The answer is in their genes.

Chronic obstructive pulmonary disease (COPD) is characterised by progressive decline in lung function, and encompasses both chronic bronchitis and emphysema. Almost 90% of COPD is caused by chronic cigarette smoking, but only 25% of long-term tobacco smokers will go on to develop COPD.

New research published yesterday in Respiratory Research from the Wake Forest School of Medicine and Saint Louis University, may shed some light on why.

The researchers looked at a disintegrin and metalloprotease (ADAM) gene known as ADAM33 in 880 long-term heavy smokers. ADAM33 is located on chromosome 20 and has been linked with asthma in previous research. This study is unique in comparing long-term smokers with COPD versus a control group of long-term smokers without COPD.

Five single nucleotide polymorphisms (SNPs), which are human DNA sequence variations, were found in ADAM33 that were more frequent in the COPD group than in the group of smokers without COPD. One particular SNP, known as S1, had a particularly strong link to lung abnormalities.

Functional studies will now be needed to evaluate the biologic significance of these polymorphisms in the pathogenesis of COPD, but the early results suggest that the abnormalities may affect the chances of developing chronic obstructive pulmonary disease (COPD) in later life.

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Sadeghnejad, A., Ohar, J., Zheng, S., Sterling, D., Hawkins, G., Meyers, D., & Bleecker, E. (2009). ADAM33 polymorphisms are associated with COPD and lung function in long-term tobacco smokers Respiratory Research, 10 (1) DOI: 10.1186/1465-9921-10-21