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FILE NAME: Norton (NORT) DATE: 1936 DOC#: NORT009 DOCUMENT DESCRIPTION: Journal Article - Clinical Aspects, Diagnosis and Treatment of Pneumoconiosis lose uaas, ntrol ealtb u and 1934. i sfliaenoy [ealtb VT-W o/ / ^ t - ; CLINICAL ASPECTS, DIAGNOSIS AND TREATM ENT OF PNEUMOCONIOSIS* W. Irving Clark from the Norton Company, Worcester, and Harvard School 0} Public Health, Boston, Matt. TH ERE are two types of dust which may cause some degree of pneumoconiosis; these have been termed inert and active dusts. m ight be called the normal breathing method. 2. Injection of suspensions o f dusts. --This consists in injecting suspen The determination as to whether or sions of dusts into various parts of not a dust is active or inert has been animals to detect the capacities of readied by pathological examination different dusts to provoke reaction in of the lungs of those dying of pneumo the tissues. Results are obtained coniosis, by clinical studies, especially more rapidly than by dusting b u t do x-ray, and by animal experimentation. n o t correctly show the natural de R eview of Animal E xperiments velopment of disease in the lungs. The dust suspendons may be intro The study by animal experimenta tion has been particularly valuable as it provides a method of determining the effect of a given dust upon the liv ing tissues and a comparison with the effect of similar exposure to other duced into the animal by: 1. Intratracheal or bronchoscopie injections. 2. Intraperitoneal injections (Mil- ler-Sayers method (2)). 3. Subcutaneous injections. dusts. The animals used have been 4. Intravenous injections--showing white rats, rabbits, guinea pigs, mon the effects of the dust on the extra- keys, fowl, cats, and, for some ex pulmonary viscera. periments, tadpoles and fish (1, p. 44). 5. Intracutaneous injections--for The methods used have been: 1. Dusting.--This consists in ex posing the experimental animal to a "high concentration of dust (up to 10 or 12 billion particles per cu. ft. of air, dark-field) to produce maximum effects in short tim e." This method gross reaction. 6. Intra-lymphatic injections--for reaction of lymph node cells (3). All animals tested either by dusting or b y injection showed a tissue reac tion to silica. This reaction was typi fied by the formation of fibrotic * Received for publication June 34, 1936. Read before the Harvard University Tercentenary Celebration, 1636-1936, Sym posium on "The Environment and its Effect upon Man," Harvard- School of Public Health, Boston, August 27, 1936. When presented, the paper was illus trated by lantern Blides showing x-rays-and specimens of pathological conditions. nodules except in the cold blooded ani mals where there was necrosis followed b y some fibrosis. Changes in sus ceptibility of animals to tuberculosis as a result of the effects of various dusts have also been studied, and the 537 . IP 'r!- phri?'.V S !- : *! P ' * i 'i| isrv-.fc Jli>ft vj3 if' -:-ir ib '.a P SC-ALL-01222 SCF-FA-0366 538 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [Oct., 1938 activating effect of silica demon Sil ic o s is iatit strated. The Committee on Pneumoconio tene The effect of the inert dusts upon the sis and the Committee on Standards of root animal tissue was fdhnd similar to th at the American Public Health Associa late of any foreign body. There was reac tion (4) adopted in 1932 the following guai tionary enlargement of lymphatic definition: "Silicosis is a disease due to eels, nodes, slight fibrotic reaction imme breathing air containing silica (SiOi) by diately surrounding the injected dust characterized anatomically by general the b u t no continuation of this fibrosis ized fibrotic changes and the develop neig and no formation of nodules. The ment of miliary nodulation in both the exact pathology noted was scattered lungs, and clinically by shortness of i off or clumped cells containing the inert breath, decreased chest expansion, i fori dust lying in the alveoli, slight inflam lessened capacity for work, absence of whi mation or no inflammation of the fever, increased susceptibility to tu the adjacent walls, a slow accumulation berculosis, (some or all of which symp the of dust-containing cells in the lymph toms may be present) and by charac the nodes with enlargement of the nodes, teristic x-ray findings." mai and a deposition of dust about the fibr lymphatics of the lung or pleura. I. Pathology o f Silicosis on, When inert substances were injected exti intravenously, intraperitoneally or D ust particles after reaching the tiss subcutaneously, there was no reaction lung alveoli may remain quiescent for con beyond th a t of .any foreign body (2). a considerable period as is the case are As a result of such experiments with the inert dusts, or they may pene of which have been repeated in many trate the lymph spaces in small num lyn parts of the world, it is believed th at of bers. The bulk, however, are phago- the all suspected dusts only silica has a cytosed, th a t is engulfed, by