Dust occupational diseases. Silicosis. Etiology, pathogenesis, clinical picture, principles of prevention.
Exposure to dust can cause both specific, so and nonspecific diseases.
The most common specific diseases are dust fibrosis (pneumoconiosis) - occupational diseases in which the respiratory surface is limited and a person’s respiratory function is impaired. The occurrence of diseases in this group is due to fibrogenic The effect of whining is that dust, entering the lungs, accumulates in the alveoli, interstitial substance, causing the proliferation of connective tissue and the development of pulmonary fibrosis. At the same time, in some places of the lung sclerosis and induration are observed, while in others emphysema develops compensatory.
In addition to the fibrogenic effect, dust can cause allergic reactions and also have a directly toxic effect (in case of inhalation of dust that is toxic in its chemical composition).
From nonspecific diseases They highlight eye lesions - conjunctivitis, inflammation of the cornea, warts, lung cancer and other diseases.
Pneumoconiosis is an occupational lung disease caused by prolonged inhalation of dust and characterized by the development of diffuse interstitial fibrosis. May occur among workers in mining, coal, asbestos, engineering and some other industries. The development of pneumoconiosis depends on the physicochemical characteristics of inhaled dust. The clinical picture of pneumoconiosis has a number of similar features: a slow, chronic course with a tendency to progress, often leading to disability; persistent sclerotic changes in the lungs
The following main types of pneumoconiosis are distinguished:
· silicosis and silicatoses,
metalloconiosis,
carboconiosis,
· pneumoconiosis from mixed dust (anthracosplicosis, siderosilicosis, etc.
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),
· pneumoconiosis from organic dust.
Silicosis, the most common and severe type of pneumoconiosis, develops as a result of prolonged inhalation of dust containing free silicon dioxide. Most often it occurs among miners of various mines (drillers, miners, fixers, etc.
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), foundry workers (sandblasters, chippers, core workers, etc.
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), workers in the production of refractory materials and ceramic products. It is a chronic disease, the severity and rate of development of which vary and are directly dependent on both the aggressiveness of the inhaled dust (dust concentration, the amount of free silicon dioxide in it, dispersion, etc.), and on the duration of exposure to the dust factor and individual characteristics of the body. The gradual atrophy of the ciliated epithelium of the respiratory tract sharply reduces the natural release of dust from the respiratory system and contributes to its retention in the alveoli. In the interstitial tissue of the lungs, primary reactive sclerosis develops with a steadily progressive course. The initial clinical symptoms are scant: shortness of breath on exertion, chest pain of an undetermined nature, a rare dry cough. Direct examination often reveals no pathology. Moreover, even in the initial stages, it is possible to identify early symptoms of emphysema, which develops mainly in the inferolateral parts of the chest, a boxy tint of percussion sound, a decrease in the mobility of the pulmonary edges and excursions of the chest, and weakening of breathing. The addition of changes in the bronchi is manifested by hard breathing, sometimes dry wheezing. In severe forms of the disease, shortness of breath bothers you even at rest, chest pain intensifies, a feeling of pressure in the chest appears, the cough becomes more constant and is accompanied by sputum production, and the severity of percussion and auscultation changes increases.
Silicates are caused by inhalation of dust from silicate minerals containing silicon dioxide associated with other elements (magnesium, calcium, iron, aluminum, etc.
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). This group of pneumoconiosis includes asbestosis, talcosis, cementosis, pneumoconiosis from mica dust, etc.
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Silicates are widely distributed in nature and are used in many industries. Silicosis can develop during work related to the extraction and production of silicates, as well as their processing and use. In silicatosis, a predominantly interstitial form of fibrosis is observed.
Metalloconiosis is caused by inhalation of dust of certain metals: berylliosis - beryllium dust, siderosis - iron dust, aluminosis - aluminum dust, baritosis - barium dust, etc. The most benign course is characterized by metalloconiosis, which is characterized by the accumulation of radiopaque dust (iron) in the lungs Eza, tin, barium) with a moderate fibrous reaction. These pneumoconioses do not progress if exposure to dust from these metals is excluded; Regression of the process is also possible due to the self-cleaning of the lungs from radiopaque dust. Aluminosis is characterized by the presence of diffuse, predominantly interstitial fibrosis. In some metalloconiosis, the toxic and allergic effect of dust with a secondary fibrous reaction (beryllium, cobalt, etc.) predominates.
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) sometimes with a severe progressive course.
