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Background: Increasing attention was focused on the β2-adrenergic receptor gene (ADRB2), whose genetic variability has been implicated as a risk factor for asthma-related phenotypes. However, only a few studies reported the associations by utilizing haplotypic approaches. We therefore examined the relationship of childhood wheezing illness with polymorphisms at codons 16 and 27, and evaluated the influence of polymorphisms individually and in combination as haplotypes. Methods: We conducted a genetic case–control study comprising 215 wheezing children and 183 nonwheezing controls, all of whom were selected from 2524 fourth- to ninth-grade schoolchildren in southern Taiwan. Results: All participants were homozygous at the ADRB2 Thr164 locus. After controlling for possible confounders, ADRB2 Glu27 allele was significantly associated with wheezing illness in all genetic models, but the risks on Arg16Gly genotypes were inconclusive. Estimated frequencies for the three main hyplotypes were Arg16/Gln27 57.2%, Gly16/Gln27 35.3%, Gly16/Glu27 7.4% in wheezing children, and Arg16/Gln27 56.3%, Gly16/Gln27 32.2%, Gly16/Glu27 10.4% in controls. The protective effect of Gly16/Glu27 haplotype remained relative to all other ADRB2 haplotypes [adjusted relative risk (aRR) = 0.58; 95% confidence interval (CI) 0.35–0.97]. As compared with children without Gly16/Glu27 haplotype, those with Gly16/Glu27 haplotype had a significantly lower risk for wheezing illness (aRR = 0.56; 95% CI 0.33–0.99). The copy numbers of Gly16/Glu27 haplotype also showed a clear dose-response relationship on the decreased risks. No significant association was found with the prevalence of wheezing illness for other haplotypes. Conclusion: We concluded that ADRB2 Glu27 allele and Gly16/Glu27 haplotype were significantly protective factors for wheezing illness in Taiwanese schoolchildren. [ABSTRACT FROM AUTHOR]

Background The β-chain of a high-affinity IgE receptor (FcℇRIβ) 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 FcℇRIβ 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 FcℇRIβ 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 FcℇRIβ 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. Conclusion The FcℇRIβ E237G allele may have a protective role in wheezing illness among Taiwanese schoolchildren, depending on airway oxidative stress levels. [ABSTRACT FROM AUTHOR]

Background: Polymorphisms at the glutathione S-transferase (GST) were associated with asthma-related phenotypes. We hypothesized that the GSTP1 and GSTM1 genotypes could modify the effects of household environmental tobacco smoke (ETS) on childhood wheezing illness. Methods: We conducted a case-control study comprised of 216 lifetime wheezing children and 185 nonwheezing controls, all of whom were selected from 2524 fourth- to ninth-grade school children in southern Taiwan. Results: Homozygous GSTP1 Ile-105 was significantly associated with current wheezing (OR = 1.78, 95% CI 1.04–3.12), but insignificantly associated with ever wheezing (OR = 1.26, 95% CI 0.82–1.94). The risks of ever or current wheezing on GSTM1 null genotype were positive but not statistically significant. Although household ETS exposure was not associated with wheezing illness, after excluding subjects having in utero ETS or active smoking habits, the adverse effects of household ETS exposure differed significantly by GSTP1-105 genotypes. In children without any ETS exposure at home, GSTP1 Ile-105 homozygosity was significantly related to increased risks for both ever wheezing (OR = 2.29, 95% CI 1.17–4.49) and current wheezing (OR = 4.86, 95% CI 1.86–12.70). In children with household ETS exposure, the risks of wheezing illness did not increase for those carrying two GSTP1 Ile-105 alleles. Children carrying any GSTP1 Val-105 allele were at a significantly greater risk of both ever and current wheezing when exposed to ETS, with a clear dose-response relationship to the number of smokers at home. Conclusion: Household ETS exposure is a modifiable cause of wheezing illness in a genetically susceptible subpopulation. [ABSTRACT FROM AUTHOR]