Pneumoconiosis

Pneumoconiosis (from the Greek pneumon - lung, conis - dust) is a reaction of lung tissue to the accumulation of dust in it.

Pneumoconiosis is a chronic lung disease caused by prolonged inhalation of industrial dust, which leads to the development of widespread fibrosis of lung tissue.

There are several types of the disease, depending on the causative factor, but the most common clinical manifestations of pneumoconiosis are still distinguished.

Thus, a person is bothered by a dry cough, increasing shortness of breath, pain in the chest, which is caused by the development of deforming bronchitis and severe respiratory failure.

In the process of diagnosing the disease, professional experience and harmful conditions that provoke damage to the lung tissue are taken into account. In addition to physical examination data, spirometry, X-ray examination, determination of the gas composition of the blood and acid-base balance are used.

The main direction in treatment is considered to be the elimination of the harmful factor that caused the development of pneumoconiosis. In addition, medications are used to alleviate the patient's condition and reduce the area of damage to the lung tissue. These include bronchodilators, expectorants, hormones, as well as the use of physiotherapy procedures, oxygen inhalations and hyperbaric oxygenation.

Among professional pathologies, pneumoconiosis occupies a leading place. Most often, it is observed in workers in the glass, machine, coal and asbestos industries, when the professional experience exceeds 5-15 years, depending on the working conditions.

Aggressive dust particles can stimulate the formation of connective tissue in the lung parenchyma. This leads to pulmonary fibrosis and respiratory dysfunction. Diseases caused by exposure to dust are usually classified as occupational diseases. Their diagnosis and treatment are carried out by occupational pathologists.

The most common cause of pneumoconiosis progression after dust exposure has ceased is its complication by tuberculosis. Silicosis occupies a central place among pneumoconioses in terms of the frequency of specific infection. The emerging disease, silicotuberculosis, is a qualitatively new nosology that has features of both silicosis and tuberculosis.

The rate of development of pneumoconiosis has changed significantly due to improved working conditions, so now progressive forms of silicosis and silicotuberculosis, which were identified in the 1950s, are very rarely diagnosed.

ICD-10 codes

Silicosis (J62)

Pneumoconiosis caused by inhalation of dust containing free silicon dioxide (SiO ₂ ) in the form of a fine aerosol with particle sizes from 0.5 to 5 microns. Silicosis is detected in workers in the mining and metalworking industries (miners, miners). The likelihood of developing silicosis depends on the amount of dust deposited in the lungs, the size, surface characteristics and crystalline structure of silicon oxide particles. As a result of the reaction of lung tissue to dust, interstitial fibrosis develops in the form of silicotic cuffs along the course of small vessels. Progression of the process leads to the formation of silicotic nodules, which can increase to 1-1.5 cm or more. Histological examination reveals fibrous and cellular-fibrous nodules with a concentric arrangement of collagen and argyrophilic fibers, with dust particles located in the center of the nodule. The same nodules are located in the regional lymph nodes. Silicosis is characterized by a progressive course even after contact with dust has ceased, and is often complicated by tuberculosis.

A separate group of diseases associated with the accumulation of dust in the lungs containing a small amount of free silicon dioxide (J.62.8) is identified: kaolinosis, cement, mica, nepheline and other pneumoconiosis.

Pneumoconiosis caused by talc dust - talcosis (J62.0). The morphological feature of the disease is the development of connective tissue without the formation of nodules in the lung parenchyma and mediastinal lymph nodes. The course of the disease is favorable.

Anthracose (J60)

Anthracosis - coal worker's pneumoconiosis; the disease is caused by coal dust accumulated in the lungs. Histological examination reveals coal dust accumulations (anthracotic nodules). The lung is gray (sometimes black). Dust deposits are found in the lymph nodes of the mediastinum, liver, and spleen.