Carboconiosis is caused by exposure to carbon-containing dust (coal, graphite, soot) and is characterized by the development of moderately expressed fine-focal and interstitial fibrosis of the lungs. Anthracosis is a carboconiosis caused by inhalation of coal dust. It develops gradually in workers with extensive work experience (15-20 years) exposed to coal dust, miners working in coal mining, workers in processing factories and some other industries. The course is more favorable than with silicosis; the fibrotic process in the lungs occurs as diffuse sclerosis. Inhalation of mixed coal and rock dust containing silica causes anthracosilicosis, a more severe form of pneumoconiosis characterized by the progressive development of fibrosis.
Pneumoconiosis from organic dust can be classified as pneumoconiosis conditionally, since they are not always accompanied by a diffuse process resulting in pneumofibrosis. Bronchitis with an allergic component develops more often, which is typical, for example, of byssinosis, which occurs from inhaling dust from plant fibers (cotton)
Prevention measures:
As with any occupational disease, the following groups of measures are distinguished in the dust pathology prevention system:
1. Technological activities: development of new production process technologies to reduce dust formation, production automation, etc.
2. Sanitary measures: sealing equipment, organizing effective ventilation (local exhaust ventilation), completely covering the place of dust formation with the help of covers, etc.
3. Organizational measures: compliance with a rational work and rest regime.
4. Use of personal protective equipment: dust respirators, gas masks, safety glasses, workwear.
5. Legislative measures - establishment of maximum permissible concentrations (MAC) for various types of pollen in industrial premises. So, for example, for dust containing more than 70% of free silicon oxide, the MPC is 1 mg/m3, from 10% to 70% - 2 mg/m3, less than 10% - 4 mg/m3, and for other types of dust - 6-10 mg/m.
6. Medical measures:
Preliminary and periodic medical examinations once every 3 months - 1 year.
Preventing people with tuberculosis, diseases of the upper respiratory tract, bronchi, lung diseases, pleura, organic diseases of the cardiovascular system and some others from working in conditions of high levels of quartz dust.
Dust occupational diseases. Silicosis. Etiology, pathogenesis, clinical picture, principles of prevention. - concept and types. Classification and features of the category "Dust occupational diseases. Silicosis. Etiology, pathogenesis, clinical picture, principles of prevention." 2017, 2018.
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 occupational lung diseases are one of the most severe and widespread types of occupational diseases throughout the world, the fight against which is of great social importance.
The main dust occupational diseases are pneumoconiosis, chronic bronchitis and upper respiratory tract diseases.
Extremely rare dust diseases include neoplasms of the respiratory system.
Pneumoconiosis- chronic occupational dust lung disease, characterized by the development of fibrotic changes as a result of prolonged inhalation action of fibrogenic industrial aerosols.
In accordance with the classification adopted in the USSR in 1976, the following types of pneumoconiosis are distinguished according to the etiological principle.
1. Silicosis is pneumoconiosis caused by inhalation of quartz dust containing free silicon dioxide, i.e. silica and its modifications in crystalline form: quartz, cristobalite, tridymite. The most common crystalline variety of silica is quartz, containing 97 - 99% free SiO 2. The effect of quartz-containing dust on the body is associated with mining, since about 60% of all rocks consist of silica.
2. Silicates - pneumoconiosis that occurs from inhalation of mineral dust containing silicon dioxide in a bound state with various elements: aluminum, magnesium, iron, calcium, etc. (kaolinosis, asbestosis, talcosis; cement, mica, nopheline pneumoconiosis, etc.).
3. Metalloconiosis - pneumoconiosis from exposure to metal dust: iron, aluminum, barium, tin, manganese, etc. (siderosis, aluminosis, baritosis, staniosis, manganoconiosis, etc.).
4. Pneumoconiosis from mixed dust: a) with a significant content of free silicon dioxide - more than 10%; b) does not contain free silicon dioxide or contains up to 10%.
5. Pneumoconiosis from organic dust: plant - byssinosis (from cotton and flax dust), bagassosis (from sugar cane dust), farmer's lung (from agricultural dust containing fungi), synthetic (plastic dust), as well as from exposure to soot - industrial carbon.
Silicosis- the most severe form of pneumoconiosis. This form of pneumoconiosis is most common among coal miners; it is also found in mining workers, especially drillers and riggers. Known diseases of silicosis in ceramic, pottery, mica production, during grinding on sandstone stones and other work associated with the formation of dust containing crystalline silicon dioxide.
