Document KaMzdXazBm6QMOB1zD0mn84w

FILE NAME: Abex (ABX) DATE: 1944 Mar DOC#: ABX004 DOCUMENT DESCRIPTION: Journal Article - Industrial Dust - The Pneumoconioses il PLAINTIFF'S ex h ib it :| | a B - 6 7 ' uy y < o /x0 Industrial Dust -- The Pneumoconioses L. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago \ yM Reprinted from Industrial Medicine, March, 1944 SPNY-000227 I I Industrial Dust -- The Pneumoconioses L. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago T HE relation between dust and certain diseases of toxic and systemic effects, but usually their main con t the lungs has been recognized for centuries, but sequence is local or irritant. They do not cause pul only in recent years has it been given the intensivme onary fibrosis, but such things as dermatitis, dental study it deserves. In the fifth century b.c., Hippocrates lesions, irritations of the nasal mucous membranes, t noted symptoms in a metal digger, comparable to those and conjunctivitis are fairly common in workers han observed among present-day miners suffering from dling these materials. Digestive disturbances have silicosis. Since that time, other investigators have been observed. Allergic symptoms may occur in those recorded their impressions and observations on the exposed to pollens, horse hair, furs and wool,- and effects of inhaled dusts and have emphasized the asso various types of wood dust are known to affect suscep ciation of these with tuberculosis. It was not until the tible persons. Bacteria such as the anthrax bacillus latter part of the nineteenth century, however, that are capable of producing cutaneous lesions, or "wool real interest in the subject was manifested. sorters' disease," when inhaled. Sappington2 has listed To South Africa must be given the credit for the over 100 occupations which may produce exposure earliest serious contribution to our knowledge of the resulting in allergy, asthma, or irritation of the skin industrial dust hazard. Here, in 1902, physical exam and upper air passages. inations were made on 3000 rock drillers and for the Fungi, such as mycelia and spores of molds, are apt first time, x-rays of the chest were used in a compre to cause rashes and painful fissures of the sldn, while hensive study of 300 cases. Diagnostic standards of cotton weavers develop a form of disease known as disease, safe limits of particle' concentration in the air aspergillosis from inhaling spores of a mildew which < of working places, and engineering methods for dust occasionally occurs on threads. f control were instituted. From 1915 on, Great Britain, The inorganic dusts which have significance in I; Germany, Australia, Italy, Canada, and the United industry are derived mainly from minerals and metals. States made further investigations, but the most note In the process of grinding, crushing, blasting and worthy progress in these countries occurred during drilling these earthy substances, dust particles ranging the last few years. in size from microscopic to visible are liberated and iI Kronenberg and Morse1 have suggested the follow remain in suspension in the air for varying periods ing classification of industrial dusts: depending on their size and settling velocity. Inhala tion of those particles which contain silica in the Table I. uncombined state produces the type of pulmonary I. Organic Dusts: II. Inorganic Dusts : fibrosis known as silicosis. Gardner8 demonstrated the A. Non-Living: A. Toxic and (or) specific action of silica and made it clear that only I 1. Toxic and (or) Irritant. silica in the "free" state is capable of causing this Irritant. B. Fibrosis Producing. type of tissue reaction. B. Living: C. Non-Fibrosis Pro- The toxic inorganic dusts are those of the heavy 1. Bacteria ducing. metals and their salts, such as lead, mercury, man 2. Fungi. ganese, etc. They are usually considered under the Generally speaking, organic dusts originate from heading of industrial poisons rather than of dusts. plants or animals, but many thousands of these sub stances are made synthetically. They may produce The te x t o f Dr. H a m lin 's L ecture a t th e Second Post-G raduate Course in In d u stria l Medicine, Loner Island College o f Medicine, B rooklyn, F riday, N ovem ber 6, 1948. SPNY 000228 T N d is c u s s in g .hazardous particles, the distinction between dust, fumes, smoke and mist is frequently overlooked. Drinker and Hatch1 state that dust is formed by reducing earthy materials to small-sized portions, sub-microscopic to the visible, the compo sition of the particles being the same as that of the parent material. Common examples are the mineral dusts derived from the disintegration of rock and the organic dusts like wheat and flour. Fumes are formed by processes like combustion, sublimation and condensation. The particle size is generally below 1 micron. ' Smoke is generally of organic origin and is char acterized by a particle size below 0.5 microns. Mists or fogs are formed by the condensation of water vapor upon suitable nuclei. The particle or drop let size varies widely, depending on the condition prevailing. The significance of these distinctions becomes ap parent when evaluating the exposure in an individual manifesting signs or symptoms of pneumoconiosis. Since men working in dusty atmospheres are fre quently exposed to a combination of these factors, the actual cause of fibrosis may be obscured, a fact which has considerable importance in cases involving litiga tion. Like "rheumatism," the term "pneumoconiosis" covers a variety of conditions. It