Fine particulate matter (PM2.5) air pollution and immune status among women in the Seattle area

Lori Williams; Cornelia M. Ulrich; Timothy Larson; Mark H. Wener; Brent Wood; Zehava Chen-Levy; Peter T. Campbell; John Potter; Anne McTiernan; Anneclaire J. De Roos

doi:10.1080/19338244.2010.539636

Fine particulate matter (PM_2.5) air pollution and immune status among women in the Seattle area

Lori Williams, Cornelia M. Ulrich, Timothy Larson, Mark H. Wener, Brent Wood, Zehava Chen-Levy, Peter T. Campbell, John Potter, Anne McTiernan, Anneclaire J. De Roos

Research output: Contribution to journal › Article › peer-review

19 Scopus citations

Abstract

Changes in immune status have been suggested as a possible biologic mechanism by which particulate matter (PM) air pollution could lead to adverse health effects. The authors studied associations between ambient PM _2.5 and immune status among 115 postmenopausal, overweight women in the greater Seattle, Washington, area. The authors evaluated 3-day, 30-day, and 60-day average PM_2.5 values in relation to inflammation markers (C-reactive protein, serum amyloid A, interleukin-6) and functional assays of cellular immunity (natural killer cell cytotoxicity, T-lymphocyte proliferation) at 3 time points for each woman during 1 year. Three-day averaged PM _2.5 was inversely associated with anti-CD3-stimulated lymphocyte proliferation. There were no notable associations between the inflammation markers and PM_2.5. If additional studies confirm our findings, then future health effect assessments for PM_2.5 should consider changes in cellular immunity as an endpoint that may lead to overt clinical disease.

Original language	English (US)
Pages (from-to)	155-165
Number of pages	11
Journal	Archives of Environmental and Occupational Health
Volume	66
Issue number	3
DOIs	https://doi.org/10.1080/19338244.2010.539636
State	Published - Jul 2011
Externally published	Yes

Keywords

air pollution
immune function
inflammation
particulate matter

ASJC Scopus subject areas

Toxicology
Environmental Science(all)
Public Health, Environmental and Occupational Health
Health, Toxicology and Mutagenesis

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1080/19338244.2010.539636

Cite this

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title = "Fine particulate matter (PM2.5) air pollution and immune status among women in the Seattle area",

abstract = "Changes in immune status have been suggested as a possible biologic mechanism by which particulate matter (PM) air pollution could lead to adverse health effects. The authors studied associations between ambient PM 2.5 and immune status among 115 postmenopausal, overweight women in the greater Seattle, Washington, area. The authors evaluated 3-day, 30-day, and 60-day average PM2.5 values in relation to inflammation markers (C-reactive protein, serum amyloid A, interleukin-6) and functional assays of cellular immunity (natural killer cell cytotoxicity, T-lymphocyte proliferation) at 3 time points for each woman during 1 year. Three-day averaged PM 2.5 was inversely associated with anti-CD3-stimulated lymphocyte proliferation. There were no notable associations between the inflammation markers and PM2.5. If additional studies confirm our findings, then future health effect assessments for PM2.5 should consider changes in cellular immunity as an endpoint that may lead to overt clinical disease.",

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author = "Lori Williams and Ulrich, {Cornelia M.} and Timothy Larson and Wener, {Mark H.} and Brent Wood and Zehava Chen-Levy and Campbell, {Peter T.} and John Potter and Anne McTiernan and {De Roos}, {Anneclaire J.}",

note = "Funding Information: The authors would like to thank the women who made this study possible by volunteering to be subjects. This work was supported by grants from the National Institutes of Health (CA 69334, DK 02860, DK 035816). Lori Williams was supported by a National Institute of Environmental Health Sciences Training Grant (T32 ES 007262-15). Peter T. Campbell was supported in part by a postdoctoral fellowship from the National Cancer Institute initiative on Transdisciplinary Research on Energetics and Cancer (TREC) (U54 CA116847). The funding sources were not involved in the study design; collection, analysis, or interpretation of data; in the writing of the report; or in the decision to submit the paper for publication.",

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AU - Campbell, Peter T.

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AU - McTiernan, Anne

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N1 - Funding Information: The authors would like to thank the women who made this study possible by volunteering to be subjects. This work was supported by grants from the National Institutes of Health (CA 69334, DK 02860, DK 035816). Lori Williams was supported by a National Institute of Environmental Health Sciences Training Grant (T32 ES 007262-15). Peter T. Campbell was supported in part by a postdoctoral fellowship from the National Cancer Institute initiative on Transdisciplinary Research on Energetics and Cancer (TREC) (U54 CA116847). The funding sources were not involved in the study design; collection, analysis, or interpretation of data; in the writing of the report; or in the decision to submit the paper for publication.

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N2 - Changes in immune status have been suggested as a possible biologic mechanism by which particulate matter (PM) air pollution could lead to adverse health effects. The authors studied associations between ambient PM 2.5 and immune status among 115 postmenopausal, overweight women in the greater Seattle, Washington, area. The authors evaluated 3-day, 30-day, and 60-day average PM2.5 values in relation to inflammation markers (C-reactive protein, serum amyloid A, interleukin-6) and functional assays of cellular immunity (natural killer cell cytotoxicity, T-lymphocyte proliferation) at 3 time points for each woman during 1 year. Three-day averaged PM 2.5 was inversely associated with anti-CD3-stimulated lymphocyte proliferation. There were no notable associations between the inflammation markers and PM2.5. If additional studies confirm our findings, then future health effect assessments for PM2.5 should consider changes in cellular immunity as an endpoint that may lead to overt clinical disease.

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