Abstract
BackgroundLung 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.MethodsWe 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 GSTOs, and level of lung function (FEV1, FEV1/FVC). Since the interactions between ETS and GSTOs 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.ResultsDaily and workplace ETS exposure was associated with significantly lower FEV1 levels. GSTO SNPs (recessive model) interacted with in utero ETS and were associated with higher levels of FEV1, whereas the interactions with daily and workplace ETS exposure were associated with lower levels of FEV1, effects being more pronounced in never smokers. The interaction of GSTO2 SNP rs156697 with in utero ETS associated with a higher level of FEV1 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.ConclusionsGSTO genotypes interact with in utero and adulthood ETS exposure on adult lung function level, but in opposite directions.
Highlights
Lung growth in utero and lung function loss during adulthood can be affected by exposure to environmental tobacco smoke (ETS)
It has been very well established that genetic factors contribute to lung function level [12], less is known about how genetic factors modify effects of ETS exposure on the level of lung function during the life-span
The directions of the interactions of in utero and workplace ETS exposure with the Single nucleotide polymorphism (SNP) found in the second sample were in line with the first sample, but effect estimates were somewhat smaller and not always significant
Summary
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. Lung function loss is common in chronic respiratory diseases like chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and interstitial lung fibrosis, and associates with all-cause and other specific mortality [1,2]. Another study could not replicate this association between rs156697 and FEV1, but found an association with COPD, defined by lower lung function [25] It is unknown whether GSTO1 and GSTO2 SNPs modify effects of ETS exposure on the level of lung function
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