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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| Published in: | Particle and fibre toxicology Vol. 12; no. 1; p. 33 |
|---|---|
| Main Authors: | , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
BioMed Central
29.10.2015
Springer Nature B.V |
| Subjects: | |
| ISSN: | 1743-8977, 1743-8977 |
| Online Access: | Get full text |
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| Abstract | 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 |
|---|---|
| AbstractList | 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 PM1 concentration at 314 mu g/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. BACKGROUNDSmoke 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.METHODSFourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM1 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.RESULTSSignificant 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.CONCLUSIONSShort-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 REGISTRATIONNCT01488500. 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 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. Fourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM1 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. 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. 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. NCT01488500. 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 PM1 concentration at 314 μg/m3 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. |
| ArticleNumber | 33 |
| Author | Rankin, Gregory Kelly, Frank J. Mudway, Ian S. Unosson, Jon Jalava, Pasi I. Sehlstedt, Maria Happo, Mikko S. Muala, Ala Pettersson, Esbjörn Boman, Christoffer Uski, Oskari Pourazar, Jamshid Nyström, Robin Hirvonen, Maija-Riitta Bosson, Jenny A. Behndig, Annelie Sandström, Thomas Westerholm, Roger Bergvall, Christoffer Blomberg, Anders |
| Author_xml | – sequence: 1 givenname: Ala surname: Muala fullname: Muala, Ala organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 2 givenname: Gregory surname: Rankin fullname: Rankin, Gregory organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 3 givenname: Maria surname: Sehlstedt fullname: Sehlstedt, Maria organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 4 givenname: Jon surname: Unosson fullname: Unosson, Jon organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 5 givenname: Jenny A. surname: Bosson fullname: Bosson, Jenny A. organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 6 givenname: Annelie surname: Behndig fullname: Behndig, Annelie organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 7 givenname: Jamshid surname: Pourazar fullname: Pourazar, Jamshid organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 8 givenname: Robin surname: Nyström fullname: Nyström, Robin organization: Department of Applied Physics and Electronics, Thermochemical Energy Conversion Laboratory, Umeå University – sequence: 9 givenname: Esbjörn surname: Pettersson fullname: Pettersson, Esbjörn organization: Department of Applied Physics and Electronics, Thermochemical Energy Conversion Laboratory, Umeå University – sequence: 10 givenname: Christoffer surname: Bergvall fullname: Bergvall, Christoffer organization: Department of Environmental Science and Analytical Chemistry, Arrhenius Laboratory, Stockholm University – sequence: 11 givenname: Roger surname: Westerholm fullname: Westerholm, Roger organization: Department of Environmental Science and Analytical Chemistry, Arrhenius Laboratory, Stockholm University – sequence: 12 givenname: Pasi I. surname: Jalava fullname: Jalava, Pasi I. organization: Department of Environmental Science, University of Eastern Finland – sequence: 13 givenname: Mikko S. surname: Happo fullname: Happo, Mikko S. organization: Department of Environmental Science, University of Eastern Finland – sequence: 14 givenname: Oskari surname: Uski fullname: Uski, Oskari organization: Department of Environmental Science, University of Eastern Finland – sequence: 15 givenname: Maija-Riitta surname: Hirvonen fullname: Hirvonen, Maija-Riitta organization: Department of Environmental Science, University of Eastern Finland – sequence: 16 givenname: Frank J. surname: Kelly fullname: Kelly, Frank J. organization: Environmental Research Group, MRC-PHE Centre for Environment and Health, King’s College London – sequence: 17 givenname: Ian S. surname: Mudway fullname: Mudway, Ian S. organization: Environmental Research Group, MRC-PHE Centre for Environment and Health, King’s College London – sequence: 18 givenname: Anders surname: Blomberg fullname: Blomberg, Anders organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University – sequence: 19 givenname: Christoffer surname: Boman fullname: Boman, Christoffer organization: Department of Applied Physics and Electronics, Thermochemical Energy Conversion Laboratory, Umeå University – sequence: 20 givenname: Thomas surname: Sandström fullname: Sandström, Thomas email: thomas.sandstrom@lung.umu.se organization: Department of Public Health and Clinical Medicine, Division of Medicine/Respiratory Medicine, Umeå University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26511835$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-123515$$DView record from Swedish Publication Index (Stockholms universitet) https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111761$$DView record from Swedish Publication Index (Umeå universitet) |
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| Keywords | Bronchoscopy Lymphocytes Neutrophils Air pollution Cytotoxicity Mast cells Biomass |
| Language | English |
| License | 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. |
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| PublicationTitle | Particle and fibre toxicology |
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Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim... 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... Background Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim... BACKGROUNDSmoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim... Background: Smoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim... |
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| SubjectTerms | Air pollution Asthma Biomass Biomedical and Life Sciences Biomedicine Biopsy Bronchoalveolar Lavage Fluid Bronchoscopy Combustion Cytotoxicity Environmental Health Exposure Health risks Human subjects Humans Indoor air quality Inhalation Exposure Lavage Lymphocytes Mast cells Nanotechnology Neutrophils Outdoor air quality Particulate matter Pharmacology/Toxicology Pneumology/Respiratory System Public Health Respiratory diseases Respiratory Function Tests Respiratory Tract Diseases - etiology Respiratory Tract Diseases - physiopathology Risk factors Smoke Wood |
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| Title | Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity |
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