wandering anc specific action upon animal tissue endothelial cells which a t first, lining stri which results in fibrotic nodulation. the wall of the alveolus, become de 1 Asbestos fibres produce a peculiar re tached, and then, having taken up the ! of I action in the lung which is different dust particles, pass by ameboid move alii from silica. Following the inhalation ment through the walls of the alveolus noi of asbestos dust there are formed into the lymph spaces. The cells now mn "cuffs of more dense connective tissue Blowly migrate to the minute lymph of about the terminal bronchioles'' (1, islands which guard the entrance to SCO p. 46). Contraction and collapse of tthhreousgmh altlhesley,mtphheantcice tvoestsheels,lympapshs 141r the alveoli supplied by the affected vessels, and finally are caught by the tia bronchioles occurs. This is followed large group of lymphatic glands which voi by induration and fibrosis of the col form p art of the hilus or root of th the lapsed alveoli, presenting the picture lung. These wandering cells are com of of diffuse fibrosis of parts of the af monly called dust cells. As fected lung with persistent fod of The piling up of cells and the reac enl normal air spaces. tion of the glands blocks the free circu- cai vol. IS, no. ] CLINICAL ASPECTS AND DIAGNOSIS OF PNEUMOCONIOSIS 539 lation of lymph so th at the dust cells tend to move slowly toward the lung roots, blocking the lymph vessels and later the minute lymph masses which guard the entrance to the lymph ves sels. The dust cells which are killed by the silica disintegrate and free the silica dust for further injury to the neighboring tissues. The reaction of the tissues to silica is the production of fibrous tissue. Thus fibrous tissue forms along the lymphatic vessels which accompany the blood vessels of the lung, invades the septa between the lobes, and spreads its shoots into the lung tissue itself. The minute masses of lymphatic tissue become fibrotic nodules and these, as time goes on, increase in number to such an extent that, combined with th e fibrous tissue of the former lymph channels, conglomerate masses of fibrous tissue are formed, blocking off large portions of the lungs. The blocking of the lym ph How toward the hilus increases th e spread of dust cells to the pleura and eventually leads to fibrosis of this structure. The fibrotic nodule is characteristic of silicosis. I t is a small, discrete hy aline mass surrounded by apparently normal lung. I t does not exceed 6 mm. in diameter. "Occasionally some of these nodules may show micro scopic foci of central necrosis" (1, p. 146). This increasing amount of fibrous tissue obliterates the alveoli and pro vokes a compensatory enlargement of th e alveoli elsewhere. This condition of enlargement is called emphysema. As the amount of air space is insuffici ent to permit the normal oxygencarbon dioxide interchange of the lungs required b y the b o d /, the effort of the heart to pump blood fast enough may promote enlargement of th at vital organ. This, however, if it occurs, is a terminal condition infrequently ob served, as the patient usually develops pulmonary tuberculosis or dies of an intercurrent disease before this stage is reached. I t m ust be remembered th a t only one-fourth of one lung is necessary for life, and th a t the amount of fibrosis m ust be enormous to re strict the lung capacity to this extent. I I . Symptoms The effect of the underlying pathol ogy upon the workman is at first too slight to be detected by physical ex amination and the worker shows no symptoms. While there is a patho logical condition, present, it is to all intents and purposes harmless, in that if it does not progress rapidly it may not provoke symptoms during a work er's life, or only during the last decade. Even respiratory disease of another nature, such as bronchite or even pneumonia, may occur with recovery during this period. As the condition progresses, how ever, more and more of the lung tissue is converted into fibrous tissue, and the patient begins to chow certain symptoms. He complains of short ness of breath when he goes up-hill and says th at he notices his heart beat on exertion. He also mentions a cough which is a t first dry and infrequent, b ut which gradually becomes moist and frequent. W ith the cough he raises scanty, stringy sputum which is some times discolored. The sputum is never large in am ount unless he catches cold and develops bronchitis. At this Sc 640 JOURNAL OF INDUSTRIAL H Y G IEN E AND TOXICOLOGY (Oct., 1936 stage an attack of bronchitis does not disappear but becomes chronic. Dur ing this period the silicotic m ay com plain of pain in the chest due to pleu risy or to epigastric pain, anorexia, and morning vomiting. While he is able to work, the victim cannot carry on his usual tasks and seeks lighter work. Slowly the shortness of breath in creases, the patient has poor lung ex pansion, and his color becomes pale and his lips bluish. At this stage pulmonary tuberculosis is a frequent complication. When this occurs, the cough