Evidence for gene-smoking interactions for hearing loss and deafness in Japanese American families

American Diabetes Association GENNID Study Group

Research output: Contribution to journalArticle

Abstract

Background: This study investigated the relationship between smoking and hearing loss and deafness (HLD) and whether the relationship is modified by genetic variation. Data for these analyses was from the subset of Japanese American families collected as part of the American Diabetes Association Genetics of Non-insulin Dependent Diabetes Mellitus study. Logistic regression with generalized estimating equations assessed the relationship between HLD and smoking. Nonparametric linkage analysis identified genetic regions harboring HLD susceptibility genes and ordered subset analysis was used to identify regions showing evidence for gene-smoking interactions. Genetic variants within these candidate regions were then each tested for interaction with smoking using logistic regression models. Results: After adjusting for age, sex, diabetes status and smoking duration, for each pack of cigarettes smoked per day, risk of HLD increased 4.58 times (odds ratio (OR) = 4.58; 95% Confidence Interval (CI): (1.40,15.03)), and ever smokers were over 5 times more likely than nonsmokers to report HLD (OR = 5.22; 95% CI: (1.24, 22.03)). Suggestive evidence for linkage for HLD was observed in multiple genomic regions (Chromosomes 5p15, 8p23 and 17q21), and additional suggestive regions were identified when considering interactions with smoking status (Chromosomes 7p21, 11q23, 12q32, 15q26, and 20q13) and packs-per-day (Chromosome 8q21). Conclusions: To our knowledge this was the first report of possible gene-by-smoking interactions in HLD using family data. Additional work, including independent replication, is needed to understand the basis of these findings. HLD are important public health issues and understanding the contributions of genetic and environmental factors may inform public health messages and policies.

Original languageEnglish (US)
Article number107875
JournalHearing Research
Volume387
DOIs
StatePublished - Mar 1 2020

Fingerprint

Asian Americans
Deafness
Hearing Loss
Smoking
Genes
Chromosomes
Logistic Models
Public Health
Odds Ratio
Confidence Intervals
Genetic Linkage
Public Policy
Health Policy
Tobacco Products
Type 2 Diabetes Mellitus

Keywords

  • Family
  • Gene-environment interaction
  • Genome-wide linkage
  • Hearing loss
  • Linkage
  • Smoking

ASJC Scopus subject areas

  • Sensory Systems

Cite this

Evidence for gene-smoking interactions for hearing loss and deafness in Japanese American families. / American Diabetes Association GENNID Study Group.

In: Hearing Research, Vol. 387, 107875, 01.03.2020.

Research output: Contribution to journalArticle

American Diabetes Association GENNID Study Group. / Evidence for gene-smoking interactions for hearing loss and deafness in Japanese American families. In: Hearing Research. 2020 ; Vol. 387.
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title = "Evidence for gene-smoking interactions for hearing loss and deafness in Japanese American families",
abstract = "Background: This study investigated the relationship between smoking and hearing loss and deafness (HLD) and whether the relationship is modified by genetic variation. Data for these analyses was from the subset of Japanese American families collected as part of the American Diabetes Association Genetics of Non-insulin Dependent Diabetes Mellitus study. Logistic regression with generalized estimating equations assessed the relationship between HLD and smoking. Nonparametric linkage analysis identified genetic regions harboring HLD susceptibility genes and ordered subset analysis was used to identify regions showing evidence for gene-smoking interactions. Genetic variants within these candidate regions were then each tested for interaction with smoking using logistic regression models. Results: After adjusting for age, sex, diabetes status and smoking duration, for each pack of cigarettes smoked per day, risk of HLD increased 4.58 times (odds ratio (OR) = 4.58; 95{\%} Confidence Interval (CI): (1.40,15.03)), and ever smokers were over 5 times more likely than nonsmokers to report HLD (OR = 5.22; 95{\%} CI: (1.24, 22.03)). Suggestive evidence for linkage for HLD was observed in multiple genomic regions (Chromosomes 5p15, 8p23 and 17q21), and additional suggestive regions were identified when considering interactions with smoking status (Chromosomes 7p21, 11q23, 12q32, 15q26, and 20q13) and packs-per-day (Chromosome 8q21). Conclusions: To our knowledge this was the first report of possible gene-by-smoking interactions in HLD using family data. Additional work, including independent replication, is needed to understand the basis of these findings. HLD are important public health issues and understanding the contributions of genetic and environmental factors may inform public health messages and policies.",
keywords = "Family, Gene-environment interaction, Genome-wide linkage, Hearing loss, Linkage, Smoking",
author = "{American Diabetes Association GENNID Study Group} and Wan, {Jia Y.} and Christina Cataby and Andrew Liem and Emily Jeffrey and Norden-Krichmar, {Trina M.} and Deborah Goodman and Santorico, {Stephanie A.} and Edwards, {Karen L.} and Eric Boerwinkle and John Buse and Ralph DeFronzo and David Ehrmann and Elbein, {Steven C.} and Wilfred Fujimoto and Kahn, {Steven E.} and Hanis, {Craig L.} and Mulivor, {Richard A.} and Beck, {Jeanne C.} and Jill Norris and Permutt, {M. Alan} and Philip Behn and Leslie Raffel and Robbins, {David C.}",
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AU - American Diabetes Association GENNID Study Group

AU - Wan, Jia Y.