Silicosis develops at different times when working under dust exposure conditions. The prevalence, speed of development of the disease and the degree of its severity depend on working conditions, dispersion, and concentration of quartz dust.
The severity of silicosis increases with increasing content of free SiO 2 in dust. In old enterprises with high dust levels, silicosis developed in miners after 3–10 years of experience, in casting cutters – 1–4 years, in porcelain workers – 10–30 years. Currently, such conditions practically do not occur and cases of silicosis are found mainly only in people with a long history of exposure to high concentrations of dust.
The pneumoconiotic process in silicosis is characterized by the development of nodular fibrosis, as well as the proliferation of fibrous tissue along the bronchi, vessels, near the alveoli and lobules. Pathological phenomena usually grow slowly, clinical symptoms do not always correspond to the severity of the pneumofibrotic process, therefore, radiological data are of primary importance for diagnosing and determining the stage of the disease. There are interstitial, diffuse sclerotic, nodular or mixed forms of fibrosis. Depending on the clinical course, nature and severity of changes in the lung tissue, 3 degrees of the disease are distinguished.
Silicosis is a general disease of the body, in which, along with respiratory dysfunction (subjectively - shortness of breath, cough, chest pain), the development of emphysema, chronic bronchitis, and cor pulmonale is observed. Changes in immunological reactivity, metabolic processes, and disturbances in the activity of the central and autonomic nervous systems are recorded.
With the development of the silicotic process, asthmatic bronchitis, bronchiectasis occur, and the most common complication is tuberculosis. A characteristic feature of silicosis is its progression even after stopping work in a dusty profession.
Silicates. Specific fibrous-sclerotic lung diseases develop from inhalation of dust containing silicon dioxide in a state associated with other elements (Mg, Ca, A1, Fe, etc.). Silicates include many minerals: asbestos, talc, kaolin, nepheline, opeine, etc.; artificial compounds: mica, cement, fiberglass, etc. Dust that causes silicates is found in many industries: fireclay-silica, rubber, cement, etc.
Mining, processing, loosening, mixing, and transportation of minerals poses a health hazard. Silicosis develops later than silicosis, and is often combined with silicosis (silicosilicosis). The effect of silicate dust is weaker than that of quartz. The most aggressive dust is magnesium silicate 3MgO 2SiO 2 2H 2 O - chrysotile asbestos - a fibrous mineral.
When inhaling asbestos dust, generalized fibrosis is observed in the lungs, classified into a special form called asbestosis. The clinical and morphological features of this disease are determined by the fibrous structure of asbestos. Asbestos fibers in the vast majority of cases are not phagocytosed; their removal by lymph is difficult due to the needle-like nature of the dust particles. They penetrate the bronchi, injure the mucous membranes, and cause an inflammatory reaction. There is also a mechanical effect of asbestos dust. The development of asbestosis occurs depending on the concentration of dust in different periods - from 3 to 11 years. Characteristic is the presence in sputum of asbestos bodies 30 - 70 microns long, pale yellow in color, shaped like fibers with club-shaped extensions at the ends.
Clinically, asbestosis is accompanied by shortness of breath, cough, initially dry and then with sputum. Emphysema, chronic bronchitis, decreased vital capacity of the lungs, and changes in the cardiovascular system are noted. There are 3 stages of asbestosis. Asbestosis is often complicated by chronic pneumonia, tuberculosis, and lung cancer.
Silicates also include talcosis, which develops in workers in textile, rubber, paper, perfume, ceramics and other industries who have been in contact with talc for 15 - 20 years. The course of talcosis is benign. Pneumosclerosis is interstitial, in a pronounced stage - diffuse interstitial fibrosis with small nodular shadows. Talcosis is often complicated by emphysema and chronic bronchitis.
Pneumoconiosis can also be caused by other types of dusts that do not contain silica. These are, for example, siderosis, aluminosis, apatitosis, baritosis, manganoconiosis, antradosis, graphitosis, pneumoconiosis from grinding dust, etc. Metalloconiosis and carboconiosis are more benign, developing 15 - 20 years after the start of work in the profession. Often there is a combination of a mildly expressed fibrotic process with chronic bronchitis, which, as a rule, is decisive in the clinical picture of the disease.
Among metalloconiosis, beryllium (pneumoconiosis from inhalation of beryllium dust and its compounds), which is particularly aggressive, and manganoconiosis (manganese pneumoconiosis) should be noted. Manganoconiosis develops when inhaling aerosols of disintegration and condensation of manganese and its compounds. Manganese oxides and salts are found during the extraction of manganese ores, smelting of high-quality steels and alloys, during arc welding, submerged arc welding, etc.
