Do risk factors act in combination in the development of COPD

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A combination of exogenous risk factors could be an alternative hypothesis to

Fig. 2.2 Epidemiological model of COPD during the life cycle. Shaded area indicates changing function: (a) during pregnancy; (b) during lung growth (age 0-20); (c) during the plateau phase (age 20-40); and (d) during lung function decline (age > 40). Adapted with permission from [3].

explain why there are susceptible smokers. Exposure to a mixture of known noxious agents, such as active plus passive smoking, and environmental pollution and occupational pollution could cause COPD. However, current data do not support the hypothesis of combinations of these risk factors as the basis for the existence of susceptible smokers [3]. A number of other risk factors have been proposed that may play a role in the development of COPD.

Some studies have suggested a link between severe childhood respiratory infections and COPD in adult life [62]. However, this association is rather weak, because it is not easy retrospectively to exclude the possibility that these infections result from lung function impairment, rather than being the cause of it. Nevertheless, viral infections may directly contribute to the development of COPD by incorporating viral DNA into the airway cells. This could alter their genetic material and thus their response to subsequent exposure to cigarette smoke. In fact, increased levels of adenoviral DNA have been found in

COPD patients in comparison with control individuals [63]. Incorporation of adenoviral DNA in animal epithelial cells has also been shown to amplify the inflammatory response on exposure to cigarette smoke [64,65]. A possible scenario might therefore be that susceptible smokers are those in whom a viral infection early in life leads to an excess load of adenoviral DNA in the epithelial cells. These cells might then orchestrate an 'abnormal' inflammatory response to cigarette smoke. However, results of this type have not been reproduced by other investigators in humans.

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