The Modifying Influences of Silicosis and Silicosis with Infection upon the Healthy Chest

Abstract

FOR years, the spectacular roentgen findings of pneumoconiosis were regarded with passive interest. More recently, because of the occupational importance of the disease and its controversial medico-legal aspects, it has received considerable recognition. At the present time, it is generally conceded that the roentgen examination when properly done is the most precise method for determining pulmonary changes in patients suspected of having pneumoconiosis. The absence of pathognomonic signs and symptoms in pneumoconiosis has placed a heavy responsibility upon physicians interpreting roentgenograms in questionable cases. It behooves these men, therefore, to become thoroughly familiar with (1) the anatomy of the chest and its physiologic changes; (2) the normal roentgenographic and fluoroscopic appearances and their permissible variations; (3) the histology of the lungs and pulmonary lymphatics; (4) the pathology of pneumoconiosis and the diseases with which it may be confused; (5) the roentgenographic appearances of pneumoconiosis and the conditions simulating it; (6) the physical background involved in the production of pneumoconiosis, and (7) the proper technic for obtaining the most diagnostic chest films. Pneumoconiosis is a general term for the condition induced by the long-continued inhalation of dust. A discussion of the entire subject is beyond the province of this report. Our remarks will be confined to silicosis, a condition of the lungs caused by the inhalation of free silica. For years, physicians have classified silicosis according to the degree of lung involvement. These classifications have overtly connoted continued activity and progressive changes as the result of the silicotic invasion. Recent experiences with workers in pure silica have led us to endorse a more simple classification. This classification divides silicosis into two large groups: (a) simple silicosis, and (b) silicosis with infection, which is more simple and probably of more practical value. The various “stages” of silicosis used in other classifications may be explained on the basis of coexisting respiratory infections and the modifying influences of respiration and other contaminating dust. According to Miller (1–4), the lymphatics of the lung may be divided into two main systems. One of them, the deep lymphatics, courses through the lung as a series of vessels which follow the bronchovascular tree toward the hilum. The other, or superficial set, runs through the pleura and empties into the tracheobronchial nodes. These two systems communicate in the periphery of the lung through a series of short lymphatic vessels containing valves which allow lymph to escape from the deep-set into the superficial lymphatics. In addition, there exist small tufts of lymphoid tissue which may be found in the walls of the primary lobule.