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Genotypes linked to increased breathing issues following early tobacco exposure

GST null mutations, GSTP1 Ile/Ile alleles more susceptible to asthma and decreased lung function

Glenview, IL– While exposure to tobacco in early life is known to have an increased risk on the development of asthma and lung function deficits in adolescents and adults, further research is needed to determine whether there are genetic factors that influence this relationship. There are few longitudinal studies that focus on gene-environment interactions and that measure outcomes and lung function as children age. Researchers from the University of Melbourne, Australia, sought to investigate the relationship between a key gene, the glutathione s-transferase (GST) gene family and early life tobacco smoke exposure and their interaction on asthma and lung function in patients between the ages of 12 and 18.

The Melbourne Atopy Cohort study (MACs) recruited children prior to birth between 1990 and 1994 and included 620 children who had at least one first-degree family member with the allergic disease. Researchers then collected data prospectively on patients’ exposures and respiratory outcomes from birth to 18 years of age. The investigators conducted follow-ups on cohort participants, recording perinatal tobacco smoke exposure, then asthma and lung function at 12 (59 percent) and again at 18 years (66 percent). Children were genotyped for GSTM1, GSTT1 and GSTP1 (69 percent).

Investigators found that GST genotypes interacted with tobacco smoke exposure on lung function outcomes (p-interaction ≤.05).  Specifically, children with GSTT1 null genotypes, who were exposed to tobacco smoke in early life were associated with an increased risk of impaired lung function at both 12 and 18 years. These children were at risk for reductions in pre-bronchodilator (pre-BD) forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) at these ages. Similar associations were not seen in children with the GSTT1 gene present.

“[Our study] provides suggestive evidence of interaction between early tobacco smoke exposure and GST genotypes on lung function,” says Ms. Xin DaI,  lead author. “These findings suggest that carriers of GST null mutations and GSTP1 Ile/Ile alleles may be more susceptible when exposed to tobacco smoke in early life. These findings support stronger recommendations to protect all infants from tobacco smoke exposure,” says Dr. Caroline Lodge, senior author.  

Full text of this article and interviews with the authors are available to credentialed journalists upon request; contact media@chestnet.org.

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