In the structure of occupational diseases, respiratory diseases (pneumocaniosis, chronic bronchitis) occupy 1st place. They are followed by diseases of the musculoskeletal system, then vibration disease and occupational skin diseases are not recorded.

The main industries that cause occupational diseases are coal, metallurgy, and engineering.

Recently, pronounced forms of chronic occupational diseases have been registered, which leads to long-term sick leave for workers. For modern production, the characteristic is an increase in psycho-emotional tension. The reasons for the low detection of occupational diseases are a change in the structure of production and the employee’s fear of losing his job. This is evidenced by cases of death of miners at work and in 26% of cases of identification of occupational diseases and persons for whom work in such conditions was contraindicated 5-6 years ago.

Urgent measures are needed to improve the situation:

Creation of a system of social and hygienic monitoring of harmful production factors;

Use of effective means of collective and individual protection, medical prevention;

Systematic analysis of occupational diseases, their causes, study of the radical features of their formation;

Scientific justification for the maximum safe working time in specific hazardous conditions;

Improvement of the regulatory framework.

36. Emergency hazard of coal mines.

The emergency hazard of production processes and mine facilities is determined by the mining-geological and mining-technical conditions of work, the effectiveness of the emergency protection system and prof. personnel preparedness.

Every year in Ukraine, about 2 thousand accidents occur with the cessation of production for more than a day and the loss of production of 10-15 million tons of coal.

The ignition of methane is caused by the occurrence of exothermic oxidation reactions. The reason is insufficient ventilation of the workings. The rate of combustion propagation and the pressure created in this case depends on many reasons, the initial temperature pressure, humidity of the working resistance, heat transfer conditions, etc.

Explosive combustion turns into detonation with a jump, its speed exceeds the speed of sound tens of times.

The main method of ignition is a source of thermal energy - the heated surface of the working body of the combine, blasting, frictional sparking, sparking in contacts, open fire.

In addition to the required temperature, sufficient time is required for ignition. When a methane explosion occurs in a mine, two impacts are observed - direct and reverse to the center of the explosion, due to the formation of low pressure there after cooling of the explosion products.

The main damaging factor in an explosion in 75% of cases is carbon monoxide poisoning or lack of oxygen, and 25% is the effect of a shock wave.

Main causes of explosions:

1. violation of ventilation due to stops of the air pump, short-circuiting of the air stream - the organizational cause of 90% of explosions;

2. frictional sparking;

3. blasting;

4. poor quality of passports;

5. spontaneous combustion of coal;

6. smoking – 5 cases.

Measurement of air composition and its consumption is carried out in mines of categories I and II - once a month; III category - 2 times a month; the rest - 3 times a month.

In formations with high gas content, where ventilation cannot achieve the established methane standards, it is necessary to degas the goaf or accompanying formations. It also needs to be carried out if methane release exceeds 2 m 3 /min in thin layers, 3 m 3 /min in medium layers, and 3.5 m 3 /min in thick layers.

To carry out degassing work in mines, special degassing areas are formed, vacuum pumping stations are installed, usually on the surface, and main gas pipelines are laid through specially drilled wells to prevent gas from entering the mine.

An important element of the gas regime is the following activities:

Use of safety explosives;

Electrical explosions;

Explosion-proof equipment and lamps;

Prohibition of open fire.

On May 8, 2010, methane gas exploded at Russia's largest coal mine, Raspadskaya, in the Kemerovo region. Four hours after the first explosion, the second one occurred.

Occupational morbidity is a generally accepted criterion of the harmful effects of unfavorable working conditions on the health of workers.

In the coal industry, this is contact with coal dust; changes in the gas composition of the air (decrease in oxygen content, increase in carbon dioxide concentration, release of methane, carbon monoxide, hydrogen sulfide, sulfur dioxide, nitrogen oxides, explosive gases, etc. into the mine atmosphere); noise and vibration; poor lighting and ventilation; forced body position; neuropsychic, visual, auditory stress; heavy physical labor, as well as an increased risk of injury. And the longer the underground experience, the higher the likelihood of health problems as a result of illness or injury.

