Document gaX0n7xNY45e1GYx0Z5pNk9Jq

FILE NAME: New York State & NY Times (NY) DATE: 1950 DOC#: NY004 DOCUMENT DESCRIPTION: Journal Article - Dust Inhalation in Relation to Pulmonary Disease [Author - Dr. Silson of NY Dept of Labor] DISEASES / 1 ' of the CHEST VOLUME XVII! JULY - DECEMBER, 1950 I4 Dust Inhalation in Relation To Pulmonary Disease^' JOHN E, SILSON, M.D.* * New yofk, New York lungs produced by dust, the term pneumoconiosis has been applied Diagnostic Factors in Pneumoconioses ^.n order to establish the diagnosis of pneumoconiosis, two factors must be present: 1) pulmonary pathology which might have beer produced by exposure to a particular dust, and 2) an occupational history of exposure to that dust. The chest physician is generally in a good position to evaluate the first factor, through the medium of signs, symptoms, x-ray inspection and laboratory tests. In de termining the second factor, he is often handicapped by his paucity of knowledge of the nature of his patient's work and the materials handled. Most physicians are aware that a rock miner or stone cutter may be exposed to free silica in amounts capable of causing silicosis. They may not be aware, however, that a worker in a soap factory, which includes in its products scouring powders, may be handling large quantities of silex. which is almost pure pulverized silica. In ,,ther instances, the etiology of the pul monary pathology may not be so readily recognized because the physician is unaware of the more obscure effects upon the iur.-s of a material such as talc or bagasse. Another factor which makes it difficult to recognize the impor tance of an^ industrial dust exposure in the pathogenesis of a pulmonary disease is the close resemblance which frequently exists w York State Chanter, ary 16. 1950. New York ISafSety Standards. New York State Department o?f<"a TM HygSiene and 562 Vol. XVIII DUST INHALATION 53 between that disease and some other pulmonary pathology of non-industrial etiology. When the x-ray picture is characteristic, /as in an obvious case of nodular silicosis, the physician is apt to inquire caiefully into the worker's occupation, and to enlist the aid of industrial hygienists or other experts in an effort to establish a dust etiology. When the clinical and sometimes even the path ological findings are almost identical with some non-occupational disease of the lungs, however, he is not so likely to seek far afiela for an occupational exposure. It was not until the unusual inci dence of workers dying irom what was presumed to be Boeck's sarcoid in a plant manufacturing fluorescent lamps was noted, that the toxicity of one of the materials which they were handling was even suspected, and that the Identity of chronic pulmonary granulomatosis due to beryllium was established.1 Recognition of the dust etiology is even more difficult when the pathology is identical with that of a non-occupat<onal disease, as for instance the primary lung carcinoma seen with increased frequency in chromate workers.2 Another way in which dust inhalation may affect pulmonary disease is by aggravation of a pre- or co-existing non-occupational disease. Today, the fact that silicosis predisposes a worker to tuberculosis, and renders that tuberculosis much more severe, is well established. We are just becoming aware, however, that some of the more innocuous dusts may adversely affect the course of tuberculosis and other pulmonary infections.3 It is no longer con sidered good practice for an individual with arrested tuberculosis to return to work in any dusty environment. We all too frequently, however, see workers with chronic bronchitis, pulmonary emphy sema or even bronchiectasis who are permitted to work In an extremely dusty atmosphere. Even the increased coughing induced by a dust, which is slightly irritant to the upper respiratory pas sages, or necessary to clear these passages of the accumulated particles, may be sufficient to aggravate a chronic pulmonarv diseased " Over and above all of these specific aspects is the general effect of dust on the aging processes of the lung. I would like to quote ;ui observation made by Dr. Edgar Mayer, in an article3 he pub lished a few years ago: " respiratory infections and . . general dust exposure eventually provoke pulmonary change-;. There exist on!, differences in degree, not In kind, between the .m-called normal amount of pulmonary fibrosis so prevalent in the ir:mra! population and those .severe fibrotic processes which destroy ;.he lungs of workers in industries wherein exposures exist to mmre concentrat 'd and continuous effect oi the same agents nnwro in greater dilution in the atmosphere of industrial centers.'' 