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Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity

BACKGROUND: Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim of this study was to determine whether exposure to wood smoke from incomplete combustion would elicit airway inflammation in humans. METHODS...

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Autores principales: Muala, Ala, Rankin, Gregory, Sehlstedt, Maria, Unosson, Jon, Bosson, Jenny A., Behndig, Annelie, Pourazar, Jamshid, Nyström, Robin, Pettersson, Esbjörn, Bergvall, Christoffer, Westerholm, Roger, Jalava, Pasi I., Happo, Mikko S., Uski, Oskari, Hirvonen, Maija-Riitta, Kelly, Frank J., Mudway, Ian S., Blomberg, Anders, Boman, Christoffer, Sandström, Thomas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625445/
https://www.ncbi.nlm.nih.gov/pubmed/26511835
http://dx.doi.org/10.1186/s12989-015-0111-7
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author Muala, Ala
Rankin, Gregory
Sehlstedt, Maria
Unosson, Jon
Bosson, Jenny A.
Behndig, Annelie
Pourazar, Jamshid
Nyström, Robin
Pettersson, Esbjörn
Bergvall, Christoffer
Westerholm, Roger
Jalava, Pasi I.
Happo, Mikko S.
Uski, Oskari
Hirvonen, Maija-Riitta
Kelly, Frank J.
Mudway, Ian S.
Blomberg, Anders
Boman, Christoffer
Sandström, Thomas
author_facet Muala, Ala
Rankin, Gregory
Sehlstedt, Maria
Unosson, Jon
Bosson, Jenny A.
Behndig, Annelie
Pourazar, Jamshid
Nyström, Robin
Pettersson, Esbjörn
Bergvall, Christoffer
Westerholm, Roger
Jalava, Pasi I.
Happo, Mikko S.
Uski, Oskari
Hirvonen, Maija-Riitta
Kelly, Frank J.
Mudway, Ian S.
Blomberg, Anders
Boman, Christoffer
Sandström, Thomas
author_sort Muala, Ala
collection PubMed
description BACKGROUND: Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim of this study was to determine whether exposure to wood smoke from incomplete combustion would elicit airway inflammation in humans. METHODS: Fourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM(1) concentration at 314 μg/m(3) for 3 h in a chamber. Bronchoscopy with bronchial wash (BW), bronchoalveolar lavage (BAL) and endobronchial mucosal biopsies was performed after 24 h. Differential cell counts and soluble components were analyzed, with biopsies stained for inflammatory markers using immunohistochemistry. In parallel experiments, the toxicity of the particulate matter (PM) generated during the chamber exposures was investigated in vitro using the RAW264.7 macrophage cell line. RESULTS: Significant reductions in macrophage, neutrophil and lymphocyte numbers were observed in BW (p < 0.01, <0.05, <0.05, respectively) following the wood smoke exposure, with a reduction in lymphocytes numbers in BAL fluid (<0.01. This unexpected cellular response was accompanied by decreased levels of sICAM-1, MPO and MMP-9 (p < 0.05, <0.05 and <0.01). In contrast, significant increases in submucosal and epithelial CD3+ cells, epithelial CD8+ cells and submucosal mast cells (p < 0.01, <0.05, <0.05 and <0.05, respectively), were observed after wood smoke exposure. The in vitro data demonstrated that wood smoke particles generated under these incomplete combustion conditions induced cell death and DNA damage, with only minor inflammatory responses. CONCLUSIONS: Short-term exposure to sooty PAH rich wood smoke did not induce an acute neutrophilic inflammation, a classic hallmark of air pollution exposure in humans. While minor proinflammatory lymphocytic and mast cells effects were observed in the bronchial biopsies, significant reductions in BW and BAL cells and soluble components were noted. This unexpected observation, combined with the in vitro data, suggests that wood smoke particles from incomplete combustion could be potentially cytotoxic. Additional research is required to establish the mechanism of this dramatic reduction in airway leukocytes and to clarify how this acute response contributes to the adverse health effects attributed to wood smoke exposure. TRIAL REGISTRATION: NCT01488500 ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-015-0111-7) contains supplementary material, which is available to authorized users.
