Prevention of occupational dust diseases should be carried out in a number of areas and includes: .
Hygienic standardization;
Technological activities;
Sanitary and hygienic measures;
Personal protective equipment;
Therapeutic and preventive measures.
Hygienic standardization. The basis for carrying out measures to combat industrial dust is hygienic standards. The requirement to comply with the maximum permissible concentrations established by GOST (Table 5.3) is fundamental in the implementation of preventive and routine sanitary supervision.
Table 5.3. Maximum permissible concentrations of aerosols of predominantly fibrogenic action.
| Name of substance | MPC value, mg/m 3 | Hazard class |
| Crystalline silicon dioxide: when its content in dust is over 7 0% the same from 10 to 70% » from 2 to 10% | 2 4 | 3 4 4 |
| Amorphous silicon dioxide in the form of a condensation aerosol: when its content in dust is over 60%, the same is from 10 to 60% | ||
| Silicates and silicate-containing dust: asbestos, asbestos cement, cement, apatite, talc clay, mica glass fiber | 2 6 4 4 | 4 4 4 4 |
| Carbon dust: diamond metallized coal containing free silicon dioxide up to 5% | 4 10 | 4 4 |
| Metal dust: aluminum and its alloys (in terms of aluminum) aluminum oxide with an admixture of silicon dioxide in the form of a condensation aerosol aluminum oxide in the form of a disintegration aerosol (alumina, electrocorundum) iron oxide with an admixture of manganese oxides up to 3% the same 3 - 6% cast iron titanium, titanium dioxide tantalum and its oxides | 6 10 10 | 4 4 4 4 4 4 4 4 |
| Dust of plant and animal origin: grain (regardless of the silicon dioxide content), flour, cotton, wood, etc. (with an admixture of silicon dioxide less than 2%), cotton, cotton, linen, wool, down, etc. (with an admixture of silicon dioxide more than 10%) with an admixture of silicon dioxide from 2 to 10% |
Systematic monitoring of the dust level is carried out by SES laboratories and factory sanitary and chemical laboratories. The administration of enterprises is responsible for maintaining conditions that prevent an increase in the maximum permissible concentration of dust in the air.
When developing a system of health-improving measures, basic hygienic requirements must be applied to technological processes and equipment, ventilation, construction and planning solutions, rational medical care for workers, and the use of personal protective equipment. In this case, it is necessary to be guided by sanitary rules for organizing technological processes and hygienic requirements for production equipment, as well as industry standards for production with dust emissions at enterprises in various sectors of the national economy.
Measures to reduce dust in production and prevent pneumoconiosis must be comprehensive and include measures of a technological, sanitary-technical, medical-biological and organizational nature.
Technological activities. Eliminating dust formation in workplaces by changing production technology is the main way to prevent dust-induced lung diseases. The introduction of continuous technologies, automation and mechanization of production processes that eliminate manual labor, and remote control contribute to significantly facilitating and improving the working conditions of a large contingent of workers. Thus, the widespread use of automatic types of welding with remote control, robotic manipulators in the operations of loading, pouring, and packaging of bulk materials significantly reduces the contact of workers with sources of dust emission. The use of new technologies - injection molding, electrochemical methods of metal processing, shot blasting, hydro- or electric spark cleaning - eliminated operations associated with dust formation in the foundries of factories.
Effective means of combating dust are the use in the technological process of briquettes, granules, pastes, solutions, etc. instead of powdered products; replacement of toxic substances with non-toxic ones, for example, in cutting fluids, greases, etc.; transition from solid fuel to gaseous fuel; widespread use of high-frequency electric heating, which significantly reduces pollution of the production environment by smoke and flue gases.
The following measures also help prevent dust in the air: replacing dry processes with wet ones, for example wet grinding, grinding, etc.; sealing of equipment, grinding areas, transportation; separating units that pollute the work area into isolated rooms with a remote control device.
The main method of combating dust in underground mines, which is the most dangerous in relation to occupational dust lung diseases, is the use of nozzle irrigation with water supply under pressure of at least 3 - 4 atm. Irrigation devices should be provided for all types of mining equipment - combines, drilling rigs, etc. Irrigation should also be used in places where coal and rock are loaded and unloaded, as well as during transportation. Water curtains are used immediately before blasting and when there is suspended dust, and the water torch should be directed towards the dust cloud.
Sanitary measures. Sanitary measures play a very significant role in the prevention of dust diseases. These include local shelters for dust-generating equipment with air suction from under the shelter. Sealing and covering equipment with continuous dust-proof casings with effective aspiration are a rational means of preventing dust release into the air of the working area. Local exhaust ventilation (casings, side exhausts) is used in cases where technological conditions make it impossible to humidify processed materials. Dust must be removed directly from dust generation areas. The dusty air is cleaned before being released into the atmosphere.
When welding metal structures and large-sized products, sectional and portable local suction is used. In some cases, ventilation is installed in combination with technological measures. Thus, in installations for dust-free dry drilling, local exhaust ventilation is combined with the head of the working tool. To combat secondary dust formation, pneumatic cleaning of premises is used. Blowing away dust using compressed air and dry cleaning of premises and equipment is not permitted.
Personal protective equipment. In cases where measures to reduce dust concentrations do not reduce dust in the work area to acceptable limits, it is necessary to use personal protective equipment.
Personal protective equipment includes: dust respirators, safety glasses, special dust-proof clothing. The choice of one or another respiratory protection device is made depending on the type of harmful substances and their concentration. The respiratory organs are protected with filtering and isolating devices. The most widely used respirator is the “Petal” type. In case of contact with powdery materials that adversely affect the skin, use protective pastes and ointments.
To protect the eyes, use closed or open glasses. Closed-type glasses with durable safety glasses are used for mechanical processing of metals (cutting, chasing, hand riveting, etc.). For processes accompanied by the formation of small and solid particles and dust, metal splashes, closed glasses with sides or masks with a screen are recommended.
