Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines

Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting sou...

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Published inParticle and fibre toxicology Vol. 9; no. 1; p. 45
Main Authors Bølling, Anette Kocbach, Totlandsdal, Annike Irene, Sallsten, Gerd, Braun, Artur, Westerholm, Roger, Bergvall, Christoffer, Boman, Johan, Dahlman, Hans Jørgen, Sehlstedt, Maria, Cassee, Flemming, Sandstrom, Thomas, Schwarze, Per E, Herseth, Jan Inge
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 23.11.2012
BioMed Central
BMC
Subjects
Air Pollutants - toxicity
Air pollution
Alveolar Epithelial Cells - drug effects
Alveolar Epithelial Cells - immunology
Atoms & subatomic particles
Cell Line
Cell Survival - drug effects
Coculture Techniques
Combustion
Combustion phase
Combustion temperature
Cytokines - metabolism
Emissions
Environmental Health and Occupational Health
Health aspects
Humans
Inflammation
Miljömedicin och yrkesmedicin
Monocytes - drug effects
Monocytes - immunology
Organic Chemicals - analysis
Organic Chemicals - toxicity
Organic fraction
Outdoor air quality
Particulate matter
Particulate Matter - toxicity
Physiological aspects
Polycyclic aromatic hydrocarbons
Risk factors
Smoke - adverse effects
Smoke - analysis
Smoke inhalation injuries
Studies
Wood
Wood smoke
Norway
Sweden
Online AccessGet full text

