In summing up the evidence bearing on the predisposing and exciting causes of pneumonokoniosis we cannot overlook the recent discoveries of Koch and his collaborators, but may conclude that although there is increasing evidence tending to show that the bacillus tuberculosis is always present in tuberculous pulmonary processes, yet its exact etiological relation cannot be considered as established. We may still hold that when large amounts of inorganic materials are taken into the lungs, particularly if the ventilation or hygienic conditions under which the dust is inhaled are imperfect, certain diverse pulmonary processes are apt to ensue. That phthisis can be thus produced is undoubted, but the nature of the irritant has less to do with the type of the resulting disease than has an inferior or scrofulous constitution, inherited or acquired, or the indulgence in habits directly damaging to the health; since an unvarying specific cause would be more destructive than has been proven, large numbers of individuals escaping any serious effects when equally exposed.
PATHOLOGY AND MORBID ANATOMY.—Whatever be the dust inhaled, the pathological processes set up by it partake of the same essential character, though differing in intensity and in the division of pulmonary tissue principally involved, while the combined inhalation of organic particles may essentially modify the results produced. Examination of the lungs has revealed deposits of various inorganic materials which have been inhaled, such as oxide of iron, indigo, snuff, silica, coal, carbon, etc. A black discoloration of the pulmonary tissue, with or without induration, enlargement, and blackening of the bronchial glands, may, however, have its origin in morbid changes independent of inhaled matter, such as defective elimination of carbon and carbonic acid, with a sort of precipitation of carbon within the tissues.
The black coloration of the lungs, especially in miners, is also partly due to the deposition of a true hæmatoidin pigment in granular form, caused by the irritating particles inhaled setting up changes in the bronchial or pulmonary tissues, resulting in the escape of the coloring matter of the blood either by rupture of capillaries or from transudation of serum. Similar discoloration is often found in cases of chronic bronchial processes independent of a dusty etiology. The most penetrating form of dust is the silicious, on account of its hard, vitreous character. German authors comment on the difference in the power of penetration of mineral coal-dust as compared with charcoal-dust, because the spiculæ of the former are elongated, sharpened splinters. The coloration of the lung from clay-dust does not diffuse itself so readily as coal-dust, yet it possesses more irritating properties and creates more damage.
The morbid anatomy of pneumonokoniosis includes nearly all the pathological processes incident to the pulmonary tissues. The bronchial lesions are those of chronic bronchitis, with thickening of the bronchial mucous membrane, associated with possible ulceration and bronchial dilatations, forming bronchiectasic cavities. These cavities are caused by combined softening of the bronchial tissues with traction from without by the newly-formed fibrous tissue. The bronchial glands may be enlarged to the size of walnuts, and are often perfectly black and gritty on section. These enlarged glands may occasion, through pressure, many changes in the pulmonary tissues. The effect of this pressure is especially manifest in the lymphatic system. The lymph-circulation is further crippled by the accumulation in the lymph-channels of the inhaled inorganic materials. These interferences with the lymph-circulation may be followed by exudation or lobular and interlobular formation of tissue; secondary to these changes the pressure upon the vesicles may cause local congestions, exudations, and even hæmoptysis. By one or all of these processes the expansile power and elasticity of the lung are slowly depreciated, emphysema develops, intertwined with the lesions of acute, subacute, or chronic bronchitis, fibroid phthisis, and atrophic emphysema. Nodules of cretaceous matter can be recognized through the lungs, which are black in anthracosis or gray in silicosis. These nodules occur from the size of a pin's head to that of a pea, and are especially found in the lungs of glass-cutters, sandstone-workers, and grinders. In these cases they consist in part of iron and in part of stone. In sandstone-workers they are composed of silica; the organ feels nodulated, very fibrous, and in some cases actually gritty. The predominant form of pulmonary change is fibroid; hardened districts of advanced cirrhosis occur measuring two inches and upward in length and width, and in depth and thickness nearly as much. These may be rounded, but are not separable from the adjacent structures, the condensation of the tissues lessening without a defining line. On section they appear tough and leathery, most pronounced along the anterior edges of the lungs, and are apt to be covered in by thickened pleura. If the nodules previously alluded to are encysted, fibrous prolongations extend from these cysts into the substance of the lung, the thickening of the lung being greatest in the septa, on the pleural surfaces, and along the course of the bronchial tubes. Sometimes subacute or chronic pleural processes coexist. The caseous masses found in tubercular fibroid phthisis are infrequent in pneumonokoniosis, but in the latter process the pathological changes may be identical with the ordinary forms of phthisis, especially in those individuals who are predisposed to pulmonary affections and those in whom the pathological processes are rapid.
