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California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity

BACKGROUND: During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM(10–2.5) (particulate matter with mass median aerodyn...

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Detalles Bibliográficos
Autores principales: Wegesser, Teresa C., Pinkerton, Kent E., Last, Jerold A.
Formato: Texto
Lenguaje:English
Publicado: National Institute of Environmental Health Sciences 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702402/
https://www.ncbi.nlm.nih.gov/pubmed/19590679
http://dx.doi.org/10.1289/ehp.0800166
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author Wegesser, Teresa C.
Pinkerton, Kent E.
Last, Jerold A.
author_facet Wegesser, Teresa C.
Pinkerton, Kent E.
Last, Jerold A.
author_sort Wegesser, Teresa C.
collection PubMed
description BACKGROUND: During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM(10–2.5) (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM(2.5) (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected. OBJECTIVES: These observations prompt a number of questions about the health impact of exposure to elevated levels of PM(10–2.5) and PM(2.5) and about the specific toxicity of PM arising from wildfires in this region. METHODS: Toxicity of PM(10–2.5) and PM(2.5) obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007. RESULTS: Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung. CONCLUSIONS: We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.
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spelling pubmed-27024022009-07-09 California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity Wegesser, Teresa C. Pinkerton, Kent E. Last, Jerold A. Environ Health Perspect Research BACKGROUND: During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM(10–2.5) (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM(2.5) (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected. OBJECTIVES: These observations prompt a number of questions about the health impact of exposure to elevated levels of PM(10–2.5) and PM(2.5) and about the specific toxicity of PM arising from wildfires in this region. METHODS: Toxicity of PM(10–2.5) and PM(2.5) obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007. RESULTS: Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung. CONCLUSIONS: We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season. National Institute of Environmental Health Sciences 2009-06 2009-02-02 /pmc/articles/PMC2702402/ /pubmed/19590679 http://dx.doi.org/10.1289/ehp.0800166 Text en http://creativecommons.org/publicdomain/mark/1.0/ Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, ?Reproduced with permission from Environmental Health Perspectives?); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.
spellingShingle Research
Wegesser, Teresa C.
Pinkerton, Kent E.
Last, Jerold A.
California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity
title California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity
title_full California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity
title_fullStr California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity
title_full_unstemmed California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity
title_short California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity
title_sort california wildfires of 2008: coarse and fine particulate matter toxicity
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702402/
https://www.ncbi.nlm.nih.gov/pubmed/19590679
http://dx.doi.org/10.1289/ehp.0800166
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