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Kanashova, T.* ; Sippula, O.* ; Oeder, S. ; Streibel, T. ; Passig, J. ; Czech, H.* ; Kaoma, T.* ; Sapcariu, S.C.* ; Dilger, M.* ; Paur, H.-R.* ; Schlager, C.* ; Mülhopt, S.* ; Weiss, C.* ; Schmidt-Weber, C.B. ; Traidl-Hoffmann, C. ; Michalke, B. ; Krebs, T.* ; Karg, E.W. ; Jakobi, G. ; Scholtes, S. ; Schnelle-Kreis, J. ; Sklorz, M.* ; Orasche, J. ; Müller, L. ; Reda, A. ; Rüger, C* ; Neumann, A.* ; Abbaszade, G. ; Radischat, C.* ; Hiller, K.* ; Grigonyte, J.* ; Kortelainen, M.* ; Kuuspalo, K.* ; Lamberg, H.* ; Leskinen, J.* ; Nuutinen, I.* ; Torvela, T.* ; Tissari, J.* ; Jalava, P.* ; Kasurinen, S.* ; Uski, O.* ; Hirvonen, M.-R.* ; Buters, J.T.M. ; Dittmar, G.* ; Jokiniemi, J.K.* ; Zimmermann, R.

Emissions from a modern log wood masonry heater and wood pellet boiler: Composition and biological impact on air-liquid interface exposed human lung cancer cells.

J. Mol. Clin. Med. 1, 23-35 (2018)
DOI
The consumption of wood fuel is markedly increasing in developing and industrialized countries. Known side effects of wood smoke inhalation manifest in proinflammatory signaling, oxidative stress, DNA damage and hence increased cancer risk. In this study, the composition and acute biological impact of emissions of state-of-the-art wood combustion compliances: masonry heater (MH) and pellet boiler (PB) were investigated. Therefore A549 cells were exposed to emission aerosols in an automated air-liquid interface exposure station followed by cytotoxicity, transcriptome and proteome analyses. In parallel, aerosols were subjected to a chemical and physical characterization. Compared to PB, the MH combustion at the same dilution ratio resulted in a 3-fold higher particle mass concentration (PM2.5) and deposited dose (PB: 27 ± 2 ng/cm 2 , MH; 73 ± 12 ng/cm 2 ) . Addi- tionally, the MH aerosol displayed a substantially larger concentration of aldehydes, polycyclic aromatic hydrocarbons (PAH) or oxidized PAH. Gene ontology analysis of transcriptome of A549 cells exposed to MH emissions revealed the activation of pro- inflammatory response and key signaling cascades MAP kinase and JAK-STAT. Furthermore, CYP1A1, an essential enzyme in PAH metabolism, was induced. PB combustion aerosol activated the proinflammatory marker IL6 and different transport processes. The proteomics data uncovered induction of DNA damage-associated proteins in response to PB and DNA double- strand break processing proteins in response to MH emissions. Taking together, the MH produces emissions with a higher particle dose and more toxic compounds while causing only mild biological responses. This finding points to a significant miti- gating effect of antioxidative compounds in MH wood smoke.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Particulate matter; Wood combustion; Log wood; Wood pellets; Masonry heater; Pellet boiler; Air-liquid interface aerosol exposure; Human lung cells; Air-Toxics; Biomarkers; Proteomics; Transcriptomics; Polycyclic aromatic hydrocarbons; Phenolic compounds; Antioxidants; CYP1A1 induction; Soot; Zinc
ISSN (print) / ISBN 2616-3632
e-ISSN 2616-3632
Journal Journal of Molecular and Clinical Medicine
Quellenangaben Volume: 1, Issue: , Pages: 23-35 Article Number: , Supplement: ,
Publisher IMR Press
Publishing Place Hong Kong
Non-patent literature Publications
Institute(s) Cooperation Group Comprehensive Molecular Analytics (CMA)
Institute for Allergy Research (IAF)
Institute of Environmental Medicine (IEM)
Research Unit Analytical BioGeoChemistry (BGC)