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  3. Epidemiology and Preventive Medicine / 流行病學與預防醫學研究所
  4. Association of Air Pollution Exposure and Interleukin-13 Haplotype with the Risk of Aggregate Bronchitic Symptoms in Children
 
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Association of Air Pollution Exposure and Interleukin-13 Haplotype with the Risk of Aggregate Bronchitic Symptoms in Children

Journal
EBioMedicine
Journal Volume
29
Pages
70-77
Date Issued
2018-03
Author(s)
YUNG-LING LEE  
Chen, Jing-Huei
Wang, Chi-Min
Chen, Mei-Ling
Hwang, Bing-Fang
DOI
https://api.elsevier.com/content/abstract/scopus_id/85042107695
10.1016/j.ebiom.2018.02.008
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/412801
URL
https://api.elsevier.com/content/abstract/scopus_id/85042107695
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 12.51μg/m3 change), O3 exposure (aOR, 1.54 95% CI, 1.05-2.27 per 8.28ppb change) and SO2 exposure (aOR, 1.19; 95% CI, 1.02-1.39 per 0.98ppb 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.
Subjects
Air pollutants; Bronchitic symptoms; Interleukin-13
SDGs

[SDGs]SDG3

Other Subjects
carbon monoxide; interleukin 13; nitrogen dioxide; ozone; small nuclear ribonucleoprotein; sulfur dioxide; interleukin 13; air pollutant; air pollution; Article; atopy; bronchitis; bronchus mucus; child; chronic cough; cockroach; cross-sectional study; environmental exposure; female; gene frequency; genotype; haplotype; human; major clinical study; male; maternal smoking; mold (soil); odds ratio; odor; particulate matter; pet animal; priority journal; questionnaire; real time polymerase chain reaction; school child; single nucleotide polymorphism; air pollution; bronchus disease; comorbidity; disease predisposition; gene linkage disequilibrium; genetics; genotype environment interaction; haplotype; health survey; prevalence; risk assessment; risk factor; syndrome; Taiwan; Air Pollutants; Air Pollution; Bronchial Diseases; Child; Comorbidity; Disease Susceptibility; Environmental Exposure; Female; Gene Frequency; Gene-Environment Interaction; Haplotypes; Humans; Interleukin-13; Linkage Disequilibrium; Male; Odds Ratio; Polymorphism, Single Nucleotide; Population Surveillance; Prevalence; Risk Assessment; Risk Factors; Syndrome; Taiwan
Publisher
ELSEVIER SCIENCE BV
Type
journal article

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