In the structure of professional morbidity among miners, according to diagnoses, the first place is occupied by diseases caused by the influence of industrial aerosols (pneumoconiosis, chronic and dust bronchitis, coniotuberculosis), the second place is occupied by diseases associated with physical overload and overload of organs and body systems (radiculopathy), the third place is diseases caused by physical factors (vibration disease, arthrosis, cataracts).

COMPARATIVE ASSESSMENT OF THE HEALTH STATE OF WORKERS OF COAL ENTERPRISES BASED ON THE RESULTS OF MEDICAL EXAMINATIONS

Kislitsyna Vera Viktorovna
Research Institute of Complex Problems of Hygiene and Occupational Diseases of the Siberian Branch of the Russian Academy of Medical Sciences
Candidate of Medical Sciences, Leading Researcher, Department of Human Ecology

COMPARATIVE EVALUATION OF THE WORKERS" HEALTH IN THE COAL ENTERPRISES BY THE RESULTS OF MEDICAL EXAMINATIONS

Kislitsyna Vera Viktorovna
Research Institute for Complex Problems of Hygiene and Occupational Diseases SB RAMS
Candidate of Medical Sciences Leading Scientific Worker of the Department of Human Ecology

Bibliographic link to the article:
Kislitsyna V.V. Comparative assessment of the health status of workers at coal enterprises based on the results of medical examinations // Modern scientific research and innovation. 2013. No. 7 [Electronic resource]..03.2019).

Russia ranks fifth in the world in terms of coal production. The Kuznetsk coal basin, located in the south of Western Siberia in the Kemerovo region, is the main coal base of the country and provides half of the total Russian coal production. High quality coal occurs here, including coking coal. Coal is mined using both underground and more advanced open-pit methods. There are 58 mines and 36 open-pit mines in operation in Kuzbass.

At the same time, occupational morbidity in the Kemerovo region remains one of the highest in Russia, 7-8 times higher than the level in the country as a whole. The main reasons contributing to the creation of unfavorable working conditions: outdated production technologies, lack of collective protective equipment, failure of employers to comply with legislative and regulatory documents in the field of occupational health. At enterprises, as a rule, work is not carried out on reconstruction and technical re-equipment, introduction of new technologies, mechanization and automation of production processes, replacement of worn-out and modernization of outdated equipment, certification of workplaces is carried out at a low pace, understaffing and insufficient volume of sanitary-industrial work are often found laboratories. At a number of coal enterprises, there have been no positive changes in the field of medical prevention of occupational diseases.

When working at coal enterprises, the employee’s body is exposed to numerous adverse factors. These include: contact with coal dust, changes in the gas composition of the air (decrease in oxygen content, increase in carbon dioxide concentration, release of methane, carbon monoxide, hydrogen sulfide, sulfur dioxide, nitrogen oxides, explosive gases, etc. into the mine atmosphere) , noise and vibration, irrational lighting and ventilation, forced body position, neuropsychic, visual, auditory strain, heavy physical labor, as well as an increased risk of injury.

Research methods

This study was carried out at coal industry enterprises (mine and open pit) in the south of Kuzbass, developing one deposit.

To assess and predict the occupational risk of health problems based on the results of medical examinations using the methodology of the Institute of Occupational Medicine of the Russian Academy of Medical Sciences, an integral index of occupational diseases was calculated, which included ranked categories of risk and severity and made it possible to simultaneously evaluate different nosological forms of diseases. Table 1 shows the categories of risk of occupational diseases according to their posterior probabilities with gradations according to identified cases of occupational diseases and early signs of their subclinical forms, while the risk is assessed for the average period of development of an occupational disease or its early signs.

The categories of severity of occupational diseases given in Table 2 were developed by authors from the USA and Finland based on materials from compensated cases of occupational diseases according to the Institute of Occupational Medicine in Helsinki.

This classification is based on the International Classification of Impairments, Causes of Disability and Disability, as well as the International Classification of Diseases.

