Gene-Environment Interaction between the IL1RN Variants and Childhood Environmental Tobacco Smoke Exposure in Asthma Risk

Yongzhao Shao, Yian Zhang, Mengling Liu, Maria-Elena Fernandez-Beros, Meng Qian and Joan Reibman
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Yongzhao Shao: Division of Biostatistics, Department of Population Health, School of Medicine (SOM), New York University, New York, NY 10016, USA
Yian Zhang: Division of Biostatistics, Department of Population Health, School of Medicine (SOM), New York University, New York, NY 10016, USA
Mengling Liu: Division of Biostatistics, Department of Population Health, School of Medicine (SOM), New York University, New York, NY 10016, USA
Maria-Elena Fernandez-Beros: Division of Pulmonary and Critical Care Medicine, Department of Medicine, SOM, New York University, New York, NY 10016, USA
Meng Qian: Division of Biostatistics, Department of Population Health, School of Medicine (SOM), New York University, New York, NY 10016, USA
Joan Reibman: Division of Pulmonary and Critical Care Medicine, Department of Medicine, SOM, New York University, New York, NY 10016, USA

IJERPH, 2020, vol. 17, issue 6, 1-16

Abstract: (1) Background: Variants of the interleukin-1 receptor antagonist ( IL1RN ) gene, encoding an anti-inflammatory cytokine, are associated with asthma. Asthma is a chronic inflammatory disease of the airway influenced by interactions between genetic variants and environmental factors. We discovered a gene–environment interaction (GEI) of IL1RN polymorphisms with childhood environmental tobacco smoke (ETS) exposure on asthma susceptibility in an urban adult population. (2) Methods: DNA samples from the NYU/Bellevue Asthma Registry were genotyped for tag SNPs in IL1RN in asthma cases and unrelated healthy controls. Logistic regressions were used to study the GEI between IL1RN variants and childhood ETS exposures on asthma and early onset asthma, respectively, adjusting for population admixture and other covariates. (3) Results: Whereas the rare genotypes of IL1RN SNPs (e.g., GG in SNP rs2234678) were associated with decreased risk for asthma among those without ETS exposure (odds ratio OR = 0.215, p = 0.021), they are associated with increased risk for early onset asthma among those with childhood ETS (OR = 4.467, p = 0.021). (4) Conclusions: We identified a GEI between polymorphisms of IL1RN and childhood ETS exposure in asthma. Analysis of GEI indicated that childhood ETS exposure disrupted the protective effect of some haplotypes/genotypes of IL1RN for asthma and turned them into high-risk polymorphisms for early onset asthma.

Keywords: gene and environment interaction; environmental tobacco smoke; IL1RN variants; early onset asthma; SNP genotypes; risk haplotypes; case-control association study; population admixture; ancestral informative markers; inflammation (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2020
References: View references in EconPapers View complete reference list from CitEc
Citations: View citations in EconPapers (3)

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