GSTM1, GSTP1, prenatal smoke exposure, and atopic dermatitis

Ann Allergy Asthma Immunol. 2010 Aug;105(2):124-9. doi: 10.1016/j.anai.2010.04.017. Epub 2010 Jun 11.

Abstract

Background: The increase in the prevalence of atopic dermatitis (AD) is likely to involve changes in specific environmental exposures among genetically susceptible individuals.

Objective: To evaluate the effect of glutathione S-transferase (GST) genotype polymorphisms and prenatal smoke exposure on pediatric AD on the basis of the cord blood cotinine levels.

Methods: We conducted a case-control study composed of 34 children with AD and 106 non-AD controls, all of whom were selected from 483 participants in the Taiwan Birth Panel cohort study. Cord blood samples and information on perinatal factors of children were gathered at birth. At 2 years of age, information about the development of AD and environmental exposures was collected. We compared AD with non-AD children for GTM1 and GSTP1 polymorphisms stratified by the cotinine level. Multiple logistic regressions were performed to estimate the association of genotype polymorphisms and cotinine levels with AD.

Results: GSTM1 null and GSTP1 Ile/Ile genotypes showed a significant increase in the risk of AD (odds ratio [OR], 3.61; 95% confidence interval [CI], 1.40-9.31; and OR, 3.11; 95% CI, 1.30-7.46; respectively). In children with a cotinine level less than 0.1 ng/mL, the risk of AD increased for those carrying 2 GSTP1 Ile-105 alleles (OR, 6.63; 95% CI, 1.46-30.18). In children a with cotinine level of 0.1 ng/mL or greater, the GSTM1 null genotype was significantly related to AD (OR, 5.21; 95% CI, 1.32-20.58).

Conclusions: Within groups of children, genetic polymorphisms in GSTM1 and GSTP1 may be responsible for differences in susceptibility to AD with regard to prenatal smoke exposure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Child, Preschool
  • Cotinine / blood
  • DNA Mutational Analysis
  • Dermatitis, Atopic / blood
  • Dermatitis, Atopic / epidemiology
  • Dermatitis, Atopic / genetics*
  • Female
  • Follow-Up Studies
  • Genetic Predisposition to Disease
  • Glutathione S-Transferase pi / genetics*
  • Glutathione Transferase / genetics*
  • Humans
  • Infant
  • Infant, Newborn
  • Male
  • Polymorphism, Genetic
  • Pregnancy
  • Prenatal Exposure Delayed Effects / blood
  • Prenatal Exposure Delayed Effects / epidemiology
  • Prenatal Exposure Delayed Effects / genetics*
  • Prevalence
  • Smoking*

Substances

  • GSTP1 protein, human
  • Glutathione S-Transferase pi
  • Glutathione Transferase
  • glutathione S-transferase M1
  • Cotinine