Abstract
BackgroundA number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma.MethodsA case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale.ResultsAfter excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant.ConclusionsIn the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma.
Highlights
Asthma is a common chronic airway inflammatory disorder, characterized by hyper responsiveness, obstruction and chronic inflammation of the airway [1]
The reference sequence numbers, minor allele frequencies, and Hardy– Weinberg equilibrium (HWE) tests of Single nucleotide polymorphism (SNP) included in the present study were shown in Additional file 1: Table S4
Associations between inflammation‐related genetic polymorphisms and childhood asthma We evaluated the associations between the SNPs and childhood asthma in different genetic models
Summary
Asthma is a common chronic airway inflammatory disorder, characterized by hyper responsiveness, obstruction and chronic inflammation of the airway [1]. It has emerged as a major global public health problem. The Third Nationwide Survey of Childhood Asthma in Urban Areas of China (2010) found that the prevalence of asthma in children under 14 years had increased from 2.0% in 2000 to 3.0%, and Shanghai had the highest rate of 7.6% [2]. A number of studies have examined the association between mold exposure and childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma
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