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Asbestosis (J61)

The development of asbestosis is associated with the accumulation of asbestos fibers in the lungs. Morphological manifestations are fibrosing alveolitis and interstitial fibrosis. With minor and short-term exposure to asbestos dust, individual areas of damage are detected, in these areas asbestos bodies are found.

ICD-10 identifies a large group of pneumoconioses caused by other (non-silicon) inorganic dust (J63): aluminosis (J63.0), berylliosis (J63.2), siderosis (J63.4), stannosis (J63.5), graphite fibrosis (J63.3), etc. The histological picture and clinical manifestations depend on the influencing factor.

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Pathogenesis of pneumoconiosis

Due to serious air pollution exceeding the permissible level and insufficient functioning of the mucociliary apparatus, dust particles penetrate into the alveoli of the lungs. They can then be absorbed by macrophages or penetrate into the interstitial tissue.

The pathogenesis of pneumoconiosis is based on the presence of cytotoxic action of dust particles on macrophages, resulting in the development of lipid peroxidation and secretion of lysochondrial and lysosomal enzymes. Thus, the process of fibroblast proliferation and the appearance of collagen fibers in the lung tissue are activated.

In addition, the presence of immunopathological processes in the development of pneumoconiosis has been proven. Tissue fibrosis can be characterized by nodular, nodular or interstitial localization. Nodular fibrosis consists of sclerotic nodules of macrophages filled with dust and clusters of connective tissue elements.

Interstitial pneumoconiosis is observed in the absence of fibrous tissue nodules. However, thickened alveolar septa, perivascular and peribronchial fibrosis are present.

The pathogenesis of pneumoconiosis can cause the appearance of large nodes due to the fusion of smaller ones, as a result of which a significant part of the lung loses its ventilation capacity.

The fibrous process is accompanied by emphysema (focal or widespread), which can take on a bullous character. In addition to damage to the lung tissue, pathological processes are observed in the bronchi with the development of inflammation of the mucous membrane of the bronchi and bronchioles.

Pneumoconiosis goes through several stages, in particular, it undergoes an inflammatory reaction, dystrophic and sclerotic effects.

Symptoms of pneumoconiosis

A feature of silicotuberculosis is the scarcity of clinical manifestations. In the initial stages of the process, the symptoms are poorly expressed and non-specific: shortness of breath during physical exertion, dry cough, increased fatigue can be manifestations of uncomplicated silicosis and concomitant chronic non-specific pathology.

The clinical picture of tuberculous bronchoadenitis against the background of silicosis is caused by severe intoxication: fever, weakness, sweating. The formation of a lymphobronchial fistula is accompanied by a debilitating unproductive cough. In the absence of treatment, secondary pneumonia develops, and the course of the disease worsens. With the progression of massive silicotuberculosis, pulmonary heart failure develops.

Tuberculous pleurisy in pneumoconiosis may be the first manifestation of a specific process, a complication of tuberculous bronchoadenitis or pulmonary destruction in massive silicotuberculosis.

Massive silicotuberculosis, corresponding to stage III of silicosis, is characterized by the formation of large foci of heterogeneous structure in the upper lobes of the lungs due to calcification of individual areas and the appearance of destruction zones. Unlike tuberculosis, destruction zones can remain stable for a long time. The indicated pulmonary changes are formed due to the fusion of individual foci and nodular formations or in lymphobronchial complications of tuberculous lesions of the lymph nodes. As the process progresses, the destruction zone increases, focal dissemination appears.

Pneumoconiosis in electric welders

During the process of electric welding, particles of iron and other metal dust, silicon dioxide and toxic gases are formed. When these components affect the respiratory tract, their damage is observed, including pulmonary edema.

Contact with allergens causes bronchitis with an asthmatic component. In most cases, pneumoconiosis is characterized by a benign course. In the case of welding in a closed room, the concentration of dust increases significantly, and the resulting hydrogen fluoride, with its toxic effect, provokes the development of pneumonia and frequent respiratory diseases.

