Document OE3wbNZ69kOYNE0mp31b4MDzp

FILE NAME: Abex (ABX) DATE: 1944 Mar DOC#: ABX316 DOCUMENT DESCRIPTION: Journal Article - Industrial Dust- The Pneumoconioses - Industrial Medicine M W rk are rtunity event a examee who it man. A flue a great ht; one md the us time ianged, "ure of it read walked apparn were had an lid not attural 'e only ner alwait so patient sight, -action ie were nulk of w only power as past is most e sure t id well o small e most rgans. >eak in >d, had fety. I e endividmg of this iris as irtially elf are inter for all calists of the ms of action of the eptive defer id low iprocal rpretaworkis also erfect indcrw gives f ours in the itional Vol. IS, No. 8 INDUSTRIAL MEDICINE Page S2S Chronic Carbon Disulfide Exposure --Effect on Thiamine Excretion-- HENRY H. RUBIN, M.D., Conclusion E" xposure to low concentrations of CS~ does not ap*-' pear to cause a thiamine deficiency as determined by assay of the urine. E Medical Supervisor, The Visking Corporation, Chicago References 1, H arms, L. J ., and Leonq, P . C .: V itam ins In Human N utrition, xposure to vapors of industrial solvents with their The Excretion of Vitamin Bi in Human Urine and Its Dependence on effects on the central nervous system has led to the Dietary Intake, Lancrt, 1:886 (April IS) 1986. 2. Lewey, F, H .: Neurological, Medical and Biochemical Signs and the belief that thiamine deficiencies may result. WhereSymptoms Indicating Chronic Industrial Carbon Disulfide Absorption, such exposure is prolonged and the concentration levels A nn. In t. M *d. 15:869, (November) 1941, 8. McKee. R. W ,, Kjper. C., F ountain, 3 . H,, R is k in . A. M,, and are high this situation might conceivably prevail. Ex Drinker, P . : A Solvent Vapor, Carbon Disulfide: Absorption, Elimina perimental investigation has pointed in that direction. tion, Metabolism and Mode of Action. J . A. M. A ,, 122:217 (May 22) But where systems of exhaust ventilation for the con 1948. trol of such hazards have been established and the concentration levels are within or near the permissible Industrial Dust -- The Pneumoconioses limit such a result may not be expected. Determination of thiamine deficiency by assay of the urine has been offered as a diagnostic test.1 In workers who were exposed to various degrees of chronic carbon disulfide absorptions, Lewey2 reported t. E. HAMLIN, M.D., F.A.C.S., Medical Director, American Brake Shoe Company, Chicago diminished thiamine excretion in 24-hour specimens of urine. He proffered the hypothesis that the mechan ism of chronic CS2 absorption is attributed to thiamine deficiency, possibly by way of a liver damage and by T he relation between dust and certain diseases of the lungs has been recognized for centuries, but only in recent years has it been given the intensive study it deserves. In the fifth century B.C., Hippocrates direct poisoning of the coenzymes of nerve metabolism noted symptoms in a metal digger, comparable to those and respiration. McKey et al,s in vitro manometric observed among present-day miners suffering from experiments, in which exposure concentrations approx silicosis. Since that time, other investigators have imated those of our own work, show that the systems recorded their impressions and observations on the which involve vitamin B, were not inhibited by carbon effects of inhaled dusts and have emphasized the asso disulfide. ciation of these with tuberculosis. It was not until the The objective was to examine the concentration latter part of the nineteenth century, however, that levels of CS2 exposure and to determine if an actual real interest in the subject was manifested. thiamine deficiency existed among those so exposed. To South Africa must be given the credit for the Method earliest serious contribution to our knowledge of the industrial dust hazard. Here, in 1902, physical exam T*WENTY-FOUR hour urine specimens were collected inations were made on 3000 rock drillers and for the * from workers in various partB of the plant who first time, x-rays of the chest were used in a compre were exposed to CS2 vapors. Two workers who were hensive study of 300 cases. Diagnostic standards of far removed from the operational areas were used as disease, safe limits of particle concentration in the air controls. Assays of thiamine in the urine were made of working places, and engineering methods for dust by the thiochrome method. Checks of CS2 in the air control were instituted. From 1915 on, Great Britain, were made of the various plant areas in which each Germany, Australia, Italy, Canada, and the United worker was located. All of the workers had been em States made further investigations, but the most note ployed in their present jobs for one or more years. worthy progress in these countries occurred during the last few years. Data Kronenberg and Morse1 have suggested the follow Micrograms ing classification of industrial dusts: Worker p.p.m. CS2 Thiamine in Maximum Readings 24-hr. Specimens T a b u e I, 1 20 142.8 I. Organic D u s t s : , II. I n o r g a n ic D u s t s : 2 25 101.5 A. Non-Living: A. Toxic and (or) 8 20 74.6 1. Toxic and (or) Irritant. 