Document Qgbmqv7ND4g2oMweYJgQNp9x8

***. 19H SAFETY ENGINEERING t ^g5jTIJHKIfMCIB THE PATHOLOGY of VARIOUS'MINERAL DUST br LEROY U. CAADNEX. M.D,, d Lftborsfery for Xhm Sfudf d Tubrcv4ou DISEASES U/ tS# Uiti'iii / . / Xlinimf d: Mttdimrftrd a, lrk CLy, F 13, HE lung \% an organ developed to permit an ro- work ia very dusty atmosphere for long peri: T tercHange of jai between the blood and the protective devices cannot cope with the nruatxr trtemai air. Being is free communication with mechanisms are themselves damaged and tin the exterior it. is more or leia exposed to the action opfarticles coliea where the air should be. atmospheric impurities, both paniculate and paseoua. The folio* Yg discussion will be conEned to particuLaie contaminates. Certain mechanisms are provided to protect the lungi# from the accumulation of such foreign panicles. 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 nails which trap many smaller panicles. In addition, the nasal cavities and the remaining ponions 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 cany panicles lodging on their surface away from the lung and back toward the surface. Panicles 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 cany the foreign panicles out of the air spaces and into a special drainage system, knoycn xs the lymphatics. The lymphatics are minute Lungs Can Absorb Much Dust However, even excessive quantities of most 1= dust are tolerated by the lungs. Loss of function to occur Dot from accumulations of particles iosi air spaces, or alveoli, but only after changes have place io the walls of these spaces. Such changes fere with the permeability of the alveolar walls t. gen and carbon dioxide and destroy their norma ticity, so that the lung as a whole cannot expan contract with respiration. - Of the common inorganic dusts tb be found dustry only silica and some of the silicates, like tos. are known to produce dangerous reactions walls of the air spaces and the (ramework of the Other substances apparently may accumulate ie large amounts and not result in incapacitation, may produce pigmentation and perhaps cause tht neetivo tissues along the lymphatics to thicken what, but these changes do not interfere with fur Th. Toxicity of Silica Attention is therefore centered upon silica a_> compounds. Silica in sufficient concentrations has 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 panicles in the functionaf port of the lungs. If an individual continues to shown to be a cell poison, hnvtlloidal form it it toxic and when injected irCKc^e #f0ses it may about active cdl destruction ztt3 even death. O silica poisoning causes the connective tissue ce multiply and form scar tissue. Particulate silic produce the same effects, if it is in a sufficient! state of subdivision, which suggests that its act chemical in nature. Absolute proof of solution i PLAINTIFF'S EXHIBIT Vi-QOt.a<5 The finest dust respirators in all safety history will be introduced on this page in May. t*.V wifi out-perform even the present Pulmosan Dustpruf Respirators . . . themtelves rated as the outstanding respirators by leading industrial plants. Many refinements and improvements have been added, to Increase safety__ comfort--breathing ease--and working efficiency. <r&` //: PULMOSAN SAFETY EQUIPMENT CORPORATION 176 JOHNSON ST.. BROOKLYN, N. Y. Industrial Safety Eq uipment Aji'n. PLAINTIFFS ' EXHIBIT : 239 193" 0T : Or-! "Gi SDA83 03NI KOiWBSBcJ: QI t3:8T T6.-8I-99W w^pcidetit Preoeation Health CctueruaHcn . ' Thirty-third Veer---The Pioneer PubUctdiod la lie Field i " -- Fire Prevent.ion'.;1 SAFETY EMGIMEERING! '. .. "The Magazine of Safety" ` '' i wfti which has bate combined: Rrotoetlee EnfiroerUg, ' CoflMrvrtion ind Flratrevention. ARTHUR C. CARR OTHERS, Editor HARRY deG. ARMAND, 8usin Manager Vol. LXVDYNo. 3 COniEIlTS March, 1934 EDITORIAL OBSERVATIONS, HEALTH, Industry Must Organize Againit Occupational ' Disease ....................................... A Challenge to the Automobile Industry .. 88 New York Gty's Drive Again*,) Tenement Fire Traps .................................t'................ 89 . As Explanation ...................................................69 The Pathology of Various Dust Diseases-- ' 8b7y- LeRoy U. Gardner, MJD........................... 109 The Diagnosis of Silicosis--by Adelaide Rofs Smith, 1LD..................................................... 113 Controlling Dusts in the Drilling of Rode-- by R. A. Brackett............. ;.......................... 116 ACCIDENT. ' ' An Analysis of Automobile Accidents In 1933 .................................................................. 91 The French Meet the Problem of Accident How Compensable Is Disease?--By F. Rob ertson Jones ............................... ,................... 117 Misleading Factors in Respirator Efficiency ' Teats--by Philip Drinker................... 119 Prevention ....................................................... 96 Protection of Workers in the Soviet Republic .--by Henry W. Alexander ............;........... 97 Drive*, Occupant and Pedestrian .................. 99 Workmen's Compensation for Silicosis (Con tinued from February) ............................. 120 New A. S. A. Standards Required in P. W. A. Contracts--by Cyril Ainsworth.............. 100 INDUSTRIAL NURSING, . ' Ladder Accidents--byJohn Russell, Jr............101 Searching for the Truth ................................. 123 FIRE. The Family Hijtnry' ................................. 123 Fire Losses Decline as Property Values Go Down............................... 1'............. .. 103 The Crippling Effect of Intangible Fire Losses ............................................................ 107 ' Ao Outstanding Hazard in Industry 123 Tuberculosis Among Food-Handlers............... 123 Infectioo Following Accidental Injury .... 