentration dependencies under different environmental conditions.
"Building on the new model and exposure-response relations, we can further elucidate which substances and processes are most important for the adverse health effects of air pollutants. This knowledge will help to develop efficient air quality control strategies in different environments and to understand the large-scale and long-term effects of regional and global air pollution on public health in the Anthropocene,“ explains Ulrich Pöschl, director at the Max Planck Institute for Chemistry in Mainz.
In the course of the Anthropocene, which is the present era of globally pervasive and steeply increasing anthropogenic influence on planet Earth, the average concentrations of ozone and fine particulate matter in populated areas have increased to levels that are multiple times higher than in pre-industrial times. The large increase of air pollutants has been estimated to cause millions of premature deaths every year, and it is likely to enhance not only mortality but also chronic inflammatory diseases. A subject of particular interest to the researchers is the impact of air pollution on the development of and increasing prevalence of allergies, which they investigate together with biomedical colleagues in the Mainz Center for Chemical Allergology (MCCA) and international partners. To fully unravel and quantify these and other adverse health effects of air pollution, further research including both experimental investigations and model studies will be required, for which the modeling approach and exposure-response relations developed in this study provide a baseline and promising directions.
Chemical exposure-response relationship between air pollutants and reactive oxygen species in the human respiratory tract
Pascale S. J. Lakey, Thomas Berkemeier, Haijie Tong, Andrea M. Arangio, Kurt Lucas, Ulrich Pöschl and Manabu Shiraiwa
Scientific Reports 6, 8 September 2016, doi:10.1038.
Dr. Pascale Lakey
Max Planck Institute for Chemistry
Prof. Manabu Shiraiwa
Department of Chemistry, University of California Irvine, Irvine, CA 92697, USA
Prof. Dr. Ulrich Pöschl
Max Planck Institute for Chemistry
Dr. Susanne Benner | Max-Planck-Institut für Chemie
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