Bhattacharjee et al. earlier studied the polymorphism of a 1- antitrypsin gene in the population of the same area where we have taken up the study. COPD is the consequence of an abnormal inflammatory response due to inhalation of noxious agents such as cigarette smoking, occupational or NIDA-41020 environmental exposure. In fact only a portion of heavy smokers develops a clinically detectable disease. Antioxidants and other less well understood protective mechanism may also be important in preserving normal lung function in the face of a lifetime exposure to potentially injurious environmental factors. Oxidative injury may also play an important role in the pathogenesis of COPD,. Such injury, resulting from an imbalance between free radicals and protective mechanisms, can alter the conformation of protease inhibitors and Necrostatin-7 reparative enzymes, injure cell membranes, and may result in mutagenesis. Free radicals appear in the lungs through inhalation from the environment or by its release from inflammatory cells inside the body. Genetically controlled antioxidant defence systems may also play an important role in determining susceptibility, both to free radicals released by inflammatory cells and to oxidants inhaled from the environment. The lung possesses several enzymatic scavengers including glutathione which are under genetic control. The observation that the enzymatic antioxidants are under genetic control and the allelic variations of these antioxidants alter their abilities to reduce free radicals, suggests that genetic factors may place some individuals at greater risk for oxidant injury. The glutathione system is the major antioxidant mechanism in the airways. The increased oxidative stress in the airways of COPD patients may play an important pathophysiological role in the disease development by amplifying the inflammatory response in COPD. COPD is characterized by progressive development of airflow limitation that is not fully reversible. It encompasses chronic obstructive bronchitis, with obstruction of small airways, and emphysema with enlargement of air spaces and destruction of lung parenchyma, loss of lung elasticity and closure of small airways.