The logical stage in the development of the concept of assessing occupational diseases by risk and severity was the complementary combination of rating systems through the reciprocal of their product in the form of a single-numeric indicator - the index of risk and severity of occupational disease (Iz):

where the values ​​of K p and K t are given in the corresponding tables. The value of the integral indicator for one occupational disease is within 0.06 and 1.0. If there is a probability of developing several occupational diseases simultaneously, the indices are summed up:

And sum = , (2)

Research results

Based on clinical data from medical examinations, the risk and severity of occupational diseases were assessed. Occupational diseases of subclinical forms, which are causally associated with production factors, and general somatic diseases, which can probabilistically be associated with a complex of occupational and production factors and partially with one or another specific factor, were identified. For example, vegetative-vascular dystonia and chronic gastritis in the literature are usually associated with occupational stress (noise, vibration, infrasound, night shifts) and quite often with intense noise. In the literature, diseases of the female genital area are often associated with exposure to general vibration.
Tables 3, 4 show the results of calculations of risk categories and severity of occupational diseases.

Based on the specific influence of factors (high probability of dust bronchitis and hearing loss), the occupational disease index was 0.23 for open-pit workers and 0.58 for mine workers. For general somatic diseases comparable to a complex of production factors, the sum of the indices was 0.5 for open-pit workers and 0.92 for mine workers. The total sum of indices for all nosologies is 0.73 for open-pit workers and 1.5 for mine workers.

Chapter 25

OCCUPATIONAL DISEASES

Occupational diseases are a group of diseases that arise exclusively or predominantly as a result of exposure to unfavorable working conditions and occupational hazards on the body.

There is no uniform classification of occupational diseases. The most accepted classification is based on the etiological principle. The following occupational diseases caused by exposure are distinguished:

Industrial dust;

Chemical production factors;

Physical production factors;

Biological production factors.

Many occupational factors in modern conditions have a complex effect, so the clinical picture and morphology of some occupational diseases may differ from the described “classical” forms.

This lecture discusses some occupational diseases that most often develop in industrial regions.

Relevance of the problem topic

Occupational diseases, which represent one of the most numerous groups of diseases, cause not only the highest level of disability in people, but also one of the most common causes of mortality among the working population on the globe. Occupational diseases caused by various occupational hazards should not be considered as an inevitable phenomenon. The occurrence of occupational diseases largely depends on the imperfection of the technological process and equipment. The problem of occupational pathology is not only a medical problem, it is also a social and economic problem. The study of occupational pathology is necessary for doctors of both therapeutic and medical-preventive and dental profiles, on the one hand, to provide competent pathogenetically based therapy, and on the other, to take appropriate measures aimed at improving the scientific and technical process and introducing preventive measures.

The purpose of training – be able to determine macro- and microscopic manifestations of occupational diseases, explain their causes and mechanism of development, assess the outcome and determine the significance of probable complications for the body.

Why you need to be able to:

Identify visible macro- and microscopic signs of acute manifestations of occupational hazards, explain the causes, mechanism of development, outcome and evaluate their significance;

Identify visible macro- and microscopic signs of chronic manifestations of occupational hazards, explain the causes, mechanism of development, outcome and evaluate their significance;

Determine the morphological signs of the main occupational diseases, explain the causes, mechanism of development, outcome and evaluate their significance.

OCCUPATIONAL DISEASES CAUSED BY EXPOSURE TO INDUSTRIAL DUST (PNEUMOCONIOSIS)

Pneumoconiosis(from lat. pneumon- lungs, Sonya- dust) - dust lung diseases. The term “pneumoconiosis” was proposed in 1867 by Zenker. Industrial dust is the name given to the smallest particles of solid matter formed during the production process, which, entering the air, remain suspended in it for a more or less long time. A distinction is made between inorganic and organic dust. TO inorganic dust include quartz (on 97-99% consisting from free silicon dioxide), silicate, metal. TO organic - plant (flour, wood, cotton, tobacco, etc.) and animal (wool, fur, hair, etc.). There is mixed dust, for example, containing coal, quartz and silicate dust in varying proportions, or iron ore dust, consisting of iron and quartz dust. Particles industrial dusts are divided into visible (more than 10 microns in diameter), microscopic (from 0.25 to 10 microns) and ultramicroscopic (less than 0.25 microns), detectable using an electron microscope. The greatest danger is posed by particles smaller than 5 microns that penetrate into the deep parts of the lung parenchyma. The shape, consistency of dust particles and their solubility in tissue fluids are of great importance. Dust particles with sharp jagged edges injure the mucous membrane of the respiratory tract. Fibrous dust particles of animal and plant origin cause chronic rhinitis, laryngitis, tracheitis, bronchitis, and pneumonia. When dust particles dissolve, chemical compounds arise that have irritating, toxic and histopathogenic effects. They have the ability to cause the development of connective tissue in the lungs, i.e. pneumosclerosis.