564 JOHN E. SILSON D ec.. 1950 Dust Characteristics A pre-requisite to the understanding of the effects of dust inha lation upon the lungs is a knowledge of the type of material under discussion. We have chosen to cover in this paper all forms of solid particulate matter generated in the course of industrial operations, because in so many instances their effects are similar or even identical. Fibers and fumes as well as dusts have therefore been included. Since some uncertainty exists as to the exact mean ing of these terms in industrial hygiene, v/e shall start with a few definitions. The term dust Ls applied to the solid particles produced by handling, cutting, crushing, grinding or pounding organic or inorganic materials such as rock, ore, metal, coal, wood, grain, etc. Fibers are the particles similarly produced from organic or in organic material composed of thread-like or slender elements such as cotton, wool, fur, bagasse or asbestos, and are also created in such operations as stripping, spinning and weaving. Fume is a term limited to the solid particles created by condensation from, a gaseous state, generally after volatilization from molten metals, and often accompanied by a chemical reaction such as oxidation. Contrary to general usage, it does not refer to condensations to a liquid droplet form, which are called mists, or to a uniform gaseous dispersion, whether visible or invisible, which is referred to as a vapor or gas. The common denominator of all these materials is thus the fact that they are present in the atmosphere as solid particles. An important characteristic of these particles is their size.1'1 It has been shown both theoretically and experimentally that on inhala tion those which are too large do not reach the lungs, but are filtered out in the upper respiratory passages. Particles which are too small, on the other hand, do not settle cut, and are there fore theoretically not retained in the alveoli but are re-exhaled. The question of the Innocuousness of these sub-microscopic par ticles has recently been open to question. It is a generally accepted principle, however, that the particles exert their greatest dele terious effect upon the lungs when they are between 0.5 and 3 microns in diameter. Tire other important factor determining the reaction of a dust upon the lungs is its composition, that is, its chemical and phys ical characteristics.7 Where it is a mixture of several different compounds, such as the dust created in a granite quarry, the percentage of the most active ingredient (in this instance free silica) is of the utmost importance. Even where the mixture is man-made and not a natural product, its composition has to be taken into consideration. For example, the sand used in an Iron Vol. XVIII DUST INHALATION 565 foundry may consist of almost pure silica, but the dust released in a shake-out operation will have a much lower silica content because a large part of it comes from the iron oxide particles separated from the surface of the casting. The particle structure also appears to play a role: crystalline silica has long been con sidered a far more active substance than the amorphous form. Fumes from a melting operation are frequently much more reac tive than the same material ,,reated as a dust by grinding or crushing. In some instances even the shape of the particles has significance, particularly when their effects are dependent to a large extent upon local mechanical irritation. Protective Mechanisms There are a number of mechanisms by which the lung paren chyma is protected from inhaled dust.7 Many of the particles may be filtered out by the coarse hairs guarding the entrance to the nose, or trapped by the moist walls of the turbinates. Particles deposited on the surface of the mucous membranes of the trachea and bronchi are carried back towards the pharynx by the wave like vibrations of the cilia, and also by the cough reflex induced by the irritation to the lining membranes. Particles which succeed in passing these barriers and gain en trance into the alveoli are ingested by macrophages which ..rise from the alveolar walls and are commonly referred to as "dust cells." Some of these phagocytes, laden with dust, may pass up < into the bronchioles and eventually be carried off in the sputum; the others pass through