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 (URT).

Extremely rare dust diseases include neoplasms of the respiratory system.

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 - 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 SiO2. 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, berylliosis, staniosis, manganoconiosis, etc.). 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.

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.

In addition, industrial dust can lead to the development 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 is becoming the most common type 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.

The term silicosis was first proposed by the Italian anatomist Visconti in 1870. It is used to this day to designate a peculiar, mainly nodular, fibrosis of the lungs from inhalation of silica dust - free silicon dioxide (SiO2).

A broader collective concept, pneumoconiosis, was introduced even earlier, in 1866, by Zenker to designate pulmonary fibrosis that develops as a result of inhalation of various types of dust.

Depending on the type of dust that caused the development of pneumoconiosis, the corresponding types of pneumoconiosis are distinguished. Thus, silicosis is called pneumoconiosis caused by exposure to silicon dioxide, silicosis - exposure to dust of various silicates (in particular, kaolin - kaolinosis, talc - talcosis, asbestos - asbestosis, etc.), anthracosis - coal, siderosis - iron-containing dust, etc. d. Mixed forms of pneumoconiosis are designated taking into account the composition of the dust, for example, silicoanthracosis, silicosiderosis, etc. The combination of pneumoconiosis with pulmonary tuberculosis is designated as coniotuberculosis; at the same time, depending on the type of dust, the terms “silicotuberculosis”, “anthracotuberculosis”, etc. are used.

Particular attention should be paid to such types of metal dust as dust of beryllium, vanadium, molybdenum, tungsten, cobalt, niobium and their compounds, under the influence of which not only peculiar damage to the lungs is observed, but also pronounced changes in other organs and systems. Dust of these metals can most likely be classified as a group of substances that have general toxic and toxic-allergic effects. The main sections of the new classification of pneumoconiosis are: I - types of pneumoconiosis, II - clinical and radiological characteristics of pneumoconiosis.

The following types of pneumoconiosis have been identified, taking into account the etiological principle:

1. Silicosis - pneumoconiosis caused by inhalation of quartz dust containing free silicon dioxide.

2. Silicosis - 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 pneumoconiosis, etc.).

3. Metalloconiosis - pneumoconiosis from exposure to metal dust: iron, beryllium, aluminum, barium, tin, manganese, etc. (siderosis, berylliosis, aluminosis, baritosis, staniosis, manganoconiosis, etc.).

4. Carboconiosis - pneumoconiosis from exposure to carbon-containing dust: coal, coke, graphite, soot (anthracosis, graphitosis, soot pneumoconiosis, etc.).

5. Pneumoconiosis from mixed dust. These include the following two subgroups: 1) pneumoconiosis caused by exposure to mixed dust containing a significant amount of free silicon dioxide (10% or more), for example anthracosilicosis, siderosilicosis, silicosilicosis, etc.;

2) pneumoconiosis caused by exposure to mixed dust that does not have free silicon dioxide or with its insignificant content (up to 5-10%), for example, pneumoconiosis of grinders, electric welders, etc.

6. Pneumoconiosis from organic dust. This type includes all forms of dust lung diseases observed when inhaling various types of organic dust, the clinical picture of which includes not only a disseminated process with the development of diffuse fibrosis, but also bronchitis and allergic syndromes (chronic dust bronchitis, bronchial asthma).

These included diseases caused by exposure to plant fibers, various types of agricultural dust, dust from synthetic substances, such as bagassosis (from exposure to sugar cane dust), byssinosis (from cotton and flax dust), the so-called “farmer's lung” (from various types of agricultural dust, containing mushrooms).

In 1996, the State Research Institute of Occupational Medicine of the Russian Academy of Medical Sciences proposed a new classification of pneumoconiosis, set out in guidelines No. 95/235 of the Ministry of Health and Medical Industry of the Russian Federation.

