Based on this rationale, the present study was designed to test the hypothesis that the EPHX1 polymorphism increases the risk of COPD development in individuals who smoke, while CHRNA3/5 polymorphisms contribute to increased tobacco intake, thereby acting synergistically to accelerate the onset and severity of smoking-related pulmonary disease [10,11,12,13,14]. This evidence concerns the gene EPHX1 and chronic obstructive pulmonary disease.