Occupational exposure to diesel engine exhaust and alterations in immune/inflammatory markers: a cross-sectional molecular epidemiology study in China

• Published in: Carcinogenesis (New York) Vol. 38; no. 11; pp. 1104 - 1111
• Main Authors: Bassig, Bryan A, Dai, Yufei, Vermeulen, Roel, Ren, Dianzhi, Hu, Wei, Duan, Huawei, Niu, Yong, Xu, Jun, Shiels, Meredith S, Kemp, Troy J, Pinto, Ligia A, Fu, Wei, Meliefste, Kees, Zhou, Baosen, Yang, Jufang, Ye, Meng, Jia, Xiaowei, Meng, Tao, Wong, Jason YY, Bin, Ping, Hosgood, H Dean, Hildesheim, Allan, Silverman, Debra T, Rothman, Nathaniel, Zheng, Yuxin, Lan, Qing
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 26.10.2017
• Subjects: Adult; Air Pollutants, Occupational - adverse effects; Biomarkers - metabolism; Cancer Biomarkers and Molecular Epidemiology; Carcinogens; Case-Control Studies; China; Cross-Sectional Studies; Gasoline - adverse effects; Humans; Inflammation - chemically induced; Inflammation - metabolism; Lung - metabolism; Lung Neoplasms - etiology; Lung Neoplasms - metabolism; Male; Molecular Epidemiology - methods; Occupational Exposure - adverse effects; Prospective Studies; Risk Assessment; Vehicle Emissions
• ISSN: 0143-3334; 1460-2180; 1460-2180
• DOI: 10.1093/carcin/bgx081

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.