Background: Studies that examine a link between long-term exposure to ambient particulate matter (PM) and atopic dermatitis (AD) in children are lacking. This longitudinal study aimed to investigate the effect of long-term exposure to PM on AD in infants. Methods: A total of 150 infants diagnosed with AD before age 2 were enrolled and followed until age 3 in Seoul, Korea. Long-term exposures to ambient PM with an aerodynamic diameter ≤10 μm (PM 10) from birth to age 3 were assessed at an individual level. Effects of long-term exposure to PM 10 on AD persistence and sensitization to aeroallergens were evaluated using Cox proportional hazard regression models after adjusting for potential confounders. Results: Out of 150 infants, 54 (36.0%) showed remission of AD at age 3. The risk of AD persistence at age 3 significantly increased with an increase in long-term exposure to PM 10 [Hazard Ratio (HR) = 1.07, 95% Confidence Interval (CI): 1.01−1.12, p = .017 per 1 µg/m 3]. Moderate-to-severe AD at enrollment was more likely to persist at age 3 with increased exposure to PM 10 ( p < .05), whereas the persistence of mild AD was not influenced by PM 10 exposure. Long-term exposure to PM 10 increased the risk of sensitization to pollen (HR = 1.14, 95% CI: 1.02−1.27, p = .021). However, it did not affect sensitization to house dust mites or pet allergens. Conclusions: An early-life long-term exposure to ambient PM 10 in infants with AD decreases remission and increases sensitization to pollen at age 3.

Background: The effect of prenatal secondhand smoke (SHS) exposure on childhood atopic dermatitis (AD) remains controversial. We aimed to investigate the association between prenatal SHS and childhood AD in a general population-based birth cohort. Methods: Patients included 2,360 mother–child pairs from the Cohort for Childhood Origin of Asthma and Allergic diseases (COCOA), stratified into 0–3, 4–6, and 7–9 years age groups. Prenatal SHS exposure was assessed using questionnaires. AD diagnosis and symptom assessments were conducted through annual visits by pediatric allergists. Skin prick tests for 18 allergens were conducted. Serum total IgE and eosinophil levels were measured at birth and ages 3 and 7 years. Maternal urine cotinine concentrations were measured at week 36 of gestation. Multivariate logistic regression was performed. Results: Children aged 7–9 years exposed to prenatal SHS were significantly more likely to have an AD diagnosis (aOR 1.670, 95% CI: 0.995–2.804) and current AD (aOR 1.823, 95% CI: 1.051–3.161). This association in AD diagnosis was stronger in children with sensitization (aOR 2.205, 95% CI: 1.048–4.642). Higher maternal urine cotinine levels increased the risk of current AD at ages 4–6 (aOR 2.816, 95% CI: 1.053–7.529). Children exposed to prenatal SHS were more likely to have a late-onset phenotype of AD (aOR 1.663, 95% CI: 1.038–2.664). Conclusion: SHS exposure during pregnancy was associated with late childhood AD. Prevention of prenatal SHS exposure is necessary to reduce the risk of AD in schoolchildren.

Background: Although atopic dermatitis (AD) is associated with certain gene variants, the rapidly increasing incidence of AD suggests that environmental factors contribute to disease development. In this study, we investigated the association of AD incidence and phenotype with antibiotic exposure within 6 months of age, considering the dose administered and genetic risk. Methods: This study included 1,637 children from the COCOA birth cohort. Pediatric allergists assessed the presence of AD at each visit and obtained information about antibiotic exposure for more than 3 days. IL-13 (rs20541) polymorphism was genotyped by the TaqMan method. We stratified the AD phenotypes into 4 groups and used multinomial logistic regression models for analysis. Results: Antibiotic exposure within 6 months of age was found to increase the risk of AD within 3 years of life (aOR=1.40, 95%, CI 1.09–1.81) in dose-dependent manner. Antibiotic exposure more than twice increased the risk of the early-persistent AD phenotype (aOR=2.50, 95% CI 1.35–4.63). There was a weak interaction between genetic polymorphisms and environmental factors on the development of AD (p for interaction=0.06). Children with the IL-13 (rs20541) GA+ AA genotype have a higher risk of the early-persistent AD phenotype when exposed to antibiotics more than twice than those with the IL-13 (rs20541) GG genotype and without exposure to antibiotics (aOR=4.73, 2.01–11.14). Conclusion: Antibiotic exposure within 6 months was related to the incidence of early-persistent AD and a dose-dependent increase in the incidence of AD in childhood, whose effect was modified by the IL-13 (rs20541) genotype.