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r PLAINTIFF'S I EXHIBIT l AB-67 ^^ZJU. '/x3 Industrial Dust --The Pneumoconioses L B. HAMLIN, M.D,, FA.C.SW Medical Director, American Brake Shoe Company, Chicago Reprinted from Industrial Medicine, March, 1944 SPNY *000227 Industrial Dust --The Pneumoconioses L E. HAMLIN, M.D., F.A.C.S., Medico/ Director, American Brake Shoe Company, Chicago he relation between dust and certain diseases of toxic and systemic effects, but usually their main con Tthe lungs has been recognised 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 recorded their impressions and observations on the exposed to pollens, horse hsir, 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. Sappington1 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 skin, while hensive study of 300 cases. Diagnostic standards of cotton weavers develop & 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. _ control were instituted. From 1916 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 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: 11. Inorganic Dusts: A. Non-Living: A. Toxic and (or) 1. Toxic and (or) Irritant fibrosis known as silicosis. Gardner1 demonstrated the specific action of Bilica and made it dear that only 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 during. metals and their salts, such as lead, mercury, man 2. Fungi- 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 The text of Dr. Hamlin's Lecture at the Second Poet-Graduate Course in Industrial MedieJne, Lon; Island College of Medicine, Brooklyn, Friday, November 6, INS, SPNY 000228 IN_ DISCUSSING -hazardous particles, the distinction offers a fair standard. between dust, fumes, smoke and mist is frequently . ^overlooked. Drinker and Hatch' state that dust is ' Table II. formed by reducing earthy materials to small-sized Permissible Dubt Concentrations in Various Industries portions, aub-micro3copic to the visible, the compo sition of the particles being the same as that of the parent material. Common examples are the mineral Induct ry 1 PeteeaUf* SUiea is the Du,l Perraieeihle Duet Coceeotnttoa Mince per Cable tiat dusts derived from^he 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 So-itb Alrio*....................... OflUrio Cold MiMt*........... AuetralU SaadcW&e*........... GnxUt**.,,................. Peaneytouia Aathradtc Cod Mine***. IS 13 6 Broktti fllU* Attttrmli**........ 00 tn t0 S to 10 10 to IS *0 14 acterized by a particle size below 0.5 microns. EUttd ttpotk ttfiowiflc practice. Mists or fogs are formed by the condensation of **B--ed upon djpicwi tudin. __ water vapor upon suitable nuclei. The particle or drop Of the dusts studied up to the present time, only let size varies widely, depending on the condition silica and asbestos produce definite pulmonary fibrosis. prevailing. All the other types of pneumoconiosis exhibit the same The significance of these distinctions becomes ap general kind of tissue change with a similar pattern parent when evaluating the exposure in an individual of shadows on the roentgenogram. Gardner states that manifesting signs or symptoms of pneumoconiosis. the pattern in this instance consists of a mere accen Since men working in dusty atmospheres are fre tuation of the normal branching, tree-like shadows cast quently exposed to a combination of these factors, the chiefly by the pulmonary blood vessels. It represents a actual cause of fibrosis may be obscured, a fact which simple benign type of linear fibrosis and is difficult to has considerable importance in cases involving litiga distinguish from the mild accentuation of linear mark tion. ings sometimes seen in x-rays of individuals with no Like "rheumatism," the term "pneumoconiosis'* known history of dust exposure. covers a variety of conditions. It has been defined as Various terms are used to indicate special types of a "chronic pulmonary fibrosis due to the inhalation of pneumoconiosis. For instance, "anthracosis" desig irritating dusts which produce a proliferative reac nates a condition of the lungs found among coal miners tion" (Johnson*), or a condition due to "the effects due to the inhalation of coal dust. "Siderosis" de upon the lungs of the inhalation of excessive quantities scribes the tissue reaction occurring in some iron ore of dust, manifested by structural changes in the lung miners, and such terms as "byssinosis," and "tobac- tissue and entirely distinct from the action of poison osis" refer to the pulmonary changes resulting from ous dust such as lead or mercury, in which case the exposure to dust from cotton and tobacco. While such lungs act merely as the point of entrance into the body distinctions do not add much to our knowledge of dis without definite local influence" (Pancoast0). Perhaps eases due to dust, nevertheless it is desirable to have a the simplest way of stating it would be to say that the general conception of the important physical and terra refers to a condition of the lung3 resulting from roentgenological features of each for the sake of diag the prolonged inhalation of dust whether harmful or nosis. inert. In this connection it is advisable to mention the Pneumoconiosis includes such specific diseases as status of the silicates. The term "silicatosis" has been anthracosis, asbestosis, siderosis, silicosis, etc. used from time to time to describe changes observed in the chest x-ray of persons exposed to dust from TM RECENT years few diseases have received more at such substances as talc, soap stone, mica, feldspar, tention and publicity than those due to dust The garnet, etc.; but the exact role played by these silicates . work of the United States Bureau of Mines in the in the production of pulmonary change has not yet Tri-State Lead and Zinc