the walls and into the regional lymphatics. Some of the latter are arrested locally in the peribronchiolar tissue, but the remainder pass onward into the peribronchial and perivascular lymphatics, and are finally trapped in the lymph nodes at the root of the lung. Types of Pathology The type of pulmonary pathology which may be caused by the inhalation of a specific dust is determined by the manner in which this lung cleansing mechanism is disturbed, and by the type of reaction which results. Probably the best known is the fibrotic reaction produced by exposure to silica and similar materials.8 This reaction represents a specific cellular response to the material. The particles engulfed by the dust cells stimulate the production of fibroblasts in any area where they are congregated; and these fibroblasts are eventually replaced by dense fibrous tissue. In the case of dusts other than silica, this fibrosis is usually fairly gen eralized: but with silica, it tends to nodular formations distributed along the lymphatics. In either cKse, the net effect is to make the lungs less elastic, increase their bulk while decreasing then capacity, ad decrease pulmonary circulation anu aeration of the blood. Less characteristic is the action of those dusts which act as general irritants,9 particularly on the respiratory passages, but do not exhibit a specific fibrosing action. Included in this category are most of the organic dusts. Workers first exposed to them respond by sneezing and coughing, but usually quickly become acclimatized so that the irritant action is no longer found trouble some. Continued inhalation of these dusts, however, may resuit in chronic inflammatory changes in the mucous membranes with secondary hyperplasia or atrophy. Degenerative changes have also been noted, with disappearance of the ciliated columnar epithelium and its replacement by a cuboidal or squamous form.10 The chronic cough induced by these irritants may also be responsible for em physema and other secondary changes in the lungs. In addition to this generalized irritant action, certain dusts may elicit a specific inflammatory response.9 This may be of a chemical nature,, as in the case of beryllium or Thomas slag, or may be infectious, due to bacteria or fungi carried in by the dust. In both instances, the pathology of the response depends upon the material producing it, and may be acute or chronic, reversible or perma nently damaging. With some materials, for instance beryllium, the pathology is quite characteristic. With others, particularly those transporting micro-organisms, it may be indistinguishable from non-occupational infections of the pulmonary tract, and only a careful investigation of the patient's occupation will elicit the offending material. Even when the dust particles exert no irritant action whatso ever, there may be slight pulmonary changes due to their mech anical effects.11 Pulmonary allergy is a type of response observed with certain organic dusts,12 particularly those of plant or animal origin. The picture is one of a typical asthma, and only the occupational history differentiates it from identical reactions so commoniy seen from pollens or house dusts. The distinction often can only be made by natch testing or similar procedures, which will demon strate that the responsible antigen is present m the man occupa tional rather than non-occupational environment. Primary carcinoma of the lung has at one Lime or another been ascribed to a great many of the industrial dusts produced in industry. Proving or disproving the carcinogenic properties of any particular material is often an extremely difficult procedure, because the pathology in no way differs from that of a lung cancer of unknown etiology. Merely demonstrating the co-existence Vo!. XVIII DUST INHALATION 567 of cancer and some other pulmonary disease such as silicosis, is not sufficient, since there is no reason why the incidence of malignancy in silicotics should be any lower than it is in nonsilicotics. The only satisfactory proof of such carcinogenicity is the uniquivocal demonstration of an incidence of cancer in workers exposed to a particular dust which is sufficiently higher than that of a comparable group of non-exposed workers to have statistical significance. Great care must be taken in selecting the control group to insure that all extraneous factors, such as age distri bution, sex and non-industrial environment, are identical. The high incidence of lung cancer in the uranium mines of