The first signs of manganoconiosis appear after 4 - 5 years of work. Mangaioconiosis, unlike berylliosis, is accompanied by a benign course, but is combined with chronic manganese poisoning, manifested in predominantly damage to the nervous system.
Byssinosis(“byssos” - textile fiber) is an occupational disease that develops as a result of prolonged exposure to dust from cotton, flax, hemp, jute, kenaf among workers of cotton gin and cotton spinning factories, flax mills, etc. Dust generated during production operations with coarse, low-grade raw materials, may be contaminated with bacteria and fungi.
The main symptom in the clinical picture of byssinosis is bronchial obstruction, which develops under the influence of bronchial constrictors contained in cotton, flax and other types of plant dust. In addition, fungal and bacterial contamination of organic plant dust is a source of protein substances that have a sensitizing effect. The main complaints are tightness in the chest, difficulty breathing, shortness of breath during physical exertion, cough, weakness. Initially, these symptoms are observed only when performing work after a break - the “Monday symptom”, and later they become permanent, complicated by persistent disorders of the bronchopulmonary apparatus and pulmonary-heart failure.
Pneumoconiosis caused by the action of organic dusts (byssinosis, etc.) is rare.
Pneumoconiosis from mixed dusts. Pneumoconiosis of this type includes electric welding pneumoconiosis, pneumoconiosis of gas cutters, refractory workers, steelworkers, grinders, emery workers, etc.
Electric welding pneumoconiosis develops in electric welders during prolonged work in poorly ventilated areas, when a high concentration of welding aerosol containing iron oxide, manganese or fluorine compounds is created. Pneumoconiosis progresses favorably. Complaints of shortness of breath with significant physical exertion, dry cough. Diffuse enhancement and deformation of the pulmonary pattern with numerous small focal compactions are revealed. In the 2nd stage of the disease, chronic bronchitis and emphysema are added.
In all cases of the development of pneumoconiosis, the severity of the pneumofibrotic process depends on the structure and composition of the exposed dust. For example, anthracite dust is more coniogenic than soft brown coals and shale. The admixture of silica increases the danger of coniosis.
Pneumoconiosis in severe stages is often complicated by pulmonary tuberculosis. This combination is usually called coniotuberculosis. The following types of coniotuberculosis are distinguished: silicotuberculosis, anthracotuberculosis, siderotuberculosis, etc. Taking into account the clinical features, they are considered as independent nosological forms of the disease.
The state system of measures to combat silicosis has led to a significant improvement in working conditions and a decrease in the level of dust in the air at mining, metallurgical, engineering and other industries. As a result, the incidence of pneumoconiosis, including its most severe type, silicosis, has decreased.
Industrial dust can lead to the development of occupational bronchitis, pneumonia, asthmatic rhinitis and bronchial asthma. Some of the dust settles on the mucous membrane of the nose and bronchi. Depending on the nature and concentration in the air, it causes different reactions in the nasal mucosa. Hypertrophic and atrophic rhinitis develops. Chromium compounds and nickel sulfate cause ulcerative-necrotic lesions of the mucous membrane and even perforation of the nasal septum. Dust lingers in the respiratory tract, causing local processes: bronchitis, bronchiolitis.
Dust bronchitis becoming the most common types of pathology. As dust levels decrease, the incidence of pneumoconiosis and bronchial asthma decreases, and small concentrations of dust cause dust bronchitis. Dust bronchitis occurs when inhaling moderately aggressive mixed dusts of coarse dispersion (metal, plant, cement, etc.). The prevalence and timing of the development of the disease depend on the concentration and chemical composition of the dust; most often, bronchitis develops after 8 - 10 years of work at the relevant enterprise.
Bronchitis from allergenic dusts is accompanied by bronchospasms and complicated by asthma. Plant dust - cotton, flax, jute - causes bronchitis of an asthmatic nature with exacerbations after a day off. In the future, they are complicated by emphysema and pneumosclerosis. Bronchial asthma is caused by ursol and some other types of dust that have an allergenic effect.
Dust and pneumonia. Slag pneumonia occurs in the production of fertilizers among workers engaged in grinding waste containing phosphorus salts. There are indications of the severity of such pneumonia with a high percentage of the development of emphysema, sometimes with death.
Lipoid pneumonia develops in workers exposed to significant concentrations of highly dispersed oil aerosols (oil mists).