Mining districts (1924-1927) been definitely established. They constitute a group of and the Metropolitan Life Insurance Company7 di numerous minerals which find widespread use in in rected attention to other industries where disabling dustry, but with the exception of asbestos, their pulmonary diseases were known to exist- Other inves capacity to produce fibrosis has not been demonstrated. tigations were* made by the U. S. Public Health Petrologists warn against the potential hazard from Service, and in 1933 Gardner and Cummings, of the silicates but experiments so far have produced no evi Saranac Laboratory, began extensive studies in the dence of connective tissue proliferation as a result of iron ranges of Northern Michigan, and Wisconsin. their use. On the other hand, it should not be assumed Since that time, many industries, here and abroad, that lack of such evidence indicates absolute i> xrtneas. have established clinics and laboratories for further The changes observed in the chest x-rays of persons, research and control of the hazard. exposed to silicate dust have been theoretv :ally ex The pathology of these diseases was definitely estab plained as a mild silicosis arising from silica ieft after lished by Dr. Leroy U. Gardner,* Director of the Sara- the body fluids have leached the bases out of the sili -nac laboratory, in 1934. He demonstrated the effects cotic molecule. A representative group of 24 silicates of various dusts on the lungs of laboratory animals and used in industry, listed by Gardner, appears in Lanza's studied the part played by tuberculosis in the progress book, "Silicosis and Asbestosis." The inert dusts, of the disease. The etiology, physical signs and symp which include most of the silicates, are relatively un toms, x-ray and laboratory findings were fully de important because of their non-disabling character. scribed and many other details of a technical nature A few of these materials are limestone, marble, talc, determined. During this period also, concentration chalk, calcined magnesium for insulation, furnace lin codes, representing "safe" limits of air borne dust, ings, carbon dust, iron dust, tobacco dust, cement, were recommended. These vary in different locations cotton, molds, fungi, etc. but, generally speaking, the following table, set up by Anthraco-silicosis results from excessive exposure to the Committee on "Prevention of Silicosis Through coal dust which contains amounts of free silica. Since Medical Control" of the National Silicosis Conference, 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 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 in industrial medicine is important, but judging from the comparatively small number of persons exposed in 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. pROM 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 ing air containing silica {Si 02), characterized an atomically by generalized fibrotic changes and the de velopment of military nodulation in both lungs, and clinically by shortness of breath, decreased chest ex pansion, lessened capacity for work, absence of fever, increased susceptibility to tuberculosis (some or all of which symptoms may be present) and by character istic x-ray findings.". Gardner14 points out that an objection to this definition is that it recites symptoms which are not always present except in advanced cases. He suggests the following as being more simple and adequate: "Silicosis means a disease of the lungs due to breathing air containing uncombined silicon dioxide (Si 02) dust, characterized anatomically by general ized nodular fibrotic changes throughout both lungs which are demonstrable by x-ray examination and by autopsy and resulting from any process of occupation involving inhalation of silicon dioxide dust." The disease has been known as a clinical entity since the year 1871, but not until recent years was it recog nized in industries other than hard rock mining. Silica is a most abundant constituent of rocks and minerals. With its compounds, it makes up 65% of the earth's crust. It occurs in two forms, free and combined. The combined forms are known as silicates (previously referred to). Probably no other mineral is more widely used than silica and its compounds. Some of the more common occupations providing exposure are mining, tunneling, processing ores, quarrying, stone cutting and polish ing, manufacture of abrasives, sand blasting, and grinding. For a complete list of the uses to which silica may be put see the table "Occupational Environment" by LaDoo. To appreciate the pathological changes occurring in silicosis, it is well to recall the natural mechanism of defense in the respiratory tract itself. Nature has provided a barrier to dust and foreign particles at the point of entry into the body. The fine hairs of the nostrils and the mechanical arrangement of the upper Diagrammatic npmKitatin of pathway of daft partida Htuttfating factor* iavohrad in natural dilmn machanluR at tha body respiratory tract offer considerable resistance to large particles and provide a very effective means of pro tection against all but the very fine dusts. Probably the greater part of the inhaled particles are eliminated by the upward current created by the ciliated epi thelium of the trachea and bronchi. Beyond this point, the alveolar phagocyte or "dust cell" provides further elimination by transporting particles to the point where the cilia become effective. It is believed that the particles from 0.6 to S microns in size are the only ones capable of producing pulmonary fibrosis. Those above 8 microns are elim inated by the upper respiratory tract while few of those below 0.5 micron actually remain in the alveoli. In the actual production of fibrosis, the