Angiotensin-converting-enzyme gene polymorphisms, smoking and chronic obstructive pulmonary disease

Abstract

While tobacco smoking is the main risk factor for chronic obstructive pulmonary disease (COPD) only a fraction of smokers go on to develop the disease. We investigated the relationship between the insertion (I) – deletion (D) polymorphisms in the Angiotensin converting enzyme (ACE) gene and the risk of developing COPD in smokers by determining the distribution of the ACE genotypes (DD, ID and II) in 151 life-long male smokers. 74 of the smokers had developed COPD (62 ± 2 years; FEV₁ 44 ± 6 % reference) whereas the rest retained normal lung function (56 ± 2 yrs; FEV₁ 95 ± 3 % reference). In addition, we genotyped 159 males recruited randomly from the general population. The prevalence of the DD genotype was highest (p = 0.01) in the smokers that developed COPD and its presence was associated with a 2-fold increase in the risk for COPD (OR 2.2; IC95% 1.1 to 5.5). Surprisingly, the 151 individuals in the smoking population did not demonstrate Hardy-Weinberg equilibrium unlike the 159 recruited from the general population. Our results suggest that ACE polymorphisms are associated with both the smoking history of an individual and their risk of developing COPD.

Keywords:

• chronic bronchitis
• COPD
• dopamine
• drug addiction
• emphysema

Acknowledgements

Supported, in part, by FIS 00/0437, FIS 02/3008and RTIC C03/11 (Red Respira); CICYT PB98-1084, SEPAR and ABEMAR.

Notes

XB and NGM equally contributed to this work.