PNEUMOCONIOSIS

1. PNEUMOCONIOSIS Conf. Dr. Brandusa Constantin

2. Definition: "Pneumoconiosis is the accumulation of mineral dust in the lung and the tissue reaction to its presence". Classification • Collagenous pneumoconiosis is characterized by: - permanent alteration or destruction of alveolar architecture - collagenousstromal reaction of moderate to maximal degree - permanent scarring of lung. • Examples: silicosis, asbestosis.

3. Complicated coalworkers' pneumoconiosis or progressive massive fibrosis (PMF) is an altered tissue response to a relatively non-fibrogenic dust. • Non-collagenouspneumoconiosis is caused by a non fibrogenic dust ("inert" dust) and has the following characteristics: - the alveolar architecture remains intact - the stromal reaction is minimal and consists mainly of reticulin fibres - the lesion is potentially reversible examples are those caused by pure dusts of barium sulphate (barytosis), kaolinite, titanium dioxide, ferric oxide, glass; - iron dust if inhaled in sufficient quantities can lead to pneumoconiosis - known as siderosis. The disease is seen in metal polishes, arc-welders, but above all among iron mines. In some iron mines, the presence of free silica leads to mixed-dust pneumoconiosis. Siderosis is observed after long exposure 15-25 years. The radiological appearance of siderosis is discrete, we may find punctiform images, rarely micronodular and never macronodular or pseudotumoral after exposure has ceased, the images are seen to precede somewhat in the course of the years.

4. SILICOSIS • Silicosis is a pulmonary fibrosis caused by the inhalation of dust containing free silica. • It is the most common and severe of all pneumoconiosis. • Silicosis remains a difficult problem for the entire world.

5. Etiology • Silicosis is caused by the inhalation of free crystalline silica (SiO2). • In nature, free silica is found in a variety of forms, the most important and widespread being quartz. Even in its normal state quartz is highly silicogenic but, when heated to temperatures in excess of 100o C it is converted to, its allotropic forms, trydimite and cristobalit, which are even more pathogenic.

6. The silicosis hazard is encountered in a wide variety of occupations: • underground mining and tunneling in quartz-bearing rock • extraction and cutting of quartzite, granite and slate • manufacture of refractory materials and silicous abrasives • foundry operations: sand preparation, knocking-out, fettling and sand-blasting).

7. The level of risk depends on 3 factors: - concentration of dust in the atmosphere - the percentage of free silica in the dust - the exposure time. The dangerous free silica particles are those with a diameter of less than 3 m called "respirable fraction". • The retention maximal in the alveoli is for particles with a diameter of 1-2 m; the retention break down for particles of less than 1 m and it is null for particles of 0.3-0.5 m that have a Brownian movement. For smaller particles of less than 025 m, the retention grows and become 100% through the diffusion mechanism. • The retention and absorption of free silica particles depend to the integrity of the mechanisms of elimination of dust - out of alveoli.

8. Pathogenie • Whereas the aetiology of silicosis is well defined, its pathogenesis still has to be elucidated. There are many hypothesis, but the immunological theory by Pernis and Vigliani is recognised being the best. • the free silica particles are phagocytised by the macrophages. • the death of macrophages release, arise the proliferation of fibroblasts and collagenous fibres • the plasma cells proliferation and gamma globulin synthesis. It is a specific antibody autoimmune response to tissue antigens (the rest of protein macrophages become "non self") or a heteroimmuneresponse to different antigens arrived to the interstitial with macrophages.

9. Pathology • The silicotic nodule has an unmistakable histological appearance, being rounded. The centre is composed of fibro-hyaline tissue either whorled or resembling a ball of wool, and sometimes aggregated to a homogenous form. The rim consists of a cellular halo, often clearly delimited from the hyaline centre, that contains, in varying proportions, reticular fibres, macrophages, fibroblasts and immunocytes (plasma cells and lymphocytes) at varying stages of maturity. The cellular halo may be very large, the larger the halo, the more active, that is progressive, the lesion; sclero-hyaline nodules with virtually no cell haloes can be regarded as inactive.

10. The nodules may aggregate to form round masses ranging from a few millimetres to 1 cm in diameter; in more serious cases a number of nodules coalesce or form large hyaline masses. The coalescing of several nodules is almost always caused by additional factors, of which infection, often tubercular, or rheumatoid factor seem to be the most important. • The pulmonary parenchyma between the aggregated silicotic nodules and between the silicotic masses invariably displays a high degree of emphysema.

