Professional dust from dust disease. Prevention of professional dust disease

19.11.2018 7:20:00

Production dust is one of the adverse factors affecting human health. The first information about the possibility of developing diseases of the lungs as a result of inhalation of dust in mining works is found in the ancient Greek and ancient Roman literature. However, according to the descriptions presented at that time, it is still difficult to say what specific forms of dust diseases of the lungs were discussed. It can be assumed that most likely it was pneumoconiosis, coni-tuberculosis, chronic dusty bronchitis.

Only from the middle of the last century began to gradually accumulate observations, which allowed to identify the nosological forms of dust diseases of the lungs.

Among domestic scientists and doctors are a great contribution to the study of pathogenesis, clinics, diagnosis, prevention and treatment of pulmonary diseases, I. N. Kavalerov, D. A. Karpilovsky, I. M. Pancy, I. G. Gelman, N. A. Vigdornchik, S. M. Genkin, M. A. Kovnatsky, P. P. Dvizhkov, M. V. Evgenova, K. P. Molokanov, etc.

In various industries and agriculture, many production processes are associated with the formation of dust. This is a mining, coal-mining industry; Metallurgical, metalworking and machine-building enterprises; production of building materials; Electric welding work; labor in textile enterprises; Processing of agricultural products (grains, cotton, flax, etc.).

Production dust in its composition, physical properties and chemical nature is very diverse. The physicochemical properties of dust largely determine the nature of the impact on a person. Therefore, it is necessary to take into account the form, solubility, structure (amorphous or crystalline), adsorption ability, electrostability and dimensions of dust particles. The chemical nature of dust is important. In terms of composition, dust is inorganic, organic and mixed. Dust consisting of minerals or metals belongs to inorganic. Organic dust contains particles of plant or animal origin, as well as microorganisms that are usually on them, and their livelihoods. Various - both inorganic and organic particles or a mixture of inorganic and organic particles may be included in the mixed dust.

Some solid toxic substances, such as lead, phosphorus, arsenic, antimony, boron, etc., may be in the dusty state. However, they are not believed to the group of dust factors, so they are not considered in this section. In production conditions, dust penetrates into the human body through the respiratory tract and accumulates in the lungs. At the same time, for a clinical picture of dust diseases, the lesion of pulmonary fabric or respiratory tract with development or pneumosclerosis, or chronic bronchitis, or bronchial asthma, as well as various combinations of these forms, is characterized. When penetrating into light dust of toxic substances, lesions of lung tissue and airways are not always noted (this can be observed on the example of lead dust).

Pneumosclerosis, resulting from inhalation of dust, in 1866, suggested calling "pneumoconiosis", which in Greek refuses the lungs (Pneumon - light, conion - dust). Pneumoconiosis occurs mainly when exposed to dust of various minerals, including silica dioxide, silicates (kaolin, talc, asbestos, cement), an antrahylic is called pneumoconiosis when exposed to stone coal dust, metal coniosis arises from the effect of dust with the content of some metals (iron, aluminum, barium , Tin, etc.). It is especially necessary to allocate dust with the content of vanadium, beryllium, molybdenum, tungsten, niobium, cobalt. Less often, pneumoconiosis arises from organic dust (grain, cotton, wood, linen dust, etc.) and mixed dust (electric welding aerosol, a mixture of quartz-containing and metal dust, etc.).

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Depending on the type of dust, which caused the development of pneumoconiosis, distinguish between the corresponding types of pneumoconiosis. Thus, the silicosis is called pneumoconiosis due to the effect of silica dioxide, silicate - the effects of various silicates (in particular, kaolin - the kaolinosis, talca - talcosis, asbestos - asbestosis, etc.), sideriosis - iron-containing dust and mixed forms of pneumoconiosis are denoted by the composition dust, for example, silicoanracecosis, silicosiderosis, etc. The combination of pneumoconiosis with pulmonary tuberculosis is denoted as a coni-tuberculosis; At the same time, depending on the type of dust, silicotuberculosis distinguish, antrachuberculosis, etc.

Clinical manifestations of pneumoconiosis

Pneumoconiosis belongs to the very common form of chronic dust diseases of the lungs. For all pneumoconiosis, it is necessary to have a pneumophybrusic process. However, the current, the clinical radiological and pathological pattern of various types of pneumoconiosis have some features, in many ways depending on the composition of production dust, which caused the development of lung fibrosis.

Modern classification of pneumoconiosis:

1. Silicosis - occurs when inhalation of silicon dioxide.

2. Silicatosis - arises from inhalation of dust of silicon dioxide minerals due to other elements (cement, mica, nephower pneumoconiosis).

3. MetalOll cycle - pneumoconiosis from inhalation of metals. There are sedresses, aluminia, barytosis, manganoanokoniosis (the impact of manganese).

4. Carboconiosis - pneumoconiosis from inhalation of carbon-containing dust (coal, coke, graphite, soot).

5. Pneumoconiosis from inhalation of mixed dust. Divided into two groups:

1) consisting of 10% and more silicon;
2) As part of 5-10% silicon or its absence.

6. Pneumoconiosis from inhalation of organic dust. This includes diseases from the effects of sugar cane dust (Bagassoz), from cotton and flax dust (bissing), "Easy farmer" - when contacting organic material infected with fungus.

By the nature of the flow, the following forms of pneumoconiosis are distinguished:

A) rapidly progressive;
b) slowly progressive;
c) late;
d) regressive.

Figrogressing pneumoconiosis. I stage of the disease can be detected in 3-5 years after the start of work in contact with dust, the progress of the pneumoconiotic process, i.e. The transition of pneumoconiosis in II stage is observed in 2-3 years. To this form of pneumoconiosis, in particular, the so-called acute silicosis should be attributed, which is essentially a rapidly progressive form of silicose.

Slowly progressive forms of pneumoconiosis are usually developing 10-15 years after the start of work in contact with dust, and the transition from I to the II stage of the disease lasts at least 5-10 years.

Pneumoconiosis, developing in a few years of cessation of contact with dust, is called late.

According to radiological studies, the regression forms of pneumoconiosis are found only when accumulated in light X-ray-contrast particles of dust, which create the impression of a more pronounced stage of lung fibrosis in such patients. With the termination of the contact of the patient with dust, it is usually a partial removal of X-ray-repeat dust from the lungs. This explains the "regression" of the pneumoconiotic process.

Silicatozes and silicatosis

The most common and usually severe form of pneumoconiosis. It is characterized by sclerotic (connecting) rebirth of lung tissues. Accompanied by education in the lungs of nodules. Silicose is also characterized by emphysema of the lungs. It should be noted that with severe changes in the lungs, emphysema and expansion of bronchi may occur, which are not accompanied by the development of purulent processes.

Often with silicosis, especially in the pronounced stages of the disease, the extended heart is diagnosed. Typical silicotic nodules in rare cases can be found in the kidneys, in the bone marrow of tubular bones, liver and spleen.

With silicotuberculosis, changes are largely dependent on the shape and predominance of the silicotic or tuberculosis process. Change specific for tuberculosis is usually localized in the field of pulmonary tops and in the subclavian regions, while silicotic - in the middle and lower lungs.

The clinical picture depends on the degree of severity of the pneumophybosis, concomitant emphysema of the lungs, the presence and nature of complications. The working conditions of the patient (the composition of dust, its dispersion, degree of dustiness) and the duration of work in contact with dust are also important. Silicosis, being a chronic disease, is usually developing slowly and often for a long time does not bother patients. Early, although not permanent, signs of it may be pain in the chest, shortness of breath and cough.

Chest pain in the form of tingling, mainly in the field of blades and under the blades, as well as in the form of a sense of constraint and stiffness in such patients are due to changes in the pleura due to microtraumamation of it and the formation of adhesions in the pleural cavity by penetrating through the lymphatic system of light dust. The causes of the occurrence of shortness of shortness of silicosis are pneumosclerosis, lung emphysema and bronchitis. Therefore, in the early stages of the disease in the absence of severe emphysema of lungs and bronchitis, shortness of breath is observed only with a large physical voltage.

In the future, as the pneumoconiotic process and the occurrence in the light sections of massive fibrosis, shortness of breath can be marked with a small physical voltage and even at rest. Acceding chronic bronchitis, especially with impaired bronchial patency, and bronchial asthma contribute to the strengthening of shortness of breath. It should be noted that with the uncomplicated silicosis of the pain in the chest and shortness of breath are sometimes absent not only in the early, but also in the pronounced stages of the disease. Passion or cough in patients with silicosis is mainly due to irritation of the mucous membrane of the upper respiratory tract of dust. The cough is predominantly non-permanent, dry or with a separation of a small amount of sputum mucosa. The presence of a large amount of sputum and purulent nature usually indicate the joining chronic bronchitis.

The most common silicatosis are asbestosis and talcosis. Less often meet the kaolinosis, nephelinoatite pneumoconiosis, etc.

