Abstract
On Lung Function and Interactions Using Genome-Wide Data
Highlights
Smoking is the most wellstudied and established lifestyle risk factor for respiratory diseases, not all smokers develop diseases such as asthma or chronic obstructive pulmonary disease (COPD) [6]
As the effects of gene-smoking interactions on lung function have not been extensively studied in large data sets so far, the paper by Hancock et al in this issue of PLOS Genetics adds value to the current literature in many ways [11]
The authors present a large scale gene–environment interaction study based on genome-wide association studies (GWASs) data, smoking status, and lung function outcomes in over 50,000 adults from 19 studies primarily from the CHARGE and SpiroMeta consortia (Figure 1)
Summary
Smoking is the most wellstudied and established lifestyle risk factor for respiratory diseases, not all smokers develop diseases such as asthma or COPD [6]. IL13 single nucleotide polymorphisms (SNPs) have been shown to modulate the adverse effects of long-term cigarette smoking on pulmonary function [7]. MMP12, a protease involved in tissue degradation, has been associated with lung function and risk of COPD, but only in high-risk populations such as smokers and asthmatics [8].
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