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PLAINTIFF'S EXHIBIT U'-fy'fi'l Industrial Dust -- The Pneumoconioses L. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago v. S' :>> l Reprinted from Industrial Medicine, March, 1944 SPNY -000227 Industrial Dust -- The Pneumoconioses L. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago _ . THE relation between dust and certain diseases of toxic and systemic effects, but usually their main con 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, 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 9 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, slsthma, or irritation of the akin 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 skin, while hensive study of 300 cases. Diagnostic standards of cotton weavers develop a form of disease known as I 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. control were instituted. From 1915 on, Great Britain, The inorganic dusts which have significance in \ 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 Kronenberg and Morse1 have suggested the follow remain in suspension in the air for varying periods ing classification of industrial dusts: depending on their Bize and settling velocity. Inhala tion of those particles which contain silica in the Table I. uncombined state produces the type of pulmonary' I. Opxanic Dusts: A. Non-Living: 1. Toxic and (or) Irritant. II. Inorganic Dusts: A. Toxic and (or) Irritant. B. Fibrosis Producing. fibrosis known as silicosis. Gardner3 demonstrated the specific action of silica and made it clear that only silica in the "free" state is capable of causing this type of tissue reaction. B. Living: 1. Bacteria 2. Fungi. C. Non-Fibrosis Producing. The toxic inorganic dusts are those of the heavy metals and their salts, such as lead, mercury, man ganese, etc. They are usually considered under the heading of industrial poisons rather than of dusts. Generally speaking, organic dusts originate from plants or animals, but many thousands of these sub stances are made synthetically. They may produce Th text of D*. Kakuk`8 Lecture *t the Second Port-Grdu*te Course in Induitri&l Medicine. Lon? Iiknd College of Medicine, Brooklyn, Friday. November 6. 194S. SPNY 000228 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 is shortness of breath, fre quently associated with productive cough. More ad vanced cases complain of weakness, chest pain, gastric disturbs, ces and hemoptysis. Sayers8 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 iron ore miners.) He notes such physical signs as dyspnea, prolenged 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-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, 641 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'KE 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 thar. the lungs. While the action of free silica :s chemical, that of asbestos is mechanical. The typical lesions, observed microscopically, show large macrophages in the distal portions of the bronchia] 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 363 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. Y*r> at Work Cues Ex&reiotd Showing Fibroei* Per Cent 0 to 4 ............ 5 to 9 ............ .......... 141 .......... 10 to 14 .......... 16 to 19.......... .......... 28 .......... 20 and over ... .......... 21 ....'.. .......... 17 ................. ___ 90.9 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 asbestos 'a 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 in industrial medicine Is important, but judging from the comparatively small number of persons exposed ir. this country, the actual amount of disability re sulting from the disease is not great. In one of our plants where considerable asbestos is used In the manufacture of automobile brake linings, a recent survey of 189 employees exposed to variable amounts of dust, revealed no actual cases of fibrosis. A few men's films showed haziness which suggested evidence of the disease, but they were not sufficiently typical to warrant a diagnosis of asbestosis. However, it should be stated that the hazard in this particular plant is well controlled by adequate exhaust ventila tion. From the mass of evidence accumulated during the past 25 years, it now seems definitely established that silica is the public enemy No. 1 of those engaged in dusty occupations. By itself and in combination with other dusts, it offers a harmful exposure to a conservatively estimated 600,000 workers in the United