4 25 49.1 Irritant. B. Fibrosis Producing. 5 25 124.2 B. Living: 1. Bacteria. C. Non-Fibrosis Pro ducing, 6 5 103.2 2. Fungi. 7 5 106.8 8 (control) 0 9 (control) . 0 128.8 71.4 Generally speaking, organic dusts originate from plants or animals, but many thousands of these sub Results T he normal output of a healthy adult on an adequate 1 diet is between 50 and 150 micrograms of thiamine per day. Only one worker showed a reading below the lower limit for normal, although the difference was so slight that it cannot be considered as subnormal. The permissible limit of CS2 in the breathing zone of workers is given as 10 parts per million. However, in short exposures this limit is raised to 20 parts per million. At the time of air sampling, the concentration stances are made synthetically. They may produce toxic or systemic effects, but usually their main con sequence is local or irritant. They do not cause pul monary fibrosis, but such things as dermatitis, dental lesions, irritations of the nasal mucous membranes, and conjunctivitis are fairly common in workers han dling these materials. Digestive disturbances have been observed. Allergic symptoms may occur in those exposed to pollens, horse hair, furs and wool, and various types of wood dust are known to affect suscep- levels were slightly above the upper limit for Bhort exposures for workers 2, 4 and 5. The tex t of Dr. H amlin's L ecture a t th e Second Post-G raduate Coorte In Industrial Medicine, Long Island College of Medieine. Brooklyn, Friday, November 6, 1948. are capable of producing cutaneous lesions, or "wool 1 tention and publicity than those due to dust, ine I sorters' disease," when inhaled. Sappington2 has listed work of the United States Bureau of Mines in the over 100 occupations which may produce exposure Tri-State Lead and Zinc Mining districts (1924-1927) i resulting in allergy, asthma, or irritation of the skin and the Metropolitan Life Insurance Company7 di i andFuunpgpie, rsuacihr pasasmsaygceesl.ia and spores of molds, are apt rpeucltmedonaarttyendtiisoenasetos woethreerkninowdunsttroieesxiwsth. erOethdeirsaibnlviensg to cause rashes and painful fissures of the skin, while tigations were made by the U. S. Public Health cotton weavers develop a form of disease known as Service, and in 1933 Gardner and Cummings, of the aspergillosis from inhaling spores of a mildew which Saranac Laboratory, began extensive studies in the occasionally occurs on threads. ' iron ranges of Northern Michigan and Wisconsin. The inorganic dusts which have significance in Since that time, many industries, here and abroad, industry are derived mainly from minerals and metals. have established clinics and laboratories for further In the process of grinding, crushing, blasting and research and control of the hazard. drilling these earthy substances, dust particles ranging The pathology of these diseases was definitely estab in size from microscopic to visible are liberated and lished by Dr. Leroy U. Gardner,8 Director of the Sara remain in suspension in the air for varying periods nac Laboratory, in 1934. He demonstrated the effects depending on their size and settling velocity. Inhala of various dusts on the lungs of laboratory animals and tion of those particles which contain silica in the studied the part played by tuberculosis in the progress uncombined state produces the type of pulmonary of the disease. The etiology, physical signs and symp fibrosis known as silicosis. Gardner* demonstrated the toms, x-ray and laboratory findings were fully de specific action of silica and made it clear that only scribed and many other details of a technical nature silica in the "free" state is capable of causing this determined. During this period also, concentration type of tissue reaction. codes, representing "safe" limits o f air borne dust, The toxic inorganic dusts are those of the heavy were recommended. These vary in different locations metals and their salts, such as lead, mercury, man but, generally speaking, the following table, set up by ganese, etc. They are usually considered under the the Committee on "Prevention of Silicosis Through heading of industrial poisons rather than of dusts. Medical Control" of the National Silicosis Conference, offers a fair standard. g N discussing hazardous particles, the distinction I ly.