The following types of workwear are used: dust-proof overalls - women's and men's with helmets to perform work associated with large formation of non-toxic dust; suits - men's and women's with helmets; self-contained spacesuit for protection from dust, gases and low temperatures. For miners engaged in open-pit mining and for quarry workers during the cold season, special clothing and footwear with good heat-protective properties are issued.
Treatment and preventive measures. In the system of health-improving measures, medical monitoring of the health status of workers is very important. In accordance with the order of the Ministry of Health No. 700 of June 19, 1984, it is mandatory to conduct preliminary medical examinations upon entry into work and periodic medical examinations. Contraindications to employment associated with exposure to dust are all forms of tuberculosis, chronic diseases of the respiratory system, cardiovascular system, eyes and skin.
The main task of periodic examinations is the timely detection of the early stages of the disease and the prevention of the development of pneumoconiosis, determining professional suitability and carrying out the most effective treatment and preventive measures. The timing of inspections depends on the type of production, profession and the content of free silicon dioxide in the dust. Examinations by a therapist and an otolaryngologist are carried out once every 12 or 24 months. depending on the type of dust with mandatory chest x-ray and large-frame fluorography.
Among the preventive measures aimed at increasing the body's reactivity and resistance to dust damage to the lungs, the most effective are UV irradiation in fotariums, which inhibits sclerotic processes, alkaline inhalations, which promote the sanitation of the upper respiratory tract, breathing exercises, which improve the function of external respiration, a diet with the addition of methionine and vitamins
Indicators of the effectiveness of anti-dust measures are a decrease in dust levels and a decrease in the incidence of occupational lung diseases.
Dust is an occupational and household irritant that causes dangerous human diseases. Entering the body through the lungs, mucous membranes of the eyes, nasal cavity, skin, the smallest solid particles floating freely in the air have:
- poisonous effect;
- allergenic;
- fibrogenic.
The dust may contain helminth eggs, plant pollen, mold microfungi, and particles of dead insects.
Lung diseases caused by dust
The effect of dust on parts of the respiratory system is determined by the shape and size of the particles. Particularly dangerous are poorly soluble particles less than 0.3 microns in elongated diameter. Some types of dust are naturally removed from the lungs over time, while others remain in the body forever, causing illness. The latter include silicates, natural and synthetic asbestos, asbestos rubber, and aluminosilicates.
Pneumoconiosis
Pneumoconiosis is a group of lung diseases caused by the penetration of dust particles into the respiratory tract. The name of the disease comes from the Greek pneumōn, “lungs,” and konía, meaning “dust.” In addition to mechanical trauma to the mucous membranes of the bronchi, trachea, and lungs, the ability of a number of substances entering the respiratory tract to dissolve in body fluids to form toxic compounds is dangerous. Silicon dioxide, silicates, beryllium, and some types of organic particles cause the proliferation of connective tissue and lead to pneumosclerosis.
Dust bronchitis, tracheitis, asthma
The occurrence of the disease is facilitated by:
- intense physical labor in a dusty environment;
- smoking;
- age;
- aerosol spraying;
- infectious lung diseases.
The disease in the initial stages is asymptomatic, manifested only by a dry cough. Subsequently, the cough intensifies, becomes paroxysmal, then shortness of breath, weakness, and sweating occur.
Conjunctivitis
Dust particles of various natures mechanically irritate the mucous membrane of the eyes, causing dryness, foreign body sensation, redness, swelling of the eyelids, and inflammation in the cornea. Contact with dust of microfungi in the eyes can cause purulent conjunctivitis with the formation of yellowish films, nodular infiltrates of leukocytes and mucous epithelial cells involving eye tissue in the pathological process.
In addition to mechanical irritation, dust can cause allergic conjunctivitis. Seasonal exacerbations of the disease during the flowering of some plants cause particular harm to health. The patient experiences photophobia, pain, burning in the eyes, and lacrimation.
Dermatoconiosis
The action of cement dust, fiberglass particles, tobacco, talc, flour and other damaging agents on the skin leads to the appearance of skin rashes, erythematous spots, blisters, and bloody crusts. The disease is accompanied by itching and redness of the affected area. The course of the disease depends on the condition of the skin, dustiness and humidity of the environment. Good room ventilation, elimination of dust sources, and hygienic clothing prevent the occurrence of dermatoconiosis.
The name “pneumoconiosis” (from the Greek pneumon - “lungs”, konis - “dust”) combines a number of diseases caused by the ingestion of a large number of dust particles into the lungs over a long period of time. The term “pneumoconiosis” was proposed by F.A. Zenker (1866). These diseases belong to the group of occupational processes. Pneumoconiosis is found in some workers who inhale various types of dust for 5-15 years or more. Small dust particles entering the respiratory tract cause a reaction in the interstitial connective tissue, resulting in the development and progression of pulmonary fibrosis.
The negative impact of industrial dust on humans is determined by its total toxicological effect on various organs. The respiratory organs, skin, eyes, blood and digestive tract are most affected by dust.
When dust is inhaled, pneumoconiosis occurs, which is associated with the deposition of dust in the lungs and the reaction of the tissue to its presence.
Along with the chemical composition of dust, other factors are also important: the shape and size of the particles, their solubility, degree of hardness, distribution of electron density over their surface, etc. Industrial dust particles are divided into visible (more than 10 microns in diameter), microscopic (from 0 .25 to 10 µm) and ultramicroscopic (less than 0.25 µm), 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.
The nature of the resulting pneumoconiosis, the features of its course, possible complications, and prognosis depend on the characteristics and concentration of dust entering the respiratory system during work. The most dangerous is dust containing free silicon dioxide, in particular in the form of small crystals, i.e. quartz particles. This dust has the most pronounced fibrogenic properties. Dust containing most silicates has similar, but much less pronounced properties; The fibrogenic activity of dust of some metals, in particular beryllium, is even lower (but still noticeable). The fibrogenic properties of most types of organic dust are weakly expressed. When dust of different compositions 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 with 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 are 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.
