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The genetics of smoking in individuals with chronic obstructive pulmonary disease Obeidat, Ma’en; Zhou, Guohai; Li, Xuan; Hansel, Nadia N.; Rafaels, Nicholas; Mathias, Rasika; Ruczinski, Ingo; Beaty, Terri H.; Barnes, Kathleen C.; Paré, Peter D.; Sin, Don D.

Abstract

Background: Smoking is the principal modifiable environmental risk factor for chronic obstructive pulmonary disease (COPD) which affects 300 million people and is the 3rd leading cause of death worldwide. Most of the genetic studies of smoking have relied on self-reported smoking status which is vulnerable to reporting and recall bias. Using data from the Lung Health Study (LHS), we sought to identify genetic variants associated with quantitative smoking and cessation in individuals with mild to moderate COPD. Methods: The LHS is a longitudinal multicenter study of mild-to-moderate COPD subjects who were all smokers at recruitment. We performed genome-wide association studies (GWASs) for salivary cotinine (n = 4024), exhaled carbon monoxide (eCO) (n = 2854), cigarettes per day (CPD) (n = 2706) and smoking cessation at year 5 follow-up (n = 717 quitters and 2175 smokers). The GWAS analyses were adjusted for age, gender, and genetic principal components. Results: For cotinine levels, SNPs near UGT2B10 gene achieved genome-wide significance (i.e. P 

Item Metadata

Title
The genetics of smoking in individuals with chronic obstructive pulmonary disease
Creator
Obeidat, Ma’en; Zhou, Guohai; Li, Xuan; Hansel, Nadia N.; Rafaels, Nicholas; Mathias, Rasika; Ruczinski, Ingo; Beaty, Terri H.; Barnes, Kathleen C.; Paré, Peter D.; Sin, Don D.
Contributor
University of British Columbia. Centre for Heart Lung Innovation; St. Paul's Hospital (Vancouver, B.C.)
Publisher
BioMed Central
Date Issued
2018-04-10
Description
Background: Smoking is the principal modifiable environmental risk factor for chronic obstructive pulmonary disease (COPD) which affects 300 million people and is the 3rd leading cause of death worldwide. Most of the genetic studies of smoking have relied on self-reported smoking status which is vulnerable to reporting and recall bias. Using data from the Lung Health Study (LHS), we sought to identify genetic variants associated with quantitative smoking and cessation in individuals with mild to moderate COPD. Methods: The LHS is a longitudinal multicenter study of mild-to-moderate COPD subjects who were all smokers at recruitment. We performed genome-wide association studies (GWASs) for salivary cotinine (n = 4024), exhaled carbon monoxide (eCO) (n = 2854), cigarettes per day (CPD) (n = 2706) and smoking cessation at year 5 follow-up (n = 717 quitters and 2175 smokers). The GWAS analyses were adjusted for age, gender, and genetic principal components. Results: For cotinine levels, SNPs near UGT2B10 gene achieved genome-wide significance (i.e. P 
Subject
Cessation; Smoking; GWAS; eCO; Cotinine
Genre
Article
Type
Text
Language
eng
Date Available
2018-04-11
Provider
Vancouver : University of British Columbia Library
Rights
Attribution 4.0 International (CC BY 4.0)
DOI
10.14288/1.0365551
URI
http://hdl.handle.net/2429/65274
Affiliation
Medicine, Faculty of; Other UBC; Non UBC; Medicine, Department of
Citation
Respiratory Research. 2018 Apr 10;19(1):59
Publisher DOI
10.1186/s12931-018-0762-7
Peer Review Status
Reviewed
Scholarly Level
Faculty
Copyright Holder
The Author(s).
Rights URI
http://creativecommons.org/licenses/by/4.0/
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Attribution 4.0 International (CC BY 4.0)