becomes more severe and continuous, the sputum free and moist, areas of dulness to percussion are noted, riles are heard over the chest on physical examina tion, and cavitation may be detected. Tubercle bacilli may or may n ot be present in the sputum. M any of these cases are able to carry on light work for years before finally succumb ing. Hemorrhage from th e lungs oc casionally occurs. During the early stages when peri vascular, peribronchial, lymph node reaction is present there are only in definite physical signs. Irvine (5) de scribes these as follows: 1. Acertain lack of elasticity of the chest wall during movements of respiration to gether with 2. A somewhat reduced air entry, and 3. A characteristic alteration of the in spiratory murmur from the normal vesicular character to a higher pitched or "harehened," thinned and commonly somewhat shortened type, the expiratory murmur although somewhat prolonged remaining fainter than the inspiratory. There is little change in these signs as the disease progresses. "The per cussion note is somewhat flattened w ithout being definitely dull especially posteriorly. Breath sounds have more definite characteristic thinning, the expiration bring longer and fainter" (6). W ith the advent of tuberculosis the physical signs are those of that disease. I I I . X-ray The most im portant evidence of silicosis B obtained b y x-ray. While a flat film gives valuable information, an accurate diagnosis requires a stereo scopic set of films. Iu many cases a lateral film is desirable in order to de termine the amount of emphysema present and the rise of the heart. Fluoroscopic examination is of inter est in cases where diaphragmatic ad hesions are suspected or shown on the film. The old classification into first, sec ond and third stages has been recently changed to a more descriptive nomen clature. The conditions noted on the film are now called: 1. Stage of perivascular, peribron chial, lymph node proliferation. Ir regular exaggeration of linear mark ings. 2. Stage of nodulation. 3. Stage of fibrosis w ith conglomer ate masses. 4. Any of above stages complicated by shadows characteristic of tubercu losis. The first is n ot considered as diag nostic of silicosis as it m ay occur in persons who are in good health or in a number of pathological conditions which have nothing to do with silicosis. The stage of nodulation is pathog nomonic of silicosis b u t may be con fused w ith films of miliary tuberculosis. vol. I I j T1 ate ; 1 broil t i1 ! D 1. j mat i dust ! 2. | 3. 4. 1 sisa ! 0 ' are i mos ! whe i Abs ; weij i sugj ! chef T the ! cas< ! bac S has Thi pro cau "E ma cer tiss cei fib: 3 gei ub ve) `T sili etc vol. 18, no. 8] CLINICAL ASPECT8 AND DIAGNOSIS OF PNEOMOCONIOSIS 541 The stage of fibrosis with conglomer ate masses may be confused with fi broid phthisis. TV. Diagnosis Diagnosis is made upon: 1. Occupational history with esti mated length of exposure, quality of dust and quantity of dust. 2. Physical examination. 3. X-ray examination. 4. Presence or absence of tuberculo sis as a complication. Of these measures the first and third are most important. Probably the most difficult thing to decide is whether or not tuberculosis is present. Absence of fever and maintenance of weight, with absence of physical signs suggesting active inflammation in the chest, is indicative of simple silicosis. The absence of tubercle bacilli from the sputum is inconclusive, as many cases of silico-tuberculosis fail to show bacilli in the sputum. V . Progress Silicosis once established in the lung has a strong tendency to progress. This appears to be owing to the toxic properties of the silica particle. What causes this toxic action is still in doubt. "Experiments and human pathological material indicate that in high con centrations silica is .toxic and kills tissue; prolonged action of lower con centrations cause proliferation and fibrosis" (1, p. 46). In spite of the fact that quartz is generally recognized as relatively insol uble, there is great rapidity of de velopment of body reactions to silica. "Possibly. unexplored properties of silica, electrical charge, adsorption etc., are concerned" (1, p. 48). This progressive tendency has been noted by Irvine, Bhme, Bussell and others (1, P- 28). The question is not what is the pres ent condition, of the silicotic, but how rapidly it will advance and how far. This is a serious problem in industry, for a worker having no symptoms and an early stage pathology by x-ray, may develop a disabling silicosis or a com plicating tuberculosis. I t is, there fore, possible for a worker to contract his disease while working for one em ployer and to develop symptoms many years later while working for another. If the work he is doing for the second employer involves exposure to an in ert dust the employer may have diffi culty in proving that this was not the cause of disability. One of the striking differences be tween the effects of the inert dusts and silica dust is the lade of progress of pathology in the former as compared with the latter. Bhme (7) found th at silicosis progressed after removal from exposure in 20 per cent of the cases diagnosed as having silicosis grade 1, in 40 per cent of the cases in grade 2 and in practically all the cases in grade 3. The experience of the State of Wisconsin, however, suggests th at silicosis detected at an early stage in many cases will not progress if the worker is transferred to nondusty work (8) though the reports of Watkins-Pitchford (9) and Britton and Head (10) make this somewhat doubtful. Infection may play a part in the de velopment. In fact, it is the frequent and serious complication of silicosis, and of the common infections, pulmon ary tuberculosis is by far the most serious. 