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      Toxicity of wood smoke particles in human A549 lung epithelial cells: the role of PAHs, soot and zinc.

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          Abstract

          Indoor air pollution is associated with increased morbidity and mortality. Specifically, the health impact of emissions from domestic burning of biomass and coal is most relevant and is estimated to contribute to over 4 million premature deaths per year worldwide. Wood is the main fuel source for biomass combustion and the shift towards renewable energy sources will further increase emissions from wood combustion even in developed countries. However, little is known about the constituents of wood smoke and biological mechanisms that are responsible for adverse health effects. We exposed A549 lung epithelial cells to collected wood smoke particles and found an increase in cellular reactive oxygen species as well as a response to bioavailable polycyclic aromatic hydrocarbons. In contrast, cell vitality and regulation of the pro-inflammatory cytokine interleukin-8 were not affected. Using a candidate approach, we could recapitulate WSP toxicity by the combined actions of its constituents soot, metals and PAHs. The soot fraction and metals were found to be the most important factors for ROS formation, whereas the PAH response can be mimicked by the model PAH benzo[a]pyrene. Strikingly, PAHs adsorbed to WSPs were even more potent in activating target gene expression than B[a]P individually applied in suspension. As PAHs initiate multiple adverse outcome pathways and are prominent carcinogens, their role as key pollutants in wood smoke and its health effects warrants further investigation. The presented results suggest that each of the investigated constituents soot, metals and PAHs are major contributors to WSP toxicity. Mitigation strategies to prevent adverse health effects of wood combustion should therefore not only aim at reducing the emitted soot and PAHs but also the metal content, through the use of more efficient combustion appliances, and particle precipitation techniques, respectively.

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          Author and article information

          Journal
          Arch. Toxicol.
          Archives of toxicology
          Springer Nature
          1432-0738
          0340-5761
          Dec 2016
          : 90
          : 12
          Affiliations
          [1 ] Karlsruhe Institute of Technology, Campus North, Institute of Toxicology and Genetics, Hermann-von-Helmholtz-Platz 1, 76344, Eggenstein-Leopoldshafen, Germany.
          [2 ] Joint Mass Spectrometry Centre-Comprehensive Molecular Analytics, Helmholtz Zentrum München, Ingolstädter Landstraße 1, D-85764, Neuherberg, Germany.
          [3 ] Joint Mass Spectrometry Centre-Chair of Analytical Chemistry, Institute of Chemistry, University of Rostock, Dr.-Lorenz-Weg 1, 18051, Rostock, Germany.
          [4 ] Karlsruhe Institute of Technology, Campus North, Institute for Technical Chemistry, Hermann-von-Helmholtz-Platz 1, 76344, Eggenstein-Leopoldshafen, Germany.
          [5 ] Karlsruhe Institute of Technology, Campus North, Institute of Toxicology and Genetics, Hermann-von-Helmholtz-Platz 1, 76344, Eggenstein-Leopoldshafen, Germany. carsten.weiss@kit.edu.
          Article
          10.1007/s00204-016-1659-1
          10.1007/s00204-016-1659-1
          26838041
          57952e21-049a-439b-ba47-5eaf3e64d032
          History

          Lung epithelial cells,Metals,Particulate matter,Polycyclic aromatic hydrocarbons,Soot,Wood smoke

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