Lecture 2.

OCCUPATIONAL DISEASES
RESPIRATORY ORGANS
The main industries associated with the formation of industrial dust.
Many industries are associated with dust formation. Mineral dust of rocks occurs during the
construction of tunnels, mines, mining, production of cement and other building materials.
Dust from metal particles and their oxides accompanies the production and processing of
metals.
Organic dust arises from the production and processing of plastics, storage and industrial
processing of agricultural products.
Types of industrial dust that cause dust lung disease.
Dust arising in the process of industrial production is differentiated into inorganic, organic,
mixed.
Dust lung disease
Occupational lung diseases caused by harmful effects of dust include pneumoconiosis,
byssinosis, and chronic occupational dust bronchitis. Professional bronchial asthma arising from
inhalation of allergenic dust, in accordance with the approved List of occupational diseases,
belongs to the group of allergic diseases.
The value of the physical and chemical properties of various
types of dust and associated adverse factors of the working environment. Dust inhaled by a
person can penetrate into the respiratory paths to different depths depending on the size of
the dust particles. Large particles, the size of which exceeds 20 microns, are deposited on the
mucous membrane of the upper respiratory tract, large bronchi. Dust about 10 µm in size can
settle on the surface of medium and small bronchi. If the size of the dust particles is not
exceeds 5-7 microns, they are able to reach the alveoli. However, they cannot be deposited in
normal alveoli, since the electrostatic charge of the alveolar wall creates a repulsive sip that
exceeds the force of gravity of these particles.
For the occurrence of professional dust damage to the lungs, the composition of dust particles
is of great importance, as well as the concentration of dust in the air surrounding a person. The
dust concentration in the air is measured in mg / m3. The maximum permissible concentration
(MPC) of dust depends on its pathogenicity, primarily on fibrogenicity - the ability to cause
pulmonary fibrosis. For highly fibrogenic dusts, the maximum permissible concentration is 1 mg
/ m3, for moderately fibrogenic dusts - 4-6 mg / m3, for weakly fibrogenic ones - 8-10. For plant
dust that does not have fibrogenicity, the MPC is determined the number of fibers of the
respiratory fraction (fiber length more than 5 microns, thickness less than 3 microns) in 1 m3 of
air.
The unfavorable factors of the working environment, contributing to the formation of
occupational dust diseases, include extremely high or low air temperature, dehydration.
Occupational diseases caused by dust factors are caused by safety violations at work, work on
worn out, outdated equipment, use of faulty collective (ventilation) and personal (respirators)
respiratory protection, untimely replacement of air filtering elements in dust protection
equipment.

Classification of pneumoconiosis
Pneumoconiosis is the general name for chronic occupational diseases with respiratory damage
caused by prolonged exposure to industrial dust, which leads to
the occurrence of fibrosing lesions of the lungs, pulmonary insufficiency.
There are 6 main groups of pneumoconiosis, depending on the composition of the dust that
caused the occupational disease:
1. Silicosis - from inhalation of dust containing free silicon dioxide (silica dust).
2. Silicatosis - from inhalation of silicon hydroxide dust (silica tov):
• Asbestosis - from inhalation of asbestos dust;
• Apatigoz - from inhalation of apatite dust;
• Talcosis - from inhalation of talcum dust;
3. Carboconiosis - from inhalation of dust containing free carbon:
• Anthracosis - from the inhalation of coal dust.
• Graph igos - from inhalation of graphite dust.
4. Metalloconioses - from inhalation of dust containing metals and their water-insoluble salts:
• Siderosis - from inhalation of iron dust;
• Aluminosis - from inhalation of aluminum dust.
• Barigosis - from inhalation of dust from barium compounds.
• Manganoconiosis - from inhalation of manganese dust.
5. Mixed - from inhalation of multicomponent inorganic dust:
• Sverosilicosis - from inhalation of dust containing free silicon dioxide and iron;
• Silicoangracosis - from inhalation of dust containing free silicon dioxide and carbon.
• Pneumoconiosis of electric welders.
6. Developing from inhalation of organic dust:
• Amylosis - from inhalation of flour dust.