12+ A Model Labor Code...................................... 124 The Death Penalty for Arson......... ............. 108 A Spray Painting Code in New York ......... 124 W* I SBMBEXCZu Rubflrhed Meothly by Safely KrTaqozin* Ptrb lilkinq Co rpopolion , Editorial and general offices, 45 John Street, New York, N. Y. Publication office, 34 N, Crystal St., E. Stroudsburg, Pa. ARTHUR C CAJUtUTHERS, President HARRY d.C. AJtMANC, Secretary AUSTIN f. HANCOCK, Y1e Preilden. Contents ol previous hjvini oI Safety Engineering cm be found by consulting (be ledu.frill Art, Index in yo*r Dbriry. Ir/areli ** ^few'^ Cli.( Wider finusry 7, 1930, if the post office at list Stroud,burg, Pi., under the id of March 3, 1879. 5UISCRIPTIONJ; 33 i yeer In adraace. In Caned*. J4.00. Fereift subscription. J4.50. Hfltle cople., 25c PLAINTIFF'S EXHIBIT ! "0d 1907 01 ten T3i SDActS OJNI H3>fy9E3a:ai S:S1 IE 1 i <rr o exhibit _ I fe <*- 5- . THE PATHOLOGY of VARIOUS MINERAL DUST LIBRARY AND INFORMATION CENTER GEORGIA INSTITUTE Of TECHNOLOGY ATLANTA, GA. 30332-0900 DISEASES , fay LEROY U. CARDNER. W.D.. of the Saranac Laboratory for the Study of Tuberculosis Pretented before the American Intlitute of Mining & Metallurgical Enginccrt, York City, February 19, 1934. HE lung is an organ developed to permit an in work in very dusty atmosphere for long periods, his T terchange of gas between the bloo.d-and the external air. Being in free communication with protective devices cannot cope with the situation, the mechanisms are themselves damaged and the dust the exterior it is more or less exposed to the action opfarticles collect where the air should be. atmospheric impurities, both particulate and gaseous, v following discussion will be connned to particulate , .minates. "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 man}' smaller particles. In addition, the nasal cavities and the remaining portions of the upper respirator}' tract, the pharynx, the trachea and the bronchi are lined by cells covered with minute vibrator}' 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, W'hich come out of the partitions between the spaces for the purpose. These cells are capable of independent 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 panicles 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 clas-> 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 verylarge 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. movement. They tend to carry the foreign particles out The Toxicity of Silica f the air spaces and into a special drainage system, Attention is therefore centered upon silica and its known as the lymphatics. The lymphatics are minute compounds. Silica in sufficient concentrations has been vessels which drain into sedimenting basins known as shown to be a cell poison. In colloidal form it is very ivmph nodes. They arc situated along the course of the toxic and when injected in large dose; it may bring Is and bronchi, and at the root of the lung wheie about active cell destruction and even death. Chronic trachea divides into the two main bronchi. silica poisoning causes the connective tissue cells to Tor oidinar}' amounts of atmospheric pollution these multiply and form scar tissue. Particulaie silica will protective mechanisms are adequate to prevent the sig- produce the same effects, if it is in a sufficiently fine nincnm accumulation of foreign particles in the func- state of subdivision, which suggests that its action is Hor.nl part of the lungs. If an iiuitv.dual continues to chemical m nature. Absolute proof of solution in the 1*-* rT AN ENLARGED LYMPH NODULE CHOKING OFF A LYMPHATIC VESSEL body is still lacking although this is interred from 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 >*he lung there is no connective tissue reaction. But un ! rtunately silica particles act upon the phagocytes that ^..ave 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 en tirely 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. If 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 connective tissue cells. The result is scar tissue so dense that gases can no longer pass between the air 'ace 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- LCi to such an extent that the lymphatic system is ob structed, new nodules begin to appear in the thin walls of the air spaces. I'nder unusual conditions, where the atmospheric concentration of very tine silica is ex cessive, nodule formation and diffuse generalized thick ening of the air space walls may constitute the fir<i re action. Apparently so much dust enters the lung that physiological mechanisms are quite inadequate. The lymphatic drainage system cannot begin to remove the particles fast enough to prev ent an immediate effect in the functioning part of the lung. These effects can be visualized in an X-ray film of a living subject being exposed to silica dust. In the early 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 forma tion of new connective tissue about the lymphatics which course through the walls of the blood vessels. The beading 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 l>ecause of enlargement of the lymph nodes in this re gion. Later, when diagnosable silicosis has developed, the lung fields themselves are studded with great num bers of nodular shadows. As the latter increase in size 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 has been inhaled to initiate nodule formation, each fo cus continues to enlarge until finally a state of equili brium is established. Nodules, which may not be visible by X-ray when a man leaves a silica industry, may sub sequently increase in size so that they are readily de tectable some years later. The progression of the process is favored and accelerated by the development of pulmonary infection. Frequency of Complicating Tuberculosis World wide experience with different groups of sili cotic human beings has repeatedly demonstrated