11. Symptoms at the beginning of this century (in Romania at 1950-1960 years), fatal cases of silicosis with a rapid evolution (1-3 years) so-called "acute silicosis" were not uncommon among workers who inhaled enormous quantities of dust with a high quartz content (for example the mining Lesu-Ursului with 90-96% silica free in atmosphere). • Now, this rapidly evolving form has been replaced by slowly developing silicosis (12-15-20 years or more). But still exist the case with small exposure - 5-7years, that occurs especially in foundry. • The symptoms are untypical. • The first symptom of silicosis is dyspnoea on exertion. In serious cases, the dyspnoea occurs even on very slight exertion or when the patient is at rest. Cough with sputum is an indication of bronchitis and chronic bronchitis is frequently associated with advances silicosis.

12. Complications • Pulmonary tuberculosis is, even today, still the cause of death in a quarter of cases and is the most frequent complication. It has recently been proved that tubercle bacilli grow and multiply far more actively in macrophages that have phagocytised silica particles than in those that have not done so, perhaps because the former have suffered a loss of vitality and are no longer capable of destroying the tubercle bacilli. • Respiratory insufficiency is largely due to massive emphysematous and fibrotic changes. These are sometimes accompanied by chronic obstructive pulmonary disease resulting by the destruction of a large part of the vascular bed and spasm of the pulmonary capillaries brought about by hypoxemia. • Acute broncho-pulmonary infection is often epiphenomenal of chronic bronchitis associated with advanced silicosis.

13. Diagnosis is based on: • medical and occupational history, • clinical examination, • radiology and • respiratory tests-function. The radiographic examination must be carried out using a suitable technique.

14. Differential diagnosis • Tuberculosis especially in its disseminated miliary form. • Endogenous hemosiderosisdue to mitral stenosis • Boeck'ssarcoidosis, especially in nodular form. • Some forms of pulmonary metastasis of carcinoma • Idiopathic interstitial pulmonary fibrosis (seaman Rich type) • Some collagen diseases (scleroderma rheumatoid arthritis).

15. The radiographs are classified in 4 level of quality: 1. Good; 2. Acceptable; 3. Mediocre; 4. Unacceptable. • It is accompanied by a new set of 22 standard radiographs selected after international trials. It is mandatory to read the film comparatively with standard films. The short classification • - film quality • - small opacities rounded Profusion. Category • 0 - absent • 1 - small opacities present, but relatively few in number • 2 - small opacities - numerous • 3 - small opacities - very numerous Type: • p - rounded opacities up to about 1.5 mm diameter • q - rounded opacities exceeding about 1.4 mm and up to about 3 mm diameter • r - rounded opacities exceeding about 3 mm and up to about 10 mm diameter

16. Small opacities irregular • Profusion. Category: 1, 2, 3 • Type: • s - fine irregular or linear opacities • t - medium irregular opacities • u - coarse (blotchy) opacities Large opacities • A - an opacity with greatest diameter between 1 cm and 5 cm or several such opacities the sum of whose greatest diameters does not exceed 5 cm • B - one or more larger or more numerous than thosse in category A, whose combined area does not exceed one-third of the area of the right lung • C - one or more large third of the area of the right lung

17. Obligatory symbols • Plc - pleural calcification • pl - pleural thickening • ax - suspect coalescence of small rounded opacities • bu - bullae • ca - suspect cancer of lung or pleura • cn - calcification in small opacities • co - abnormality of cardiac size of shape • cp - suspect COPD • cv - cavity • di - marked distortion of the intrathoracic organs • ef - epanchement pleural • em - marked emphysema • es - eggshell calcifications • fr - fracture of rim fracture • tu - marked enlargement of hilar shadows • ho - honey comb lung • id - diaphragm ill defined • kl - Kerley line • od - other significant disease • pi - pleural thickening of interlobarescissure of mediastin • px - pneumothorax • rp - rheumatoid pneumoconiosis • tb - tuberculosis

18. The stages in silicosis: • I 1p, 1q, 1r stage • I/II 2p, 2q, 2r stage • II 3p, 3q, 3r stage • II/III 3p, 3q, 3r ax • III A, B, C

19. Treatment • Etiologic: interruption of the occupational exposure to free crystalline SiO2 • Pathogenic: it does not exist because the ethiopathogenical mechanism is not known

20. Symptomatic: • bronchodilators; • expectorants; • respiratory gymnastics; • respiratory infection prevention; • chemoprophylaxis with HIN: 15 mg/body,6 months. • Silico-tuberculosis treatment lasts at least 3 years. • Complications (silico-tuberculosis, chronic obstructive pulmonary disease) treatment • Aerosols • Vitamins