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Background Little is known about the effect of postnatal maternal psychologic problems on the development of childhood atopic disorders. Objectives To assess the association between early life maternal psychologic problems and atopic dermatitis ( AD) in children in a national birth cohort. Methods We used multistage, stratified systematic sampling to recruit 24,200 mother-newborn pairs from the Taiwan national birth registration. Maternal psychologic problems and potential confounders were gathered by the standard questionnaire at 6 months old. At 3 years of age, information about the development of AD was assessed by International Study of Asthma and Allergies in Childhood via home interviews. Multiple logistic regression analysis was performed to estimate the association of postnatal maternal psychologic problems (postpartum depression (PPD) and maternal mental health index) and AD. Results The prevalence of physician-diagnosed AD was 10.5%. PPD increased the risk of subsequent physician-diagnosed AD in children after adjusting for potential confounders and other maternal mental health index ( aOR = 1.42, 95% CI = 1.21-1.66). We observed that the risk of AD associated with PPD was not confounded by other social demographic factors such as maternal AD, maternal education, family income, breastfeeding, day care, and number of siblings. Conclusions Postpartum depression increased the risk of childhood AD even when other maternal mental health index and social demographic factors are considered. Early intervention of PPD might be helpful for AD prevention. [ABSTRACT FROM AUTHOR]

Background Hereditary and environmental factors contribute to the occurrence of atopic dermatitis (AD). However, the interaction of these two factors is not totally understood. Objectives To evaluate the early risk factors for infantile AD at the age of 6 months and to develop a predictive model for the development of AD. Methods In 2005, a representative sample of mother and newborn pairs was obtained by multistage, stratified systematic sampling from the Taiwan national birth register. Information on hereditary and environmental risk factors was collected by home interview when babies were 6 months old. Multivariate regression analysis was applied to determine the risk factors for AD in the infants. Results A total of 20 687 pairs completed the study satisfactorily. AD was diagnosed in 7·0% of 6-month-old infants by physicians. Parental asthma, atopic dermatitis and allergic rhinitis, and maternal education levels were risk factors for AD in infants. Among environmental factors, fungus on walls at home and renovation/painting in the house during pregnancy were significantly associated with early infantile AD. Using these factors, the probability of having infantile AD was estimated and grouped into low, high and very high. With five runs of tests in mutually exclusive subsets of this population, the likelihood of AD for 6-month-old infants was consistent in all the groups with the predictive model. The highest predicted probability of AD was 70·1%, among boys with maternal education levels > 12 years, both parents with AD, renovation and painting of the house during pregnancy and fungus on walls at home. The lowest probability was 3·1%, among girls with none of the above factors. Conclusions This investigation provides a technique for predicting the risk of infantile AD based on hereditary and environmental factors, which could be used for developing a preventive strategy against AD, especially among those children with a family history of atopy. [ABSTRACT FROM AUTHOR]

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 Parental atopy and environmental exposure are recognized risk factors for atopic eczema (AE) in childhood. However, the relative contributions of specific risk factors and the overall contributions of hereditary and environmental exposure remain unexplored. Objectives To identify risk factors, estimate the population attributable risk (PAR) of environmental exposure, and compare the AE data for boys vs. girls in primary-school children. Methods During a February to June 2001 cross-sectional, Taiwan-based questionnaire survey, we investigated 23 980 children from 22 primary schools, all located within 1 km of an air-monitoring station. Results The 12-month prevalence of AE was reported as 6·1% in boys and 4·9% in girls. In both sexes, the risk of AE was strongly associated with parental atopy and perceived ambient air pollution. The presence of cockroaches [odds ratio (OR) 1·18, 95% confidence interval (CI) 1·00–1·40] and visible mould on walls at home (OR 1·46, 95% CI 1·22–1·70) were also significantly related to AE for girls; however, only visible mould on walls (and not the presence of cockroaches) at home was related to AE for boys (OR 1·40, 95% CI 1·18–1·66). While mutually adjusted models were applied, we found adjusted ORs and PARs were similar in boys and girls in hereditary and outdoor environmental factors. The PAR of indoor environmental factors was higher in girls (8·4%) than in boys (5·5%). There was no interaction between parental atopy and environmental factors. Conclusions Parental atopy contributed more to AE than indoor or outdoor environmental factors. Girls may be more susceptible to indoor environmental factors than boys. [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]