Pneumoconioses

PNEUMOCONIOSES, diseases of the lungs, caused by changes in lung tissue under the influence of prolonged dust inhalation in connection with professional factors. (P. is included in the list of professional diseases compiled by the State Insurance Fund for disability insurance.) Changes in lung tissue consist mainly in disseminated progressive fibrosis, most often caused by the presence of silica in the dust. If fibrosis does not form, then there is no P. Not all types of dust are capable of causing fibrosis in the lungs. Such properties—as this is proven by clinical observations and experimental research—are possessed only by inorganic types of dust, and to varying degrees. The name P. was first introduced into world medical literature by Zenker in 1866. He proved the presence of iron in the lung of a worker in iron ore mines, called this condition 'siderosis pulmonum,' and proposed the name P. for lung diseases caused by inhalation of various types of dust. Of all types of dust, only mineral dust and 'artificial' dust (obtained in the manufacture of glass, enamel, brick, cement, iron, steel, chemical preparations, paints, etc.) cause fibrosis, which depends mainly on the greater or lesser content of silicate particles in them. Organic types of dust, which include all types of dust of animal and vegetable origin, causing irritation of the upper respiratory tract in the form of catarrhal inflammation of the mucous membrane of the trachea, bronchi, can lead to the development of various types of bronchitis, bronchial asthma, emphysema, but do not cause the development of connective tissue in the lungs, i.e., fibrosis, and therefore do not lead to P. by themselves. If ^nevertheless, even if not sharply expressed degrees of fibrosis occur, then these 'organic' types of dust are obliged to this admixture of 'inorganic' dust, which is often present in them. The smaller the particles, the more easily they penetrate into the lung parenchyma. According to Mavrogordato, dust particles larger than 5 μ have relatively little significance, from 5 to ¹/₄ μ are dangerous, and from ¹/₄ to ¹/₁₂ μ have no significance. Particles larger than 10 μ cannot penetrate into the alveoli (for more details—see Dust). To understand all the diversity of P. depending on the irritating effect of different types of dust, it is important to note the difference in the reaction of bronchial, and mainly—lung tissue, especially at the very first stages of irritation. When inhaling coal dust, swelling and coal pigment are found in some cells of the alveolar epithelium. Later, in the alveoli, there accumulates desquamated alveolar epithelium with a large amount of pigment, detritus, and fine dust particles. The latter can be found even earlier in the walls of the alveoli and around the bronchi. In a later stage—after several years of work in a coal mine—much more swollen alveolar epithelial cells containing coal pigment are found, more detritus from the breakdown of these cells, leukocytes, more pigment in the walls and in the connective tissue between the lobules [see separate table (pp. 239-240), fig.]; connective tissue is somewhat more than normal, bronchial and mediastinal glands are black and enlarged in volume. If work in the mine continues for many years but was stopped long before death, then swollen alveolar epithelial cells are not found: the epithelium is normal; no pigment is found in the cells or alveoli, but dust is contained in the walls of the alveoli, in the partitions, and in the peribronchial connective tissue.—The condition of cells and dust in the lungs of dusty rabbits has been well studied in the same direction and at various stages of irritation with lime dust (research of Iszard). It turned out that the longer the animal was exposed to dust, the more pronounced was the desquamation of the epithelium and the number of macrophages filled with dust particles and located in the interalveolar tissue increased. Autopsies of animals a month and later after cessation of dusting showed less and less macrophages loaded with dust. The most light is shed on all the complex questions about the solubility and absorption of mineral dust by the research of Mavrogordato and other researchers (Gye, Purdy, Kettle, Cummings).^vAccording to Mavrogordato, depending on the type of silicate dust, 'dust cells' form in the lungs, which at first lie in the alveoli. In Mavrogordato's opinion, these cells do not originate from the bronchial epithelium, but most likely from the cells of the vascular and lymphatic endothelium. Many researchers (Zeman, Pesa-khovich, Sheinin) disagree with this assertion, believing that the alveolar epithelium also actively participates in the formation of dust cells. With coal and slate dust, phagocytes quickly die, the dust remains lying extracellularly in the tissue and mainly on the outer part of the blood vessel. These types of dust can cause catarrhal inflammation of the mucous membrane, which expels them from the lungs. 