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.