542 JOURNAL OF INDUSTRIAL H Y G IEN E AND TOXICOLOGY \Oct., 1936 Tuberculosis may develop early or late in the disease. In those who have an inactive focys in the lung, the silica dust may change the condition to one of activity, or in cases of well-de veloped silicosis, tuberculosis may be superimposed upon the silicotic fibrosis. Thus Kettle writes, "harmful dusts if inhaled into the lung may excite to activity a latent tuberculosis infec tion; they may exaggerate an active tuberculosis lesion or a coincident in fection; and they may render the lung less able to cope with a superimposed infection" (11). The course of silicosis with a second ary tuberculosis is usually slow and without the usual symptoms of in toxication and may be carried for years without serious impairment of working capacity. While tuberculosis is the most fre quent complication and cause of death, other infections do occur. On the Rand pneumonia is a common cause of disability and death. Pope and Zacks found pneumonia occurring with great frequency among foundry workers in Massachusetts. Proskc and Sayers have confirmed Cummingp' discovery of fuso-epirochetal organisms as a cause of infection among miners in Picher, while chronic bronchitis with asthm a is fairly common (12, p. 47). Collis and Yule (13) compared the mortality experience of an occupa tional group exposed to silica dust with th at of the general population, and w ith th a t of an occupational group exposed to dust not containing silica. As a result of the study, they con cluded th a t silica is a body poison like lead. Even though it exerts its primary injurious effects on the re spiratory tract, the silica slowly invades the body, involving the circulatory system, the nervous system, the diges tive organs, the kidneys and liver, and eventually causes death through its harmful effect upon one or another of these organs. A sbesto sis "Asbestosis is a pneumoconiosis caused by the inhalation of asbestos dust. I t is distinct from silicosis both in its pathology and clinically. As bestos is a hydrated magnesium sili cate containing no free silica b u t about 44 per cent of combined silica, 43 per cent magnesium, nearly 13 per cent of water and traces of iron and nickel" (14). I . Pathology of Asbestosis Asbestos dust differs from other inhalable dusts in th a t it exists in thread like fibres in which the diameter may be very small (5 microns or less) but which m ay be many microns in length. These dust fibres do not appear to enter the alveoli. They are stopped a t the neck of the alveolus where they are phagocytosed or penetrate the tissues. Acting specifically or merely as a foreign body they become sur rounded first by mononuclear phago cytes, later by giant cells and last by fibrous tissue. There is no migra tion in d ust cells to the lymphatics and lymph nodes as is seen in silicosis. The newly formed fibrous tissue con tracts, constricting the neck of the al veolus so th a t no air can enter. Col lapse of the alveolus follows and subsequent fibrosis. In this way the lower parts of the lungs are filled with interstitial fibro sis and the air space markedly dimin- sol. iehe maj lun; the alw. con 1 con fret 1i bod (15 dri< luc dm are int occ dut dia cor exj the pn wh ! tos I Tfc ca; i vit T1 ! lot ou be by bj i ge fri fii ta sb vades afcory diges- and ;b it$ ier of aiosis estos both Asi siliJ)OUt i per cent jkel" t in* eadmay but gth. ir to Jped they the rely 8UTagot by graitics osis. coni alColand the brooin* vol. 18, no. 8] CLINICAL ASPECTS AND DIAGNOSIS OF PNEUMOCONIOSIS 543 ished. A compensatory emphysema may occur in the upper part of the lungs. Thickening of the pleura over the lover half of the chest is almost always present. Tuberculosis as a complicating factor is not common. The asbestos fibre after it has be come fixed at the neck of the alveolus frequently develops into a "curious body," the asbestosis body of Cooke (15). This is a long, narrow, cylin drical body, golden yellow and trans lucent, often with rounded ends like a dumbbell. These asbestosis bodies are found on autopsy and occasionally in the sputum. As similar bodies may occur in lungs not exposed to asbestos dust, the finding of these bodies iBnot diagnostic of asbestosis unless ac companied by a definite history of exposure to asbestos dust. I I . Symptoms of Asbestosis The symptoms