Pathogenesis of dust lung diseases. There are several theories of the mechanism of action of dust and the main ones are: mechanical, toxic-chemical and biological. Proponents of the mechanical theory tried to explain the development of fibrosis by the physical properties of dust, believing that the harder the dust particles and the sharper their edges, the more aggressive they are. However, carboreside dust, being more hard than quartz, does not cause pneumoconiosis. The toxic-chemical theory explained the fibrogenic properties of silicon dioxide dust by its solubility in the body's media and its toxic effect. But there is no direct relationship between the degree of quartz solubility and the degree of fibrogenicity. The solubility of amorphous silicon is approximately 2 times greater than the solubility of crystalline quartz and tridymite, but tridymite has the greatest fibrogenicity, followed by crystalline quartz and the least - amorphous silicon.
B.T. Velichkovsky put forward a hypothesis about the connection between the fibrogenic properties of silicon dioxide and the microstructure of the surface of quartz particles and the formation of silanol groups on it. When the quartz crystal lattice is mechanically damaged on the silica fracture surface in the presence of water vapor contained in the air, chemical active radicals SiOH and silanol groups are formed. The latter, reacting with tissue proteins, cause their destruction and the development of fibrotic changes.
It is now generally accepted that the leading role in the development of silicosis is played by macrophages that phagocytose silica dust particles. The death of macrophages is considered the first stage in the development of other pneumoconiosis, as well as chronic dust bronchitis.
It has been established that without a sequential change in the processes of phagocytosis, death, and disintegration of coniophages, dust, even quartz, does not have a direct fibrogenic effect. For the fibrogenic properties of dust to manifest, direct contact of dust particles with the membrane of the phagocytic cell is necessary. The contents of dead macrophages activate fibroblasts, inducing the development of fibrosis in the lungs. The effect of fibrogenic dusts on the macrophage is due to the cytotoxic effect, which consists in the rapid destruction of phagolysosomes containing particles absorbed by the cell. The further development of dust pathology is associated with the destruction products of coniophages, which affect the body in three directions: they mobilize an additional number of cells necessary for the processes of self-cleaning of dust from the lungs, cause immunological changes, stimulate fibroblasts and collagen formation.
From the standpoint of this theory, it is possible to most convincingly connect the clinical manifestations of dust lung diseases with quantitative indicators of dust content, their chemical structure and the physicochemical properties of dust.
Modern dust pathology of the respiratory system is defined as a combination of numerous body reactions to dust, such as interstitial fibrosis, emphysema, reflex bronchospasm, chronic asthmatic bronchitis, etc.
Due to their size, large dust particles measuring 5 - 7 microns or more penetrate into the bronchial tree, causing a mechanical traumatic effect on the alveolar wall and causing the development of dust bronchitis. Dust particles 0.5 - 2 microns in size penetrate the alveoli and exhibit a cytotoxic effect, and also contribute to the development of nodular forms of pneumoconiosis. Finely dispersed dusts, with a grain size of 0.3 - 0.02 microns, entering the lungs for a long time, accumulate 7 - 10 in macrophages and only then exhibit a cytotoxic effect as an effect of decompensation of hypertrophied coniophages. Such dust contributes to the formation of diffuse sclerotic changes in the lung tissue. This may explain the mechanism of action of dusts that have low cytotoxicity, such as anthracosis.
The location of formation of dust nodules depends on the fibrogenicity of the dust and the level of dust content. Thus, with a high concentration of quartz dust, increased decay of microphages with dust is observed in the cavity of the alveoli, around which silicotic nodules are formed, with a decrease in dust content - in the pulmonary parenchyma in the area of peribronchial and perivascular lymphatic follicles. With a low dust content in the air, nodules form in the regional lymph nodes, and diffuse sclerotic changes predominate in the lungs.
Viral infection and other causes that reduce the immunobiological reactivity of the body inhibit the activity of macrophages, inhibit the self-cleaning of dust from the lungs and thereby contribute to the earlier development of dust diseases.
Wikipedia interprets the concept of “dust” as the smallest dry particles of something floating in the air. She is so familiar and yet still mysterious. We don't see it, but it is a constant source of trouble for housewives and a headache for allergy sufferers.
Manifestations of allergies to dust, according to statistics, are observed today in 40% of the world's population. Moreover, today it is considered the most common allergen.
The symptoms of a dust allergy are well known: sneezing, watery eyes, and runny nose.
Chemical analysis of house dust shows that it is habitable. Scientists find in the dust the smallest grains of desert sand and microparticles of meteorites, not to mention various household, ash, wool components and dead scales of our skin.