• Tobacco - from inhalation of tobacco dust.
• Farmer's lung - from inhalation of hay dust, straw containing fungi.
Silicosis
Silicosis is a pneumoconiosis caused by inhalation of dust containing more than 10% of highly
fibrogenic microcrystals of silicon dioxide, with the formation of interstitial and nodular
pulmonary fibrosis, impairment of the ventilation function of the lungs, predominantly of a
restrictive type.
Theories of the pathogenesis of silicosis:
Dust particles ranging in size from 7-10 microns and more are deposited on the bronchial
mucosa. Dust grains less than 5-7 microns in size sweep to penetrate into the alveoli. But in the
absence of obstacles to the movement of air through the small bronchi, they leave from there.
Surface active polarized substances - surfactants, create an electric charge that prevents the
deposition of small particles that have penetrated into the alveoli, including bacteria and fungi.
When working in dusty conditions, regardless of the type of dust, endobronchitis necessarily
occurs. With a long course of endobronchitis, the ciliated epithelium of the bronchi atrophies.
The drainage function of the bronchial mucosa is impaired. Periodically occurring obstruction of
small bronchi cause microatelectasis, providing contact of the walls of collapsed alveoli with
small particles of silicon dioxide. Dust microparticles from the surface of collapsed alveoli are
captured by alveolar macrophages and with their help are transported to the lymphatic
capillaries of interstitial tissue of the lungs. , have the ability to chemically combine with
proteins through sipone groups. Protein-silicon structures are perceived by the immune system
as foreign antigens. However, the enzymatic systems of macrophages that have absorbed such
antigens are unable to destroy silicon dioxide crystals in either early neutral or late acidic
phagoluosomes. In this, there is a certain similarity between acid-fast silicon dioxide crystals
and acid-fast Mycobacterium tuberculosis. Macrophages, unable to degrade phagocytosed
crystals of silicon dioxide, destroy themselves by autophagy, and particles of silicon dioxide are
again phagocytosed by other macrophages, which also die, being unable to destroy them.
Release of proinflammatory cytokines by activated macrophages, autoangigesh from the
cytosol of destroyed macrophages attracts cells to these places other cells of the mesenchymal
line (monocytes, macrophages). Around the focus of the presence of silicon dioxide crystals, a
circle of local cells (monocytes, granulocytes) forms a protective immune barrier - granuloma.
Morphologically, it practically does not differ from the granulema formed by the mycobacteria
of tuberculosis that invaded the tissue. Inflammatory mediators released at the site of the
granuloma activate the processes of fibrogenesis, as a result of which the granuloma is
subsequently replaced by fibrous tissue. Granuloma-fibrous foci give a characteristic X-ray
picture of nodular lesions of the lungs. The type of granulomatous reaction depends on the
ingestion of the dust. Inhalation of highly fibrogenic dust containing more than 10% free silicon
dioxide, the granuloma consists of mainly from macrophages. When exposed to dust with toxic
and coallergic properties, granulomas are formed from epigelioid cells.
Thus, the ingress of silicon dioxide crystals into the interstitial lung tissue is a triggering factor
that stimulates the processes of inhalant or focal fibrosis of the lung tissue. It is in connection
with the autoimmune nature of the inflammatory process in patients with silicosis that there is
not ezzobron chit, which is more characteristic of weakly fibrogenic pneumoconiosis, but
mainly peribronchig with granulomatous inflammation of the interstitial tissue surrounding the
bronchi. In connection with the blockade of lymphatic capillaries, matrix-forming and fibrocytes
(they surround themselves with a kind of matrix - fibrin clots, protecting them from the
proapoptotic effect of the passage of needle cytokines, primarily from tumor necrosis factor-
alpha) pleural lesions are one of the typical complications of silicosis.
Clinic and diagnostics
When working in an extremely high concentration of silicon dioxide dust in the inhaled air,
"acute" silicosis can form during the year. It is characterized by a stubbornly progressing
current, rapid formation of massive fibrosis of the lungs. Currently, due to the improvement of
industrial safety and, for this reason, the lack of conditions for its occurrence, this variant of
silicosis does not occur. Silicosis can proceed in the following forms:
- Rapidly progressive silicosis. The clinical course is close to "acute" silicosis. It develops 3-5
years after the onset of contact with silicon dioxide dust. Transitions from the initial to the next
stages of the disease occur in 2-3 years.
