Air pollution and childhood bronchitis: Interaction with xenobiotic, immune regulatory and DNA repair genes
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
26655675
DOI
10.1016/j.envint.2015.10.002
PII: S0160-4120(15)30068-4
Knihovny.cz E-resources
- MeSH
- Asthma epidemiology MeSH
- Bronchitis * epidemiology immunology MeSH
- Child MeSH
- Genotype MeSH
- Incidence MeSH
- Gene-Environment Interaction * MeSH
- Polymorphism, Single Nucleotide MeSH
- Air Pollutants adverse effects analysis MeSH
- Humans MeSH
- Adolescent MeSH
- Random Allocation MeSH
- DNA Repair genetics MeSH
- Particulate Matter adverse effects analysis MeSH
- Polycyclic Aromatic Hydrocarbons adverse effects analysis MeSH
- Child, Preschool MeSH
- Immunity, Innate drug effects MeSH
- Xenobiotics adverse effects analysis MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Child, Preschool MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Czech Republic MeSH
- Names of Substances
- Air Pollutants MeSH
- Particulate Matter MeSH
- Polycyclic Aromatic Hydrocarbons MeSH
- Xenobiotics MeSH
BACKGROUND: Gene-environment interactions have been investigated for diseases such as asthma, chronic obstructive pulmonary disease, cancer etc. but acute disease like bronchitis has rarely been studied. We investigated interactions between air pollution (polycyclic aromatic hydrocarbons (PAH) and particulate matter <2.5 μm (PM2.5)) and single nucleotide polymorphisms (SNP) in EPHX1, IL10, STAT4 and XPC genes in relation to bronchitis in children aged 0-2 years. METHODS: A stratified random sample of 1133 Czech children, born between 1994 and 1998 in two districts, were followed since birth, of which 626 were genotyped. Pediatrician-diagnosed bronchitis episodes were obtained from the medical records. Central-site monitors measured air pollution exposure. We used multivariable logistic regression and estimated coefficients using generalized estimating equations. Interaction was assessed between pollutants and genes and associations in genotype-specific strata were presented. False discovery rate was used to adjust for multiple comparisons. RESULTS: There were 803 episodes of bronchitis with an incidence rate of 56 per 1000 child-months. We found significant gene-environment interaction between PAH and four SNPs (EPHX1, (rs2854461), STAT4 (rs16833215), XPC (rs2228001 and rs2733532)), which became non-significant after adjusting for multiple comparisons. PM2.5 interactions with two XPC SNPs (rs2228001 and rs2733532) remained significant after accounting for multiple comparisons and those with CC alleles had a more than doubling of odds, OR=2.65 (95% CI: 1.91, 3.69) and 2.72 (95% CI: 1.95, 3.78), respectively, per 25 μg/m(3) increase in exposure. CONCLUSION: The findings suggest that the DNA repair gene XPC may play an important role in the air pollution-induced pathogenesis of the inflammatory disease bronchitis.
References provided by Crossref.org
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