8 weeks after cessation of dusting animals, mineral dust free from silica was found scattered in the cells and in the tissue. A completely different picture is obtained 8 weeks after inhaling 'free silica.' Dust particles lie in the cells, but these cells are not scattered in the tissues, but lie in heaps, together, so they can be called 'pseudotubercles.' Dust-filled cells move first of all toward the subpleural lymphatic network, and therefore dust is found much earlier there than in the bronchial glands. According to English and American researchers, silica acid first has a kind of preservative effect on cells, delaying their autolysis and transition to the lymphatic system, but after they get there, unlike other types of dust, they block the lymphatic network. In the perivascular spaces, increasingly dense fibers are formed, in which these dust-filled cells are embedded, and ultimately the vessel with its accompanying lymphatic spaces turns into a bundle. Thus, as a result of the initial irritation in silicosis, pleural and freely lying pseudotubercles and obliteration of lymphatic pathways are formed. It is important to note that dust-laden cells themselves turn into fibers, but fibrosis develops mainly due to pseudotubercles and obliterated lymphatic pathways. Based on experimental research by Golden, coal dust that entered the lungs of an animal completely disappears from there in several weeks, while silicate dust remains in the lungs. What this difference depends on is the main question of the problem of P., which has not yet been resolved. Gye and Purdy experimentally obtained significant development of fibrosis in the liver, enlargement of the spleen, interstitial nephritis when injecting rabbits for several weeks with small doses of orthosilicic acid Si(OH)₄. By injecting under the skin to mice the same Si(OH)₄, as well as insoluble SiO₂, they caused in both cases (but faster in the first) coagulation necrosis, which was gradually replaced by organized inflammatory fibrosis. Kettle, by inserting under the skin to rabbits collodion bags containing one—insoluble preparation, and others—solution of calcium chloride, proved that the reaction around the bag with SiO₂ was much stronger. According to Kettle, SiO₂ is a protoplasmic poison. The research of Pesa-khovich is instructive in this regard, who, by inserting collodion bags with various types of dust into the subcutaneous tissue of infected (tuberculosis) animals, could not detect preferential damage to tuberculosis tissues surrounding the bags with silicate dusts. The tissue reaction around collodion bags with silicate dust shows the low solubility of these dusts, but when silicate dusts are introduced into the body without a bag, part of them is hydrolyzed (porcelain dust), causing local necrotic lesions, while others (flint, sand) do not hydrolyze at all, and finally some are poorly hydrolyzed (chamotte dust). Studying the phagocytosis of various dusts, Pesa-khovich comes to the conclusion that the biological harmfulness of dust depends on the rate of phagocytosis of its particles, and not on their solubility. Cummings in vitro proved that colloidal silica acid significantly weakens the bactericidal properties of blood and delays the complement formation reaction. Fenn (Keppe) also in vitro proved that coal particles are phagocytosed by leukocytes 3 times faster than quartz particles. All these data provide sufficient support for the assertion that silicate dust causes much more changes in the lungs than other types of dust. All types of conioses are now considered as conioses caused by their origin primarily by the main part of the dust—SiO₂, and then by other constituent parts. So, for example, anthracosis, which until recently received so much attention and was described as the main type of P., has yielded first place to silicosis. Anthracosis affects coal districts and different mines to a far from equal degree. From the experience of the Donbas and coal regions of Germany and Sweden, it is known that so-called

"Soft" and "smoky" varieties of coal do not cause a sharply expressed fibrosis in the lungs, and conversely, "anthracite" when inhaled for a long time gives a picture characteristic of P. This difference is due to the different content of silica in the composition of coal from different regions. The same can be said about other types of coniosis, where silica is a component of the dust causing them. Regarding the clinical diagnosis of P., the differential diagnosis with tbc, there is currently no unified opinion. Most adhere to the view that the picture of not only "early", but also "medium" and "expressed" forms of P. presents nothing characteristic, differs in no way from the picture that occurs in developed forms of chronic bronchitis, emphysema without disturbance of cardiac compensation in some cases and with disturbance in others. Another group of authors describes a certain symptom complex. All researchers consider the most characteristic discrepancy between the relatively small data of stethacoustic character and the very "rich" X-ray picture. Among individual symptoms, dyspnea has special significance, which gradually increases and intensifies as the disease progresses. If it is possible to detect these qualitative changes, manifested primarily by dyspnea, in quantitative indicators (serial changes in spirometry, breath-holding tests), then it is partially possible to establish a parallelism between the intensification of dyspnea and the increase of coniotic changes in the lungs. According to the opinion of the All-Ukrainian Institute of Hygiene and Occupational Pathology, a reliable diagnosis of P. can be made on the basis of a triad of signs: a) a consistent professional history and professional experience in dusty production, b) the symptom complex obtained in "medium" and "expressed" forms of P. by physical methods of investigation and by assessment of functional tests of the cardiovascular and respiratory systems, c) a technically flawless X-ray. The diagnosis is presumptive in the presence of two components of the indicated triad: either a consistent professional history and experience and clinical data, or a consistent professional history and professional experience and a positive X-ray, with the second combination giving the diagnosis greater certainty than the first. As for the symptom complex in "medium" and "expressed" forms of G.G., it is based in general on the reaction of lung tissue to the introduced dust, i.e. a) on general emphysema, b) on fibrosis and c) on the subsequent vicarious emphysema. This is a high-pitched and continuing to the lower parts boxy shade of percussion sound, weakened or harshly-weakened breathing, presence of symmetrically located areas of dullness, detectable with the weakest percussion according to Veme in the axillary area on both sides (according to the research of workers of the Institute of Pathology and Hygiene of Labor in Kharkov - in the middle third of the scapulae or below the angle of the scapulae also symmetrically), presence in these places of a small amount of moist rales and pleural changes from the very delicate to the very rough friction noise, more often on the right. This symptom complex, if to it are added data from the cardiovascular system in the form of a pulse wave, slowed in some and accelerated in others cases, usual intensification of the 2nd tone on the pulmonary artery, blood pressure without special characteristic changes for this disease, expansion of the heart borders to the right, and subsequently also to the left in far-advanced forms, does not represent anything specific, sharply highlighting this disease from other similar ones (first of all from expressed forms of emphysema). Individual symptoms and some of their groupings enter into the composition of this or that disease, but if the presence of professional history and professional experience is added, then the diagnosis can already be made presumptively. Final confirmation should be given by the X-ray, on the basis of which most researchers distinguish three stages of P. To understand the nature of pneumoconiotic changes on the X-ray plate, one must proceed from the reaction of lung tissue to the dust introduced into the lung tissue and from the sequence of changes occurring in it, keeping in mind that the anatomical substrate determines the nature of the X-ray picture. Part of the dust, as is known, is excreted through the respiratory tract, another part remains in the alveoli, irritating the cells of the reticulo-endothelial system, as a result of which the production of macrophages and young fibroblasts increases. These cells with captured dust particles rush into the lymphatic spaces, perivascularly, peribronchially, as well as into the subpleural lymphatic plexuses leading to the lymphatic nodes and the root of the lung. Changes in the lung tissue consist of the following stages: blocking of the lymphatic pathways by cells grouped together (coniotic nodule) impregnated with silicon; development from these cells of fibers (first microscopic fibrosis of lymphatic pathways, primary lobules, branches of the pulmonary artery, venous roots and bronchi, then proliferation of interalveolar tissue and interlobular septa, further increase and fibrosis of the tracheo-bronchial lymphatic glands), finally development of interlobar, subpleural, perivascular and peribronchial fibrosis. At the same time, microscopic fibrous nodules scattered throughout the lung, in places of lymphoid formations located at the confluence of perivascular and peribronchial channels, begin to noticeably increase, reaching the size from a pinhead to a pea, i.e. from 1 to 5 mm. As difficulties for lymph outflow to the roots of the lungs increase, its flow in the reverse direction, i.e. along the subpleural lymphatic network, intensifies. Lymph outflow also causes corresponding changes here in the form of fibrous nodules, thickening and adhesions. The described changes are limited to the area of the root of the lung or also involve the central parts of the lungs, to which the largest part of dusty air reaches; in this case, nodules are located in a small number radiating from the enlarged roots. The next phase consists in the fusion of individual nodules into large conglomerates and in a sharp intensification of interstitial fibrosis. Usually the pleura is also involved in the process; this is manifested in the formation of adhesions not only with the diaphragm, but also in the area of the mediastinal and interlobar visceral pleura. From the point of view of the X-ray picture, three stages of P. are distinguished. The first stage is characterized radiologically by a clear increase, intensification of the root shadows and the appearance of linear striation in the form of a network structure of the peripheral zone. The intensification of the stem shadows is most noticeable in the inner part at the base of the lung, and then in the supraclavicular area. The outer part at the base of the lung is less affected because its lymphatic