Schnee berg and Joachimsthal has been known for some time.13 More recently, an increased incidence of pulmonary malignancy has been demonstrated in workers exposed to chromate dusts,2 al though the statistical significance of the data which have been collected on this material is still being investigated. Both silica and asbestos have on many occasions been indicted as predis posing to lung cancer; but in the case of silica, it has never been demonstrated statistically, while accumulating evidence points more and more strongly to asbestos as a carcinogenic agent.14 Pulmonary Disease Due to Silica Having presented the general types of pulmonary pathology Which may be produced by dusts, I would like to devote the re gaining time to a brief description of the specific pulmonary effects produced by certain materials. As has been previously pointed out, undoubtedly the most important of these is silica. This is the oxide of the element silicon, and is widely distributed, both free and combined, in the earth's crust. Crystalline silica occurs pure as quartz and as beach sand, and is also scattered in varying percentages throughout many forms of rock, such as granite, marble and sandstone. Dusts containing free silica can be created industrially in a multitude of ways, such as drilling and blasting operations in the course of mining and quarrying, cutting and shaping of stone, rock crushing, sand blasting or any other operations in which quartz, sand or silica-containing rock is processed. The disease8 is characterized anatomically by gen eralized fibrotic changes and the development of miliary nodula tion throughout the lung fields, and clinically by cough and pro gressive shortness of breath. Chest x-ray films show at first an exaggeration of the lung markings and lymph node enlargement, which is followed by nodulation, and finally by coalescence and conglomeration. Tuberculosis may be super-imposed *at any stage, and is believed by some to be present in all areas where coalescence has taken place. As a rule, there is no fever or weight loss in 563 J O H N E. SIL30N D ec., 11)1)0 simple siliaosis, and these signs may be indicative of a complicating tuberculosis. The patient tends to go downhill very rapidly vviui the development of an active tuberculous lesion. Many observers have been of the opinion that silicosis could be caused only by the crystalline form of silica, but evidence is accumulating to the effect that the amorphous form as well is capable of producing pulmonary damage. Observations upon the effects of amorphous silica15 have been made largely on workers exposed to diatomaceous earth, which is a light fluffy material formed by the accumulation of skeletons or shells of diatoms. It has a wide use in industry as filters, fillers and absorbents. In contrast to crystalline silica, it produces fibrosis of the lungs without discrete nodulation. The fibrosis is much more marked when the exposure is to calcined material, during which process microcrystals of chrystobalite may be formed. Disability appears to be less marked than with silica, and the fibrosis seems to dim inish rather than enhance susceptibility to tuberculosis. Another possible example of pulmonary damage due to a non crystalline form of silica occurs in workers fusing bauxite in electric furnaces in the manufacture of alumina abrasives.18 The fumes given off in tiiis operation consist17 of 25 to 10 per cent silicon dioxide and 40 to 60 per cent aluminum oxide, together with small amounts of iron oxide and numerous other impurities. Under the electron microscope they are revealed as fused par ticles varying in size from 1/100 to 1/2 micron in diameter. A high percentage of the workers exposed to these fumes have developed cough with expectoration, weight loss, anorexia, tight ness in the chest, and dyspnea on exertion. X-ray inspections show a lace-like or granular increase in the lung markings, be ginning at the apices. These gradually extend to involve the entire lung fields, and may be accompanied by pleural adhesions causing distortion of the thoracic contents. Spontaneous pneumothorax is a common complication. While the aluminum oxide has gen erally been advanced as the etiological agent responsible lor this disease, it seems quite possible that this may be a response to silica fume with a particle size far lower than that generally considered injurious, especially since more than one form of silica have been shown to be damaging to the lungs, while aluminum oxide has