A study of 14 healthy adult subjects was undertaken to determine whether brief exposure to 0.5-0.6 ppM of ozone would increase bronchial reactivity to inhaled irritants, as reflected by the rise in airway resistance provoked by aerosol challenge with weak solutions of histamine or methacholine. An additional study of 9 subjects with nonasthmatic allergic diseases was also undertaken to determine the effects on ozone on bronchial reactivity in atopic subjects. Subjects from both the non-atopic groups were exposed to ozone on several occasions to determine whether tolerance develops to the sensitizing effects of ozone on bronchial responsiveness. The results indicate that exposure to 0.6 ppM of ozone for 2 hours increases bronchial reactivity to histamine in both normal and atopic subjects and that the increase in responsiveness is blocked by pretreatment with atropine, suggesting that postganglionic cholinergic mechanisms are involved. Bronchial reactivity returned to control levels in 1-7 days in most subjects, but tolerance to repeated exposures to ozone was not observed.
The mechanism of airflow obstruction was investigated in 21 patients with tracheal stenosis using tantalung tracheograms and pulmonary function studies, including flow-volume (FV) loops. In 4 patients with severe obstructive pulmonary disease, FV loops failed to demonstrate radiographically visible tracheal stenosis. In 17 patients, both FV loops and tracheograms demonstrated central airway obstruction. In three of the 17 patients, the stenotic segment was a rigid lesion at the thoracic outlet with similar limitation of inspiratory and expiratory flow. In nine of the 17 patients, the lesion was extrathoracic (rigid in 6 patients and pliable in 3). The 3 pliable extrathoracic lesions produced marked limitation of inspiratory flow but normal expiratory flow. Three rigid extrathoracic lesions produced inspiratory flow that was more limited than expiratory flow, suggesting dynamic inspiratory compression of the normal extrathoracic trachea. The one rigid intrathoracic lesion caused expiratory flow limitation greater than inspiratory flow limitation, suggesting dynamic compression of the intrathoracic trachea on expiration. The position of the obstructing lesion and dynamic compression of the normal, compliant trachea may be the major determinants of the difference in flow limitation between expiration and inspiration in some patients.
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