the fre quency of complicating tuberculosis. In South Africa it is estimated 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, presents none of its usual manifestations and merely modifies the character of the reaction to inhaled silica dust.. In others it develops simultaneously with the sili cotic reaction with a more or less typical localization in the upper portion of the lungs. Such cases may exhibit none of the characteristic symptoms of tuberculous in toxication for many years and are often only discovered in routine roentgenograpbic examinations of large 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 grams show so much evidence of tuberculosis that the unexplained reason regularly produced progressive tu characteristic features of silicosis are obscured. Never berculosis in animals infected in various ways with at theless they have had long exposures to dust and post tenuated bacilli! * mortem examination will reveal the nodular fibrosis There are four possible explanations for the progres ' ---educed by silica. These cases, like those of the pre- sion. of the tuberculous infection: (1) alterations in ana 'g group, run a definitely chronic course and may tomical structures of the lungs like the lymphatic sys Jie of their infection until the fifth or sixth decade, tem which may favor retention of bacilli as they are 'finally, there is another group, with well developed accidentally inhaled; (2) alteration of the tissues to of nodular silicosis, who apparently have never had a tu fer a more f?."Qr-ab!e soil for the grov-th of the bac berculosis infection. Such men become infected, de teria; (3) depression of the normal immunity mecha velop a rapidly progressive tuberculosis and die within nisms in the body, or (4) alteration of the bacilli so six months. In them the symptoms of intoxication are that they take on undue virulence. more acute but badlli may be veiy difficult to detect in F_xperiments at the Saranac Laboratory and else . their sputa and even in the lungs removed at autopsy. where have quite conclusively demonstrated that bacilli Laboratory Animals Show Function of Tuberculosis 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 fonn 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 infected by the inhalation of small numbers of such recovered from silicotic lungs arc not permanently al tered. The attenuated organism which grows so vig orously in a silicotic environment will not produce pro gressive disease when transferred in bits of such tissue to a normal animal. Outside the silicotic lung it re sumes its norma! characteristic appearance and diseaseproducing capacity. Experiments to test the effect of silicosis on immunity are now in progress. Silica's Reaction is Easily Demonstrated tubercle bacilli and immediately subjected to a pro longed period of silica dust inhalation the animals de velop a chronic tuberculo-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 "Van silicotics of the first group. If the infection is ; listered first and the dust inhalation is commenced ar~uiffercnt 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 chronic 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 partiallyhealed tuberculosis infections. Finally animals, which are first rendered silicotic by' exposure to silica for 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 pans of the body, but if the animal is killed after several days 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 he very hard a year 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. The rapid tuberculosis which develops in the presence f preestablished silicosis has its counterpart in the last class of the human cases mentioned. Effect on Tuberculosis Not Understood "1 he cause for this effect of silicosis upon tubercu:s not known. It is apparently quite specific, for :, soft coal, aluminum oxide, gypsum, and hema- ^-uusts have so far failed to influence the course of Such infection. Asbcslos. a silicate or magnesium, excn$ a slichliy stimulating effect but the resultant tuberuil.w; jy rarc|v progressive and has usually healed af- EARLY STAGE. DUST CELLS HAVE MASSED IN LYMPH NODULES ALONG THE COURSE OF A VEIN .  illV.il -- **- ----------- - It siiica is added to artificial culture media on which tubercle bacilli are to be grown the results are not so .clearly defined. It seems as it this slow growing organ ism begins to develop more rapidly w hen 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 nodulation of silicosis the fibrosis of asbestosis probably dis ables its victim more rapidly. The general thickening of the walls cf the air spaces prevents interchange of _ gases throughout large portions of the lungs and brings about a state of deficient o.x}'genation 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, 'tibout the tube and as this contracts it constricts the bronchiole. Air is thereby prevented from entering the peripheral rami fy fications of the tube and these portions then collapse. 1 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 int'ec- 5ILICOTIC NODULE IN RABBIT LUNG. AFTER 13 MONTHS OF QUARTZ DUST EXPOSURE. 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. P. Jones. While it is too 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 exoerinients 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-siliccous 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 taint 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 undulv prev alent in certain dusty industries. In how far the dust is responsible is not proved. The carbide of silicon produces similar, non-progres sive, chronic inflammatory changes in the normal lung. In experimental animals this dust has regulariy 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 land a limited number of the silicates are known to pro puce 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.