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Article: Occupational exposure to diesel engine exhaust and serum cytokine levels

TitleOccupational exposure to diesel engine exhaust and serum cytokine levels
Authors
Keywordsdiesel engine exhaust
inflammatory biomarkers
molecular epidemiology
occupational exposure
Issue Date2018
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009058
Citation
Environmental and Molecular Mutagenesis, 2018, v. 59 n. 2, p. 144-150 How to Cite?
AbstractThe International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross-sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-1β, and monocyte chemotactic protein (MCP)-1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP-1β were significantly reduced by ∼37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM2.5 concentrations in all subjects (Ptrend  < 0.001) as well as in exposed subjects only (Ptrend  = 0.001). Levels of IL-8 and MIP-1β were significantly lower in workers in the highest exposure tertile of PM2.5 (>397 µg/m3 ) compared to unexposed controls. Further, significant inverse exposure-response relationships for IL-8 and MCP-1 were also found in relation to increasing PM2.5 levels among the DEE exposed workers. Given that IL-8, MIP-1β, and MCP-1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144-150, 2018.
Persistent Identifierhttp://hdl.handle.net/10722/281188
ISSN
2019 Impact Factor: 3.131
2015 SCImago Journal Rankings: 1.326
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorDai, Y-
dc.contributor.authorRen, D-
dc.contributor.authorBassig, BA-
dc.contributor.authorVermeulen, R-
dc.contributor.authorHu, W-
dc.contributor.authorNiu, Y-
dc.contributor.authorDuan, H-
dc.contributor.authorYe, M-
dc.contributor.authorMeng, T-
dc.contributor.authorXu, J-
dc.contributor.authorBin, P-
dc.contributor.authorShen , M-
dc.contributor.authorYang, J-
dc.contributor.authorFu, W-
dc.contributor.authorMeliefste, K-
dc.contributor.authorSilverman, D-
dc.contributor.authorRothman, N-
dc.contributor.authorLan, Q-
dc.contributor.authorZheng, Y-
dc.date.accessioned2020-03-09T09:51:21Z-
dc.date.available2020-03-09T09:51:21Z-
dc.date.issued2018-
dc.identifier.citationEnvironmental and Molecular Mutagenesis, 2018, v. 59 n. 2, p. 144-150-
dc.identifier.issn0893-6692-
dc.identifier.urihttp://hdl.handle.net/10722/281188-
dc.description.abstractThe International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross-sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-1β, and monocyte chemotactic protein (MCP)-1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP-1β were significantly reduced by ∼37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM2.5 concentrations in all subjects (Ptrend  < 0.001) as well as in exposed subjects only (Ptrend  = 0.001). Levels of IL-8 and MIP-1β were significantly lower in workers in the highest exposure tertile of PM2.5 (>397 µg/m3 ) compared to unexposed controls. Further, significant inverse exposure-response relationships for IL-8 and MCP-1 were also found in relation to increasing PM2.5 levels among the DEE exposed workers. Given that IL-8, MIP-1β, and MCP-1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144-150, 2018.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009058-
dc.relation.ispartofEnvironmental and Molecular Mutagenesis-
dc.rightsPreprint This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. Postprint This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectdiesel engine exhaust-
dc.subjectinflammatory biomarkers-
dc.subjectmolecular epidemiology-
dc.subjectoccupational exposure-
dc.titleOccupational exposure to diesel engine exhaust and serum cytokine levels-
dc.typeArticle-
dc.identifier.emailXu, J: xusunjun@hku.hk-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/em.22142-
dc.identifier.pmid29023999-
dc.identifier.pmcidPMC6438621-
dc.identifier.scopuseid_2-s2.0-85031087232-
dc.identifier.hkuros309321-
dc.identifier.volume59-
dc.identifier.issue2-
dc.identifier.spage144-
dc.identifier.epage150-
dc.publisher.placeUnited States-

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