Evidence map›Paper›PMID 25673341›Full record

ArticleOccupational and environmental medicine2015

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 and 12 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Occupational and environmental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Urinary Amino-PAHs in relation to diesel engine emissions and urinary mutagenicity.International journal of hygiene and environmental health · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 10 institutions in 5 countries.

Qing LanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
Roel VermeulenInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.
Yufei DaiKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Dianzhi RenChaoyang Center for Disease Control and Prevention, Chaoyang, China.
Wei HuDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
Huawei DuanKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Yong NiuKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Jun XuHong Kong University, Hong Kong, Hong Kong.
Wei FuChaoyang Center for Disease Control and Prevention, Chaoyang, China.
Kees MeliefsteInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.
Baosen ZhouChina Medical University, Shenyang, China.
Jufang YangChaoyang Center for Disease Control and Prevention, Chaoyang, China.
Meng YeKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Xiaowei JiaKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Tao MengKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Ping BinKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Christopher KimDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
Bryan A BassigDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
H Dean HosgoodDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Division of Epidemiology, Albert Einstein College of Medicine, New York, New York, USA.
Debra SilvermanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
Yuxin ZhengKey Laboratory of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Nathaniel RothmanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
Chinese Center For Disease Control and Prevention · CNDivision of Cancer Epidemiology and GeneticsNational Cancer Institute · USNational Institute for Occupational Health and Poison Control · CNCenter for Disease Control · TWUtrecht University · NLAlbert Einstein College of Medicine · USBeijing Chaoyang Emergency Medical Center · CNChina Medical University · CNUniversity of Hong Kong · HK

Funding

Occupational Exposure AssessmentZIACP010122 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI FRIESEN, MELISSA · 2009 to 2025
$8.6M
STUDIES OF OCCUPATIONAL CANCER--WOMEN AND MINORITIESZ01CP010123 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI CHOW, WONG · 1996 to 2008
$1.8M
Intramural NIH HHS Z01 CP010123
6 · The paper itself

Abstract

backgroundThe 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.

methodsWe 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.

resultsThe 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).

conclusionsOur 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.

Indexed as

Air Pollutants, OccupationalVehicle EmissionsAdultB-LymphocytesCarbonCarcinogensCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCross-Sectional StudiesHumansInflammationLung NeoplasmsLymphocyte SubsetsMiddle AgedMotor VehiclesOccupational ExposureAir Pollutants, OccupationalCarbonCarcinogensVehicle EmissionsDiesellymphocyte subsetoccupational exposuretoxicity

Identifiers

PMID25673341
PMCPMC6438624
OpenAlexW2124712113

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.