Pneumoconiosis is a very common form of chronic dust lung diseases. For all types of pneumoconiosis, the presence of a pneumofibrotic process is mandatory. However, the course, clinical, radiological and pathological patterns of various types of pneumoconiosis have some features, largely depending on the composition of the industrial dust that caused the development of pulmonary fibrosis.
It is believed that the destruction of alveolar macrophages by dust plays a significant role in the development of pulmonary fibrosis, which is most noticeable when inhaling dust containing quartz, as well as coal and asbestos dust. In addition, the action of dust stimulates the formation of a significant amount of collagen. A common feature of all types of pneumoconiosis is the development of interstitial fibrosis, however, each type of pneumoconiosis has its own characteristics, determined by histological examination.
In addition to the nature and amount of inhaled dust, the occurrence and development of the disease is also influenced by the previous state of the respiratory system, immunological status, allergic reaction, etc.
This explains the differences in the health status of workers exposed to similar occupational conditions for the same amount of time.
Classification
Based on the nature of the course, the following types of pneumoconiosis are distinguished:
regressing.
rapidly progressing;
slowly progressing;
With a rapidly progressing form of pneumoconiosis, stage I of the disease can be detected 3-5 years after the start of work in contact with dust or when the pneumoconiotic process progresses, i.e. the transition from stage I of pneumoconiosis to stage II is observed after 2-3 years. This form of pneumoconiosis, in particular, includes the so-called acute silicosis, which is essentially a rapidly progressing form of silicosis.
Slowly progressive forms of pneumoconiosis usually develop 10-15 years after the start of work in contact with dust, and the transition from stage I to stage II of the disease lasts at least 5-10 years.
Pneumoconiosis that develops several years after cessation of contact with dust is usually called late.
Regressive forms of pneumoconiosis occur only when radiopaque dust particles accumulate in the lungs, which create the impression of a more pronounced stage of pulmonary fibrosis according to X-ray studies. When the patient stops contact with dust, partial removal of radiopaque dust from the lungs is usually observed. This explains the “regression” of the pneumoconiotic process.
Depending on the nature of the inhaled dust, various types of pneumoconiosis are distinguished.
Silicosis is a disease caused by inhalation of dust containing free silicon dioxide (SiO2).
Silicates (asbestosis, talcosis, cement, mica, nepheline, olivine and other silicates, kaolinosis). Silicates occur when inhaling silicate dust containing silicon dioxide in a bound state.
Metalloconiosis (berylliosis, siderosis, aluminosis, baritosis, staniosis, pneumoconiosis caused by dust from rare earth hard and heavy alloys).
Carboconiosis (anthracosis, graphitosis, soot pneumoconiosis). These diseases are a consequence of inhaling carbon-containing dust.
Pneumoconiosis caused by inhalation of mixed dust containing free silicon dioxide (anthracosilicosis, siderosilicosis, silicosilicosis), with a small content of it (pneumoconiosis of grinders, electric welders) and not containing silicon dioxide.
Pneumoconiosis caused by inhalation of organic dust (cotton, grain, cork, reed pneumoconiosis).
According to the international classification of diseases ICD-10, the following types of lung diseases caused by external agents are distinguished (J60-J70).
J60. Coal miner's pneumoconiosis.
Anthracosilicosis.
Anthracosis.
Coal miner's lung.
J61. Pneumoconiosis caused by asbestos and other mineral substances.
Asbestosis.
Excluded: pleural plaque.
J92.0. With asbestosis.
J65. With tuberculosis.
J62. Pneumoconiosis caused by dust containing silicon.
Included: silicate fibrosis (extensive) of the lung.
J65. Excluded: pneumoconiosis with tuberculosis.
J62.0. Pneumoconiosis caused by talc dust.
J62.8. Pneumoconiosis caused by other dusts containing silica.
J63. Pneumoconiosis caused by other inorganic dusts.
J65. Excluded: with tuberculosis.
J63.0. Aluminosis (lung).
J63.1. Bauxite fibrosis (lung).
J63.2. Beryllium.
J63.3. Graphite fibrosis (lung).
J63.4. Siderosis.
J63.5. Stannoz.
J63.8. Pneumoconiosis caused by other specified inorganic dusts.
J64. Pneumoconiosis, unspecified.
J65. Excluded: with tuberculosis.
J65. Pneumoconiosis associated with tuberculosis.
Any condition listed in sections J60-J64 in combination with tuberculosis classified in sections A15-A16.
J66. Respiratory tract disease caused by specific organic dust.
J67.1. Excluded: bagassos.
J67.0. Farmer's lung.
J67. Hypersensitivity pneumonitis caused by organic dust.
J68.3. Reactive airway dysfunction syndrome.
J66.0. Byssinosis.
Respiratory disease caused by cotton dust.
J66.1. Flax ripper disease.
J66.2. Cannabinosis.
J66.8. Respiratory disease caused by other specified organic dusts.
J67. Hypersensitivity pneumonitis caused by organic dust.
Included: allergic alveolitis and pneumonitis caused by inhalation of organic dust and particles of fungi, actinomycetes or particles of other origin.
J68.0. Excluded: pneumonitis caused by inhalation of chemicals, gases, fumes and vapors.
J67.0. Lung of a farmer (agricultural worker).
Reaper's lung.
Mower's lung.
A disease caused by moldy hay.
J67.1. Bagassoz (from sugar cane dust).
Bagassoznaya (s):
pneumonitis
J67.2. Poultry farmer's lung.
Disease, or lung, of a parrot lover.
Disease, or lung, of the pigeon fancier.
J67.3. Suberosis.
Disease, or lung, of the balsa wood processor.
Disease, or lung, of a cork worker.
J67.4. The lung of someone working with malt.
Alveolitis caused by Aspergillus clavatus.
