title: GSTM1, GSTP1, prenatal smoke exposure, and atopic dermatitis.
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.
authors.affiliation: Department of Pediatrics, Taipei Hospital Department of Health, Taipei, Taiwan.
authors.forename: I-Jen
authors.initials: IJ
authors.lastname: Wang
authors.forename: Yueliang Leon
authors.initials: YL
authors.lastname: Guo
authors.forename: Tien-Jen
authors.initials: TJ
authors.lastname: Lin
authors.forename: Pau-Chung
authors.initials: PC
authors.lastname: Chen
authors.forename: Yu-Nian
authors.initials: YN
authors.lastname: Wu
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D002675:Child, Preschool; D003367:Cotinine / Q000097:blood; D004252:DNA Mutational Analysis; D003876:Dermatitis, Atopic / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease; D051549:Glutathione S-Transferase pi / Q000235:genetics*; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011110:Polymorphism, Genetic; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D015995:Prevalence; D012907:Smoking
chemical_list: D003367:Cotinine; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; C496556:GSTP1 protein, human