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.

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.