of asbestosis, like those of silicosis, are cough and dys pnea. With the cough there is sputum which may or may not contain asbes tosis bodies. Hemoptysis is rare. There is loss of weight in the advanced cases, and marked reduction in the vital capacity and in chest expansion. The patient's face has an "earthy" look. In advanced cases the dyspnea is out of proportion to the physical signs, being very severe, and is accompanied by blueness of the lips and occasionally by clubbing of the fingers. The fin gers frequently show "asbestos corns" from the penetration and irritation of fine spicules of asbestos which are de tached from the asbestos in handling. I I I . Physical Examination The patient, if an advanced case, shows loss of weight. The chest is emphysematous, and respiration is shallow, expansion being frequently less than 1 inch. The percussion note is one of dull tympany but with no definite dullness. The breath sounds are distant and expiration prolonged. The heart is normal in size, but lateral x-ray may show an anteroposterior enlargement. IV . X-ray This shows a fine mottling of a "ground glass" quality over the lower half of the chest. There is often an obliteration of the costophrenic angle and pleural thickening, shown par ticularly in the interlobular pleural on the right. The lateral view may show well-marked compensatory emphy sema. A spot of tuberculosis at either apex is occasional but rare. Still later in the course of the dis ease the appearance is that of a very fine stippling th at obliterates most of the natural markings. The pleural shadow is definitely thickened. In some of the advanced eases the heart is enlarged and radiating from it into the lung fields is a series of heavy fi brous bands. This picture has been re ferred to as "porcupine heart." A nthhaco-Siu c o s ib This disease occurs among hard coal miners and is commonly known as miners' asthma. I t is caused by the inhalation of large amounts of dust consisting of a mixture of anthracite coal and quartz, the quartz coming from the rock in which the coal is imbedded. The pathology consists of a clogging of the lymph spaces with carbon par ticles which invade the upper lobes especially. Accompanying this is a linear or nodular fibrosis due to the 544 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [Oct., ISSe inhaled silica particles. 'When large areas of the lung are involved there is a compensatory emphysema. I. Symptoms of Anthraco-SUicosis The cardinal symptom of anthracosilicosis is shortness of breath, which explains the term "miners' asthma." With this there is cough and sputum. The cough may be dry and the sputum scanty bu t if infection in the form of bronchitis is present, the sputum is muco-purulent and colored with coal dust. As in silicosis, tuberculosis is a frequent complication. The physical signs are similar to those of simple silicosis or of silicosis with infection. Diagnosis is made largely by x-ray which gives a picture very similar to th at of simple silicosis. The U. S. Public Health study on this problem (16) suggests that the true lung injury is due to the silica inhaled rather than to the carbon particles. Carbon has been found to be harmless when inhaled in the form of smoke and by animal experiment. Inset Dusts I . Pathology The inert dusts are relatively harm less. They may increase the fre quency of respiratory disease when inhaled in large amounts, but this has not as yet been proved statistically. Workers inhaling these dusts develop a mild fibrosis which follows the course of the lymphatics along the bronchoarterial tree and is accompanied by enlargement of the trachial lymph nodes. This reaction which is very slow, after a number of years may progress to a moderate amount of in terstitial thickening. The pleura may be thickened and there may be diar phragmatic adhesions. These later manifestations only appear after many yearn of constant exposure to a high concentration of dust. I I . Symptoms Caused by Inert Dusts The symptoms of the pneumoconio sis of inert dusts are negligible. If the exposure has been long and the dust discharge abnormally heavy, there may be some dyspnea on moderate working. This is not usually severe enough to interfere with the worker's normal activities and may be caused by degenerative changes of the heart due to advancing age, as much as to the pathology of the lung. There is no evidence th a t the inert dusts, un less mixed with an active dust, can produce disability. I I I . X -ray Picture, Physical Examina tion and Diagnosis The x-ray picture is that of peri vascular, peribronchial, lymph node thickening which does not progress. Some diaphragmatic adhesions may show in cases with long exposure to heavy concentrations of dust. Serial pictures fail to show nodulation or the massive areas of fibrosis which char acterize silicosis. The physical examination of those exposed to inert dusts is usually nega tive. In' a few cases where there has been prolonged exposure to great quan tities of dust there may be some re striction of chest expansion