Asbestosis

Asbestos is a mineral having a peculiar fibrous structure, it is also called "mountain flax". There are two types of asbestos: cornea (amphibol) and serpentine (chrysotyl). The latter is mainly used in industry. Due to the fibrous structure of asbestos, dust, in addition to sclerosing action, causes a more pronounced mechanical damage to the mucous membrane of the respiratory tract and pulmonary fabric than other types of dust. This, apparently, partly can be explained by some features of the clinical and radiological picture, flow and complications of asbestosis. The pronounced changes of the pleura, bronchi and the presence of lung fibrosis are characteristic. In the chest detects pleural spikes. Pleverra thickened, sclerized.

The lungs are sealed, asbestos tales are visible. Determined by the exciting eyebreaker fabric, interdollastic and alveolar partitions, sclerosis, often marked lung emphysema. The nodules characteristic of silicose are absent during asbestos. In the areas of the accumulation of asbestos dust there are chambers consisting of cells. In large, small bronchops and bronchioles there are expansions with a sharp rise in the glaired sheath gland. In the pronounced stages of the disease, sometimes occasional in the cartilage of the bronchi is observed. Lymphatic nodes are dense, contain a large amount of dust. The lung cancer during asbestos is developing from the epithelium of small bronchi. In tumors, it is often contained a large number of asbestos taurus and asbestos fibers.

The symptom complex of chronic bronchitis, emphysema of lungs and pneumophibrosis, in which the leading role belongs to chronic bronchitis and lung emphysema. Already in the initial stages of the disease, there is often severe clinical symptoms. Early appears shortness of breath, arising with small physical stresses and even alone; The bogged cough was first dry, then with a difficultly separated viscous sputum; Pain in the chest, especially intense when coughing. The general well-being of patients is noticeably violated: sharp weakness, weight loss, weakness, fast fatigue, headache. The type of patient changes: they lose weight, there is a gray-earth painting of skin with a cyanotic hint of the face and lips. Signs of chronic bronchitis and lung emphysema are determined. Peculiar signs, but not always encountered, are the presence of patients with asbestos fibers and a calf, as well as education on the skin of asbestos warts.

The appearance of asbestos fibers in sputum is a consequence of self-cleaning of the lungs from asbestos penetrating into the respiratory tract. Therefore, only in the wet asbestos, asbestos cannot be diagnosed with asbestosis. Asbestos shoulders are the formation of a variety of shapes: in the form of threads with thickened ends, drum sticks, gymnastic weights. The color of their golden yellow, brown-yellow.

Talcosis

Talcosis (talc pneumoconiosis) refers to a favorable pneumoconiosis form. It occurs after 15-20 years or more after the start of work in contact with the talcova dust, slowly progresses. Preferably there is Talcosis I stage, less often of stage II. Talcosis III stage is usually observed when mixed dust containing talc in combination with other types of silicates (for example, with kaolin dust) or with SiO2 dust.

The long-term study of talcosis testifies to the development of the sclerotic process in the lungs with the lesion of the alveolar partitions, the incombous and the occasional fabric. In places in the lungs there are point or larger sclerotic sections, located isolated or merging with thickened alveolar partitions. These sites have accumulation of talc dust with numerous giant cells. The plasma of the latter shows shiny talc fibers. Unlike silicotic nodules, there are no concentric structure and a downward trend. In addition, connecting tissue is poorly expressed in them.

Clinical picture. With talcosis I stage in patients, minor complaints. The emerging small shortness of breath during physical stress, dry cough and tingling in the chest in the field of blades usually little bother patients. The appearance of the patients is not changed. Objectively marked non-permanent fried dry wheels. The respiratory function is not violated or there are hidden signs of respiratory failure that are detected during load.

On radiographs, moderate amplification and deformation of the vascular-bronchial drawing are noted throughout both lungs. Vascular shadows in places have a clear look. A few shades of a nodule character of 1-2 mm are visible, which are localized mainly in the middle and lower lungs. These shadows have uneven, but rather clear contours. The roots of the lungs are somewhat expanded and sealed.

When talcosis II stage, the specified complaints and changes in the lungs are more pronounced. In addition to dry wheezes, the noise of the friction of the pleura in the lower lung departments can be brought. There are non-letters of pronounced signs of respiratory failure. The tuberculosis of light talcosis is rarely combined.

Pneumoconiosis from cement dust

Cement is obtained by firing a mixture of clay, limestone or natural megrels. The main types of cement are Portland cement, Slagoportland cement, Pozzolana Portland cement, acid-resistant cement. In its chemical structure, they relate to silicates, which, regardless of the type of cement, may contain: SAO, CA (OH) 2, MGO, A12O3, Feo, Fe2O3, SO3, MNO, SiO2, alkali. In addition, some types of cement contain a large amount of silicon dioxide. Cement is mainly used in construction as a binder and for the manufacture of building blocks and various parts. The clinical and radiological picture, the flow and complication of pneumoconosis caused by the effects of cement dust depend on the content of free silicon dioxide.

Types of cement containing a small amount of silicon dioxide cause the development of good-quality forms of pneumoconiosis. Patients with such forms of pneumoconiosis complaints almost do not prevent, there are no changes in the lungs; Functions of external respiration are not violated, on radiographs moderate amplification and deformation of the pulmonary pattern. The roots of the lungs are blurred, the progression of the fibrous process in the lungs is usually not observed for a long time.

When cement dust contains a large amount of silicon dioxide, the development of the nodular form of pneumoconiosis is possible, which, according to the clinicorentgenic picture and the flow resembles silicos and can be attributed to silicosilicatosis. Along with the pneumoconiosis, the cement workers are often observed bronchial asthma, as well as skin damage (dermatitis or eczema).

Pneumoconiosis from slags

The pneumoconiotic process progresses relatively slow. The severity of the course of the disease is mainly determined by the severity of chronic bronchitis, emphysemic lungs and complications - chronic pneumonia. If the glass fiber gets into the skin, it is irritated with its subsequent development of dermatitis. In the clinical picture of certain types of pneumoconiosis (asbestosis, pneumoconiosis, due to inhalation of dust of glass wool and cement) there is a combination of a fibrous process in the lungs with chronic bronchitis. Therefore, such patients, first of all, need the treatment of chronic bronchitis, which often predetermines the severity of the course of the disease and its forecast.

Patients with silicatosis of stage I in the absence of complications and concomitant diseases may be left in their former work if the air dusting in the workplace does not exceed the maximum permissible concentrations. In cases where the stage I silicates are combined with chronic bronchitis, expressed emphysens, respiratory failure or other complications, is contraindicated with work in contact with dust, irritant substances, in adverse meteorological conditions and with significant physical stress.

Silicatosis patients stage II need rational employment, and having complications such as, for example, severe chronic pneumonia, lung cancer, etc., accompanied by severe respiratory and heart failure, can be considered disabled. For persons exposed to silicate dust, depending on the type of dust and the nature of the work performed, the following deadlines for periodic medical examinations are established:

— mining of chrysolite and amphibole asbestos ores, wet enrichment of asbestos ores, the use of asbestos in the production of asbestos-cement, electrical insulating and other materials - 1 time in 24 months;
— dry enrichment of asbestos ores, asbestosectile production - 1 time at 12 months;
— production and processing Talc, Kaolina, Cement, Olivina, Nethelin, Apatity, Slouds and other natural silicates - 1 time in 24 months.
— production and use of glass wool, mineral fiber, mineral wool - 1 time in 24 months;
— production of fiberglass, fiberglass, glass solids and other glass-containing materials— 1 time in 24 months

Carboconiosis

Carboconios include pneumoconiosis caused by inhalation of the coarse dust. The most common type of pneumoconiosis of this group is an antrahylic, the development of which is due to the impact of stone coal (anthracite, brown coal) or soft coal coal. Antrazes occurs mainly in workers of coal mines engaged in the production and loading of coal, much less often - in the manufacture of coal electrodes and in workers of coke-chemical plants. Therefore, it is sometimes called the pneumoconiosis of coalsels.

However, the miner-coal miners are preferably a mixed type of pneumoconiosis - anractor silicos, and often silicos, which depends on the minogeneous conditions of the location of the mine and the nature of the work performed. For example, an antrahylic prevails from the designers, the vublotbers and carriers of cut cars, the work of which is associated with the predominance of coal dust. In the penetrations and drillers engaged in the development of mine rocks containing a high percentage of SiO2, silicosis develops. Anaturaxicosis is more likely to have miners operating on breed and coal.

The clinical radiological and pathological picture of antracosis and antraksilicosis have some features that distinguish these diseases from silicose. This is largely due to the property of coal dust to increase the activity of the cells of the immune system, which contributes to a more enhanced than in silicosis, the removal of dust, as well as strengthen the secretion of the glance of the bronchi mucous membrane. Therefore, the antrazes is characterized by relatively slow development. It usually occurs 15 years later and more after the start of contact with coal dust and is often combined with chronic dust bronchitis, which can precede the appearance of clinical and radiological signs of the pneumoconiotic process.