has been defined as a "chronic pulmonary fibrosis due to the inhalation of irritating dusts which produce a proliferative reac tion" (Johnson5), or a condition due to "the effects upon the lungs of the inhalation of excessive quantities of dust, manifested by structural changes in the lung tissue and entirely distinct from the action of poison ous dust such as lead or mercury, in which case the lungs act merely as the point of entrance into the body without definite local influence" (Pancoast0). Perhaps the simplest way of stating it would be to say that the term refers to a condition of the lungs resulting from the prolonged inhalation of dust whether harmful or inert. Pneumoconiosis includes such specific diseases as anthracosis, asbestosis, siderosis, silicosis, etc. TN recent years few diseases have received more at tention and publicity than those due to dust. The work of the United States Bureau of Mines in the Tri-State Lead and Zinc Mining districts (1924-1927) and the Metropolitan Life Insurance Company7 di rected attention to other industries where disabling pulmonary diseases were known to exist. Other inves tigations were made by the U. S. Public Health Service, and in 1933 Gardner and Cummings, of the Saranac Laboratory, began extensive studies in the iron ranges of Northern Michigan and Wisconsin. Since that time, many industries, here and abroad, have established clinics and laboratories for further research and control of the hazard. The pathology of these diseases was definitely estab lished by Dr. Leroy U. Gardner, Director of the Sara nac Laboratory, in 1934. He demonstrated the effects of various dusts on the lungs of laboratory animals and studied the part played by tuberculosis in the progress of the disease. The etiology, physical signs and symp toms, x-ray and laboratory findings were fully de scribed and many other details of a technical nature determined. During this period also, concentration codes, representing "safe" limits of air home dust were recommended. These vary in different locations but, generally speaking, the following-table, set up by the Committee on "Prevention of Silicosis Through Medical Control" of the National Silicosis Conference offers a fair standard. T able II. P ermissible Dust Concentrations in Various I ndustries Industry S o jth A frica*.......................... O ntario Gold M ines*........... A ustralis Sandstone*........ Barr* G ranite*.................... Prnnsylvania Anthracite Coal Broken Hill. Australia*. Percentage SUica in the Duet M ines**. 86 13 6 Baaed upon engineering practice. Breed upon clinical itudiea. Permiaelble Duet C o ncantra tion snllllone par Cubic Root <K SK s S t o 10 lO to 16 60 14 ^Of the dusts studied up to the present time, only silicp and asbestos produce definite pulmonary fibrosis. AH the other types of pneumoconiosis exhibit the same general kind of tissue change with a similar pattern of shadows on the roentgenogram. Gardner states that the pattern in this instance consists of a mere accen tuation of the normal branching, tree-like shadows cast chiefly by the pulmonary blood vessels. It represents a simple benign type of linear fibrosis and is difficult to distinguish from the mild accentuation of linear mark ings sometimes seen in x-rays of individuals with no known history of dust exposure. Various terms are used to indicate special types of pneumoconiosis. For instance, "anthracosis" desig nates a condition of the lungs found among coal miners due to the inhalation of coal dust. "Siderosis" de scribes the tissue reaction occurring in some iron ore miners, and such terms as "byssinosis," and "tobac- osis" refer to the pulmonary changes resulting from exposure to dust from cotton and tobacco. While such distinctions do not add much to our knowledge of dis eases due to dust, nevertheless it is desirable to have a general conception of the important physical and roentgenological features of each for the sake of diag nosis. ' In this connection it is advisable to mention the status of the silicates. The term "silicatosis" has been used from time to time to describe changes observed in the chest x-ray of persons exposed to dust from such substances as talc, soap stone, mica, feldspar, garnet, etc.; but the exact role played by these silicates in the production of pulmonary change has not yet been definitely established. They constitute a group of numerous minerals which find widespread use in in dustry, but with the exception of asbestos, their capacity to produce fibrosis has not been demonstrated. Petrologists warn against the potential hazard from silicates but experiments so far have produced no evi dence of connective tissue proliferation as a resulf of their use. On the other hand, it should not be assumed that lack of such evidence indicates absolute inertness. The changes observed in the chest x-rays of persons texposed to silicate dust have been theoretv sally ex plained as a mild silicosis arising from silica left after the body fluids have leached the "bases out of the sili cotic molecule. A representative group of 24 silicates used in industry, listed by Gardner, appears in Lanza's book, "Silicosis and Asbestosis." The inert dusts, which include most of the silicates, are relatively un important because of their non-disabling character. A few of these materials are limestone, marble, talc, chalk, calcined m agnesium fo r insulation, furnace lin ings, carbon dust, iron dust, tobacco dust, cement, cotton, molds, fungi, etc. ' Anthraco-silicosis results from excessive exposure