and signs of emphysema. The diagnosis is made by physical examination, occupational history, and x-ray. A typical inert dust is th at of the artificial abrasive, aluminum oxide. This material is widely used in grind- 193$ iter any ugh i sis j aio~ : the , lust sere 1 .'ate rere : er's \ : ;art j i to ; e is un | can [ i i en- ode ess. nay * to rial i the iar iose igahas lanreigns ical and the ide. nH- ml. 18, no. *1 CLINICAL ASPECTS AND DIAGNOSIS OF PNEUMOCONIOSIS 545 ing wheels and for polishing, sand paper, etc. In the year 1929 over 71,000 tons were sold or used in plants in the United States and Canada (17). The use of aluminum oxide creates a certain amount of dust. The effect of this dust has been studied by Clark (18) and Simmons clinically and by Gardner (19) on the experimental animal. In a factory where artificial abrasives and grinding wheels are manufactured, Clark has studied the effects of inhalation of this substance for 25 years. He believes th a t in factories which provide proper dust removal, the continuous inhalation of artificial abrasive dust extending over many years of work does not produce the symptoms or present the x-ray findingg of crippling fibrosis of the lung; th a t the number of cases of pulmonary tuberculosis does not greatly exceed the number normally present in the community; and th at workers using wheels made of artificial abrasive or using this substance for polishing or other purposes run b u t slight risk of pneumoconiosis if excessive dust is removed by exhaust systems. In spite of the fact that clinical and experimental evidence points to the relative harmlessness of the inert dusts, an effort should be made to keep the dust count around 20 million particles per cubic foot of air. This will make working conditions much more satisfactory to the worker and will reduce the hazard of respiratory disease. T reatment of P neumoconiosis The only method of treatment of the pneumoconioses is prevention. Dust in quantity must be eliminated from industry wherever possible, and in most operations this is feasible. In a few where it is not, protective devices such as respirators or positive air pressure helmets must be used by the worker. When a worker is found upon examination to have lung fibrosis it is wise to keep him at work in a nondusty department. While his lung condition, if it is due to silica or to asbestos dust, will progress slowly, many years of profitable work are before him unless infection intervenes. As dyspnea increases, lighter work must be provided- If tuberculosis complicates the picture and the patient develops tubercle bacilli in the sputum, he must be isolated from other workers, b ut even then may be able to do fight outdoor work. In more severe cases where there is temperature, all work must, of course, be stopped, Exposure The rapidity of development of silicosis and of asbestosis depends upon the amount of dust inhaled and the percentage of free silica (SiO*) or of asbestos in the dust. In men exposed to heavy dust clouds with a high concentration of silica, silicosis has developed in as little as 2 years, but under the usual exposures of mining and of industry where the free silica usually varies from 13 to 35 per cent, the development is slow and symptoms do not appear for 15 or more years, In the case of asbestosis, the de velopment of symptoms is more rapid, g to 8 yeare be^g the usual required time of exposure, Efforts are now being made to corre- late the exposure with the pathology, as shown by x-ray, and with the physi- 546 JOURNAL OF INDUSTRIAL H Y G IEN E AND TOXICOLOGY [Oct., 19S6 cal signs. In other words, an effort is being made to determine standards' of permissible amounts of dust in the working air for both the inert and the harmful dusts. Such standards will be of the greatest value to industry in its effort to reduce its dust hazard to a mininmim E pidemiology I . Silicosis The danger of inhaling inorganic dust has been recognised for centuries, but careful study of the effect of such inhalation was first instituted in South Africa and culminated in the Inter national Conference on Silicosis held in Johannesberg in 1930. In 1933 V an Siclen (20) published an estimate of the health hazard from dust in the mines and allied industries of the United States. In his study he found th a t of 7722 men examined in the Tri-State zinc-lead district of southwest Missouri in 1927-28, 5704 were classified as negative for lung dis ease, 1362 had signs of first stage sili cosis, 253 had second stage, and 32 had third stage. The remainder showed signs of tuberculosis with or w ithout silicosis. In B utte mines (M ontana), of 1018 miners 42.4 per cent showed definite signs of dust injury to the lungs. In the Lead-Deadwood district mines in South D akota the sickness rates per thousand for respiratory dis ease was two and a half times greater than in general industry, while the tuberculosis rate was almost ten times greater. Grouping the various industries studied, Van Siclen found th a t in m etal mining about 62,228 workers were ex posed while among those engaged in non-metallic mining or quarrying, 23,665 had a respiratory hazard. T he prevalence of silicosis in the general population was studied by Lanza and Vane in 1934 (21). They cite the following occupations as con stituting a definite silicosis hazard: 1. Anthracite-coal and metal min ing, quarrying. 