Are there cigarette smokers who are susceptible to COPD

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It is well known that less than 20% of smokers develop clinically significant chronic obstructive pulmonary disease (COPD) [1-3]. From a number of epidemiological studies, it has become apparent that there are susceptible smokers who will develop COPD [1,3]. However, the characteristics of such susceptible individuals are not known [4]. The questions 'Is there a distinct group of susceptible smokers?' and 'What is the distribution (bimodal or unimodal) of susceptible individuals?' are extremely difficult to answer on the basis of the current scientific knowledge.

According to a new working definition developed by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) group, COPD is a 'disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and results from an abnormal inflammatory response of the lungs to noxious particles and gases' [5]. It is likely that the reason why fewer than 20% of smokers develop COPD is connected with an abnormal inflammatory response to noxious agents. COPD is the result of an environmental insult and a response by the host that is primarily genetically predetermined.

Another mystery concerning the pathogenesis of COPD is why some patients develop predominantly parenchymal disease (emphysema), while others mainly develop airways disease (chronic bronchitis). This suggests the possibility of subgroups of susceptible individuals, some primarily with defects at the level of the major airways and others with defects at the level of the parenchyma. Are these defects genetically determined? [4].

A brief summary of the pathogenesis of the disease will be presented here first, with a review of the current literature. The environmental insults (noxious agents) concerned will then be discussed, as well as possible genetic risk factors.

Fig. 2.1 Schematic presentation of the pathogenesis of chronic obstructive pulmonary disease (COPD) as a result of host exposure to environmental risk factors. Abnormal inflammation may play a significant role in the pathogenesis (for more details, see text).

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