Silicoanthracosis

Silicoanthracosis, silicanthrocosis - chronic dust bronchitis, the most common disease of the respiratory tract among miners in various industries, develops over a large area of ​​the lungs, slowly progresses, and is accompanied by signs of bronchitis and emphysema. Ultimately, in severe cases, the disease becomes life-threatening. Silicoanthroclesis can be not only an occupational disease, but also a consequence of the unfavorable environmental situation in cities with a developed metallurgical industry.

Etiology. Silicolluidogenic, the process rarely develops without exposure to harmful substances (dust and gases). Still, antigenically altered cells of foreign origin apparently play a role. The reasons for the development of silicosis in the anamnesis are varied: as a result of the presence of mineral particles in the air (dust, sand, smoke), irritation of the mucous membranes of the respiratory tract constantly occurs, but, as a rule, the development of the disease is associated with prolonged exposure to substances of an inorganic nature: when inhaling large silicate powder, metal slag etc. over a long period of time (during the work of mining professions, steelworkers) or when inhaling coal tar, ash, oily chips, fiberglass, etc. etc. (during textile work), less often under the influence of industrial, silicon-hydrogen gases from the exhaust gases of cement kilns, miner's tar, dust from chalk and cement mortars, concrete mixers and construction cranes.). It has been proven that with uniform grinding of raw materials, the mechanism of transfer of nanoparticles through epithelial cells is similar to the mechanism of transfer of organic acid anions. On the surface of silicate particles, macromolecules and mesotheliocyte tissue begin to “bind tightly,” and phagocytes turn into mast cells. After the onset of fibrosis, in the interalveolar “impregnation” phase, fairly rapid metaplasia occurs, although the accumulation of iron by interstitial cells determines the relative continuity of the dissemination process. A pronounced dynamic interaction of protein subcomponents of the blood (coagulation and fibrinolysis) is not observed under these conditions, since microphagocytosis of atypical pneumocytes is weakly expressed due to aspiration of mucus and profound changes in the surfactant apparatus. One can imagine the picture observed on histological preparations of foci of pneumofibrosis in chronic silicosis: certain areas of lung tissue are devoid of parenchymal elements and are characterized by a massive proliferation of connective tissue structures, leading to a significant expansion of the lumen of the pulmonary alveoli and bronchioles.

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