In addition to all this, it represents a kind of biocenosis in which there are millions of bacteria, fungi, microalgae and dust mites. Particularly many dust mites are found in beds, upholstered furniture, and carpets.
Human housing is the best habitat for these invisible monsters. The most favorable climate for them is: temperature – 25۫°С, humidity – 75%. Dust mite waste often serves as an allergen.
If, when you wake up in your bed in the morning, you feel a constant stuffiness in your nose and your eyes are watery, most likely you have an allergy to house dust.
Considering that a person’s skin renews itself every 28 days, about 700 g of dead scales accumulate per year, which serve as a food source for ticks.
What diseases can dust cause?
An allergy to house dust not only causes a runny nose and sneezing in children, but also serves as a provoking factor in the development of diseases such as skin rashes, bronchitis, and pneumonia.
In adults and children, contact with house dust can cause concomitant diseases.
- Chronic rhinitis. Rhinitis caused by dust always begins acutely, accompanied by endless sneezing, tearfulness and wet discharge from the nose. The child usually also complains of an itchy nose and a burning sensation in the throat.
- Conjunctivitis. It is also accompanied by lacrimation, the eyes turn red, they stop seeing well, and swelling occurs. In a child, conjunctivitis may occur with mucus-like discharge from the eyes.
- Bronchial asthma. The most serious consequence of the penetration of allergens into the human body is bronchial asthma. In young children, this disease can be fatal, so treatment should be started immediately. It also causes a lot of trouble for adults: from shortness of breath to breathing spasms.
An allergy to paper dust gives exactly the same symptoms. Pollen from domestic plants can also be an allergen.
For the treatment and prevention of skin diseases and the appearance of acne and warts, our readers successfully use the Monastic Collection of Father George. It contains 16 useful medicinal plants, which are extremely effective in treating skin diseases and cleansing the body as a whole.
But cement and asbestos dust are especially dangerous, as they lead to a gradual accumulation of particles of the substance in the lungs, which are then impossible to remove. Such an allergy may not manifest itself for years, but eventually the disease asbestosis may develop, which is incurable.
How to deal with allergies
There are two main ways to combat allergies caused by house dust.
1. Avoid contact with the source of allergens. To do this:
- Ventilate the apartment as often as possible. On the street, oddly enough, the air is almost 10 times cleaner than at home.
- Do wet cleaning of your home more often than vacuuming. When you vacuum your apartment, some microorganisms are released back into the air.
- do a general cleaning of the house, removing excess garbage and old things that litter the rooms.
- change bedding: mattresses, pillows, blankets at least once every few years and replace down elements with modern hypoallergenic materials.
- change bedding more often, use air purifiers.
- Do not keep many books open. The concentration of living elements in the dust of old libraries is simply off the charts. Try to limit paper and book dust to closet space.
2. Take antihistamines. The most popular and publicly available: “Suprastin”, “Tavegil”, “Eris”. For children, it is better to use drops such as “Aquaramis”, “Aqualor”, “Salin”. For adults, Tafen and Nasal are recommended for topical use.
Treatment for dust allergies is not quick, so be prepared for the fact that you will need a lot of strength and patience to get rid of unpleasant symptoms.
Let's sum it up
To prevent the problem of allergies to house dust from affecting you and your child, try to always keep your home clean and ensure constant access of air to the apartment. Furnish your home using modern hypoallergenic materials. Young children are especially susceptible to house dust, so the children's room should be free, easy to clean, and free of bulky furniture and old carpets. It is better to buy modern bright microfiber rugs for children that are easy to wash and knock out. It is impossible to get rid of dust in the house, but any housewife can control its level.
If the allergy problem has already affected you and your child, then the best solution would be to visit a doctor. This disease requires long-term monitoring and serious diagnostics to determine the allergen, so only a doctor can prescribe effective treatment.
Lecture 13. Industrial dust and industrial poisons as a hazard factor. Main productions. Specific and nonspecific occupational dust diseases and poisonings, measures for their prevention.
Industrial (industrial) dust– dust generated at workplaces of manufacturing enterprises as a result of the technological process, which can enter the air of the working area and have a negative effect on the worker’s body.
There are several classifications of industrial dust:
1) by origin
Organic;
Inorganic;
Mixed.
Organic dust is divided into natural And artificial. TO natural Organic dust includes dust of plant and animal origin, wood, cotton, linen, wool, etc. Artificial organic dust is dust from plastics, rubber, resins, dyes, etc.