For anthratracosis, it is primarily characterized by deposition in light coal dust (pigment), which gives them a gray-black color, the intensity and localization of which depend on the amount of dust and stage of the disease. In the initial stages, the deposition of coal pigment is observed mainly in the lower lobes. These shares become more dense. In the alveolar partitions, around vessels and bronchi there is an arrangement of connective tissue with a small amount of cellular elements. In places, cell accumulations with particles of coal dust are determined, which ranked the name of anthratic chairs.

In contrast to silicotic nodules, they do not contain concentric and "vortical" connective tissue beams. When merging small devils, larger sections of sclerosis (antratic nodes) may form. Pneumoscleotic changes are usually combined with emphysemic lungs, chronic bronchitis, and sometimes with bronchiectasses. In places of deposit of a large amount of dust, the death and softening of the pulmonary fabric are sometimes observed, which is the cause of cavity formation (anthratic cavities). The emergence of the latter contributes to both violations of local blood circulation due to the growth of the connective tissue around the vessels. With anractor siliciasis, in addition to the specified changes, typical silicothic nodules are found in the lungs.

Clinical picture. The clinical symptoms of antracosis largely depends on the combination of it with chronic dust bronchitis. In patients with antrahylic, as in silicosis, pain in the chest and shortness of breath can appear. At the same time, with an antrazosis, a constant and more pronounced cough with the release of sputum mucosa is significantly more often observed, which sometimes acquires dark color due to the content of carbon dust particles. Objectively, such patients are early marked signs of the emphysema of the lungs (the expansion of the chest, the omission of the lower boundaries of the lungs and the limitation of their mobility, the box sound). In the lungs against the background of weakened or harsh respiration, dry or wet wipes are often listened.

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In cases where an antrahyld is not combined with chronic bronchitis, complaints and objective clinical data are almost absent. Anaturaxicosis is essentially the most common form of pneumoconiosis in working coal mines, since under the underground work miners have to have a permanent or periodic contact with mixed dust containing various amounts of coal and silicon dioxide. The presence of particularly large quantities of silicon dioxide in coal dust significantly affects the nature and flow of the fibrous process.
In the lungs.

Anaturaxicosis has a number of similarities both with antrahylic and silicosis. In most cases, it develops after 10 years or more after work in contact with dust. As with the animance, there is a symptom complex of chronic bronchitis and lung emphysema, however, they are somewhat less pronounced and developed mainly against the background of the already existing lung fibrosis. Therefore, with anaturaxicosis, mainly in the initial stages of the disease, clinical signs are scanty. The well-being of patients remains quite satisfactory.

MetalOll cycle

Many types of metal dust can cause the development of the pneumoconiotic process. At the same time, it should be noted that the metal coniosis is rare comparatively, since under production conditions, the dust of metals usually contains various impurities, including metals. Therefore, pneumoconiosis from inhalation of such types of dust essentially should be attributed to mixed forms of pneumoconiosis.

The so-called pure metal conizes are characterized mainly by slow development and lack of trends towards the progression of pulmonary fibrosis. According to radiological features, they mainly correspond to the I or II stage of pneumoconiosis. When exposed to some metals (zinc, copper, etc.), there is sometimes a casting fever. It occurs when inhaled aerosol of metals generated during their melting. Siderosis and aluminia are most common from metal con kindas.

Siderosis is mainly in working blast furnaces and agglomerating factories. The clinical picture of his scanty. For a long time, such patients may have complaints and objective signs indicating lung defeat. The respiratory function is not violated. Only on radiographs of the lungs there are non-timbbled fibrosis and scattered contrasting fine-mesel shadows with rather clear contours, which are ferrous to the accumulation of metal dust. Therefore, the diagnosis of sederosis sometimes has to be installed only on the basis of x-ray data, taking into account the composition of dust, available in production, where the patient works.

Complications for sideriosis are practically not observed. Patients with an uncomplicated form of sederosis in most cases do not need treatment. The ability to be fully saved. With careful medical observation, they can remain in their own former work.

The clinical picture of sederosilicosis is very similar to that with silicose. Questions of treatment and working capacity of patients are solved in the same way as in Silicose. Aluminous is observed predominantly in persons working with powdered aluminum, which is used in pyrotechnics and for the manufacture of paint, as well as in working electrolytic workshops to obtain aluminum from bauxite. The clinical-radiological picture of aluminose, in contrast to sederosis, is characterized by more pronounced symptoms. With aluminous, already in the initial stages of the disease, complaints of shortness of breath may appear, pain in the lungs. The painting of aluminose there is a development in the light of interstitial sclerosis with the growth of connective tissue in the inter-vololar partitions. In the lumets of the alveoli find containing particles of dust cells and aluminum accumulations. The basic principles of treatment and workability examination with aluminia are the same as for silicose.

Pneumoconiosis from organic dust

In addition to inhalation of organic dust, in addition to chronic bronchitis, bronchial asthma and pneumoconiosis, peculiar diseases of the respiratory apparatus may develop, in the clinical picture of which the bronchial asthma lesions are noted in the type of bronchial asthma (yes Easy farmer "). For dust bronchitis due to the effect of organic dust, the presence in the clinical picture of the spasm of the bronchi and the increased secretion of the glanes of the bronchi mucosa.

Therefore, the function of external respiration is early disturbed and the lung emphysema is developing. In addition, chronic bronchitis in such patients is often complicated by the respiratory tract infection, which contributes to a more severe flow of it and the emergence of bronchiectasis. Pneumoconiosis from the effects of organic dust occurs infrequently; It is mostly arising against the background of chronic dust bronchitis. Due to the fact that the composition of organic dust often contains various impurities, including SiO2, in persons working in contact with it, mixed forms of pneumoconiosis can be observed.

The pneumoconiotic process caused by the impact of organic dust usually does not tend to progression, and therefore rarely encounters the II stage of the disease. This flow is mainly observed in the presence of SiO2 in organic dust.

Bissinosis is made to designate the disease of the lungs, which occurs when inhaling the dust of cotton, flax and hemp. It is believed that these types of dust contain biologically active substances that directly act on the smooth muscles of the bronchi and cause bronchospasm, accompanied by the attacks of choking. Usually, the most severe attacks of churning appear on Mondays ("Monday Symptom"), and by the end of the week they become much less pronounced or disappear at all.

In the clinical picture of Bissinosis, the main syndrome is the bronchospaist component. Depending on the degree of severity, it is distinguished by three stages of the disease.

With the I stage, the attacks of bronchospasm arise a few hours after the start of work, and at the end of the work, it is usually stopped soon. These attacks are characterized by a difficult breathing, a feeling of gravity in the chest, an incision and dryness in the throat. Cough appears, general weakness, fast fatigue. In the lungs listen dry wheezing. Sometimes there is a slight increase in body temperature.

For stage II, more pronounced and pronounced attacks of difficulty breathing are characterized, especially on Mondays. The patients are worried about the permanent cough - dry or with the allocation of a small "amount of hardwood sputum. Increased shortness of a shortness of stroke.
In the lungs, harsh respiration with a large number of dry wheezes, which are often audible at a distance. The emergence of attacks of suffocation is provoked not only inhalation of organic dust, but also changes in meteorological conditions, physical stress, smoking.

Bissinosis III stages are essentially a transitional form in heavy chronic bronchitis, combined with emphysema lungs. At the same time, respiratory failure, a pulmonary heart and is often joined by chronic pneumonia.

According to clinical and radiological data, there are already signs of the emphysema of the lungs during Bissinoma I stage. Depending on the stage of bissing and the severity of the bronchospast component, such patients have a periodic or more constant violation of the respiratory function. For bissinosis, uncharacterically presence in the wet elements.

In the presence of chronic dust bronchitis I stage, when a little expressed clinical manifestations of the disease and there are no violations of the functional ability of the lungs, the worker can be left in the same place under the condition of careful dynamic observation and prophylactic treatment. The transition of the disease to the next stage or the presence of even minor signs of pulmonary failure is the basis for the translation of the worker to the place outside contact with dust, adverse meteorological factors and without physical tension. Patients with moderately pronounced bronchitis recommend rational employment or retraining, which is of particular importance for young people.

Berylliosis

Beryllium - Metal from a group of rare earth. In its pure form in nature is not found. It is part of some minerals, of which beryl or aluminosilicate beryllium are most common, as well as chrysoberyill and phenakite.

Beryllium crystals are precious stones. So, the beryl of the green color was called the emerald, blue-green - Aquamarina, Golden - Helidor. Beryl is mined from granite pegmatites, which are a large-crystalline rock. Pure beryllium is a silver-gray metal, light (relative density 1.85-1.86), with a high melting point (1,280 ° C), characterized by heat resistance and non-corrosion when heated to 400-500 ° C.

Thanks to valuable qualities (high strength, hardness, the ability to increase the electrical conductivity, slowing down oxidation to form an oxidized film that protects against water reaction) Beryllium is widely used in industry: mechanical engineering, reactor construction, in the manufacture of electronic equipment, X-ray tubes, radiolamps, manufacture of fire-resistant ceramic paints and fluorescent compositions. Currently, beryllium alloys with copper, nickel, aluminum, manganese, magnesium, fluorine and other elements received great distribution.

