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“Pneumoconiosis” is the general name for occupational lung diseases caused by exposure to industrial dust and characterized by the gradual development of sclerotic changes in the pulmonary parenchyma. Their development depends on the amount of inhaled dust; the size, shape and buoyancy of aspirated particles (dust particles); solubility and physico-chemical reactivity of dust particles; possible concomitant effects of other irritants (e.g. tobacco smoke).

The amount of dust held in the lungs is determined by its concentration in the ambient air, the duration of aspiration and the effectiveness of clearance mechanisms. Any violation of the integrity of the mucociliary apparatus of the airways predisposes to the accumulation of dust in the lungs, and the most dangerous are particles with a diameter of 1-5 microns, which allows them to reach terminal bronchioles, alveoli and settle on the epithelium. In normal lungs, there is always a small pool (pool) of alveolar macrophages, capable of rapidly increasing with the massive entry of dust particles into the alveoli. However, macrophage protection from dust, carried out mainly due to phagocytosis of particles, can be suppressed by large masses of respirable dust (in industry, construction), as well as using specific chemical interactions of dust particles and macrophages.

The solubility and cytotoxic quality of respirable dust particles, largely determined by their size, can affect the nature of changes in lung tissue. The smaller the particles, the higher the ratio of their surface area to mass, and the more likely and with greater speed toxic substances brought in by dust will accumulate in the tissue fluid of the lungs. Larger particles are poorly soluble and can persist in the lung parenchyma for many years. They cause fibrosing pneumoconiosis, characteristic, for example, of silicosis. The tissue reaction to crystalline silica (silicon dioxide, Si02) used in the manufacture of glass, ceramics, concrete and other products and existing in nature in the form of quartz shows how important the physicochemical reactivity of dust particles is in the development of pneumoconiosis. Quartz can directly damage tissue and cell membranes when they interact with free radicals and other chemical groups on the surface of dust particles. The resulting damage to the membranes ends in cell death. However, more important is the ability of quartz to induce alveolar macrophages to secrete products that cause an inflammatory response and ensure the proliferation of fibroblasts and the deposition of collagen. The role of mediators of inflammatory reactions and fibrosis is also crucial in the pathogenesis of asbestosis. Many of the neurotransmitters and cytokines that were discussed when discussing the pathogenesis of diffuse interstitial fibrosis may have some significance in tissue reactions to aspirated dust.

Part of the dust particles can penetrate into epithelial cells or pass through the barrier of the lining and interact directly with fibroblasts and interstitial macrophages. Some particles reach the regional lymph nodes via drainage pathways with lymph or inside macrophages and, thus, cause an immune response to dust components and / or their own proteins modified by the particles. As a result, local reaction intensifies. Smoking aggravates the effects of aspiration of any kind of mineral dust; the combination of smoking and asbestosis is especially harmful.

Pneumoconiosis of coal miners. It can be simple and complicated (progressive massive fibrosis). Coal - medium-grade fossilized coal containing 75–97% carbon in the combustible mass. Anthracite - fossil coal of the highest stage of coalification contains 93–97% of carbon. Despite the fact that currently the main types of fuel have become cheaper liquid and gaseous types, fossil coal retains a large, and in some places predominant importance due to the high heat during combustion. The spectrum of changes in the lungs of coal workers (mainly miners) has three groups of options: asymptomatic anthracosis, in which pigment accumulates without a noticeable cellular reaction; simple pneumoconiosis of coal miners, in which macrophages accumulate, but impaired lung function is small or absent; complicated pneumoconiosis, or progressive massive fibrosis with a threatening decrease in organ function. Technological improvements aimed at reducing the dustiness of coal mines and reducing the level of dust aspiration have led to a significant decrease in the incidence of miners with pneumoconiosis, but not in all countries. About 10% of miners with simple pneumoconiosis of coal miners survive to form complicated pneumoconiosis in them.

The pathogenesis of complicated pneumoconiosis and, in particular, the causes of the progression of simple pneumoconiosis to complicated have not been studied. An admixture of silica in coal dust can enhance this progression. But still, in most cases, the main cause of the disease is coal dust itself. With a complicated form, the miners' lungs contain relatively large amounts of coal dust compared to those with a simple form of pneumoconiosis.

Anthracosis. This is the most harmless coal lung injury. Aspirated particles of coal (not only anthracite) are absorbed by alveolar and interstitial macrophages. The latter accumulate in the stroma along the lymphatic vessels, as well as in the parabronchial lymph nodes or in the area of ​​the root of the lung. In a pathological study, all places of deposition of coal pigment are clearly visible in the form of black stripes or asterisks in the lung tissue or in the form of black and slightly enlarged lymph nodes.

