Document Exvnyg9bDy0zOG5X0Ov2Zae9n

FEBH23-B00S 07:09P FROM: TO:1618S5 IOK MUCOSIS AND OTIICR FIOROTIC PNEUMOCONIOSES Patholog i and morbid anatomy of asbestosis In cru ihing operations, fiberizing and disintegrating, in opening, spinning, weaving and the filing of asbestos mattresses, production of fine thistledown dust occurs This consists of fine needles nr spicules of asbestos, which are inhaled by the workmen Most of the dust inhaled never reaches the lungs, bpt Is arrested in the upper respiratory tract and trachea, from which it is rejected in the nasal mucus and sputum Whereas only the minute parljiclcs of silica gain entrance and are retained within the lungs, much larger particles of usbestos, when mhulod, because of their physical form, arc mechanically trapped. Fibres up to 200 microns have been delected in the air passages, but dangerous fibres measure up to 20 microns. In the lung no local necrosis results, nor is there any leucocytic reaction. As a result of mechanical irritation the pulmonary epithelial cells are desquamated, and fibroblasts appear round bronchioles and alveoli, in interlobular septa and in the subpleural tissue. Finally, collagenous fibres appear around the distal raraificajtions of the bronchial tree. Gtardner and Cummings (1931) have shown, by animul-inoculniion ex* perimems, that the chief site of asbestos-dust localisation is the respiratory bronchiple. They describe the curly lesion, in the guinea-pig exposed to inhalation of asbestos dust, as follows: " The asbestos dust is carried by the Inspired air only to the distal respiratory bronchioles . . . The mononuclear phagocytes from the adjacent connective tissues enter the lumen of the air passages and engulf the particles. ;The|phagocytes with their contained fragments of dust are frequently pushed nsidc into the alveoli which pouch out of the sides of the bronchioles, where many of them remain Indefinitely. More dust entering the lung is held up by the partial obstruction created, and further reaction is largely proximal la ihc point of original localization." At 60 days the authors describe the dust-cells of the terminal bronchioles as being increased, and the lumina of some of the lateral alveoli completely blocked with mononuclear phagocytes und giant cells At the end of 2 months small asbcslosis bodies appear. After 90 days' exposure it was found that the amount af cellular reaction had not kept pace with the number and size of the asbcslosis bodies Hyperplasia of the lymphoid tissues was now visible. At the end of a ypar the wails of the bronchioles proximal to the alveolar ducts were thickened fijom excessive local accumulation of phitgooyies, but definite proliferation of fibroblasts was not noted until after 550 days. This was confined to the walls of the air spaces adjacent to the deposlli or dust phagocytes. Ai ihe end of n further 100 days a true fibrosis developed, contracting the air spaces, which now appeared to be filled with compact masses of dust cells and phagocytes, fibres and bodies. After 2 years the mischief had reached the periphery of the lung, and sub-pleural greyish-white nodules were uniformly distributed over the surface. King. Clegg and Roe (1946) have recorded the results of experiments in rabbits exposed io the inlriuruchcnl injection of usbestos fibres of varying length. In P:6'13 animals treated comparable wji with short fihia of powdered al Post-mortem app Microscopicalji> The morbid ap above for siljeosi The pleural chm of pneumoconio advanced long-st sheath like a pla folds, and it io frequently the \ completely obliti as is shown on p The asbestosis fibrotic charactei Ftc. 19.--Fern lung showm theTower pol Dt II Wyi