For the special technical qualities of Beryllium, the name "Miracle Metal" was named, and for insidious toxicity in a number of works of German authors, he is referred to as "Metal damn". The volume of beryllium consumed in industrial production is constantly increasing, respectively increase the number of persons subjected to beryllium, and the danger of environmental pollution.

Beryllium was opened in 1798 by L. Voklen. For a long time, the toxic properties of beryllium remained unknown. The first clinical descriptions of diseases caused by contact with beryllium compounds appeared only in the XX century. The first scientists who studied berylliosis were German researchers Weber and Engelgard, domestic clinicians I. G. Gelman, B. E. Israel.

The most toxic beryllium compounds are beryllium peroxide, fluoride and beryllium chloride. Along with the local irritant action, these compounds have high overall toxicity. Contact with beryllium and its compounds is possible in obtaining metal beryllium from ores, in the process of manufacturing its alloys, their processing, in a number of other industries.

Beryllium and its compounds can flow into the body in the form of vapors and dust through respiratory organs, in relatively rare cases - through the gastrointestinal tract with food. A peculiar form of pathology develops when cells of beryllium with skin surface contact. Unlike other occupational diseases, the flow of berylliosis and the severity of its clinical manifestations are not in direct connection with the concentration of toxic substance. There are often cases when the severity of intoxication inadequate the number of connections entered into the body.

The first manifestations of intoxication can occur on different terms of contact - from several days to 10 years and more. Sometimes for the development of the disease is quite short, even random (not more than 20 minutes), contact, for example, when collecting scrap metal. It is possible to develop berylliosis in individuals who do not have direct contact with beryllium. Cases of diseases of family members of workers in contact with beryllium compounds are described when washing at home workwear, keeping the house of work clothing, etc. Heavy cases of the disease, often with fatal exodus, are found in the living in close proximity (at a distance of 1-2 km) from beryllium production and by the nature of the work in contact with the connections of beryllium. Berylliosis sick face of different ages. Cases of diseases of children under 7 years old, whose parents worked with Beryllium.

Changes in the lungs with berylliosis at the autopsy are characteristic. When extracting from the chest, the lungs are not falling down, preserving the form due to the significant development of the connective tissue. The mass of them reaches 200-800. The surface of the lungs is fine-grained. When feeling, multiple small, dense to the touch nodules, having a type of fine-fought grayish-white formations on the cut.

The picture in chronic beryllium is characterized by changes in alveolar partitions, bronchioles, interdoolesale partitions, bronchops and vessels. The pulmonary process is evenly affecting both lungs, but most expressed in the middle and lower shares, where even necrotic changes are developing. In most cases, with berylliosis in the nodules there are so-called conchoid (sink-shaped) calves with a diameter of 6 to 10 microns. The evolution of the development of the granulomatous process during berylliosis is characterized by the formation of small sclerotic nodules, which, merging, form large granulomatous nodes. Granulomas of the same structure can be found in lymph nodes, liver, skin, spleen, kidneys, muscles (more often than breathing), myocardium, pleura. The first cases of professional intoxication beryllium were described in 1933 in Germany. In 1935, the Italian scientist Fabroni offered the term "berylliosis".

The incidence of berylliosis among persons with contact with beryllium and its compounds is 0.3-7.5%. There are sharp and chronic forms of berylliosis, or beryllium disease. Acute intoxication causes soluble beryllium compounds, chronic states are insoluble. All forms of beryllium lesions, even with their clinical manifestation by one body or system, are the disease of the whole organism. This is a confirmation of the beryllium observed with all types of beryllium, as well as the formation of a granuloma in chronic berylliosis not only in the lungs, but also in other organs.

Acute intoxication. The defeat of the respiratory tract during acute poisoning varies from rhinitis to the hardest pneumonites. The nature of the lesion depends on the nature of beryllium compounds, their physical condition (smoke, dust, fog) and from the individual sensitivity of the body. With acute intoxication, beryllium is distinguished by several basic syndromes. Sharp catarrhal rhinitis, pharyngitis, trachetes are relatively easy. Inflammation of the mucous membrane of the upper respiratory tract is determined by the irritating properties of beryllium connections. When removing contact, these changes are completely disappearing after 24-48 hours even without special treatment. The acute tracheobronchitis syndrome is characterized by a dry cough, shorthand during exercise, pains for the sternum. With an objective examination, hyperemia of the mucous membrane of the upper respiratory tract is noted. Dry wheezing wheezing are listened to the lungs, the radiograph is determined by the amplification of the bronchomicious pattern.

With the defeat of deep departments of the respiratory tract, bronchoobronchite and toxic pneumonia are developing. They are characterized by a rapid beginning. Patients complain of shortness of breath, difficulty breathing, cough with scarlet sputum, indefinite pain in the chest. The lungs are listened to a large number of different-caliber medium and fine-grained wet wheezes. As you involve in the pathological process, the Alveol joins a crunch in the lungs.

Thus, in the acute period of severe intoxication, the leading symptom is pneumonia. The outcome of it may be different:

— recovery with full normalization of the X-ray picture;
— the development of pneumosclerosis with the seal of intermediate lung tissue;
— transition to chronic shape;
— Death at the height of intoxication or in the coming deadlines.

Mortality for beryllium pneumonia is quite high. The fatal exodus often occurs on the 2-3rd week of the disease, however, with an extremely serious course, patients die in the first day due to the paralysis of the respiratory center.

Xronic beryllio. Chronic granulomatosis of the lungs is more often observed in working with luminous paints, in the manufacture of fluorescent lamps, three contacts with zinc-beryllium silicate, the effects of metallic beryllium and its low-soluble compounds - oxide (veto) and hydroxide vehicles (it) 2. The disease may occur as the outcome of the acute intoxication of beryllium connections or as a primary chronic form. Unlike most professional diseases, the concentration of the toxic substance does not play the main role in the development of chronic berylliosis.

The clinical picture of the disease can develop in a few months or even years after the cessation of contact with beryllium, often without a history of sharp intoxications. "Interesting and at the same time terrible" called German authors the ability of beryllium to cause late manifestations: a few years later there are the first symptoms of the so-called protracted toxic beryllium pneumonia. The duration of the latent period varies in very wide limits from a few weeks to 15 years. More often this period is ½-2 years.

It is noted as if the inverse relationship between the duration of the latent period and the severity of clinical manifestations of the disease: in patients with a long-lasting latent period there is a relatively more common course of the disease, with a tendency to stabilization. Clinical options for chronic berylliosis are extremely diverse. The beginning of the disease can be gradual, with a small number of complaints or heavy, rapidly progressive, with bright clinical symptoms.

The earliest sign of changes in the functional state of the lungs is the extension of the alveolar-capillary gradient or the difference in the partial tension of oxygen on both sides of the alveolar-capillary membrane, the so-called alveolar-capillar block. The noted feature is a consequence of a peculiar disorder of gas exchange with a violation of the diffusion of gases through the alveolar-capillary membrane. Clinical manifestations of the disease largely depend on the severity and progression of this process.

For the initial manifestations of the disease, weakness, fatigue, shortness of breath, during exercise, dry bakery cough is characterized. There are often complaints against cheerful pain in the chest without a clear localization, fast weight loss, fever. Dyspnea gradually increases and is the leading, most characteristic symptom of the disease. In a short time, patients lose 8-10 kg.

The disease is often combined with the intolerance to a number of drugs. The appointment of antibiotics may worsen the general condition. There are cases when the first manifestations of the disease coincided with the use of antibiotics. The rapidly progressive variants of chronic berylliosis is often inherent in a sharp start with a fever, at which the temperature reaches 39-40 ° C, chills, severe overall well-being, pronounced breath and sharp weight.

Patients complain of a sweetish taste in the mouth, stubborn, multiple vomiting, there is sharp cyanosis. Temperature of the body usually falls gradually. With the development of the process, cyanosis takes a spilled character, a peculiar "cast-iron" shade. The box sound, a symmetrical limitation of mobility of pulmonary edges, scattered dry and fine-duct wet wets, mainly in the lower lungs are determined. Often, the noise of friction of the pleura is listened.

In pronounced cases, chronic beryllium, as a rule, is complicated by the hypertension of a small circle of blood circulation, followed by the development of chronic pulmonary heart and pronounced worldwide failure. In the development of this symptom, the emphysema of the lungs is of great importance.

The disease can accompany the pronounced articular and hepatic seleasonal symptom. In some cases, skin thickening are developing. It is possible to defeat bone tissue with the thickening of the assault ribs and long tubular bones.

In the study of the external respiratory function, quite peculiar deviations are stated: indicators reflecting the state of ventilation capabilities are usually close to normal values \u200b\u200band do not correspond to the degree of shortness of breath and cyanosis. At the same time, the coefficient of utilization of oxygen of the ventilated air is dramatically reduced.

Periodic medical examinations are held 1 time in 6 months. With the obligatory participation of the therapist and the radiologist. According to the testimony, the otolaryngologist, dermatologist, oculist, neuropathologist are involved.

