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FILE NAME: Engineering (ENG) DATE: 1934 Mar DOC#: ENG021 DOCUMENT DESCRIPTION: Trade Journal Article - The Pathology of Various Mineral Dust Diseases O ccident Prevention Health Conservation Thirty-third Year-- The Pioneer Publication in It Field Fire Prevention SAFETY ENGINEERING "The Magazine of Safely" with which has been combined: Protection Engineering. Conservation and Fire Prevention. Voi. LXVII, No. 3 ARTHUR C CARRUTHERS, Editor HARRY deC. ARMAND, Business Manager C O n T E T IT S W i DO OUR PART March, 1 9 3 4 EDITORIAL OBSERVATIONS: HEALTH: Industry Must Organize Against Occupational I Disease ............................................................. 87 The Pathology of Various Dust Diseases-- by LeRoy U. Gardner, M.D............................ 109 A Challenge to the Automobile Industry .. 88 New York City's Drive Against Tenement The Diagnosis of Silicosis--by Adelaide Ross Fire Traps ........................................................ 89 Smith, M.D...................................................... 113 An explanation .................................................. 89 Controlling Dusts in the Drilling of Rock-- ACCIDENT : by R. A. B rack ett............................................ 116 How Compensable Is Disease ?--By F. Rob An Analysis of Automobile Accidents in ertson Jones ..................................................... 117 1933 ................................................................... 91 Misleading Factors in Respirator Efficiency The French Meet the Problem of Accident Tests--by Philip Drinker ............................. 119 Prevention ........................................................ 96 Protection of Workers in the Soviet Republic Workmen's Compensation for Silicosis (Con --by Henry W. Alexander ......................... 97 tinued from February) ............................... 120 Driver, Occupant and Pedestrian ................. 99 New A. S. A. Standards Required in P. W. A. Contracts--by Cyril Ainsworth ............... 100 I.adder Accidents--by John Russell, J r ......... 101 INDUSTRIAL NURSING: FIRE: Searching for the Truth .................................. 123 The Family History .......................................... 123 Fire Losses Decline as Property Values Go Down ................................................................. 103 The Crippling Effect of Intangible Fire Losses ............................................................... 107 The Death Penalty for Arson ........................ 108 An Outstanding Hazard in Industry ......... 123 Tuberculosis Among Food-Handlers ............. 123 Infection Following AccidentalInjury ____ 124 A Model Labor Code ........................................ 124 A Spray Painting Code in New York .......... 124 Publish! Monthly by Safety M aq azin e Publislrinq Corporation Editorial and general offices, 45 John Street, New York, N. Y. Publication office, 34 N. Crystal St., E. Stroudsburg, Pa. ' ARTH UR C. CARRUTH ERS, President HARRY deC. ARM AN D, Secretary A U S T IN F. H A N C O C K , Vice President Contents of previous issues of S a fe t y E n g in e e r in g can be found by consulting the Industrial Arts Inde c n i c r B i i T i n u c * * * Matter January 7, 1930, at the post office at East Stroudsburg, Pa., under the act 0 S U B S C R IP T IO N S ; S3 a year in advance. In Canada, $4.00. Foreign subscriptions, $4.50. Single copies, 25 in your library. March 3, 1879. --" --' * l U i iiiy THE PATHOLOGY of VARIOUS MINERAL DUST by LERO Y U. GARDNER, M.D., of the Saranac Laboratory for the Study of Tuberculosis DISEASES Presented before the Am erican Institute o f M ining & M etallurgical Engineers, New York City, F eb ru ary 19, 19.14. TH E lung is an organ developed to permit an in terchange of gas between the blood and the external air. Hcing in free communication with the exterior it is more or less exposed to the action of atmospheric impurities, both particulate and gaseous. The following discussion will be-confined to particulate contaminates. Certain mechanisms are provided to protect the lungs from the accumulation of such foreign particles. The nose, through which the respiratory tract opens onto the surface of the body, is guarded by a coarse filter of hair. Behind this is a series of tortuous passages with moist walls which trap many smaller particles. In addition, the nasal cavities and the remaining portions of the upper respiratory tract, the pharynx, the trachea and the bronchi are lined by cells covered with minute vibratory hairs, the cilia. Wave-like vibrations of these hairs tend to carry particles lodging on their surface away from the lung and back toward the surface. Particles which succeed in passing these barriers and penetrate to the terminal air spaces of the lung are in gested by wandering scavenger cells, or phagocytes, which come out of the partitions between the spaces for the purpose. These cells are capable of independent movement. They tend to carry the foreign particles out of the air spaces and into a special drainage system, known as the lymphatics. The lymphatics are minute vessels which drain into sedimenting basins known as lymph nodes. They are situated along the course of the vessels and bronchi, and at the root of the lung where the trachea divides into the two main bronchi. For ordinary amounts of atmospheric pollution these protective mechanisms are adequate to prevent the sig nificant accumulation of foreign particles in the func tional part of the lungs. If an individual continues to work in very dusty atmosphere for long periods, his protective