vessels flow through the pulmonary ligament into the pleural lymph nodes, and not into the root ones, as in the other lung areas. The changes of the first stage are not specific for P.; they can also be caused by chronic bronchitis, blood stasis and tbc. The second stage is characterized by the appearance on the X-ray plate of nodules of various sizes - from a pinhead to a pea [see separate table (pp. 223-224), figure 8], then on both lung fields against the background of phenomena of the first stage a typical mottling appears, capturing them more or less uniformly, while the apices and the posterior and lower parts are less affected. The first nodules appear in the right lung around its root. The localization of nodules and the sequence of occurring changes depend on the size and direction of the bronchial tree. Therefore, as was indicated, the right lung is more and more strongly affected. The apices, usually poorly ventilated, remain little or completely unchanged. As for the posterior and lower parts, in addition to the indicated cause, certain peculiarities of their lymphatic system play a certain role. Nodules located laterally from the enlarged roots, de la Camp compares with the form of a butterfly, and Ikker - with the form of wings. Often in this stage a decrease in the root shadows can occur, explained by the reverse flow of lymph along the subpleural system. The third stage of pneumoconiosis, designated as large-nodular, is characterized by diffuse fibrosis, fusion of individual nodules into more or less large irregular masses and the appearance of clouded areas. These signs may occur simultaneously or each separately. In the unilateral development of indurated areas, a tumor-like form of pneumoconiosis arises, which can be distinguished from a true tumor only by the presence of other signs characteristic of this stage. On the other hand, if the shadow of the indurated area has considerable size, irregular shape and indistinct borders, then this gives grounds to suspect the presence of tuberculous infection. Most researchers believe that the development of coniotic changes in the lungs owes its origin to a previous, existing even in a latent state tuberculous infection.

Many of the adherents of this view attribute this origin only to 'expressed' forms of P., admitting that for initial and moderately expressed forms such a combination is not necessary. Hilbschman entirely joins the long-expressed position of Ribbert that 'most anthracotic foci represent the result of healed tuberculous foci.' As for the histological structure of the nodules, the study of which researchers attached great importance, hoping in this way to find the key to clarifying the complex question of the relationship between coniosis and tuberculosis, Mavrogordato distinguishes three forms of nodules: a) 'blockade nodules' along the course of the 'blocked' lymphatic network, b) sharply defined, occurring in normal or almost normal lung tissue 'pseudotuberculosis' and c) inflammatory nodules, 'similar to Pülmonary foci,' surrounded by an atelectatic zone of lung tissue—'infectious nodules'—owing their origin to the action of both factors: 1) infection, mainly and almost exclusively tuberculous, and 2) dust. All developed forms of P., which on the x-ray show significant fibrous hardening, and especially accompanied by areas of enlightenment, in his opinion have a 'coniotuberculous character.' Such a view with respect to developed forms of P. is extended by some to the entire problem of P. Among Soviet researchers, Karpilovsky adheres to this very view. Holst, on the basis of his dynamically traced material, comes to the conclusion that only two stages can be attributed to P.—this according to the x-ray picture stages I and II—and that stage III of P. does not exist, since this is always tuberculosis. The one-sidedness of this view is indisputable. Morphological similarity does not yet mean similarity in substance—the functional evaluation and the clinical picture, the course of the process, are of much greater importance, which these researchers do not sufficiently take into account. In opposition to this view, other researchers (among whom from the Soviet camp are Sheinin, Gottlieb), on the basis of also dynamically traced material, taking into account the same immunobiological reactions, x-ray data, clinical course of the process, biological tests (injection of sputum of doubtful cases into guinea pigs), etc., come to the conclusion that not only the so-called initial forms of coniosis, but also medium and well-developed ones can be and are, owing their origin to the action of dust alone, that to these expressed forms very often a tuberculous infection is added, or that under their influence old tuberculous foci are exacerbated and provide grounds for classifying them as coniotuberculous. 