*'t between dust, fumes, smoke and m ist is frequently T a b l e II. I. S overlooked. Drinker and Hatch4 state that dust is P e r m is s ib l e D u s t Co n c e n t r a t io n s i n V a r io u s I n d u st r ie s formed by reducing earthy materials to small-sized Percentage Silica Permissible Dust Concentration portions, sub-microscopic to the visible, the compo In the millions per sition of the particles being the same as that of the Industry Dust Cubic Foot parent material. Common examples are the mineral i < dusts derived from the disintegration of rock and the organic dusts like wheat and flour. h Fumes are formed by processes like combustion, sublimation and condensation. The particle size is generally below J. micron. South Africa*.................... ...................... 80 Ontario Gold Mines*......................about 88 (in the rock) Australia Sandstone*........ B a m Granite*.................. ...................... 31 to 38 Pennsylvania Anthracite Coal Mines**. 35 13 5 Broken Hill, Australis* .. ...................... 10 to 17 8K 6 00 to 20 to 10 10 to IS 50 14 Smoke is generally of organic origin and is char acterized by a particle size below 0.5 microns. *Based upon engineering practice. **Based upon clinical studies. Mists or fogs are formed by the condensation of Of the dusts studied up to the present time, only t water vapor upon suitable nuclei. The particle or drop silica and asbestos produce definite pulmonary fibrosis. ' let size varies widely, depending on the condition All the other types of pneumoconiosis exhibit the same prevailing. general kind of tissue change with a similar pattern The significance of these distinctions becomes ap of shadows on the roentgenogram. Gardner states that parent when evaluating the exposure in an individual the pattern in this instance consists of a mere accen manifesting signs or symptoms of pneumoconiosis. tuation of the normal branching, tree-like shadows cast Since men working in dusty atmospheres are fre chiefly by the pulmonary blood vessels. It represents a i r quently exposed to a combination of these factors, the simple benign type of linear fibrosis and is difficult to actual cause of fibrosis may be obscured, a fact which distinguish from the mild accentuation of linear mark r htiaosn.considerable importance in cases involving litiga iknngoswnsohmisettoimryesofsedeunstinexxp-orsauyrse.of individuals with no -i Like "rheumatism," the term "pneumoconiosis" Various terms are used to indicate special types of covers a variety of conditions. It has been defined as pneumoconiosis. For instance, "anthracosis" desig a "chronic pulmonary fibrosis due to the inhalation of nates a condition of the lungs found among coal miners irritating dusts which produce a proliferative reac due to the inhalation of coal dust. "Siderosis" de tion" (Johnson8), or a condition due to "the effects scribes the tissue reaction occurring in some iron ore upon the lungs of the inhalation of excessive quantities miners, and such terms as "byssinosis," and "tobac- of dust, manifested by structural changes in the lung osis" refer to the pulmonary changes resulting from tissue and entirely distinct from the action of poison exposure to dust from cotton and tobacco. While such \f : oluunsgds uasctt smuecrhelaysalseathde oproimnterocfuernyt,rainncwe hinictho tchaesebotdhye deaissteisncdtuioentso ddousnto, tnaedvdermthueclehsstoitoiusrdkensiorwablelde gteo ohaf vdeisa without definite local influence" (Pancoast*). Perhaps general conception of the important physical and the simplest way of stating it would be to say that the roentgenological features of each for the sake of diag term refers to a condition of the lungs resulting from nosis. ! .. the prolonged inhalation of dust whether harmful or In this connection it is advisable to mention the inert. status of the silicates. The term "silicatosis" has been Pneumoconiosis includes such specific diseases as used from time to time to describe changes observed nthracosis, asbestosis, siderosis, silicosis, etc. in the chest x-ray of persons exposed to dust from * . t i _ ___________________ _____ '*/ '.'IMP> ion at* 4 The in the 1-1927) iyT di sabling invesHealth of the in the eonsin. ibroad, urther estab Saraeffects ils and ogress symply de nature ration dust, ations up by rough rence, e JDiaft ate oPo*tr .