Simple pneumoconiosis. It is characterized by the presence of coal spots (diameter 1-2 mm) and several larger coal (koniotic) nodules. Carbon spots consist of macrophages containing particles of coal dust, and nodules, in addition, also from a delicate network of collagen fibers. Despite the diffuse nature of the changes in both lungs, the upper lobes and upper zones of the lower lobes are more severely affected. Nodules are localized mainly along the respiratory bronchioles, i.e. in places of initial dust accumulation. Over time, the adjacent alveoli expand, similar to what happens with centrilobular emphysema (see above). However, with emphysema, destruction of the alveolar walls occurs, the presence of which with pneumoconiosis is not proven.

Complicated pneumoconiosis. The disease develops on the basis of simple pneumoconiosis of coal miners. For this, as a rule, many years of continuous professional exposure to coal dust are necessary. With progressive massive fibrosis in the lungs, multiple intensely blackened scars 3-10 cm long are found. Under the microscope, a dense scar tissue rich in carbon pigment is visible. Necrosis occurs in the center of the scars, apparently due to local ischemia. With developed complicated pneumoconiosis based on pulmonary hypertension, a pulmonary heart often appears. In addition, patients with this form are particularly susceptible to the incidence of tuberculosis, chronic bronchitis, emphysema and bronchopulmonary cancer.

Kaplan's syndrome (A.Caplan). This combination of pneumoconiosis with rheumatoid arthritis is particularly rapid in the development of nodular lesions of the lungs. Like rheumatoid nodules (see chapter 24), nodular lesions in Kaplan syndrome in the center can have a zone of necrosis, which is surrounded by macrophages, fibroblasts and collagen fibers. The syndrome also occurs with asbestosis and silicosis.

Silicosis. Silicosis is a pulmonary disease caused by inhalation of particles of crystalline quartz (silicon dioxide) and is the most common occupational disease in the world. Being a slowly progressive, nodular, fibrosing pneumoconiosis, silicosis develops, as a rule, tens of years after the start of silicon dust aspiration. Workers using sandblasting machines employed in the stone and foundry industries, hard rock processing and construction work are at risk of getting sick. The risk group also includes miners mining minerals. Occasionally, with especially intense dustiness of the lungs, acute forms of silicosis occur.

Silica is found in crystalline and amorphous forms, however, quartz is the most fibrogenic, which indicates the pathogenetic importance of the physical form and surface properties of silicon dioxide particles. Immediately after aspiration, the particles interact with epithelial cells and macrophages.
Then damage occurs, after which fibrosis develops.

Despite the fact that pulmonary macrophages that absorb quartz dust particles ultimately become victims of the cytotoxic effect of dust particles, quartz activates macrophages - macrophages secrete mediators: IL-1, TNF, and free oxygen radicals.

In the early stages of development, silicosis is macroscopically characterized by the presence in the upper zones of the lungs of tiny tiny pale or blackish (if there is an admixture of coal dust) nodules. As the disease progresses, such nodules can merge into dense scars rich in collagen. In some nodules, the central part softens, then a cavity forms in it. This may be due either to ischemia of the nodule or to layering of tuberculosis infection. The lung tissue between the secondarily changed nodules is compressed or becomes airy, thus forming a honeycomb (cellular) lung. However, a sclerotic type of change is more common. Fibrosis is also noted in the basal lymph nodes and pleura. In some patients, the regional lymph nodes contain thin spherical or hemispherical plates of lime, which on the radiographs look like an egg shell. In the late stages of silicosis, the picture is identical to complicated pneumoconiosis (see above). Under the microscope, it can be seen that nodular lesions consist of concentric layers of hyalinized collagen fibers surrounded by a dense capsule of even denser collagen. Examination of nodules in a polarizing microscope (polarized light) helps to identify quartz particles with birefringence.

Diseases associated with asbestos exposure. “Asbestos” is a generalized name for minerals from crystalline hydrated silicates forming fine-fiber aggregates. More often use chrysotile asbestos. Like other types of asbestos, it has fire resistance (melting point about 1500 ° C), resistance to bases and acids, conducts poorly electric current. Chrysotile asbestos is used as a filler in plastics (textolites, fibers, etc.), asbestos cement and materials for production of fire-resistant and heat-insulating products. Inhabitants of old urban residential buildings, children studying in old school buildings, may be exposed to sprayed asbestos fibers, but this effect is at least 100 times less than the minimum for industrial conditions. Professional pathology observed in workers engaged in the production of asbestos products is expressed in the occurrence of focal fibrous plaques on the pleura, less often diffuse pleural fibrosis; pleural effusion; diffuse interstitial fibrosis (asbestosis) of the lungs; bronchogenic carcinoma; mesothelioma (tumors from the pleural mesothelium); neoplasms of the larynx and, possibly, other organs (in particular, the colon).