always been considered a non-fibrosing agent. Silica, when present only in combined form as a silicate, has usually been regarded as relatively inert. Considerable evidence, however, has been accumulating against this concept. Probably the best known of the silicates producing severe pulmonary damage is asbestos.18 This is a mineral silicate occurring in the form of long fibers, which renders it capable of being carded, spun, and Vol. XVIII DUST INHALATION 5G9 woven into threads and cloth, or bonded with cement into building shapes. Inhalation of these fibers in the course of mining or processing asbestos has been shown to be responsible for the de velopment of progressive pulmonary fibrosis with diffuse thick ening of the alveolar walls. The outstanding symptoms are dyspnea and dry cough. Emphysema, pulmonary Infections, and secondary caidio-vascular changes due to increased pulmonary resistance are the most common sequelae. Chest x-ray films show a "ground glass" haziness, rather than the reticulation and nodulation of silicosis. Another combined silicate which has been shown to be not completely inert is talc, a hydrated magnesium silicate used exensiveiy in its powdered form as a dusting agent. It may contain variable percentages of free silica; and when these are high the classical picture of silicosis has been observed in workers mining m!riVlni5' gnndmg or otherwise handling it. Even when it contain^ r 1 per cent free silica, however, as is usually the case the mmoonnaaiiwy ffibhromsihsalseimd'ilaSr CtaoP&abslbeestfospisr.o1duIctint?enadsfitnoe bdeifdfuissaeb'lpinugland is frequently accompanied by dyspnea, cough and fatigue In cution deposits of x-ray opaque material on the pleural sur faces m the form of plaques have been observed. Still another silicate showing definite effects upon the lungs mica, which is a double silicate of aluminum and either potas- ThiS minera1' because ifc splite int0 thin sheets tranSparent' and have a high dielectric constant, has innumuable uses m industry, particularly in the manufacture ox electrical equipment. For some time, it has been believed S i the chest pathology so prevalent where it is mined was due to e fiee sinca present in the rocks in which mica deposits occur Even among workers exposed solely to pure mica dust in grinding operations, however, there has been observed- a high iticidence o increased pulmonary fibrosis, with cough and dyspnea The buT'less SymPt TM are the same as Ul03e occurring in silicosis, but less severe. X-ray films show a fine granulation of uneven density wnh coalescence of the lesions in more advanced cases. u/hh11 T 686 exposure3' the common denominator has been silica i ther free or combined. Recently, however, carborundum, which n almost pure silicon carbide containing less than 1 per cent f te sihea. has been suspected of being an agent capable of causing pulmonaiy changes identical with silicosis.21 This has been ex P amed theoretically by the possible oxidation of the material in , l lung. This may be the explanation for the occasional occur- 01 S!llC0sls among workers using carborundum grinding 570 JQJIN E. SILSON Dec., 1950 wheels, which have been considered a completely "safe" substitute for the far more hazardous sandstone wheels. Pulmonary D iseases of Non-Sllicotic Origin The pulmonary changes seen in coal miners has long been at tributed to the free silica content of the shale through which they had to dig to get at the coal. Recent large scale studies in Wales have indicated,33 however, that exposure to very heavy concentrations of coal dust with a negligible percentage of free silica, such as occurs among the coal trimmers on the docks, leads to a form of pneumoconiosis differing from the anthraco-siiicosis of miners. There is a massive fibrosis of the lungs with nodular deposits of anthracotic pigment scattered throughout. The prin cipal symptoms are due to the marked secondary emphysema, and the cardiac changes produced by pulmonary hypertension. Susceptibility to tuberculosis is increased. The x-ray picture is one of reticulation rather than Modulation, because of the lack of opacity of the nodules. Specific pulmonary pathology has also been shown to be pro duced by exposure to fumes and dusts of certain of the metals, notably beryllium and cadmium. Both these substances actually are systemic poisons, but since Industrial exposure to them occurs primarily by Inhalation, the principal pathology is usually present in the lungs. Beryllium is responsible