{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T03:34:50Z","timestamp":1777347290590,"version":"3.51.4"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,10,12]],"date-time":"2017-10-12T00:00:00Z","timestamp":1507766400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Environ and Mol Mutagen"],"published-print":{"date-parts":[[2018,3]]},"abstract":"<jats:p>The 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\u2010sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM<jats:sub>2.5<\/jats:sub> and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)\u20101, IL\u20106, IL\u20108, tumor necrosis factor (TNF)\u2010\u03b1, macrophage inflammatory protein (MIP)\u20101\u03b2, and monocyte chemotactic protein (MCP)\u20101 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP\u20101\u03b2 were significantly reduced by \u223c37% in DEE exposed workers (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) and showed a strong decreasing trend with increasing PM<jats:sub>2.5<\/jats:sub> concentrations in all subjects (<jats:italic>P<\/jats:italic><jats:sub>trend<\/jats:sub>\u2009&lt;\u20090.001) as well as in exposed subjects only (<jats:italic>P<\/jats:italic><jats:sub>trend<\/jats:sub>\u2009=\u20090.001). Levels of IL\u20108 and MIP\u20101\u03b2 were significantly lower in workers in the highest exposure tertile of PM<jats:sub>2.5<\/jats:sub> (&gt;397 \u00b5g\/m<jats:sup>3<\/jats:sup>) compared to unexposed controls. Further, significant inverse exposure\u2010response relationships for IL\u20108 and MCP\u20101 were also found in relation to increasing PM<jats:sub>2.5<\/jats:sub> levels among the DEE exposed workers. Given that IL\u20108, MIP\u20101\u03b2, and MCP\u20101 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 PM<jats:sub>2.5<\/jats:sub> exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144\u2013150, 2018. \u00a9 2017 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/em.22142","type":"journal-article","created":{"date-parts":[[2017,10,12]],"date-time":"2017-10-12T07:46:45Z","timestamp":1507794405000},"page":"144-150","source":"Crossref","is-referenced-by-count":19,"title":["Occupational exposure to diesel engine exhaust and serum cytokine levels"],"prefix":"10.1002","volume":"59","author":[{"given":"Yufei","family":"Dai","sequence":"first","affiliation":[{"name":"Key Laboratory of Chemical Safety and Health National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention Beijing China"},{"name":"Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics National Cancer Institute. 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