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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]

Nuclear grade 316LN stainless steel with different surface states are prepared: electropolished and ground to 240 grit. Surface topography, surface Volta potential distribution, and nanohardness distribution on cross-sectional surface are investigated, respectively. Oxide films on the ground and electropolished samples after immersion in high temperature pressurized (HTP) water for 0.1, 168, and 366 h were studied using various methods. Distinct from electropolished surface, the ground surface is featured by a rugged surface and a heterogeneous distribution of surface Volta potential. A thicker (∼28 μm) cold-worked layer was introduced by grinding.More crystallites were precipitated on the ground surface, resulting from the existence of high-energy sites with higher residual strain and higher electrochemical activity and a less protective inner layer. The oxidation rate was reduced by electropolishing and a thinner oxide film was formed, due to the formation of a more protective oxide film with higher content of chromium (Cr). The mechanism of oxide film formation was further discussed. [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 Attempts to identify predictors of atopic dermatitis (AD) have focused on genetic and immunologic factors. However, the role of neuro-mediators remains to be elucidated. Objective To evaluate nerve growth factor (NGF) and vaso-active intestinal peptide (VIP) in predicting paediatric AD and assess their correlation with intrinsic and extrinsic types of AD. Methods We performed a nested case–control study in the prospective Taiwan birth panel cohort study. Cord and maternal plasma and questionnaires were gathered at birth. During follow-up, we identified 40 available AD cases, which were matched to 80 unaffected controls chosen from this cohort. The concentrations of IgE, NGF, and VIP in cord and maternal plasma of these subjects were performed by ELISA. Receiver-operating characteristic (ROC) curves were generated to see how well each biomarker could predict AD. Results The NGF levels were significantly higher in AD patients than controls (mean±SD: 65.47±44.45 vs. 49.21±12.18 pg/mL for cord plasma and 89.68±41.04 vs. 66.96±23.05 pg/mL for maternal plasma) ( P<0.05). VIP levels were also higher but not statistically significant. Plasma NGF may be a better biomarker than IgE in detecting paediatric AD (area under the ROC curve=0.65 vs. 0.61 for cord plasma and 0.69 vs. 0.61 for maternal plasma). Maternal NGF levels were significantly higher in patients with both intrinsic (96.18±48.15 pg/mL) and extrinsic (86.18±37.23 pg/mL) types of AD compared with controls (66.96±23.05 pg/mL) ( P<0.05). We assessed a significant correlation between self-reported stress during pregnancy and maternal NGF levels ( r=0.22, P=0.02). Conclusion Our results suggest that NGF is a good alternative biomarker in predicting children with a risk of AD. [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]

Previous studies of predictors of atopic dermatitis (AD) in Asia have had limited sample size and small numbers of variables focused primarily on family history or dietary exposures. The purpose of this study was to evaluate the influence of various environmental risk factors for early infantile AD. We used multistage, stratified systematic sampling to recruit 2048 mother–child pairs from the Taiwan national birth registration in 2003. Information on environmental risk factors for infant AD gathered by questionnaire were available from 1760 infants at 6 months of age. Multiple logistic regression was used to estimate adjusted odds ratios (aORs) and their 95% confidence intervals (CIs) for risk factors for AD after adjusting for potential confounders. AD was noted in 118 of 1760 (6.7%) of the infants. After adjusting for maternal age and education, family history of atopy, infant gender, and gestational age, fungi on walls of the house [aOR 2.14 (95% CI 1.41–3.22)] and frequent use of microwave oven at home [aOR 1.71 (95% CI 1.13–2.58)] increased the risk of early infantile AD. This study suggests that environmental factors do play a role in early infantile AD. Fungi, a kind of aeroallergen, are especially important in humid climate as in Taiwan and their impacts might be felt at the early infant stage. The hazards of microwave use should be paid more attention. [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]

Background: Increasing attention was focused on the beta2-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.

This presentation focuses on the four most important skin diseases in Taiwan thought to be of environmental and/or occupational origin. The majority of work-related dermatoses are contact dermatitis patients. Among occupational contact dermatitis patients, 58.5% involved irritant and 41.5%, allergic dermatitis. Electronics, hairdressing, medical practice, and construction were the most important occupations causing contact dermatitis. An endemic occurrence of chronic arsenism causing hyperpigmentation, keratosis, and cancer has been reported in Taiwan. Arsenical skin cancers present as multiple lesions at different disease stages. The skin cancers are usually found in non-sun-exposed areas. UVB exerts an inhibitory effect on the proliferation of arsenical cancers; this may explain its non-sun-exposed nature. An outbreak of premalignant and malignant skin lesions was reported among paraquat manufacturers in 1985. The skin lesions were mainly distributed over the sun-exposed areas. Photodamage and photocarcinogenesis revealed a strong association with exposure to bipyridines among paraquat manufacturers. In 1979, a mass poisoning occurred in Taiwan from cooking oil contaminated by polychlorinated biphenyls (PCBs). Over 60% of patients were in grades O-II by the Japanese classification. The blood PCB levels of the Taiwanese patients were found to be higher than those of the Yusho subjects.

In 1979, a mass poisoning involving some 2,000 persons occurred in central Taiwan from cooking oil contaminated by polychlorinated biphenyls (PCBs) and their heat-degraded byproducts, including polychlorinated dibenzofurans (PCDFs). The responsible health department registered cases for clinical purposes between 1979 and 1983. The exposed persons are referred to as the "yucheng" (oil disease) cohort. PCBs and PCDFs are toxic chemicals widely dispersed in the environment and in human tissue, which persist long after exposure. The consequences of exposure to these agents are not well understood. We traced the cohort through December 31, 1991, and compared overall and cause-specific mortality of 1,837 "yucheng" subjects with age, gender, and calendar time-specific mortality rates for the Taiwan general population. Eighty-three deaths were identified from 23,404 observed person-years. Even though the overall standardized mortality ratio (SMR) was 0.8 (95% confidence interval (CI) 0.7-1.0), there was a substantial elevation in the mortality rate for chronic liver disease and cirrhosis (10 deaths, SMR = 2.7, 95% CI = 1.3-4.9). Mortality from malignant neoplasms and other causes was not significantly different from that of the Taiwan population. PCB/PCDF exposure appears to promote the development of severe liver disease, perhaps in combination with known risk factors such as infection with hepatitis B virus. Further follow-up of this young cohort is necessary to see if the consequences include hepatic cancer.