J67.5. The lung of someone working with mushrooms.
J67.6. Lung of maple bark harvester.
Alveolitis caused by Cryptostroma corticale.
Cryptostromosis.
J67.7. Lung in contact with air conditioning and humidifiers.
Allergic alveolitis caused by fungal mold, thermophilic actinomycetes and other microorganisms that multiply in ventilation (air conditioning) systems.
J67.8. Hypersensitivity pneumonitis caused by other organic dust.
Cheese washer's lung.
Light coffee grinder.
Lung of a worker at a fish flour factory.
Lung of a furrier (furrier).
The lungs of someone working with sequoia.
J67.9. Hypersensitivity pneumonitis caused by unspecified organic dust.
Allergic alveolitis.
Hypersensitivity pneumonitis.
J68. Respiratory conditions caused by inhalation of chemicals, gases, fumes and vapors.
To identify the cause, use an additional external cause code (class XX).
J68.0. Bronchitis and pneumonitis caused by chemicals, gases, fumes and vapors.
Chemical bronchitis (acute).
J68.1. Acute pulmonary edema caused by chemicals, gases, fumes and vapors.
Chemical pulmonary edema (acute).
J68.2. Inflammation of the upper respiratory tract caused by chemicals, gases, fumes and vapors, not classified elsewhere.
J68.3. Other acute and subacute respiratory conditions caused by chemicals, gases, fumes and vapors.
Reactive airway dysfunction syndrome.
J68.4. Chemical respiratory conditions caused by chemicals, gases, fumes and vapors.
Emphysema (diffuse) (chronic).
Obliterating bronchitis (chronic) subacute.
Pulmonary fibrosis (chronic) of smoke and vapors.
J68.8. Other respiratory conditions caused by chemicals, gases, fumes and vapors.
J68.9. Unspecified respiratory conditions caused by chemicals, gases, fumes and vapors.
J69. Pneumonitis caused by solids and liquids.
P24. Excluded: neonatal aspiration syndrome.
J70. Respiratory conditions caused by other external agents.
To identify the cause, use an additional external cause code (class XX).
J70.0. Acute pulmonary manifestations caused by radiation.
Radiation pneumonitis.
J70.1. Chronic and other pulmonary manifestations caused by radiation.
Lung fibrosis due to radiation.
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When conducting an X-ray examination, plain radiographs of the lungs reveal an increase and deformation of the pulmonary pattern, against which numerous nodule-like formations measuring about 3 mm, round in shape with clear contours, are visible. These nodules are scattered against the background of a deformed pulmonary pattern and are accompanied by symmetrical changes in the structure of the roots of the lungs. Analysis of radiographs of patients with aluminosis shows that after 10-15 years...
In most asthma patients, physical activity leads to increased symptoms of the disease along with other triggers. However, in some patients it is the only triggering factor. If, in this case, spontaneous disappearance of obstruction occurs 30-45 minutes after physical activity, such asthma is usually characterized as exercise-induced asthma. When studying FEV1, you can find that after stopping...
Patients experience symptoms characteristic of silicosis and symptoms of tuberculosis. The emergence or increase of tuberculosis intoxication indicates a complication of silicosis with tuberculosis. When interviewing a patient, you should carefully study your professional history: work with quartz-containing dust, contact with bacillary tuberculosis patients, tuberculosis in the past. The most typical complaints for patients with silicotuberculosis are increasing weakness, shortness of breath, cough with mucopurulent sputum, ...
The basic principles of treatment and examination of temporary disability for aluminosis are the same as for silicosis. However, I would like to mention homeopathic treatment. As you know, every poison has an antidote. Thus, various aluminum compounds in homeopathic dilutions (sold in homeopathic pharmacies) can serve as a kind of antidotes for “aluminum disease”. Due to the microdose they are not toxic (in one homeopathic grain...
Preventive measures include the following: patient education; continuous monitoring of respiratory function using a home peak flow meter and regular spirometry in a medical facility; control over environmental triggers; identification and treatment of concomitant diseases, such as chronic sinusitis, nasal polyposis, allergic rhinitis, gastroesophageal reflux, heart rhythm disturbances, which can worsen the course of asthma; prevention of side effects (cataracts,...
The X-ray picture of silicotuberculosis is polymorphic. The characteristic symmetry of silicosis rashes is disrupted with the development of silicotuberculosis. Asymmetrically located lesions or foci with vague contours appear in the apical-subclavian areas. Most often, silicotuberculosis lesions occur in segments I, II and VI. X-ray can detect a cavity. Against the background of silicosis stages I and II, the cavities have a round shape, with silicosis III ...
An important feature of inflammation in bronchial asthma is that it has a unique origin that, according to most researchers, is not related to bacterial infection. Therefore, antibiotics, especially the penicillin series, due to their allergenic properties, can only be used according to strict indications (for radiologically proven pneumonia, sepsis, purulent sinusitis, infectious foci in other areas). Respiratory viral infection...
Treatment of patients with silicotuberculosis is a difficult task. Basically, it is carried out according to the same principles as the treatment of patients with tuberculosis. When choosing a treatment method, it is necessary to take into account large morphological changes in the lungs, pneumosclerosis, which limit the penetration of drugs into the pathological focus. Patients who have received a large number of chemotherapy drugs, with symptoms of drug intolerance, as well as with a progressive process can be recommended...
Pneumoconiosis is a dust lung disease.
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.
When dust of different composition enters the lungs, the lung tissue may react differently.
The localization of the process in the lungs depends on the physical properties of the dust. Particles of small 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.
Among pneumoconiosis, anthracosis, silicosis, silicosis, metalloconiosis, carboconiosis, pneumoconiosis from mixed dust, pneumoconiosis from organic dust are distinguished.
1) 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. 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.
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.
2) Silicosis
Silicosis or chalicosis 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.
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 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. 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. Diffuse emphysema, bronchial deformation, various forms of bronchiolitis, and bronchitis develop.