The manifestation of the carcinogenic effect of asbestos fibers is facilitated by the potentially toxic compounds adsorbed on the surface of these fibers. For example, the adsorption of carcinogens from tobacco smoke on asbestos fibers is important in the combined induction of bronchogenic cancer in asbestos workers. Back in the 80s, it was shown that occupational exposure to asbestos increases the incidence of bronchogenic carcinoma by 5 times compared with the incidence in representatives of other professions, and in smokers by 55 times!

Chronic aspiration (and sedimentation) of asbestos fibers and sustained release of mediators ultimately lead to generalized interstitial inflammation and interstitial fibrosis. Specific fibrogenic cytokines detected by reactive (macrophage) changes in response to asbestosis include fibronectin, platelet growth factor, and insulin-like growth factor I. It is not yet clear why silicosis is a nodal fibrosing process, and asbestosis is diffuse interstitial. Apparently the diffuse nature is due to the ability of asbestos fibers to reach the alveoli or to penetrate the epithelial cells, or both.

With asbestosis, diffuse interstitial pulmonary fibrosis develops. Changes with it are indistinguishable from those with other types of diffuse interstitial fibrosis. Essentially, the only difference is asbestos bodies. The latter under the microscope look like golden brown, fusiform sticks (Fig. 15.21) or needles with thickenings in the form of strung beads. The central part of these sticks is translucent, and they themselves are composed of the finest asbestos fibers coated with iron-containing material. They appear when macrophages try to phagocytize asbestos fibers. Other inorganic particles are also capable of being coated with similar complexes of iron and protein.

Asbestosis begins with fibrosis around the respiratory bronchioles and alveolar passages. Further, the adjacent alveolar sacs and alveoli are involved in the process. Fibrous tissue distorts the usual architectonics of the lung. Enlarged air spaces appear, enclosed in thick fibrous walls. Gradually, the affected areas take the form of cellular (cellular) tissue. Unlike pneumoconiosis and silicosis, asbestosis begins in the lower lobes and subpleural zones. However, as fibrosis progresses, the middle sections and upper lobes of the lungs are involved in the process. At the same time, fibrous thickening of the visceral pleura and the formation of adhesions with parietal pleura are observed. Some individuals with a competing disease - rheumatoid arthritis - may develop large nodes similar to those that develop with Kaplan syndrome (see above). In the final stages of fibrotic changes in the lungs due to narrowing of the arteries and arterioles by scar tissue, pulmonary hypertension occurs and the pulmonary heart forms.

The most common manifestations of asbestosis are pleural plaques - limited by dense collagen masses, often containing lime. Usually they develop on the anterior and posterolateral surfaces of the parietal pleura and above the dome of the diaphragm. Plaques do not contain asbestos bodies and are extremely rare in people who do not have professional contact with asbestos. Sometimes with asbestosis there is a pleural effusion, usually serous, less often with a hemorrhagic component. Workers in asbestos plants may develop bronchogenic cancer and pleural or peritoneal mesothelioma. The incidence of rare tumors such as mesothelioma (2-17 observations per 1 million people) in workers who are constantly in contact

Fig. 15.22.

Chronic berylliosis, stage of fibrosis


In the lung, among fibrous tissue, conchoidal (shell-like) bodies.

those with asbestos is increased by 1000 times compared with that in healthy people. It is known that if smoking contributes to the development of cancer with asbestosis, then it does not affect the incidence of mesothelioma.

Berylliosis. Occupational exposure to dust or fumes of metallic beryllium or its oxides, alloys or salts can lead to acute pneumonitis. Longer exposure at low doses causes pulmonary or systemic granulomatous lesions resembling sarcoidosis. Acute forms of berylliosis are practically not encountered at present. Workers in nuclear power and the aerospace industry that use beryllium alloys are at greatest risk of developing chronic berylliosis.

Chronic berylliosis occurs with the induction of cell-mediated immunity. Since it occurs in only 2% of people in contact with beryllium, it is believed that a genetic predisposition is necessary to stimulate the immune response. The development of delayed hypersensitivity leads to the formation in the lungs and regional lymph nodes of non-caseizing (i.e. not subject to cheesy necrosis) granulomas. Less commonly, granulomas also occur in the spleen, liver, kidneys, adrenal glands and lymph nodes distant from the lungs. Pulmonary granulomas undergo progressive fibrosis (Fig. 15.22) and then become noticeable with chest fluoroscopy. Lymphadenopathy of basal lymph nodes is observed in approximately 50% of patients.

Chronic berylliosis often occurs latently for many years. Then shortness of breath, cough, weight loss and arthralgia appear. В некоторых случаях патологический процесс стабилизируется, иногда болезнь прогрессирует вплоть до дыхательной недостаточности. Эпидемиологические данные свидетельствуют о связи между бериллиозом и развитием бронхиолоальвеолярной карциномы.

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