'Pure' forms in a developed state occur, although not often; more often they are of a mixed coniotuberculous character, but this by no means means that all P. is only fibrous degeneration and calcification of 'secondary tuberculosis.' Even in cases of mixed coniotuberculous character, the entire clinical picture speaks against 'secondary tuberculosis.' According to the opinion of Sheinin and Gottlieb, pneumoconiotic changes strongly predispose to the development of a tuberculous process, which can in some cases join the initial coniotic changes, in others—to much later ones. The entire course of development of the coniotuberculous process, which (according to data from the Institute of Pathology and Occupational Hygiene in Kharkov) appears sometimes as a tuberculous process joining a coniotic one, sometimes as a coniotic process superimposed on a tuberculous one, is schematically depicted as follows. From the first hours of stay and work in a dusty production until the end of their working life in it, the worker daily remains for a number of hours in an atmosphere densely saturated with dust. Its particles, thanks to their physical and chemical properties, settle throughout the respiratory tract down to the alveoli and cause the formation of inflammatory foci and foci with all the resulting pathological-anatomical and clinical consequences. With a high degree of probability, it should be assumed that during the development of P., very suitable conditions are often created for the introduction and development of tuberculous infection or reinfection, especially if this is facilitated by one or another predisposing factors (contact, general weakness, etc.). And indeed, upon examination, especially of a dynamic nature, one can be convinced that a significant contingent of these workers at a young age and with a relatively short length of service (1-2 years) suffer from tuberculosis—most often—in a subcompensated form. This corresponds to the period when 'fresh' coniotic changes apparently consist only in catarrhal irritation of the upper respiratory tract and blocking of the lymphatic network in the lungs. In this state, a significant part of the affected young workers leave the production. But a significant part of workers remain intact with respect to tuberculosis, despite the presence sometimes of extremely predisposing pathological-anatomical changes in the lungs. Not all young workers who contract tuberculosis 'leave' the production. The tuberculous process in them sometimes proceeds extremely unusually in connection with the course of development of coniotic changes in the lungs. With the passage of time, 'fresh' changes in the lung tissue are more and more replaced by scar processes, i.e., abundant proliferation of connective tissue. The process that began in the early years of working and professional стаж proceeds over a long period (decades) benignly, according to the type of the so-called 'favorable' cirrhotic form of pulmonary tuberculosis. But gradually, as the developing scar tissue more and more reduces the respiratory surface, constricts blood vessels and lymphatic vessels, and thereby hinders blood circulation and causes disturbance of nutrition, and later destruction of lung tissue, the coniotuberculous process acquires a malignant course. When during prolonged stay in the body's resistance and adaptability decrease, the danger of new tuberculosis and exacerbation of old tuberculous process arises. Approximately at that time, i.e., in older workers with the longest length of service, it is possible to establish the clinical picture characterizing the exacerbation of old tuberculosis, so to speak, the 'reverse wave' of increase in tuberculosis morbidity. The thus exacerbated tuberculous process no longer proceeds as favorably as before; there are no suitable conditions either in the whole organism or in the lungs in particular. The organism apparently perishes earlier than in ordinary cirrhotic pulmonary tuberculosis without accompanying P. It should be borne in mind that for prognosis and judgment on residual working capacity, one must not proceed from morphology alone, but mainly from the evaluation of the general functional state, from data of various functional tests. Among the latter, along with the return of pulse, blood pressure to normal after exertion, serially conducted spirometry, reduced to tests of Dreyer (for growth), West-Peabody (for body surface area) and the breath-holding test by Stange and Sabrazes, acquire great importance. That stage III on the x-ray does not always correspond to worse functional test results than in P. stage II or even I-II, is known to many researchers of the P. problem. In cases of coniotuberculosis in judging prognosis and residual working capacity, one should proceed mainly from the clinical picture under the sign of tuberculous intoxication. Here, prognosis is usually always doubtful, even in cases with closed tuberculosis; it becomes very poor, even hopeless in cases of open forms of coniotuberculosis. As for the disabling effect of P., here one must first note that 'pure' forms of P. rarely disable, that in such cases the disabling factor is the high degree of emphysema and cardiovascular changes. Cases of mixed, coniotuberculous character disable much more, and the more so, the more the corresponding types of dust cause coniotic changes in the lungs and predispose to tuberculosis by exogenous route or by endogenous reinfection. These cases are encountered much more often in productions with the predominant action of silicate dust (porcelain-faience production, quarries, metal grinding, etc.), than for example in the coal mines of Donbas (especially with bituminous coal, not anthracite) or in the iron ore region of Krivoy Rog. The main line of the struggle with P. goes along the line of improving dusty productions (see Dust).