`0 '0 S only rosis, same ttern that <ecens east >nts a lit to nark<h no es of esig'iners " de n ore obaefrom such f dis ave a and diag- the been rved rrom * w yi> 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 result 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 exposed to silicate dust have been theoretically 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 magnesium for 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 duBts, it seems reasonable 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 disturbances 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 iron ore miners.) He notes such 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-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 eause 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 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 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 in oblitera tion of the lung structure. The alveoli have literally become plugged, and the function of the lung impaired mechanically. Merewether and Price12 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. Year a t Work Caaee Examined Showing Fibroai* Pei Cent 0 to * ............ .......... 89 .......... . . . . . . 0 . . . . . . . . . . . . . . 0*0 6 to 9 ............ .......... 141 .......... .......... 8 ................. . . . . 26.6 10 to 14 .......... .......... 84 .......... .......... 21 .................... . . . . KM 16 to 19 .......... .......... 28 .......... .......... 16 ................. . . . . 68.6 20 and ov*r___ .......... 21 ........ .. .......... 1? ................. . 0.9 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 socalled asbestos bodies. Cook18 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 Page Si6 INDUSTRIAL MEDICINE March, 19U 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 asbestos is. 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 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. Tj'ROM the mass of evidence accumulated during the " past 25 years, it now seems definitely established that silica is the public enemy No. I of those engaged in dusty occupations. By itself and in combination with other dusts, it offers a harmful exposure to a conservatively estimated 500,000 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 0 2), 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 Diagram m atic reprM M tation of pathw ay of 4 partid* ' fllurtnrttnf 'factors lnvcly#d In natural dafaata mcchanitm 1 o f the body 2 1 breathing air containing uncombined silicon dioxide ; (Si 0 2) dust, characterized anatomically by general- * ized nodular fibrotic changes throughout both lunp 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). H 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 haire of the nostrils and the mechanical arrangement of the upper 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 0.5 to S microns in size are the only ones capable of producing pulmonary fibrosis. Those above 3 microns are elin- tl - dioxide generalth lungs i and by cupation ity since it recogg. Silica ninerals. " earth's ned. The eviously -ed than common nneling, i polishng, and ch silica onment" xurring rhanism 'ure has *s at the ^ of the ie upper to large of prorobably minated ted epi:s point, f urther u>. point .5 to 3 during e elim Vol. 18, No. 8 INDUSTRIAL MEDICINE Page 27 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 nodes 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 Bepta 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 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 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 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 Dlicrat nodulation of oocond dogroo *Ilicoi< (uncompRcatod) in on Iron minor 1 rock miners will show & 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 actording 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 Bhow surprising resistance and may be comparatively active up till a few hours before death, 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. ! 1.5 h\ i * c i -V* : h fr-; INDUSTRIAL MEDICINE March, 19U 4 f ''t'r' %?*^ ?'*jV?fm- j ' ASBESTOS SILICOSIS X-rays demonstrating M w i in n i n t t i i t and advanced silicosis Because of the lack of physical signs and symptoms, Certain other conditions such as fungus infections, a classification of the stages of silicosis is only practi miliary tuberculosis, miliary calcification and miliary cal when based on x-ray findings. Various observers carcinoma produce shadows in the roentgenogram have made their own tabulations, but the one worked which may be confused with those of silicosis. In these out by Sampson15 affords a practical and satisfactory instances careful study of the film and previous occu grouping: pational history will usually be sufficient to make an __________________________T a b l e IV.___________________ A . U ncom plicated S il ic o sis: 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.) Si--Second degree nodulation (Nodules 2,to 4 mm. in diameter.) S--Third degree nodulation (Nodules over 4 mm.) B. Co m p l ic a t e d S i l i c o s i s : 1. Silicosis with fresh infection. 