for two types of respiratory disease.31 One is an acute inflammatory reaction varying from a mild phar yngitis or bronchitis to a massive pulmonary edema, which occurs principally among workers exposed to soluble salts in the beryl lium refining industry, The other Is a chronic pulmonary granu lomatosis developing after a delay of several months to years, which occurs primarily among workers exposed to dusts and fumes of the metal, oxide, and certain-complex silicates (fluorescent compounds). It is characterized by a nodular fibrosis giving a characteristic x-ray picture, and a diffuse thickening of the al veolar walls. The outstanding symptoms are dyspnea, fatigue, anorexia, severe weight loss and intractable cough. The mortality is high, and some degree of permanent disability remains among nearly all those who survive. Interrelations between the acute and chronic forms, and the occurrence of an intermediate sub acute type, indicate that they are probably all widely different m an ifestation s of the sam e disease process. The pulmonary pathology due to cadmium34 is generally en countered when workers unwittingly create cadmium fumes with out adequate protection: for example, in flame cutting or welding Vu!. XVIII DUST INHALATION 571 cadmium plated iron. It first causes a cough ana dryness of the throat, which then progresses to severe constricting chest pain and dyspnea, dizziness, chills and prostration. The pathological picture is that of pulmonary congestion and edema, with intersti tial pneumonitis, hemorrhage and cellular infiltration. The term siderosis25 has been applied to a benign pneumoco niosis due to exposure to dust and fumes of iron and its oxides, usually seen among hematite miners, welders and other iron work ers. Pathologically, siderosis consists of a deposition of phagccytized iron particles distributed in nodular fashion along the lymphatics. Outside of the mechanical effects of excessive pul monary accumulation previously discussed, its importance lies chiefly in the necessity of differentiating it from silicosis, with which it had frequently been confused in the past, particularly among foundry workers. The nodules in siderosis are more discrete and sharply defined on x-ray, and there is no tendency to con fluent nodulation or hilar enlargement. Organic Dust Diseases A few materials of organic origin have been found to be re sponsible for specific types of pulmonary pathology. Notable among these is bagasse,26 which is the residue of sugar cane after extrac tion. This material has been extensively used in the manufacture ,of insulating board and other building materials. It shreds readily ` when handled dry, with the production of a fibrous dust. A high percentage of workers exposed to these fibers have developed, after about two months, an acute bronchiolitis with high fever, extreme dyspnea, productive cough, weakness and weight loss. X-rays show scattered miliary shadows throughout the lung fields which may go on to a confluent pneumonia. The disease usually clears up, but may be fatal or result in chronic fibrosis or bronchiectasis. Both acute and chronic pulmonary diseases have been reported among cotton workers. The former" consists of an acute febrile illness with productive cough and dyspnea, resembling an acute bronchitis. It usually resolves completely, but may occasionally result in chronic bronchitis. It is believed to be due to the dust of the fungi or bacteria which grow on damp, unsterilized cotton. The chronic disease,28 known as byssinosis, consists of a progres sive fibrosis, usually associated with emphysema and bronchiec tasis, which develops after many years of inhalation of cotton fibers. It is not yet known whether it is a specific fibrotic response, an allergic reaction, or the end result of repeated subclinical acute infections. \ 572 JOHN E. SII.SON Dec., I960 * SUMMARY . There are a number of types of pulmonary pathology which can be caused by the Inhalation of excessive quantities of particulate matter, varying from specific fibrotic reactions with a charac teristic picture to an increased incidence of a form of pathology usually considered non-industrial in origin. Size, composition and structure of the particles are all factors determining the nature of the response. Pathological reactions generally result when the capacity of the filtering and phagoeytlzing mechanisms'of the respiratory tract are exceeded. These reactions may be fibrotic, inflammatory, degenerative, allergic, carcinogenic