Localized Inflammatory Pulmonary Disease in Subjects Occupationally Exposed to Asbestos (12)

DeVuyst et al reported granulomatous inflammation in the lung tissue from a 32-year-old chemist who had worked for eight years in a dusty environment containing aluminum powders. They indicated that the pathologic changes in the lung biopsy specimens were similar to those of berylliosis and sarcoidosis, but demonstrated that the patient had neither of those diseases. We have observed granulomatous inflammation in open lung biopsy specimens in two persons exposed to aluminum dusts, and in both cases, analytical analysis of lung tissue showed significantly elevated concentrations of aluminum compared with control lung tissue. The report by DeVuyst et al and our own observations suggest that other mineral dusts, such as aluminum as well as asbestos, can induce granulomatous inflammation in the lung.
Case 8 is of significance because of the recent report by Rom and Travis of lymphocyte-macrophage alveolitis in nonsmoking individuals occupationally exposed to asbestos. Open lung biopsies were done in two patients described in their report, and showed changes essentially identical to what we observed in case 8. Pathologically these changes are similar to those seen in hypersensitivity pneumonitis, although there is no evidence that asbestos causes a hypersensitivity type pneumonitis. Also of interest is the report of Sprince et al who reported an increase in T lymphocytes in bronchoalveolar lavage fluid from patients with occupational asbestos exposure.
In summary, the cases reported herein suggest that asbestos may cause localized lesions in the lung that clinically and radiographically can be misinterpreted as cancer. Pathologically, these localized nodular lesions show either BOOP, localized nonspecific scarring and inflammation, granulomatous inflammation, a desquamative interstitial pneumonitis type pattern, or a nonspecific fibroinflammatory reaction with numerous eosinophils. Our findings also suggest that asbestos may cause a lymphocyte-plasma cell interstitial infiltrate. We believe that our findings reported herein expand the spectrum of pathologic changes potentially caused by asbestos.