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.

Abstract Background: The level of pollen in Korea has increased over recent decades. Research suggests that pollen-food allergy syndrome (PFAS) may be more frequent in childhood than previously recognized. We aimed to investigate the prevalence and characteristics of PFAS in children aged 6–10 years from a general population-based birth cohort. Methods: We analyzed 930 children from the COhort for Childhood Origin of Asthma and allergic diseases (COCOA) birth cohort. Allergic diseases were diagnosed annually by pediatric allergists. The skin prick tests were performed with 14 common inhalant allergens and four food allergens for children aged 3 and 7 years. Results: Of the 930 eligible children, 44 (4.7%) aged 6–10 years were diagnosed with. The mean age at onset was 6.74 years. PFAS prevalence was 7.2% among children with allergic rhinitis (AR) and 19.1% among those with pollinosis, depending on comorbidity. PFAS was more prevalent in schoolchildren with atopic dermatitis, food allergy, and sensitization to food allergens and grass pollen in early childhood. In schoolchildren with AR, only a history of food allergy before 3 years increased the risk of PFAS (aOR 2.971, 95% CI: 1.159–7.615). Conclusion: Food allergy and food sensitization in early childhood was associated with PFAS in schoolchildren with AR. Further study is required to elucidate the mechanism by which food allergy in early childhood affects the development of PFAS.

Background: Phthalates can cause respiratory and immunological disorders. However, little is known about the role of serum periostin and YKL-40 levels in mediating the effects of phthalates. We investigated the mediating role of these biomarkers in the relationship between phthalates and airway dysfunction. Methods: A total of 487 children (aged 10 to 12 years-old) were examined. Four high-molecular-weight phthalate (HMWP) [Σ4HMWP] metabolites and 3 low-molecular-weight phthalate (LMWP) [Σ3LMWP] metabolites in urine samples were measured. Serum periostin and YKL-40 levels were measured. Airway function was measured using impulse oscillometry. A mediation model was used to quantify the mediating effects of periostin and YKL-40 on airway dysfunction. Results: After adjustment for height, gender, BMI z-score, aeroallergen sensitization, secondary smoking, and vitamin D level, the level of urinary Σ3LMWP metabolites was significantly associated with respiratory system resistance at 5 Hz (Rrs5; adjusted β: 0.020, 95% CI: 0.005 to 0.034; P = .010). The levels of urinary Σ4HMWP and Σ3LMWP metabolites were significantly associated with periostin level, but not with YKL-40 level. In addition, the periostin level was associated with Rrs5 (adjusted β: 0.048, 95% CI: 0.015 to 0.081; P = .005) and Rrs20-5 (adjusted β: 0.040, 95% CI: 0.011 to 0.069; P =.007). Serum periostin level had a significant effect in mediating the relationship between Σ3LMWP and Rrs5 (13.9%, 95% CI: 10.7 to 77.0; P < .001). Conclusion: Exposure to LMWPs was significantly associated with airway dysfunction, and this effect was partially attributable to increased serum periostin level.

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.

Background The association between dyslipidemia and atopic dermatitis in children is unclear. This study investigated the association between dyslipidemia and atopic dermatitis in children by analysis of disease onset, risk factors, and disease severity. Methods Subset I examined 7 year-old children in elementary school (n = 248) and Subset II was a retrospective long-term follow-up hospital based-study (n = 52,725) conducted from 1986 to 2016 that used propensity score matching. In the Subset I Study, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) were determined, and the severity of atopic dermatitis was determined using SCORing Atopic Dermatitis (SCORAD). In the Subset II Study, the time of atopic dermatitis onset was determined for asymptomatic subjects whose TC levels were below or above 170 mg/dL. Results Our Subset I Study indicated that children with atopic dermatitis (n = 69, 27.8%) had significantly higher levels of TC and TG, and that disease severity had significant associations with high levels of TC and TG, and a low level of HDL-C. Our Subset II Study (1,722 with high TC and 6,735 with normal TC after propensity score matching) indicated the high TC group had a greater hazard ratio (HR) for the onset of atopic dermatitis (consensus-based HR: 2.47; 95% CI: 1.23, 5.06, P = 0.012) during 5 years. Conclusion An abnormal blood lipid profile in children is associated with the presence and severity of atopic dermatitis. The risk of atopic dermatitis onset was significantly greater with high levels of TC.