Document ormoJrXKdLJk88060Da7Gxw8

FILE NAME: CERAMICS (CER) DATE: 1950 DOC#: CER045 DOCUMENT DESCRIPTION: US Dept of Interior - Review of Literature Dusts ) ) UNITED STATES DEPARTMENT OF THE INTERIOR J . A. K R U G . S ecretary BUREAU OF M INES JAMES BOYD, D irector BULLETIN 478 REVIEW OF LITERATURE ON DUSTS By J . J . FORBES, SARA J. DAVENPORT, an d GENEVIEVE G. M ORGIS W \/ UNITED STATES GOVERNMENT PRIN TIN G OFFICE W ASHINGTON i IMO For b y tWe S u p e r in t e n d a n t of D o c u m e n t , U . S. G< it P r t n l t n v QffVre ) ) JUL 6 - CONTENTS In tro d u c tio n ___________________ S u m m a ry ............................................ C onclusions_________________ -- Definition and classification of d u s t s , . ............ ............................ E xposure to d u s t......... .................... Physiological cfTects of b re ath in g d u s t . ............................. -- H istorical r t s u m i ........... . -- Incidence of dust d ise ases____ G re a t B rita in ....... ......... ........... G erm an y _______________ -- A frica_____________________ South A frica......................... W est A frica. ........................ U nited S ta te s ...................... -- M in in g ................................ G rinding in d u s try ___ . . . G ranite in d u s try ..........-- F o u n d ries..... ............. ........... Cement industry.. P o ttery in d u s try ................. Silica and fire-brick indus trie s.............. A ustralia. __ C a n a d a . .............. -- N e th e rla n d s .. .......................... D e n m a rk ............. F ra n c e ....................... In d ia ............................................ I t a l y ............. H usain... ...................... - South America . . . B rasil___ .. -- ... C hile_______ _ _________ P e ru ......... ............................... S p a in ................................... Sw eden........................................ S w itzerland..... . . . . .. T ypes of dust injurious to h e a lth . Term inology of bust diseases .. P neum oconiosis. S i l i c o s i s ......................... D efinition................. S y m p to m s. .................................... P a th o lo g y .............. . ... S ta g e s................... . D iagnosis...................... .............. Roentgenological aspects of silicosis........ ............................. .. How fibrosis of tho lungs is p ro d u c ed ........................................... Page I Prevention o f dust diseases_____ 1 Principal dust factors pro- 10 ducing pulmonary patliol- o g v ........................................ .. 12 Silica d u s t........... .. -- 15 Chem ical properties of s i l i c a .................. - . 18 Occurrence of silica in 18 n a tu r e ______ _______ 2222 In d u stria l uses of silic a ---S c r ic ite ............................. 20 Carbon dioxide theory -- 32 N a tu re of silica d u s t.......... 32 Particle size of dangerous 34 d u s t ..................................... 34 Q uantity of dust required 35 t o produce silicosis___ _ 39 Length of dust exposure 40 required to produce sili 42 c o s is ................................. .. 44 D eterm ination of dust in a ir -- 45 Dust-sam pling m eth o d s.. . . C o n d e n sa tio n ........................ 45 F i l tr a t io n ._______ _____ 40 W ashing ................................. 40 O p tic a l...................... 40 S e d im e n ta tio n ................... .. 51 Electrostatic m eth o d s.... 51 R esistance.................. . . . 52 Im pinging m eth o d s............ 53 P etro g rap h ic m e th o d s----- 55 D ust-counting cells............ 55 Physiological m ethods. ._ 55 Engineering control in preven 55 tion of du st d iseases__ 50 D ust control in m ining in 50 d u stry . ....................... 50 Sources of dust in m ine a ir 57 M ethods of controlling 58 d u st product inn iu 00 m ines.............................. 00 W a te r_____ _ . . . . . . 03 D u st tra p s ............. . . 03 D ust respirators 04 D u st filters.............. 05 D u st control in industries 74 oilier than m in in g .. . . . 77 Abrasives amt grinding in d u strie s.......................... 70 F oundry in d u s try ............... G ranito in d u stry . . ______ 85 D ust-collecting d e v ic es____ in rsge 03 93 04 94 94 95 1O02f. 103 104 107 110 125 127 127 129 132 132 133 135 135 130 146 147 148 150 155 158 105 168 174 184 188 100 101 104 am 201 2 REVIEW OF LITERATURE ON DUSTS A summary of some of the points mentioned or discussed follows: 1. Dust has been defined ns solid particles (usually dry, but they may be wet) ranging in size from less than 1 micron (1/1000 mm. or approximately 1/25000 inch) to about 150 microns. 2. Physiologically, there arc almost, ns many different classifications of dusts as there are authors on the subject; these classifications prob ably are not particularly important, because in daily practice m in dustry the harmful effect, is produced more frequently (alm ost invari ably) by dusts of mixed origin. An attem pt to group dusts under the headings "active" and "inert" (w ith reference to effect on health) has proved unsatisfactory; the further the subject is investigated, the more it becomes apparent th at virtually all dusts m ay be harm ful if breathed in large amounts over long periods. 3. The extent or the dust hazard in industry in the U nited States is not known definitely, and exact d ata on the num ber of persons exposed are not available although some rough estim ates have been made. 4. So far as known at present, silica dust apparently is the most harmful of the dusts ordinnrily encountered. Silicosis (so-called), the disease caused by breathing silica dust, is a widespread industrial hazard which probnbly is increasing and affects appreciably the death rate among industrial workers exposed. The Silicosis (MedicalArrangements) Committee of G reat B ritain reported in 192!) th at "silicosis is more widespread than is generally Relieved and occurs to some extent in a number of industries and occupations whoro its gresence has not been suspected." Some authorities in the United tates, particularly lawyers who have handled any considerable num ber of (fust cases legnlly, have expressed essentially the same opinion. 5. Vnrious writers on industrial disenses have referred to harmful effects of exposure to dust for centuries, nt lenst as fnr back as 75 A. IX, when Pliny referred to it. 6. Dust diseases are found nmong workers in dusty trades all over the world but are more prevalent., or a t lenst have received maximum attention, in such industrial countries as Great B ritain, Germany, Australia, South Africa, Canada, and the United States. 7. In the United States dust disense, usually designated "silicosis," is more or less common nmong workers in the m ining, grinding, granite, and foundry industries; it also is found to some extent in more than 100 other occupations or industries. 8. As regards types of dust injurious to health, it appears that any dust insoluble or difficultly soluble in the fluids o f the respirntory pnssages and in sufficiently finely divided form to flont in the air nnd be breathed by workers in considerable quantities over long periods ultimately will be linrmfiil. Although free silica dust (S iO ,) has been considered the most, harmful, silicates (fo r example, asbestos) linvo been found almost, ns hnrinful, nnd other dusts certainly linvo a detri mental effect upon health under certain conditions. 9. The following forms are commonly used to describe dust dis eases of the lungs: (a) "Pneumoconiosis" (from Greek pncvmon. lung, and konti, dust), a gcnornl term for nil dust diseases of the lungs; (ft)"silicosis," a condition of the lungs due to inhalation of silicon dioxide or free silica; (c) "silicatosis,' a disoaso of the lungs thought ) ) SUMMARY 3 to be caused by silicates; (d) "anthracosis," a dust disease of the lungs of coal miners; ( e) "siderosis," a diseased condition of the lungs of metal workers, particularly in iron or ores of iro n ; and (f) " asbestosis," a lung disease caused by breathing asbestos dust. The generic term " pneumoconiosis'' or possibly the sim pler one "dust disease'' ap pears to represent more accurately the common types of dust disease, because numerous dusts usually are involved. 10. Silicosis is characterized by fibrotic changes in the lungs which are said to be more clearly noticeable and easier to diagnose than changes due to other dust diseases of the lungs. The dust of free silica is considered more dangerous than other dusts, chiefly becauso its victims are thought to be more liable to contract tuberculosis than persons exposed to nonsiliceous dusts. 11. The symptoms of silicosis nre shortness of breath (dyspnea), pains in the chest, cough, expectoration (coughing and spitting ma terial), hemoptysis (spitting blood), night sweats, loss of strength, and gastrointestinal symptoms; most of these symptoms also accom pany disenses caused by at least some other dusts. 12. As outlined by Panconst, the pathological features of silicosis are: (a) E ntrance of dust; (b) "dust cell" ; (c ) entrance of dust, cell info the lymphatic system of the lungs ns a carrier of silica particles; (rf) influence of deposited, silica in the production of fibrous tissue; (c) action of silica; (/) elimination of dust; (y) predisposition of the fibrotic and silica-saturated lung to respiratory infections, espe cially tuberculosis. 13. The mechanisms provided to protect the lungs from accumula tion of foreign particles nre the mouth and nose, through which the respiratory tract opens to the surface of the body, the latter of which is guarden by a conree filter of h air; behind this n series of tortuous passages with moist walls which trap ninny sm aller particles; and cells covered by the cilia (minute vibratory hairs) which lino the nnsal cavities, portions of the upper respiratory tract, the pharynx, the trachea, and bronchi. The wavelike vibrations of the cilia tend to carry (articles lodging on their surface away from the lungs and back toward the surface. These mechanisms, with others, are ade quate to protect against ordinary amounts of atmospheric pollution, but if work is continued in n very dusty atm osphere to r long periods, they cannot cope with the situation, the devices themselves aro dam aged, and the dust particles collect where the a ir should bo or possibly prevent air from going where it is expected to go and is needed. 14. In some count lies silkosis has been divided arb itrarily into tlireo stagas for convenience of description and possible compensa tion purposes: In the first stage (as designated in the United States) the symptoms are few and often indefinite, and the working capacity is not noticeably im paired; in the second stage a definite shortness of breath on exVbtion is usually experienced, work cannot ho performed as well as formerly, and the chest expansion is noticeably decreased; in the third stngo the shortness of breath is marked and distressing on slight exertion, tho cough is moro frequent, tho capacity for work is seriously and permanently im paired, chest expansion is greatly decreased, flesh is likely to be lost, pulse rate may lie increased, the heart may become dilated, and usually tuberculosis has intervened. 6 REVIEW OF LITERATURE ON DU8T8 cations may ensue in 2 years or even less from the date of first exposure to heavy concentrations under unfavorable conditions of temperature, humidity, noxious gases, exposure, etc. 26. Determination of dust in air breathed by workers is held to be necessary before measures can be taken to prevent dust disease; more over, it is economically im portant as evidence of the extent of the dust hazard involved in dusty processes and ns a measure of the efficiency of protective devices introduced to mitigate the hazard. The various methods that have been nnd are being used are described. The final choice of an instrument for Rampling dust depends on its efficiency, its relative freedom from errors in analysis, its ruggedness, portability, and weight, and the difficulty or ease with which tne snmples obtained may be analyzed. The instrument or method should eliminate as far as possible variation or errors due to the "human equation"--a difficult requirement and one apparently not yet reached. A suitable instru ment or method for determining air dustiness in one industry may not necessarily lie applicable to conditions in another, though, as far as feasible, instruments nnd methods should be kept standard r all industries to permit correlation of results. 27. Engineering met Ik ds of controlling dust in the mining, abrasive, grinding, foundry, and granite industries are discussed. 28. Textbooks on ventilation nnd engineering handbooks devote little or no space to methods of controlling industrial dust; less than <per cent of the articles in an extensive bioliography on dust diseases deals with engineering control. 20. No definite, absolutely reliable standards of allowable dustiness are known; therefore the nim in the prevention of dust disease should be to eliminate dust from the atmosphere breathed by workers or at least to reduce the dust content to the lowest figure feasible. Consid ering the many uncertain! ies of the present day, standards--especially in legal requirements--should be tentative and flexible rather than permanent and rigid. 30. The remedy for the apparently concerted effort to hide the facts. regarding dust diseases in industry 9 education of workers in the* necessity of taking available precautions, including physical exami nations; of employers in recognizing the seriousness of the situation and in providing devices and methods to reduce or prevent the inci dence of disense and. if necessary, force their adoption on the workers; of doctors in correctly diagnosing disense, giving publicity to its prev alence, seriousness, preventive remedies, etc., and assigning in death certificates dust disease as the cause if such is the enso; and of mer chants, newspnjiers, nnd other influences in the community in trying to prevent the disense rather than to hide its existence. 31. Employers should not conclude that they have eliminated the danger of silicosis or of any typo of pneumoconiosis simply beenuse the air is seemingly free from dust; ns far ns now known, the pnrticles likely to do the most harm are invisible nnd remain long in suspension in the air unless the latter is replenished by fresh, puro air nt frequont intervals through ventilation. 