AU - Cataby, Christina

AU - Liem, Andrew

AU - Jeffrey, Emily

AU - Norden-Krichmar, Trina M.

AU - Goodman, Deborah

AU - Santorico, Stephanie A.

AU - Edwards, Karen L.

AU - Boerwinkle, Eric

AU - Buse, John

AU - DeFronzo, Ralph

AU - Ehrmann, David

AU - Elbein, Steven C.

AU - Fujimoto, Wilfred

AU - Kahn, Steven E.

AU - Hanis, Craig L.

AU - Mulivor, Richard A.

AU - Beck, Jeanne C.

AU - Norris, Jill

AU - Permutt, M. Alan

AU - Behn, Philip

AU - Raffel, Leslie

AU - Robbins, David C.

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N2 - Background: This study investigated the relationship between smoking and hearing loss and deafness (HLD) and whether the relationship is modified by genetic variation. Data for these analyses was from the subset of Japanese American families collected as part of the American Diabetes Association Genetics of Non-insulin Dependent Diabetes Mellitus study. Logistic regression with generalized estimating equations assessed the relationship between HLD and smoking. Nonparametric linkage analysis identified genetic regions harboring HLD susceptibility genes and ordered subset analysis was used to identify regions showing evidence for gene-smoking interactions. Genetic variants within these candidate regions were then each tested for interaction with smoking using logistic regression models. Results: After adjusting for age, sex, diabetes status and smoking duration, for each pack of cigarettes smoked per day, risk of HLD increased 4.58 times (odds ratio (OR) = 4.58; 95% Confidence Interval (CI): (1.40,15.03)), and ever smokers were over 5 times more likely than nonsmokers to report HLD (OR = 5.22; 95% CI: (1.24, 22.03)). Suggestive evidence for linkage for HLD was observed in multiple genomic regions (Chromosomes 5p15, 8p23 and 17q21), and additional suggestive regions were identified when considering interactions with smoking status (Chromosomes 7p21, 11q23, 12q32, 15q26, and 20q13) and packs-per-day (Chromosome 8q21). Conclusions: To our knowledge this was the first report of possible gene-by-smoking interactions in HLD using family data. Additional work, including independent replication, is needed to understand the basis of these findings. HLD are important public health issues and understanding the contributions of genetic and environmental factors may inform public health messages and policies.

AB - Background: This study investigated the relationship between smoking and hearing loss and deafness (HLD) and whether the relationship is modified by genetic variation. Data for these analyses was from the subset of Japanese American families collected as part of the American Diabetes Association Genetics of Non-insulin Dependent Diabetes Mellitus study. Logistic regression with generalized estimating equations assessed the relationship between HLD and smoking. Nonparametric linkage analysis identified genetic regions harboring HLD susceptibility genes and ordered subset analysis was used to identify regions showing evidence for gene-smoking interactions. Genetic variants within these candidate regions were then each tested for interaction with smoking using logistic regression models. Results: After adjusting for age, sex, diabetes status and smoking duration, for each pack of cigarettes smoked per day, risk of HLD increased 4.58 times (odds ratio (OR) = 4.58; 95% Confidence Interval (CI): (1.40,15.03)), and ever smokers were over 5 times more likely than nonsmokers to report HLD (OR = 5.22; 95% CI: (1.24, 22.03)). Suggestive evidence for linkage for HLD was observed in multiple genomic regions (Chromosomes 5p15, 8p23 and 17q21), and additional suggestive regions were identified when considering interactions with smoking status (Chromosomes 7p21, 11q23, 12q32, 15q26, and 20q13) and packs-per-day (Chromosome 8q21). Conclusions: To our knowledge this was the first report of possible gene-by-smoking interactions in HLD using family data. Additional work, including independent replication, is needed to understand the basis of these findings. HLD are important public health issues and understanding the contributions of genetic and environmental factors may inform public health messages and policies.

KW - Family

KW - Gene-environment interaction

KW - Genome-wide linkage

KW - Hearing loss

KW - Linkage

KW - Smoking

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