When dust of different composition enters the lungs, the lung tissue may react differently. The reaction of the lung tissue can be:

Inert, for example, with common pneumoconiosis - anthracosis of coal miners;

Fibrosing, for example, with massive progressive fibrosis, asbestosis and silicosis;

Allergic, for example, with exogenous allergic pneumonitis;

Neoplastic, for example, mesothelioma and lung cancer with asbestosis.

The localization of the process in the lungs depends on the physical properties of the dust. Particles less than 2-3 microns in diameter can reach the alveoli; larger particles are retained in the bronchi and nasal cavity, from where they can be removed from the lungs by mucociliary transport. An exception to this rule is asbestos, particles of which 100 microns in size can settle in the terminal parts of the respiratory tract. This occurs as a result of the fact that asbestos particles are very thin (about 0.5 microns in diameter). Dust particles are phagocytosed by alveolar macrophages, which then migrate into the lymphatic vessels and are directed to the hilar lymph nodes.

Classification. Among pneumoconiosis, anthracosis, silicosis, silicosis, metalloconiosis, carboconiosis, pneumoconiosis from mixed dust, pneumoconiosis from organic dust are distinguished.

Anthracosis

Inhalation of coal dust is accompanied by local accumulations of it, invisible until massive pulmonary fibrosis forms. The accumulation of coal in the lungs, referred to as “pulmonary anthracosis,” is typical for residents of industrial cities. It can be observed in almost all adults, especially smokers. Dust particles are found in macrophages, in the lumen of the alveoli, in and around the bronchioles, and in the lymphatic drainage system. In city dwellers, this pigmentation is not toxic and does not lead to the development of any respiratory disease.

Only coal miners who stay for many years and for a long time in mines, especially heavily dusty ones, can experience a number of serious consequences.

There are two main forms of coal miners' anthracosis:

Benign anthracosis pulmonary fibrosis, or “spotted anthracosis”;

Progressive massive fibrosis.

In the mildest benign form of anthracosis fibrosis, or “spotted anthracosis,” the lung contains only localized areas of blackish pigmentation separated by wide zones of healthy tissue. This focus of blackish pigmentation is called an “anthracite spot.” It consists of an accumulation of carbon-filled macrophages around the respiratory bronchioles, pulmonary arterioles and veins. Similar cells are found in the lymphatic vessels and lymph nodes of the roots of the lungs. Fibrosis is mild, but local dilatation of the respiratory bronchioles is often detected, which is a manifestation of local centrilobular emphysema. These changes can develop not only as a result of only inhalation of coal dust, but concomitant smoking. Depending on the number of “anthracite spots”, the severity of chronic bronchitis, bronchial ectasia and local emphysema, patients will have clinical manifestations of respiratory disorders. As spotted anthracosis progresses, nodules with a diameter of up to 10 mm appear, which are clearly visible on x-ray films. This variety is called the nodular form of spotted anthracosis. At this stage, there is also no pronounced fibrosis, and the impairment of lung function is insignificant.

Progressive massive fibrosis (PMF) represents a further continuation of the disease and is usually considered secondary, arising from the superposition of intercurrent complications. At the same time, pigmentation becomes much more intense. In these miners, the anthracite spots are larger and more numerous (“black lung disease”) and are gradually surrounded by fibrous tissue. Progressive massive fibrosis characterized by the formation of large fibrosis nodes of irregular shape; these nodes are more than 10 mm in diameter and can reach significant sizes. These fibrous nodules may have liquefaction in the center and when cut open, a viscous, inky-black liquid will ooze out. In these cases, the clinic may experience hemoptysis and symptoms reminiscent of tuberculosis, which gives rise to the name “black consumption” for this form. The nodes may undergo contraction, which leads to the development of mixed emphysema around the scar. Large nodes are usually located in the upper and middle parts of the lung, often bilaterally. Concomitant emphysema is usually severe, sometimes with the formation of bullae (large-volume abnormal air cavities). Progression of the disease leads to fibrosis and destruction of lung tissue.

