EPIDEMIOLOGIC EVIDENCE FOR DIFFERENT TYPES OF CHRONIC AIR-FLOW OBSTRUCTION

There would appear to be a large body of evidence suggesting that there are at least two different types of chronic airflow limitation in our population sample in Tucson, Arizona. One develops in subjects whose clinical syndrome is characteristic enough of asthma that they are quite aware of having this disease. The likelihood of the diagnosis is very closely related to the serum IgE level, although in older age groups this is apparent only if one accounts for the changes in IgE level that occur with age in the population as a whole. Among subjects with active asthma, the severity of FEV1 impairment between acute attacks was closely related to the severity of wheezing complaints and increases with age. As yet unpublished data from our study show that in these subjects there is little if any relationship of lung function impairment to cigarette consumption, presumably because those with the most severe asthma tend not to smoke or to quit relatively quickly if they do begin. This type of disease, which we have called chronic asthmatic bronchitis, appears to conform well with the Dutch hypothesis. An allergic constitution seems essential for its development, and a predisposition to bronchial hyperresponsiveness may also be required for an allergic reaction in the airway to lead to frank airway obstruction. However, at least in our data, there is no evidence that the usual form of COPD developing in heavy smokers has any relationship to an asthmatic constitution. In the absence of known asthma, the degree of FEV1 impairment is closely related to the quantity of smoking and shows no relationship to any evidence of allergy. Many of these subjects appear to have an insidious development of ventilatory impairment with few respiratory symptoms, and many have not seen a physician for their disease. Their diffusing capacities tend to decline with the development of CAO, suggesting an emphysematous component in their disease. There is at least a strong suspicion that the development of an emphysematous type of COPD depends on the status of the lungs' proteolytic-antiproteolytic mechanisms (18). There is no reason to believe that this is determined by the presence or absence of an asthmatic constitution. Unfortunately, practical criteria for distinguishing chronic forms of asthma from COPD in epidemiologic studies have not yet been described, and the problem is complicated by the likelihood that overlap syndromes with features of both types of illness almost certainly occur. Also, it would seem highly likely that a person with mild or even subclinical asthma who does continue to smoke would be especially prone to develop severe chronic airway obstruction. From our data, however, this does not appear to be the usual manner in which COPD develops in heavy cigarette smokers. We believe that at least two forms of CAO are present in our population and that they differ with regard to their risk factors, pathogenic mechanisms, physiologic characteristics, and clinical courses. An attempt should be made to distinguish these types of disease when examining possible risk factors for CAO or when describing the clinical courses of patients with CAO.