The contraindication to the reception to work in contact with beryllium are the following diseases:

— diseases of allergic genesis (allergic rhinitis, bronchial asthma, urticaria);
— chronic diseases of the respiratory organs (laryngotrachiteitis, chronic bronchitis, bronchiectatic disease, pneumosclerosis, lung emphysema, tuberculosis and other diseases of the bronchopulmonary apparatus);
— cardiovascular diseases: heart defects, myocardits, hypertensive disease, expressed atherosclerosis;
— chronic liver diseases;
— ulcerative disease of the stomach and duodenum, chronic gastritis, colitis;
— chronic kidney diseases;
— organic diseases of the central nervous system;
— endocrine-vegetative diseases;
— blood disease and blood-forming organs;
— chronic skin diseases;
— chronic diseases of the organs of vision.

Professional bronchial asthma

Bronchial asthma refers to the number of common forms of occupational diseases. The etiological factors in the development of professional bronchial asthma are various allergens with which the patient had to have contact in the process of his work. Production allergens can be a substance of both organic and inorganic origin, which in the form of dust, aerosol or vapor penetrate the body mainly respiratory.

Organic allergens are many types of vegetable dust: grains, flour, cotton, flax, tobacco; Pollen plants, dust of various wood breeds, natural silk, hair, animal wool, feathers, scales of the epidermis, etc. In addition, organic allergens can perform essential oils, some products of life insects, worms, worms, etc. Bronchial asthma, due to the impact of these allergens, is usually found among workers in agriculture and produces for processing and use as raw materials products of vegetable and animal origin (in mucomols, workers of cotton and woodworking, flax and silk-peeling enterprises, speeds, etc. ), as well as veterinarians, hairdressers, cosmetic staff staff, etc.

Among the production allergens there are a wide variety of chemical structure and composition of the substance. These include metals (nickel, chrome, platinum, cobalt, etc.) and their compounds, some nitroquras, ursol, rosin, formalin, etchlorohydrin, bitumen, synthetic polymers, etc. These substances are used in many industries, and therefore professional asthma May meet from representatives of a number of professions.

Various drugs (antibiotics, sulfonamides, hypyakuana, analgesics, aminazine, some balms, hormones, vitamins, etc.) are also industrial allergens. Professional bronchial asthma from drugs can be observed in the working chemical-pharmaceutical industry, among workers of pharmacies and medical personnel who have contact with drugs.

Many types of industrial dust, aerosols and vapors have
Not only allergic properties, but also the ability to mechanically injury, as well as cause irritation of the mucous membranes of the respiratory tract. Therefore, by the nature of the action on the respiratory organs, they are distributed to the following groups:

1. Substances with a pronounced sensitizing effect. For example, drugs (antibiotics, sulfonamides, vitamins, aminezine, etc.), rosin, some types of wood dust, bitumen, etc.
2. Sensitizer substances that simultaneously possess
and the locally excluding effect, and some of them cause the development of pneumophibrosis. These include chromium, nickel chloride, chlorine, ursol, formaldehyde, some types of dust (from flour, cotton, tobacco, wool, cement), electric welding aerosol, etc. Being sensitizers, they cause the development of bronchial asthma.

At the same time, depending on the chemical structure and physical properties of such allergens in the clinical picture, the respiratory apparatus may be initially observed in the form of chronic toxic or dust bronchitis, toxic pneumosclerosis or pneumoconiosis. In the future, on the background of these lung diseases, bronchial asthma is possible.

Clinical picture. It is characterized by a capture due to dysfunction of the respiratory system with common bronchospasm and increased secretion of the bronchiole mucous membrane, bronchiole musculat, edema. Professional bronchial asthma often arises against the background of full health during operation, suddenly. When the contact with sensitizing substances is stopped. First, the attack is quickly fastened when taking bronchodiolitical substances. Pronounced suffocation can provoke previous rhinitis, supercooling. In the clinical picture, two main periods can be distinguished: the attack and intercreant.

For the attack period, a whistling breathing is characterized, which is heard at a distance. The patient takes a forced sedental pose. Chest expanded. Lips, nail beds, Skin skin. The mobility of the lower edges of the lungs is limited. When attacking the sound over the light box. Breathing hard, with an elongated exhalation; There is a rich number of scattered dry wheezes on inhale and exhale. Due to the blockage of bronchiole with clots of sputum, breathing in the respective lung sites is not auditioned.

In extremely severe cases, respiratory noises may generally be absent ("Some light"). The heavy and long-term course of the attack of bronchial asthma (Status AsthMaticus), as well as the widespread blockage of bronchioles, mating mocrine can be the immediate cause of the patient's death.

In the interconceptional period, clinical symptoms of bronchial asthma may be completely absent. It is more often observed in the initial stages and light forms of the disease. A more pronounced forms of bronchial asthma in the intergreacar period are often accompanied by several difficult breathing, moderate shortness of breath, mainly with physical voltage, cough, sometimes with a separation of a small amount of sputum mucosa. In the lungs in such patients there are hard breathing, they are often scattered dry wheezing, especially with a forced exhale.

Disruption of the function of external respiration, hemodynamics of a small circle, as well as changes in some laboratory indicators, are often found. Already in the early stages of the development of bronchial asthma, especially in the attack period, respiratory failure is revealed. For the diagnosis of lung emphysema, pneumosclerosis and pulmonary heart, additional radiographic and electrocardiographic methods should be used.

For bronchial asthma, eosinophilia in the peripheral blood and the appearance of a small number of vitreous sputum mucosa appears. More often, they appear at the height of the attacks, and in the interconception period may be absent. According to the nature of the flow, there is a light, medium and severe degree of bronchial asthma,

For the prevention of bronchial asthma, a thorough professional medical selection of persons arriving on production, where possible contact with production allergens is possible. Therefore, a list of medical contraindications for work with substances with sensitizing action includes various diseases of both allergic and non-allergic nature, which can contribute to the development of professional bronchial asthma.

Significant preventive activities in professional bronchial asthma are the early detection of initial signs of the disease and rational employment outside contact with production allergens. In such cases, it is sometimes possible to prevent the further development of bronchial asthma and preserve the ability of the patient.

D.M. Huseynov A.A.

From the history of the question

Until the middle of the XIX century. lung diseases
caused by dust that
observed at miners and
Kamenotesov, were known under
names "mountain illness", "mountain
Asthma "," CHAKHOTE OF RUDOPOKOV ".
For pulmonary fibrosis arising
from inhalation of various types of dust,
German doctor K. Basker in 1866
The collective concept of pneumoconiosis was introduced.

Factors defining dust pathogenicity

Particle sizes:
- large (6-25 microns) - settle, the main
way in the nasal cavity
- "Average" (0.5-6 microns) - in bronchi
- 0.1-5 μm - the cause of pneumoconiosis
- less than 0.1 - smoke
The most dangerous - from 0.1 to 5.0 microns
Geometric properties (better
spherical particles penetrate)
Penetrating ability
The form
Radioactivity

Definition

Pneumoconiosis - (Pneumon - Light and Konia dust), a group of diseases of lungs
(irreversible and incurable) caused by
Long inhalation production
dust and characterized by development in them
fibrous process; refer to
Professional diseases.
Found in workers mining,
coal, engineering and some
other industries.

Terms of development:
1. Dust type.
2. Profmashrut:
3.
4.
5.
6.
7.
8.
Duration of exposure:
4-6 years of work (\u003e 70% quartz dust);
12-15 years of work (30-70% of quartz dust).
Sanitary and hygienic characteristics of working conditions:
Dust concentration in the workplace:
\u003e 70% quartz dust - MPC 1 mg / m3
30-70% quartz dust - MPC 2 mg / m3
The presence of a respirable fraction (1-5 microns).
The presence of incorporation of dust in light.
Dust removal efficiency (bronchogenic,
lymphogenic path).
Use of personal protective equipment (PPE).
Genetic predisposition.
Harmful habits (smoking, alcohol consumption).

Pathogenesis of pneumoconiosis

Pathogenesis theories:
- mechanical
- toxico-chemical
- biological,
-imnunological.
Currently recognized
Immunological theory.

Stages of pathogenesis:

inhalation of dust particles in bronchioles, Alveola;
Dust Elimination Violation and Education
"Dust depot" in lungs and lymph nodes;
Absorption (phagocytosis) dust particles with diameter
less than 5 microns alveolar macrophages;
Activation and death of macrophages with release
active forms of oxygen;
The release of the contents of the dead cells, in
TCD cytokines and dust particles;
Repeated phagocytosis of dust particles by others
macrophages and their death;
Toxic action of oxidants on the pulmonary
Fabric (connecting fabric, proteins, lipids,
DNA, surfactant);

Stages of pathogenesis 2.

excess mediators
inflammation, chemohotontes,
Fibronctin;
Activation and proliferation of others
Effector cells inflammation
(neutrophils, fat cells, lymphocytes and
fibroblasts);
enhancing the synthesis of fibroblasts,
collagen, elastin and fibrosis
in the lungs;
appearance in focus fibrous focus
hyalinized connective tissue
(Formation of pneumoconiotic
nodules).