Antibodies, most often IgA, are detected in nodular fibrous pulmonary lesions, and at the same time they increase in the blood serum. In this regard, an association has been noted between the development of rheumatoid polyarthritis and progressive massive fibrosis in coal miners, which is called Kaplan and Koline syndrome.

It is known that in a group of mine workers with the same work experience, some may develop PMF, while others may develop only a slight impairment of pulmonary function. The reason for this observation is unknown. It is assumed that the following factors may influence this case:

The amount of silicon and quartz inhaled with coal dust, as well as the type of coal (bituminous coals are more dangerous in terms of fibrosis than charcoal);

Concomitant infection with tubercle bacilli or atypical mycobacteria;

The development of hypersensitivity reactions caused by the death of macrophages and the release of antigens;

Development of fibrosis associated with deposition of immune complexes.

However, neither theory has been proven, and some researchers believe that only the amount of dust absorbed is the determining factor.

At the end of the disease, the lungs have the appearance of a honeycomb, and the formation of a pulmonary heart is observed. Patients die either from pulmonary heart failure or from the addition of intercurrent diseases.

Silicosis (from lat. silicium- silicon), or chalicosis(from Greek chalix- limestone) is a disease that develops as a result of prolonged inhalation of dust containing free silicon dioxide. Most of the earth's crust contains silica and its oxides. Silicon dioxide occurs naturally in three different crystalline forms: quartz, cristobalite and tridymite. . The non-combined forms of silicon dioxide are called “free silicon”, and the combined forms containing cations make up the various silicates. Silicon dust is found in a variety of industrial processes, including gold, tin and copper mines, stone cutting and polishing, glass production, metal smelting, pottery and porcelain production. In all these industries, particle size matters. Sand usually contains 60% silica. However, its particles are too large to reach the periphery of the lungs. Only small particles entering the bronchioles and alveoli can cause damage. Silicon, especially its particles 2–3 nm in size, are a powerful stimulator of the development of fibrosis. The amount and duration of exposure to silicon also plays a large role in the development of silicosis. Approximately 10-15 years of work in dusty industrial conditions without respirators can cause silicosis. But if the dust concentration is significant, then its acute form may occur within 1-2 years (“acute” silicosis). In some cases, the disease may appear several years after exposure to industrial dust ends. (“late silicosis”). The risk group for this disease includes workers in the professions mentioned above.

Pathogenesis. Currently, the development of silicosis is associated with chemical, physical and immune processes that occur during the interaction of dust particles with tissues. At the same time, the importance of the mechanical factor is not excluded.

According to modern concepts, the pathogenesis of silicosis includes the following stages:

Inhalation of silicon particles with a diameter of less than 2 microns with their penetration into the terminal sections of the airways (bronchioles, alveoli);

Uptake (phagocytosis) of these silicon particles by alveolar macrophages;

Death of macrophages;

Release of the contents of dead cells, including silicon particles;

Repeated phagocytosis of silicon particles by other macrophages and their death;

The appearance of fibrous hyalinized connective tissue;

Possible development of further complications.

The exact nature of the factor or factors causing fibrosis has not yet been determined. Unlike coal dust, silicates are toxic to macrophages and lead to their death with the release of proteolytic enzymes and unchanged silicate particles. Enzymes cause local tissue damage followed by fibrosis; the silicate particles are reabsorbed by macrophages and the cycle repeats endlessly. According to this theory, we are talking about the leading role in the pathogenesis of silicotic fibrosis of the death of coniophages, followed by stimulation of fibroblasts by the decay products of macrophages. It is believed that hydrogen bonds between the released silicic acid, formed when it is absorbed by the lysosomes of macrophages and the phospholipids of the phagosome membrane, lead to membrane rupture. Rupture of the phagosome membrane leads to the death of macrophages. All resulting macrophage derivatives are capable of stimulating fibroblastic proliferation and activation of fibrillogenesis. Since plasma cells and immunoglobulins are detected in the lesions, it is assumed that immune reactions are involved in fibrillogenesis, however, the mechanism of their development in silicosis is not yet clear. According to the immunological theory, when tissues and cells are exposed to silicon dioxide, autoantigens appear during their breakdown, which leads to autoimmunization . The immune complex that arises from the interaction of antigen and antibodies has a pathogenic effect on the connective tissue of the lungs, resulting in the formation of a silicotic nodule. However, no specific antibodies were detected.

