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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]

Prior studies in hairless mice have demonstrated that acute barrier disruption by acetone treatment increases the molecular weight (MW) cutoff of polyethylene glycol (PEG) penetration through the skin. The objective of the present study was to further investigate the dependence of permeability on MW with different forms of barrier disruption. A series of PEGs ranging in MW from near 300 to over 1000 Da were used to study the effects of tape stripping and sodium dodecyl sulfate (SDS) treatment on the MW permeability profiles of mouse skin in vitro. The 12-h percutaneous penetration of all the PEG 300, 600, and 1000 oligomers generally increased as a function of transepidermal water loss (TEWL) of the skin, either tape-stripped or SDS-treated. In addition, the total penetration of PEG oligomers across control skin, and skin tape-stripped and SDS-treated to different degrees of barrier disruption progressively decreased with increasing MW. There were no significant differences in the percutaneous penetration of the PEG oligomers between skin tape-stripped and SDS-treated to the same degree of barrier disruption. The penetration enhancement relative to control skin was more prominent with larger molecules. The MW cutoff for skin penetration increased with the degree of barrier disruption irrespective of the treatment applied, and was 986 Da (tape stripping) and 766 Da (SDS treatment) at TEWL levels in the range 10–20 g/m2 per h in comparison with 414 Da for control skin. In accordance with previous findings in acetone-treated mouse skin, the results strongly suggest that, irrespective of the form of barrier disruption applied, not only higher amounts but also more varieties of chemicals (larger molecules) may penetrate skin with a compromised barrier than normal skin. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that permeability barrier disruption by acetone treatment significantly enhances skin permeability to both hydrophilic and amphipathic compounds, but not to highly lipophilic compounds. The purpose of the present study was to investigate the dependence of permeability on molecular weight (MW) in acetone-disrupted hairless mouse skin in contrast to normal skin. Penetration of polyethylene glycol (PEG) 300, 600, and 1000 over 12 h was measured using diffusion cells. High-performance liquid chromatographic methods with refractive index detection were used to separate and quantitate the individual oligomeric species in the PEG samples. Percutaneous penetration of PEGs exhibited slightly steeper MW dependency at a transepidermal water loss (TEWL) of 30–41 g/m2 per h in comparison with TEWLs of 0–10 (control skin), 10–20, and 20–30 g/m2 per h, with a higher percentage of smaller oligomer PEGs penetrating than larger ones. Increasing the TEWL of the skin increased the penetration of all the PEG oligomers, and the degree of the enhancement relative to penetration through control skin increased with MW and was maximal for oligomers with a MW ranging from 326 to 414 Da. Within the limit of quantitation of the assay, the MW cut-off for PEG penetration across mouse skin with TEWLs of 0–10, 10–20, and 20–30 g/m2 per h was 414, 590, and 942 Da, respectively, while all the measurable oligomers up to MW 1074 Da were able to penetrate skin with TEWLs in the range 30–41 g/m2 per h. The results suggest that not only higher amounts but also more varieties of chemicals may penetrate skin with a compromised barrier than normal skin, implying a higher risk of intoxication and hypersensitization by environmental agents through diseased skin with impaired barrier function. [ABSTRACT FROM AUTHOR]

The intercellular lipid lamellae of the stratum corneum (SC) is believed to provide the permeability barrier of the epidermis. Previous functional studies have demonstrated an increase in the transepidermal water loss (TEWL) after long-term use of topical corticosteroids (TCS); however, direct morphological confirmation of this barrier abnormality is still lacking. The aim of this study was to determine whether any abnormality could be detected in the structure of the SC intercellular lipid lamellae in patients after long-term TCS. Atrophic skin and untreated normal skin of 10 patients after long-term TCS were examined by transmission electron microscopy using ruthenium tetroxide-fixed tissue for the multilamellar lipid sheets of SC, and oil red 0 stain for neutral lipids of the SC. Layers of the SC were evaluated by 0.1% methylene blue slain after alkaline expansion, and TEWL was measured by Evaporimeter EP1. The TCS-treated atrophic skin had fewer layers of horny cells, mean 9.4 layers, than the normal control skill, 18 layers (P<0.001) and increased TEWL of 21.3 g/m² compared with the control skin TEWL of 6.7 g/m² (P<0.01). The mean neutral lipid content of the SC was also significantly lower (P<0.001). Moreover, ultrastructural studies revealed a marked decrease in both the numbers of intercellular lipid lamellae of SC and membrane-coating granules of stratum granulosum in the atrophic skin. These results suggest that the diminution in the SC intercellular lipid lamellae and SC cell layers play an important part in the pathogenesis of barrier dysfunction after long-term use of TCS. [ABSTRACT FROM AUTHOR]