32. The following methods of reducing dust in South African mines are said to linve l>ecn effective in preventinp the incidence of dust diseases for the past several years: Wet drilling, water spraying (by 1 ) SUMMARY 7 water blast), filtration, requiring adequate time between blasting and return to the working face, air sampling, ventilation, and wearing of masks. 33. The main sources of dust in metal-mine air in the order of im portance are: Dry-drilling holes for blasting, blasting, shoveling or ``mucking" very fine dry material at the working face which is usually poorly ventilated, loading cnrs from chutes, dumping loaded cars into chutes, nnd timbering. Dry crushing and other occupations in metal-mine mills are also likely to be dangerously dusty. 34. The most dangerously dusty occupation in coal mines is cutting or loading dry coal by machines; blasting, shoveling, drilling, nnd rock dusting by machinery are also very dusty operations. In addition to the miners and their helpers, rockworkers nnd timbennen nnd drivers who must enter the miners' workplaces when the air is particularly dusty are exposed to relatively large amounts of dust. 35. The best remedy for the dust menace in mines, other than pre venting its formation, appears to be the universal coursing of currents of air to remove the dust, as it has been proved that the very fine, most dangerous dust in metal mines remains suspended in still air for several hours. Dust-prevention devices of proved success, such as the present-day self-rotating wet stoper and other wet-drilling equipment, should supplant dry drilling; their use should be enforced upon both miners and operators in metal mines. Care should be taken, however, that holes are not started or "collared" dry. To date no workable device is available for removing dust in dry drilling in underground mines. 30. Various "dust traps" to prevent dissemination into the atmos phere of dust produced by drilling in rock with pneumatic percussion drills are described; these devices are used in mines in tire United States to only n very limited extent. 37. The advantages nnd disadvantages of dust respirators are dis cussed. On August 20, 1034, the Federnl Bureau of Mines issued an approval schedule for dust respirntors describing the procedure for testing filter-type dust, fume, and mist respirntors for permissibility; a number of respirators have been approved under this schedule. 38. Dust filters developed in South Africa for removing dust pro duced in ore bins and at tipple stations are said to have dust-catching efficiencies of 08 percent or more. 30. In industries other than mining the processes used vary so widely nnd call for such different treatment that each must lie studied separately. Methods recommended for eliminating dust are: Local exhaust ventilation to remove the dust at point of origin ; substitution of non-silicosis-producing material ns a metal abrasive for sand, iinnsiliceous parting eoiiqiomids for molds in foundries, nnd clay instead of flint in bedding poiterywnre for baking; enclosure and segregation of dusty processes, ns the use of sandblasting cabinets; suppression of dust by water spray and steam; general mechanical ventilation; plant clennliness, which is ns important ns upkeep of protective equip ment; protection of workers by masks and helmets, nlthough such devices should be considered only emergency equipment ns dustiness should by all menus be controlled by such measures ns dust-collecting equipment nnd exhaust fans if feasible; medical supervision with 8 REVIEW OF LITERATURE ON DUSTS periodical physical examinations of workers; education of workers; and dust counting to check the efficiency of the measures. 40. If much progress is to be expected engineers, operating officials, and doctors must cooperate in the control or dust diseases. The most important measure in tho medical control of dust diseases is physical examination of workers before employment and at stated intervals thereafter. It has been found tbnt certain defects and diseases are predisposing causes of silicosis. According to German investigators, workers with poor nasal filtration nre more susceptible to dust diseases. A man with a good, sound physique and with good reserve respiratory capacity is snid to bo best-suited for underground work in mines. Age is also imj>ortaiit; a mar. with n good chest and good reserve enn carry without inconvenience or loss of health enough fibrosis to seri ously affect one with poor reserve or a chest becoming rigid with age. All persons with signs of tuberculosis taint or tendency should be rig orously excluded from dust.y occupations, irrespective of silica content of the dust. 41. A plan for medical control includes establishment of a medical department adequately equipped, routine examination of applicants for employment, rating and placement of applicants, periodical physi cal examinations, and provision for the disabled. Methods of con ducting examinations are outlined. 42. No cure is yet. known for silicosis. At. one time it was thought th at removal of the victim from further contact with dust would arrest the condition at the |*>int of development reached when dis covered; although this practice is effective in some instances, generally it is not now considered the solution, and in some mining localities the removal system is not utilized. 43. Earlier investigators believed that so-called " protector" dusts would cause excretion from the lungs of such harmful dusts as silica by exciting the physiological process of elimination and that these protective dusts acted in some way to prevent the. development of tu berculosis; some still hold this opinion. Coni dust, iron-ore dust, clay lust, and dusts of calcium minerals hnve been suggested and tried in he treatment of silicosis; there has been great divergence of opinion if various investigators regarding the liarmfillness or linrmlessness if these dusts and their efficacy in preventing silicosis and tuberculosis, vhen mixed with dusts definitely agreed upon as harmful, or their larmfulness when breathed alone. However, the belief is growing hat any dust or combination of dusts if breathed in large onough inantity over a long enough period will cause diseases of the respira- ory organs. 44. Experiments by Canadian investigators led to the suggestion hat the inhalation of aluminum dust might prevent if not cure sili- osi8. The method of application was develoj>ed at tho M clntire lines. Ltd., of Canada and is being tried at a number of mints in the Jnited States and some other countries. The theory of aluminum horany in silicosis is bnsed on the hypothesis that chemical action, ot physical irritation by silica, is the ennse of silicosis. It was bserved by some investigntors that, aluminum almost completely n- ibited solution of siliceous material. ) unwiu w v m m m w i SUMMARY 9 45. Animal experiments indicate that the prophylactic use of alumi num^ inhibits the toxic action of relatively pure quartz. The th era peutic use in man appears to relieve symptoms m some cases. As human silicosis develops slowly, only prolonged, unbiased observation, with adequate control cases, will demonstrate its value in the treatment and prevention of silicosis. 46. I t has been recommended that general application of aluminum therapy in industry be delayed until adequately and impartially con trolled clinical observation demonstrates its effectiveness in preventing or alleviating silicosis in man. Meanwhile, there should be no slack ening in the control measures that have been found effective in re ducing the incidence of dust diseases in industry. 47. I t is recognized that, in extending compensation coverage to occupational diseases, the subject is much more complex than th at of accidents. In 1948, 39 States included silicosis in their occupational disease compensation laws. 48. The status of compensation for silicosis in the United Stntes, Cnnnda, Great Britain, South Africa, and Australia is summarized, and the important fentures of the laws and methods of enforcing them are more or less briefly described. 49. The main effectiveness of the preventive aspects of silicosis schemes is said to lie in their power to set up a standard of physique for new entrants into the industries, based on periodical medical ex amination; this procedure would hnve ramifications affecting safety, production, and probably other plinses of industrial work also. 50. The pressure of occupational disease (especially dust disease) on insurance companies increased so much ns to threaten finnncinl ruin in some instances; consequently, insurance companies are decidedly active in connection with investigations, research, and nil other phases of occupational disease, especially dust disease. 51. Much of the information regarding the cost, of legal compensa tion for silicosis has been obtained from foreign countries, especially the British Empire, ns most of the silicosis-compensation laws in the United States nre too recent to determine the cost of their operation. 52. The most complete figures available are probably those for South Africa. The total amount pnid for silicosis compensation since enact ment. of the miners' phthisis laws of South Africn to 1934 exceed 14,000,000 (about $70,000,000). The cost per ton of ore milled was nbout. 6d. (al)out 12 cents) and per ounce of gold recovered, Is. 7d. (about 38 cents) ; the cost per underground European shift was nbout 4s. ($ 1). In Canada in 1931 the cost of silicosis compensation was 1*4 percent of the total mine p a y roll, although only 2</. percent of the men employed by the mining conipnnies were actually exposed.' The estimated t>ost o f each case to the company wns $ 11,000 to $12,000. It wns also snid that, for every $5 spent in mining and concentrating 1 ton of gold ore, $1 wns required for silicosis. 53. The cost of cases of silicosis in Wisconsin for 1942 was $122,039; for 1913, it was $30,199; for 1944, it wan $44,837; and for 1945, it was $18.H98. 54. No question offers grenter difficulty in the administration of workmen's compensation laws than that of determining the nature and extent of disability in silicosis. It is known, however, that silicosis ) ) 10 REVIEW OF LITERATURE ON DUSTS cwi be present in diagnosable form in a person who will still possess enough capacity to permit full employment. Information is given on various methods for the determination of vital capacity and working capacity. CONCLUSIONS The literature on the efTect of breathing dusts abounds in various experimental, theoretical, nnd factual data; it comas from nearly all civilized countries; it covers nenrly all plinses of the subject but lacks conclusivencss in almost any or every phase except possibly that barm to health can be expected from prolonged breathing of excessive amounts of dust. There npnenrs to be good reason to believe that this applies to virtually any or all dust or combination of dusts, organic or inorganic. Almost innumerable uncertainties are connected with the harmful ness of dust, but du=t is now generally believed to be detrimental to health through its effect of one kind or another on throat, bronchial passages, lungs, stomach, and other internal organs, as well as eyes, ears, nose, other external organs, and the skin covering the entire body. Many <lus*s (metal, mineral, and organic) aro explosive; others fire spontaneously with moro or less readiness under vnrying conditions; and virtually all dusts have almost universally detrimental effects upon settlement, whether in the home, in the office, or on the external sur faces of buildings or on the ronds, streets, or sidowalks. All of these facts (and others enn be added) make dust one of the real scourges of present-day life, and certainly no sane person can deny that a most determined effort should be mndn to reduce dust or at least to confine it in such manner as to minimize its numerous harmful effects. It now seems probable th at the most harmful of the ordinnry lusts is that of silica; on the other hand, not even free silica (supposedly the most detrimental of the silica dusts) is harmful unless it is breathed in considerable quantities and over comparatively long periods; no human being has ever lived any length of time without breathing silica dust (free silica dust), yet by no means all of tho j>eoplo of the world have or liavo had silicosis. In othor words, tho quantity of dust taken into the respiratory organs is a controlling factor in dust respiratory harm fill ness, nnd common sense indicates that quantity of dust breathed is one of tho dominant factors ns to possible hnrmfulness from any kind of nir-borno dust. AVhat constitutes that quantity limit no one knows, notwithstanding the fact that numerous so-called threshold limits are now l>eing announced, some of them embodied in State regulations or lnws. Predicating dust respirntory lmrmfulness on a sliding scale in proportion to the freo-silica content of tho dust is anything but logical; in the fii-st place, no one knows whether a dust of 1-pcrcent silica is or is not moro harmful than a dust of 2- or .A- porcent or ovon of .AO-percent. Moreover, air with a certain number of dust particles per cubic, foot with a silica content of 1 percent (or nny other percentage) probably would Iw far moro harmful to a pc-son working on a contract basis than to ono on a day-pay basis, or moro harmful to n jierson working in an atmosphere of 8!> or !