Among inorganic dust is distinguished mineral And metal. TO mineral dust includes quartz, silicate, asbestos, cement and other types of dust. Metal dust is zinc, iron, copper, lead and other types of dust.
Mixed dust is a multiphase, heterogeneous dispersed system containing various components.
2) by method of education:
Aerosols of disintegration;
Aerosols of condensation;
Mixed aerosols.
Aerosols disintegration are formed during mechanical grinding, crushing and destruction of solid particles.
Aerosols condensation are formed during thermal processes of sublimation of solids, cooling and condensation of metal and non-metal vapors.
Mixed aerosols are formed during grinding, polishing, and sharpening work.
3) by particle size:
Visible dust (>15µm);
Microscopic (0.25 – 10 µm);
Ultramicroscopic (<0,25мкм).
Industrial dust can have the following effects on workers:
Fibrogenic;
Annoying;
Allergenic;
Toxic.
The main role is played by the concentration of dust in the inhaled air, dispersion, electrical charge, and the shape of dust particles. Disintegration aerosols with dust grain sizes of 1–2 microns and condensation aerosols with particles less than 0.3–0.4 microns, which penetrate most deeply and linger in the lungs, have the greatest fibrogenic activity. In the etiology of dust bronchitis, particles over 5 microns are the least active.
When assessing the effect of dust on the body, the shape of the particles, their hardness, sharpness of edges, fibrousness, and solubility are of certain importance.
The shape of dust particles affects their behavior in the air, accelerating (rounded) or slowing down (fibrous, plate-like shape) their settling. Elongated and spindle-shaped particles (asbestos) penetrate into the deep parts of the respiratory tract and cause injury.
The specific surface area (cm 2 /g) of dust is also important. Burnt products (perlite, expanded clay, vermiculite), having a surface area 3 times larger than the raw materials used for their production, have a more pronounced fibrogenic effect on lung tissue. The greatest fibrogenic activity is exhibited by quartz-containing dusts, disintegration aerosols with dust particle sizes up to 5 microns (fractions of 1–2 microns are especially dangerous) and condensation aerosols with particles less than 0.3–0.4 microns.
The toxic effect of dust depends largely on the chemical structure of the dust, rather than on the size and shape of the dust particles.
The electrical properties of dust particles have a great influence on the time they remain in the air and the deposition process. With opposite charges, particles are attracted to each other and quickly settle out of the air. With the same charge, dust particles, repelling one another, can remain in the air for a long time.
Quickly dissolving dusts are easily removed and have a weak pathological effect. Poorly soluble dusts linger in the respiratory tract for a long time and have a more pronounced effect. In particular, quarium-containing dust lingers in the respiratory tract for a long time and slowly dissolves in the biosphere, forming silicic acid, which is one of the leading factors in the development of silicosis.
A number of dusts have adsorption properties; dust particles are capable of carrying gas molecules (carbon monoxide, carbon dioxide, methane), which can be a source of intoxication.
In addition, dust can be a carrier of microorganisms, helminth eggs, fungi, mites, and mold. Cases of pulmonary anthrax have been described in workers at meat processing plants who inhale wool dust, as well as in workers at knitting factories who inhale dust from processed raw materials.
Cotton dust, grains, and flour contain a significant amount of bacteria and fungi. In the production of citric acid, the dust may consist entirely of fungi, and cases of allergenic reactions are often detected among workers.
The number of production processes in which intense dust emissions can occur is extremely large. The most dust-hazardous are many operations in the mining and coal industries, in mechanical engineering (electric welding, iron, copper and steel foundries, especially chipping and grinding), in the porcelain and earthenware, textile, flour-grinding industries, etc.
In production conditions, dust can lead to the development of occupational diseases - specific And nonspecific. Systematic work in dusty conditions leads to an increased incidence of workers with temporary disabilities (colds, bronchitis, pneumonia, etc.), which is associated with a decrease in the overall reactivity of the body.
TO specific Occupational diseases associated with dust inhalation include 2 groups of diseases. These are pneumoconiosis and allergic diseases (in the event that the allergen is precisely identified, and the worker came into contact with this substance at work; in addition, the content of this allergen in the air of the working area is established to exceed the maximum permissible concentrations).
TO nonspecific Dust injuries include chronic respiratory diseases, eye diseases and skin diseases.
