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Background  Lung growth  in utero  and lung function loss during adulthood can be affected by exposure to environmental tobacco smoke (ETS). The underlying mechanisms have not been fully elucidated. Both ETS exposure and single nucleotide polymorphisms (SNPs) in  Glutathione S - Transferase  ( GST )  Omega  genes have been associated with the level of lung function. This study aimed to assess if  GSTO  SNPs interact with ETS exposure  in utero  and during adulthood on the level of lung function during adulthood.    Methods  We used cross-sectional data of 8,128 genotyped participants from the LifeLines cohort study. Linear regression models (adjusted for age, sex, height, weight, current smoking, ex-smoking and packyears smoked) were used to analyze the associations between  in utero , daily and workplace ETS exposure,  GSTO  SNPs, the interaction between ETS and  GSTO s, and level of lung function (FEV 1 , FEV 1 /FVC). Since the interactions between ETS and  GSTO s may be modified by active tobacco smoking we additionally assessed associations in never and ever smokers separately. A second sample of 5,308 genotyped LifeLines participants was used to verify our initial findings.    Results  Daily and workplace ETS exposure was associated with significantly lower FEV 1  levels.  GSTO  SNPs (recessive model) interacted with  in utero  ETS and were associated with higher levels of FEV 1 , whereas the interactions with daily and workplace ETS exposure were associated with lower levels of FEV 1 , effects being more pronounced in never smokers. The interaction of  GSTO2  SNP rs156697 with  in utero  ETS associated with a higher level of FEV 1  was significantly replicated in the second sample. Overall, the directions of the interactions of  in utero  and workplace ETS exposure with the SNPs found in the second (verification) sample were in line with the first sample.    Conclusions   GSTO  genotypes interact with  in utero  and adulthood ETS exposure on adult lung function level, but in opposite directions.

GST-omega genes interact with environmental tobacco smoke on adult level of lung function