Pathological anatomy. In the chronic course of silicosis, atrophy and sclerosis are found in the mucous membrane and submucosal layer of the nasal concha, larynx, and trachea. In humans, the histological evolution of silicic lesions is not well known, since autopsy reveals an already advanced form of the disease. According to the study of silicosis in animals and cases of acute disease, the following has been established. The first response to the appearance of silicon in the acini is the accumulation of macrophages. If the dust is massive, then macrophages fill the lumen of the bronchioles and surrounding alveoli. It is possible that the development of a serous inflammatory reaction is similar to that which can be observed with alveolar proteinosis. In some cases, a picture similar to gray hepatization of the lungs in lobar pneumonia has been described. With the slow development of the process, in the early stages, multiple tiny nodules are detected in the lung tissue, mainly in the upper sections and in the hilum area, which give the lung parenchyma a fine-grained appearance, as if the entire tissue is strewn with sand. During this period, the formation of granulomas occurs, represented mainly by macrophages, surrounded by lymphocytes and plasma cells. These granulomas are found around bronchioles and arterioles, as well as in paraseptal and subpleural tissues. During the process of evolution, the size of the nodules increases, some of them grow together and then they are visible to the naked eye. The nodules become larger and larger, denser and denser, and then large areas of the lungs turn into scar layers, separated from each other by foci of mixed emphysema. The pleural layers grow together with dense cicatricial cords. Lymph nodes undergo similar changes and become nodular and fibrotic.

In the lungs, silicosis manifests itself in two main forms: nodular and diffuse sclerotic (or interstitial).

In the nodular form, a significant number of silicotic nodules and nodes are found in the lungs, which are miliary and larger sclerotic areas of round, oval or irregular shape, gray or gray-black (in coal miners). In severe silicosis, the nodules merge into large silicic nodes, occupying most of the lobe or even the entire lobe. In such cases, they speak of a tumor-like form of pulmonary silicosis. The nodular form occurs when there is a high content of free silicon dioxide in the dust and with prolonged exposure to dust.

In the diffuse sclerotic form, typical silicotic nodules in the lungs are absent or there are very few of them; they are often found in the bifurcation lymph nodes. This form is observed when inhaling industrial dust with a low content of free silicon dioxide. With this form in the lungs, connective tissue grows in the alveolar septa, peribronchially and perivascularly. Diffuse emphysema, deformation of the bronchi, various forms of bronchiolitis, bronchitis (usually catarrhal-desquamative, less often purulent) develop. Sometimes they find mixed form pulmonary silicosis. Silicotic nodules may be typical or atypical. The structure of typical silicotic nodules is twofold: some are formed from concentrically located hyalinized bundles of connective tissue and therefore have a rounded shape, others do not have a rounded shape and consist of bundles of connective tissue, swirling in different directions. Atypical silicotic nodules have irregular outlines and lack a concentric and vortex-like arrangement of connective tissue bundles. In all nodules there are many dust particles lying freely or in macrophages, which are called dust cells, or coniophages. Silicotic nodules develop in the lumens of the alveoli and alveolar ducts, as well as at the site of lymphatic vessels. Alveolar histiocytes phagocytose dust particles and turn into coniophages. With prolonged and heavy dusting, not all dust cells are removed, so their accumulations form in the lumens of the alveoli and alveolar ducts. Collagen fibers appear between the cells, and cellular fibrous nodule. Gradually, the dust cells die, the number of fibers increases, resulting in the formation of a typical fibrous nodule. In a similar way, a silicotic nodule is built at the site of a lymphatic vessel. With silicosis, in the center of large silicotic nodes, connective tissue disintegrates with the formation silicotic cavities. Disintegration occurs due to changes in the blood vessels and nervous apparatus of the lungs, as well as as a result of instability of the connective tissue of silicotic nodules and nodes, which differs in biochemical composition from normal connective tissue. Silicotic connective tissue is less resistant to collagenase compared to normal tissue. In the lymph nodes (bifurcation, hilar, less often in peritracheal, cervical, supraclavicular) a lot of quartz dust, widespread sclerosis and silicotic nodules are found. Occasionally, silicotic nodules are found in the spleen, liver, and bone marrow.