Pneumoconiosis in electric welders most often develops after 15 years. Typical forms of silicosis are observed in workers who come into contact with dust containing silicon dioxide.

Uncomplicated pneumoconiosis is characterized by cough with scanty sputum, chest pain, and shortness of breath during physical activity. In addition, pharyngitis, rhinitis, dry wheezing, and signs of emphysema are detected during a more detailed examination.

Pneumoconiosis in electric welders is registered after an X-ray examination. Unlike silicosis, the image shows radiopaque iron dust. After contact with dust has ended after 3-5 years, pneumoconiosis can be "cured" by cleaning the iron dust. However, these cases are possible only in the absence of complications in the form of obstructive bronchitis and tuberculosis.

Stages of pneumoconiosis

The development of pneumoconiosis can be characterized by a slowly or rapidly progressing, late or regressive course. Slow development of the pathology occurs as a result of exposure to dust over 10-15 years.

A more rapidly progressing form begins to manifest itself after several years (up to 5 years) from the beginning of contact with the dust factor with an increase in symptoms over 2-3 years. The late form is characterized by the onset of manifestations only after several years have passed since the end of contact with the pathological factor. Regression of pneumoconiosis is noted in the case of removal of dust particles from the respiratory organs after the end of exposure to dust.

Despite the various causes of pneumoconiosis, the stages of development in most cases have similar characteristics. The initial stages of pneumoconiosis are shortness of breath, dry cough or cough with scanty sputum, pain syndrome when moving the chest, under and between the shoulder blades.

As the process progresses, in the second stage of pneumoconiosis, the pain becomes constant. In addition, weakness increases, temperature appears (from 37.0 to 37.9 degrees), sweating increases, weight gradually decreases and shortness of breath increases.

At the third stage of pneumoconiosis, coughing is constant, sometimes paroxysmal, shortness of breath is noted at rest, respiratory failure increases, “blueness” of the lips is noted, and changes in the shape of the fingers and nail plates are noted.

Then pulmonary heart disease develops and the pressure in the pulmonary artery increases. Complications include chronic bronchitis (obstructive, with an asthmatic component), tuberculosis (silicotuberculosis), damage to the walls of blood vessels with pulmonary hemorrhage, and the formation of bronchial fistulas.

In addition, in some cases, bronchiectatic lesions, emphysema, asthmatic component, spontaneous pneumothorax and systemic diseases (rheumatoid arthritis, scleroderma) can be detected. The presence of silicosis or asbestosis increases the likelihood of developing bronchial or lung cancer, as well as pleural mesothelioma.

Types of pneumoconiosis

Based on the damaging factor, it is accepted to distinguish some types of pneumoconiosis, for example, silicosis, carboconiosis, silicosis, metalloconiosis. In case of exposure to mixed dust, anthracosilicosis, siderosilicosis, as well as diseases due to damage by organic dust are distinguished.

The most common and severe disease is silicosis, which occurs as a result of exposure to dust containing silicon dioxide. This type of pneumoconiosis is observed in workers in foundries, mines, and in the manufacture of refractory materials and ceramics.

Silicosis is a chronic pathology, the severity of which is determined by the duration of exposure to an aggressive factor. At first, shortness of breath during physical activity, chest pain, and periodic dry cough are observed.

As it progresses, signs of emphysema join in, the cough becomes harsher, wheezing appears, and the pain bothers even at rest. Gradually, the cough becomes frequent and wet with sputum.

Based on the X-ray examination, the degree and form of pathology are determined. It is customary to distinguish 3 degrees of severity, as well as nodular, nodular and interstitial forms of silicosis.

In the absence of treatment and the presence of an influencing damaging factor, complications may develop. Among them, the most common are respiratory and cardiovascular failure, bronchial asthma, tuberculosis, obstructive bronchitis and pneumonia.

The next type of pneumoconiosis is asbestosis, which is caused by asbestos dust. In addition to the chemical effects of dust, damage to lung tissue by asbestos particles is noted.

