1. Association of Air Pollution Exposure and Interleukin-13 Haplotype with the Risk of Aggregate Bronchitic Symptoms in Children
- Author
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Yungling Leo Lee, Jing-Huei Chen, Chi-Min Wang, Bing-Fang Hwang, and Mei-Ling Chen
- Subjects
Male ,Taiwan ,lcsh:Medicine ,Comorbidity ,Logistic regression ,Polymorphism, Single Nucleotide ,Risk Assessment ,Linkage Disequilibrium ,General Biochemistry, Genetics and Molecular Biology ,03 medical and health sciences ,0302 clinical medicine ,Gene Frequency ,Air pollutants ,Risk Factors ,Interquartile range ,Air Pollution ,Environmental health ,Odds Ratio ,Prevalence ,medicine ,Humans ,030212 general & internal medicine ,Child ,lcsh:R5-920 ,Air Pollutants ,Interleukin-13 ,business.industry ,lcsh:R ,Phlegm ,Confounding ,Haplotype ,Bronchial Diseases ,Environmental Exposure ,Syndrome ,General Medicine ,Odds ratio ,Bronchitic symptoms ,Haplotypes ,030228 respiratory system ,Population Surveillance ,Population study ,Female ,Gene-Environment Interaction ,Disease Susceptibility ,medicine.symptom ,lcsh:Medicine (General) ,business ,Research Paper - Abstract
Interleukin-13(IL-13) might play an important role in driving aggregate bronchitic symptoms pathogenesis. However, none of the studies assessed the interaction between air pollutants exposure and IL-13 gene on the risk of aggregate bronchitic symptoms in non-asthma children. To assess the independent and joint effects of the exposure to air pollution and IL-13 haplotypes on the risk of aggregate bronchitic symptoms, we conducted a cross-sectional study and focused on non-asthma children. The study population consisted of 2944 children. The effect of each air pollutant on the risk of aggregate bronchitic symptoms was estimated as odds ratios per interquartile range (IQR) change. In the multiple logistic regressions, adjusted for confounding factors, the risk of chronic phlegm was associated with PM2.5 exposure (aOR, 1.59; 95% CI, 1.07–2.37 per 12.51 μg/m3 change), O3 exposure (aOR, 1.54 95% CI, 1.05–2.27 per 8.28 ppb change) and SO2 exposure (aOR, 1.19; 95% CI, 1.02–1.39 per 0.98 ppb change). Our study further provides the evidence that gene-environment interactions between IL-13 haplotype and O3 exposure on chronic phlegm (95% CI for interaction, 1.01–1.38). Identifying children who are more sensitive to air pollution helps us to provide them an efficient prevention to avoid aggregate bronchitic symptoms., Highlights • Limited studies explored the interactions between IL-13 gene and air pollutants exposure on the risk of bronchitic symptoms. • Genetic susceptibility of IL-13 may interact with O3 exposure causing the pathogenesis of bronchitic symptoms. • Identifying children susceptible to air pollutants helps us to provide them an efficient prevention of bronchitic symptoms. Genetic susceptibility may interact with specific environmental factors causing the pathogenesis of aggregate bronchitic symptoms. Limited studies have explored the interactions between Interleukin-13 (IL-13) gene and air pollutants exposure on the risk of aggregate bronchitic symptoms. Our study further provides the evidence that gene-environment interactions between IL-13 gene and O3 exposure may play an important role in aggregate bronchitic symptoms. Identifying children who are more sensitive to air pollutants helps us to provide them an efficient prevention to avoid aggregate bronchitic symptoms.
- Published
- 2018
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