Qing Lan1, Roel Vermeulen2, Yufei Dai3, Dianzhi Ren4, Wei Hu1, Huawei Duan3, Yong Niu3, Jun Xu5, Wei Fu4, Kees Meliefste2, Baosen Zhou6, Jufang Yang4, Meng Ye3, Xiaowei Jia3, Tao Meng3, Ping Bin3, Christopher Kim1, Bryan A Bassig1, H Dean Hosgood7, Debra Silverman1, Yuxin Zheng3, Nathaniel Rothman1. 1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA. 2. Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. 3. Key Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China. 4. Chaoyang Center for Disease Control and Prevention, Chaoyang, China. 5. Hong Kong University, Hong Kong, Hong Kong. 6. China Medical University, Shenyang, China. 7. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Division of Epidemiology, Albert Einstein College of Medicine, New York, New York, USA.
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/m(3)) 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. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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/m(3)) 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. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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