4 research outputs found
Traditional Market Revitalization Using Design Thinking Methods & Sense-Making
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Evidence for Large-Scale Gene-by-Smoking Interaction Effects on Pulmonary Function
Background: Smoking is the strongest environmental risk factor for reduced pulmonary
function. The genetic component of various pulmonary traits has also been demonstrated, and
at least 26 loci have been reproducibly associated with either FEV1 (forced expiratory volume in
1 second) or FEV1/FVC (FEV1/forced vital capacity). Although the main effects of smoking and
genetic loci are well established, the question of potential gene-by-smoking interaction effect
remains unanswered. The aim of the present study was to assess, using a genetic risk score
approach, whether the effect of these 26 loci on pulmonary function is influenced by smoking.
Methods: We evaluated the interaction between smoking exposure, considered as either ever
vs. never or pack-years, and a 26 SNPs genetic risk score in relation to FEV1 or FEV1/FVC in 50
047 participants of European ancestry from the CHARGE and SpiroMeta consortia.
Results: We identified an interaction ( = −0.036, 95% confidence interval, -0.040 – -0.032,
P=0.00057) between an unweighted 26 SNPs genetic risk score and smoking status (ever/never)
on the FEV1/FVC ratio. In interpreting this interaction, we showed that the genetic risk of falling
below the FEV1/FVC threshold used to diagnose chronic obstructive pulmonary disease is higher
among ever smokers than among never smokers.
Conclusions: This study highlights the benefit of using genetic risk scores for identifying
interactions missed when studying individual SNPs, and shows for the first time that persons
with the highest genetic risk for low FEV1/FVC may be more susceptible to the deleterious
effects of smoking
Genetic loci associated with chronic obstructive pulmonary disease overlap with loci for lung function and pulmonary fibrosis
Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality worldwide1.
We performed a genetic association in 15,256 cases and 47,936 controls, with replication of select
top results (P < 5x10-6) in 9,498 cases and 9,748 controls. In the combined meta-analysis, we
identified 22 loci at genome-wide significance, including 13 new associations with COPD. Nine of
these 13 loci have been associated with lung function in general population samples2-7; however, 4
(EEFSEC, DSP, MTCL1, and SFTPD) are novel. We noted 2 loci shared with pulmonary fibrosis8,9
(FAM13A and DSP) but with opposite risk alleles for COPD. None of our loci overlapped with
genome-wide associations for asthma; however, one locus has been implicated in the joint
susceptibility to asthma and obesity10. We also identified genetic correlation between COPD and
asthma. Our findings highlight novel loci, demonstrate the importance of specific lung function loci
to COPD, and identify potential regions of genetic overlap between COPD and other respiratory
diseases
Genome-wide association analysis identifies six new loci associated with forced vital capacity
Forced vital capacity (FVC), a spirometric measure of pulmonary function, reflects lung volume and is used to diagnose and monitor lung diseases. We performed genome-wide association study meta-analysis of FVC in 52,253 individuals from 26 studies and followed up the top associations in 32,917 additional individuals of European ancestry. We found six new regions associated at genome-wide significance (P < 5 × 10(-8)) with FVC in or near EFEMP1, BMP6, MIR129-2-HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease