A single asbestos body was identified in the frozen section specimen, and asbestos digestion analysis of the lung tissue showed 4,666 asbestos bodies per gram of wet lung tissue, 819 X 10^ chrysotile fibers per gram of dry lung tissue, and 20 X 106 tremolite fibers per gram of dry lung tissue. The authors discussed the experimental and clinical studies, suggesting that asbestos could cause such a lesion, but they did not comment on the association of desquamative interstitial pneumonitis with cigarette smoking.
In case 5, at postmortem examination, approximately one third of the right upper lobe was involved by a fibrotic process with associated cystic changes in which necrotic material was present in the dilated cystic spaces. Histologically, there was necrotizing granulomatous inflammation (culture and microorganism special stain negative), in which asbestos bodies were easily identified and seemed to be concentrated in the areas of necrosis. The pathogenesis and morphogenesis of this change is uncertain, although the pathologic changes suggested a fungal or mycobacterial infection.
In case 6, the necrotizing granulomatous inflammation in association with fungal hyphae resembling Aspergillus is of interest in that Hillerdal and Heckscher reported Aspergillus infection in four persons with asbestos-related lung changes, two of which had localized lung masses. The authors cited one previous case of an aspergilloma in association with asbestosis, and indicated that asbestos can lead to cylindric bronchiectasis and fibrotic narrowing of bronchi. They also discussed how asbestos can affect the immune system, and suggested Aspergillus infection may be related to a malfunction of immunologic surveillance.