Tuberculosis is often associated with silicosis. Then they talk about silicotuberculosis, in which, in addition to silicotic nodules and tuberculous changes, so-called silicotuberculous foci are found. The right half of the heart is often hypertrophied, up to the development of a typical pulmonary heart. Patients most often die from progressive pulmonary heart failure.
3) Asbestosis
The onset of asbestosis varies widely. 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, are thin, so they penetrate deeply into the alveoli in the basal regions 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.
The carcinogenicity of asbestos depends not on its type, but on the length of the fibers. Thus, large fibers do not have carcinogenic properties, while small fibers 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.
4) Beryllium
Beryllium dust and vapors are very dangerous and can cause lung damage and the development of systemic complications.
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. as a result. Microscopically, such pneumonia has the character of “acute chemical pneumonia.” 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.
Chronic berylliosis is often called "granulomatous berylliosis" because it is characterized by the development of small granulomas resembling those of tuberculosis or sarcoidosis.
Unlike asbestosis, beryllium does not cause a predisposition to lung cancer. In chronic berylliosis, along with kidney damage, granulomatous changes are observed in the liver, kidneys, spleen, lymph nodes and skin. When beryllium particles enter through damaged skin, granulomatous inflammation develops with the formation of long-term non-healing wounds.
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Ministry of Education and Science of Ukraine
Ukrainian Engineering and Pedagogical Academy
on the topic: « Occupational diseases caused by exposure to industrial dust»
Kharkoin 2013
Introduction
The topic of this essay is very relevant in our time, when heavy industry is very developed. In post-Soviet countries, they are accustomed to violating safety regulations, which leads to numerous accidents, and even more people suffering from occupational diseases. Therefore, I will try to study diseases caused by long-term contact with dust. At the moment, science is developing rapidly, but in the wrong direction. Therefore, I believe that the research conducted in this essay will be useful, firstly for managers, and secondly for the workers themselves who come into contact with dust.
I will try to explore pneumoconiosis from a medical point of view, their manifestations and symptoms, their treatment and prevention.
PNeumoconiosis
Under the name “pneumoconiosis” (from the Greek pneumon - “lungs”, konis - “dust”) they combine a number of diseases caused by the ingestion of a large number of dust particles into the lungs over a long period of time. The term “pneumoconiosis” was proposed by F.A. Zenker (1866). These diseases belong to the group of occupational processes. Pneumoconiosis is found in some workers who inhale various types of dust for 5-15 years or more. Small dust particles entering the respiratory tract cause a reaction in the interstitial connective tissue, resulting in the development and progression of pulmonary fibrosis.
The negative impact of industrial dust on humans is determined by its total toxicological effect on various organs. The respiratory organs, skin, eyes, blood and digestive tract are most affected by dust.
When dust is inhaled, pneumoconiosis occurs, which is associated with the deposition of dust in the lungs and the reaction of the tissue to its presence.
Along with the chemical composition of dust, other factors are also important: the shape and size of the particles, their solubility, degree of hardness, distribution of electron density over their surface, etc. Industrial dust particles are divided into visible (more than 10 microns in diameter), microscopic (from 0 .25 to 10 µm) and ultramicroscopic (less than 0.25 µm), 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.
The nature of the resulting pneumoconiosis, the features of its course, possible complications, and prognosis depend on the characteristics and concentration of dust entering the respiratory system during work. The most dangerous is dust containing free silicon dioxide, in particular in the form of small crystals, i.e. quartz particles. This dust has the most pronounced fibrogenic properties. Dust containing most silicates has similar, but much less pronounced properties; The fibrogenic activity of dust of some metals, in particular beryllium, is even lower (but still noticeable). The fibrogenic properties of most types of organic dust are weakly expressed. When dust of different compositions enters the lungs, the lung tissue may react differently.
The reaction of the lung tissue can be:
1. inert, for example with ordinary pneumoconiosis - anthracosis of coal miners;
2. fibrosing, for example with massive progressive fibrosis, asbestosis and silicosis;
3. allergic, for example with exogenous allergic pneumonitis;
4. neoplastic, for example with 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 are 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. Pneumoconiosis is a very common form of chronic dust lung diseases. For all types of pneumoconiosis, the presence of a pneumofibrotic process is mandatory. However, the course, clinical, radiological and pathological patterns of various types of pneumoconiosis have some features, largely depending on the composition of the industrial dust that caused the development of pulmonary fibrosis. It is believed that the destruction of alveolar macrophages by dust plays a significant role in the development of pulmonary fibrosis, which is most noticeable when inhaling dust containing quartz, as well as coal and asbestos dust. In addition, the action of dust stimulates the formation of a significant amount of collagen. A common feature of all types of pneumoconiosis is the development of interstitial fibrosis, however, each type of pneumoconiosis has its own characteristics, determined by histological examination. In addition to the nature and amount of inhaled dust, the occurrence and development of the disease is also influenced by the previous state of the respiratory system, immunological status, allergic reaction, etc.
This explains the differences in the health status of workers exposed to similar occupational conditions for the same amount of time.
Classification
Based on the nature of the course, the following types of pneumoconiosis are distinguished:
1. rapidly progressing;
2. slowly progressing;
3. late;
4. regressing.
With a rapidly progressing form of pneumoconiosis, stage I of the disease can be detected 3-5 years after the start of work in contact with dust or when the pneumoconiotic process progresses, i.e. The transition from stage I of pneumoconiosis to stage II is observed after 2-3 years. This form of pneumoconiosis, in particular, includes the so-called acute silicosis, which is essentially a rapidly progressing form of silicosis.
Slowly progressive forms of pneumoconiosis usually develop 10-15 years after the start of work in contact with dust, and the transition from stage I to stage II of the disease lasts at least 5-10 years.
Pneumoconiosis that develops several years after cessation of contact with dust is usually called late.