>0 F., rela tive humidity 00 or flfi jiercent, than to one working in nn ntmosphero of 00 F., rolntivo humidity 00 percent. Numerous other moro or less * i i 1 CONCLUSIONS 11 similar contributing factors make unworkable or futile the establish ment of regulations as to allowable number of dust particles on a sliding scale in proportion to silica content of the dust. In some in dustries, such as metal mining and tunneling, there may be as many different percentages of silica in the mine air as there are working places, and in many metnl mines it is very unlikely that the percentage of silica in the air of a working place today will be at all close to the percentage of silica in that same place tomorrow; to apply to most metal mines the sliding scale of allowable number of dust particles in the air in proportion to silica content would be utterly impossible of enforcement or fulfillment. Much should be done to clarify numerous uncertainties as to airdust harmfulness before any attem pt is made to establish more or less rigid air-dust standards by legal means. At present there is a definite lack of knowledge as to the size of air-borne lust- likely to be harmful, and present-day so-called standards of air dustiness are built on numerous uncertain premises on this point alone. Different author ities have found, in the lungs of deceased silicotics, varying maximum and minimum sizes of dust, ranging from as small as 0.2 micron to ns large as 10 microns; this fact lenils to the conclusion that, as fnr as harm to the lungs is concerned, the dust to be avoided is that, from 0.2 to 0.5 micron on the low side to Cor even as high ns 10 microns on the high side; this leaves much leeway, because nn air-dust sample con taining 10,000,000 particles (0.5- to 0-micron size) per cubic foot of air might easily have 30,000,000 particles 0.2 to 10 microns in size. More over, if the solution theory of dust hnrmfulness to the lungs is correct, there is the best of reasons to think that pnrticles much smnllcr than 0.2 micron are very likely to be harmful. To hold that the only harmful sizes aro those found in the lungs is anything but. good reasoning, beenuse certainly dusts ranging from 10 to 100 microns or more when floating in the air are drawn into the nostrils and other protective nir passages nnd if in huge numbers soon clog theso protective agencies and passages, permitting virtually free unobstructed entrance of the so-called harmtul dusts (say, 0.2- to 10-micron sizes) into the lungs to perform maximum injury. I t does not seem logical to disregard these larger sizes entirely, as is now done almost universally in the so-called dost standards l>cing considered nnd announced. Again, the present-day instruments nnd methods of sampling nir- borno dust ami determining the number of pnrticles present, are any thing but accurate or definite, even when handled by technically trained experts, and methods or instruments applied to certnin in dustrial conditions nro wholly unsuited to others. A condition ns to nir dustiness found in ono sample in a certain place is unlikely to l>o anything like nnother sample taken immediately afterward in the snmo place nnd in the same manner; this is true where the sampling is done instniunneously by grnb method or over a period of several minutes. In other words, the technic of determining quantity of dust pnrticles in nir is by no means definite, accurate, fair, or depend able, not only ns regards conditions between different plants but lietween different time periods in the same place in any one plant. In the face of all these (ns well ns numerous others) uncertainties ns to airborne dust, the attempt to embody in lnws aim regulations having ) 12 REVIEW OF LITERATURE ON DUST8 the force of law rigid standards as to air dustiness would seem to be a travesty on justice. I f o lantity standards as to air-borne dust are * made, they certainly should be labeled tentative, and the technic of taking the air samples and making the particle determinations should be outlined and enforced very carefully; otherwise, much injustice can be inflicted through inexperience or the malice of the persons making the determinations. This review of the voluminous liternture on harm to health caused by breathing inorganic dusts has been confined to readily available data and almost wholly to respiratory disease, chiefly lung affections. It gives little or no consideration to the numerous ill effects to human organs, other than the lungs, due to breathing more or less insoluble dust or the harm to other internal organs (stomach, liver, kidneys, etc.) or to the nose, tlironf, and bronchial tubes from breathing more or lees soluble or so-called poisonous dusts; nor does it take into con sideration the numerous hnznrds to human beings in breathing organic dusts, with accompanying hay fever and kindred ills. Moreover, nu merous dusts, both organic and inorgnnic, havo harmful effects of vari ous kinds on eyes, ears, and other paits of the body and on the skin from external contact; indeed, some dusts cause hnrm to health by absorp tion through the skin. Hence, while pulmonary disease due to tne breathing of air-borne dust is unquestionably of great importance, its various ramifientions (pneumoconiosis, silicosis, anthracosis, or these combined with tuberculosis), while vitally important., constitute by uo means the only detrimental effect to human beings in coining in contact with dust, externally or internnlly. Close analysis of the stntus of dust, in industry (and in general life outside of industry also) indicates that, numerous--one might almost say innumerable--uncertainties still exist as to specific features con nected with dust, linrmfulness. So numerous and far-reaching are these uncertainties (only a few of which have been indicated in these conclusions) that almost the only dofinito fact is that dust is a menace and that all kinds of it likely to come in contact with human beings should be reduced to a minimum or at least bo held under positive control until much well-plnnnrd, well-correlated research and investi gation (field and laboratory) have been conducted on almost every phase of tho subject. DEFINITION AND CLASSIFICATION OF DUSTS According to Welister's Unabridged Dictionary, dust may be de fined as fine, dry particles of earth or other matter so comminuted that they may lie raised and wafted by the w ind; th at which is ernVnbled to minute portions; fine powder. In 1870 Richardson ( /) 1 included in tho term "dusts" all those fine, solid particles thrown off from various substances in the processes of manufacture or treatment of articles in common use in daily life. Drinker () in 10.10 defined dusts as solid particles rnnging in sixe from lessthnn 1 micron "to nbout 150 microns; this definition is probably ns applicable ns can bo had insofar ns con cerns respiration. M fa llrit 1 number In |* r n !h c * r* rttr-r in H M Injrrnphy 1 rn<! o f b u lle tin . A w lcroo 1 1 /1,000 mm nr ap p ro x lm n lrlj- I/21UKK) Inch. ) ) w DEFINITION AND CLASSIFICATION OF D ISTS 13 i Physiologically, there are almost ns many different classifications of dust as there are authors on tho subject, Richardson (/) suggested the following: (a) Cutting dusts, formed of minute, hard, crystallized particles with sharp, cutting, and pointed edges and composed of iron or steel, stone, sand, or glass, dried silicates in earthenware, lime, and pearl. (b ) Irritant dusts, derived from woods, ivory, textile fabrics, fluffs of wool, silk, cotton, flax, hemp, hair, and clay. i (c) Inorganic poisonous dusts charged with arsenical salts, derived from poisonous chemicnl compounds used for coloring artistic prod- i nets or for preserving organic substances, such ns furs. (d) Solw le saline dusts, organic poisonous dusts thrown off during the mnking of tobacco into cigars and snuff and enrrying with them particles of the dried tobacco plant. (e) Obstructive, and irritating dusts composed of carbon, fine par ticles of coal dust, scrapings of carbon or soot, dust of rouge, and flour. Ilaskerville ($) in li)12 classified dusts ns: (a) Insoluble inorganic dusts, including metals (antimony, nrsenic. type metal, brass, bronze, copper, aluminum, iron, steel, lead, rnnngn- , nese, vanadium and ferrovnnadium, silver, tin, zinc, and solder) in a state of fine division (dusts, atomized metals, and metallic powders) ; , flue dusts; various ore dusts (iron oro) ; silicn; sand, emery, flint, ami glass powders; carbon graphite, diamond, coal, and soot; brick dust, marble, granite, cement, nnd terra cotta; lime, gypsum, plaster, and meerschaum; phosphates; nnd gunno. (b) Soluble inorganic dusts, including substances likely to be swallowed nnd absorbed, such ns metal particles, including lead, brass, copper, zinc, arsenic, mercury, and silver, ns well ns soluble inorganic salts. (c) Organic dusts, comprising such widely varying materials ns saw dust, fur, skins, feathers, broomstrnw, grains, flours, jute, flax, hemp, cotton, wool, carpet d u s t, street sweepings, tobacco-box dust, hides and leather, felts, rags, pnper, and horsehair. In 1918 Hoffman (4) considered the following classification to be in strict accord with tho fncts as they were known nnd understood at that tim e: (a) Inorganic dusts, including metallic dust, mineral dust, nnd lusts of the mineral industries. (b) Organic and miscc/laneouw dusts, including vegetable-fiber dust, animal and mixed-fiber dust, organic lust, and mixed orgnnic nnd inorganic (public) lusts. 'Thompson (b) classified lusts as: (<i) Insoluble inorganic dusts (irritating the respiratory pnssnges), as flint, silicn. sand, carbon (coal soot), brick lust, marble, grnnite. terra cotta, cement, asphalt, enamel, glassvqunrtz, limo (gyirsum, lilnster), meerschaum, phosphate (fertilizers), gunno. emery, liamonil dust, metal tilings (lead, brass, iron, steel, etc.), pumice, nnd nshes. (b) Soluble inorganic dusts (liable to be swallowed nnl absorbed), ns soluble arsenic, mercury, lead nnd silver compounds, metnl filings of lead, brass, and zinc. Rn.vjin ni> - 2 14 REVIEW OF LITERATURE ON DUSTS (c) Organic dusts and pb'rrs arising from handling or manufacture of wood, l>one, and shell, fur. skins, hides and leather, feathers, brooms and straw, flour and grain, jute, (lax (linen), hemp, cotton, wool (worsted, etc.), tobacco, felt, carpets, rags and paper, horsehair, and street sweepings. De Balsnc and Agasse-Lafont (ff) suggested the following classi fication : (a) Active dusts, which are immediatley disseminnted and radiate beyond their point of application; toxic dusts (lead, arsenic, and mercury); caustic dusts, chromates, etc.; infectious dusts. (b) Inert dusts, soft, flexible felting (lusts (wool, cotton, nnd leath ers) ; hard, troublesome, wounding dusts (ligneous, metallic, stone, and coal dusts). Schurmann (7) differentiated dust, according to origin, into animal, plant, nnd mineral dusts nnd dust from artifacts. Animal dust is evolved with the working of ivory, horn, whalebone, bones, mollier-of-pearl, hides, leather, bristles, sheep's wool, hair (horse, rabbit, nnd cow), and feathers. Plant- dv.it originates in industries working with grain, medicnl powders, spices, cotton, hemp, jute, ffnx, tobncco, wood, thick-shelled nuts, bark of plants (tanning industry), rags, shoddy, and paper. Mineral dust is formed in working hard coal, marble nnd other lime stones, and in connection with clay nnd porce'ain industries, also pumice, sandstone, granite, nnd sintes. Dust from artifacts is encountered in the glnss, glazing, enameling, tile, cement, Thomas sing, celluloid, iron, steel, bronze, gnhilith, nnd lead-alloy industries nnd in (he chemical (especially dye) industry. Schurmann (7) defined mixed dust ns a mixture of polishing mate rials and the fragments of the object being polished. According to Drinker (2) nil these classifications linve little prac tical importance, since in daily practice in industry the harmful effect is exercised more frequently liy dusts mostly of mixed origin. Most important, moreover, is tho physical nnd chemicnl constitution of the dusts and consequently their action on the human system. An effort, has been made to group under the bending "Inert" a certain number of dusts: but tho milliner is liecoming more and more reduced since certain ousts, such as talc and asbestos nnd even coal dust, until re cently considered ns inert nevertheless have caused serious organic lesions among certain classes of workers. The majority of experts admit that, the so-called inert dusts are not. renlly inert when considered from tho pathogenic point of view. Although at the outset Ilieso dusts are not harmful nn<l even when present in the workroom in large quantities some of them enuse only transitory discomfort, (sneezing, watering of tho eyes, and rough), it is certain that, ns the organic reactions diminish nnd tho system seeins to linve recovered from the efforts, they nevertheless finally nttnek it in n subtle innnner, sometimes oven seriously. Tho mucous membrane of tho nose, the conjunctiva, first tho upper nnd Inter the lower respiratory passages, tho teeth, the skin, nnd often tho digestive tract are subjected to the harmful action of these dusts. As indicated by the above discussion, an absolute classification for dusts is difficult. Opinion regarding so-cnllcd inert or harmless dusts ) ) EXPOSURE TO DUST 15 has changed as further investigation has proved some of them to be injurious. A convenient classification, according to physical charac teristics and physiological effect, lias been used by Sayers (8). He classified dusts info the two main categories of orgnnic and inorganic. The organic he divides into nonliving and living organic dusts, with further subdivision of the nonliving into toxic and (or) irritant dusts and allergic dusts and the bving into bacteria and fpi. The inor ganic dusts are subdivided into toxic and (or) irritant, fibrosis-produc ing, and non-fibrosis-producing dusts. EXPOSURE TO DUST Prehistoric man, who originated the trade of making stone imple ments, probably started the first industrial hazard, the extent and severity of which the medical profession, ns well ns the industries con cerned, has begun to realize only comparatively recently. In fact, dust ns a factor in the causation of disease had not received much attention before 1000. At the site of one of the Swiss lake dwellings where flint implements were found, although the flint must have come from a distance (probably from the south of France), the chippings of material were m such profusion ns to imply that the implements were manufactured on the spot. In other words, a prehistoric flint- knapping factory was probably located there (#). Some of the per sons who prepared these implements no doubt suffered from respira tory diseases. According tot'ollis (10), the (lint knappers of Brnndon, flic lineal occupational representatives of this oldest, of industries, who still use tools similar in shape to the dcerliorn picks of their prehistoric ancestors, suffer n terrible mortalit v from phthisis induced by flint dust generated in their work. The work is carried on in small workshops at the back of cottages in the rural district bordering Norfolk and Suffolk, where large flints or pot.stones arc found; the district has been known from remote antiquity for the manufacture of arrowheads and other prehistoric implements, tinder