to coal dust which contains amounts of free silica. Since carbon is one of the inert dusts, it seems reasonable SPNY 000229 to assume that the fibrosis is simply the result of the action of free Bilica 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 is shortness of breath, fre quently associated with productive cough. More ad vanced cases complain of weakness, chest pain, gastric disturbs: ces and hemoptysis. Sayers states that in a U. S. Public Health Survey of anthracite miners in Pennsylvania in 1933, fever and night sweats were seldom mentioned. (This is true of silicosis cases in 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 Price12 examined 868 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. iron ore miners.) He notes such physical signs as dyspnea, prolonged expiration, change in contour of T a b le III. the chest, decreased chest expansion, clubbing of the Year* a t Work Coses Exam ined Showing Fibrowe Per Cent 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. _ g9 .................. 0 ................... . . . . 0-0 6 to 9 ............. ____ 26.6 JU ..................27 ..................... ........ 82.1 16 to 19 ........... 28 ......... 16 ..................... ____ 68.6 Z0 and ov*r -- ........... 21 ........................ .................. ........ 90.9 The pathology of anthraco-silicosis 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-silicosis 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. As 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 origina 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 T h e 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 is 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 will 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 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 t J , Table V. X-Ray Appearance _________ ASBESTOSIS___________ ___________SILICOSIS___________ Diffuse lesions limited to lower helves i of lungs--Hyperventilation in.upper portions. Obliteration of the diaphragm. Nodular lesions distributed more in upper and mid-lung fields or general ized-emphysema in lower halves. Shortening of long diameter of chest with adhesions and tenting of dia By the same token, extreme care should be taken to eliminate contact with tuberculosis from these work ers. This can only be accomplished by repeated chest x-rays of all those exposed to hazardous dust and removal of the ones showing evidence of infection. Bibliography 1*. K ronenberg a n d Morse: H ealth H a za rd s o f O ccupational E n phragm. v ironm ents. D e p a rtm e n t o f Public H e alth C ircular 154. . No nodulation. " Ground glass*1appearance. May be u n ila te r a l.________________ Marked nodulation. Discrete nodulation to massive con glomerate shadows. Bilateral.________ . 2. Sappincton, C. O .: Essentials of Industrial H ealth. U p p in co tt. 1943, p p . 186-187. ,, ,,, . 8. Gardner, L. U .: Pathology o f Silicosis, Second Symposium on Silicosis, S a ra n a c L ake, N ew Y ork, 1935. 4. Drinker a n d H a t c h : In d u stria l D ust. M cGraw-Hill Book Com pany, Inc., N ew Y ork, 1936, p. 2. , Certain other conditions such as fungus infections, miliary tuberculosis, miliary calcification and miliary 6. J ohnstone, R. T . : Occupational Diseases. W . B. Saunders. P hila delphia, 1942, p . 804. 3 r 6. P ancoast, H . K .: Silicosis an d Asbestosis-- In tro d u ctio n , L anza. carcinoma produce shadows in the roentgenogram O xford Medical Publications, 1938. , _ which may be confused with those of silicosis. In these 7. Lanza, A. J . : Silicosis and Asbestosis, O xford Medical Publica tions, 1938. ,, _ . , A_. instances careful study of the film and previous occu 8. Gardner, L. U .: Symposium on Silicosis, Saranac Lake, 1934. pational history will usually be sufficient to make an 9 Sayers. R. R .: R eaction to Mixed D usts: A tm ospheric and Clin ical Findings in H ard Coal M ining. Fourth Saranac Laboratory Sym II accurate diagnosis. posium on Silicosis, 1989. , T As in all diseases due to dust, treatment is an en 10. D ressen, W . G., D allavalle, J . M., E dwards. T. I.. Miller. J . W ,, Sayers. R. R .: A Study of Asbestosis in the Asbestos Textile In gineering problem rather than a medical one. Once dustry. U nited States Public H ealth Bulletin--241, 1938. fibrosis is established in the lungs, it is permanent. Progression of the disease is very slow and chronic, 11. Gardner, L. U .: R ecent D evelopm ents in R elation to Silicosis. in d u stria l M edicine, 9:45. F ebruary. 1940. __ , 12. Merewether, E . R . A ., an d P rice, C. W .: R ep o rt on Effects of except in some instances where infection occurs. Con Asbestos D ust on th e Lungs and D ust Suppression in the Asbestos In tinued exposure to hazardous dust appears to be the d ustry. H . M. S ta t. Office. London. 1930. 13. Cook W . E . : A sbestos D ust an d th e " C urious Bodies F o u n d in biggest factor in the advancement of fibrosis. When Pulm onary Asbestosis. B ritish Medical Journal, 2:578, 1929. ^ I dust is kept at a safe concentration in the air of work 14. Gardner, L. U .: Saranac Lake, New York, Personal Communica ing places, there is no good reason why a person with tion, 1943. * n r i 15. Sampson, H. L .: T hird Symposium on Silicosis. Saranac *-*ake, uncomplicated silicosis cannot continue his occupation. New York. 1937. SPNY 000233 Y A. Chest Conditions Simulating Silicosis L. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago , f Reprinted from Industrial Medicine, 15 : 6, 376 - 381, June, 1946 SPNY 000234