Regressive forms of pneumoconiosis occur only when radiopaque dust particles accumulate in the lungs, which create the impression of a more pronounced stage of pulmonary fibrosis according to X-ray studies. When the patient stops contact with dust, partial removal of radiopaque dust from the lungs is usually observed.
This explains the “regression” of the pneumoconiotic process.
Depending on the nature of the inhaled dust, various types of pneumoconiosis are distinguished.
1. Silicosis is a disease caused by inhalation of dust containing free silicon dioxide (SiO2).
2. Silicoses (asbestosis, talcosis, cement, mica, nepheline, olivine and other silicoses, kaolinosis). Silicates occur when inhaling silicate dust containing silicon dioxide in a bound state.
3. Metalloconiosis (berylliosis, siderosis, aluminosis, baritosis, staniosis, pneumoconiosis caused by dust from rare earth hard and heavy alloys).
4. Carboconiosis (anthracosis, graphitosis, soot pneumoconiosis). These diseases are a consequence of inhaling carbon-containing dust.
5. Pneumoconiosis caused by inhalation of mixed dust containing free silicon dioxide (anthracosilicosis, siderosilicosis, silicosilicosis), with an insignificant content of it (pneumoconiosis of grinders, electric welders) and not containing silicon dioxide.
6. Pneumoconiosis caused by inhalation of organic dust (cotton, grain, cork, reed pneumoconiosis).
According to the international classification of diseases ICD-10, the following types of lung diseases caused by external agents are distinguished (J60--J70).
J60. Coal miner's pneumoconiosis.
Anthracosilicosis.
Anthracosis.
Coal miner's lung.
J61. Pneumoconiosis caused by asbestos and other mineral substances.
Asbestosis.
Excluded: pleural plaque.
J92.0. With asbestosis.
J65. With tuberculosis.
J62. Pneumoconiosis caused by dust containing silicon.
Included: silicate fibrosis (extensive) of the lung.
J65. Excluded: pneumoconiosis with tuberculosis.
J62.0. Pneumoconiosis caused by talc dust.
J62.8. Pneumoconiosis caused by other dusts containing silica.
J63. Pneumoconiosis caused by other inorganic dusts.
J65. Excluded: with tuberculosis.
J63.0. Aluminosis (lung).
J63.1. Bauxite fibrosis (lung).
J63.2. Beryllium.
J63.3. Graphite fibrosis (lung).
J63.4. Siderosis.
J63.5. Stannoz.
J63.8. Pneumoconiosis caused by other specified inorganic dusts.
J64. Pneumoconiosis, unspecified.
J65. Excluded: with tuberculosis.
J65. Pneumoconiosis associated with tuberculosis.
Any condition listed in headings J60--J64, in combination with tuberculosis classified in headings A15--A16.
J66. Respiratory tract disease caused by specific organic dust. J67.1. Excluded: bagassos.
J67.0. Farmer's lung.
J67. Hypersensitivity pneumonitis caused by organic dust.
J68.3. Reactive airway dysfunction syndrome.
J66.0. Byssinosis.
Respiratory disease caused by cotton dust.
J66.1. Flax ripper disease.
J66.2. Cannabinosis.
J66.8. Respiratory disease caused by other specified organic dusts.
J67. Hypersensitivity pneumonitis caused by organic dust.
Included: allergic alveolitis and pneumonitis caused by inhalation of organic dust and particles of fungi, actinomycetes or particles of other origin.
J68.0. Excluded: pneumonitis caused by inhalation of chemicals, gases, fumes and vapors.
J67.0. Lung of a farmer (agricultural worker).
Reaper's lung.
Mower's lung.
A disease caused by moldy hay.
J67.1. Bagassoz (from sugar cane dust).
Bagassoznaya (s):
pneumonitis
J67.2. Poultry farmer's lung.
Disease, or lung, of a parrot lover.
Disease, or lung, of the pigeon fancier.
J67.3. Suberosis.
Disease, or lung, of the balsa wood processor.
Disease, or lung, of a cork worker.
J67.4. The lung of someone working with malt.
Alveolitis caused by Aspergillus clavatus.
J67.5. The lung of someone working with mushrooms.
J67.6. Lung of maple bark harvester.
Alveolitis caused by Cryptostroma corticale.
Cryptostromosis.
J67.7. Lung in contact with air conditioning and humidifiers.
Allergic alveolitis caused by fungal mold, thermophilic actinomycetes and other microorganisms that multiply in ventilation (air conditioning) systems.
J67.8. Hypersensitivity pneumonitis caused by other organic dust.
Cheese washer's lung.
Light coffee grinder.
Lung of a worker at a fish flour factory.
Lung of a furrier (furrier).
The lungs of someone working with sequoia.
J67.9. Hypersensitivity pneumonitis caused by unspecified organic dust.
Allergic alveolitis.
Hypersensitivity pneumonitis.
J68. Respiratory conditions caused by inhalation of chemicals, gases, fumes and vapors.
To identify the cause, use an additional external cause code (class XX).
J68.0. Bronchitis and pneumonitis caused by chemicals, gases, fumes and vapors. Chemical bronchitis (acute).
J68.1. Acute pulmonary edema caused by chemicals, gases, fumes and vapors.
Chemical pulmonary edema (acute).
J68.2. Inflammation of the upper respiratory tract caused by chemicals, gases, fumes and vapors, not classified elsewhere.
J68.3. Other acute and subacute respiratory conditions caused by chemicals, gases, fumes and vapors.
Reactive airway dysfunction syndrome.
J68.4. Chemical respiratory conditions caused by chemicals, gases, fumes and vapors.
Emphysema (diffuse) (chronic).
Obliterating bronchitis (chronic) subacute.
Pulmonary fibrosis (chronic) of smoke and vapors.
J68.8. Other respiratory conditions caused by chemicals, gases, fumes and vapors.
J68.9. Unspecified respiratory conditions caused by chemicals, gases, fumes and vapors.
