An analysis of genetic data revealed new associations between lung function and smoking behavior. The findings provide new insight into the underlying mechanisms for COPD, tobacco addiction and airflow obstruction, researchers wrote.
Researchers evaluated 50,008 unique samples from the UK Biobank for both heavy smokers and participants who have never smoked.
They found significant genetic sharing between heavy smokers and participants who have never smoked and low FEV1, as well as overlapping genetic causes for low FEV1 between participants with doctor-diagnosed asthma and no asthma.
In addition, researchers found six genetic-wide significant signals of association for low FEV1, which included signals at new loci, such as KANSL1, TSEN54, TET2, and RBM19/TBX5. Extremes in FEV1 were associated with the number of copies in a 150 kb region containing the 5’ end of KANSL1, according to Wain and colleagues.
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