boxes, and in later years flints for flintlock guns. Carozzi ( / / ) has ouestioned the hypothesis of an occupational pneumoconiosis in prehistoric man. The conditions requisite for the development of this oeeupnt ions I disease do not seem to Carozzi to hnvo been present in that distant epoch. For example, if it is true that even today, in dusty industrial surroundings, a long period of exposure to the dust is necessary, and if it is true that the average duration of life did not exceed 10 years, it is doubt fill tlint mortality from a form of p n e u m o c o n i o s i s attained a high value, Cnrozzi ( / / ) states, however, that, it is certain that prehistoric man suffered from a disease of the n aturenf tiil>qycnlosis. Dusts of vnrious kinds are carried in the atinosphero in all parts of the world; and the inhalation of these dusts over periods of years in evitably nroduces changes in the lungs, as, for example, the pigmented lung of t lie city dweller ( 12 ). The following tnhle by Landsberg (/./) indicates the amount of dust that inay be present in the air under dif ferent conditions: ) 16 REVIEW OF LITERATURE ON DUSTS Particle* per ruble Kind of Ir: centim eter (large particle* only) M ountain_______________________________________________________ 2 City, renlilentlnl f|unrtori<_________________________________________ ir> City, iiuslnpflfl re n to r__ . . . ______________________________________ 100 Cement fnetnr.v---------------------------- __ . _ ______________________1,200 Granite ru ttln ir____ _______ 2,10) Bltumlnous-con I m ine_______________________________ 3,900 Anthracite m ine-----------------------------------------------------------------------------4,400 Grinding hope____________________________________________________ 0,700 Lnndsborg (/.?) lifts estimated thni llie nir inhaled by a normal person during a working dnv contains roughly 12 billion lust, particles. Pfnff (H ), however, found the values for city dust in Snnrbriioken, Germany, to lie bet ween 2.r>0 nnd 2,800 pnrticlcs per cubic centimeter; in streets with heavy traffic he found 4,000 particles. This difference in results probably is due, at least in part, to the size of particles; Lnndsberg (/.?) states that he counted "large particles only" but does not say how large, while PfaiT (lh) counted those for the most part under 1/ 1! micron. Tho composition of the dust is not given in cither instance. Soper's ( lit) report on tho air and dust, in tho 21-mile subway of the Interborouiih Rapid Transit Rnilrnnd of New York City, published in 190(5, likewise deals with general exposure to dusts. Chemical analysis of the dust underground showed that it col `nined Cl.1)0 percent of iron, nearly all of which was in the metallic state, 21.94 percent of organic mntter of vegetable nnd animal origin, 15.58 percent of silica and other matters insoluble in ncid; nnd 1.18 percent of oil. There were, on the average, Cl.fi mg. of dust in 1,000 cubic feet of nir; the maximum weight was 204 mg. Tho dust, in the air of tho subway w as 11 to SIX) percent heavier than that in the street nir. Alth.iugh some of this dust was carried in from the streets, much of it wns of underground origin from gradual wear nnd tear of tho wood, cement, and other materials used in constructing the subway and from opornting the trains; tho largest, percentage wns iron dust from the grinding action of (lie powerful brakes on the cars. The loss of weight in brake shoes alone was estimated ns about 1 ton per mile of track per month, nnd when the loss from the wheels nnd tho railway track is added to this, the origin of the metallic dust, is explained. The men had not been employed underground long enough at flint time to show the effect on health of inhalation of the dust. Although no se rious disensa wns found among them, many suffered from iiillnmmatory affect ions of (he nose, throat, and windpipe and from "dry pleu risy" unaccompanied by pain. iloffmnn <i) prepared an occupational grouping to emphasize in a general way the principal dust hazards in 118 occupations or groups of employment, which he said was in strict necord with the facts as they were known and understood at. that time (1918). Under tiro heading "Organic and miscellaneous dusts" he listed 05 occupa tions; under the bending " Inorganic dusts" hn listed 52 occupations. Using 1ho United States census for 1919, ho estimnted that. .'5,928,978 persons were employed in the dusty trades; of these 1,007,181 were listed ns employed in occupations exposed to metallic nnd mineral dust and dust in tho mineral industries. He considered thnt quant itatively EXPOSyRE TO DUST 17 the most important kind of metallic dust encountered under typical industrial conditions is the dust of iron and steel, which, however, is generally more or less intermixed with dust of other metallic, or minora! substances. Exposure to mineral dusts is most common in the stone industry, among potters, in cement manufacture, and in mining. In a paper on the extent and severity of file health hazard from dust in mines and allied industries in the United States van Siclen (16) gave the following estimates, based on the 1929 decennial Fed eral census, of the number of men exposed to dust hazard in various types of mining and industries working in metals and minerals: Totn I tcnrkrr* txpantfl Metal m in in g ____________________ -- ------------------- - -- l2. 2d.s Nnnmotalllcs mining, excluding tunnel and foundation excavations -- 23. 5 BUumln<ms-conl mining, underground - - -- -------- --------- 4r*o, fits ftlttiniirmus-conl min ing. n|xn p i t -- - - - - - -- --- 8 .2 M AAnntthhrraacciittee mmiinniinngg,, uUnudleejrxguruoluenudt _w__u_s_h_er-les - -,, --------------------------------------------------- --- Uli.tINx<l Smelting, non fe rr o u s p l a n t s --------------- ----------------------------------------- -- 13. 300 Smelting, fe rr o u s p l a n t s ____________ ___________________ ________ - - - 24. POO Cement p l a n t s ___________________ ___ Abrasive In d u s tr y ____________ _______ -- -- --------------- ---------......... .......................-- --- - -- Asbestos pr<ducts __ _ _________ _______________ _____ ._______ ----- Olay p ro duct-- ___ ___ - ........................................................ - - - - C u t l e r y _______________________________________ _________ -- ------ - - - Clas s m a n u f a c t u r e _______________________ ____ -- ------- -- -- - - (Jranlte, sla te, marble, nn<l oflier stone product*.,.................. - ------ -- Hones, wh t*toues, am i s i m i l a r p ro d u cts____ -- - --------- Iron ami ste e l____________ ________ . ..... __.......................................... - - Mineral f e r t i l i z e r s . -------- --------------- ------------------- ----------- ---------- - - - Mineral an d e a r t h s , g m u n d .............. - ........... - -------------------------- Non fernm s-m etn I alloys a n d product*-.- - ---------------------------- -- Pottery , Including p o r c e l n l n w a r e . . . . __ ... -- -- - -- Sand-lime b r ic k ____ _______________ _______ _______________________ -- 3.873 S, 0*J1> 0 3 ,33d 14.001 07.527 28.715 37 4 30,007 20,0-2 1.070 70.383 33.400 no In his conclusion lie stated : No t o ta lin g of the nmrd>er of woikm en cxjMised to the d u st h a z a r d In the mining and allied in d u stries In th e I 'nlted States, a n e stim ated In the preceding pages, h as Imi'm u n d e r t a k e n , t h st Imviiuso th e e s tim a te d figures them se lves a r e subject to revision after more detailed study of the mineral industries and manufactures, and wound, because the degree of the dust hazard varies with the several Industries, w ith the manifold occupations In each Industry, and |Nt\veea s im ila r imaUlotm in different p lan ts of th e sa m e Industry* A lump-sum total would therefore have no real meaning. The separate totals, however, are sufllelent to Indicate the wide extent of tills kind of hazard. in 1047 the weekly average employment in the hard-coal mines of Great Britain (/7) exclusive of ancillary plant and office workers was "Ifi.000. During (lie same year 320,000 men were employed in (lie hard-coal mines of France nnd lfiO.OOOin the mines of Belgium. As of l)eceml)or 31, 1040^ about 100,000 men were employed in iho coal ami metal mines of South Africa {IS). Probably lf>0,0tX) persons were employed in 19JJ0 in the quarrying, cement, pottery, and stoneware industries of Germany (JO). Of 217,000 men employed in the coal mines of the Ruhr district in 1033, 11,500 were said (20) to have been employed in work involving exposure to rock dust. In 1047 the average daily employment in the British zone of Germany wns2S7,000 and in tho American zone 8,000; 41,000 were employed in the Saar, ) ) is RF.V1EW OF LITER ATtJRE ON DUSTS .?i>,(XX) in flip hard-coal mines of flie Netherlands, and 27,000 in the Italian mines ( 17). The above figures on number of employees in the dusty trades are given merely to indicate the possible exposure to the dust hazard; they are in no way complete and, of course, do not show the actual num ber subjected to the hnziml. In 1034 Lanza and Vane (21) stated that silicosis was associated with certain industries as a major hnzard. nnd the number of persons engaped in these industries could be estimated with some degree of reliability. In a great'many other industries, however, isolated jobs or processes might involve exposure to silica dust, and only a guess could bo hazarded regarding the number of workers in these proc esses. From a summary of the facts, these authors concluded that, approximately 450.000 workers nre exposed to silica dust in the chief mining,quarrying, nnd manufacturing industries, and 100,000 in other industries and processes; the >00,000 they gave ns a final conservative estimate of the number of workers in the United States exposed to silica dust to a harmful degree probably is still applicable. It is apparent, therefore, thnt silicosis has been nnd still is a widespread industrial hazard, is probably increasing, nnd affects appreciably the death rate among industrial workers exposed. Only dusts encountered in the mining nnd allied industries nnd the diseases caused by them nre considered in this paper. PHYSIOLOGICAL EFFECTS OF BREATHING DUST HISTORICAL RESUME Following is a brief reference to some of the ninny nut hors who have added to our knowledge, of the history of silicosis. For n more detailed and complcto historical rt\sum6, the reader is referred to Cnrozzi's contribution covering the period from the 27th century II. C. to 1871 A. D. (//). Probably the oldest published statement regarding the harmful ness of exposure to dust is one by Pliny (22) : Minium w l l n w In tin fnctorv envelop t h e i r f n r e s w i t h loose Mnritler*, which enable them to my* w ith o u t Inlmlhic th o f a t a l dust. IIipj>ocrnte3 (&?), wlio \vns born nbout 4CO B. 0., called nttention to the difficult breathing of the metal digger. C-elsus, a Roman medical writer who lived in the first century, staled : n.r far the most t er rib le fo rm of e m a c i a t i o n la tlm t wlilrli th e Dreeka rail phtidsls. It spread* to t h e lime*. Oil to p of (Ida, u lceratio n iM-cnra anil a alow ferer which at tlmea dlsa|i|ieara and at other times reapiiears. In quoting this passage Mavrogordnto (2i) said tlmt when early writers discussed dust, plithisis one may assume that the d!*ence (hry had in mind wnsof the nature mentioned by Celsus. In 1551 Amatus Lusitaniis (7) reported thnt most workers occupied with the preparation of gypsum nnd lime died of lung phthisis. Agricola (14!)1-l.r>55), in his Do Ro Metallic (W), published in 1550, descrilted mining as-- A. perilous orrujinllon to pu reu e l*ornue t h e m iner* n r e Mitnetlmofl ktllrtl by the peatllentlnl n!r which they brent h e ; Rometlmes their lung* rot nwny. ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST *. * * Some mine* nrp ver y d r y nnd th e m n p t n n t dut ont^r* th e Mood find hings, producing flip difficulty of brent hint; the (irccks m i l nstlunn. When the dust Is corrosive it ulcerntes tlip lung* mid produt*os consum ption; hence. It is tlint in th e ('n rp n t h i n n Mountain tiicre a r e wom en w h o hn v e n m r rl e d seven huslmnds. nil of whom fids dreadful disease has brought to an early grave. In the sixteenth century, accordinp to Georpius Apriooln. it was known that permanent injury to the limps resulted from exposure to certain kinds of dust but not to all kinds (25). Two kinds of in jurious dusts were recopnized--a corrosive and a noncorrosive type. Each of these classes was associated with a different, kind of limp ehnnpe. "simple" and "infective" silicosis, respectively, described in the 191G General Report of the Miners' P hthisis Prevention Commit tee of South Africa. Paracelsus, a Swiss alchemist and physician, in his hook (2(1) on miners' phthisis and other miners' diseases, described especially (he chronic limp (roubles of miners as "bmp consumption," "asthma, ' and "dyspnea.' lie was the first to lit briefly the occupational diseases of miners and smelters as well ns the first in the world literature to prepare a monopraph on industrial medicine (26). From 15.11 to lM i Paracelsus revisited the mines and smelters of Scliwaz in the Tyrol, where he had worked as a laborer between 1510 and 1Trill, and wrote Jus hook, which was published in 1567 after his death. He found that -- M iners tn motnt mines, when they a r e occui>iwl tn (tigging, sm elting , a n d washIhit gold. silver, suit, jilum, iilphur, lend, ci*iiH*r, zinc. Iron, m u l quoklUor In flic refining of vitriol, suffer from various disturbances of the lungs, sfonmcli. and IntoMthics; thc\ arc thou said to hnve " miners* diseases." However, there Is nothing found In the works of the old w r ite rs In re g a rd to these diseases. His theory was that lung licenses contracted above ground depended upon cliinaf io eotidit inns as influenced by the rays of the stars. Sim ilarly, pulmonary disease of nutlet's underground was caused by mineral rays. Ilowever, he philosophically reminded his tenders that -- We need m etals nud, therefore, we lim'd risk life mid health for them, since every w here In n a tu r e good and e ill lie together. As th e crocodile distresses a n d kills men hy hW b r e a th , likewise aNo th e v a p o r s Mine d u s t ? ) o f su ch niet/ds kill tts. * * T h e organism must Ih` p r e v e n te d fro m com ing In co n tact with