The idea that increases in airways responsiveness--either as a result of exposure to cigarette smoke and/or pre-existing increases in bronchial responsiveness, possibly genetically mediated--might be causal in the pathogenesis of the development of COPD in cigarette smokers presents an attractive hypothesis. The fact that a relatively small proportion of cigarette smokers develop COPD begs for specific susceptibilities as an explanation of selective pathogenesis. In our view, the evidence for modest increases in airways responsiveness in cigarette smokers who do not have asthma or allergies is convincing. Such increases in bronchial responsiveness are modest when compared to patients with asthma and may have a different mechanism. However, the demonstration by Verma et al that two types of patients with cigarette smoke-induced COPD, "bronchitis" patients and "emphysematous" patients, have virtually identical alterations in bronchial responsiveness, and that these alterations appear to be a function of airways caliber, has led us to believe that the changes in airways tone in patients with COPD may be reflective more of changes in airways geometry imposed by the development of disease rather than a measurement of a risk factor in the development of COPD. Of the epidemiologic studies that have emerged throughout the 1980s, problems of possible inclusion of asthmatic subjects in the study groups and of baseline airflow rates as a function of bronchial responsiveness have limited the ability of data to implicate increases in airways responsiveness as a risk factor in the development of COPD.(ABSTRACT TRUNCATED AT 250 WORDS)