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 Although the development of allergic rhinitis (AR) is associated with multiple genetic and hygienic environmental factors, previous studies have focused mostly on the effect of a single factor on the development of AR. This study aimed to investigate the combined effect of multiple genetic and hygienic environmental risk factors on AR development in school children. Methods We conducted a cross-sectional study, comprising 1,797 children aged 9–12 years. Weighted environmental risk score (ERS) was calculated by using four hygienic environmental factors, including antibiotic use during infancy, cesarean section delivery, breast milk feeding, and having older siblings. Weighted polygenic risk score (PRS) was calculated by using four single nucleotide polymorphisms (SNPs), including interleukin-13 (rs20541), cluster of differentiation 14 (rs2569190), toll-like receptor 4 (rs1927911), and glutathione S-transferase P1 (rs1695). Multivariable logistic regression analysis was used. Results More than three courses of antibiotic use during infancy increased the risk of current AR (adjusted odd ratio [aOR], 2.058; 95% confidence interval [CI]: 1.290–3.284). Having older siblings, especially >2 (aOR, 0.526; 95% Cl: 0.303–0.913) had a protective effect. High ERS (>median; aOR, 2.079; 95% Cl: 1.466–2.947) and PRS (>median; aOR, 1.627; 95% Cl: 1.117–2.370) increased the risk of current AR independently. Furthermore, children who had both high ERS and PRS showed a higher risk of current AR (aOR, 3.176; 95% Cl: 1.787–5.645). Conclusions Exposure to multiple hygienic risk factors during early life increases the risk of AR in genetically susceptible children. Key words: Allergic rhinitis, Hygiene, Genes, Risk factors, Child, Gene-environment interaction, Anti-bacterial agent

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.