Evidence map›Paper›PMID 19860819›Full record

Trial reportClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2009

The interaction of glutathione S-transferase M1-null variants with tobacco smoke exposure and the development of childhood asthma.

A J Rogers, C Brasch-Andersen, I Ionita-Laza, A Murphy, S Sharma, B J Klanderman, B A Raby

Abstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Copy Number Variation in Asthma: An Integrative Review.Clinical reviews in allergy & immunology · 2025
    Review
  5. Article
  6. Genetics of Asthma and Allergic Diseases.Handbook of experimental pharmacology · 2022
    Article
  7. Review
  8. Second-hand smoke and NFE2L2 genotype interaction increases paediatric asthma risk and severity.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Article
  9. Review
  10. Article
  11. Air pollutants and early origins of respiratory diseases.Chronic diseases and translational medicine · 2018
    Article
  12. Outdoor air pollution and asthma.Lancet (London, England) · 2014
    Review
  13. Article
  14. Article
  15. Article
  16. Copy number variation prevalence in known asthma genes and their impact on asthma susceptibility.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2013
    Article
  17. Review
  18. Review
  19. Review
  20. Unravelling gene-by-environment effects in asthma and allergy: the glutathione pathway as an early success story.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2011
    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

7 authors.

A J RogersChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. reajr@channing.harvard.edu
C Brasch-Andersen
I Ionita-Laza
A Murphy
S Sharma
B J Klanderman
B A Raby

Funding

THE PHARMACOGENETICS OF ASTHMA TREATMENTU01HL065899 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI TANTISIRA, KELAN G, WEISS, SCOTT T · 2000 to 2014
$38.5M
SYSTEMS APPROACHES TO THE EPIDEMIOLOGY, GENETICS AND GENOMICS OF LUNG DISEASEST32HL007427 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI DAWN L DEMEO, Edwin K Silverman · 1985 to 2026
$13.6M
Statistical GeneticsP01HL083069 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LANGE, CHRISTOPH · 2007 to 2011
$12.2M
Genetics and Gene Expression Profiling in AsthmaR01HL086601 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI RABY, BENJAMIN ALEXANDER · 2007 to 2015
$6.8M
Structural Genetic Variation in AsthmaR01HL093076 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI RABY, BENJAMIN ALEXANDER · 2008 to 2011
$3.5M
CLINICAL CENTER FOR CAMPN01HR016049 · HR · BRIGHAM AND WOMEN'S HOSPITAL · PI WEISS, SCOTT T · 1991 to 2000
$1.0M
NHLBI NIH HHS N01 HR016049NHLBI NIH HHS N01 HR16049NHLBI NIH HHS P01 HL083069NHLBI NIH HHS R01 HL086601NHLBI NIH HHS R01 HL093076NHLBI NIH HHS T32 HL007427NHLBI NIH HHS T32 HL07427NHLBI NIH HHS U01 HL065899
6 · The paper itself

Abstract

backgroundThe glutathione S-transferase M1 (GSTM1)-null variant is a common copy number variant associated with adverse pulmonary outcomes, including asthma and airflow obstruction, with evidence of important gene-by-environment interactions with exposures to oxidative stress.

objectiveTo explore the joint interactive effects of GSTM1 copy number and tobacco smoke exposure on the development of asthma and asthma-related phenotypes in a family-based cohort of childhood asthmatics.

methodsWe performed quantitative PCR-based genotyping for GSTM1 copy number in children of self-reported white ancestry with mild to moderate asthma in the Childhood Asthma Management Program. Questionnaire data regarding intrauterine (IUS) and post-natal, longitudinal smoke exposure were available. We performed both family-based and population-based tests of association for the interaction between GSTM1 copy number and tobacco smoke exposure with asthma and asthma-related phenotypes.

resultsAssociations of GSTM1-null variants with asthma (P=0.03), younger age of asthma symptom onset (P=0.03), and greater airflow obstruction (reduced forced expiratory volume in 1 s / forced vital capacity, P=0.01) were observed among the 50 children (10% of the cohort) with exposure to IUS. In contrast, no associations were observed between GSTM1-null variants and asthma-related phenotypes among children without IUS exposure. Presence of at least one copy of GSTM1 conferred protection.

conclusionThese findings support an important gene-by-environment interaction between two common factors: increased risk of asthma and asthma-related phenotypes conferred by GSTM1-null homozygosity in children is restricted to those with a history of IUS exposure.

Indexed as

HomozygotePhenotypeAsthmaChildFemaleFollow-Up StudiesForced Expiratory VolumeGene DosageGlutathione TransferaseHumansMaleTobacco Smoke PollutionGlutathione TransferaseTobacco Smoke Pollution

Identifiers

PMID19860819
PMCPMC2773694

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Registered trials

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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.