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Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets
  1. Qing Lan1,
  2. Roel Vermeulen2,
  3. Yufei Dai3,
  4. Dianzhi Ren4,
  5. Wei Hu1,
  6. Huawei Duan3,
  7. Yong Niu3,
  8. Jun Xu5,
  9. Wei Fu4,
  10. Kees Meliefste2,
  11. Baosen Zhou6,
  12. Jufang Yang4,
  13. Meng Ye3,
  14. Xiaowei Jia3,
  15. Tao Meng3,
  16. Ping Bin3,
  17. Christopher Kim1,
  18. Bryan A Bassig1,
  19. H Dean Hosgood III1,7,
  20. Debra Silverman1,
  21. Yuxin Zheng3,
  22. Nathaniel Rothman1
  1. 1Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA
  2. 2Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
  3. 3Key Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China
  4. 4Chaoyang Center for Disease Control and Prevention, Chaoyang, China
  5. 5Hong Kong University, Hong Kong, Hong Kong
  6. 6China Medical University, Shenyang, China
  7. 7Division of Epidemiology, Albert Einstein College of Medicine, New York, New York, USA
  1. Correspondence to Dr Qing Lan, Occupational & Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, 9609 Medical Center Drive, Room 6E138, Rockville, MD 20850, USA; qingl{at}mail.nih.gov

Abstract

Background The International Agency for Research on Cancer recently classified diesel engine exhaust (DEE) as a Group I carcinogen based largely on its association with lung cancer. However, the exposure–response relationship is still a subject of debate and the underlying mechanism by which DEE causes lung cancer in humans is not well understood.

Methods We conducted a cross-sectional molecular epidemiology study in a diesel engine truck testing facility of 54 workers exposed to a wide range of DEE (ie, elemental carbon air levels, median range: 49.7, 6.1–107.7 µg/m3) and 55 unexposed comparable controls.

Results The total lymphocyte count (p=0.00044) and three of the four major lymphocyte subsets (ie, CD4+ T cells (p=0.00019), CD8+ T cells (p=0.0058) and B cells (p=0.017)) were higher in exposed versus control workers and findings were highly consistent when stratified by smoking status. In addition, there was evidence of an exposure–response relationship between elemental carbon and these end points (ptrends<0.05), and CD4+ T cell levels were significantly higher in the lowest tertile of DEE exposed workers compared to controls (p=0.012).

Conclusions Our results suggest that DEE exposure is associated with higher levels of cells that play a key role in the inflammatory process, which is increasingly being recognised as contributing to the aetiology of lung cancer.

Impact This study provides new insights into the underlying mechanism of DEE carcinogenicity.

  • occupational exposure
  • toxicity
  • Diesel
  • lymphocyte subset

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