or merely mech anical impairment of function. The best known cause of pneumoconiosis is free crystalline silica, but amorphous silica, silicates, and even silicon carbide have been shown to exert deleterious effects. Coal dust, certain metals, and a few organic compounds, have also been indicated as the cause of specific lung pathology. A careful evaluation of both the clinical picture and the occupational history is necessary in every case of chronic pulmonary disease to rule out a possible etiological or aggravating factor in the patient's working environment, and to ensure an optimum prognosis by eliminating all future exposure to any harmful atmospheric agents found. RESUMEN La inhalacin de cantidades excesivas de particulas de materia puede causar ciertos tipos de alteraciones pulmonares patolgicas, que varan de reacciones fibrosas especficas, con un cuadro carac terstico, a una forma patolgica, de incidencia creciente, que ge neralmente no se considera ser de origen industrial. El tamao, la composicin y la estructura de las particulas son factores que determinan la naturaleza de la reaccin. Generalmente resultan reacciones patolgicas cuando se excede la capacidad de los me canismos de filtracin y fagocitosis del aparato respiratorio. Estas reacciones pueden ser fibrosas, inflamatorias, de degeneracin, alrgicas, carcingenas o, solamente, impedimentos mecnicos de la funcin. La causa ms conocida de la neumoooniosis es la slice cristalina libre, pero se ha demostrado que la slice amorfa, los silicatos y an el carburo de silicio pueden causar efectos nocivos. Se ha sospechado que el polvo de carbn, ciertos metales y algunos com puestos orgnicos tambin causan cambios patolgicos especficos del pulmn. Es necesario avaluar cuidadosamente tanto el cuadro clnico como los daros de las ocupaciones en todo caso de iieurr.opata crnica a fin de determinar si existe un posible factor etio- Vol. XVIII DUST INHALATION 573 lgico o agravante en el ambiente de trabajo del paciente, y para asegurar el mejor pronstico posible mediante la eliminacin de la futura exposicin a cualquier agente atmosfrico nocivo que se haya descubierto. REFERENCES ' 1 Hardy. H. L. and Tabershaw, I. R.: "Delayed Chemical Pneumonitis in Workers Exposed to Beryllium Compounds," J. Indust. Hyg. and Toxicol., 28:197, 1946. 2 Maehle, W. and Gregorius, F.: "Cancer of the Respiratory System in the United States Chromate-Producing Industry," Public Health Re ports, 63:1114, 1948. . 3 Jotten. K. W.: "Pneumoconiosis and Tuberculosis in Dusted Lungs," Beihefte z. Zentralbl. f. Getverbehyg., 15:146, 1930. 4 Dernehl. C. U. and Nau, C. A.: "Some New Aspects and Approaches to the Problem of Dust Diseases," Indust. 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Med., 20:255, 1944. 13 Hamilton. A. and Hardy, H. L.: "Industrial Toxicology," Second Ed., p. 481, Hoeber, 1949. 14 Asbestosis and Cancer of the Lung," (Editorial), J.A.M.A., 140:1219 1949. .15 Johnstone. R. T.: "Occupational Medicine and Indus,nial Hvgiene." p. 382, Afos?/, 1948. ' *16 Shaver. C. G. and Riddell, A. R.: "Lung Changes Associated with the * Manufacture of Alumina Abrasives," J. Indust. Hyg. and Toxicol, 29 145. 1947. 17 Jephcott. C. M.: "Fume Exriosure in the Manufacture of Alumina Abrasives." Occuv. Med., 5:701, 1948. 18 Stone, M. J.: "Clinical Studies in Asbestosis," Am. Rev. Tuberc., 41:12, 1940. 19 Siegel. W,, Smith, A. R. and Greenburg, L.: "The Dust Hazard in Tremolite Talc Mining," Am. J. Roentgenol., 49:11, 1943. 20 Vestal. T. F., Winstead. J. A. and Joliet, P. V.: "Pneumoconiosis Among Mien and Pegmatite Workers." Indust. Med., 12:11, 1943.. 21 Smith, A. R. and Perir.a, A. E.: "Pneumoconiosis from Synthetic Abrasive Materials," Med., 5:390, 1948. 22 Gough, J.: "Pneumoconiosis in Coal Workers in Wales," Occicp. Med., 4:86, 1947. 23 Silson. J. E,, Beniamin, L. P. and Wilson, S. C.: "The Use of Beryllium in New York State," Monthly Review, Div. of Indust. Hyg., N. Y. State Dent, ol Labor, 28:13. 1949. 24 Spolyar, L. W.. Kepder, J. F. and Porter, H. G.: "Cadmium Poisoning in Industry: Report of Five Cases. Including One Death," J. Indust. Hyg. and Toxicol.. 26:232, 1944. 25 Sander. O. A.: "Benign Pneumoconiosis Due to Metal Fumes and Dusts," Am. J. Roentgenol., 58:277. 1947. 26 Sodemnn, W. A.: "Bagasse Disease of the Lungs," Arch. Int. Med., 73: 365. 1944. 27 Middleton. E. L.: "Weavers' Cough," J. Indust. Hyg. and Toxical., 3: 428, 1926. . 28 Bolen, H. L.: "Byssinosis," J. Indust^Hyg. and Toxicol., 25:215, 1943.