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HERO ID
3160340
Reference Type
Journal Article
Title
Toxicity of wood smoke particles in human A549 lung epithelial cells: the role of PAHs, soot and zinc
Author(s)
Dilger, M; Orasche, J; Zimmermann, R; Paur, HR; Diabaté, S; Weiss, C
Year
2016
Is Peer Reviewed?
Yes
Journal
Archives of Toxicology
ISSN:
0340-5761
EISSN:
1432-0738
Publisher
SPRINGER HEIDELBERG
Location
HEIDELBERG
Volume
90
Issue
12
Page Numbers
3029-3044
Language
English
PMID
26838041
DOI
10.1007/s00204-016-1659-1
Web of Science Id
WOS:000387697600010
URL
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84991578052&doi=10.1007%2fs00204-016-1659-1&partnerID=40&md5=f55861c4ee699e2296f01afbe6b1f559
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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.
Keywords
Lung epithelial cells; Metals; Particulate matter; Polycyclic aromatic hydrocarbons; Soot; Wood smoke
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