SILICOSIS (silicosis; lat. silex, silicis flint + - osis) — the disease of lungs developing at inhalation of the dust containing free silicon dioxide. The page represents the most widespread and heavy look pneumoconiosis (see), practically is always an occupational disease.
people were ill S. still in the ancient time. The silikotichesky changes in lungs found at a research of the Egyptian mummies which perhaps served as a cause of death testify to it. Long time of S. was identified with tuberculosis, calling by its tuberculosis scabblers or miners, and only by the end of 19 century idea of S. as the independent disease of lungs caused by inhalation of dust forms. The term «silicosis» was offered in 1870 to Visconti.
Gained the greatest distribution of S. in the end 19 and in 20 century of hl. obr. in connection with development of ore mining and mechanical engineering industry. According to researchers of a number of the countries, S.'s incidence in the mentioned industries continued to remain high up to the 60th years of the current century. So, in England in 1955 the number of the patients who received pension in connection with S.'s disease made apprx. 40 thousand. Approximately as much patients in the same years it was registered in the USA and Germany. And only in the last decades S.'s incidence in the advanced countries decreased. In the Soviet Union in connection with carrying out systematic preventive measures the indicator of incidence of S. constantly decreased, in recent years at many enterprises new cases of diseases do not come to light.
S. develops at inhalation of the dust containing free silicon dioxide (Si02), a thicket at workers of ore mining industry (drillers, drifters, coalminers, timberers, blasters, etc.), machine-building (sandblasters, blaster operators, obrubshchik, etc.), by production of refractories, grind of sand, a driving of tunnels, processing of granite. In the nature dioxide silicon (see) meets in three crystal versions more often — in the form of quartz, tridymite, cristobalite. As a rule, the disease results from influence of dust of quartz and is very rare — aerosols of condensation (see. Aerosols ) silicon dioxides, possessing considerably smaller fibrogenny action.
S.'s incidence is in direct dependence on quantity, disperse composition of the inhaled dust and content of quartz in it. Particles from 0,5 to 5 microns in size possess the most fibrogenny action.
Maximum allowable concentration of the dust containing more than 70% of crystal silicon dioxide — 1 mg/m3, from 10 to 70% — 2 mg/m3, from 2 to 10% — 4 mg/m3; Maximum allowable concentration of the dust containing more than 70% of amorphous silicon dioxide — 1 mg/m3, from 10 to 70% — 2 mg/m3. In former years the disease usually developed under unfavorable conditions of work in the first
5 — 10 years of work.
the Pathogeny in many respects is still not clear. It is established that S.'s development is impossible without phagocytosis (see) quartz motes macrophages (see), to-rye as a result of absorption of quartz crystals perish. Phagocytosis of dust particles is necessary premises of developing of a disease. However there are not clear causes of death of the macrophages who absorbed dust particles (coniophages), and the fibrosis developing in the subsequent. On sovr. to representations, on a coniophage difficult biochemical, enzymatic and electronic and exchange mechanisms are the cornerstone of cytotoxic action of a quartz particle. Damage of a coniophage is connected at the same time with emergence on fracture surface of quartz of the hydroxylic groups creating active centers of a crystal lattice. Change of electronic structure and electronic potential, in turn, can lead to free radical activity (see. Radicals free ) and to change of structural components of cellular membranes. On a nek-eye to data, from the perishing macrophages the certain, yet not known fibrogenny factor stimulating a fibrogenesis and a kollage-noobrazovaniye can be allocated. Along with it there are facts testimonial of the fact that take part in S.'s pathogeny also immunopathological, including autoimmune, mechanisms. A certain part is assigned to the individual predisposition which is perhaps connected with genetic features of an organism, including and immunological homeostasis.
The pathological anatomy
S. is characterized by development of the specific progressing kletochnopylevy and fibrous silikotiches-ky small knots in easy and regional limf, nodes against the background of diffusion intersticial changes, is more rare in upper airways, a trachea, bronchial tubes, is exclusively rare in other bodies. The Silikotichesky small knot at the beginning of process differs in a concentric or vorticose arrangement argyrophil, further the dense hyalinized collagenic fibers which are completely forcing out coniophages. These small knots can be miliary at a diffusion form C. Groups them, merging, form in lungs large nodes of dense gray-whitish fabric (nodular, nodal and tumorous forms), sometimes with disintegration (silikotichesky cavities), sometimes with adjournment of lime in the center or for the periphery of nodes; small knots can develop also around vessels, squeezing them. On spodogramma (see) or in slantwise incident light of a dark field of a microscope in silikotichesky small knots, especially on the periphery, the shining quartz motes are found. At S., as a rule, develop an adhesive pleuritis, hron. preferential atrophic bronchitis, diffusion intersticial pneumosclerosis (see), emphysema of lungs (see). Patients perish from cardiopulmonary insufficiency at a pulmonary heart and a muscat liver or from the joined tuberculosis.
