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O18-5 Occupational exposure to diesel exhaust and alterations in immune/inflammatory markers
  1. Qing Lan1,
  2. Bryan A Bassig1,
  3. Roel Vermeulen2,
  4. Yufei Dai3,
  5. Dianzhi Ren4,
  6. Wei Hu1,
  7. Huawei Duan3,
  8. Yong Niu3,
  9. Jun Xu5,
  10. Meredith Shiels1,
  11. Troy J Kemp6,
  12. Wei Fu4,
  13. Kees Meliefste2,
  14. Baosen Zhou7,
  15. Jufang Yang4,
  16. Meng Ye3,
  17. Xiaowei Jia3,
  18. Tao Meng3,
  19. Ping Bin3,
  20. Christopher Kim1,
  21. Dean H Hosgood8,
  22. Allan Hildesheim1,
  23. Debra T Silverman1,
  24. Yuxin Zheng3,
  25. Nathaniel Rothman1
  1. 1Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, USA
  2. 2Institute for Risk Assessment Sciences, Division of Environmental Epidemiology, Utrecht University, Utrecht, The Netherlands
  3. 3Key Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Centre for Disease Control and Prevention, Beijing, China
  4. 4Chaoyang Centre for Disease Control and Prevention, Chaoyang, China
  5. 5Hong Kong University, Hong Kong, China
  6. 6HPV Immunology Laboratory, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, USA
  7. 7China Medical University, Shenyang, China
  8. 8Division of Epidemiology, Albert Einstein College of Medicine, New York, USA


Introduction Diesel engine exhaust (DEE) is a known lung carcinogen in humans (IARC Group 1). However, the biological mechanism underlying this association is unclear. Given the suspected relationship between inflammation and lung carcinogenesis, we evaluated associations between DEE exposure and a multiplex panel of immune markers in workers exposed to DEE and unexposed workers in China.

Methods A cross-sectional molecular epidemiology study was conducted among 54 workers exposed to DEE in a diesel engine testing facility, and 55 unexposed workers who were employed in separate factories. Repeated personal exposure measurements of elemental carbon (EC) were taken from workers before blood collection. Serum levels of immune markers were analysed using a Luminex bead-based assay. Linear regression was used to evaluate differences in marker concentrations between DEE exposed vs. unexposed workers, and to explore exposure-response trends with EC.

Results Four markers were significantly associated with DEE exposure in analyses of exposed vs. unexposed workers (P-value < 0.05). Significant monotonic trends in relation to increasing EC levels were observed for CXCL-11/I-TAC (19% reduction in exposed workers overall) and CCL15/MIP-1D (21% increase in exposed workers overall). Analyses of DEE exposed vs. unexposed workers stratified by smoking status found that an additional marker (CCL2/MCP-1) was significantly increased in workers exposed to DEE among never and former smokers, but not current smokers (Pinteraction = 0.01).

Conclusions Recent evidence suggests that higher levels of CCL15/MIP-1D and CCL2/MCP-1, two markers in the CC chemokine subfamily that attract white blood cells to sites of inflammation, are associated with increased risk of lung cancer in Asian never-smoking women. Alterations in these markers in the same direction among workers exposed to DEE in our study may provide mechanistic insight into the relationship between DEE and lung carcinogenesis.

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