This type is found in workers involved in the production of pipes, slate, brake tapes, as well as in the shipbuilding, aviation and construction industries.

Clinical symptoms are expressed by chronic bronchitis, emphysema and pneumosclerosis. Most often, the symptoms are cough with sputum production, where "asbestos bodies" are found, increasing shortness of breath and asbestos warts are present on the skin.

Possible complications include pneumonia, severe respiratory failure, and the formation of neoplasms in various locations - pleura, lungs, or bronchi.

Such types of pneumoconiosis as talcosis, which develops as a result of inhaling talc dust, are usually considered relatively benign silicosis. This pathology is characterized by the appearance of bronchitis, the severity of which is significantly less than with asbestosis. In addition, talcosis is less prone to progression, but not in the case of inhaling cosmetic powder.

Metalloconiosis is caused by damage to the lung tissue by beryllium dust with the development of berylliosis, iron - siderosis, aluminum - aluminosis or barium - baritosis. Metalloconiosis, the cause of which was radiopaque dust (barium, iron, tin), has a benign form of the course.

In this case, moderate fibrosis develops, the progression of which is not observed. In addition, when the negative impact of dust is eliminated, regression of the disease is observed as a result of self-cleaning of the lungs.

Aluminosis is characterized by interstitial fibrosis of diffuse form. As for beryllium and cobalt, toxic and allergic lung damage is possible due to their influence.

Carboniosis occurs as a result of inhalation of carbon-containing dust, such as soot, graphite or coal. It is characterized by moderate fibrosis of the lung tissue in small focal or interstitial localization.

Carboniosis, caused by exposure to coal dust with the development of anthracosis, is singled out separately. The pathology is observed in workers of the enrichment plant or mines after 15-20 years of work experience.

The fibrous process has the appearance of widespread sclerosis. However, with combined damage from coal dust and rock, the development of anthracosilicosis is noted, which is a more severe form with progressive fibrosis.

Damage to lung tissue as a result of exposure to organic dust is only conditionally related to pneumoconiosis, due to the fact that in some cases there is no diffuse process with the development of pneumofibrosis. Most often, bronchitis with an allergic component is observed, for example, when inhaling cotton dust.

An inflammatory nature with elements of allergy can be observed in cases of exposure to flour dust, sugar cane, plastic products, as well as agricultural dust with the presence of fungi.

Complications of pneumoconiosis

In case of prolonged contact with a harmful factor and the absence of full treatment of pneumoconiosis, the risk of complications increases. They aggravate the clinical picture of the pathological process and, as it progresses, involve new tissues in the process.

Complications of pneumoconiosis include the development of pulmonary heart disease, pneumonia, obstructive bronchitis, bronchial asthma, the formation of bronchiectasis, and the occurrence of cardiac and pulmonary failure.

Tuberculosis is often observed to join the pathological process, which causes silicotuberculosis. The most important thing is differential diagnostics of these diseases, on which the patient management tactics and treatment measures depend.

It is important to remember that tuberculosis is a contagious disease, which leads to infection of people around. A person with an open form of tuberculosis is subject to isolation and specific treatment.

In silicosis, there are no clinical symptoms of intoxication, manifestations from the respiratory system of moderate activity, and a typical clinical picture is observed.

Complications of pneumoconiosis in rare cases can also be expressed in transformation into a malignant process. Tumor-like silicosis differs from cancer by its slow growth and relatively satisfactory condition of the patient.

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Diagnosis of pneumoconiosis

The diagnosis of pneumoconiosis is established on the basis of several diagnostic criteria:

• professional history data:
• assessment of dustiness of the working area:
• X-ray picture at the time of examination and in dynamics over several years,
• indicators of external respiratory function.

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Laboratory diagnostics of pneumoconiosis

In active silicotuberculosis, the leukocyte formula and biochemical blood parameters change: moderate increase in ESR, shift in the leukocyte formula to the left, lymphopenia, increased levels of γ-globulins, haptoglobin, and protein.