devices cannot cope with the situation, the mechanisms are themselves damaged and the dust particles collect where the air should be. Lungs Can Absorb Much Dust However, even excessive quantities of most kinds of dust are tolerated by the lungs. Loss of function seems to occur not from accumulations of particles inside the air spaces, or alveoli, but only after changes have taken place in the walls of these spaces. Such changes inter fere with the permeability of the alveolar walls to oxy gen and carbon dioxide and destroy their normal elas ticity, so that the lung as a whole cannot expand and contract with respiration. Of the common inorganic dusts to be found in in dustry only silica and some of the silicates, like asbes tos, are known to produce dangerous reactions in the walls of the air spaces and the framework of the lung Other substances apparently may accumulate in ven large amounts and not result in incapacitation. They may produce pigmentation and perhaps cause the con nective tissues along the lymphatics to thicken some what, but these changes do not interfere with function. The Toxicity of Silica Attention is therefore centered upon silica and its compounds. Silica in sufficient concentrations has been shown to be a cell poison. In colloidal form it is verv toxic and when injected in large doses it may bring about active cell destruction and even death. Chronic silica poisoning causes the connective tissue cells to multiply and form scar tissue. Particulate silica will produce the same effects, if ic is in a sufficiently fine state of subdivision, which suggests that its action is chemical in nature. Absolute proof of solution in the '110 SAFETY ENGINEERING ,, , M arch, 19H4 A N ENLARCED LYM PH NODULE CHO KING OFF A LYM PH ATIC VESSEL Lody is still lacking although this is inferred iron, the available evidence. To excite reaction in the connective tissues the silica particles must be concentrated in considerable amounts in immediate contact with cells of this variety If the particles remain scattered through the air spaces of the lung there is no connective tissue reaction. But un fortunately silica particles act upon the phagocytes that have ingested them to bring about concentration of the irritant at the very point where it can exert its harmful effect. Phagocytes containing silica seem to move much faster than cells containing other types of dust particles. As a consequence silica is rapidly concen trated in the lymph nodes, both those inside the lung and those at its root. These structures contain connec tive tissue, which is stimulated, increases in amount and is gradually transformed into scar. The reaction in the nodes encroaches upon the lymph vessels associated with them; the lymphatic channels are narrowed or co in ely blocked. Sheaths of new connective tissue de velop about the damaged vessels. As this tissue matures it contracts and still further compresses the enclosed lymphatics. The result is a progressive impairment of the pulmo nary drainage system. J f more particles are now inhaled they cannot be eliminated. They either remain inside the air spaces or they are carried into the walls of these structures. Here again they stimulate overgrowth of co n n ect,vc tissue cells. The result is scar tissue so dense that gases can no longer pass between the air space and the capillary blood vessel in its walls. Nodules Form First in Lymph Nodes The characteristic effect produced by silica is a no dule of very dense, glassy scar tissue. In ordinary sili- COS1S ot the lungs such nodules first form in the lvnmh nodes as already described. After they have developed to such an extent that the lymphatic system is ob-s ucted, new nodules begin to appear in the thin walls the a,r spaces. Under unusual conditions, where the atmospheric concentration of very Hue silica is ex cessive, nodule formation and diffuse generalised thick ening of the air space walls may constitute the first re action Apparently so much dust enters the lung that physiological mechanisms are quite inadequate. The ymphatic drainage system cannot begin to remove the particles fast enough to prevent an immediate effect in the functioning part of the lung. These effects can be visualized in an X-ray him of a living subject being exposed to silica dust. Jn the ca y stages, before it is customary to diagnose the con dition as definite silicosis, the roentgenogram reveals an undue prominence and beading of the radiating shadows cast by the blood vessels. This is due to the formamn ot new connective tissue about the lymphatics wh.eh course through the walls of the blood vessels C bca(ll"ff is a visualization of small nodules in the associated lymph nodes. At the same time the shadow cast by the structures at the root of the lung is widened because of enlargement of the lymph nodes in this re gion. Later when diagnosable silicosis has developed he lung i.elds themselves are studded with great num bers of nodular shadows, As ,ho latter io e r L e in a "c and number they soon tend to obliterate the previously prominent linear blood vessel markings. Silicosis a Progressive Disease Silicosis is a progressive disease. If enough silica lias been inhaled to initiate nodule formation, each folus continues to enlarge until finally a state of equili>r,imi is established. Nodules, which may not be visible bv X-ray when a man leaves a silica industry, may sub sequently increase in size so that they are readily de lectable some years later. The progression of the process ,s favored and accelerated by the development ot pulmonary infection. Frequency of Complicating Tubrculos World wide experience with different groups of sili cotic human beings has repeatedly demonstrated the fre quency of complicating tuberculosis. In South Africa 11. 