Abstract
Introduction: In utero tobacco exposure is associated with reduced lung function in infancy, an effect influenced by glutathione-s-transferase (GST) genotype. GST enzymes are involved in detoxification of xenobiotics, activity levels being dependent on the genotype. Null GSTT1 and GSTM1 polymorphisms are associated with zero production of their respective enzymes. We hypothesised that GST genotype would continue to exert an influence on the negative effect of in utero tobacco exposure on lung function from infancy into adulthood.
Methods: In the Perth Infant Asthma Follow up study (n=253), in utero smoking history was collected from parents antenatally and the children had lung function measured at 1, 6, 12 months, 6, 11, 18 and 24 years of age. GSTM1 and GSTT1 genotype was assessed by PCR in 179 of the cohort. Longitudinal analysis was done using linear mixed modelling.
Results: Exposure to maternal in utero tobacco was associated with lower FEV1 and FVC from 6 to 24 years (mean deficit -4.9% predicted, p=0.016 and -6% predicted, p=0.003 respectively). However, among those exposed to in utero tobacco, those with GSTT1 null had a 15% predicted deficit in FVC compared with those with GSTT1 non-null (p=0.001) and a 10% deficit in FEV1, although this did not meet statistical significance (p=0.059).
Conclusion: Our data suggest that gene-environment interactions in utero have lifelong consequences on the respiratory health of children and adults. Anti-oxidant treatment targets in utero offer a potential preventative strategy which requires further study.
Footnotes
Cite this article as: European Respiratory Journal 2018 52: Suppl. 62, OA3586.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2018