10. Features of pathogenesis:

The severity of inflammatory processes
Determined by the properties of affecting
dust, degree of dust load and
Feature effector response
Immune system with the inclusion of 4 types
Immune inflammation.
Against the effect of dust factor series
Researchers celebrate high frequency
Secondary immunological
Insufficiency.

11.

12. Classification of pneumoconiosis by type of industrial dust:

Silicosis - pneumoconiosis due to inhalation,
quartz dust containing free dioxide
Silicon.
Silicatosis - pneumoconiosis arising from
Inhalation of dust of minerals containing dioxide
silicon in the associated state with different
elements: aluminum, magnesium, iron,
Calcium et al. (Kaolina, Asbestosis, Talcosis,
Cement, saliva pneumoconiosis, etc.).
Metallokoniosis - Pneumoconiosis from exposure
dust of metals, iron, beryllium, aluminum, barium,
tin, manganese, etc. (Siderosis, Berilliosis,
Aluminia, etc.).
Carboconiosis - pneumoconiosis, from exposure
Carbon-containing dust: coal, coke,
graphite, soot (antrase, graphitosis, scenic
Pneumoconiosis, etc.).

13. Classification of pneumoconiosis by type of industrial dust 2:

Pneumoconiosis from mixed dust:
a) pneumoconiosis due to the impact of mixed dust,
having a significant amount of free
silicon dioxide (from 10% or more), for example, antrachocycosis,
Siderosilicosis, silicosilicatosis, etc.;
b) pneumoconiosis due to the impact of mixed dust,
no free silicon dioxide or with
insignificant content (up to 5-10%), for example
Pneumoconiosis of grinders, etc.
Pneumoconiosis from organic dust. In this species
included all forms of dust lung diseases that
observed when inhaling various types of organic dust
(cotton, grain, cork, cane). This includes
Diseases caused by the effects of plant fibers,
various agricultural dusts, including so
Called farm lung.

14. In 1996, a new classification of pneumoconiosis was adopted

1. Pneumoconiosis arising from exposure to high and
moderately fibrogenic dust (with a free dioxide content
Silicon more than 10%): Silicosis, antrachocyciasis, sederosilicosis,
Sylikosilicatosis. These pneumoconiosis are most common
Among sandblastiers, bubbles, peckers, agricultures,
refractories. They are prone to fibrous progression
process and complication of tuberculosis infection.
2. Pneumoconiosis arising from exposure
weaklyobrogenic dust (with a free dioxide content
Silicon less than 10% or not containing it): silicatosis
(asbestosis, talcosis, coalinosis, pneumoconiosis from exposure
cement dust), carboconiosis (antrase, graphitosis, scenic
Pneumoconiosis, etc.), Pneumoconiosis of grinders and
sandrafts, metal coniosis or pneumoconiosis from
X-ray-contrast dust species (siderosis, including
aerosol with electrical welding or gas cutter of iron products
Baritosis, Staniosis, etc.). They are characterized by moderately pronounced
pneumophybroke, benign and slow-stroke
the flow is often complicated by nonspecific infection,
Chronic bronchitis.

15. New classification of pneumoconiosis 2

3. Pneumoconiosis arising from
The effects of aerosols of toxico-allergic
Actions (dust containing allergen metals,
Components of plastics and other polymeric
materials, organic dust, etc.), - beryllio,
Aluminous, "Easy Farmer" and others
Hypersensitive pneumonites. In the initial
The disease stages are characterized by clinical
Picture of the chronic bronchipoly, alveolitis
Progressive flow with outcome in fibrosis.
The concentration of dust does not have a decisive value in
Development of this group of pneumoconiosis.
The disease occurs with insignificant, but
long and constant contact with an allergen.

16. International Classification of Diseases of the 10th Review (ICD-10)

J60. Pneumoconiosis of the coil.
J61. Pneumoconiosis caused by asbestos and other minerals.
J62. Pneumoconiosis caused by dust containing silicon. Included:
Silicate fibrosis (extensive) lung. Excluded: Pneumoconiosis with
tuberculosis (J65).
J62.0 Pneumoconiosis caused by talc dust.
J62.8. Pneumoconiosis caused by another dust containing silicon.
J63. Pneumoconiosis caused by other inorganic dust.
J63.0. Aluminous (lung).
J63.1. Boxing fibrosis (lung).
J63.2. Berilliosis.
J63.3. Graphite Fibrosis (Lung)
J63.4. Siderosis.
J63.5. Stannas
J63.8. Pneumoconiosis caused by other unspecified inorganic dust.
J64. Pneumoconiosis is unspecified.
J67. Hypersensive pneumonite caused by organic dust.
Included: Allergic Alleolitis and Pneumonite caused by inhalation
Organic dust and particles of mushrooms, actinomycetes or other particles
Origin.

17. The main sections of the new classification of pneumoconiosis:

I - types of pneumoconiosis;
II - Clinical X-ray characteristic
Pneumoconiosis.
In the diagnosis of pneumoconiosis leading role plays
X-ray research method.
In X-ray classification, small and
Big blackouts. Small darkening of rounded shape
Clear contours, middle intensity. They
monomorphic, diffusely arranged mainly in
Upper and middle lung sections. Small linear
Dimming incorrect form reflect
Peribronchial, perivascular and intermediate fibrosis.
They have a mesh, cellular or tired-cellular shape and
Located mainly in the middle and lower departments
lungs.
Large dimming (the result of a merger of rounded dimming
on the site of atelectasis, pneumonic focus, with
Complicating tuberculosis). Based on x-ray
Characteristics allocate interstitial, nodule and
Nodular forms of pneumoconiosis.

18.

19.

20.

21.

22. Classification of pneumoconiosis

Clinical X-ray characteristic:
Interstitial - I Stage
Nodule - nodules 1-10 mm - stage II
Nodal (nodes\u003e 10 mm) - stage III
Clinical and functional characteristic:
Chronic bronchitis, bronchiolitis.
Emphysema of the lungs.
Days I, II, III.
Chronic pulmonary heart.
HSN I, II, III.

23. Classification of pneumoconiosis 2

Course of the disease:
slowly progressive;
quickly progressive;
regressive;
Later development.
Complications:
tuberculosis, pneumonia, bronchial
asthma, rheumatoid arthritis, SLE,
Sclerodermia, tumors (asbest),
Pneumothorax, etc.

24. Diagnosis criteria:

1.
2.
3.
4.
5.
6.
PROFMSRUT (work experience in conditions
dust formation).
Sanitary hygienic characteristic
working conditions (dust with the exceedment of the PDC when
Pneumoconios from highly moderate and
weaklyobrogenic dust, work more than 20% in shift
In conditions of dust).
X-ray - fibrosis of lungs of varying degrees
expression
Pneumoconiosis.
The clinical picture of the defeat of the respiratory organs.
Functional disorders - respiratory
Insufficiency, pulmonary heart (FVD, ultrasound
Hearts, USDG of the Vessels of the Small Circle, ECG, Gas
blood composition).
Survey study (probability of complication
tuberculosis).

25.

26.

27.

28. Treatment:

No specific treatment methods.
Treatment methods are used
Related chronic
Bronchitis.

29.

30. Prevention of pneumoconiosis

1.
2.
3.
4.
5.
6.
Reducing the level of dusting in the source of its formation
Fighting smoking
Development and implementation of the most effective means
Individual protection against dust
Timely
Holding
preliminary
and

Wet and salt-alkaline inhalations, UFO, rational
meals, food vitaminization, organization of labor regime and
rest, shortened working day, extra
Paid vacation and earlier retirement
According to the Order of the Ministry of Health of the Russian Federation No. 90 of 1996 and No. 405 of 1996
years in contact with quartz dust periodic
Medical examinations of workers spend 1 time in 12 months
Therapist.
and
otorinolarningologist
from
Mandatory
Lung Radiography and Research Function External
breathing

31. Opportunity Examination

All patients who are first diagnosed
Pneumoconiosis, subject to the direction in the institution
Medical and social
Examination
for
Examination
and
establishment
Groups
Professional disability and / or degree of loss
professional working capacity in need
medical
Social
and
Professional
rehabilitation, which regulates "Resolution
Government of the Russian Federation of October 16, 2000 No. 789 "
DEVICE OF LOSS OF PROFESSION
Installed as a percentage, based on the loss assessment
abilities
Patient
realize
Former
Professional activities in the same amount

32. Silicosis. Definition

Silicosis is the most common and hard
flowing view of pneumoconiosis, professional
Light disease due to long
Inhalation of dust containing free dioxide
Silicon. Characterized by diffuse arrangement
in lung connective tissue and education
Characteristic nodules. This foreign tissue reduces
The ability of lungs to recycle oxygen.
Silicos causes the risk of tuberculosis diseases,
bronchitis and emphysema lungs. Silicosis is
irreversible and incurable disease, and
The impact of quartz can promote development
Light cancer.

