Xin Dai1, Gayan Bowatte1, Adrian J Lowe1,2, Melanie C Matheson1, Lyle C Gurrin1, John A Burgess1, Shyamali C Dharmage1,2, Caroline J Lodge3,4. 1. Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Level 3 207 Bouverie Street, Melbourne, 3010, Australia. 2. Murdoch Childrens Research Institute, Melbourne, Australia. 3. Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Level 3 207 Bouverie Street, Melbourne, 3010, Australia. clodge@unimelb.edu.au. 4. Murdoch Childrens Research Institute, Melbourne, Australia. clodge@unimelb.edu.au.
Abstract
PURPOSE OF REVIEW: Glutathione S-transferase (GST) genes are involved in oxidative stress management and may modify the impact of indoor air pollution. We aimed to assess the influence of GST genes on the relationship between indoor air pollution and allergy/lung function. RECENT FINDINGS: Our systematic review identified 22 eligible studies, with 15 supporting a gene-environment interaction. Carriers of GSTM1/T1 null and GSTP1 val genotypes were more susceptible to indoor air pollution exposures, having a higher risk of asthma and lung function deficits. However, findings differed in terms of risk alleles and specific exposures. High-exposure heterogeneity precluded meta-analysis. We found evidence that respiratory effects of indoor air pollution depend on the individual's GST profile. This may help explain the inconsistent associations found when gene-environment interactions are not considered. Future studies should aim to improve the accuracy of pollution assessment and investigate this finding in different populations.
PURPOSE OF REVIEW: Glutathione S-transferase (GST) genes are involved in oxidative stress management and may modify the impact of indoor air pollution. We aimed to assess the influence of GST genes on the relationship between indoor air pollution and allergy/lung function. RECENT FINDINGS: Our systematic review identified 22 eligible studies, with 15 supporting a gene-environment interaction. Carriers of GSTM1/T1 null and GSTP1 val genotypes were more susceptible to indoor air pollution exposures, having a higher risk of asthma and lung function deficits. However, findings differed in terms of risk alleles and specific exposures. High-exposure heterogeneity precluded meta-analysis. We found evidence that respiratory effects of indoor air pollution depend on the individual's GST profile. This may help explain the inconsistent associations found when gene-environment interactions are not considered. Future studies should aim to improve the accuracy of pollution assessment and investigate this finding in different populations.
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