2. Certain manufacturing industries such as potteries, glass works, and plants manufacturing granite, sand blasting. 3. Construction work--rock drill ing, handling sand and gravel. Their rough estimate of the num ber of workers exposed to silica dust to a harmful degree in the United States is upward of 500,000. A careful study of 2,600 granite and foundry workers has recently been made by Pope an d Zacks (22) in which correlation of the duration of exposure to d ust mid th e incidence of silicosis was determined: Their conclusions are as follows: 1. In representative groups of both granite and foundry workers in Massa chusetts the frequency of silicosis and of silicosis with tuberculosis wss found to be positively correlated with the duration of exposure to dusts containing free silica and to concentration of such dusts in the occu pational environment. 2. Among the granite workers examined silicosis alone was found in 15.2 per cent and silicosis complicated with tuberculosis in 7.6 per cent. 3. Tuberculosis is the cause of death in over one-third of all granite workers, a proportionate mortality three times that in foundry workers and four times th a t in all males of 20 years and ov.ef. In 1907 SummonB of the Miners' Phthisis Committee of Australia re ported th a t gold miners there who contracted silicosis died of tuberculosis (23) by star autl the Iosif .rate B of Bar grai beli tho tub SUi Sili Asi Asl i f chf i i ha T1 du fo: "( nc be i t ai w lo OI p> Cf Cf A vol. 18, no. I CLINICAL ASPECTS AND DIAGNOSIS OF PNEUMOCONIOSIS 647 (23). "The initial studies of silicosis by workers in South Africa were started by a demand made upon health authorities to determine the cause of the excessive mortality from tubercu losis which was increasing a t a rapid .rate among the miners there." Russell found an excessive number of deaths from tuberculosis in his Barr, Vermont study of the health of granite workers (24) and Gardner (25) believes th at a t least 75 per cent of those who develop silicosis contract tuberculosis. berculoas is so often associated with asbestosia th a t it seems probable, that the association is more than acci dental". Gardner (1, p. 51) says th a t many autopsies show a combination of tu berculosis with asbestosis and other silicate dusts but "th at surveys of liv ing American workmen show no great excess of this infection" , while Lanza (28) in a study of dust conditions in asbestos mines and mills in Canada and in fabricating plants along the Atlantic seaboard found in his study TABLE 1 Silicosis and Asbestosis in Great Britain, through 1934* mnoiBor PBiTBB TBRAOB Mmnoir or bmfloykch* DV TSARS AOl ATD1ATB MsTTsemp Miniaran A m i Silicosis...................................................... 261 55.4 60 2.3 34.8 Silicosis with tuberculosis......................... 315 52.5 67 2.0 32.0 Asbestosis................................................... 41 41.0 27 1.5 12.9 Asbestosis with tuberculosis..................... 26 38.0 29 0.8 9.9 * J. C. Bridge: Report o( Chief Inspector of Factories and Workshops, London, 1034, chapter 3. 11. Incidence o f Asbestosia The health hazard of asbestos dust has only been recently recognized. The Regulations for the Asbestos In dustry in England have been in force for only 4 years. Bridge (26) says: "Over a number of years" (number not specified) "the deaths from as bestosis reported to the Department and compiled in 1934 numbered 41 while those from asbestos and tubercu losis numbered 26" . (See Table 1.) Wood and Gloyne began their studies on pulmonary asbestosis in 1928 and published results of the study of 100 cases in 1934 (27). Most of these cases worked in the same factory. According to Wood, " pulmonary tu- of 126 workers by x-ray th a t 67 were diagnosed as having asbestosis in some form, but th at no predisposition to tuberculosis due to asbestos dust was indicated. Clark and Drinker (29) in gumming up present beliefs say th a t while a secondary tubercular in fection is not uncommon in asbestosia, it is far less frequent as a complica tion than in silicosis. SUMMABY 1. Pneumoconiosis is a disease re sulting from the inhalation of inor ganic dust. 2. The two pneumoconioses which produce disability are silicosis and as bestosis. 4 i'1.***v g w ii 1 i ;a . f| f, .'i jj iIlIlI jS:| IS S il. t \I Ii '1 f f [111. IlinftHgt r , IjS, l II}I'S r=<: IIif ] w} 548 JOURNAL O F IN D U STR IA L H Y G IEN E AND TOXICOLOGY [Oct., 1938 3. T he pathology of silicosis is char acterized by the,,presence of fibrotic nodules scattered through both lungs, and th a t of asbestosis is characterized by a n interstitial fibrosis involving the lower half of both lungs. 4. T he sym ptom s of silicosis and as bestosis are similar, the m ost im portant being dyspnea. 