title: Associations of FcepsilonRIbeta E237G polymorphism with wheezing in Taiwanese schoolchildren.
abstract: BACKGROUND
  The beta-chain of a high-affinity IgE receptor (FcepsilonRIbeta) has been proposed as a candidate gene for atopic diseases, but previous studies have come to inconsistent conclusions. Because some air pollutants would produce oxidative stress, increase serum IgE, and trigger T-helper type 2 (Th2)-type airway inflammation, the associations of FcepsilonRIbeta polymorphism with wheezing illness may vary by their exposures and variants of oxidant defence genes. The purpose of this study was to investigate the association of FcepsilonRIbeta E237G polymorphism with wheezing illness and to determine whether these associations vary with air pollution and glutathione S-transferase (GST) P1-105 and M1 genotypes.
  
  
  METHODS
  In 2001, we conducted a case-control study comprised of 214 children with any history of wheezing and 185 non-wheezing controls, all of whom were selected from 2558 fourth- to ninth-grade schoolchildren in southern Taiwan. We examined differences in associations with ambient air pollution and by GST genotypes.
  
  
  RESULTS
  Compared with the FcepsilonRIbeta EE genotype, children with the G allele had a significantly reduced risk of lifetime wheezing with low-ozone exposure [adjusted odds ratio (aOR)=0.25, 95% confidence interval (CI) 0.08-0.69]. The risk was not reduced in children living in high-ozone communities (aOR=0.98, 95% CI 0.57-1.67). This difference in genotypic effects between low- and high-pollution environments was statistically significant. The reduction of the protective effect from the G allele with higher air pollution was most marked in the GSTP1-105 Ile/Val or Val/Val and GSTM1 null groups.
  
  
  CONCLUSIONS
  The FcepsilonRIbeta E237G allele may have a protective role in wheezing illness among Taiwanese schoolchildren, depending on airway oxidative stress levels.
authors.affiliation: Department of Occupational and Environmental Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
authors.forename: Y-L
authors.initials: YL
authors.lastname: Lee
authors.forename: F D
authors.initials: FD
authors.lastname: Gilliland
authors.forename: J-Y
authors.initials: JY
authors.lastname: Wang
authors.forename: Y-C
authors.initials: YC
authors.lastname: Lee
authors.forename: Y L
authors.initials: YL
authors.lastname: Guo
mesh_terms: D000397:Air Pollution; D000483:Alleles; D016022:Case-Control Studies; D002648:Child; D004781:Environmental Exposure; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D018698:Glutamic Acid; D005998:Glycine; D006801:Humans; D008297:Male; D010126:Ozone; D011110:Polymorphism, Genetic; D017455:Receptors, IgE / Q000235:genetics*; D012135:Respiratory Sounds / Q000235:genetics*; D018570:Risk Assessment; D012574:Schools; D013624:Taiwan
chemical_list: C502447:MS4A2 protein, human; D017455:Receptors, IgE; D018698:Glutamic Acid; D010126:Ozone; D005998:Glycine