An absolute sign of silicotuberculosis is the presence of mycobacteria tuberculosis in the patient's sputum, detected bacterioscopically or by sowing on nutrient media, however, the proportion of bacteria excreting bacteria does not exceed 10%.

Immunological changes: a decrease in the absolute number of T-lymphocytes due to the CD4 population, sometimes an increase in the content of IgA and IgM.

The information content of provocative tests with tuberculin is insufficient for a confident diagnosis of silicotuberculosis.

X-ray examination methods for pneumoconiosis

The darkenings resulting from coniotic pneumofibrosis are classified by shape, size, location and intensity. The stage of the process is determined by comparing the resulting radiographs with standards: depending on the severity of the process, four categories are distinguished (0, I, II, III).

For a detailed assessment of the condition of the lung parenchyma, vessels of the pulmonary circulation, mediastinal lymph nodes, and pleura, CT of the chest organs is mainly used.

Limited (minor) forms of silicotuberculosis: focal tuberculosis, limited disseminated tuberculosis, limited infiltrate and tuberculoma. If the above changes are detected in a patient with the interstitial form of silicosis, there are no difficulties in establishing a diagnosis. Diffuse interstitial changes in the lung parenchyma and areas of emphysema indicate pneumoconiosis, and a limited process in the form of small and large foci or foci that have arisen on an intact pulmonary field is regarded as a manifestation of tuberculosis. Further clinical and radiological observation allows us to confirm the diagnosis.

When new focal or focal changes are detected, localized in the apical-posterior segments of the lungs, against the background of silicosis, it is necessary to clarify what caused such changes: progression of silicosis or its complication by tuberculosis. To establish a diagnosis, archival documentation is studied and the dynamics of the process (the rate of development of new elements and growth of the focal formations themselves) is assessed: the faster the changes occur, the higher the probability of tuberculous etiology. The progression of the silicotic process is usually uniform in all parts of the lungs. The appearance of asymmetry, an increase in the severity of changes in the posterosuperior sections indicate the addition of a specific process. CT reveals signs of destruction, which do not occur with small sizes of silicotic nodes. The dynamics of the process are assessed under the influence of the prescribed specific treatment for 3 months or more.

Silicotuberculoma against the background of nodular silicosis is a special form of damage (does not correspond to the classification of silicosis), detected against the background of diffuse nodular pneumoconiosis in the form of rounded formations. They are formed due to the fusion of individual foci, localized more often in the cortical parts of the lungs. A distinction is made between tuberculoma in a stable state (its size does not change, and a fibrous capsule is formed along the periphery). In the active phase, using CT, a destruction zone is detected closer to its lower inner pole. The progression of silicotuberculoma is accompanied by an increase in the decay zone, the appearance of focal dissemination and an increase in the focus of the lesion.

Bronchological research methods in pneumoconiosis

In the diagnosis of silicotuberculosis, bronchological examination is sometimes used in combination with cytological and cytochemical examination of lavage fluid.

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Diagnosis of lymph node lesions

Tuberculosis of the intrathoracic lymph nodes is a frequent complication of silicosis, usually undiagnosed for a long time. Both silicosis and silicotuberculosis are characterized by damage to all groups of intrathoracic lymph nodes, but the number of calcification foci and the nature of calcium deposition differ. Tuberculous and silicotic processes in the lymph nodes occur simultaneously, and the specific process quickly undergoes hyalinosis, so even by biopsy it is not always possible to confirm the diagnosis; however, a massive increase in the lymph nodes mainly in one or two groups, the presence of a lymphobronchial fistula, and the further development of inflammatory stenosis of the bronchus indicate a complex lesion. To confirm the diagnosis, it is necessary to establish the fact of bacterial excretion and re-examine (dynamically) the endoscopic picture. In the presence of a fistula, sanitation is constantly carried out to prevent the development of secondary inflammation in the pulmonary parenchyma. Sometimes, with silicotuberculosis, multiple fistulas are detected, the healing of which occurs with the formation of characteristic pigmented, retracted scars.