th e m etal e m a n a t i o n s ; for If the o r g an ism I* once In ju re d t h e r e Is no cure. The mi timely dent It of Paracelsus was attributed to injuries to health received dnrinp his activities in the inininp and metnllnrpical indiist ries. Pnuconst, n more recent ant her (27), likewise referred to the incrensinp interest in the subject a s a recopnition of the eomliton of pneu moconiosis a more or less maessiuy risk of commercial development in the progress of civilization in recent years. Pnnsn, in 10I4,vwas t lie first to discuss in detail limp disease of miners and (lie asthma of prniii measurers (7). Ill 1G4!) Van Diemorbroek was reported (2S) to have made the lirst section of a stonecutter's limp which, in a case of fatal asthma, revealed " limp vesicles completely flopped with line dust" ; as i|iu>!cd by Raninzzini (2.0), he found siicli heaps of sand t bat in vtuminp the knife throuph the pulmonary vesicles lie tliouplit bo was cut t iup some sandy body. 20 REVIEW OF LITERATURE ON DUSTS Carozzi (11) quoted Fourcroy regarding this incident as follows: In (ltBRecttng a t the hospltnl the domestic of a lapidary, who died of osthm a, he found the pulmonary vessels Ulled with dust of the diamond. In 16.r>2, Ursinns (1C18-C4) described (30) the lung disens" that attacked especially the miner but also the smelter. H e divided lung diseases into two clnsses--one was caused by poison, and the other was not. The principal symptoms were coughing and shortness of breath. Etiology was a question of brenthing dust, catching cold, fatigue, injury, and the like. He said the long disease due to "poison" was not so clear and wns unknown liefore I'nrncelsns. In his book published in 16T>G. Stochnusen (SI) defined miners' phthisis ns "difficult breathing, chest asthma with disagreeable hard tough and considerable hoarseness, which effects generally degenerate into fatal consumption." He attributed these symptoms to metallic vapors, dust, and meteorological conditions, from which miners suffer more ot less and call "miners consumption" because the affliction arises especially in connection with mining. The actual causes, he said, were-- especially thick, lowering clnmls anil mine ilnmpnesa, w atery hum idity, all aorta of rapora of earth and metal, various fumea and smoke, different dusts and dirt. He also said that much dust arose from grinding, so thnt workers were forced tocovor nose and mouth with cloths. Etmiiller, 1648-82, a professor at Leipzig about 1670, described (32) a case of a miner who-- wan seized drat with rough and then with g re at anxiety and dldleulty of hrt nthlog. especially at night; he used to Jump out o t bed and open the window for fresh air. In 1600 Li'mneiss (.7.7), referring to miners, gave the morbid sequence of events as follows: The dust anil stones full upon the lungs, the men have lung disease, breathe with dldleulty, and at last take consumption. Ramuzzini (?) wns the first to recognize the social significance of industrial diseases from chemical substances. In bis (took published in 1700, he mentioned the harmful effect of dust on the respiratory organs. For information he went to tlio workers in tho occupations, entered tho mines, ascended the mine shafts, and collected tho experi ences of his occupational collcngues. His book was based on n study coveriiigmorothnn 40yenrs. Flint dust has long Iicon recognized in England as injurious; a patent for grinding flints by a wet method wns granted in 1713 to Thomas Ilcnson, of Newcastle-under-Lyme (34); liefore this date, flints had been pounded dry, winch pion-ss proved very destructive to mankind, insomuch thnt any person, ever so nealthy and strong, work ing in that, business, could not possibly survive over 2 years, occasioned by the dusk sucked into bis laxly by the nir be breathed. In 1770Scliefller (.72), a mine physician in Saxony, wrote that, miners were attacked hv an nstlnnntio condition which he called sicum-drum nfitlunn. According to the Mining .lournnl (32), the older mine physi cians called it. asthma metnllicmn or moutniuim-metal or mountain asthma. PHYSIOLOGICAL EFFECTS OF BREATHING DUST 21 Scheffier (35) realized that the description of miners' phthisis riven bv previous medical men was insufficient. His conception of it was a cnronic slow fever with hardening of the glnnds nnd obstruction of the lungs, with lack of elaboration, secretion, nutrition, and apposition which, through the arsenical or other dusts, dries out the soft lymph of the glands in the lungs and air passages. The symptoms were slight fever, loss of appetite, cough, shortness of breath, and swollen feet, the imtients finally becoming bedfast ar pulse, sleeplessness, dry skin, and showing great weakness, usually constant fever, often irregubloody sputum, hemorrhage, sweating, and diarrhea until death claimed then. Von Linn (17H7-78) reported (3ft) from his travels in Dubinin in 1734 that the stone workers in O rs a , ns a result of their health- destroying work, seldom attained a greater age than 20,30, or 40 years. In 1727 Wepfer (3d) pointed out that there must be a connection between the phthisis from which the stone worker sulfered ami tho dust, particles which each breathed with the exercise of his activity. In 1771Hubbe (30) described the ``Seeberger stone breakers'disease." In 1780 Ackerman ( 17.rC--1801J referred (37) to miners' phthisis as the most " frequent and specific' mine workers' disease and said that physicians did not agree regarding the true definition of this disease. As a result of a special inouiry into the prevalence of dust phthisis Allison (1790-18.r>!)), a professor of medicine at Edinburgh, found (33) that rarely did a mason, regularly employed in hewing stones in Edinburgh, live free from phthisical symptoms to the ape of n0. According to Mavrogordato (~ f), he established the association be tween dust phthisis and tuberculosis, that is, l*et ween dust phthisis and true phthisis. Not dust per se but a secondary complication was re sponsible for (he "ulccratio'' of Celstis. '1 he corrosive dust of sixteenth-century Agricoin and eighteenth-century Hamazzini became the "tuberculosis" of Allison. Allison, like Lacnnec, knew of tho anatomical tnbeivie but not of the tuberole bacillus. Hugh Miller (!!>), the famous writer, geologist, and stonemason, described his own narrow escape: T h o <luMt of tho Htom wlilt h 1 hml Imvii h ew in g for flu* !nt 2 your* h ad hoenn to affect my lung*, hm they hml hren afrcct<<l In Ih e last a u t u m n of my a p p r e n ticeship, hut much mon Ncvcrely; mill l w a s too paljaibly sin k in g In first an d s tr e n g t h to re n d e r It sa fe for mo to e u m u n t e r tho consequences of a n o t h e r sensun of hard work as a stomvnlter. From the stage of tho malady at which 1 h ad a l r e a d y a rriv ed , |aor wor km en, utmhlo to to wlmt t <tht, th ro w them se lv es loose f ro m ttiolr em ploym en t, mid sink In <1 o r 8 m o nth Into tho g r a v e --some at a n oarllor. some at a lator |M*rlod of life ; hilt ho g e n e r a l la th o afTivthui t h a t few of mir Kdlnlnirgh stonecutters puss (hoir fortieth your unscathed, ami not 1 out o f every f><) of t h e i r nmnltcr over reaches hla forty -fifth y ear. In 1783 IIofTnmn ( stated Mint metal fumes nml vapors, ns well as dust, mused the disease picture of "miners' phthisis," but Iletikol (41) in 1745 attributed the disease to such external causes as dust from stones and metals, lack of air, bud air, or bad fumes or vapors. Thackrah ( 178(>-1H33) wrote the first general work on occupational medicine in English (7 /), with the execution of tho translations of Unmazzini's treatise. lie (42) claimed that, such generalization was not justified--that "dust of every kind irritates but not in an equal degree"--but recognized that masons minding particles of sand nnd ) 22 REVIEW OF LITERATURE ON DUSTS I dust which arise from chipping stone were short-lived, generally dying before they attained the age of 40. He also discussed the prevalence of phthisis among the metal grinders of Sheffield and quoted Knight's opinion that fork erinding ought to be confined to criminals. A few years later Holland (46) portrayed the conditions of fork grinders-- a picture of wTetchedneim w hich h a s no parallel In the annala of any country, or In the record of any trade. Fiction can add no color or touches to a picture like this. Truth transcenda the sandy embellishments of Im agination. The distempered fancy has here no room to exercise h e r powers. INCIDENCE OF DDST DISEASES According to Greenbnrg (44), data oil prevalence of occupational \ disease in different countries at different, periods of time must be interpreted with the grentest caution, because industrial processes differ so widely nnd change so frequently. To be conclusive, such data should be available in the form of nctual death rates, based upon knowledge of the population exposed as well as on the number of deaths occurring, and properly corrected for the age distriburio jf trroup involved. A brief summary of some of the voluminous information available on the incidence of dust disenscs in some of the principal mining ountries of the world follows. l or more detniled information, the render is referred to Carozz.i's Bibliographic Contribution to the ITisorv of the Pneumoconiosis "Silicosis" {11), published in 1941^42, and 0 Kosen's interesting nnd comprehensive History of Miners' Diseases (46), published in 1943. (UIF.AT I lil T M K Statements published in England ()6 ) before 1860 indicate that ninors apparently suffered more with pulmonary complaints than ither population groups nnd that the mean duration of life of miners vas less than the average duration for the imputation ns a whole, rhe Mining Journal {46) for 18.r>8contains the following report.; At the age of 20, the total average nlrknem of coat m inera exceeds th a t of (tier people by 4 percent ; a t (he age of 30, It rlsca 70 percent; at 40, It Is 78 orront ; at 00, they have an excess of 7U percent ; and a t the nge of (Ml about fill o rc en t Between the ages of 10 nnd 20, one-third of the deaths among coal dnera are due to dlaonsoa of the respiratory organs, wbltp one-third of the mil "rs le a violent death. It la an undeniable fnct tlint the average duration of life of m iners Is only 7.7 years, while ngrlcnltiiriil w orkers nttnln nn average nge of 42.8 years. In 1892 royal commissioners "eve appointed in England ( 10) to nquiro into the hcnlth of men employed in metalliferous mines. Not withstanding the evidence of several witnesses, particularly the miners hemselvos, that- dust, was far worse than nnything else with which hey had to contend, the commissioners conducted in 11virtually unnniiious medical opinion (hat the influence of dust was subsidiary to the inny other adverse conditions of ventilntion, exposure to fumes of cplosivea, and variations of temprature which at that time were 1revalent in tlio mining industry. Collis {10) snid that (his condit ion was unfortunnto, ns tho provalor.ee of phthisis in cortnin indus- ) ) tfU M M B B W PHYSIOLOGICAL EFFECTS OF BREATHING DUST 23 tries was attributed to imperfect hygienic conditions rather than to dust inhalation, a point then in dispute. In 1902 a departmental committee {10), of which Haldane was a PC' member, was appointed to reinvestigate the cause of the still per sistently high phthisis mortality among Cornish tin miners. This committee decided that-- So far na the Cornish m iners are concerned It seems evident enough thnt stone dn st which they Inhale produces perm anent Injury of the lungs--gradually In the case of ordlnnry m iners, and rapidly In the case of m achine drllltnen--nnd thnt th is Injury, while It la apparently capable of gradually producing by Itself great Impairment of the respiratory functions, and Indirectly of the general health, also predisposes enormously to tul>eroulosls of the lungs, so th n t a large propor tion of miners die from tubercular phthisis. T hat the prim ary Injury to the lungs In due solely to Inhalation of stone dust would seem to be practically certain. From February 1, 1919, when the first silicosis scheme of compen sation for the refractories industry became effective, until the end of 1928 compensation awards were made in England in 423 enses, includ ing 121 deaths (46). During the period 1921-23, 328 deaths were recorded in England and Wales under the generic title "chronic interstitial pneumonia", which included such diseases as fibroid phthisis, fibrosis of the lungs, silicosis, and miners' phthisis, when returned ns nontliberations {47). In 192G the question was raised in Parliam ent (48) as to the number of men not affected by the Silicosis Act, but when examined by officers of the Home Office during the preceding 5 years had been found suffering from the disease. The reply was thnt the medical in spectors had made no routine examination of workers in factories except sample examinations in connection with special inquiries into the grinding nnd other industries. Of 1,106 workers employed in processes involving silion dust so examined, 556 were found to be affected by fibrosis of the lungs; 528 of these men were employed in the grinding industries ami 28 at steel works. A memorandum on industrial silicosis nnd nsbesfosis issued by the Home Office in July 1932 (40) contained the following statement: The Incidence of silicosis continues to tie serious nnd w idespread, ns Is shown by the following figures of enses In which com |iensntlon hns been paid under the S|ieclnl schemes mmle under section 47 of the W orkm en's Com pensation Act. 1!2T>. D uring the Inst ,'t yenra there hnve been 80 enses. Including 30 dentils, am ongst workmen employed In gnnlsler mines nnd sllleh brick w o rk s; 1711 eases. Including 23 deaths. In the getting nnd m nnlpulntlon of ruimlstone nt qonrrles o r on prem ises worked In conjunction th erew ith : 322 caw's. Including 87 dentils. In the pottery Industry ; 81 eases. Including 32 dentils. In the m etal Industries, Including metnl grinding nnd snndhlnstlng; nnd PI enses. Including 20 deaths. In coni mines. t v The numlior of silicosis enses (fatal cases excluded) in Great Britain receiving Kompensntion in different industries in 1933, 1935, and 1938 is given in table 1. The compensation in these cases was grnnted under section 47 of the Workmen's Compensation Act, 1925, as amended by tho net of 1930 (!