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Background: Hereditary and environmental factors have been related to the occurrence of atopic dermatitis (AD) in early childhood. However, the role of prenatal and early postnatal exposure to air pollutants has not been totally elucidated., Objectives: To evaluate the association between prenatal air pollutant exposure and occurrence of AD., Methods: In total 24 200 infant-mother pairs were recruited to participate in the Taiwan Birth Cohort Study in 2005 using multistage stratified sampling. Medical history, including physician-diagnosed AD, was inquired by questionnaire at the infant's age of 6 months. Monthly averages of five criteria air pollutants - NO2 , CO, O3 , SO2 and PM10 - were retrieved from 66 air-quality-monitoring stations, and interpolated to all administrative districts using the kriging method. Exposure data during each of the three gestational trimesters and three months after birth were calculated for each study subject, and odds ratios (ORs) of AD occurrence were calculated by logistic regression., Results: Among the participants, 16 686 mother-infant pairs were qualified for and included in the analysis. Among them, 1206 infants (7·2%) had been diagnosed as having AD before the age of 6 months, and the prevalence was higher in boys (8·3%) than in girls (6·1%). The occurrence of AD was significantly associated with CO exposure during the whole gestational period [adjusted OR (aOR) 1·37, 95% confidence interval (CI) 1·06-1·78] and the first trimester (aOR 1·51, 95% CI 1·16-1·97). We did not observe any significant association among the other air pollutants during either the whole gestational period or any period of the three trimesters and 3 months after birth., Conclusions: Our study found a relationship between AD occurrence and gestational exposure to CO, where exposure during the first trimester seemed to be the most important., (© 2015 British Association of Dermatologists.)

Background: Polymorphisms at the glutathione S-transferase (GST) P1 locus were associated with asthma-related phenotypes and bronchial hyper-responsiveness., Objective: This study investigated whether GSTP1 genotypes and outdoor air pollution were interactive risk factors on childhood asthma., Methods: Four hundred and thirty-six subjects were recruited for oral mucosa samplings from 2853 fourth- to ninth-grade schoolchildren from three districts with different air pollution levels in southern Taiwan. PCR-based assays were performed by oral mucosa DNA to determine GSTP1 genotypes. We also conducted a nested case-control study comprising 61 asthmatic children and 95 controls confirmed by International Study of Asthma and Allergies in Childhood questionnaire results and methacholine challenge test. Multiple logistic regression was used to adjust for potential confounding factors., Results: All participants were homozygous at the Ala-114 locus. Although only a marginally significant association existed between the frequency of homozygosity at the Ile-105 locus and asthma when air pollution was not considered, we found a significant gene-environmental interaction between GSTP1-105 alleles and air pollution after adjusting for confounders (P=0.035). Specifically, we found that compared with participants carrying any Val-105 allele in low air pollution, those who are Ile-105 homozygotes in high air pollution district had a significantly increased risk of asthma (adjusted odds ratio (AOR)=5.52, 95% confidence interval (CI)=1.64-21.25). Compared with participants carrying any Val-105 allele, in high air pollution district, children with Ile-105 homozygotes had a significantly increased risk of asthma (AOR=3.79, 95% CI=1.01-17.08), but those who carried two Ile-105 alleles in low or moderate air pollution districts did not show similar tendencies. The risk of asthma also revealed a clear dose-response relationship with outdoor air pollution in children with Ile-105 homozygotes., Conclusion: Our result suggests a gene-environmental interaction between GSTP1-105 genotypes and outdoor air pollution on childhood asthma.

This study compared the prevalence of asthma with climate and air pollutant data to determine the relationship between asthma prevalence and these factors. We conducted a nationwide survey of respiratory illness and symptoms in middle-school students in Taiwan. Lifetime prevalences of physician-diagnosed asthma and of typical symptoms of asthma were compared to air monitoring station data for temperature, relative humidity, sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with aerodynamic diameter [less than/equal to] 10 microm (PM(10)). A total of 331,686 nonsmoking children attended schools located within 2 km of 55 stations. Asthma prevalence rates adjusted for age, history of atopic eczema, and parental education were associated with nonsummer (June-August) temperature, winter (January-March) humidity, and traffic-related air pollution, especially carbon monoxide and nitrogen oxides, for both girls and boys. Nonsummer temperature, winter humidity, and traffic-related air pollution, especially carbon monoxide and nitrogen oxides, were positively associated with the prevalence of asthma in middle-school students in Taiwan.

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: There is evidence that long term exposure to ambient air pollution increases the risk of childhood asthma, but the role of different sources and components needs further elaboration. To assess the effect of air pollutants on the risk of asthma among school children, a nationwide cross sectional study of 32 672 Taiwanese school children was conducted in 2001. Methods: Routine air pollution monitoring data for sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (O3), carbon monoxide (CO), and particles with an aerodynamic diameter of 10 μm or less (PM10) were used. Information on individual characteristics and indoor environments was from a parent administered questionnaire (response rate 93%). The exposure parameters were calculated using the mean of the 2000 monthly averages. The effect estimates were presented as odds ratios (ORs) per 10 ppb changes for SO2, NOx, and O3, 100 ppb changes for CO, and 10 μg/m3 changes for PM10. Results: In a two stage hierarchical model adjusting for confounding, the risk of childhood asthma was positively associated with O3 (adjusted OR 1.138, 95% confidence interval (CI) 1.001 to 1.293), CO (adjusted OR 1.045, 95% Cl 1.017 to 1.074), and NOx (adjusted OR 1.005, 95% CI 0.954 to 1.117). Against our prior hypothesis, the risk of childhood asthma was weakly or not related to SO2 (adjusted OR 0.874, 95% CI 0.729 to 1.054) and PM10 (adjusted OR 0.934, 95% CI 0.909 to 0.960). Conclusions: The results are consistent with the hypothesis that long term exposure to traffic related outdoor air pollutants such as NOx, CO, and O3 increases the risk of asthma in children. [ABSTRACT FROM AUTHOR]

To investigate whether changes in outdoor air pollutants, meteorology data, certain personal or environmental factors explain the changing prevalence of current wheeze, ever wheeze and physician-diagnosed asthma among Taiwanese middle-schools children.Data from two cross-sectional national surveys between 1995 and 2001 were used. Study population was limited from 22 middle schools located within one-kilometer catchment areas of 22 air-monitoring stations in Taiwan. The main outcome measures were physician-diagnosed asthma, lifetime wheezy symptoms, and wheeze in current 12 months, as reported by parents. The effects of several personal and environmental factors on the change of three diseases were assessed by multiple logistic regression. Changes in air pollutants and meteorology data in communities were also compared with estimated prevalence changes of three diseases.44,118 data from 1995 survey and 11,738 data from 2001 survey were left for final analysis. The prevalence of ever wheeze and physician-diagnosed asthma increased from 1995 to 2001 in both sexes. Prevalence of current wheeze decreased significantly in boys but not in girls. Three diseases were more commonly reported among children of lower age, higher parental education level, higher parental reported ambient air pollution level, and those who were exposed to ETS or incense, performed less exercise, and suffered from atopic eczema. When adjusted for these factors, the relative odds of three diseases (2001 to 1995) did not show significant changes. Communities with lower decreasing rate in sulfur dioxides level had higher increasing percentage in prevalence of three diseases.Changes in listed personal and environmental factors did not seem to explain any of the observed changes in prevalence. However, correlates of these factors which have changed over time may still underlie recent changes in diseases. Sulfur dioxides may play an essential role as an indicator in trends of three diseases. [ABSTRACT FROM AUTHOR]