TY - JOUR
T1 - Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets
AU - Lan, Qing
AU - Vermeulen, Roel
AU - Dai, Yufei
AU - Ren, Dianzhi
AU - Hu, Wei
AU - Duan, Huawei
AU - Niu, Yong
AU - Xu, Jun
AU - Fu, Wei
AU - Meliefste, Kees
AU - Zhou, Baosen
AU - Yang, Jufang
AU - Ye, Meng
AU - Jia, Xiaowei
AU - Meng, Tao
AU - Bin, Ping
AU - Kim, Christopher
AU - Bassig, Bryan A.
AU - Hosgood, H. Dean
AU - Silverman, Debra
AU - Zheng, Yuxin
AU - Rothman, Nathaniel
PY - 2015/5/1
Y1 - 2015/5/1
N2 - 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.
AB - 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.
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U2 - 10.1136/oemed-2014-102556
DO - 10.1136/oemed-2014-102556
M3 - Article
C2 - 25673341
AN - SCOPUS:84928139677
SN - 1351-0711
VL - 72
SP - 354
EP - 359
JO - Occupational and Environmental Medicine
JF - Occupational and Environmental Medicine
IS - 5
ER -