>0). *f 24 REVIEW OF LITERATURE ON DUSTS Table 1 Compensation acbems D isablem ent cmwe receiving eotnpe&antloo; total, and new cases In eaeh year < Number * Percent*** 1033 1038 1038 1033 1036 1088 til (0) *> (4) (6) (6) O) JUtiwrtcrto Industrie Schem a._____ __ _________-- Sandstone Industry Ocheroe........................................ -- MeUl-Orlndtni Industrie and Various Industries Scbetnni China and earthenware In d u s try ............................. Metal Industries........................... ................................ Oaal mlnlnr Industry.................................................. BaiMer. e l e ............................ .......... ............-- -- Miscellaneous *................. 'IVrfal 770 03) M3 (7) Ml (00) 4 0) 320 0) M (48) 123 (73) l.M S (44D) 774 (8) 00 (75) 293 (00) et (17) 646 017) 123 () 101 (38) 1,730 (462) 262 71.7 16.8 10.4 (0) (3 0) (1.8) 0 .4 ) 372 10.4 . 3 14.8 (60) (17.0) (16.6) (10. 7) M0 7) 66 (U) 1.770 * 110 (21) 180 <w> 2,617 (<M> 10.4 (22.1) 3.7 (3. 6) 18.4 <. i) 7.6 (10.0) 0.0 das) 100.0 (100.0) 16.3 (16.8) 3.6 (3.8) 31.4 (01.0) 7.1 (6. 2) 6.8 (S.W 100.0 (100.0) 0 0 (7.3) 2 2 (2 2) 30 8 (08.7) 4 4 (3 3) 7 6 (8 6) 100.0 (100.0) tT b e onbracketed numbers and peroentares are tbe total case of disablem ent (th a t Is. new cases--eases continued from previous years) In which compensation was paid In the given year; tb e bracketed Agures are the new case only, i including metalliferous m in . Bo o k s : n o n e OfTVco (1033, m \ 10M) Fatal cases are not included in table 1. However, in an analysis by Bridge (60), based upon data from death certificates supplied by the Registrar-General, and upon investigations of occupational history of deceased persons, carried out. by tbe Factory Department of the Home Office, 41/2 percent of the deaths attributed to silicosis in Eng land and Wales in 1!>U8 were assigned to the coal-mining industry. Since 1D29, when compensation for silicosis first, became payable to men employe in tbe coal-mining industry, the numlter of disablement cases among coal miners has increased rapidly until pulmonary dis ease in this industry has come to dominate the silicosis problem of Great. Britain (f>0). According to Stewart (6f), in districts of Lancashire County, where the industry of coal mining predominates f40 percent of the occupied males being engaged in mining) the male death rate from pulmonary tuberculosis is higher thnn the corresponding rate for the whole administrative county. Siaddon (62) stated that, during the 4 years 1025-28. ho had ex amined Ilie bodies of 20 coal minors; 1 hnd advanced silicosis and 7 bad slightly degrees of the condition (62). Since 1929, G3 examina tions were made, 27 of which showed definite and serious degrees of silicosis and 10 others slighter degrees. In a discussion of Prof. S. Lyle Cummins' paper, The Need for Dust-Prevention Measures in the Coal Industry, at a meeting of the South Wales Institute of Engineers, December 1031, the Colliery Guardian quoted IlaUlano (62) ns follows: ) ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 25 D r. J. 8. H aldane (Oxford) said the opinions be had already expressed were largely In agreem ent with those brought forw ard by Prof. Lyle Cummins. The m ain new point th at had emerged was that In a quite appreciable proportion of colliers who had never worked In stone, nor, in sotue cases, ever passed along stoneKlusted roads. X-ray appearances Indicative of scattered fibrosis and sim ilar to the appearances In undoubted silicosis could be found a fte r long service In an appreciable proportion of apparently healthy colliers, among whom no tendency to tubercular Infection could be discovered. But when they came to the Inter pretation of the fact there was a divergence of opinion. The m ortality among colliers from both phthisis nml bronchitis, as well ns from nlmost every other cause, had fallen steadily during the last 70 years, but so had the corresiKmdlng death rates among the general population, though not In the same ratio, till a fte r about 1000. In the Inst de<-ennlul returns published th ere w as still, how ever, a well-tnnrki'd excess of denths from bronchitis among colliers nbove about 55. H e could not find, however, nn.v Justification In th e official sta tistic s fo r D r. T ath am 's statem ent th at bronchitis had IiutcusihI since' about 1800. T h ere had been a steady decrease all the time. In the anthracite districts of South Wales, for Instance, the death rntes were unusually high ; anil this suggested that there m ight be som ething specially Irr'ta tln g In anth racite dust. The recent X-ray Investigations described by I'rof. Lyle Cummins seemed to confirm this and also showed th a t It wns not uncommon to find among elderly colliers of all sorts scattered fibrosis due to dust. lie would like to know wlmt the death rate from bronchitis was among the rest of the population la the anthracite area. Almost the otdy point In which he did not agree w ith Prof. Lyle Ciniunlns wns In extending the term "silicosis" to cover any form of fibrosis due to the Inhalation of dust. This seemed Inadvisable since there was no evidence thnt various forms of actual fibrosis were In fact due to Inhalation of free silica and not to other forms of dust, such ns coal dust or abate dust, which produced no tendency toward tubercular phthisis. It seemed preferaldp to distinguish these latter forms an "pneumoconiosis," since the word 'silicosis'' hnd come to have a very sinister significance. Tile 1930 report of the Chief Inspector of Workshops and Factories (S3) stated: By a recent arrangem ent the Factory-Inspection Service receives copies of nil death certificates In which death resulted from pulm onary dlsensc Involving flbrosln of the lungs. Of TOO such certificates received la lOfiO. 241 gave silicosis a s the cause of death, and In the great mnjorlt.v of cases It wns found th a t the previous ocetipatlon of the iiersons eoneerned wns one In which there wns recognized exposure to si Ilea dust. The industries furnishing tho greatest number of such cases were the pottery trade, ,r>2; sandstone, 49 ; coal mining, 39; sandblasting, 10; tin mining, 10; and other industries, 90. The report also said that recent investigations of the effects of exposure to asbestos dust had resulted in the adoption of measures to control dust in the textile branch of the asbestos industry. Data regarding 20 fatal cases of asbestosis without tuberculosis show a serious hazard in continued exposure to '-avy concentrations of asbestos dust. Tho frequency of silicosis in English porcelain plants wns referred to in 1920 ny Sutherland and Bryson, quoted by Bruce (3G), who ex amined 508 porcelain workers, 250 with roentgen ray. Silicosis wns determined among 87 workers employed in the slip and molding departments nVid in tho kiln house. Middleton reported, quoted by Bruce (36), in 1930 on 35 porcelain workers whose death was referred to silicosis. In 17 enses tho occupa tional disenso was complicated by tuberculosis. Three of tho deceased had an exposure timo of 20 to 29 years; 7, 30 to 39 years; 18, 40 to 49 years; and 7 had an exposure timo of more than 50 years. > 26 REVIEW OF LITERATURE ON DUSTS Iii 1931 Wood and Gloyne (6>i) were prompted by the recent dis covery that asbestos workers nre often the victims of occupational disease to determine whether pulmonary asbestosis also paves the way for a tuberculous invasion of the lunes or aggravates an existing infection. They studied 57 cases of pulmonary asbestosis, including 18 males and 39 females, 8 of whom were young girls from 18 to 21 years old; 12 of the 57 cases showed evidence of pulmonary tubercu losis, 4 of the 12 died, nnd on post, mortem examination evidence of obsolescent tuberculosis was found in 2 and of active tuberculosis in 2. Meriwether, quoted by Gloyne (66), found 4 nctive cases of tubercu losis and 33 inactive on e.xnminntion of 374 asbestos operatives while at work. According to Sparks (60), 2,000 workers in England are exposed to asbestos dust. An inquiry by Sutherland nnd Bryson (67) on the occurrence of silicosis among sandstone workers in England since February 1, 1929, under the Workmen's Compensation Act of 1925, disclosed that one of every four men at work appeared to have "mason's disease." As only men at work were examined, cases as far advanced as third stage ana many in second stage, not being at work, were not included in the survey. The outstanding feature of Ferguson's (68) investigation on the occurrence of silicosis among snndstone workers in Scotland and the North of England was tlie high degree of pulmonary morbidity exist ing throughout the industry. O f 1,000 working people examined, 433 showed clinical evidence of pulmonnry fibrosis. Radiological exami nation of all the workers snowing clinical evidence of fibrosis was impracticable but. doubtless would have disclosed other cases of sili cosis; most of the cases X-rnyed by Ferguson were those thnt showed the severest fibrosis and those that gnve the most renson for suspecting tlie presence of silicosis. One hundred nnd seventy-three of these workers showing clinical evidence of pulmonary fibrosis were X-rnyed; 97 showed first-stngc and 12 second-stage silicosis (advanced noaulcs coalescent). The report of the Chief Inspector of Workshops and Factories in Great Bntnin for 1932 (69) considered particularly 42 deaths from asbestosis or asbestosis with tuberculosis and 281 deaths from silicosis or silicosis with tuberculosis distributed nmong the industries ns fol lows: Pottery, 147; snndstone, (50; grinding materials, 30; sandblast ing. 23; scouring powder, 5; miscellaneous, 16. Under Parliamentary Intelligence, the Colliery Guardian (00) on August 4, 1933, published the following: In tlie Ilouso of Commons on Friday, on the motion for the sum m er adjourn ment, Mr. It. Dnvles Introduced a discussion on the annual rejiort of the Chief lns|ieetor of Factories, In the course of which Mr. T inker raised a iiiiiiiImt of quesii/.na r ,lsllhx In Industrial diseases nnd the solvency of employers, ns a remedy for which lie demanded n system of compulsory Inaurance. Mr. R. T. Evans bur. (tested that the hronehlal dlseaaes isirtlcularly affecting minera should tie placed In a separate category and dealt with hy the Mines D epartm ent under a new order. Mr. H. Williams complained th a t scores of men had died from alllcosls In South Wales, whose dependents had not received a farthing: of compensation nnd th at there were also scores who were dying but were not receiving comiicnsatlon after having worked for years In h ard ground because the rock did not contain a certain amount of silica. He also urged th a t anthrncoals should be schc . ilod as sn Industrial disease. ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 27 On February 10, 1904, the Colliery Guardian (fit) published ft statement from the Home Ollice that, since June 1. 1901. when the coal mining industry first came within the scope of the general medical board under the silicosis-compensation scheme,402 men in the industry had lieen certified by the board ns disabled or having died from silicosis or from silicosis accompanied by tuberculosis and that 085 of these cases occurred in the South Wales coal field. Earlier comparable figures were not available. On March Hi. 1904, the Iron and Coal Trades Review (62) quoted the following statement by 1'rof. J. S. Haldane from the British Medical Journnl: of Mllrosts in the s4no norm ntly Accepted end nenrly nltvnya In denth from phtllN. nnd If there wen* Actually n large num ber of cases of real silicosis In this sense among South W ales collier**, th eir p h thisis denth ra te would In* rnnshlernhly lncresHl nbov* the norm al figure. T here seems to le in wmml rensn for tsdieving that many more cases of real silicosis xvur am ong South W ales colliers than niuoiig other colliers, nnd l think the w idespread alarm pro<luci*t| In the South Wales colliery district by tlie num erous certified canon silicosis hns no suhstantlai basis so fa r ah silicosis Is concerned. However, Harper (66), a radiologist practicing in the South Wales coal field, in a letter to the British Medical Journal published in May 19.'54, said that, when the full facts were known, there was little mystery in the many cases of silicosis in that part of South Wales. Deductions are made from the pay of the coal mind's at the colliery offices in behalf of the medical men in the district; the workmen can therefore have roentgenological examinations if the family doctor is doubtful of their condition, and silicosis at present is the fashionable disease in the area. H arper (66) believed that more colliery workmen bad been X-rayed in this area (linn in any other part of the coal field; hence, more eases of silicosis had lieen found than in other areas where no such examina tions were made. This course partly explains why there were more known eases here. In fact, Harper said, there were more eases of silicosis than had lieen oil her examined or passed by the board because some refused to he examined, preferring to continue at work regard less of 11io cost to their health rather than lie retired by compulsion with partial eompensation of nbout i`l a week to meet the necessities of life and no further hope of employment. Kettle (12) said that nearly all the specimens sent to the board from this nrea were those of infective silicosis, and the infecting organism was most commonly the tubercle bacillus (66). Harper considered this statement much more reliable tlmn any returns of (lie Registrar General. Therefore tliero would seem to he no difference between the silicosis in South Wales and the commonly accepted type, and he could find no roentgenological difference liotweon cases of silicosis in South Wales nnd cases he had soon in tlio lioljrjnn HoMc In March 19.'t(i, the Chief Medical Officer of the Silicosis Medical Hoard (50) informed the committee that (he claims for compensation made by coal miners in South Wales were increasing in number. The total claims in 19:111. 19114, nnd I9.'I5 were 2:$4, IIIPi, and 1198, respect ively. Cases and incidence of certified silicosis among coal miners under ground in various parts of the British coni Helds during tho period 1SiltI--117 are listed (50) in table 2. 28 REVIEW OF LITERATURE ON DUSTS T aim.ic 2 OoalfleM 0) Total number o? new CMN 1 (J) Arenurenum her of men employed undentround Arenure an nual incidentrata per 1.000 employ! underground * (3) (4) A othm rtte mine# of ftouth Weir*................................................. 