Literature DB >> 19860819

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

A J Rogers1, C Brasch-Andersen, I Ionita-Laza, A Murphy, S Sharma, B J Klanderman, B A Raby.   

Abstract

BACKGROUND: The 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.
OBJECTIVE: To 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.
METHODS: We 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.
RESULTS: Associations 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.
CONCLUSION: These 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.

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Year:  2009        PMID: 19860819      PMCID: PMC2773694          DOI: 10.1111/j.1365-2222.2009.03372.x

Source DB:  PubMed          Journal:  Clin Exp Allergy        ISSN: 0954-7894            Impact factor:   5.018


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