- Slowly progressive silicosis. It develops with prolonged, for 10-12 years, inhalation of dust with
a relatively low content of silicon dioxide. In the initial stages, it is usually clinically latent.
Transitions between the stages of the disease last 5-10 years.
- Late silicosis. It occurs several years after the termination of contact with silicon containing
dust. It is characterized by progressive fibrosing lung damage, respiratory failure.
There are three stages in the clinical development of silicosis:
Stage I silicosis corresponds to diffuse sclerotic changes in the lungs. At this stage, clinical
manifestations are very scarce. Patients may complain of a rare dry cough, chest pain,
shortness of breath on exertion.
Objective research may not reveal anything. Only in some cases, with percussion of the chest, it
is possible to detect expansion of the roots of the lungs, harsh breathing.
Stage II of silicosis corresponds to the nodular form of the disease. At this stage, inspiratory
dyspnea becomes noticeable in patients. Disturbed by dry cough, chest pain. Objective data are
usually the same as in stage I sily goat. Sometimes a pleural friction noise can be heard. A box-
shaped percussion tone may appear above the inferior lateral regions of the lungs.
Stage III silicosis corresponds to massive, large nodular fibrosis of the lungs. Despite the gross
changes in the lungs, the general well-being of patients at this stage of the disease can remain
relatively good. The main concern is shortness of breath with difficult inhalation, less often -
inhalation and exhalation, dry or low-productivity cough with pain in the chest. The increase in
the severity of the clinical manifestations of the disease is usually associated with
decompensation
chronic pulmonary heart disease. In such cases, peripheral edema appears, the liver enlarges,
and ascites occurs. On objective examination over all fields of the lungs, percussion sound with
a box shade, pleural friction noise, unsonic crepitations, indicating the formation of widespread
emphysema, dry pleurisy, pneumosclerosis. The boundaries of the heart expand.
Complications
Typical complications of silicosis are:
• pulmonary tuberculosis (silicotuberculosis%
• silicoarthrig (Kaplan's syndrome);
• scleroderma;
• chronic dusty bronchitis;
• pulmonary emphysema;
• pleurisy;
• bronchial asthma;
• cor pulmonale;
• spontaneous pneumothorax.
Silicoarthritis or Kaplan's syndrome is a combination of most often interstitial or nodular
silicosis with rheumatoid arthritis. Quite often, with sypicoargriga in the peripheral parts of the
lungs, rounded infiltrative formations with sizes from 0.5 to 2 cm in diameter are revealed. Joint
lesions do not differ from those arising in classic rheumatoid arthritis. Arthritis begins with a
symmetrical bilateral lesion
small joints of the hands. Less often, the pathological process begins with a symmetrical lesion
of other joints. Patients are worried about morning or persistent stiffness, arthralgia, swelling,
limited mobility of the affected joints. X-ray images reveal the usurs of the articular surfaces -
typical for rheumatoid arthritis signs of erosive ankylosing lesions of the joints.
Silicatoses
Silicatoses are pneumoconiosis resulting from inhalation weakly fibrogenic silica dust containing
less than 10% free dioxide silicon. The main component of such dusts is silicon hydroxide and its
compounds - silicates. Natural silicates are minerals asbestos, talc, nephilin, kaolin, mica,
olivine. Artificial silicates are glass and cement. Silicates are widely used in industry. Therefore,
silicatoses are one of the most common dust occupational diseases of the lungs. They are
characterized by slowly progressive and, therefore, usually mild fibrosis, rarely leading to fatal
decompensation of lung function. The aggravation of the condition of patients with
occupational silicosis is facilitated by
the appearance of obstructive dust bronchitis, pulmonary emphysema. The most common
silicosis are asbestosis and talcosis.
Abestosis
The disease is caused by inhalation of asbestos dust, a natural mineral of the fibrous structure.