In the diagnosis of silicotuberculosis bronchoadenitis, timely bronchological examination of the patient and collection of material for research (bacteriological, cytological and histological) are of great importance.

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Formulation of diagnosis for pneumoconiosis

There is currently no generally accepted classification of silicotuberculosis. Doctors use a descriptive formulation of the diagnosis, which includes a statement of the presence of the disease and subsequent characteristics of the silicotic and tuberculous process in accordance with the current classifications of these diseases.

The formulation of the diagnosis of pneumoconiosis includes an assessment of the X-ray morphological changes in the lungs, the prevalence and intensity of the lesion, the stage of the process, the functional characteristics of external respiration, the course of the disease and the presence of complications, for example:

Silicotuberculosis. Silicosis of the first stage (s). Infiltrative tuberculosis of the second segment of the right lung in the phase of decay and dissemination (BC+).

This approach to formulating a diagnosis has a number of limitations: if at the initial stages of the development of the process the radiological picture of silicotuberculosis is practically no different from its classical manifestations, then at stages II and III it is often impossible to differentiate between the silicotic and tuberculous process (disseminated and conglomerate silicotuberculosis).

Acute silicosis is a special form of the disease (a rapidly progressing process that develops after inhalation of finely dispersed silicon particles in very high concentrations).

Treatment of pneumoconiosis

An important aspect in the treatment of pneumoconiosis is the elimination of the harmful factor that caused the development of the disease. Treatment of pneumoconiosis consists of slowing down or completely stopping the progression of the pathological condition, reducing the activity of the process, reducing clinical symptoms and preventing the development of complications.

Significant importance is attached to the nutritional regime, which must be enriched with protein products and vitamins. In order to increase the body's resistance to infection, it is necessary to increase immune protection. For this purpose, it is recommended to take immunomodulators of plant origin (echinacea, Chinese magnolia vine).

Treatment of pneumoconiosis must necessarily include health and hardening procedures, for example, therapeutic exercise, massage, various types of showers - Charcot, circular.

Uncomplicated pneumoconiosis responds well to treatment using ultrasound, electrophoresis with calcium and novocaine on the chest.

To improve expectoration, bronchodilators and expectorants are used to reduce the viscosity of bronchial secretions and activate the mucociliary apparatus. In addition, it is advisable to use inhalations with bronchodilators and proteolytic enzymes, as well as oxygen therapy (HBO, oxygen inhalations).

A preventive course to prevent the progression of pneumoconiosis is carried out twice a year in a hospital or sanatorium. In case of complicated course of the disease, additional use of hormonal drugs is required to reduce the severity of the inflammatory reaction and for antiproliferative purposes.

As respiratory and cardiac failure increases, it is advisable to use diuretics, bronchodilators, cardiac glycosides and anticoagulants that affect blood clotting.

Prevention of pneumoconiosis

Specific prevention of pneumoconiosis consists of upgrading equipment at the production site to reduce the time a person spends in contact with the damaging factor. In addition, a set of measures should be developed to improve working conditions and ensure industrial safety.

Individual protection means using dust respirators, glasses and special clothing. It is also necessary to take care of collective protection in the form of supply and exhaust ventilation, ventilation and humidification of premises in production.

Prevention of pneumoconiosis requires mandatory regular preventive examination of people who are constantly in contact with the harmful factor. In addition, before employment in production, it is necessary to undergo a medical examination for contraindications.

They include the following diseases: allergic pathology, chronic bronchial diseases, deviated nasal septum, chronic dermatoses, as well as congenital anomalies of the cardiac and respiratory systems.

Pneumoconiosis is an occupational pathology caused by industrial dust. Depending on working conditions and length of service, the degree of damage to the lung tissue may vary. Despite this, some types of pneumoconiosis are still treatable, but only if the harmful factor is eliminated.