Dataset Information

Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets.

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.

SUBMITTER: Lan Q

PROVIDER: S-EPMC6438624 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature

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Publications

Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets.

Lan Qing Q Vermeulen Roel R Dai Yufei Y Ren Dianzhi D Hu Wei W Duan Huawei H Niu Yong Y Xu Jun J Fu Wei W Meliefste Kees K Zhou Baosen B Yang Jufang J Ye Meng M Jia Xiaowei X Meng Tao T Bin Ping P Kim Christopher C Bassig Bryan A BA Hosgood H Dean HD Silverman Debra D Zheng Yuxin Y Rothman Nathaniel N

Occupational and environmental medicine 20150211 5

<h4>Background</h4>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.<h4>Methods</h4>We conducted a cross-sectional molecular epidemiology study in a diesel engine truck testing facility of 54 workers exposed to ...[more]

PMID: 25673341

Similar Datasets

Project description:BackgroundDiesel engine exhaust (DEE) exposure causes lung cancer, but the molecular mechanisms by which this occurs are not well understood.ObjectivesTo assess transcriptomic alterations in nasal epithelium of DEE-exposed factory workers to better understand the cellular and molecular effects of DEE.MethodsNasal epithelial brushings were obtained from 41 diesel engine factory workers exposed to relatively high levels of DEE (17.2-105.4 μg/m3), and 38 unexposed workers from factories without DEE exposure. mRNA was profiled for gene expression using Affymetrix microarrays. Linear modeling was used to identify differentially expressed genes associated with DEE exposure and interaction effects with current smoking status. Pathway enrichment among differentially expressed genes was assessed using EnrichR. Gene Set Enrichment Analysis (GSEA) was used to compare gene expression patterns between datasets.Results225 genes had expression associated with DEE exposure after adjusting for smoking status (FDR q < 0.25) and were enriched for genes in pathways related to oxidative stress response, cell cycle pathways such as MAPK/ERK, protein modification, and transmembrane transport. Genes up-regulated in DEE-exposed individuals were enriched among the genes most up-regulated by cigarette smoking in a previously reported bronchial airway smoking dataset. We also found that the DEE signature was enriched among the genes most altered in two previous studies of the effects of acute DEE on PBMC gene expression. An exposure-response relationship was demonstrated between air levels of elemental carbon and the first principal component of the DEE signature.ConclusionsA gene expression signature was identified for workers occupationally exposed to DEE that was altered in an exposure-dependent manner and had some overlap with the effects of smoking and the effects of acute DEE exposure. This is the first study of gene expression in nasal epithelial cells of workers heavily exposed to DEE and provides new insights into the molecular alterations that occur with DEE exposure.

Dataset Information

Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets.

Background

Methods

Results

Conclusions

Impact

Publications

Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets.

Similar Datasets

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