Document 85918M4n5XaDVJNOgmaXXL8Ro

to assume that the fibrosis is simply the result of the action of free silica which is present in sufficient con centration to induce proliferative cell reaction. Be cause it occurs chiefly in hard coal miners, it has been known for many years as "miner's asthma." The cardinal symptom 1b shortness of breath, fre quently associated with "productive cough. More ad vanced cases complain of weakness, chest pain, gastric disturbs: cea and hemoptysis. Sayers* states that in a U. S. Public Health Survey of anthracite miners in Pennsylvania in 1938, fever and night sweats were seldom mentioned. (This is true of silicosis cases in iron ore miners.) He notes Buch physical signs as dyspnea, prolonged expiration, change in contour of the chest, decreased chest expansion, clubbing of the fingers, change in breath sounds, altered fremitus and impaired resonance. Where infection complicated the picture, the symptoms were more marked and included cyanosis and loss of weight and strength. The pathology of anthraco-silieosis is characterized by accumulations of coal dust in the lungs associated with varying degrees of pulmonary fibrosis. The lungs are gray and firm and may show dark colored markings on the pleural surfaces. On section, areas of black pigmentation appear scattered throughout the lung fields. Coalescence of the nodules produces larger areas, particularly in the hilar regions, but many large discrete nodules appear throughout the;parenchyma. Fibrous hyperplasia can be seen along the lym phatics. Microscopic section reveals deeply pigmented areas of fibrous connective tissue with dust laden macrophages around the outer -border of the nodule. The earliest x-ray evidence of anthraco-silieosis con sists of exaggeration of the linear markings which increases with continued exposure, until the general pattern is obscured and replaced by definite nodulation. Further progress of the disease will be evidenced by more massive conglomerate shadows which may be complicated by the presence of infection. Asbestosis as an occupational disease has been rec ognized only in recent years. Forty-one deaths were reported from this cause in England up to 1934. In this country it has been estimated by Lanza that approximately 10,000 persons are exposed to asbestos dust. In a study by Dressen, Edwards and Miller10 of the U. S. Public Health Service, 541 asbestos workers were examined. No cases of asbestosis were found among workers exposed to dust concentrations below 2,500,000 particles per cubic foot of air. 'T'HE greatest occupational hazard exists in mining, handling and crushing crude asbestos, making in sulation and the carding and weaving of asbestos. In other industries such as the compounding of mate rials for automobile brake linings, the hazard is recog nized but the disease is uncommon. Asbestos is a hydrated magnesium silicate. It is the one silicate which does produce a fibrosis, but this differs pathologically and roentgenologically from the nodular reaction of silica. Industrial asbestos dust is comprised of very small fibres. Only the larger ones, over 2 microns in length, are thought to be capable of producing fibrosis. Gardner11 iB of the opinion that inhaled asbestos fibres are irritating not because they are silicates, but because they are stiff fibres which mechanically irritate the lungs. When the fibres used in animal experiments were finely ground (under 2 microns), the irritating property of asbestos practi cally disappeared. Unlike the free silicas, these miner als wilt not stimulate fibroblasts in any part of the body other than the lungs. While the action of free silica is chemical, that of asbestos is mechanical. The typical lesions, observed microscopically, show large macrophages in the distal portions of the bronchial tree, the formation of the asbestos giant cell, and the generalized fibrosis surrounding the bronchioles, alve oli, air sacs and blood vessels. This results ip oblitera tion of the lung structure. The alveoli have literally become plugged, and the function of the lung impaired mechanically. Merewether and Price1* examined 863 workers ex posed to practically pure asbestos dust In factories in Great Britain. The following table indicates their find ings as regards exposure and fibrosis. Table III. Ynti *t Work Cuts EnuLaod Showfac Fibrooi* Per C*ni 0 to 4............. ........... 89 ........... ........... 0........ ..... ____ ........... 141 ........... ...........86 ........ fu ........... ...........Ti .................... 16 to 19............ .......... 8........... ...........16..................... Z0 mad over..,, .......... ti ...... ........... 17 .................. 0.0 Aa in cases of fibrosis produced by other dusts, there is no typical symptom of asbestosis. Dyspnea is the most striking feature of the disease. The onset is grad ual, and the symptoms increase as the condition ad vances. Cough, expectoration, cyanosis, loss of weight, and emaciation are late occurrences probably associ ated with infection. A feature of asbestosis is the occurrence of -so- called asbestos bodies. Cook1* states that "the `curious bodies' so characteristic of pulmonary asbestosis are found in the alveoli and bronchioles and in the fibrous and necrotic areas. They measure 20 to 100 microns in length. One or both ends are bulbous, giving a clubbed or dumb-bell appearance. The shafts are either homogeneous or segmented crosswise. They are golden yellow to brownish in color. They do not stain but give a Prussian blue reaction to iron. From a diagnostic standpoint, it is generally agreed that the 'curious bodies* signify exposure to asbestos dust but cannot be depended upon for a diagnosis of asbestosis." Ap parently the asbestos body is formed from the original fibre by a tissue reaction, the nature of which is still obscure. The fact that segmented figures are not found in crude asbestos or asbestos dust indicates that they are formed only after the fibres have come in contact with living tissue.. Another interesting skin lesion found in this dis ease is the "asbestos corn" due to the penetration of fibres into the superficial layers of the skin. To establish a diagnosis, a history of exposure to asbestos dust is essential. The length of this exposure is important and should be correlated with the chest roentgenogram in which the "ground glass appear ance" is characteristic. The lesions are limited to the lower halves of the lungs and there is hyperventilation in the upper portions. The cardiac outline becomes blurred and the domes of the diaphragm obliterated. The appearance of the heart and lower chest may sug gest cardiac disease which should be definitely ruled out in a worker in an asbestos plant before diagnosing his condition as asbestosis. The diagnosis of asbestosis from the x-ray is not an easy matter, but the follow ing features are fairly characteristic: 1. Lesions basal in character. 2. Hyperventilation in upper lobes. 3. Blurred cardiac outline. 4. Obliteration of the diaphragm, 5. No nodulation. 6. "Ground glass" appearance. 7. May be unilateral. The occupational hazard of asbestos is not par ticularly significant. Its recognition as a clinical entity , SPNY 000230