The new classification identifies three main groups of pneumoconiosis:

1. Pneumoconiosis developing from exposure to highly and moderately fibrogenic dust (with a free silicon dioxide content of more than 10%) - silicosis, anthracosilicosis, silicosiderosis, silicosilicosis. These pneumoconiosis are most common among sandblasters, chippers, tunnelers, farmers, core workers, refractory workers, and among workers in the production of ceramic materials. They are prone to progression of the fibrotic process and complications from tuberculosis infection.

2. Pneumoconiosis developing from exposure to weakly fibrogenic dust (with a free silicon dioxide content of less than 10% or not containing it) - asbestosis, talcosis, kaolinosis, olivinosis, carboconiosis, siderosis, etc.). They are characterized by moderately severe pneumofibrosis, a benign and slowly progressive course, often complicated by a nonspecific infection, chronic bronchitis, which mainly determines the severity of the disease.

3. Pneumoconiosis, developing from exposure to aerosols of toxic-allergic action (dust containing allergenic metals, components of plastics and other polymeric materials, organic dust, etc.) - berylliosis, aluminosis, “farmer's lung” and other hypersensitivity pneumonitis. In the initial stages of the disease, they are characterized by a clinical picture of chronic bronchiolitis, progressive alveolitis with outcome in fibrosis. Dust concentration is not critical in the development of this group of pneumoconiosis. The disease occurs with minor, but prolonged and constant contact with an allergen.

In the International Classification of Diseases, 10th revision (ICD-10), the following categories are allocated to pneumoconiosis (/60-65 - associated with exposure to inorganic, /67 - organic dust):

/60. Coal miner's pneumoconiosis.

/61. Pneumoconiosis caused by asbestos.

/62. Pneumoconiosis caused by silica-containing dust, including silicosis, silicotic and silicate (massive) fibrosis of the lung, and pneumoconiosis caused by talc.

/63. Pneumoconiosis caused by other inorganic dusts. /63.0. Aluminosis (lung).

/63.1. Bauxite fibrosis (lung).

/63.2. Beryllium.

/63.3. Graphite fibrosis (lung).

/63.4. Siderosis.

/63.8. Pneumoconiosis caused by other non-refined inorganic dusts.

/64. Pneumoconiosis, unspecified.

/65. Pneumoconiosis associated with tuberculosis.

/67. Hypersensitivity pneumonitis caused by organic dust (exogenous allergic alveolitis).

In the diagnosis of pneumoconiosis, the leading role is played by the x-ray method. The radiological classification includes:

Small and large blackouts

1. Small opacities are characterized by shape, size, profusion (numerical density per 1 cm2) and distribution over the zones of the right and left lung.

a) rounded (nodular): p - 1.5 mm;

q - 1.5-3 mm; r - up to 10 mm;

b) linear dimming:

s - thin, linear - up to 1.5 mm wide; t - average linear - up to 3 mm; and - rough, spotted, irregular - up to 10 mm.

Small round-shaped darkenings have clear contours, medium intensity, monomorphic, diffusely located mainly in the upper and middle parts of the lungs.

Small linear opacities of irregular shape reflect peribronchial, perivascular and interstitial fibrosis, have a mesh, cellular or cellular-cellular shape and are located mainly in the middle and lower parts of the lungs.

Symbols are written twice (p / p, q / q, r / r) or (p / q, q /1, p/s, etc.).

The saturation density or concentration of small shadows per 1 cm2 of the lung field is encrypted in Arabic numerals:

1) single, pulmonary bronchovascular pattern can be traced;

2) a few small shadows, the pulmonary bronchovascular pattern is partially differentiated;

3) multiple small shadows, the pulmonary bronchovascular pattern is not differentiated.

For example, 0/0, 0/1, 1/0, 3/3, etc. Numerator - basic forms, denominator - others.

2. Large darkening (the result of the merging of rounded darkening at the site of atelectasis, pneumonic foci, when complicated by tuberculosis): A - up to 50 mm; B - up to 100 mm; C - more than 100 mm.