In anthracosis the lung is large and increased in weight; the surface of the pleura has a bluish-black color, contrasting with the coal-black color of the lungs, which are universally pigmented and contain nodules of pigment. When only small quantities of pigment are present, it presents the appearance of dark lines running between the lobules; on section these are very hard and distinct, being about the size of a millet-seed. They are universally distributed throughout the lung, and in some places appear like small masses of charcoal. Upon squeezing the organ a blackish fluid exudes which stains the hands, but the discharge which is found lying in the bronchial tubes is often yellow and muco-purulent, although the sputa during life is more or less discolored. When the distribution of the discoloration of anthracosis is investigated, it is found to closely correspond with the lymphatic distribution of the lung, and the conclusion is probably well founded that all other irritating particles pursue the same course through the pulmonary tissues. When particles of coal or pigment enter the bronchi with the air, they cannot pass through its mucous membrane, because the basement membrane and fibrous coat underlying it present an obstacle to their lodgment, whilst the cilia of the epithelium tend to prevent their retention in the bronchi; they therefore enter the vesicles, and may be found sticking to the walls. In this way the exemption of the bronchi from pigmentation, even down to the smallest ramifications, can be explained. The interlobular septa ate also the seat of great pigmentation. The germinating epithelium elevates the cells slightly above the surface, and in the interspaces between them the pigment insinuates itself, and thus enters the underlying plasmatic or lymphatic spaces; or the pigment may be incorporated into the epithelial cells, which transfer it to the underlying lymph-space. Once the pigment has found entrance to these lymphatic channels, it is carried by them through the lymphatic vessels in the sheath surrounding the bronchial tubes and the small branches of the pulmonary artery, and in the interlobular septa to the bronchial glands. In this manner the special distribution of the coloring matter in these situations is explained. The special deposit around the small branches of the pulmonary artery is owing to the double set of lymphatics, the peribronchial and the perivascular, which form an anastomosis. The perivascular set is the larger; consequently the pigment passes into them more readily, forming the nodules. Pigment is also found in small quantities around the bronchi, which can be accounted for by the anastomosis of the lymphatics. The bluish-black appearance of the pleura and the distribution of the pigment only in the deeper layers of the visceral pleura are susceptible of a similar explanation, because the deeper layers of the pleura contain lymphatic vessels which are directly continuous by means of the lobular septa with the large perivascular branches of the lymphatic system.
The consequences of the obstruction to the lymphatic and pulmonary-artery circulation may be very serious. In grave cases the lung breaks down, forming a gangrenous-like cavity, which differs from an ordinary cavity in not being rounded; it is more like a gangrene or slough. In a few cases the pathological appearances indicate phthisis, chiefly interstitial, with formation of cavities; sometimes traces of cavities are found which have cicatrized. More commonly oedema is developed in the lung and the bronchial passages. As a consequence of combined bronchial irritation from continuous inhalation of inorganic particles, and the consequent oedema, a continuous germination and shedding of the bronchial epithelium—a chronic bronchitis—associated with emphysema, is maintained. The mechanical cause of this bronchitis—more or less impediment to the vascular and lymphatic circulations by the pigment deposit—is capable of explaining the persistence of various forms of bronchial processes in anthracosis and in other forms of pneumonokoniosis after the patient has ceased working in a dusty atmosphere.
SYMPTOMATOLOGY.—Pneumonokoniosis does not present a special symptomatology. The course of the various morbid processes is insidious and slowly progressive: the development of any of the forms of pulmonary disease depends largely upon the degree of exposure to the exciting causes, or the inherited tendencies, or the susceptibility to influences liable to diminish general vitality or affect the personal hygiene.
The earliest objective symptom of pulmonary lesion is cough, especially recurrent in winter, accompanied by expectoration, which is whitish, frothy, or stringy in character. Gradually the physical signs, taken together with the symptoms, indicate the various forms of bronchitis, acute, subacute, or chronic, sometimes associated with emphysema, bronchorrhoea, or bronchial dilatation. In other cases the symptomatology is that of asthma, either purely spasmodic or secondary to emphysema or cardiac degeneration. In true anthracosis dyspnoea is a marked symptom, and perhaps the accumulation of pigment may interfere with the oxygenation of the blood, or dyspnoea may be due only to an emphysematous pulmonary tissue. The sputa will be black so long as the subject is working in an atmosphere loaded with pigment.
Fibroid phthisis is frequently associated with atrophic emphysema, and the clinical history corresponds with that which is commonly observed in these diseases. Hæmoptysis is rare, but if it occurs it suggests the addition of some tubercular element; a purulent nummular sputa is a suspicious sign of similar import. The symptoms and physical signs of dry pleurisy are to be expected whenever any form of the phthisical process supervenes. The cavities in the lungs are usually bronchiectasic, unless tubercular phthisis occurs as a complication, and the physical signs need no comment. Subacute and chronic laryngitis with ulceration complicate certain cases, particularly those which have inherited or acquired a tubercular tendency.
DIAGNOSIS.—The diagnosis involves a comparative examination of the etiology and the physical signs.