States alone. In spite of this fact, most ob servers are now of the opinion that silicosis, uncom plicated by infection, is not a disabling disease. How ever, the fertile field it affords for the development of tuberculosis makes it imperative to disregard its be nign characteristics and view it with suspicion until otherwise proven innocent. ' The Committee on Pneumoconiosis of the Industrial Hygiene Section of the American Public Health As sociation defines silicosis as "a disease due to breath Diagrammatic rprcintation af pathway of dutt partidt illustrating facton involved in natural dafinw mochaniun of th body ing air containing silica (Si 02), characterized an atomically by generalized fibrotic changes and the de respiratory tract offer considerable resistance to large velopment of military nodulation in both lungs, and particles and provide a very effective means of pro clinically by shortness of breath, decreased chest ex tection against all but the very fine dusts. Probably pansion, lessened capacity for work, absence of fever, the greater part of the inhaled particles are eliminated increased susceptibility to tuberculosis (some or all by the upward current created by the ciliated epi of which symptoms may be present) and by character thelium of the trachea and bronchi. Beyond this point, istic x-ray findings.", Gardner14 points out that an the alveolar phagocyte or "dust cell" provides further objection to this definition is that it recites symptoms elimination by transporting particles to the point which are not always present except in advanced cases. where the cilia become effective. He suggests the following as being more simple and It is believed that the particles from 0.6 to 3 adequate: microns in size are the only ones capable of producing "Silicosis means a disease of the lungs due to pulmonary fibrosis. Those above 3 microns are elim breathing air containing uncombined silicon dioxide inated by the upper respiratory tract while few of (Si 02) dust, characterized anatomically by general those below 0.5 micron actually remain in the alveoli. ized nodular fibrotic changes throughout both lungs In the actual production of fibrosis, the phagocytes, which are demonstrable by x-ray examination and by which probably originate from the inner surface of autopsy and resulting from any process of occupation the air sac or the lining of the capillary blood vessels, involving inhalation of silicon dioxide dust." pick up the fine dust and pass to the lymph spaces to be The disease has been known as a clinical entity since transported to more distant points by the lymph ves the year 1871, but not until recent years was it recog sels along the normal course of drainage towards the nized in industries other than hard rock mining. Silica hilum of the lung. In this process, particles become is a most abundant constituent of rocks and minerals. deposited ir. t^ie interlobular tissue and rodes along the With its compounds, it makes up 65% of the earth's vessels. Here, it is thought, the body fluids produce a crust. It occurs in two forms, free and combined. The slow chemical reaction which results in the death of combined forms are known as silicates (previously the dust cells and necrosis of the surrounding tissue. referred to). This stimulates the proliferation of fibroblasts and the Probably no other mineral is more widely used than ensuing scar inhibits the further removal of dust. The silica and its compounds. Some of the more common interference with the flow of lymph causes a spread of occupations providing exposure are mining, tunneling, the phagocytes toward the pleura, and fibrosis appears processing ores, quarrying, stone cutting and polish in the interlobular septa and along the lymphatics ing, manufacture of abrasives, sand blasting, and which accompany the blood vessels. As the process grinding. For a complete list of the uses to which silica goes on, small nodules of fibrous tissue become scat may be put see the table "Occupational Environment" tered throughout the lung giving rise to the so-called by LaDoo. noduar condition typical of silicosis. These nodules To appreciate the pathological changes occurring may increase in size and eventually coalesce, forming in silicosis, it is well to recall the natural mechanism massive fibrotic areas which destroy the air sacs and of defense ir. the respiratory tract itself. Nature has result in compensatory enlargement of neighboring provided a barrier to dust and foreign particles