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Occupational exposure to diesel engine exhaust and serum cytokine levels
Author(s) -
Dai Yufei,
Ren Dianzhi,
Bassig Bryan A.,
Vermeulen Roel,
Hu Wei,
Niu Yong,
Duan Huawei,
Ye Meng,
Meng Tao,
Xu Jun,
Bin Ping,
Shen Meili,
Yang Jufang,
Fu Wei,
Meliefste Kees,
Silverman Debra,
Rothman Nathaniel,
Lan Qing,
Zheng Yuxin
Publication year - 2018
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.22142
Subject(s) - diesel exhaust , diesel engine , occupational exposure , environmental health , diesel fuel , toxicology , medicine , automotive engineering , environmental science , biology , engineering
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‐sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM 2.5 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 PM 2.5 concentrations in all subjects ( P trend < 0.001) as well as in exposed subjects only ( P trend = 0.001). Levels of IL‐8 and MIP‐1β were significantly lower in workers in the highest exposure tertile of PM 2.5 (>397 µg/m 3 ) compared to unexposed controls. Further, significant inverse exposure‐response relationships for IL‐8 and MCP‐1 were also found in relation to increasing PM 2.5 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 PM 2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144–150, 2018. © 2017 Wiley Periodicals, Inc.