Air pollution and childhood bronchitis: Interaction with xenobiotic, immune regulatory and DNA repair genes

Rakesh Ghosh, Pavel Rossner, Katerina Honkova, Miroslav Dostal, Radim J. Sram, Irva Hertz-Picciotto

Research output: Contribution to journalArticle

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Abstract

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)) and single nucleotide polymorphisms (SNP) in EPHX1, IL10, STAT4 and XPC genes in relation to bronchitis in children aged 0-2years. 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 25μg/m3 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.

Original languageEnglish (US)
Pages (from-to)94-100
Number of pages7
JournalEnvironment International
Volume87
DOIs
StatePublished - Feb 1 2016

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xenobiotics
repair
atmospheric pollution
DNA
gene
PAH
pollution exposure
asthma
particulate matter
cancer
logistics
allele
polymorphism
genotype
pollutant
comparison
rate

ASJC Scopus subject areas

  • Environmental Science(all)

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Air pollution and childhood bronchitis : Interaction with xenobiotic, immune regulatory and DNA repair genes. / Ghosh, Rakesh; Rossner, Pavel; Honkova, Katerina; Dostal, Miroslav; Sram, Radim J.; Hertz-Picciotto, Irva.

In: Environment International, Vol. 87, 01.02.2016, p. 94-100.

Research output: Contribution to journalArticle

Ghosh, Rakesh ; Rossner, Pavel ; Honkova, Katerina ; Dostal, Miroslav ; Sram, Radim J. ; Hertz-Picciotto, Irva. / Air pollution and childhood bronchitis : Interaction with xenobiotic, immune regulatory and DNA repair genes. In: Environment International. 2016 ; Vol. 87. pp. 94-100.
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abstract = "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)) and single nucleotide polymorphisms (SNP) in EPHX1, IL10, STAT4 and XPC genes in relation to bronchitis in children aged 0-2years. 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 25μg/m3 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.",
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AU - Sram, Radim J.

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AB - 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)) and single nucleotide polymorphisms (SNP) in EPHX1, IL10, STAT4 and XPC genes in relation to bronchitis in children aged 0-2years. 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 25μg/m3 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.

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