at the alveoli, or in other words, emphysema. point of entry into the body. The fine hairs of the Microscopically, the typical nodule of mature form nostnis and the mechanical arrangement of the upper consists of concentric whorls of dense hyaline collagen SPNY 000231 fibres. The border is sharply defined with no exudate in the adjacent air spaces. The nodule.may contain black pigment distributed either about the periphery or in focal collections in the interior. Symptoms in silicosis depend largely upon whether the disease is complicated by infection (tuberculosis) or not. In simple or uncomplicated silicosis, they are absent or very few. In a great many instances people with well developed nodulation are entirely unaware that anything is wrong with their lungs. The com monest symptom iB "shortness of breath," but fre quently this complaint has to be elicited from the indi vidual, and then he will often qualify it by stating that "he is not as young as he used to be." In some cases the actual dyspnea as observed by exercise tests, is less than the amount complained of. These discrepan cies demonstrate the need of looking for causes of shortness of breath other than silicosis. Fever, cough, expectoration and rales are rarely encountered. If they are met with in moderate pulmonary fibrosis, they are probably due to an acute respiratory infection. Some Bilicotics tolerate colds and even pneumonia with sur prising resistance. Physical signs are usually lacking. When the disease progresses, however, and if the individual does snow evidence of his condition, the symptoms and signs can be more definite. The short ness of breath is practically constant and is often associated with palpitation of the heart. The appear ance of dry cough, sputum, loss of appetite, and in creased fatigue should arouse suspicion of infection. "Complicated silicosis" in the vast majority of cases means silico-tuberculosis. It is what the older men knew as "miners' complaint" or miners' consumption. The susceptibility of silicotics to tuberculosis is well known, but the reason for it is still obscure. The fatal outcome in pract:cally_ all cases of death from silicosis is usually due to tuberculosis. Not bo many years ago it was believed that persons with silicosis and tuber culosis would inevitably die. There is now reason to believe that this is not necessarily true. In my own experience, I have seen cases with well marked nodu lation develop infection and show a positive sputum which later became negative after a period of hospi talization. A survey of practically any group of hard rock miners will show a considerable number with evidence of healed tuberculosis. However, the' fact remains that once tuberculosis becomes superimposed on silicosis, the prognosis is extremely serious. In chronic silico-tuberculosis the lungs, on gross appearance, are leathery or rubber-like in consistency, pigmented, and show areas of fibrous pleurisy where the lesions extend to the surface. The nodular fibrosis which is the characteristic feature can be felt imme diately beneath the pleura. On section, the cut surface, is rough and gritty, and the normal lung tissue has been practically replaced by extensive fibrosis or large masses of very dense, heavily pigmented scar tissue. The pleura is thickened and adherent. Emphysema is present. In active silico-tuberculosis, caseation and pneumonia of tuberculous origin may be present. On microscopic section this can be seen about the nodule. Infection may be active or "fresh,'' healed or "old," and indeterminate. Symptoms will vary according to the stage of the disease. As the condition advances, the patient may exhibit the characteristic phthisic symptoms and signs, such as cough, loss of weight, dyspnea, chest pain, night sweats, tubercle bacilli in the sputum, and haemorrhage. He dies a charac teristic tuberculous death. This is not always the case, however. Many individuals with far advanced silicotuberculosis shew surprising resistance and may be comparatively active up till a few hours before death, Dticrat* nodulation of Mcond dogroo silica tit (uncompGcattd) in an iron minor which may come rather suddenly and easily. I have seen such individuals and talked with them shortly before their demise .and have anticipated no sudden termination of existence. Progression of silicosis is extremely slow. Some times even in the presence of infection, it does not appear to advance very rapidly, but in certain in stances the disease proceeds