phagocytes, which probably originate from the inner surface of the air sac or the lining of the capillary blood vessels, pick up the fine dust and pass to the lymph spaces to be transported to more distant points by the lymph ves sels along the normal course of drainage towards the hilum of the lung. In this process, particles become deposited in the interlobular tissue and rodes along the vessels. Here, it is thought, the body fluids produce a slow chemical reaction which results in the death of the dust cells and necrosis of the surrounding tissue. This stimulates the proliferation of fibroblasts and the ensuing scar inhibits the further removal of dust. The interference with the flow of lymph causes a spread of the phagocytes toward the pleura, and fibrosis appears in the interlobular septa and along the lymphatics which accompany the blood vessels. As the process goes on, small nodules of fibrous tissue become scat tered throughout the lung giving, rise to the so-called noduar condition typical of silicosis. These nodules may increase in size and eventually coalesce, forming massive fibrotic areas which destroy the air sacs and result in compensatory enlargement of neighboring alveoli, or in other words, emphysema. Microscopically, the typical nodule of mature form 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 deveioped*hodulation are entirely unaware that anything is wrong with their lungs. The com monest symptom is "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 silicotics tolerate colds and even pneumonia with sur prising resistance. Physical signs are usually lacking. When the disease progresses, however, and if the individual does show 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 practically all cases of death from silicosis is usually due to tuberculosis. Not so 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 nodulation 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 oh 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 silico- tuberculosis show surprising resistance and may be comparatively active up till a few hours before death, Dncnt Mtlulatiwi ef MMd dtjrM (Okatit <uftcoMpBcat4) in on iron mintr 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 Bpeed. Silicosis takes time to develop. Experience in South Africa indicates that approximately eight years are required for the condition to progress from a presilicotic Btage 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 Sampson1 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 differential diagnosis: SPNY 000232 1 I l I SILICOSIS X-ray* dwnonttraling iSadow* lit atbtoiit and advancnd lilkotii , Table V. X-Ray Appearance ASBESTOSIE SILICOSIS Diffuse lesions limited to lower halves t Nodular lesions distributed more in of lungs--Hyperventilation-in upper upper snd mid-Jung fields or general- 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. portions. Usd-emphysema in lower halves. Obliteration o{ the diaphragm. No noduiation. "Ground glass" appearance. Shortening ol long diameter of chest with adhesions and tenting of dia phragm. Marked noduiation. Discrete noduiation to massive con Bibliography 1. SMHiNiEtc mod Morse t Httltb Hmids of Occupation*! En vironments, Department of Public Health Circular---164, 2. SAmNcrox. C. O.: Emntlals of Industrial Health. Lippincott op. i&e-m. glomerate shadows. 8. Gardner, L. U.: Pathology of SlUeosis, Second Symposium on May be unilateral. Bilateral. Silicosis. Saranac Lake, New York, 1935. 4. Drinker and Batch : Industrial Dust, McGraw-Hill Book Com Certain other conditions such as fungus infections, pany, Inc,. New York, 1935, p. 2, 5. Jobnkohe. &. T.; Occupational Diseases. TV-B. Saundets. Phila miliary tuberculosis, miliary calcification and miliary delphia, 1942. p. 104. carcinoma produce shadows in the roentgenogram 5. Paxooast, H. K.: SUieosla and Aabestosi*--Introduction. Labia. Oxford Medical Publications, 1913, which may be confused with those of silicosis. In these instances careful study of the film and previous occu pational history will usually be sufficient to make an 7. LANZA, A. J.: SHieoai* and Asbestoaii, Oxford Medical Publica tions, 1918, 8. Gardner, L. U.: Symposium on Silicosis. Saranac Lake, 1934. 9. Sayers. R. fL: Reaction to Mixed Dusts: Atmospheric and Clin accurate diagnosis. As in all diseases due to dust, treatment is an en ical Findings In Hard Coal Mining. Fourth Saranac Laboratory Sym posium on Silieoti*. 1989. 10. Djbssen, W. G.s Dallavalle, I, M,, Edwards. T. I., Miller. j. gineering problem rather than a medical one. Once fibrosis is established in the lungs, it is permanent. Progression of the disease is very slow and chronic, W,, Sayers, R. ft,: A Study of Aabestosls in the Asbestos Textile In dustry. United States Public Health Bulletin--241. Ifl38. 11. Gardner, L, U.: Recent Development* in Relation to Silicosis. Industrial Medicine, 9:45, February, 1949. except in some instances where infection occurs. Con tinued exposure to hazardous dust appears to be the 12. Merewether* E. R. A., and Price. C- W.; Report on Effect! of Asbestos Dust on the Lungs and Dust Suppression in the Asbestos In dustry. H. M. Stat. Office. London. 1930. biggest factor in the advancement of fibrosis. When 13. Coox. W. E.: Asbestos Dust and the "Curious Bodies" Found In I 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. Pulmonary AsbestosU. British Medical Journal, 2:678. 1929. 14. Gardner, L. U.: Saranac Lake. New York, Personal Communica tion. 1943. . 15. Sampson, H, L.: Third Symposium on Silicosis. Saranac Lake, New York, 1937. l SPNY 000233 / oo Chest Conditions Simulating Silicosis L. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago , Vju Reprinted from Industrial Medicine, is : 6, 376 - 381, June, 1946 SPNY 000234