Evidence map›Paper›PMID 12566517›Full record

ArticleJournal of medical genetics2003

Effect of TNF and LTA polymorphisms on biological markers of response to oxidative stimuli in coal miners: a model of gene-environment interaction. Tumour necrosis factor and lymphotoxin alpha.

R Nadif, A Jedlicka, M Mintz, J-P Bertrand, S Kleeberger, F Kauffmann

Open access · bronzeAbstract read
In one paragraph

Article in Journal of medical genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Understanding the pathogenesis of occupational coal and silica dust-associated lung disease.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  4. Review
  5. Article
  6. Article
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  8. 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

6 authors at 3 institutions in 3 countries.

R NadifINSERM U 472-IFR69, Villejuif, France. nadif@vjf.inserm.fr
A Jedlicka
M Mintz
J-P Bertrand
S Kleeberger
F Kauffmann
Johns Hopkins University · USInserm · FRService de Santé des Armées · FR

Funding

Trial of Behavioral Changes in Home Exposure ControlP01ES009606 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI DIETTE, GREGORY B · 1999 to 2008
$6.8M
Particle-induced Cardiopulmonary Injury In Mice: Genetic SusceptibilityZ01ES100563 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2002 to 2008
$1.2M
Gene-environment Interaction And Pulmonary Disease: Translational StudiesZ01ES100564 · NIEHS · ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2002 to 2007
$488k
NIEHS NIH HHS ES-09606
6 · The paper itself

Abstract

introductionInteraction between genetic background and oxidative environmental stimuli in the pathogenesis of human lung disease has been largely unexplored.

methodsA prospective epidemiological study was undertaken in 253 coal miners. Intermediate quantitative phenotypes of response to oxidant exposure, including erythrocyte glutathione peroxidase (GSH-Px) and catalase activities, were studied. Oxidant exposures studied were smoking habits and cumulative dust exposure assessed by job history and ambient measures. Disease phenotypes included subclinical computed tomography score at the first survey and x ray profusion grades twice, five years apart, to assess established coal workers' pneumoconiosis (CWP). Miners were genotyped for common functional polymorphisms in the gene for tumour necrosis factor alpha (TNF) and lymphotoxin alpha (LTA), two proinflammatory cytokines that have been implicated in the pathogenesis of chronic lung diseases.

resultsRegarding gene-environment interaction on intermediate phenotypes, results showed interaction of a promoter polymorphism at the -308 position in TNF with occupational exposure on erythrocyte GSH-Px activity with a significant association in those with high exposure (p=0.003), whereas no association was observed among those with low exposure (interaction p=0.06). Regarding gene intermediate phenotype interaction on clinical outcome, results showed an association of CWP prevalence with an NcoI polymorphism in LTA in those with low catalase activity (p=0.05), whereas no association was observed in those with high activity (interaction p=0.03). No other significant association was observed.

conclusionThe results suggest that interactions of genetic background with environmental exposure and intermediate response phenotypes are important components in the pathogenesis of CWP.

Indexed as

Coal MiningCatalaseEnvironmental ExposureErythrocytesFranceGenotypeGlutathione PeroxidaseHumansLongitudinal StudiesLymphotoxin-alphaMiddle AgedOccupational ExposureOxidantsOxidative StressPhenotypePneumoconiosisCatalaseGlutathione PeroxidaseLymphotoxin-alphaOxidantsTumor Necrosis Factor-alpha

Identifiers

PMID12566517
PMCPMC1735359
OpenAlexW2049173899

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.