2. Silicosis with old infection. 8. Silicosis with indeterminate infection. accurate diagnosis. As in all diseases due to dust, treatment is an en 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, except in some instances where infection occurs. Con 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. 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 . 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: 1. Kronen berg and Morse: H ealth H axards of Occupational En vironm ents. D epartm ent of Public H ealth Circular--15*. 2. SArriNOTON, C. O .: Essentials of Industrial H ealth. LIppineott 194$, pp. 1M-1ST. . i : g. Gardner, L. U .: pathology o f Silicosis. Second Symposium <* Slileoeta, Saranac Lake. New York, 1995, I i T able V. X -R ay A ppearance 4. D rinker and H atch: Industrial Dust. McGraw-Hill Book Com pany, Inc., New York, 1988, p. 2. 8. J ohnstone. R. T .: Occupational Diseases. W. B. Saunders, Phils- delphia, 1942. p. 894. ASBESTOSiS Diffuse lesions limited to lower halves t of kings--Hyperventilation in upper portion*. Obliteration of the diaphragm. SILICOSIS Nodular lesions distributed more In upper and mid-lung (ield* or general ised-emphysema in lower halves. Shortening of long diameter ot cheat -with adhesions and tenting of dia phragm. P anooAST, H . K .: Silicosis and Asbeatoait--Introduction, La. Oxford Medical Publications, 1938. 7. Lanza, A. J . : Silicosis and Asbestoais, Oxford Medical Publin- tions, 1988. ' 8. Gardner, L. U ,: Symposium on Silicosis, S aranac Lake, 1934. 8. Sayers, R, R .: Reaction to Mixed D u sts: Atm ospheric and Clin ical Findings in H ard Coal Mining. F ourth S aranac Laboratory Sym posium on Siticosis, 1939. No nodulation. "Ground glass" appearance. May be unilateral.__________________ Marked nodulation. Discrete nodulation to m a s t va con glomerate shadows. Bilateral, 19. Dressen. W. G.. Dallavalle. J . i t . . Edwards, T . I., Milixr. 1 w ,, Sayers, R. R .: A Study o f Asbestoais in the Asbestos Textile todustry. United S tates Public H ealth Bulletin--241, 1938. IX. Gardner, L. U .s Recent Developments in Relation to Silicosb industrial Medicine, 9:48, February. 1940. ch, actions, miliary nogram n these 18 occuake an an en. Once nanent. hronic, R. Con be the When >f workon with ipation. aken to work 'd chest ist and ion. oruU En* ppincott, osinm on ok Comrs. Philo- ii, Lanza. : Pnbliea. 1984. and Clin* o ry Sym* AILLEE, J . cxtile In* Silicosis- Vol. 13, No. 8 INDUSTRIAL MEDICINE Page Zt9 12. X E U K R i m , E. R. A., und P u c b . C. W .: Bcport on ESoeU of Aabesto* Dust on the Lunge and Duet Suppreealon in the Aebeetoe In dustry. H. V . Btat. Oftce. London. 1980. 15. Coox, W. E .: Aebeetoe Duet and the "Curious Bodice" Found in Pulmonary Aebeetocie. B ritish M edical J o u rn a l, 2:678, 1929. 14. Gadnkx. L. U .: Saranac Lake, New York. Pereonal Communica tion. 194S. ' . , 16. SaurooK, H . L.: Third Symimaium on Siltcoeie. Saranac Ike, New York, 19S7. __________ Second, the further procedure under the workmen's compensation laws would be simplified, with the great est possible justice to all concerned. Later decisions regarding compensability in cases of lumbago, spon dylosis, BpondylolisthesiB, osteomyelitis and others can be based upon the recorded thorough examination immediately following the accident, instead of upon Workmen's Compensation Procedure --The Weak Link-- differing expert opinions when the problem of "ag gravation of pre-existing disease" comes up for de cision weeks or usually months after the accident. HENRY H. JORDAN, M.D., Orthopedic Surgeon, Manhattan State Hospital; Associate Orthopedic Surgeon, Lenox Hill Hospital, New York For all these reasons, the management of disabil ities covered by workmen's compensation should be organized in such a way that within 48 hours follow ing the accident, the nature and extent of the injuries can be determined, and a plan for the most efficient T h e shortcoming of the present procedure for the treatment can be outlined. This requires early exam treatment of disabilities covered by workmen's ination of the injured workman by an expert or compensation cannot be blamed on the lack of cooperspecialist who, for obvious reasons, should be neither ation of the medical profession. The fee-splitting employed by the insurance carrier nor permitted to scandals which have attracted so much publicity in treat the cases which he has examined. At the same the State of New York, regrettable as they are, are time, it is necessary that a short cut be found by the not peculiar to workmen's compensation. They can insurance carrier for quick determination of com hardly be held responsible for the unsatisfactory man pensability