In industry, chrysotile asbestos is used as a heat resistant insulating material, consisting of a
complex compound of silicic acid with salts of magnesium, aluminum, iron. This mineral usually
contains a small amount of free silicon dioxide. In addition to its moderate fibrogenic effect,
asbestos dust has a pronounced irritant effect on the respiratory tract. Asbestosis is
characterized by changes in the lungs in the form of diffuse fibrosis with the involvement of
peribronchial, perivascular interstitial tissue, interlobular and alveolar septa. lungs are formed
asbestos little bodies. Numerous pleural adhesions occur. A large number of asbestos particles
accumulate in the compacted bifurcation and hilar lymph nodes.
dust brought here by macrophages through the lymphatic capillaries. In asbestosis, the nodules
typical of highly fibrogenic silicosis do not develop in the lungs. Unlike other pneumoconissocks,
asbestosis, bronchiectasis is very often formed. Asbestosis can
cause the formation of squamous cell carcinoma from the epithelium of the mucous membrane
of small bronchi.
The clinical picture of asbestosis is formed from the symptoms of chronic dusty bronchitis and
pneumofibrosis. The sputum contains asbestos fibers and bodies. In histological preparations of
lung tissue, asbestos bodies are also found - linear microstructures with thickened ends in the
form of weights, drumsticks - modified particles of asbestos fibers exposed to the action of
immune factors. Asbestos grooves can appear on the skin - an inflammatory-proliferative
reaction to the introduction of asbestos fibers into the epidermis.
Diagnostics
The diagnosis of asbestosis is based on the following circumstances:
• Professionals route confirming long-term work in industries related to the extraction,
processing, use in the production of asbestos mineral.
• The results of a hygienic examination, indicating that the maximum permissible concentration
of asbestos dust in the air at the workplace of the sick person has been exceeded.
• Typical clinical manifestations and diseases.
• Detection of asbestos fibers and bodies in sputum.
• The results of the study of the function of external respiration, X-ray diffraction, ECG and
other methods, confirming the presence in the patient of changes in the structure of the lungs,
respiratory failure, signs of pulmonary heart disease characteristic of asbestosis.
Talcosis is caused by long-term inhalation of talcum powder. Talc is a magnesian silicate. It is
widely used in rubber, paper, electrical industry, in medicine as a component of powders.
Talcum dust contains very little free silica and is therefore weakly fibrogenic, causing only
benign forms of the clinical course of pneumoconiosis. The disease is formed when very long, at
least 15-20 years of work experience in dusty conditions. Talcosis is usually associated with
chronic dusty bronchitis and pulmonary emphysema, which are usually less pronounced,
according to compared with asbestosis. Talcum powder causes interstitial perivascular and
peribronchial interalveolar sclerosis in the form of miliary areas. In places of pneumosclerosis,
accumulations of talc dust particles, macrophages with the inclusion of talc fibrous structures in
cytoplasm (occurs when dust is inhaled, a fibrous variety of talc - thermolite).
Pneumoconiosis caused by talc dust usually proceeds in a benign form, most often it is limited
to stage I of the disease, less often to stage II. Talcosis stage III reaches extremely rarely.
This usually occurs when mixed dust containing, in addition to talc, free silica is inhaled.
At stage I of talcosis, patients rarely complain of poor health. Only in some cases are slight
shortness of breath during physical activity, dry unproductive
cough, minor chest pain. When percussion over the lungs, a box-shaped sound is determined.
Harsh breathing, intermittent, scattered dry wheezing are heard. On
radiographs moderate expansion, compaction of the roots of the lungs. The pulmonary pattern
is enhanced. The walls of the bronchi are thickened. In some places, vascular shadows have a
distinct shape. Diffuse interstitial fibrosis is determined, against which in the middle and
in the lower parts of the lungs, a few nodules with a diameter of 1-2 mm are visible. Patients
with stage II of talcosis complain of a deterioration in general health, shortness of breath on
exertion, dry cough, chest pain. They start to lose weight. With physical examination over
the lower parts of the lungs can hear a pleural friction noise, dry wheezing. Radiographically
revealed expansion, deformation, compaction of the roots of the lungs, diffuse inerstitial
fibrosis in combination with multiple nodularformations.