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spelling pubmed-46254452015-10-30 Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity Muala, Ala Rankin, Gregory Sehlstedt, Maria Unosson, Jon Bosson, Jenny A. Behndig, Annelie Pourazar, Jamshid Nyström, Robin Pettersson, Esbjörn Bergvall, Christoffer Westerholm, Roger Jalava, Pasi I. Happo, Mikko S. Uski, Oskari Hirvonen, Maija-Riitta Kelly, Frank J. Mudway, Ian S. Blomberg, Anders Boman, Christoffer Sandström, Thomas Part Fibre Toxicol Research BACKGROUND: Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim of this study was to determine whether exposure to wood smoke from incomplete combustion would elicit airway inflammation in humans. METHODS: Fourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM(1) concentration at 314 μg/m(3) for 3 h in a chamber. Bronchoscopy with bronchial wash (BW), bronchoalveolar lavage (BAL) and endobronchial mucosal biopsies was performed after 24 h. Differential cell counts and soluble components were analyzed, with biopsies stained for inflammatory markers using immunohistochemistry. In parallel experiments, the toxicity of the particulate matter (PM) generated during the chamber exposures was investigated in vitro using the RAW264.7 macrophage cell line. RESULTS: Significant reductions in macrophage, neutrophil and lymphocyte numbers were observed in BW (p < 0.01, <0.05, <0.05, respectively) following the wood smoke exposure, with a reduction in lymphocytes numbers in BAL fluid (<0.01. This unexpected cellular response was accompanied by decreased levels of sICAM-1, MPO and MMP-9 (p < 0.05, <0.05 and <0.01). In contrast, significant increases in submucosal and epithelial CD3+ cells, epithelial CD8+ cells and submucosal mast cells (p < 0.01, <0.05, <0.05 and <0.05, respectively), were observed after wood smoke exposure. The in vitro data demonstrated that wood smoke particles generated under these incomplete combustion conditions induced cell death and DNA damage, with only minor inflammatory responses. CONCLUSIONS: Short-term exposure to sooty PAH rich wood smoke did not induce an acute neutrophilic inflammation, a classic hallmark of air pollution exposure in humans. While minor proinflammatory lymphocytic and mast cells effects were observed in the bronchial biopsies, significant reductions in BW and BAL cells and soluble components were noted. This unexpected observation, combined with the in vitro data, suggests that wood smoke particles from incomplete combustion could be potentially cytotoxic. Additional research is required to establish the mechanism of this dramatic reduction in airway leukocytes and to clarify how this acute response contributes to the adverse health effects attributed to wood smoke exposure. TRIAL REGISTRATION: NCT01488500 ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-015-0111-7) contains supplementary material, which is available to authorized users. BioMed Central 2015-10-29 /pmc/articles/PMC4625445/ /pubmed/26511835 http://dx.doi.org/10.1186/s12989-015-0111-7 Text en © Muala et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Muala, Ala
Rankin, Gregory
Sehlstedt, Maria
Unosson, Jon
Bosson, Jenny A.
Behndig, Annelie
Pourazar, Jamshid
Nyström, Robin
Pettersson, Esbjörn
Bergvall, Christoffer
Westerholm, Roger
Jalava, Pasi I.
Happo, Mikko S.
Uski, Oskari
Hirvonen, Maija-Riitta
Kelly, Frank J.
Mudway, Ian S.
Blomberg, Anders
Boman, Christoffer
Sandström, Thomas
Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
title Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
title_full Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
title_fullStr Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
title_full_unstemmed Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
title_short Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
title_sort acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625445/
https://www.ncbi.nlm.nih.gov/pubmed/26511835
http://dx.doi.org/10.1186/s12989-015-0111-7
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