5. The m ost common complication is pulm onary tuberculosis which in silicosis is a frequent cause of death. 6. T he diagnosis of both silicosis and asbestosis is made'largely b y a correla tion of history and symptoms with the x-ray examination. 7. The treatm ent of pneumoconio sis is preventive and symptomatic. 8. The course of silicosis and of as bestosis is slow b u t eventually leads to incapacity due either to the dis ease itself or to a complication, fre quently chronic pulmonary tubercu losis. 9. The number of workers exposed to harmful mineral dusts in mining and in industry in the United States has been estimated as 500,000. BIBLIOGRAPHY 1. Gardner, L. U.: Second symposium on silicosis a t Saranac Lake, N. Y., 1935. Employers' Mutuals, Wausau, Wis., 1935. 2. Miller, J. W., and Sayers, R. R.: Microscopic appearances of experi mentally produced dust nodules in the peritoneum. U. 8. Pub. Health Repts., 60,1619 (1935). 3. D rinker, C. K ., F ield, M. E ., and D rinker, P .: Tbe.cellular response of lymph nodes to suspensions of crystal line silica and to two varieties of eericite introduced through lym phatics. T his J our., 18, 296 (1934). 4. L ana, A. J.: The etiology of silicosis. J. A. M. A., 101, 583 (1933). 5. I rvins, L. J.: Report upon the work of the Miners' Phthisis Medical Bureau over the year ended July 31, 1928. Pretoria, 1929. 6. Sayers, R. R.: The clinical manifesta tions of silicosis. J. A. M. A., 101, 580 (1933). 7. B ohme, A.:Die Prognose der Staublungenerkrankung (SilikoBe). Beitr. a. Klin. d. Tuberc., 84, 119 (1933). Abstr. in T his J our., 18, 57 (1934). 8. N elson, H. A.: Silicosis problem solved in Wisconsin. Am. Labor Legis. Rev., 94, 53 (1936). 9. Watkins-Pitchtord, W.: The silicosis of the South African gold mines, and the changes produced in it by legisla tive and administrative efforts. T his J our., 9 ,110 (1927). 10. Britton, J. A., and Head, J. R.: Pneu moconiosis, the delayed development of symptoms. J. A. M. A., 98, 1938 (1931). 11. Kettle, E. H.: The action of harmful dusts. Inst. Min. & Met. (London), June 24,1934. Abstr. in T his J our., 18, 125 (1934). 12. F irst Symposium on Silicosis, Saranac Lake, 1934. Employers' Mutuals, Wausau, Wis., 1935. 13. Co l u 8, E. L., and Yule, G. U .: The m ortality experiences of an occupa tional group exposed to silica dust, compared with th a t of the general population and an occupational group exposed to dust not containing silica. T his J our., 16, 395 (1933). 14. L anza, A. J .: Asbestosis. J . A. M. A., 108, 368 (1936). 15. Cooke, W. E .: Pulmonary asbestosis. Brit. Med. J., 2, 1024 (1927). 16. Sayers, R. R., et al.: Anthraco-silicosis among hard coal miners. U. S. Pub. Health Bull. no. 221 (1935). 17. Roush, G. A.: The mineral industry, its statistics, technology and trade during 1934. McGraw-Hill Book Co., New York, 43, 9 (1935). 18. Clark, W. I.: The duBt hazard in the abrasive industry. I, II, and III. T his J our., 7,345 (1925); 11,92 (1929); and 13, 343 (1931). 19. Gardner, L. U., and Cummtnq s , D. E .: The reaction to fine and medium sized quartz and aluminum oxide particles. >k.\' eol. IS, 21. L* 24. R let., m e cdth the oconio- atic. 1 of asr leads tie dis, freibercur xposed mining States PneuJpment B, 1938 armful ndon), Jotrn., aranae ituals, The :eupadust, eneral group silica. tl. A., itosis. U .S . istry, trade :Co., l the in. 829); '. E. : lized des. vol. 18, no. 8J CLINICAL ASPECTS AND DIAGNOSIS OF PNEUMOCONIOSIS 549 Silicotic cirrhosis of the liver. Am. J. Path., 9 (whole no. 64) 751 (1933). 20. Van Sic le n , M .: H ealth hazard from dust in the mines and allied industries of the United States--Initial survey of the extent and severity. Am. Inst. Min. & Met. Engin., Contribution no. 46 (1933). 21. L anza, A. J., and Van, R. J . : The prev alence of silicosis in the general population and its effects upon the incidence of tuberculosis. Am. Rev. Tuberc., 9, 8 (1934). 22. P ope, A. S., and Zacks, D .: Epidemio logical aspects of silicosis and tuber culosis. Ibid., SB, 229 (1936). 23. Summons, W. E .: Report of miners' phthisis submitted by the Committee of the Bendigo Hospital, Victoria, 1907. 24. R ussell, A. E ., B ritten, R . H ., T hompson, L. R ., and B loomfield, J. J . : The health of workers in dusty trades. II. Exposure to siliceous dust (granite industry). U. 8. Pub. H ealth Bull. no. 187 (ig29). 26. Gardner, L. U.: Silicosis and its rela tion to tuberculosis. Am. Rev. Tuberc., 9, 1 (1934). 26. B ridge, j . C. : E xtract from Annual R eport of the Chief Inspector of Factories and Workshops, 1934. (CMD) 4931, Chap. 3, Health, p. 12-13. 27. Wood, W. B., and Glotne, S. R .: Pul monary asbestosis: A review of 100 cases. Lancet, t , 1383 (1934). 28. L anza, A. J., McC onnell, W. J., and F bhnel, J. W. : Effects of the inhala tion of asbestos dust on the lungs of asbestos workers. U. S. Pub. Health Repts., 60,11 (1935). 29. C lare, W. I., and D rinker, P .: In dustrial medicine. National Medical Book Co., New York, 1935 (p. 119). ,V 3. '-I! ,.?ij u. 1 m