with astounding speed. Silicosis takes time to develop. Experience in South Africa indicates that approximately eight years are required for the condition to progress from a pre- silicotic stage to a silicotic one. Because of the lack of physical signs and symptoms, a classification of the stages of silicosis is only practi cal when based on x-ray findings. Various observers have made their own tabulations, but the one worked out by Sampson18 affords a practical and satisfactory grouping: ^ Table IV. A. Uncomplicated Silicosis: N --Normal chest Pi--Stage of peritruncal exaggeration. Pi--Stage of marked peritruncal exaggeration. ' (Pre-Silicosis) Si--First degree nodulation--(Linear mark ings obliterated and nodules up to 2 mm. in diameter present.) S:--Second degree nodulation (Nodules 2 to 4 mm. in diameter.) . S--Third degree nodulation (Nodules over 4 mm.) B. Complicated Silicosis: 1. Silicosis with fresh infection. ' 2. Silicosis with old infection. 3. Silicosis with indeterminate infection. In silicosis the x-ray appearance of the chest differs considerably from that of abestosis. In the accom panying table the more characteristic features of each are tabulated as an aid in differentia! diagnosis: SP NY 000?3;> TM I i! t ASBESTOS'S SILICOSIS X-ray* d.mon.trating thadow* in atbntoti* and advanced *llica*it r .7 Table V. X-Ray Appearance __________ asbestosis____________ ____________SILICOSIS____________ Difluae lotion* limited to lower helve* t Modular leeiont distributed more in of lunp--Hyperventilation in .upper upper and mid-lung fields or generai- 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. iI portion*. Obliteration of the diaphragm. ixed-tmphysemt in lower halves. Shortening of long diameter of chest Bibliography with adhesions and tenting of dia phragm. 1. Kronenberc and Mouse: Health Hazards of Occupational En vironments. Department of Public Health Circular--184. No noduletion. Marked noduletion. 2. SArriNCZON. C. O.: Essentials of Industrial Health. Llppineott, "Ground glass" appearance. Discrete noduletion to massive con glomerate shadows. 1943, pp. 186-187. 4 8* Gasdhdu L. U.: Pathology of Silicosis. Second Symposium on May be unilateral.__________________ BUateraL ______ SUieosis. Saranac Lake, New York. 1938. 4. Drinker and Hatch : Industrial Dust. McGraw-Hill Book Com- pan?, Inc., New York. 1936. p. 2. Certain other conditions such as fungus infections, 6. JoHKeTONX, R. T.: Occupational Diseases. W. B. Saunders. Phila miliary tuberculosis, miliary calcification and miliary delphia, 1942, p. 804. carcinoma produce shadows in the roentgenogram 6. PancoAST, H. EL: SUieosis and Asbestosis--Introduction. Lanza. Oxford Medical Publications. 1938. which may be confused with those of silicosis. In these 7. Lanza, A. J.: Silicosis and Asbestosis, Oxford Medical Publica instances careful study of the film and previous occu tions, 1988. 8. Gaxdner,,L. U.: Symposium on Siliet-sis, Saranac Lake. 1934. pational history will usually be sufficient to make an 9. Sayers. R. R.: Reaction to Mixed Dusts: Atmospheric and Clin 1 accurate diagnosis. , ical Findings in Hard Coal Mining. Fourth Saranac Laboratory Sym posium on SlUcosis, 1939. As in all diseases due to dust, treatment is an en 10. Dremen, W. G.. Dallavalu:. J. M.. Edwards. T. I., Miller. J. gineering problem rather than a medical one. Once fibrosis is established in the lungs, it is permanent. W.. Sayers. R. R.: A Study of Asbestosis in the Asbestos Textile In dustry. United States Public Health Bulletin--241. 3038. 11. Gardner. L. V.: Recent Developments in Relation to SUieosis. Progression of the disease is very 6low and chronic, except in some instances where infection occurs. Con Industrial Medicine, 9:45. February, 1940. 12. Me^vethex. E. R. A., and Price. C. W.: Report on Effects of Asbestos Dust on the Lungs and Dust Suppression in the Asbestos In l i I ! tinued exposure to hazardous dust appears to be the biggest factor in the advancement of fibrosis. When dust is kept at a safe concentration in the air of work ing places, there is no good reason why a person with uncomplicated silicosis cannot continue his occupation. dustry. H. M. Stat. Office. London. 1930. 13. Cook, w. E.; Asbestos Dust and the "Curious Bodies" Found in Pulmonary Asbestosis. British Medical Journal, 2:676. 1929. 14. Gardner. L. U.: Saranac Lake. New York. Personal Communica tion. 1943. . 15. SAursoN, H. L.: Third Symposium on Silicosis. Saranac Lake. New York. 1937, ii I SPNY oon;m