1S ^ `niated that at least seventy-five per cent of miners with fully developed silicosis will die of this in fection. in some cases the infection remains latent, piesents none of its usual manifestations and merely modifies the character of the reaction to inhaled silica dust. Jn others it develops simultaneously with the sili c o n reaction with a more or less typical localization in lhe upper portion of the lungs. Such cases may exhibit none of the characteristie symptoms of tuberculous in toxication for many years and are often only discovered m routine roentgenographic examinations of lai-e groups of active employes. Ultimately these men de velop symptoms, expectorate tubercle bacilli and finally die of tuberculosis, but the course of their disease is J r L i i LINL.1INLERING 111 protracted. There are still others whose roentgeno grams show so much evidence of tuberculosis that the characteristic features of silicosis are obscured. Never theless they have had long exposures to dust and post mortem examination will reveal the nodular fibrosis produced by silica. These cases, like those of the pre ceding group, run a definitely chronic course and may not die of their infection until the fifth or sixth decade. Finally, there is another group, with well developed nodular silicosis, who apparently have never had a tu berculosis infection. Such men become infected, de velop a rapidly progressive tuberculosis and die within six months. In them the symptoms of intoxication are more acute but bacilli may be very difficult to detect in their sputa and even in the lungs removed at autopsy. Laboratory Animals Show Function of Tuberculosis ter a year or more. The carbide of silicon has for some unexplained reason regularly produced progressive tu berculosis in animals infected in various ways with at tenuated bacilli. ' There are four possible explanations for the progres sion of the tuberculous infection: (1) alterations in ana tomical structures of the lungs like the lymphatic sys tem which may favor retention of bacilli as they are accidentally inhaled; (2) alteration of the tissues to of fer a more favorable soil for the growth of the bac teria; (3) depression of the normal immunity mecha nisms in the body, or (4) alteration of the bacilli so that they take on undue virulence. Experiments at the Saranac Laboratory and else where have quite conclusively demonstrated that bacilli recovered from silicotic lungs are not permanently al Approximations of these various conditions of in fection in the human being have been reproduced ex perimentally in silicotic animals. By using an attenu ated form of tubercle bacillus which produces only a transitory, self-limited infection in normal guinea pigs, it has been possible to show that silica dust specifically alters the course of such infection. If guinea pigs are tered. The attenuated organism which growls so vig orously m a silicotic environment wall not produce pro gressive disease when transferred in bits of such tissue to a normal animal. Outside the silicotic lung it re sumes its normal characteristic appearance and diseaseproducing capacity. Experiments to test the effect of silicosis on immunity are now' in progress. infected by the inhalation of small numbers of such tubercle bacilli and immediately subjected to a pro longed period of silica dust inhalation the animals de velop a chronic tubrculo-silicosis. This reaction makes its appearance after some five or six months exposure to the dust (eight hours daily) but the animals do not die for a year or two. They are comparable to the human silicotics of the first group. ' If the infection is administered first and the dust inhalation is commenced at different intervals thereafter it has been shown that the healing tubercles are reactivated and again become progressive. This result follows as long as the lung con tains living bacilli. The disease produced is likewise chrome in its course and only kills its victims after many months. These animals may be compared to hu man beings who enter a silica industry with partially healed tuberculosis infections. Finally animals, which' arc first rendered silicotic by exposure to silica for Silica's Reaction Is Easily Demonstrated There is no difficulty in demonstrating that silica pro duces a reaction in the body which specifically favors the multiplication of tubercle bacilli. Kettle injected a definite quantity of fine silica particles beneath the skin of one flank of a white mouse, and in the opposite flank, the same quantity of aluminum oxide particles. A large dose of tubercle bacilli was then injected into the tail vein of the animal. The blood distributes these bacilli quite uniformly to all parts of the body, but if the animal is killed after several davs large masses of them will be found at the site of the injected silica. Where the alumina particles have localized the ba cilli are no more numerous than in any other part of the body. Apparently the reaction set up by the silica produces a favorable medium for the growth of these bacteria but later they disappear and may be very hard a \ear or more and then infected by the attenuated tubercle bacilli, develop an acute tuberculosis which terminates fatally in a few months. Normal control guinea pigs, never exposed to dust, infected at the same time, never develop progressive tuberculosis. Their tubercles heal almost completely and they either die of other causes or must be killed two or three years later. 