| Literature DB >> 28968774 |
Bryan A Bassig1, Yufei Dai2, Roel Vermeulen3, Dianzhi Ren4, Wei Hu1, Huawei Duan2, Yong Niu2, Jun Xu5, Meredith S Shiels1, Troy J Kemp6, Ligia A Pinto6, Wei Fu4, Kees Meliefste3, Baosen Zhou7, Jufang Yang4, Meng Ye2, Xiaowei Jia2, Tao Meng2, Jason Y Y Wong1, Ping Bin2, H Dean Hosgood8, Allan Hildesheim1, Debra T Silverman1, Nathaniel Rothman1, Yuxin Zheng2, Qing Lan1.
Abstract
The relationship between diesel engine exhaust (DEE), a known lung carcinogen, and immune/inflammatory markers that have been prospectively associated with lung cancer risk is not well understood. To provide insight into these associations, we conducted a cross-sectional molecular epidemiology study of 54 males highly occupationally exposed to DEE and 55 unexposed male controls from representative workplaces in China. We measured plasma levels of 64 immune/inflammatory markers in all subjects using Luminex bead-based assays, and compared our findings to those from a nested case-control study of these markers and lung cancer risk, which had been conducted among never-smoking women in Shanghai using the same multiplex panels. Levels of nine markers that were associated with lung cancer risk in the Shanghai study were altered in DEE-exposed workers in the same direction as the lung cancer associations. Among these, associations with the levels of CRP (β= -0.53; P = 0.01) and CCL15/MIP-1D (β = 0.20; P = 0.02) were observed in workers exposed to DEE and with increasing elemental carbon exposure levels (Ptrends <0.05) in multivariable linear regression models. Levels of a third marker positively associated with an increased lung cancer risk, CCL2/MCP-1, were higher among DEE-exposed workers compared with controls in never and former smokers, but not in current smokers (Pinteraction = 0.01). The immunological differences in these markers in DEE-exposed workers are consistent with associations observed for lung cancer risk in a prospective study of Chinese women and may provide some insight into the mechanistic processes by which DEE causes lung cancer. Published by Oxford University Press 2017.Entities:
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Year: 2017 PMID: 28968774 PMCID: PMC5862277 DOI: 10.1093/carcin/bgx081
Source DB: PubMed Journal: Carcinogenesis ISSN: 0143-3334 Impact factor: 4.944