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Abstract Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
AbstractList Doc number: 45 Abstract Background: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. Results: WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. Conclusion: The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
BACKGROUND: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in northern countries during the winter season. The overall aim of this study was therefore to investigate the cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. RESULTS: WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. CONCLUSION: The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
Background: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. Results: WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. Conclusion: The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
Abstract Background Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles’ physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. Results WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. Conclusion The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
Background Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles' physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. Results WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. Conclusion The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs. Keywords: Particulate matter, Inflammation, Wood smoke, Combustion phase, Combustion temperature, Organic fraction
Audience Academic
Author Sehlstedt, Maria
Sallsten, Gerd
Herseth, Jan Inge
Totlandsdal, Annike Irene
Boman, Johan
Sandstrom, Thomas
Braun, Artur
Westerholm, Roger
Schwarze, Per E
Bølling, Anette Kocbach
Dahlman, Hans Jørgen
Cassee, Flemming
Bergvall, Christoffer
AuthorAffiliation 6 Department of Respiratory Medicine and Allergy, University of Umeå, Umeå, Sweden
2 Department of Occupational and Environmental Medicine, Sahlgrenska University Hospital and Academy, University of Gothenburg, Gothenburg, Sweden
7 National Institute for Public Health and the Environment, Bilthoven, the Netherlands
3 Laboratory for High Performance Ceramics, Empa, Swiss Federal Laboratories for Materials Science and Technology, Dübendorf, Switzerland
4 Department of Analytical Chemistry, Arrhenius Laboratory, Stockholm University, Stockholm, 106 91, Sweden
1 Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway
5 Department of Chemistry, University of Gothenburg, Gothenburg, Sweden
8 Faculty of Health Sciences, Oslo and Akershus University College of Applied Sciences, Oslo, Norway
AuthorAffiliation_xml – name: 7 National Institute for Public Health and the Environment, Bilthoven, the Netherlands
– name: 8 Faculty of Health Sciences, Oslo and Akershus University College of Applied Sciences, Oslo, Norway
– name: 3 Laboratory for High Performance Ceramics, Empa, Swiss Federal Laboratories for Materials Science and Technology, Dübendorf, Switzerland
– name: 4 Department of Analytical Chemistry, Arrhenius Laboratory, Stockholm University, Stockholm, 106 91, Sweden
– name: 2 Department of Occupational and Environmental Medicine, Sahlgrenska University Hospital and Academy, University of Gothenburg, Gothenburg, Sweden
– name: 1 Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway
– name: 6 Department of Respiratory Medicine and Allergy, University of Umeå, Umeå, Sweden
– name: 5 Department of Chemistry, University of Gothenburg, Gothenburg, Sweden
Author_xml – sequence: 1
  givenname: Anette Kocbach
  surname: Bølling
  fullname: Bølling, Anette Kocbach
  email: Anette.Kocbach@fhi.no
  organization: Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway. Anette.Kocbach@fhi.no
– sequence: 2
  givenname: Annike Irene
  surname: Totlandsdal
  fullname: Totlandsdal, Annike Irene
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  surname: Sallsten
  fullname: Sallsten, Gerd
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  surname: Braun
  fullname: Braun, Artur
– sequence: 5
  givenname: Roger
  surname: Westerholm
  fullname: Westerholm, Roger
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  surname: Bergvall
  fullname: Bergvall, Christoffer
– sequence: 7
  givenname: Johan
  surname: Boman
  fullname: Boman, Johan
– sequence: 8
  givenname: Hans Jørgen
  surname: Dahlman
  fullname: Dahlman, Hans Jørgen
– sequence: 9
  givenname: Maria
  surname: Sehlstedt
  fullname: Sehlstedt, Maria
– sequence: 10
  givenname: Flemming
  surname: Cassee
  fullname: Cassee, Flemming
– sequence: 11
  givenname: Thomas
  surname: Sandstrom
  fullname: Sandstrom, Thomas
– sequence: 12
  givenname: Per E
  surname: Schwarze
  fullname: Schwarze, Per E
– sequence: 13
  givenname: Jan Inge
  surname: Herseth
  fullname: Herseth, Jan Inge
BackLink https://www.ncbi.nlm.nih.gov/pubmed/23176191$$D View this record in MEDLINE/PubMed
https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-84098$$DView record from Swedish Publication Index
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-66809$$DView record from Swedish Publication Index
https://gup.ub.gu.se/publication/168382$$DView record from Swedish Publication Index
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ContentType Journal Article
Copyright COPYRIGHT 2012 BioMed Central Ltd.
2012 Bølling et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright ©2012 Bølling et al.; licensee BioMed Central Ltd. 2012 Bølling et al.; licensee BioMed Central Ltd.
Copyright_xml – notice: COPYRIGHT 2012 BioMed Central Ltd.
– notice: 2012 Bølling et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
– notice: Copyright ©2012 Bølling et al.; licensee BioMed Central Ltd. 2012 Bølling et al.; licensee BioMed Central Ltd.
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Snippet Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The...
Background Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving...
Doc number: 45 Abstract Background: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological...
Background: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving...
BACKGROUND: Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving...
Abstract Background Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms...
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StartPage 45
SubjectTerms Air Pollutants - toxicity
Air pollution
Alveolar Epithelial Cells - drug effects
Alveolar Epithelial Cells - immunology
Atoms & subatomic particles
Cell Line
Cell Survival - drug effects
Coculture Techniques
Combustion
Combustion phase
Combustion temperature
Cytokines - metabolism
Emissions
Environmental Health and Occupational Health
Health aspects
Humans
Inflammation
Miljömedicin och yrkesmedicin
Monocytes - drug effects
Monocytes - immunology
Organic Chemicals - analysis
Organic Chemicals - toxicity
Organic fraction
Outdoor air quality
Particulate matter
Particulate Matter - toxicity
Physiological aspects
Polycyclic aromatic hydrocarbons
Risk factors
Smoke - adverse effects
Smoke - analysis
Smoke inhalation injuries
Studies
Wood
Wood smoke
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Title Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines
URI https://www.ncbi.nlm.nih.gov/pubmed/23176191
https://www.proquest.com/docview/1269153908
https://search.proquest.com/docview/1285097569
https://pubmed.ncbi.nlm.nih.gov/PMC3544657
https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-84098
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-66809
https://gup.ub.gu.se/publication/168382
https://doaj.org/article/f0a47dbfceba4c4fb40f97fdf983600c
Volume 9
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