Anthracosis
Anthracosis is a pneumoconiosis resulting from the inhalation of weakly fibrogenic dust
containing mainly carbon particles (coal, graphite, soot). It is found in workers in the coal
mining industry, in the production of graphite, coal electrodes, and in coke plants. Anthracosis
is characterized by the accumulation of coal dust in the lung tissue, which causes the
characteristic black coloration of the lung. In places where coal dust is concentrated,
macrophages congregateThe severity of pulmonary fibrosis in anthracosis directly depends on
the presence of highly fibrogenic silicon dioxide impurities in the carbon dust.
In the presence of more than 10% silicon dioxide in the dust, another, less favorable
pneumoconiosis, angracosilicosis, arises.
Anthracosis usually develops after 10-12 years of constant work in conditions of high carbon
dust content in the environment air.
Clinic
Anthracosis is a relatively clinically favorable pneumoconiosis. His clinical picture is largely
determine concomitant chronic dust bronchitis, emphysema lungs. It is for this reason that the
leading symptoms of anthracosis are shortness of breath, dry cough with discharge of dark,
even black
sputum. An objective examination reveals the symptoms of the lungs (percussion sound with a
box-shaped oplogen), chronic obstructive bronchitis (harsh breathing, dry wheezing).
Diagnostics
The diagnosis of anthracosis can be proven in the following circumstances:
• professional route confirms the fact of many years
the patient's work in the coal mining industry, on
enterprises associated with the processing and use in
production of coal, graphite;
• the results of the hygienic examination of the patient's workplace reveal the excess of the
maximum permissible concentration of coal dust;
• there are clinical manifestations of the disease characteristic of anthracosis;
• in the sputum, a large number of particles of coal
dust;
• X-ray results, confirm the presence of the patient
changes in the structure of the lungs characteristic of anthracosis.

Metalloconioses
Metalloconiosis - diseases of the respiratory system caused by
prolonged inhalation of weakly fibrogenic dust of various metals
and their water-insoluble salts. Dust of non-ferrous metals and their compounds can have a
pronounced toxic-allergic effect.
In accordance with the metal present in the dust, which caused the formation of
metalloconiosis, there are:
• siderosis - from inhalation of iron dust;
• Beryllium - from inhalation of beryllium dust.
• aluminosis - from inhalation of aluminum dust.
• barigosis — from inhalation of barium dust.
• manganoconiosis — from inhalation of manganese dust.

Siderosis is pneumoconiosis arising from the inhalation of weakly fibrous iron dust and its
insoluble salts. This occupational disease occurs among workers at blast furnaces and steel-
making furnaces, in sintering factories.
Features of the clinical picture
Siderosis is a relatively benign disease. The clinical manifestations of this disease are poorly
expressed.
Usually there are no complaints, there are no objective symptoms of damage
respiratory organs, respiratory failure. Sputum may contain iron particles. X-ray examination
lungs in patients with siderosis, diffuse, mild peribronchial and perivascular fibrosis, scattered
on all pulmonary fields are small, with clear, uneven contours
X-ray congruous foci of accumulation of iron particles.
Diagnostics
In favor of hemosiderosis is evidenced by:
• professional route, confirming the fact of many years of work of the patient at steel works
and sintering 76
milling factories, in other industries, the technological processes of which are associated with
the formation of iron containing dust;
• the results of a hygienic examination of the patient's workplace, which revealed an excess of
the maximum permissible concentrations of metal dust;
• minimal clinical manifestations of the disease characteristic of anthracosis;
• a large amount of a particle of iron-containing dust is detected in the sputum;
• X-ray results revealing changes in the lung structure characteristic of siderosis in the patient.

Beryllium disease is a toxic-allergic pneumoconiosis caused by

an agent that does not have fibrogenic activity - dust or aerosols of the rare earth metal
beryllium or its compounds.
Beryllium is a part of precious stones (beryl,
emeralds, aquamarine, etc.), is widely used in the form of alloys with other metals in industry.