The clinical picture
In 1930 at the I International conference on a silicosis in Iokhanesburge was accepted S.'s classification considering as rentgenol. data, and wedge, symptomatology. This classification gained wide recognition in a number of the countries. In the subsequent international classifications preferential radiological (skialogichesky) symptoms of a disease are considered and detailed (character and density of blackouts on a x-ray film). In the classifications accepted in the USSR for all pneumoconiosis including for S. (1958 and 1976), were considered along with radiological a wedge, symptoms of a disease. The last and current classification provides three stages (I, II, III) and three forms C. (nodular, intersticial and nodal).
The nodular form C. (fig. 1) is characterized by existence in lungs of the small roundish accurately outlined same shadows. Depending on a phase of development of a small knot (a cellular, fibrous phase, a phase of a hyalinosis or calcification) intensity and homogeneity of nodular shadows changes. In size allocate 3 types of small knots: to 1,5 mm (r), from 1,5 to 3 mm (q), from 3 to 10 mm (r).
At an intersticial form C. strengthening and deformation of the pulmonary drawing caused by perivascular and peribronchial fibrosis are defined. On the nature of intersticial changes allocate thin lineynosetchaty changes of the pulmonary drawing (s), tyazhisty, wrong linear shadows (t), grubotyazhisty, wrong, with places cellular melkopyatnisty blackouts (u). Lineyno-tyazhistye changes are observed from two parties, have diffusion widespread character that is most expressed in average and lower parts of easy (fig. 2).
Fibrous educations are characteristic of a nodal form C. (fig. 3). In size of nodal educations distinguish small nodular — diameter of nodes from 1 to 5 cm (A), macronodular from 5 to 10 cm (V) and massive — more than 10 cm (C). Nodal educations can be one-or bilateral, roundish or irregular shape, with accurate and indistinct contours.
The I stage of a nodular form C. is characterized by existence against the background of an intersticial pneumosclerosis of a small amount of small knots (code designation: r — 1,2; q — 1; — 1), and the I stage at an intersticial form — moderate bilateral diffusion strengthening of the pulmonary drawing with visible lineynosetchaty and linearly-tyazhistymi changes (s — 1,2; t — 1,2; u — 1,2).
Rentgenol. the signs defining transition of process to the II stage are generally caused by strengthening of an intersticial and nodular pneumosclerosis. At the II stage of a nodular form the pulmonary drawing is badly differentiated, are visible numerous symmetric and evenly located small - or sredneuzelkovy shadows (r — 3; q — 3 — 3). The silicosis of the II stage at an intersticial form differs in big density of an arrangement linearly - mesh and grubotya-zhisty shadows per acre at more expressed strengthening and emergence of deformation of the pulmonary drawing (s — 3, t — 3, u — 3). At the same time in most cases also small ochazhkovo-nodular blackouts of irregular shape are defined; III, or final, nodular or intersticial S.'s stage is characterized by increase in quantity of fibrous small knots, their merge, formation of shadows of massive fibrosis (And, In, C).
Sick S., as a rule, show few complaints. Most often they note a moderate asthma, cough (dry and with a phlegm) and a stethalgia. A wedge, S.'s manifestations accrue in process of development of fibrous process in lungs, but full parallelism with rentgenol. a picture is absent. Cough and short wind at S. can be connected not only with expressiveness of fibrosis, but depend as well on degree accompanying a silicosis bronchitis (see), to-ry has preferential atrophic character. The general condition of patients long enough can remain satisfactory.
The thorax is more often than a usual form, but in process of increase of emphysema of lungs extends with increase in its perednezadny sizes. Typically rigid breath, non-constant dry rattles are sometimes listened, small-bubbling rattles and a pleural rub are more rare in lower parts. In the III stage of a silicosis sites of shortening of a percussion sound and rigid breath of a bronchial shade can be found. In process of progressing of a disease the picture can develop pulmonary heart (see).
The wedge, blood test at S. is more often without special deviations. From biochemical researches the greatest value has blood test on protein fractions; S.'s progressing can be followed by a hypergammaglobulinemia. Function of breath is more often changed unsharply, in an onset of the illness moderate obstructive disturbances are possible, on to-rye in process of progressing of process restrictive usually accumulate.
S.'s current progressing at the same time development of fibrosis occurs in different terms. Distinguish S. which is slowly progressing, remaining at one level sometimes decades (intersticial is more often); quickly progressing — an aggravation of symptoms can occur in 7 — 8 years and quicker; so-called late S. — developing many years later after the contact with dust taking place. In the past acute S.'s cases were described under especially unfavorable conditions of work when the disease developed quickly and proceeded especially zlokachestvenno. In a crust, time acute S. in our country does not meet.
