Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets

Qing Lan, Roel Vermeulen, Yufei Dai, Dianzhi Ren, Wei Hu, Huawei Duan, Yong Niu, Jun Xu, Wei Fu, Kees Meliefste, Baosen Zhou, Jufang Yang, Meng Ye, Xiaowei Jia, Tao Meng, Ping Bin, Christopher Kim, Bryan A. Bassig, Howard D. Hosgood, Debra Silverman & 2 others Yuxin Zheng, Nathaniel Rothman

Research output: Contribution to journalArticle

10 Citations (Scopus)

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<sup>3</sup>) 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 (p<inf>trend</inf>s<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.

Original languageEnglish (US)
Pages (from-to)354-359
Number of pages6
JournalOccupational and Environmental Medicine
Volume72
Issue number5
DOIs
StatePublished - May 1 2015

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Vehicle Emissions
Lymphocyte Subsets
Occupational Exposure
Lung Neoplasms
T-Lymphocytes
Carbon
International Agencies
Molecular Epidemiology
Lymphocyte Count
Motor Vehicles
Carcinogens
B-Lymphocytes

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Medicine(all)

Cite this

Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets. / Lan, Qing; Vermeulen, Roel; Dai, Yufei; Ren, Dianzhi; Hu, Wei; Duan, Huawei; Niu, Yong; Xu, Jun; Fu, Wei; Meliefste, Kees; Zhou, Baosen; Yang, Jufang; Ye, Meng; Jia, Xiaowei; Meng, Tao; Bin, Ping; Kim, Christopher; Bassig, Bryan A.; Hosgood, Howard D.; Silverman, Debra; Zheng, Yuxin; Rothman, Nathaniel.

In: Occupational and Environmental Medicine, Vol. 72, No. 5, 01.05.2015, p. 354-359.

Research output: Contribution to journalArticle

Lan, Q, Vermeulen, R, Dai, Y, Ren, D, Hu, W, Duan, H, Niu, Y, Xu, J, Fu, W, Meliefste, K, Zhou, B, Yang, J, Ye, M, Jia, X, Meng, T, Bin, P, Kim, C, Bassig, BA, Hosgood, HD, Silverman, D, Zheng, Y & Rothman, N 2015, 'Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets', Occupational and Environmental Medicine, vol. 72, no. 5, pp. 354-359. https://doi.org/10.1136/oemed-2014-102556
Lan, Qing ; Vermeulen, Roel ; Dai, Yufei ; Ren, Dianzhi ; Hu, Wei ; Duan, Huawei ; Niu, Yong ; Xu, Jun ; Fu, Wei ; Meliefste, Kees ; Zhou, Baosen ; Yang, Jufang ; Ye, Meng ; Jia, Xiaowei ; Meng, Tao ; Bin, Ping ; Kim, Christopher ; Bassig, Bryan A. ; Hosgood, Howard D. ; Silverman, Debra ; Zheng, Yuxin ; Rothman, Nathaniel. / Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets. In: Occupational and Environmental Medicine. 2015 ; Vol. 72, No. 5. pp. 354-359.
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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.",
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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, Howard D.

AU - Silverman, Debra

AU - Zheng, Yuxin

AU - Rothman, Nathaniel

PY - 2015/5/1

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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.

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