The clinical manifestations of silicosis depend on the extent of the lesion and its severity. If we are talking about extensive damage, shortness of breath may appear after several years. It is caused by silicoprotein pneumonia. If the affected area is smaller, then the onset of the disease is asymptomatic and manifestations of silicosis can be detected by systematic x-ray examination. On X-ray images you can see a picture of the so-called “snow storm”, indicating the dissemination of fibrous nodules. Tuberculosis is often associated with silicosis. Then they talk about silicotuberculosis, in which, in addition to silicotic nodules and tuberculous changes, the so-called silicotuberculosis foci. The right half of the heart is often hypertrophied, up to the development of typical pulmonary heart. Patients most often die from progressive pulmonary heart failure.

Asbestosis

The word “asbestos” comes from the Greek word for “indestructible.” About 6 million tons of this mineral are extracted annually around the world. There are several types of asbestos: serpentine or white asbestos (the most commonly used industrial variety is chrysotile) and amphiboles or blue asbestos such as crocidolite and amosite. All of them are pathogenic and have a fibrosing effect. Asbestos contains many fibrous minerals composed of hydrated silicates. Asbestos fibers exhibit birefringence in polarized light, which can be used in microscopic diagnostics. They are often found in combination with silicates. In these cases, they contain calcium, iron, magnesia and soda. Asbestos has been used for centuries as it is fire resistant as insulation material, bitumen coatings, industrial structures, audio products, brake clutches and steering wheels, and a variety of other products that are potentially hazardous. The disease is widespread in Canada, which ranks first in the world in terms of asbestos reserves. Approximately 5 million people come into contact with asbestos every day on construction sites alone. Among them there is a group of insulation workers, of whom 38% are affected by asbestosis. It is interesting to note that these individuals had 150 million asbestos particles per 1 cubic meter, which for a long time was considered a safe upper limit. It must be emphasized that the impact of asbestos can also be indirect, for example, on spouses and members of their family of people who work with asbestos. It is generally accepted that crocidolite, which has the thinnest fibers, causes the development of mesotheliomas of the pleura or peritoneum, as well as carcinoma of the bronchi and gastrointestinal tract. According to most authors, the carcinogenicity of asbestos depends not on its type, but on the length of the fibers. Thus, fibers larger than 5 microns do not have carcinogenic properties, while fibers smaller than 3 microns have a pronounced carcinogenic effect. The risk of lung cancer in patients with asbestosis increases approximately 10 times, and if we are talking about smokers, then 90 times. Patients with asbestosis are twice as likely to have cancer of the esophagus, stomach, and colon. It has now been proven that asbestos potentiates the effects of other carcinogens.

The onset of pneumoconiosis varies. It happens that pulmonary manifestations occur after 1-2 years of contact with asbestos, but most often - after 10-20 years. The pathogenesis of pulmonary fibrosis is unknown.

Asbestos fibers, despite their large length (5-100 microns), have a small thickness (0.25-0.5 microns), so they penetrate deeply into the alveoli in the basal parts of the lungs. Fibers are found not only in the lungs, but in the peritoneum and other organs. The fibers damage the walls of the alveoli and bronchioles, which is accompanied by small hemorrhages, which serve as the basis for the formation of hemosiderin inside the macrophages. Sets consisting of asbestos fibers, sometimes coated with proteins, but most often with glycosaminoglycans, on which iron-containing grains of hemosiderin are deposited, are called “asbestos bodies”. In an optical microscope, they appear as reddish or oblong yellowish structures, shaped like rings or stringed pearls, reminiscent of the appearance of “elegant dumbbells.” In an electron microscope, their appearance is even more specific: their outer contours are represented by roughness, reminiscent of the steps of a staircase and their axis contains parallel lines. These bodies (10-100 microns long and 5-10 microns wide) are found in sputum and help differentiate asbestosis from fibrosing alveolitis. Histologically, interstitial fibrosis is observed in the lungs. Macroscopically, the lungs in the later stages have the appearance of a honeycomb. Pulmonary fibrosis and emphysema are detected mainly in the basal regions of the lungs. Patients die from pulmonary and pulmonary-heart failure.

