To assess the role of chest radiography in the differential diagnosis of bronchiolitis obliterans organizing pneumonia (BOOP) and usual interstitial pneumonia (UIP), records of 34 patients with biopsy-proved BOOP (16 patients) or UIP (18 patients) were reviewed. Chest radiographs taken before biopsy were available in 26 patients, clinical information in 33, and pulmonary function data in 22. These data were reviewed independently, without knowledge of the pathologic diagnosis. The clinical symptoms of BOOP were similar to those of UIP, although the duration of symptoms was longer in UIP (P less than .05), and the prevalence of systemic symptoms was higher in BOOP (P less than .025). The physical findings were similar except that finger clubbing was more common in patients with UIP than in those with BOOP (P less than .01). There was no significant difference in lung volumes, flows, or diffusing capacity between BOOP and UIP. The chest radiograph showed distinguishing features between UIP and BOOP in 23 of 26 patients. The most characteristic radiologic finding in BOOP was the presence of patchy areas of air-space consolidation (eight of 11 patients).

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Using a large animal model of radiation lung injury--the sheep exposed to bilateral thoracic irradiation--we have recently shown the development of sustained pulmonary hypertension during the first 4 weeks following radiation. This is the period prior to the onset of pneumonitis and pulmonary fibrosis. In the present study, we have examined biopsy and autopsy lung tissue from these same sheep and assessed the sequential changes in lung morphology. Six unanesthetized sheep received bilateral thoracic irradiation (a total of 15 Gy); control sheep were sham irradiated. Lung biopsy tissue was taken prior to and at weekly or biweekly intervals during the 4 weeks immediately following radiation. The lungs were also removed at autopsy for light and electron microscopic examination. Our results show early (Week 1) interstitial and progressive intraalveolar edema accompanied by endothelial and epithelial injury. A gradual increase in number of interstitial mononuclear cells was evident from Week 1, both in the lung tissue and in perivascular cuffs. The number of peripheral lung interstitial mononuclear cells was twice baseline from Week 3 and included accumulation of lymphocytes, fibroblasts, and intravascular macrophages. The increased numbers of mononuclear cells paralleled the development of chronic pulmonary hypertension, perhaps suggesting their involvement in the pathogenesis of this disease. Alternatively, it may be that increased mononuclear cell number represents a stage of lung repair.

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