The amount of beryllium mined is growing all the time. Accordingly, the number of people in
contact with this metal, potentially capable of contracting beryllium disease, is also growing.
Beryllium most often enters the body through the respiratory system in the form of vapors,
dust, and aerosols. Less commonly, it can enter through the digestive tract, penetrate by
diffusion through intact skin. About 50% of the beryllium ingested by the body is excreted
through the kidneys and intestines. 25% is deposited in lung tissues,
liver, kidney, and another 25% are fixed in the bones, replacing magnesium there. Beryllium is
most firmly and lastingly fixed in bones and lung tissue.
Unlike other pneumoconiosis, beryllium disease develops upon inhalation of minimal
concentrations of aerosols containing metallic beryllium or its compounds. The maximum
permissible concentration of beryllium in the ambient air is 0.001 mg / m3. For the formation of
beryl lyose, even a short contact, within a few minutes, with minimal beryllium concentrations
is sufficient.
Clinical picture
The disease can occur in acute and chronic forms.
The acute form of Bershliov, when metal aerosols enter through the respiratory tract, is
manifested by a number of rather characteristic syndromes:
• acute tracheobronchig. It is caused by the irritating effect of beryllium vapors and aerosols. It
manifests itself as a dry cough, shortness of breath, chest pains, aggravated by coughing.
Revealed hyperemia of the mucous membranes of the upper respiratory tract. X-ray diffraction
reveals an increase in the pulmonary pattern;
• acute broncho-bronchiolitis and / or toxic pneumonig. It is characterized by a severe general
condition with fever, chills, shortness of breath, paroxysmal unproductive cough,
thoracalgia. Auscultatory in the lungs of crepitus, moist
wheezing. Conjunctivitis, dermatitis, cutaneous erythema may occur at the same time.
Clinical manifestations of acute beryllium intoxication persist for 2-3 months. The lethal
outcome did not occur at 2-3 weeks, the disease enters the resolution phase with subsequent
recovery. With repeated contact with beryllium, relapses of acute beryllium are possible.
The chronic form of berialiov is formed after 1-2 years from the moment of the first contacts
with this metal. The disease begins with shortness of breath, which progresses rapidly,
becomes painful,
accompanied by bouts of dry cough, suffocation. Disturbed by chest pains. Recurrent fever
appears.
An objective examination reveals diffuse warm cyanosis. The terminal phalanges of the fingers
have the form of "drum sticks", the nails - "watch glasses". In the lungs, over all the fields,
unsonic crepitations are heard, similar to the "crackling of cellophane", dry and
moist fine bubbling rales. The borders of the heart are expanded, the tones are muffled. On
auscultation, the accent II tone above the pulmonary artery is determined. With the further
development of the disease,
signs of pulmonary heart decompensation: hepatomegapia, ascites, edema.
Diagnostics
Diagnosis of beryllium disease includes a number of the following mandatory steps:
• Study of a professional route to confirm the fact of the patient's work in industries related to
the production and processing of beryllium and its compounds.
• The results of a hygienic examination of the patient's workplace, in order to identify possible
ways of contact of the patient with
beryllium in connection with possible violations of technological processes and safety
measures, determination of the concentration of beryllium aerosols in the ambient air.
• Clinical manifestations characteristic of beryllium disease
diseases.
• Positive results of cutaneous drip and application tests with beryllium sulfate.
• Results of radiography, other instrumental studies, confirming the presence of the patient's
characteristic
for beryllium disease, changes in the structure of the lungs, respiratory failure, cor pulmonale.
PNEUMOCONIOSIS FROM MIXED DUST
Pneumoconiosis from mixed dusts is one of the most widespread. Depending on the amount of
free silicon dioxide contained in the replaced dust, its fibrogenic activity changes. The presence
in the mixed dust of a large amount of silicon dioxide, toxic-allergenic components (beryllium)
can significantly aggravate the severity of the clinical manifestations of the disease.
Vits of pneumoconiosis from mixed dust
The most common pneumoconiosis caused by mixed dust includes:
• Svderosilicosis,
• Silicoangracosis.
• Pneumoconiosis of electric welders.
