Evidence map›Paper›PMID 36200867›Full record

ArticleCarcinogenesis2022

Association between diesel exhaust exposure and mitochondrial DNA methylation.

Wei Jie Seow, Wei Hu, Yufei Dai, Roel Vermeulen, Hyang-Min Byun, Jason Y Y Wong, Bryan A Bassig, Batel Blechter, Huawei Duan, Yong Niu and 16 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Carcinogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 51% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

26 authors at 8 institutions in 6 countries.

Wei Jie SeowSaw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore, Singapore.ORCID 0000-0002-9114-854X
Wei HuDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Yufei DaiNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Roel VermeulenDivision of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0003-4082-8163
Hyang-Min ByunPopulation Health Sciences Institute, Newcastle University, Newcastle upon Tyne, UK.
Jason Y Y WongDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.ORCID 0000-0003-2820-2133
Bryan A BassigDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Batel BlechterDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Huawei DuanNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Yong NiuNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
George DownwardDivision of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.
Shuguang LengCancer Control and Population Sciences, University of New Mexico Comprehensive Cancer Center, Albuquerque, NM, USA.
Bu-Tian JiDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Wei FuChaoyang Center for Disease Control and Prevention, Chaoyang, Liaoning, China.
Jun XuSchool of Public Health, Li Ka Shing (LKS) Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Kees MeliefsteDivision of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.
Jufang YangChaoyang Center for Disease Control and Prevention, Chaoyang, Liaoning, China.
Dianzhi RenChaoyang Center for Disease Control and Prevention, Chaoyang, Liaoning, China.
Meng YeNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Tao MengNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Ping BinNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
H Dean HosgoodDivision of Epidemiology, Albert Einstein College of Medicine, New York, NY, USA.
Debra T SilvermanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Nathaniel RothmanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
Yuxin ZhengNational Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Qing LanDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD, USA.
National Institutes of Health · USNational Institute for Occupational Health and Poison Control · CNUtrecht University · NLUniversity of New Mexico · USAlbert Einstein College of Medicine · USNational University of Singapore · SGNewcastle University · GBUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDiesel exhaust is an established human carcinogen, however the mechanisms by which it leads to cancer development are not fully understood. Mitochondrial dysfunction is an established contributor to carcinogenesis. Recent studies have improved our understanding of the role played by epigenetic modifications in the mitochondrial genome on tumorigenesis. In this study, we aim to evaluate the association between diesel engine exhaust (DEE) exposure with mitochondrial DNA (mtDNA) methylation levels in workers exposed to DEE.

methodsThe study population consisted of 53 male workers employed at a diesel engine manufacturing facility in Northern China who were routinely exposed to diesel exhaust in their occupational setting, as well as 55 unexposed male control workers from other unrelated factories in the same geographic area. Exposure to DEE, elemental carbon, organic carbon, and particulate matter (PM2.5) were assessed. mtDNA methylation for CpG sites (CpGs) from seven mitochondrial genes (D-Loop, MT-RNR1, MT-CO2, MT-CO3, MT-ATP6, MT-ATP8, MT-ND5) was measured in blood samples. Linear regression models were used to estimate the associations between DEE, elemental carbon, organic carbon and PM2.5 exposures with mtDNA methylation levels, adjusting for potential confounders.

resultsDEE exposure was associated with decreased MT-ATP6 (difference = -35.6%, P-value = 0.019) and MT-ATP8 methylation (difference = -30%, P-value = 0.029) compared to unexposed controls. Exposures to elemental carbon, organic carbon, and PM2.5 were also significantly and inversely associated with methylation in MT-ATP6 and MT-ATP8 genes (all P-values < 0.05).

conclusionsOur findings suggest that DEE exposure perturbs mtDNA methylation, which may be of importance for tumorigenesis.

Indexed as

Occupational ExposureCarbonCarcinogenesisDNA MethylationDNA, MitochondrialHumansMaleMitochondriaParticulate MatterVehicle EmissionsCarbonDNA, MitochondrialParticulate MatterVehicle Emissions

Identifiers

PMID36200867
PMCPMC10233238
OpenAlexW4302304731

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.