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Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case-control
Yu Zhang1,2, Li Hua3, Quan-Hua Liu3
1Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Background:
A 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.
Methods:
A 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.
Results:
After 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.
Conclusions:
In 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.
Insights
Mold exposure and a specific gene variant significantly increase childhood asthma risk. This gene-environment interaction highlights the need to consider genetic factors in asthma prevention strategies.
Area of Science:
- Environmental Health
- Genetics
- Pediatrics
Background:
- Inconsistent findings exist regarding mold exposure and childhood asthma.
- Key genes influencing childhood asthma pathogenesis are often overlooked.
- Limited research explores gene-mold exposure interactions in childhood asthma.
Purpose of the Study:
- To investigate the interaction between inflammation-related genes and mold exposure on childhood asthma.
- To identify specific genetic variants that modify the effect of mold exposure on asthma risk.
Main Methods:
- A case-control study included 645 asthmatic and 910 non-asthmatic children (aged 3-12).
- Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped.
- Visible mold exposure and SNP associations with childhood asthma were analyzed using logistic regression and crossover analyses for gene-environment interactions.
Main Results:
- Visible mold exposure was associated with a 2.19-fold increased risk of childhood asthma.
- The rs7216389 SNP in the GSDMB gene showed a dose-dependent increase in asthma risk.
- Children with the rs7216389 T allele and mold exposure had a 3.21-fold increased risk of asthma, with significant interaction effects (AP=0.47, RERI=1.49).
Conclusions:
- A significant additive interaction exists between visible mold exposure and the rs7216389 SNP in childhood asthma.
- Gene-environment interactions are crucial for understanding childhood asthma risk factors.
- Future research should incorporate genetic factors alongside environmental exposures.
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