COPD is a common disease, and the major risk factor for it—cigarette smoking—has been identified. However, only a minority of smokers develop clinically relevant disease. Although significant progress has been made in understanding the pathogenesis of COPD, it remains unclear why only a few smokers develop COPD. The cornerstone of the pathogenesis of COPD is the response of the host (the smoker) to an environmental risk factor (cigarette smoke). The main effect of this response has been described as 'abnormal inflammation', but the various pathways involved are not clear. Oxidative stress, inflammation, tissue damage and tissue repair (remodeling) are parts of the complex procedure leading to COPD.

An epidemiological model has been proposed in which the emphasis is on the timing of the exposure to cigarette smoke (before birth, during lung growth, etc.). There is evidence that respiratory adenoviral infection in early life could be an important factor that characterizes the susceptible smoker. Airway hyperresponsiveness has failed to clarify the whole picture and is still a topic of debate. Differences in nutritional elements, such as vitamins or fish oil, could play a role in providing protection against the effects of oxidative stress, but cannot fully explain the existence of susceptible individuals. Genetic differences are therefore the most likely parameters for identifying susceptible smokers. The only well-established genetic risk factor so far is the aj-antitrypsin gene; other candidate genes are being investigated.

In conclusion, there are as yet no definitive answers to the basic question of why only a few smokers develop COPD. It is most likely that a number of genes are involved, affecting various pathways in the pathogenesis of the condition — but as this review shows, the genetic basis of the disease is only beginning to be elucidated. Understanding the genetic basis of COPD should lead to better methods of prevention and treatment in the future.

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