749 non ft. 33 Dim of Booth W*|r*.......................................... 60ft 4.351 .99 Cn*l min* In remainder of (I real Britain *............................... 300 507,758 .0ft i Tolu) num b* of new o w ? of cm! miner* m dlfled (under the rarlou* Industries (silicosis) schemes, 1911 tn d 1934) durtn* the period June 1911 to December 1917, to be disabled (totally or partly) or to h a re died from fllcnefe. i ATerace number of men employed underground in December of each year from 1931 to 1937. Cotonm (3) divided by column (3) and m ultiplied b y --j-j-* All nonantbradte except (or a few typical an th ra c ite mines In Scotland. Botraci: Mine* DejwMtment (1931-37, and unpublished records). It will bo soon that in 10.11-37 the absolute number of new cases from South 'Wales ns n whole wns more than six times that from the remainder of (rent Britain and that the lnnnlier of cases from the anthracite mines of South Wales was greater than from its nonanthracito mines. When these (inures are related to their respective populations, to gi vo comparative incidence rates, the geographical dif ferences are even more striking. 'I'he incident rate of certified silicosis in the anthracite mines is more (linn five times that in the other mines of South Wales nnd nearly KM) times the rate for Great Britain other than South Wales. For 1940 the total number of new ensos was ns follows: South Wales anthracite mines, `(>7; South Wales nonanthracite mines, 170; remain der of Great Britain, 41. For the South Wales sulidivisions the new cases were thus nlmut. twice the annual average for 11)31-.17, whereas for the remainder of Great Britain they wore approximately the same (M ). According to Fisher (04), for the .1years preceding 194.1 there wore 1,000 cases of dust disease annually in South Wales alone. In 1944, the first full year in which "pneumoconiosis, including the condition known ns dust, reticulation" wns certifiable for compensation, the fig ures increased enormously. In 194.9, in South Wnles, 7,37(1 coal miners applied for submission to the medical lioard and for certification ; 9,074 of these were certified ; 913 were certified ns totally disnhled, nnd 4,901 were suspended as partly disabled. In 1940 R.ROO applications were iweiveil, 3,07R of which were certified. Of tlie 3,07H certified, 327 were totally disabled nnd 3,391 were suspended as partly disabled. Fishei (0'i) stated that, although the incideiico of pneumoconiosis is much less in the country outside of South Wnles, it is nevertheless sig nificant. In 1949j 999enscs wcrecertitied, nnd up to June 30,1940, there were 310 cases. There were 13 pneumoconiosis cases certified in Not tinghamshire and 21 in Derbyshire during the period 19.32-49, 0.9 percent of which were certified during the 3 yenrs 1943-49. The numlier of applicants for examination decreased in 1947 com pared with 1940 (06). ) ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 29 From January to March 1946, 2,312 applications were received and 2,424 cases considered by the medical board, 1,230 of which were cer tified to be suffering from pneumoconiosis. The corresponding figures for 1947 were l,f>20 applications received, 2,545 cases considered by the medical board, and 840 certified. According to a statement made in April 1947 (66) by the Minister of Fuel and Power, during the pre ceding 2 years 10,500 coal miners had been certified by the Silicosis Medical Board as suffering from pneumoconiosis and suspended from work in the indust In 1720 Josiali 4 wood incorporated calcited flint with his earth enware body. In 1865 Elisa Meteyard ( / / ) wrote, in her biography of Wedgwood, that at the beginning the flint was kept in cellars nnd used parsi moniously. A history of the occurence of dust diseases in the North Stafford shire pottery industry in England was published in the Royal Sanitary Institute in October 1946 (66). According to this article, at first the calcined flints were broken by hand by men working secretly in cellars. Before World W ar II the pottery industry in North Staffordshire employed 67,000 persons, 55 percent of whom were women and girls, lie fore the industrial revolution cnrried the stigma of the exploitation of child labor, in 1863 evidence was given before a commission to the effect that each successive generation of potters became more dwarfed and less robust than the preceding one. In 1726 Thomas Henson was grunted a pntent for wet-grinding of flints (66). In his application for the patent, Henson stilted that no person could survive dry grinding for more than 2 years. Although improvement took place slowly, dry grinding had not ceased by 1936. In 1928 the Various Industries (Silicosis) Scheme ehtitled pottery workers to compensation for totnl disability or death. During the period 1931-41, 2,000 jiersons were given initial exam ination, 10 percent of whom were rejected on medical grounds. In the same period 4,000 workers were examined periodically while at work, and 490 were found to he suffering from silicosis or silicosis accompanied by tuberculosis. During the period 1929-44 the Depart ment of the Cliief Inspector of Factories recorded an nvernge of 47 deaths annually from these diseases--402 cases of silicosis anil 347 cases of silicosis with tuberculosis for the 16-year period. Great improvement has followed in recent years by tile substitution of alumina for flint nnd other siliceous materials. OKBMANY Industrial pathology in Gernmnv was developed at the b e g in n in g of the nineteenth century, simultaneously with the upward trend of Germnn industry (7). In 1781 Tissot (6i) graphically illustrated the health hazards encountered by stonemasons; in one place where the people formerly had been engaged in felling trees nnd in carving they were the "hnndsomest, strongest, nnd healthiest of persons" but for 25 yenrs--since the inhabitants had turned to stonecutting--there had been in that region the most lingering diseases. In 1804 and 1812 8<n;i6--so---- a t- ' 30 RF.VIEW OF LITERATURE ON DUSTS Goetzinger (08), in describing the mountainous part of Saxony, said that the fine dust and drink brought the stonecutter to an early death. Scliiimitimi (~) stilted in 1929 that only a few works had been pub lished on the harmful effects of iron nnd steel dust to which tho metal polisher was exposed, in spite of the fact that the works of Paracelsus, Ramazzini, and others were known in Germany, Rmnazzini's work being the sole textlmok in the field of occupntionnl disease used in Germnny up to the middle of the nineteenth century. In contrast to the English reports on the health picture of the Sheffield polishers, Hauer (GO) in 1832 reported conditions among German polishers ns not unfavorable to health. Nnsse (70) was the first to report polishers' disease; he wrote that grinding workers lusted only 12 years and recommended respiratory protection for them. The first known Ger man publication on the hnrmful effects of dust on polishers was issued by Pappenheim (71) in 1860. In 1866 Zenker (7) identified iron oxide in a lung and termed the disease caused thereby "siderosis." He designated the disenses of the lungs cnused by dust ns "pneumo coniosis.'' In a l>ook on tho cnre of health nnd medical statistics in Prnssinn mines, published in 1881, Sehlockow (73) stated that, of 942 miners exnmmed by Seltmnnn, 37.7 percent had emphysema of the lungs. Only 5 roentgenologically normal pictures were disclosed among 25 sandblasters examined by I.<ochtkeinper (74) in 1930; the remain ing 20 (80 percent) revealed vnrious stages of silicosis. In 1937 Bergerhoff (70) reported finding lung tuberculosis in 24 of 175 sand blasters examined clinically and roentgenologically. Thiele (70) found that 28 percent of the porcelain workers examined by him were affected by pneumoconiosis; Ilolzmnnn nnd Harms determined roentgenologicnlly the presence of pneumoconiosis in 75.6 percent of 41 selected porcelain workers; nnd Koelsch found 58 percent of 19 work ers affected. As given by Koelsch (77), the tulierculosis mortality rate for porcelain workers in various Bavnrian districts was 23.7 to 96.2, whereas that, for tho general population was 24 to 29. Vollrath found a tuberculosis mortality rate, of 24 nmong porcelain workers compared with 10 for the general local population in Rudolstadt nnd 57 compared with 20 in Meiningen. However, Bhme stated that only about half of the workers in porcelain factories are exposed to a severe dust hazard. Hoflmuer-h'latzeck (77) found a tulierrulosis mortality rate of 26.5 in the porcelain industrial town of Selb; 61 per cent of (hose living of (tdierciilosis had silicosis also. If this 61 per cent is subtracted, the mortality rate is scarcely higher than the aver age of 9 for the Empire; therefore, IIoflmuer-Elatzeck attributed the higher mortality entirely to injury through silieosis. Blune (78) determined pneumoconiosis in 28 percent of 184 coal cutters who had worked more than 10.years underground and in 66 percent of hard- rock miners: in another investigation he determined by X-ray exami nation that 36.2 percent of GO hard-rock miners had pneumoconiosis and by clinical examination. 17.3 |x>rcent. Komissnruk (79) examined clinically and roentgenologirnlly 40 foundry workers who had worked in dusty industries for more than 10 years; 4 definitely hnd pneu moconiosis, 5 were doubt ful, and 3 were borderline cases. In 23 cases ) ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 31 the X-ray revealed old inactive pulmonary tuberculosis, but the sputum contained no tubercle bacilli. In 1932 Lochtkemper and Teleky (80) published the results of nn extensive study on dust which covered working conditions and health of workers in many different dusty trades. The number of workers examined in each group, however, was usually too small for definite conclusions. Examination of 22 women employed in a scouringpowder factory in 1930 revealed that nil but 3 were affected by silicosis in varying degree, 6 being in stage 3. Examination of 7 workers in a sand and cement plant disclosed 1 case of silicosis in the first, stage and 2 in the third; tlie others showed no indication of silicosis or onlv slight pneumoconiosis, which the authors classified ns "silicosis 0-1. Inquiry among workers and physicians of the region revenled that 4 had died and 2 still had tuberculosis. Six of seven shell-limestone cut ters examined were diagnosed ns having pneumoconiosis 0-1 and 1 silicosis 0-1. Of 18 grnywncke workers examined, 3 were diagnosed ns negative, 4 ns having silicosis 0--I, 4 silicosis I, 3 silicosis II, 1 silicosis I--II, 1 silicosis II I , and 2 silicosis I I with tuberculosis. From nn examination of the statistics of a large sick benefit association Koelsch and Kaestle {SI) found the illness frequency, especially for tuberculosis and diseases of the respiratory organs, less foi the quarry and shell-limestone workers tlinn for the other members of the associa tion, but the mortality rates apparently were grenter for stoneworkers (0.35 percent) than for the others (0.21 percent). These investigators examined 82 persons who had worked in shell limestone only; 14 had more or less definite signs of dust lung, but it differed in appearance from the silicosis of the sandstone worker. They concluded from these examinations that under certain conditions limestone nlso can cnusc changes in the lungs within the meaning of dust lung if it can have a correspondingly long action. Dust lung wns more frequent and more pronounced among those who had worked in limestone and snndstone, the more so the closer the work in sandstone hnd followed upon that, in shell limestone. According to Landau (82), the cleaning of inetnllic castings pre sents great health hazards to the men engaged in the work. Of those examined, 09 jiercent hnd pneumoconiosis and 8 percent tuberculosis. Work with steel seemed to be much more dangerous than with cast iron, probably because compressed-air tools were used in cleaning tho steel castings, which wero cast in a mold of snnd very rich in silica. From 1929 to 1934, in the Ruhr, 332 workers died of silicosis; this figuro wns reported (83) not from the total number of workers but only from thoso working in rock, nbout 10,000 to 12,000. In 1937 Holmnnn (S/t ) published a report of extensive investigations of a lnrgo number of workers who ban worked for many years with tho purest carbon dust in the form of enrbon black, petroleum coke, tar coke, and artificial graphite without any admixture of rock dust, especially quartz. Among these workers he found a large number of dust lungs of stages I to III. According to Hollman (S4) tho dust lungs of persons exposed only to pure carbon dust could not be differentiated roentgenologically from silicosis produced by snndblnsting. O f 90 persons with severe pure carbon-dust exposure, 23 wero diagnosed as being in stage I, 10 32 REVIEW o r LITERATURE ON DUST8 in stage II, and 3 in stage H I. Of 202 workers exposed to pure carbon dust with slight admixture of carborundum, 13 had stage I dust lung. In 1939 Maaszcn nnd Biiftner (85) reported that severe silicosis as an occupational disease cost the people infinite values in health and money--costing more than nil other occupational diseases together. In 1937 these authors examined 508 workers in the largest ceramicand silica-brick factory in Germany. This factory, which hnd been in existence for several decades, was located in a small village where the employees had their homes. There was therefore little turn-over, and most of the workers hnd been employed for years. I t was possible to study all stages of silicosis nnd get a fundamental picture of the dust hazard in the silica-brick industry. Of the 508 employees examined, only 380 were actually exposed to a dust hazard; a total of 17.31 percent of the 508 were affected by various stages of silicosis, while the percentage for the 380 actually exposed to a dust hazard wns 23.15. A rn ica BOOTH AFRICA Mining wns begun in South Africn on the Witwatersrand in 1880 (85). At first the workings were shallow and in the oxidized or " freemilling" zone where the rock was relatively soft, friable, and damp. By 1892 extensi vo deep-level properties had Been operated, and drilling by machines was introduced. As long ns the mines were working in the free-milling zone very little dust was produced, as the mines were