Beryllium

Beryllium dust and vapors are very dangerous and can cause lung damage and the development of systemic complications. Due to its resistance to fracture and “wear”, this metal is widely used in alloys, tool making and aircraft construction. The risks associated with the use of this metal have been known since World War II. Beryllium was used in fluorescent lamps, and the sudden rupture of these tubes can cause occasional but noticeable harm. The use of beryllium in the luminescent industry was discontinued primarily because of beryllium.

Currently, those working in the mining of this metal, manufacturing melts and tools are at greatest risk. Beryllium infection also develops in people who live near objects that emit dust, vapors or smoke containing this metal. For unclear reasons, there is an individual predilection for berylliosis, affecting approximately 2%. Beryllium disease tends to occur most often in those who return to a risky profession that they have left for quite some time. The use of skin peels has shown that patients with berylliosis develop late positive hypersensitization to this metal, which explains the hypersensitivity in the development of toxicity. It has been proven that T lymphocytes are sensitive to beryllium. It is assumed that this metal combines with the patient’s proteins and provokes an immune reaction against itself, which allows beryllium to be considered an autoimmune disease.

The penetration of beryllium either in the form of small particles or in the form of oxides or salts is equally accompanied by the development of beryllium. Depending on the solubility and concentration of beryllium in the inhaled air, two types of pneumoconiosis develop: acute and chronic beryllium, the latter being the most common.

Acute berylliosis usually occurs when soluble acidic beryllium salts enter the body. Acute bronchopneumopathy develops. Clinically, it appears with a dry cough, difficulty breathing, fever and asthenia. Microscopically, such pneumonia has the character of “acute chemical pneumonia.” Edema is pronounced, the alveolar wall is infiltrated with polynuclear neutrophils, and the exudate contains an admixture of erythrocytes and fibrin. After a few days, macrophages and lymphocytes appear in the exudate. Then intra-alveolar organization of exudate occurs (carnification) and in parallel inter-alveolar fibrosis develops. Within a few weeks, patients may die from pulmonary failure. In less severe cases, complete recovery is observed. In acute berylliosis there are no granulomas.

People who mine coal can develop an occupational disease due to a number of factors. This occurs due to inhalation of large amounts of dust. Natural coal dust has a very bad effect on the health of miners. In order to preserve the health of miners, miners' trade unions carry out special health measures, monitor labor safety conditions, organize and distribute recreational facilities. You can read more about coal industry news at the link. First of all, it damages the respiratory system and the vascular system. Due to the increased levels of carbon dioxide, methane and other various gases, one can only imagine what diseases can arise in humans or aggravate existing ones. Below we will look at some of them.

For many years, doctors have been monitoring the most common diseases among coal industry workers, and pneumoconiosis took first place. This disease is considered to be chronic and is divided into three types: silicosis, carboconiosis and silicatosis. Treatment of such diseases is very similar to other types of bronchial pathologies. The goal of doctors is always to get rid of the disease through elimination therapy.

The next type is called vibration disease. It occurs due to high levels of equipment vibration, noise, muscle tension and being in one uncomfortable position for a long period of time. These factors are considered the main ones. It can be noted that this disease is still encountered among specialists: the engineering, metallurgical and railway industries. Doctors associate its difficult definition with the characteristics of its clinical manifestation. More often affected are: organs of the nervous system, cardiovascular, musculoskeletal and metabolism in the body. It is considered to be the most difficult when the neuro-reflex mechanisms are damaged and neurohumoral disorders appear. This disease can also affect the occurrence of instability of catelhamin metabolism, which will manifest itself in a vegetative crisis or functional jams.

The reason for the appearance of professional weakness in the body in miners is also considered to be the influence of noise. It gradually changes the level of perception of sound volume by a person, affects the nervous system and can provoke problems with the vascular systems of the body. At the same time, we should not forget that a person simultaneously inhales a large amount of dust, performs heavy physical activity and is always in one position. Due to the fact that the decebellum level exceeds the permissible norms, a person experiences some discomfort. Even if the employee gets used to it, the body does not stop suffering.