Based on the radiological characteristics, interstitial, nodular and nodular forms of pneumoconiosis are distinguished. The clinical and functional classification of pneumoconiosis includes: bronchitis, bronchiolitis, emphysema, respiratory failure, compensated, decompensated cor pulmonale. According to the course, there are slowly progressive, rapidly progressive and regressive course of pneumoconiosis, as well as late pneumoconiosis.

Also, exposure to industrial dust provokes the development of chronic dust bronchitis, which, as a rule, occurs at a lower concentration of industrial dust (also exceeding the maximum permissible concentration), when exposed to mixed dust, as well as dust with less fibrogenic activity.

Clinical example: patient Tn E.S., 57 years old, foundry worker at OJSC Kuznetsov, has been working in a foundry since 1982. Harmful production factors: exceeding the maximum permissible concentration of quartz-containing dust; heating microclimate; physical overexertion of the hands; periodic work with vibrating tools; load on the lumbar spine, shoulder and elbow joints; noise level - 79 dB, with maximum permissible concentration - 80 dB. Previously, until 1982, he worked for 9 years as an aircraft assembler and riveter at the Kuibyshev Aviation Plant in contact with noise and vibration exceeding the maximum permissible limit.

He was admitted with complaints of a sore throat, dry nose and throat, dry cough, decreased hearing, pain, numbness and chilliness of the hands, decreased strength in the hands, pain in the elbow and shoulder joints, and pain in the lower back.

When examined by an otorhinolaryngologist, sensorineural hearing loss of the second degree, chronic atrophic rhinopharyngolaryngitis was noted, with X-ray of the lungs - deformation of the pulmonary pattern, with FBS - atrophic bilateral endobronchitis, with computer pneumotachography - a decrease in expiratory flow rates, upon examination, the neurologist concluded that there was a “vegetative-sensory polyneuropathy of the hands from the combined effects of local vibration, muscle tension and microtraumatization, chronic lumbosacral radiculopathy.”

Conclusion VK: chronic dust bronchitis in the second stage, DN of the second degree. Chronic atrophic nasopharyngolaryngitis, autonomic-sensory polyneuropathy of the hands from exposure to local vibration, muscle tension and microtrauma. Chronic lumbosacral radiculopathy. Diseases are classified as occupational.

The VK did not consider it possible to associate the diagnosis of “sensorineural hearing loss of the second degree” with the profession on the basis that in the profession of a foundry worker the noise did not exceed the maximum permissible limit, and during the period of work as an aircraft assembler-riveter at the Kuibyshev Aviation Plant, hearing loss was based on an analysis of the submitted medical documentation (extract from the outpatient card and medical examination card) was not recorded, although the audiological picture indicates the role of occupational factors in the genesis of hearing loss.

Clinical example: patient Z. S.S. To date, he has worked for 50 years in various professions at the Halmer-Yu mine (Vorkuta region) for coal mining for 16 years, after joining the army. The depth of the mine reached 3-4 kilometers. Among the harmful production factors in the work of a miner, according to the sanitary and hygienic characteristics of working conditions, work with a jackhammer, exceeding the maximum permissible concentration of coal dust and dust of associated rocks (quartz), maximum permissible concentrations of vibration, noise, as well as low temperature and watering are noted.

Periodic medical examinations were carried out formally; personal protective equipment included earplugs and vibration-absorbing gloves. Respirators were practically not used. 12 years after the start of work, complaints appeared of a dry cough, shortness of breath, chilliness, numbness of the hands, whitening of the fingers, decreased muscle strength in the hands, and decreased hearing. During an examination at the occupational pathology department in 1996, chest x-rays revealed increased and deformed pulmonary patterns and pneumosclerosis; with FBS - atrophic endobronchitis; computer pneumotachography - reduction in volume and velocity parameters of forced expiration; examination by a neurologist - a decrease in pain sensitivity in the hands according to the “glove” type, an increase in the thresholds of pain and vibration sensitivity (according to algesimetry, pallesthesiometry, tuning fork test), a decrease in the muscle strength of the hands, the “cold test” is positive; examination by an otorhinolaryngologist - professional sensorineural hearing loss of the second degree.

