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Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
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2015 (English)In: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 12, article id 33Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2015. Vol. 12, article id 33
Keywords [en]
Air pollution, Biomass, Bronchoscopy, Cytotoxicity, Neutrophils, Lymphocytes, Mast cells
National Category
Environmental Sciences
Identifiers
URN: urn:nbn:se:umu:diva-111761DOI: 10.1186/s12989-015-0111-7ISI: 000363833500001PubMedID: 26511835Scopus ID: 2-s2.0-84945908415OAI: oai:DiVA.org:umu-111761DiVA, id: diva2:874099
Available from: 2015-11-25 Created: 2015-11-23 Last updated: 2023-07-07Bibliographically approved

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Muala, AlaRankin, GregorySehlstedt, MariaUnosson, JonBosson, Jenny A.Behndig, AnneliePourazar, JamshidNyström, RobinBlomberg, AndersBoman, ChristofferSandström, Thomas

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Muala, AlaRankin, GregorySehlstedt, MariaUnosson, JonBosson, Jenny A.Behndig, AnneliePourazar, JamshidNyström, RobinBlomberg, AndersBoman, ChristofferSandström, Thomas
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Pulmonary MedicineDepartment of Applied Physics and Electronics
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Particle and Fibre Toxicology
Environmental Sciences

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