J69. Pneumonitis caused by solids and liquids.
P24. Excluded: neonatal aspiration syndrome.
J70. Respiratory conditions caused by other external agents.
To identify the cause, use an additional external cause code (class XX).
J70.0. Acute pulmonary manifestations caused by radiation.
Radiation pneumonitis.
J70.1. Chronic and other pulmonary manifestations caused by radiation.
Lung fibrosis due to radiation.
Therapeutic and preventive measures include high-quality nutrition high in proteins and vitamins, proper organization of recreation, active sports, breathing exercises, smoking cessation, and water treatments.
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Various adaptogens are used among medications. They have general stimulating properties, increase nonspecific reactions of the body, and promote the rapid restoration of damaged organs. Most often, patients are prescribed tincture of eleutherococcus, pantocrine, nicotinic acid, vitamins of groups B, C and P.
If the patient does not have pronounced pulmonary insufficiency, he is recommended: potassium chloride, iontophoresis with novocaine and ultrasound on the chest. All these procedures stimulate blood and lymph circulation and significantly improve the ventilation function of the lungs. When bronchitis appears and develops, the patient is additionally prescribed expectorants and drugs that dilute sputum (marshmallow root, thermopsis, iodine preparations).
Patients with a severe stage of the disease are transferred to inpatient or sanatorium treatment of pneumoconiosis. The most widely used techniques are hyperbaric oxygen therapy and oxygen inhalation. Bronchodilators and drugs that reduce pressure in the pulmonary circulation (reserpine, papaverine, aminophylline) are effective. For decompensated cor pulmonale, patients are prescribed diuretics and cardiac glycosides. Corticosteroids are also quite widely used.
The prognosis for treatment and recovery depends on the stage of pneumoconiosis and the complications that often arise during the development of the disease. The prognosis is unfavorable for such forms as silicosis, berylliosis and asbestosis, when the progression of the disease continues even after cessation of contact with harmful compounds. The remaining forms are characterized by a benign course and favorable prognosis.
Prevention
dust pneumoconiosis therapeutic preventive
In recent years, the antifibrogenic effect of polymer drugs has been studied, the positive effect of which, according to modern concepts, is based on the protection of phagocyte cell membranes from the toxic effects of quartz and the interaction of polymers with silicon dioxide, which, when adsorbed on the polymer, loses activity. The experiment studied a number of polymer preparations, and, in particular, poly-2-vinyl-pyridine-N-oxide (polyvinoxide), which has a pronounced antifibrogenic effect and prevents the progression of silicosis, and, according to some data, contributes to the reverse development of the process. However, during a clinical trial of the drug, no positive effect was found during the progressive silicotic process. Experimental research continues in the search for new polymer drugs that undergo faster resorption in the body and have fewer side effects.
Currently used means and methods for the prevention and treatment of pneumoconiosis include general strengthening measures aimed at hardening the body and increasing its reactivity, improving the functional state of the bronchopulmonary system, preventing and treating heart failure and combating complications.
Among the measures of medical prevention of pneumoconiosis, the leading role belongs to preliminary and periodic medical examinations of workers. Of great importance in preventing dust pathology of the respiratory system is the correct organization of medical examinations using x-ray and functional diagnostic methods, ensuring early detection of respiratory pathology. During periodic examinations, workers are also selected who need preventive and therapeutic measures aimed at preventing dust diseases, and if the latter are identified, at combating complications that aggravate their course.
Long-term exposure to industrial dust often leads to changes, expressed primarily in a decrease in the functional activity of the mucous membrane of the upper respiratory tract and bronchi, as well as in changes in indicators of the general reactivity of the body. It is known that modern forms of pneumoconiosis and dust bronchitis develop on average 10 years or more after the start of work in a dust occupation, therefore persons with work experience of more than 10 years, even without any special abnormalities in the respiratory system, should be classified as a risk group for the possibility of dust pathology occurring. This group should also include those workers who exhibit individual signs of dust exposure, regarded as suspected pneumoconiosis and dust bronchitis, as well as persons suffering from chronic inflammatory diseases of the upper respiratory tract and frequent acute respiratory diseases, predisposing to the development of dust pathology of organs breathing.
Persons working in underground conditions need to carry out ultraviolet irradiation in the conditions of mine fotariums, which increases the overall reactivity of the body and resistance to infectious bronchopulmonary diseases. Irradiation is recommended to be carried out 2 times a year in the autumn-winter and spring periods, in courses of 20 sessions. When determining the dose of ultraviolet irradiation, it is necessary to take into account that with increasing underground experience, miners' sensitivity to ultraviolet rays increases, so irradiation should begin with minimal doses.
Quite widely in relation to this group of workers, various adaptogens can be used that have general stimulating properties and increase the nonspecific reactivity of the body (tincture of Eleutherococcus, Pantocrine, Chinese Schisandra in standard doses in courses of 3-4 weeks). The use of a complex of various vitamins is also indicated.
In addition to physical therapy, other health-improving activities are recommended: massage, health path, walking. Among the means of hardening, we can recommend the use of hydroprocedures, especially therapeutic showers (circular shower, Charcot shower) with a gradual decrease in water temperature. Patients with pneumoconiosis without severe pulmonary insufficiency are shown the entire complex of the above preventive measures. In addition, it is additionally advisable to prescribe currents or ultrasound to the chest, which stimulate lymph and blood circulation, as well as improve the ventilation function of the lungs. These procedures are carried out in a hospital setting, taking into account contraindications (tuberculosis, hemoptysis, hypertension, etc.). In the presence of viscous sputum, inhalation of proteolytic enzymes (lidase, hyaluronidase, ribonuclease, fibrinolysin, etc.) can also be recommended. The presence of mild signs of bronchial obstruction (complaints of paroxysmal cough or difficulty breathing, decreased expiratory power according to pneumotachometry or one-second forced expiratory volume) is an indication for inhalation of aminophylline, as well as adrenergic stimulants (ephedrine) or vagoblockers (atropine, platyphylline), taking into account the possible side effects of the latter in the form of increased blood pressure and tachycardia. It is recommended that patients in this group carry out courses of treatment and preventive measures twice a year in a sanatorium or in a hospital.