Conclusion VK: chronic dust bronchitis, stage two, pneumosclerosis, DN of the second degree, vibration disease of the second degree (vegetative-sensory polyneuropathy of the hands, peripheral anhydristonic syndrome), sensorineural hearing loss of the second degree. Diseases are classified as occupational.

Workers in most agricultural professions are constantly or during certain periods of work exposed to dust. There are organic (plant and animal origin) and inorganic dust. Agricultural workers engaged in soil cultivation (machine operators, field workers, etc.) are exposed to the influence of mixed soil and plant dust. Its composition depends on the type of soil, the plants growing on it, the admixture of mineral fertilizers and pesticides used.

Plant dust is formed during the life of thaw (pollen), during the harvesting and processing of grain and industrial crops (cotton, flax, hemp, etc.). The mechanization of the harvesting processes of industrial crops has led to an increase in the content of plant debris, consisting mainly of particles of stems, leaves, fruit bolls, bracts (leaves surrounding the fruit bolls of cotton) and weeds growing in the fields. A significant amount of dust is released into the air of the working area during various processes associated with the processing of industrial crops.

The processes of ginning, processing of cotton, its stems and other parts of plants, processing of degummed flax are characterized by the release of a significant amount of fibrous plant dust with an admixture of mineral components containing free silicon dioxide and silicates.

Getting into the respiratory system with air, soil and plant dust contributes to the development of inflammatory diseases (chronic dust bronchitis, bronchopneumonia). Certain types of fibrous plant dust are an etiological factor in the development of synovosis.

It is characteristic of organic dust that it contributes to the development of allergic reactions of the bronchopulmonary apparatus (bronchial asthma, asthmatic bronchitis). Long-term exposure (15 years or more) to fine dust of various origins, especially those containing free silicon dioxide, can cause the development of pneumoconiosis.

Research by V. S. Gumenny (1979) showed the relationship between the amount of mineral fertilizers applied to the soil and the prevalence of nonspecific respiratory diseases.

With the development of pathology of the bronchopulmonary apparatus, the chemical composition, dispersion of dust and the individual characteristics of the organism are important. In this regard, workers of the same production may develop chronic bronchitis, bronchial asthma, and neuroconiosis (E. A. Mavrina, 1972). Changes in the immunological reactivity of the body are the most important factor determining the progressive course of the disease.

Federal Agency for Education

State educational institution of higher professional education

Ulyanovsk State University

Institute of Medicine, Ecology, Physical Culture and Valeology

Faculty of Medicine

Department of Public Health, Healthcare and

public hygiene

Abstract on the topic:

Industrial dust. Occupational diseases associated with work in production with high air pollution.

Types of pneumoconiosis and their prevention

Completed.

Checked by the teacher:

Ulyanovsk

Industrial dust:……………………………………..3

What is dust ?............................................................. 3

Types of dust ………………………………………..........3

Industrial enterprises that generate dust....... 4

The impact of industrial dust on health…………...5

Pneumoconiosis:…………………………………………... 6

Definition ………………………………………..... 6

Kinds . ……………………………………………….....6

Prevention……..….…………………………………….8

Methods for determining dust content in the air........9

Conclusion……………………………………………………………...10

Literature……………………………………………………………11

Industrial dust

Anthropogenic sources of environmental pollution include industrial dusts emitted in significant quantities by many production processes. Industrial dust also has harmful effects on the human body.

What is dust?