The clinical picture of siderosilicosis, sypicoangracosis with a high (more than 10%) content of
silicon dioxide in mixed dust
corresponds to the course and clinical manifestations of silicosis.
PNEUMOCONIOSIS FROM ORGANIC DUST
The presence of organic dust in industrial conditions is the cause of the formation of
hypersensitive pneumonigas,
exogenous allergic alveolitis, including "farm lung". The pathogenic components of organic dust
are finely dispersed allergenic particles of fibrous structure of plant origin, associated with
molds and other putrefactive microorganisms (thermophilic actin and ceta, some gram-
negative bacteria).
Differential diagnosis of pneumoconiosis
For the differential diagnosis of pneumoconiosis, the most important is a professional route, a
hygienic examination of the victim's workplace, allowing sufficient
pinpoint the etiology of pneumoconiosis. Clinical examination results can provide additional
information. So, with silicosis, faster than with other pneumoconiosis, appears
severe pneumofibrosis, arises and decompensates cor pulmonale. This disease is more often
than other pneumoconiosis complicated by tuberculosis. Radiographically, silicosis is
characterized by a nodular
pneumofibrosis. Asbestosis is characterized by a predominantly interstitial type of lung damage,
dusty etsdobronchitis is expressed,
cough with tenacious, difficult to discharge phlegm. This variant of pneumoconiosis is more
often than others complicated by squamous cell bronchogenic lung cancer.
Pneumoconiosis must be differentiated from tuberculosis. Unlike pneumoconiosis,
disseminated pulmonary tuberculosis
accompanied by more striking clinical manifestations in the form of fever, intoxication,
sweating, lymphadenopathy. In miliary tuberculosis and premoconiosis, there may be similar
radiological findings. However, in tuberculosis, there are usually no interstitial peribronchial
and perivascular changes,
compaction and expansion of the roots of the lungs. Unlike pneumoconitic, tuberculous foci are
localized mainly in the upper parts of the lungs. They have pronounced polymorphism,
indistinct contours, different sizes, prone to calcification. The roots of the lungs are pulled up in
tuberculosis, which is not the case with pneumoconiosis. In addition, in tuberculosis, changes in
the lungs may regress under the influence of specific antibacterial therapy.
Clinical and radiological symptoms similar to pneumoconiosis may have a mediastinal-
pulmonary form of sarcoidosis. To distinguish between diseases, it is important to identify
extrapulmonary manifestations of sarcovdosis: fever, arthritis, hemoptysis, erythema nodosum,
peripheral lymphadenopathy,
lesions of skeletal muscles, etc. In differential diagnosis, positive tuberculin tests in patients
with sarcoidosis, a quick positive effect of glucocorticoid therapy may be of importance.
Diffuse fibrosing alveolitis often has clinical and radiological manifestations similar to
pneumoconiosis. but
with fibrosing alveolitis, X-ray changes in the lungs have a fine-mesh appearance. In
pneumoconiosis, diffuse perivascular and peribronchial fibrosis is usually revealed.
When fibrosis alveolitis often occurs hypereosinophilia, which does not happen with
pneumoconiosis.
The small focal form of lung cancer is clinically and radiologically very similar to silicosis and
other pneumoconiosis. However, with pneumoconiosis, even with very pronounced X-ray
changes in the lungs, the state of health of patients can be quite satisfactory.
Treatment of pneumoconiosis.
The main task of therapeutic measures at the initial stages of the formation of pneumoconiosis
is to improve the drainage function of the bronchial epithelium caused by chronic dusty
endobronchitis, to eliminate the functional bronchospastic component. At present, intensive
efforts are being made to develop drugs that reduce the progression of fibrosis into
lungs with silicosis and other pneumoconiosis.
Glutamic acid and potassium iodide are able to increase the resistance of alveolar macrophages
to the cytotoxic effect of coal dust, preventing the progression of pneumofibrosis.
Antioxidant therapy is recommended for patients with pneumoconiosis: vitamin complex ACE,
lipostabip. In acute and rapid troprogressive course of silicosis, a course treatment is prescribed
prednisone at a dose of up to 2-30 mg per day for 1-2 months with gradual withdrawal of the
drug.