In rapidly progressing forms of silicosis, the use of glucocorticoid hormones is justified, since they have anti-inflammatory, antiproliferative, and, according to some data, an inhibitory effect on the development of silicosis. Hormonal therapy for silicosis is carried out in courses of 1-2 months, mainly with prednisolone or urbazone in doses of 20-25 mg per day, followed by a gradual decrease. When prescribing glucocorticoids, prophylactic protection with anti-tuberculosis drugs (tubazid, PAS) is mandatory. Courses can be repeated 1-2 times a year. Instead of hormonal drugs or in addition to them, delagil, plaquinil and other quinoline drugs can be used. In terms of further research, it is promising to try to use antifibrotic drugs that have found use in pulmonological practice for the treatment of progressive forms of silicosis. These include D-penicillamine and major immunosuppressants (imuran, cyclophosphamide, etc.). It is possible that in the future drugs that have an immunostimulating effect will find their place in the treatment of silicosis.
Treatment of patients with pneumoconiosis with stage II-III pulmonary insufficiency must be carried out annually in a hospital setting, as well as in sanatoriums and sanatoriums with a specialized pulmonary profile. Pulmonary insufficiency in pneumoconiosis is restrictive in nature, which is primarily due to a decrease in tidal volumes and impaired gas exchange due to anatomical damage to the alveolar system and vessels of the pulmonary circulation. A certain role is also played by the violation of the drainage function of the bronchi, caused by their deformation and obstruction by bronchial secretions. In patients, blood oxygen saturation decreases at normal carbon dioxide tension. At the same time, the pressure in the pulmonary circulation increases and a chronic pulmonary heart is formed. Based on ideas about the pathogenesis of respiratory and cardiovascular failure: with pneumoconiosis, therapeutic measures should be aimed primarily at improving blood oxygenation, drainage function of the bronchi and reducing pressure in the pulmonary circulation. In the absence of contraindications, the above treatment complex can be used. It should be taken into account that the use of the inhalation method of drug administration is very limited in the presence of severe pulmonary insufficiency due to low tidal volumes. Oxygen therapy in the form of oxygen inhalation or, better yet, hyperbaric oxygen therapy is mandatory. Various prescriptions of bronchodilators and drugs that reduce pressure in the pulmonary circulation (aminophylline, papaverine, reserpine, etc.) are recommended. When prescribing reserpine to patients with bronchospastic syndrome, one should take into account the possible side effect in the form of increased bronchospasm. The most effective are intravenous infusions of aminophylline, which has a bronchodilator effect, reduces pressure in the pulmonary artery, and also has weak cardiotonic and diuretic properties. In the presence of chronic pulmonary heart disease in the stage of decompensation, treatment in a hospital is indicated. In addition to drugs aimed at improving the respiratory function of the lungs and reducing pressure in the pulmonary circulation, it is necessary to prescribe cardiac glycosides (korglykon, strophanthin) in combination with panangin, potassium orotate and other potassium-containing drugs that prevent intoxication with glycosides and disorders of potassium metabolism. The antialdosterone drug veroshpiron has a mild diuretic effect, removing mainly sodium. In cases of severe decompensation with peripheral edema, stronger diuretics (furosemide, diacarb, ethacrynic acid, hypothiazide, etc.) are used in short courses. Before prescribing these diuretics, it is necessary to carry out therapy with cardiac glycosides for 3-4 days, since abundant fluid secretion from the body increases the load on the heart muscle.
The normalization of metabolic processes in the myocardium is facilitated by the administration of anabolic hormones (methandrostenolone, phenobolin, retabolil), as well as B vitamins. In case of persistent edema syndrome, corticosteroid hormones are sometimes effective. In cases where it is necessary to prescribe several medications, including bronchodilators, vasodilators and cardiotonic agents, it is advisable to administer them by drip using saline solution. In this case, it is recommended to administer small doses of heparin (5000-10,000 units), which has a general resorptive effect and improves coronary blood flow. The anticoagulant properties of the drug in these dosages are insignificant. After the symptoms of decompensation are relieved, the patient can be transferred to taking lantoside, digoxin or isolanide in combination with drugs that reduce pressure in the pulmonary circulation.
Treatment of other complications of silicosis is carried out according to the usual methods and regimens for the treatment of chronic nonspecific lung diseases, taking into account the activity of bronchopulmonary infection and the severity of bronchospasm.
Conclusion
Pneumoconiosis combines a number of diseases caused by the ingestion of large amounts of dust particles into the lungs over a long period of time. These diseases belong to the group of occupational processes. They are found in some workers who inhale various types of dust for 5-15 years or more. Small dust particles entering the respiratory tract cause a reaction in the interstitial connective tissue, resulting in the development and progression of pulmonary fibrosis.
Pneumoconiosis is not particularly treatable; if the lungs are damaged, they do not recover. Therefore, the main way to fight is to prevent the disease, that is, prevention.
The basis for the prevention of pyeumoconiosis is primarily technical and sanitary measures to combat dust, described in detail in the specialized literature. They must be combined with medical measures, the first place among which is occupied by preliminary (upon entry to work) and periodic medical examinations with the mandatory use of x-ray examination.
Literature
Occupational diseases caused by exposure to industrial dust (pneumoconiosis). URL: http://www.medkurs.ru/sickness_catalog/breath_in/ (access date: 12/9/2013).
Pneumoconiosis [electronic library]. URL: http://www.eurolab.ua/diseases/1491/(access date: 12/9/2013).
Pneumoconiosis [Handbook]. URL: http://zabolevaniya.ru/zab.php?id=14045&act=fulldate of access: 12/9/2013).
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