33. Silicosis 2.

Most often silicosis develops in workers
Following industries and
Professional groups:
- Mining industry - at miners,
mining gold, tin, lead, mercury, tungsten and
Other minerals that occur in the breed,
containing quartz (drillers, penetrations,
explosives and others);
- Machine-building industry - Workers
Foundry shops (sand- and shot blasts,
Cubs, agricultures, brokers, knockers
and etc.);
- in the production of refractory and ceramic
materials, as well as in the repair of industrial
furnaces and other operations in metallurgical
industry;
- when the tunnels arete, the processing of granite, other
breeds containing free silicon dioxide
Grinding sand.

34. Pathogenesis

Pathogenesis of this complex disease
Not clear to the present.
The incidence of siliciasis is in
direct dependence on quantity
(concentration) inhaled dust and
Free dioxide content
Silicon. The greatest aggressiveness
Put particles of 0.5 to 5 microns in size,
which falling into deep branching
bronchial wood achieve pulmonary
Parenhima (bronchiole, alveol, intermediate
Fabrics) and hold in it.

35. Pathogenesis 2.

The most adopted pathogenesis theories
silicosis were mechanical, chemical,
Biological, piezoelectric and others. IN
present, according to immunological
the theory of pneumoconiosis, it is established that
Silicosis is not possible without phagocytosis of quartz
particles macrophages. The speed of death
Macrophages are proportional to fibrogenic
Dust aggressiveness. The death of macrophages is the first and mandatory stage in education
Silicatical nodal. Necessary
Prerequisite for occurrence and
the formation of the nodule is considered repeatedly
repeated phagocytization of dust, which
Release from dying macrophages.

36. Pathogenesis 3.

Active immune restructuring takes place
organism in the early stages of formation
silicotic process. Development of silicosa
accompanied by different
immunological reactions of cellular and
Humoral types associated with
Predecessors of antibodies with vlimphocytes and cells reacting
directly with tissue antigens, T-lymphocytes. In patients with silicosis,
especially when progressing the process,
There are an increase in various classes
Immunoglobulinov

37. Clinical picture

Clinical picture during sylikosis monotonne,
typical poverty subjective and objective
Symptoms.
Silicosis patients typically impose little
complaints. With a detailed survey from most of them
Receive typical for any chronic
Powerful diseases complaints: shortness of breath, cough
(which are often connected not so much with the severity
developing fibrosis, how many concomitant
Silicosis bronchitis.
The sputum can be with an admixture of dark ruby
dust particles)
Pain in the chest (usually non-intensive,
self-tapping and often related to
By changing the pleura).

38. Clinical picture 2

Clinical symptoms grow as far as development
fibrous process, so far the basis
Silicose diagnostics remains x-ray
study, while there is no direct correlation with
radiographic changes.
The general condition of patients with silicosis remains for a long time
satisfactory. Chest often ordinary shape
(with a significant emphysema can be expanded in
frontwall department). As progressing
pneumophybosis or when attaching bronchitic
Syndrome can detect the thickening of the terminal phalange
fingers and feet in combination with a change in nail shape in
The form of watch glasses.
Percussively - a box shade can be marked, especially
In the lower surface departments. With pronounced fibrosis with
forming large fibrous knots percussion sound
may be shortened, especially above the blades and in
inter-pumping area (mosaic picture).

39. Clinical picture 3

With auscultation in I and especially in the II and III stage
Diseases listen to hard breath that
Massive fibrous fields may have
bronchial tint over emphysematous
Respiratory areas are weakened. 1/3 - 1/4 patients
Listened scattered dry wheels (usually
non-permanent). Often listened
Melkushard unvivaous wet wipes and
Capital (this is due to the defeat of bronchiol,
interstitial changes, pleural
Spikes).
Percussic and auscultation mosaic
Silicose is observed mainly in
pronounced stages of the disease.

40. Clinical picture 4

Progressive forms of silicose peculiar
an increase in the total protein in the blood (especially
Large fractions - globulins).
Patients with nodules silicosis marks
Increase in the blood of protein-bound oxyproline
When reducing excretion with my urine
peptide-associated and free fractions that
characterizes the predominance of collagen synthesis in
The body over its resorption.
In the serum, SRB is often determined.
However, it should be kept due to the nonspecificity of these
analyzes (such changes may occur when
A number of other diseases - tuberculosis, COPL
and etc.).

41. Clinical Picture 5

As a rule, respiratory failure is developing,
The degree of which often does not correlate with severity
pneumophibrosis.
Respiratory disorders, in particular obstructive type,
determined the degree of severity of bronchitic
Syndrome and emphysema of the lungs, location
Silicotic nodules, mediastinal syndrome
(comprehensive mediastinal organs large l / y and
fibrous formations).
The determining factor for silicose is
The aggressiveness of dust (its concentration and dispersion,
content in it SiO2).
The disease is characterized by an unfavorable course in individuals,
Began to work in very young and middle age.
Silicosis belongs to diseases prone to spontaneous
progression and after stopping contact with dust,
What is especially typical for a nodule form.

42. Clinical picture 6

Most frequent progression option
silicotic fibrosis consider the merge of the nodules in
Large nodes with the transition to the nodal form of the disease.
The origin of these nodes can play a role
Atelectases and inflammation.
When progressing a fibrous process
consistently passes from stage I in II, from II - in
III. In the III stage, the process continues to progress
due to further distribution and increase
volume of individual seals, wrinkling,
Cyrrosis and emphysema. Gradually aggravated
Respiratory failure caused by
The development of the "pulmonary heart" and its decompensation.
Compared to nodule silicosis
interstitial fibrosis (most
Common form of modern silicose)
Progresses 2-3 times less and slower.

43. Clinical Picture 7

By flow, you can allocate:
- a slow-stroke (transition from
one stage in another takes decades),
- fast-moving (transitions from
Stages to the stage take 5-6 years and less)
- Late silicosis (Development of late
reactions to the impact of large
concentrations of quartz-containing dust through
10-20 years and more after termination
Work).

44. Clinic Silicosis

І
stage.
Dyspnea
arises
for
Significant
Physical
load
non-permanent spiny pain in the chest,
Minor dry cough. For
Radiography
lungs
Notes
Symmetric gain of the pulmonary pattern, its
deformation. Against the background of the messenger
Picture in the middle part of the pulmonary fields
Appeal
in
Little
Quantity
Nature shadows with a diameter of 1-3 mm. Roots
lungs
extended
compacted
Increased lymph nodes.

45.

46.

ІІ stage. Characteristic more pronounced shortness of breath,
which appears with a slight exercise.
Painfacing pain, dry cough or with
A small number of sputum mucosa.
When the lung radiography is determined by the amplification
Metage of pulmonary fields, increase in quantity and size
novel shadows that are placed mainly in
middle and lower lungs.
In nodule form - on the background of the mellenchy mesh
Fibrosis shows a large number of thick placed
novel shadows in the form, snow blizzes. " For
interstice - nodules are missing or in a small
quantities.

47.

48.

III stage. Clinically manifests in loss
deficiency.
Dyspnea
worried about the patient alone. Pain in chest
The cell is often intensive,
There is a cough with a wet, possible
Sunshine attacks.
Radiography
lungs
Indicates
on
Merge of native shadows into massive
homogeneous, intense shadows with unequal and
fuzzy contours that are placed
Mostly in the middle lung departments.
Meet
Massive
Pureral
layers, thickening interdolete pleura.

49.

50. Complications of Silicosa

Silicotuberculosis. With severe nodule
Silicose (III Stages) Tuberculosis complicates
The course of the disease in 60-70% of cases and more.
At stage I - at 15-20%, at stage II - in 2530%. In an interstitial form - 5-10%
patients. Purge of tuberculosis on the background
Silicotic fibrosis more often
unfavorable. Forecast of the disease depends
both from the form of tuberculosis and from the form
Silicosis and degrees of their severity.

51. Complications of Silicosis 2

Special complication of silicose is to attach
articular syndrome - silicoarthritis. Rheumatoid arthritis
precedes the development of silicose, arises with him
at the same time or (more often) in different times after establishing
Diagnosis of silicose. Silicosis in the presence of rheumatoid
Arthritis is called Colin-Kaplan syndrome. This form
Silicosis is prone to progression.
The simultaneous combination of silicosis is not excluded,
Rheumatoid arthritis and tuberculosis. For diagnosis
Silicarthritis matters in blood
rheumatoid factor in significant credits.
The combination of silicose with rheumatoid arthritis, and possibly with
systemic lupus, sclerodermy, dermatomyositis,
probably not a random coincidence, but due to generality
some mechanisms of immunoreactivity disorders due
What can it be considered as a complication.
With a combination of silicose with sclerodermia disease
Call Erasmus syndrome (by the name of the author. For the first time
described it).

52. Prevention

Visit to the pulmonologist 2 times a year.
Radiography of lungs - 1 time per year.
Antioxidants, respiratory
gymnastics.
Spa treatment.
According to experts, the only
way to prevent this disease
- Prevent inhalation
Drained air.