of an alleged accident, resulting in imme agement of an undetermined number of cases, which diate authorization of the treatment as outlined by in the final analysis results in a great loss of man the expert. power hours, and leads to unnecessary expenses for Such management of the workmen's compensation both prolonged disability and medical care. procedure is undoubtedly possible. It affords the best The crux of the problem lies in the long period of possible rehabilitation of the injured workman, sav time which frequently elapses before the correct diag ing manpower-hours and expense: it eliminates a nosis of the injuries and the compensability of the great deal of friction among claimant, insurance car alleged accident are determined. This period is of rier and physician; and it minimizes the possibility vital importance for quick and complete rehabilita of fraud and malingering. tion. Unfortunately the time is too often not utilized for the most efficient treatment. Most of the injuries are not serious enough to A Case of Onycholysis necessitate immediate hospitalization. A great many however, require more than just emergency treatment with a few follow-up visits. But without authorization the physician--general practitioner or specialist--is not permitted to apply the more expensive diagnostic procedures, e.g., roentgen examination, or to proceed with a well-planned series of physical therapy. If effi cient treatment is postponed until the compensability of the case is determined, the most valuable time for quick and complete rehabilitation is lost. Should the E. R. SATHER, M.D., Alexandria, Minnesota Miss A. M., age 42, single, working now as a house maid, appeared at my office in September, 1943, with a complaint of looseness of the finger nails, the nails becoming brittle and breaking. There was no pain whatsoever, unless the nail happened to break in to the healthy skin. She said that they used to make soap, and that occasionally the lye would get under her physician start the correct treatment immediately, nails. The condition was confined to the nails of the following only hiB professional impulse, he runs the hand, the toe-nails being unaffected. Her physical ex risk of not being able to collect his fee for services amination was essentially negative. Her tonsils had rendered, if compensability is denied later on. To been removed, and her teeth were normal. Her blood escape this dilemma, the patient is frequently referred pressure 120/80; her pulse was rapid, being 96 per to a clinic (O.P.D.) which, at least in wartime, is hard minute; her heart and lungs were negative; and her ly in a position to render the most effective treatment. sedimentation test was 17 mm. at the end of an hour. The general practitioner who sees the patient im Since Oppenheim in 1909 (recounted by H. J. Tem mediately after the accident has, as a rule, neither the pleton, in J .A M A .., December 26, 1931) presented experience nor the facilities to make a complete diag several cases of onycholysis in women doing laundry nosis of the injury. Moreover, he carries at the present work, knowledge of the incidence of this nail dystro time too heavy a burden to render the best possible phy among industrial workers has grown, schwabtz treatment, even in ambulatory cases. Superficial ex and tulipan (Occupational Disease of the Skin, Phila amination may reveal only minor injuries, such as delphia, Lea & Febiger, 1939) list bartenders, bottle contusions, sprains or superficial lacerations. Some washers, cigar makers, confectioners, farm laborers, of these, however, may eventually lead to Berious con fruit workers, gardeners, milkers, vegetable cleaners sequences, viz., Sudeck's atrophy, painful "frozen and washerwomen as prone to this disorder. Soap shoulder," late tendon or nerve injuries, traumatic makers are not listed; but the number of women who osteoarthritis, and many other conditions. make their own soap is small, and it seems possible There can be no doubt that correct and complete that thiB job could precipitate an attack of onycholysis diagnosis of the type and extent of the injuries im in a predisposed person. . mediately following the accident, with careful atten The treatment in this case consisted in having the tion to signs of pathology which are not the result patient refrain from using soap, and then applying of the injury, would have at least two advantages: a weak acid glycerine to promote healing and counter First, the injured worker would receive from the act the effects of the alkali. When last seen, she showed very beginning the most efficient treatment, based on no improvement, probably owing to the fact that Bhe correct diagnosis. is still washing dishes in soapy water.