Our hypothesis was that children with mutations in genes coding for Glutathione S-transferases (GST) have worse asthma outcomes compared to children with active type genotype. Data were collected in five populations. The rs1695 single nucleotide polymorphism (GSTP1) was determined in all cohorts (3692 children) and GSTM1 and GSTT1 null genotype were determined in three (2362 children). GSTT1 null (but not other genotypes) was associated with a minor increased risk for asthma attack and there were no significant associations between GST genotypes and asthma severity. Interactions between GST genotypes and SHS exposure or asthma severity with the study outcomes were non-significant. We find no convincing evidence that the GST genotypes studied are related to asthma outcomes.
AH Maitland-van der Zee received an unrestricted research grant for research on Pharmacogenomics in childhood asthma from Glaxo Smith Kleine. The contribution from GALA II to this work wassupported by grants from NIH to EG Burchard: The National Heart, Lung and Blood Institute (HL088133, HL078885, HL004464, HL104608 and HL117004); the National Institute of Environmental Health Sciences (ES015794); the National Institute on Minority Health and Health Disparities (MD006902); the National Institute of General Medical Sciences (GM007546). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
- glutathione S-transferase
- tobacco smoke