Pneumoconiosis.(from Greek pneumon - lung, conia - dust). This name unites all the numerous types of dust-induced pulmonary fibrosis. According to the etiological principle, 5 groups of pneumoconiosis are distinguished:
1) caused by mineral dust – silicosis, silicatosis (asbestosis, talcosis, kaolinosis, cementosis, etc.);
2) caused by metal dust – siderosis, aluminosis, berylliosis, baritosis, etc.;
3) caused by carbon-containing dust - anthracosis, graphitosis, etc.;
4) caused by organic dust - byssinosis (from cotton and flax dust), bagasosis (from sugar cane dust), farmer's lung (from agricultural dust containing mushrooms), etc.;
5) caused by dust of mixed composition - silico-asbestosis, silico-anthracosis, etc.
Allergic professional diseases (allergosis) occur upon contact with aromatic amines, nitro- and nitroso compounds, organic oxides and peroxides, formaldehyde, antibiotics, compounds of mercury, arsenic, chromium, beryllium, etc. etc. In industrial conditions, the clinical manifestations of allergosis to a certain extent depend on the route of entry of the allergen. Thus, workers at pharmaceutical plants exposed to antibiotic dust often develop bronchial asthma and urticaria; when working with penicillin solutions - eczema, dermatitis.
In the occurrence of allergies, in addition to the etiological factor, the state of reactivity of the body is of great importance; Occupational allergies occur more often in persons with a burdened allergic history, as well as against the background of neuroendocrine diseases.
TO nonspecific chronic respiratory diseases include bronchitis, pneumonia, asthmatic rhinitis, bronchial asthma (if the allergen is not clearly established).
Dust chronic nonspecific eye diseases- This
Conjunctivitis (from exposure to arsenic-containing dust, acryquin dust);
Occupational cataract (trinitrotoluene dust);
Occupational argyrosis of the conjunctiva and cornea (dust of sulfur and silver bromide salts);
Keratoconjunctivitis “pitch ophthalmia” (coal pitch dust).
Dust chronic nonspecific skin diseases. These include:
Dermatitis (arsenic, lime, superphosphate dust);
Oil folliculitis (coolant aerosols);
Allergic occupational dermatoses – eczema (cement dust);
Photodermatitis (resin, tar, asphalt, pitch).
Main directions of prevention occupational diseases in dust production are as follows:
1) hygienic standardization:
– establishment of maximum permissible concentrations of fibrogenic and other dusts in the air of the working area,
– systematic monitoring by departmental laboratories and laboratories of the Center for State Sanitary and Epidemiological Supervision of the dust content of production premises;
2) technological measures are aimed at eliminating the formation of dust in workplaces:
– continuous technologies,
Automation and mechanization of production processes,
Remote control (robots - manipulators for loading, pouring, packaging of bulk materials),
Use of granules, pastes, solutions instead of powders,
Replacing dry processes with wet ones (wet grinding),
Nozzle irrigation with pressurized water supply (mining machines, drilling rigs),
Introductory curtains (before blasting);
3) sanitary and technical measures:
– local shelter of dust-producing equipment with air suction from under the shelter,
– sealing and covering of equipment with dust-proof casings,
– local exhaust ventilation (used when it is impossible to humidify processed materials),
– moistening of processed materials, etc.;
4) the use of personal protective equipment is used in cases where measures to reduce air dust do not lead to a reduction in dust concentration in the air of the working area to the maximum permissible concentration:
Anti-dust respirators (“petal”),
Filtering and insulating gas masks,
Safety glasses (closed, open),
Masks with screen,
Anti-dust clothing (overalls with helmets, suits with helmets, autonomous spacesuit),
Protective pastes and ointments;
5) therapeutic and preventive measures:
– medical monitoring of the health status of workers - preliminary and periodic medical examinations in accordance with the requirements of the Order of the Ministry of Health No. 700 of 1984. The timing of periodic medical examinations depends on the type of production, profession and the content of free silicon dioxide in the dust. Examinations by a therapist and an otorhinolaryngologist are carried out once a year or once every 2 years with mandatory radiography or large-frame fluorography,
– UV – irradiation in fotaria (inhibiting sclerotic processes),
– alkaline inhalations (for the purpose of sanitizing the upper respiratory tract),
– breathing exercises (improving the function of external respiration),
– therapeutic and preventive nutrition (diet with the addition of methionine and vitamins).
Industrial poisons– these are chemical substances that, in the form of raw materials, intermediate, auxiliary or finished products, are found under production conditions in accordance with the technological regime and, upon penetration into the body, can cause disruptions in its normal functioning.
