Five normal human subjects were exposed for 1 h to filtered air (FA) once and to 0.3 ppm O3 on 3 separate days. Bronchoalveolar lavage (BAL) fluid was obtained less than 1 h after FA and either less than 1, 6, or 24 h after O3 exposure. FEV1 was measured before the exposures and the BAL. The first aliquot [proximal airway (PA) sample] was analyzed separately from the pooled Aliquots 2 through 4 [distal airway and alveolar surface (DAAS) sample]. The data from the PA and DAAS samples were then combined to calculate the values that would have been obtained by pooling all BAL washes. FEV1 was significantly (p less than 0.05) decreased 1 h after O3 exposure, but it returned to preexposure values at 6 and 24 h after O3. The percent of neutrophils in the PA sample was significantly elevated at less than 1 h (3.7%) at 6 h (16.5%), and at 24 h (9.2%) after O3. The percent of neutrophils in the DAAS sample and calculated pooled values were significantly elevated at 6 h (4.1 and 7.6%) and at 24 h (5.1 and 5.8%) after O3. These data demonstrate that O3-induced symptoms, FEV1 decrements, and airway neutrophilia follow different time courses and indicate that the pooling of BAL washes may obscure the detection of an O3-induced bronchiolitis. The degree of neutrophilia in the BAL did not correlate with the sensitivity of the individual subjects when measured by acute changes in FEV1, suggesting a dichotomy of pathways that result in O3-induced airway neutrophilia and pulmonary function decrements.

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Collagen in lung tissue was examined from patients with adult respiratory distress syndrome, from patients who did not have this disease but required mechanical ventilation and oxygen treatment, and from patients without overt lung disease. Cyanogen bromide peptide mapping techniques were used to determine the ratio of type I to type III collagen present in these lungs. In the fibrotic lungs from patients with adult respiratory distress syndrome a shift was found in the ratio of type I to type III from the normal value of 2:1 to a mean value of 3-4:1. In patients with normal lungs and those with other lung diseases collagen type ratios were normal. Our data suggest that (i) changes in lung collagen of patients with adult respiratory distress syndrome resemble those previously described in patients with idiopathic pulmonary fibrosis, although the changes occur much more rapidly in the former; (ii) the increased content of collagen in lungs of patients with adult respiratory distress syndrome shown by others is predominantly of type I collagen; and (iii) the stimulus to the lung to produce excess type I collagen relative to type III is not solely of iatrogenic origin-that is, resulting from oxygen or ventilator treatment.

We studied whether O3-induced pulmonary function decrements could be inhibited by the prostaglandin synthetase inhibitor, indomethacin, in healthy human subjects. Fourteen college-age males completed six 1-h exposure protocols consisting of no drug, placebo, and indomethacin (Indocin SR 75 mg every 12 h for 5 days) pretreatments, with filtered air and O3 (0.35 ppm) exposures within each pretreatment. Pretreatments were delivered weekly in random order in a double-blind fashion. Ozone and filtered air exposures, separated by 72 h, were delivered in random order in a single-blind fashion. Exposures consisted of 1-h exercise on a bicycle ergometer with work loads set to elicit a mean minute ventilation of 60 L/min. Statistical analysis revealed significant (p less than 0.05) across pretreatment effects for FVC and FEV1, with no drug versus indomethacin and placebo versus indomethacin comparisons being significant. These findings suggest that cyclooxygenase products of arachidonic acid, which are sensitive to indomethacin inhibition, play a prominent role in the development of pulmonary function decrements consequent to acute O3 exposure.

Although referring physicians and patients indicate a high level of satisfaction with telemedicine services and insurers are negotiating reimbursement policies, additional research must investigate the reasons why some payers, patients, and providers resist participation in these services.