S.'s Current is aggravated at accession of complications, the heaviest of to-rykh is tuberculosis. Pages, complicated by tuberculosis, call a tuberculosilicosis (see. Tuberculosis of a respiratory organs ).
Carry to S.'s complications also not often meeting acute and hron. pneumonia (see), bronchiectasias (see), bronchial asthma (see). The immune and autoimmune processes developing at the expressed forms C. can lead to emergence of systemic lesions like a pseudorheumatism (see) and other kollagenoz. Sometimes in lungs at S.'s combination to a pseudorheumatism (so-called silikoartrity) a peculiar picture — formation of multiple roundish blackouts is observed (see. Kaplana syndrome ); at the same time in blood it can be found rhematoid factor (see).
the Diagnosis the prof. of the anamnesis and data rentgenol establish on the basis a wedge, symptoms. researches, the Crimea belongs the main role in diagnosis of Page. All anatomic elements characterizing a silikotichesky pneumofibrosis are reflected in the roentgenogram of lungs. Along with it symmetric expansion and fibrous consolidation of roots of lungs, sometimes with skorlupoobrazny obyzvest-vlenrgy limf, nodes and adhesive pleural reaction is characteristic of S.
Differential diagnosis carry out with other pneumoconiosis and pulmonary diseases of other etiology which are followed by a syndrome of pulmonary dissimination. The general and prof. the anamnesis and a gigabyte are especially important for differential diagnosis of S. characteristic of working conditions. At differential diagnosis with the disseminated tuberculosis (see. Tuberculosis of a respiratory organs ), sarcoidosis (see), Hammen's syndrome — Rich (see. Hammena — Rich a syndrome ) consider features of a current of each of these forms, their clinicoradiological forms, absence of the typical prof. of the anamnesis. In the cases difficult in the diagnostic relation, it is possible to recommend a diagnostic bronkhoskopiya with a transbronchial biopsy.
Treatment shall be complex, directed to improvement of the general condition of an organism, the prevention of complications and progressing of diseases. Good nutrition with the sufficient content of vitamins, the respiratory gymnastics, treatment in sanatoria and dispensaries are shown. At early stages of S. physiotherapeutic methods are used: the ionophoresis with novocaine, Calcium chloratum, is more rare than UVCh on a thorax, ultrasound. According to indications appoint broncholitic drugs (an Euphyllinum, ephedrine, etc.), cardiacs, oxygen therapy. At the expressed immune and pathological manifestations accompanying S. careful purpose of small doses of glucocorticoids under protection of antibiotics is admissible, more rare appoint delagil, plaquenil. Now the question of a possibility of use at S. is studied of some polymeric drugs. Timely treatment of complications of a silicosis and first of all a tuberculosilicosis is important. At the same time the main method of treatment is the chemotherapy modern antitubercular drugs (see. Tuberculosis ). Surgical intervention is in some cases shown.
Examination of working capacity
Sick S. transfer to other work which is not followed by influence of dust, irritating and toxicants, and also adverse meteorological factors; hard physical work is contraindicated to them. In case of disability the prof. disability is established by the patient.
Prevention consists first of all in holding the hygienic and medical actions directed to reduction of dust formation and protection of respiratory tracts against dust (see. Pneumoconiosis, prevention ; Prevention primary ). Preliminary and periodic medical examinations are performed, groups of health and occupation will be organized to lay down. the physical culture, showed preventive wet and salt and alkaline inhalations and stay in dispensaries. For secondary prevention transfer of the patient in the working conditions excluding contact with dust is necessary.
in the absence of life-threatening complications and at transfer of the worker into production sites, free from dust, progressing of process at dominance of intersticial changes can stop, however the increased risk of development of inflammatory and specific damages of lungs remains. The nodular form C. quite often progresses also after the termination of contact of the worker with dust. Sick S. most often die of pneumonia, cardiovascular insufficiency or of tuberculosis.
Bibliography: Velichkovsky B. T. both Katsnelson B. A. Etiologiya and pathogeny of a silicosis, M., 1964, bibliogr.; Genkin S. M. Clinic of a silicosis, M., 1948, bibliogr.; P. P's cursors. Pneumoconiosis, M., 1965; K. P Prickly lettuces. Rehabilitation at a pneumoconiosis, M., 1977; Occupational diseases, under the editorship of E. M. Tareeva and A. A. Bezrodnykh, page 47, M., 1976; With e the Tax Code e in and the p N. A. Clinical forms of a silicosis and tuberculosilicosis, M., 1974.
N. A. Senkevich; Yu. P. Likhachev (stalemate. An.), E. A. Grigoryan (rents.).