53. Treatment

In the initial stages shown
Sanatorium-resort treatment (South
Coast of Crimea, Kislovodsk),
Catureness, physiotherapy,
Inhalation.
Oxygen inhalations are prescribed and
breathing exercises.
In the sharp form of silicose spend
Bronchoalveolar lavage.
For the treatment of obstructive syndrome
Broncholitics are prescribed.

54. Treatment 2.

For the treatment of silicotuberculeza
(combination of lung silicosis and
tuberculosis) patients appointed not
less than 3 anti-tuberculosis
drugs.
In case of severe illness with
The emergence of massive fibrosis
Doctors tend to necessity
surgical treatment that
lies in lung transplantation.

55. Treatment 3.

Forecasts for the treatment of silicose lungs depend on
The nature of the disease and its stage. Chronic
silicose form proceeds almost without
Symptoms and initial stages forecasts
Almost always favorable.
Acute or chronic progressive
The form of silicose lungs leads to development
Fibrosis of pulmonary fabrics, as well as secondary
pulmonary hypertension.
According to American specialists, the disease is inexorable and irreversible.

56. Ability to work

The question of the working capacity of patients with silicosis is solved
Differentiated with the stage, shape and flow
fibrous process in the lungs, presence and degree
severity of functional disorders, character
existing complications and concomitant diseases as well
Professions and working conditions of the patient. It should be borne in mind
that silicosis compared with other types of pneumoconiosis
characterized by the most unfavorable flow and
Often combined with pulmonary tuberculosis.
With uncomplicated silicosis I preparation
patients depend primarily from the clinical picture and form
Pneumoconiotic process. Patient interstitial
the form of silicose, which arose many years after the start
contact with dust (after 15 years or more), in the absence of
signs of respiratory and heart failure can
be left in its former work if dyingness
air in the workplace does not exceed the maximum permissible
Concentration. Periodic medical observation of such
Patients should be held at least 2 times a year.

57. Help Examination 2

Patients who have an interstitial form of silicose I
Stages developed with a small work experience in contact with
dust (less than 15 years), as well as patients with a nodule form
silicose stage I, despite the absence of their respiratory and
heart failure and complications are subject to translation
to work that is not associated with the effects of dust and substances,
possessing an irritant action. So patient

adverse meteorological factors and work,
requiring large physical stresses.
Remove from work in contact with dust patients with silicosis I
stages whose profession is associated with exposure
aggressive dust containing a large number
Crystalline silicon dioxide, i.e. With the so-called
Silico-hazard professions (drillers, peckers, etc.).
Silicosis patients stage I can be recognized
disabled when they have heavy flowing
Complications (chronic bronchitis, bronchial asthma,
lung emphysema, pulmonary heart) or accompanying
Diseases with pronounced functional disorders
(respiratory and heart failure).

58. Working Examination 3

Patients with silicosis stage II regardless of the form and
The flow of the pneumoconiotic process
Contraindicated work in the conditions of impact
Any kinds of dust. Disability of such patients
may be limited or completely
Lost, which is determined by the degree
The severity of the respiratory and heart
Insufficiency and severity of the current complications.
If the ability of the patient is recognized
limited, it should be rational
employed to work out of contact with dust
substances possess annoying
action, as well as not requiring large
physical stresses and stay in
adverse meteorological conditions.

59. Opportunity Examination 4

In silicose III stage patients usually
disabled, and some of them
need unauthorized care due to
development of severe respiratory or
heart failure, accession
active forms of tuberculosis.
However, among this contingent of patients
There are persons who throughout
Some time can be recognized
limitedly able-bodied. For them
These types of labor should be selected,
in which the impacts of any adverse factors are excluded.
production environment and large
Physical stresses.

60. Dusty bronchitis. Definition

Dusty bronchitis - chronic professional
Respiratory disease resulting from
long inhalation of industrial dust in elevated
concentrations and characterized by atrophic and
sclerotic change of all structures of bronchial
Tree with impaired Motoric Bronchi and availability
hypersecretion.
In Russia, dust bronchitis is included in the list of professional
Diseases in 1970. Dust bronchitis occurs when inhalation
predominantly moderate aggressive mixed species
dust. The diagnosis of chronic bronchitis is based on such
Clinical criteria as the presence of cough and selection
sputum not less than 3 months. For 2 years
exclusion of other diseases of the upper respiratory tract and
lungs. Potentially dangerous spheres: foundry,
mining, engineering, construction
Industry, agriculture, etc. Potentially
Dangerous professions: miners, coils, metallurgists,
Cement manufacturers, workers of weaving factories, grains,
Elevators, etc.

61. Definition 2.

The question of inclusion in
List of occupational diseases
diagnosis "chronic obstructive
Lung disease professional
Genesis "and replacing them diagnoses
"Chronic dust bronchitis (HPS)",
"Chronic bronchitis toxicochmic etiology."

62. HPB.

Causes of HPB allocation in
Independent nosological
Form:
1. High prevalence of hB
workers of various production, on
which are elevated
Dust formation.
2. 2. Growing CPB cases as
Increased work experience in conditions
Dust in production.

63. Classification of PB.

On etiology, depending on the composition and nature
Activated industrial aerosol:
* Professional dust bronchitis from exposure to conditionally
inert dust that does not have toxic and annoying
action;
* Professional toxic-dust bronchitis from exposure
Dust, toxic, irritating and allergizing substances.
According to pathorphological and endoscopic features:
* Catarval
* Catarial atrophic
* Cataro-sclerosing
On clinical and functional data:
* Unstructive bronchitis
* obstructive bronchitis
* Astmatic bronchitis
* Emphysematous bronchitis with tracheobronchial dyskinesia

64. PHB development phases

1. The initial phase (aggression) - the effect of dust causes
Response reaction from the mucous membrane
Tracheobronchial tree. The secretion of mucus increases
cover epithelium and mucous glands of bronchi with
By changing its rheological properties (increase in viscosity).
In case of long exposure to dust disturbed
Structure and functions of the cell mucosa
Tracheobronchial Tree acquire irreversible
character, and physiological methods of removal
The bronchial secret becomes insufficient.
HyperSectionage and change of the rheological properties of mucus
may be exacerbated by an irritant action of dust on
parasympathetic system of bronchial tree.
In the initial phase of the HPB, a violation is detected
Mukiciliary apparatus leading to a change in normal
functioning of the escalator mechanism drainage
Bronchi functions. This period is clinically defined as
Endobronchitis from irritation, or dust katar bronchi.

65. Flame of the development of HPS 2

2. The phase of deployed inflammation. how
The rule is noted by accession
infections are noted exudation and
infiltration. Through the porous system
The capillary channel overlook water, salt,
Fibrinogen, immune proteins. They penetrate
in the intercellular space and cause
Infiltration and swelling.
3. Recovery phase. Characterized
formation of varying degrees
Sclerosis severity with obliteration
Small bronchi.

66. Phase of the development of HPB 3

The evolution of HPB is a replacement of hypertrophic
Changes in bronchi atrophic with consistent
development of catarrhal intramural deforming
Bronchitis.
Distribution of inflammatory changes to distal
Bronchial wood departments are accompanied by violation
production of surfactant - surfankanta,
which leads to the development of bronchospasm, which contributes
The emergence of severe complications - obstructive
Emphysema lungs.
When combining bronchitis and emphysema lungs occurs
One obstruction mechanism (valve) - falling small
Bronchi in exhalation due to loss of light elastic
Properties.
The degree of obstruction is greater than defined
The predominant localization of the lesion. Basically she
Defended by the defeat of the bronchi of the middle and small caliber.
Obstructive ventilation disorders arise relatively
early.
Respiratory failure and chronic "pulmonary heart"
- Finite stages of chronic bronchitis.

67. Clinical picture

-
-
-
HPB is one of the forms of primary chronic inflammation
Bronchi. This is determined by some clinical
Features of the disease:
Slow gradual start, which is characterized
non-permanent, periodically increasing cough, as
Rule dry, sometimes with poor sputum, in the absence
Increase body temperature and substantial change
General condition.
Some types of dust (vegetable, mineral), providing
Allergizing action contribute to early violation
bronchial patency. Inflammatory process
promotes the development and progression of obstruction,
Emphysema of lightweight, respiratory failure, chronic
"Light Heart."
In the period of exacerbation, characteristic changes are noted.
laboratory indicators (leukocytosis with shift
leukocyte formula left, moderate increase in ESP).
infection and violation of bronchial patency
also contribute to the peripocal flashes of pneumonia,
prone to a protracted flow with an outcome in the carnification,
Pneumophybrosis, bronchiectase.

68. The clinical picture depends on the nature of industrial dust:

coal dust causes a pronounced reaction
The mucous membrane of the bronchi. Therefore, early
Complaints on the cough with a mocroid and
superinimation (coal professions);
Silicon-containing
dust -
changes in
bronchial trees are manifested atrophic
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Slowly progressive forms of pneumoconiosis are usually developing 10-15 years after the start of work in contact with dust, and the transition from I to the II stage of the disease lasts at least 5-10 years.

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J60. Pneumoconiosis of the coil.

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