1he rapid tuberculosis which develops in the presence of preestablished silicosis has its counterpart in the last class of the human cases mentioned. Effect on Tuberculosis Not Understood The cause for this effect of silicosis upon tubercu losis is not known. It is apparently quite specific, for marble, soft coal, aluminum oxide, gypsum, and hema tite dusts have so far failed to influence the course of such infection. Asbestos, a silicate of magnesium, ex erts a slightly stimulating effect but the resultant tuber culosis is rarely progressive and has usually heated af- |Ev m d u _d u s t CELLS H A V E M ASSED IN L Y M P H N ODULES ALO N G THE COURSE OF A VEIN 112 SAFETY ENGINEERING M arch, 1934 to find. The same seems to be true of the sputum of men with silicosis and tuberculosis. If silica is added to artificial culture media on which tubercle bacilli are to be grown the results are not so clearly defined. It seems as if this slow growing organ ism begins to develop more rapidly when the silica has been added, but the resultant quantity of growth is not much affected. Much more investigation of the whole problem of the relationship between silicosis and tuber culosis is needed. Pathological Result of Asbestos Inhalation Inhaled asbestos dust also produces fibrosis of the lungs but the scar tissue is not laid down in nodules nor does it have the peculiar glassy appearance which is characteristic of silicosis. In asbestosis one finds a widespread diffuse fibrosis throughout the framework of the lung. While not so spectacular as the nodulalion of silicosis the fibrosis of asbestosis probably dis ables its victim more rapidly. The general thickening of the walls of the air spaces prevents interchange of gases throughout large portions of the lungs and brings about a state of deficient oxygenation in the whole body. The reason for the peculiar distribution of fibrosis in asbestosis is apparently the fact that phagocytes do not transport the elongated fibres of asbestos for any dis tance. They tend to lodge along the walls of the fine cylindrical terminal bronchioles. There they cause fib rosis in the form of a collar, or cuff, about the tube and as this contracts it constricts the bronchiole. Air is thereby prevented from entering the peripheral rami fications of the tube and these portions then collapse. This in itself is a cause of fibrosis. As a result a gen eralized fibrous change involves extensive areas in the functional portions of the lungs. How far asbestosis predisposes to tubercular infec- SILICOTIC NODULE IN RABBIT LUNG, AFTER 13 M O N T H S OF Q U A R T Z DUST EXPOSURE. lion is debatable. Animal experiments have not indi cated an excessive susceptibility. Many autopsies on human beings have revealed a coexistent tuberculosis but statistical studies of large numbers of living work men together with mortality records must finally settle this point. Sericite, a Silicate, May Be Harmful Recently another silicate, sericite, has been incrimi nated in a series of papers by W. R. Jones. While it is loo soon to comment authoritatively upon his thesis, it can be definitely stated that silicotic nodules can be pro duced experimentally without sericite. Petrographic analysis of the silica employed for the animal experi ments made in the Saranac Laboratory has excluded contamination with this material. Normal crystalline quartz or, in some instances, crypto-crystalline silica have excited characteristic nodular fibrosis in guinea pigs, rabbits, white rats, cats, and domestic fowl. ' Experience with other dusts, non-siliceous, is more limited but insofar as they have been studied it would seem that they do not tend to excite serious reaction in the lungs. They are ingested by phagocytes within the air spaces and quantities of particles may remain in this location for long periods of time. The walls of the spaces involved often exhibit a mild grade of chronic inflammatory change which is apparently not suffi ciently marked to interfere with function. Many of the phagocytes leave the air spaces and enter the lymphatic system. They deposit their ingested particles in the lymph nodes within and at the root of the lung, but little or no scar tissue develops unless a sufficient quan tity of silica has also been inhaled. These non-siliceous materials may cause pigmentation of the lung as, for example, the black lung of the coal miner and the red lung of the hematite miner, but mere pigmentation is harmless. The roentgenogram may reveal a slight ac centuation of the linear blood vessel shadows and in some instances inflammatory changes in the air space walls may possibly cast a faint haze over the lung fields but none of these effects is at all definite. There is nothing to indicate that the inhalation of these non-sil iceous dusts favors the development of tuberculosis. Other infections, notably pneumonia, are unduly prev alent in certain dusty industries. In how far the dust is responsible is not proved. I he carbide of silicon produces similar, non-progres sive, chronic inflammatory changes in the normal lung. In experimental animals this dust has regularly and re peatedly increased the susceptibility to tuberculous in fection. Whether the same effect obtains in human beings has not been ascertained. In conclusion it should be reiterated that only silica and a limited number of the silicates are knowm to pro duce definite and serious pulmonary damage. In the case of silica this is associated with specific indisposi tion to tuberculosis and pneumonia. Of the silicates, as bestos is definitely recognized as a cause of pulmonary fibrosis. Its importance in predisposing to tuberculosis is not yet settled.