Dust (aerosol) are small particles of solid substances that are crushed or otherwise obtained and float (in motion) for some time in the air. This hovering occurs due to the small size of these particles (dust particles) under the influence of the movement of the air itself.

The air of all industrial premises is polluted with dust to one degree or another; Even in those rooms that are usually considered clean and not dusty, there is still dust in small quantities (sometimes it is even visible to the naked eye in a passing ray of sunlight). However, in many industries, due to the peculiarities of the technological process, the production methods used, the nature of raw materials, intermediate and finished products and many other reasons, intensive dust formation occurs, which pollutes the air of these premises to a large extent. This may pose a certain danger to workers. In such cases, dust in the air becomes one of the factors in the production environment that determines the working conditions of workers; it was called industrial dust.

Types of dust

By the nature of education Dusts are divided into groups: organic, inorganic , synthetic and mixed. Organic dust: dust of plant origin (wood, cotton, flax, various types of flour, sugar, tobacco, etc.), animal (skin, wool, hair, ground bones, feathers, fluff, etc.). Inorganic dust - dust of metals and their oxides, various minerals, inorganic salts and other chemical compounds. Synthetic dust: plastics, synthetic fibers and other organic products of chemical reactions . Mixed dust, the most common and cosmic dust.

Where dust is generated: disintegration aerosol, formed as a result of crushing or abrasion, grinding, sifting, turning, sawing, pouring; condensation aerosol resulting from evaporation followed by condensation into solid particles; combustion products (smoke), as a result of combustion with the formation of particulate matter in the air.

Dust structure: amorphous - dust particles are round in shape; crystalline - dust particles with sharp edges (formed when grinding metal); fibrous- elongated dust particles: lamellar- dust particles in the form of layered plates, etc.

Origin of dust:soluble ( sugar, flour dust ) And insoluble ( bleach dust ) in water and other liquids, including biological media (blood, lymph, gastric juice, etc.).

According to dust dispersion:visible(particles larger than 10 microns) ; microscopic(from 0.25 to 10 microns); ultramicroscopic(less than 0.25 microns), the degree of dispersion mainly determines the depth of dust penetration into the respiratory tract.

According to the effect on the body dust: toxic, containing SiO2; non-toxic, silicon-free.

Industrial plants generating dust

Enterprises in the extractive industry (mining, gas production)

Construction materials factories

Enterprises for processing materials (linen, cotton, wood, glass (grinding))

Enterprises using combustion (CHP, blast furnace industry)

The effect of industrial dust on the body

Industrial dust can have a direct or indirect effect on the body. Direct impact dust can be divided into the following groups: 1 . Effects on the respiratory tract: prolonged irritation of the nasal mucosa by dust can lead to chronic rhinitis. When large amounts of dust are inhaled, large and medium-sized bronchi can be affected (bronchitis), and lung tissue is also directly affected. Dust particles entering the alveoli are intensively captured by phagocytes; they can accumulate and die in large numbers in the lumen of the alveoli, which leads to the proliferation of connective tissue. The connective tissue wrinkles, forms scars, and compresses blood vessels. All this leads to atelectasis in some areas and emphysema in others, disrupting respiratory function. Blood circulation in the pulmonary circulation is disrupted, and stagnation occurs, and this is how the picture of pulmonary fibrosis develops - PNEUMOCONIOSIS. 2 . Effect on mucous membranes: the result of dust getting on the mucous membranes can be conjunctivitis, gingivitis, etc. 3. Effect on the skin: Industrial dust can penetrate the skin and the openings of the sebaceous glands, as a result this can lead to pyoderma and dermatitis. Indirect impact dust, as a result, dust does not act directly on the human body, but through environmental factors. An increased concentration of dust in the air leads to a decrease in the level of illumination, a decrease in air transparency, and UV cannot penetrate the dust curtain. Water (fog) can accumulate on dust particles and microorganisms can settle.

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, fasteners, 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 is disturbing 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: beryllium - 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 inhalation of 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.