shallow and probably fnirlv well ventilated, and it*is unlikely that the men were greatly affected by the dust. Very few people in South Africa suspected that mine dust wns in any way injurious to health until theGovernment. mining engineer of the Transvaal Mines i depart ment in a report in 1902 mentioned "miners' phthisis" as a disense "which seems to be peculiar to men employed in rock-drill work." This report, which covered the C months ended December 1901, stated that, of 1,377 innehinemen employed before 1899, 225 were known to have died between October 1899 and January 1902, nn average nnnunl death rate of 73 per 1,000. These facts arrested the attention of tho Government, the mining community, and the general public, nnd in December 1902 the first. (Trnnsvaal) Miners' Phthisis Commission was appointed "to intjniro into nnd report on the diseaso commonly known as miners' phthisis." A report, was issued in 1903. Tho commissioners attempted to procure a medicnl examination of all working miners, but tho returns were incomplete partly because many of tho miners were reluctant to submit, themselves to examination. O f tho 1,201 miners examined, 15.4 percent were affected by miners' phthisis, and 7.3 percent were suspected. The Report of the Medical Commission issued in February 1912 wns the second lnndmark in the medicnl history of silicosis in South Africn. The net uni examinations were more com plete than in 1903 hut. did not cover all the underground employees. A general clinical examination wns made of 3,130 working miners, supplemented by a special examination of 320 men, in which radiog raphy wns, for the first time, applied to examination of cases on a fairly extensive scale. The prevalence of the disease among the PHYSIOLOGICAL EFFECTS OF BREATHING DUST 33 working miners examined wns 26 percent, with an additional 5.5 per cent or doubtful cases. This figure is somewhat higher than that found in 1903 but probably reflects the result of a more extensive investigation. According to Irvine, Mavrogordato, and Pirow (87), 1916 was acardinal year in the history of silicosis on the Rand. It was marked by institution of the Miners* Phthisis Medical Bureau and publication of the General Report of the Miners' Phthisis Prevention Committee. The present-day system of detection and prevention of silicosis on the Rand dates from 1916. In all, 6,472 original compensation awards were made to miners for silicosis from 1912 to 1916. According to the Report Upon the Work of the Miners' Phthisis Medical Bureau (88) for the 3 years ended July 31, 1932, the average number of new cases of silicosis and tuberculosis with silicosis among the miners of the Witwntersrand wns over 8(H) annually luring the 4-year period 1912-16. The re]>ort also states that 895 cases of "prinmry-stage" silicosis were detected from 1917 to 1920; 728 cases of "antenrimnry stnge" from 1920 to 1923; 1,235 cases of "aoteprimary stngeAfrom 1923 to 1926; and 917 cases of "nnteprimnry stage*' from 1926 to 1929. In 1930-31 the number of new cases, for the first time in 8 yenrs, fell below the standard level of 251 cases, the annual average for 1920-23. The following statement by Hildick-Smith (89) summarized briefly the status of miners' phthisis in South Agrica in 1934. After minting figures showing the percentage production rate of silicosis tor the preceding 15 years he said: From a atml.v of these flauren I personally am Inclined to think tlint the tim e Is not fnr dtRtnnt when the Incidence of sllli*osls will have cease! to Ik n m utter of sorlotis concern to the Industry. Tills, I think will he iiecnmpllshed hv the elim ination. In whole or in p a rt, of the dangerous dust from the underground nlr. Old hnhlts of thought w ere inclined t<> persist In regnrd ft) the production of silicosis In the mines. T he Rc|>ort Upon th e Work of the Miners1 Phthisis Medical Rurcnei showed the rtinximum |H*r<*ent#W production rate for willronU had decreased from 14 f> percent a fte r 14 yenrs* service In the |K*riod 1618-21 to 4.5 percent a fte r 17 jours* service In UW1-.12. The graduation rntes for all miners, Including men working underground before the Inception of the Phthisis Rurenu In 1016, show th at the present inuxiniuiu production rat Im under 4 iorcent a fte r 20 years' service. Of the 157 m iners notified Inst year that they contracted silicosis more th an one-half began w ork In 1916-17, l In 1P22-21* and 1 In the following year. Since 192.1 th ere have l*oen no oases of contracted silicosis-- In other words, no new Hand m iner lias been found suffering from silicosis In the last 10 years. These results a re <*onflrmed by the fact th a t less than 50 percent of the patients at the Springkell Siinltorlum are of the m iner class W ith re g a rd to tlio em p lo y m en t o f silicotics, H ild ic k -S m ith said t l m t i n 1934, 978 w e r e e m p l o y e d b y t h e m i n e s , a n i n c r e a s e o f a b o u t 110 s i n c e N o v p m l> e r 15, 1933. The nverngepumber of miners examined annually during the j>oriod 1938-41 by the Miners' Phthisis Medicnl Bureau of the Union of South Africa (90) was 30,635, the average annual number of new cases of silicosis was 260, and the production rate per thousand was 8.50. F o r the period 1941-44, the average annual number of miners examined was 27,558, the nvomge nnmial number of new cases of silicosis for the same period wns 261, and the average annual incidence rate per thousand was 9.47 (90). > 34 REVIEW OF LITERATURE ON DUSTS During the triennial period 19.18-41 the annual average number of "new Rnnd miners" with 19 to 24 years service was 562, and they produced during that period 71 new cases; during 1941-44 the annual average of new Rand miners with 19 to 24 years service was 787, and they produced 99 new cases. T h e num ber of new cases of silicosis a m o n g new R a n d m iners has now becom e significant and m ust become m ore so as la rg e r num b ers o f them pass into the long service periods. The position as regards the general incidence of silicosis remains on the whole satisfactory, but the gradual improvement culminating in the low rates for the triennial period^ 1935-38 seems to have been checked in 1938, since when a slight rise in the rates has become apparent. WEST ArRIOA An investigation was mnde in 1940 (.9/) of the coal mines of the Tarkwa area of West Africa. Of 500 men examined^ 21 had definite silicosis, 10 without and 11 with accompanying active tuberculosis. As the incidence of pulmonary tuberculosis was higher than th at of silicosis, the authors regard tuberculosis ns the grenter menace to the health of the mine employees. At that time, nothing was being done for native minors who were suffering from cither of these diseases. In 1946 the same authors (92) reported a series of 1.002 consecutive examinations of underground employees, including the 560 referred to alove. The mines concerned are in the banket deposits of Tarkwa, the Akropong-Konongo area, the Prestea coal field, and the Ashanti Imnhot area. Of the total of 1,002 miners examined, 155 had abnormal incmise in strintion. 40 hnd definite silicosis, 19 lmd silicosis with tuberculosis, and 115 had tuberculosis alone. UNITEI STATES Dnta on the general incidence of silicosis in the United States are not available. Sucli dnta are difficult to obtain in the existing state of American vital statistics; exact knowledge of the population at risk in a given occupation, classified by age, is obtainanle only with greut difficulty and by special and intensive research m ) . In an aim lysis of statistical dutn of this kind, Grconburg ( H ) called atten tion to the importance of considering groups that are fairly compa nil do, so that the effect of industriftlluizards will not be compli cated by the influence of social and economic factors of a more general nature. He stated, for example, that in Hoffman's studies, published in 1918, ratios presented for the various dusty trades wore based on the industrial experience of the Prudential Insurance Co. but th at the ratio used ns a norm for comparison of males in the registra tion area wns obtained from dnta of the United States Census Bureau. On this basis, almost all the industries that he tabulated showed a surprisingly high tulwrculosis ratio, including many trndo designa tions of workers, such ns "iron and steel workers," who could hardly lie. considered ns generally exposed to a serious dust linznrd; his ab normally high ratios, therefore, probnhly were due to the general social and economic conditions of the wage earner's lifo Rnd to the PHYSIOLOGICAL EFFECTS OF BREATHING DUST 35 fact that the group was an industrial one. I t seemed evident to Greenburg (M) that a comparison between the Prudential figures for a given dusty trade and the Census figures for all occupied males, which gave Prudential rntios 25 to 50 percent higher for tuberculosis than those for the registration area, was not a fair one and that the conclusion reached through such a comparison was unwarranted. S everal special investigations, carried out in certnin in d u stries in the U nited S tates that have attracted attention because of th e h ig h d e a t h r a t e f r o m t u b e r c u lo s i s (93), t in d e s c rib e d b elo w . M IN IN G The first investigation of silicosis in the mining industry in the United States was made in 1914-15 by the Federal Bureau of Mines in cooperation with the United States Public Health Service in the Joplin (Mo.) mining district UU). Of 911 men examined, 04 showed plain and definite evidence of pulmonary disease, 3 were suffering from nonpulmonary disease, and 20 were seemingly well. To gain a more accurate idea of the prevalence of consumption among the miners of the Joplin district it was decided to examine a larger nmnbt r. and from May 15 to December 31. 1915, 720 miners were examined: 45.7 iiercent. had silicosis and tuberculosis and 5.3 percent had tubercu losis (.9.7). A later report (1927) of this same investigation by Lanza and Childs (96) included tl u* results of the first detaile l X-ray studies of silicosis made in the United States. Investigations of mining conditions by Harrington and Lanza (.97) in Butte, Mont., in 1921 revealed that 42.4 percent of 1,018 miners examined showed definite signs of lung damage due to dust. An ex amination in 1921 of 303 gold miners in Nevada (.9,S') disclosed that 81 percent had silicosis. In 1923 the mining companies of the Tri-State district (comprising1 the zinc- and lead-mining areas of southwestern Missouri, soiit heastern Kansas, and northeastern Oklahoma) asked the Federal Bureau of Mines to determine whether measures in use were adequate to prevent silicosis and, if not, to recommend improvements. The 1923 invest igntion (.9,9) included the examination of 309 miners, 101 of whom were found to be negative, 114 doubtful, and 94 positive cases of silicosis. Of the positive groups, 52 were in the first stnge, 22 in the second stage, and 20 in the third stage of silicosis. I' rotn July 1, 1927, to June 30. 1932, the Metropolitan Life Insur ance Co., tho Tri-State Zinc & Lend Ore Producers Association, and the Federal Bureau of Mines operated a coo|H<rafive clinic at I'icher, Okla. (100), to demonstrate to industry a workable method for diag nosing silu.oSis, to educate workers in preventive measures, nnd to serve as a model to industries presenting n dust hazard. Of 27.553 individuals examined during this period, 5,300 had silicosis, 742 sili cosis plus tuberculosis, nnd 320 uncomplicated tuberculosis. According to the United States Public Ilenlth Service (101), the percentage of anthracite miners nnd their hel]>ers showing signs of pneumoconiosis increased from 2 percent among those with less than 5 years' service to 10 percent nmong thoso with more than 15 years' service (for persons under 45 years of age). Of 95 X-rays of bitumi- ) ) 36 REVIEW OF LITERATURE ON DUSTS nous-con] miners 40 ^42 percent) showed generalized fibrosis, chiefly linesr in chnrncter. 1 lie percentage of deaths caused by all respiratory diseases among anthracite miners in Pennsylvania was definitely higher than that of other adult males in the general population--57.6 percent. in contrast with 37.2 percent among other men of the same nge in the Wilkes-Barre coal field (/OS). The following summary (JOS, 104) by the United States Public Health Service indicates the prevalence of dust diseases in anthracite mini: 1. A study of Iiealth conditions, Including the physical exam ination of 2,711 men (aland IHI |iem*nt of the nninher on the |>ny roll) was made in three repre sentative anthracltc-cnnl mines In I'ennsylranln. 2. The mt'n exim lned w ere divided Into occupational groups, lnrgely In accord ance with the proportion of free allien found In the dust to which they were expoed. M, No caaea of anthrncoalllcoHla (m iners' asthm a) were found In a control grmi|i composed of hard-coal-m ining employees whose dost exposure averaged less limn 5 million particles |n*r square foot of nlr. 4. The prevalence of iinlhracosillcosla among the entire group of employees waa found to he nhont 23 percent. 5. Among all except rm-kcvoi kora, Icrs than 2 percent of the men developed antliracnslMcnnln, when the duratio n of employment was less than 15 years, regardless of the amount of dust In the air. (I. Aruing men excised 15 to 24 y ears to d u st containing less than 5 percent free allien, 1 1 IM-reeiit of those wlm hud worked where the average ilua! count was 100 to IDS nillilo.i particles i>er cuhlc foot, 20 percent of those exposed to 200 to 209 mllll"ii particles, nml R8 |>ercent of the men who had worked for this period In mere Ilian ftOO million part Idea |>er cubic foot developed niithmcoslllcosls. 7. Among men employed for m ore Ilian 2T>years In dust containing leas th an 6 perm it free slllcn, the pro|air(lon of persona found with nnthrncoslllcosln under different concentrations of dtist wns na follow s: 5 to Ik) million particles, 7 per cent : 100 to 1!HI million particles, 54 tie rc c a t; 2t8t lo tit) in IIIIon |>nrtlclcs, 71 pere c n l: .`It) or more mlIIloti particles |>er enhle fiwit, 81) [>ori-ent. 8. With the exi-cptlon of m iners, th eir liel|>ers, ami roekworkers, nlHiat 25 pereent of nil of Ihe men employed underground developed niilhriicosllleosls a fte r a working (sulod of more Ilian 25 years. This group wns exposed to dust having a qu arts content of nluuit 13 jien'ent. II. The prevalence of iiuthrncoMlIlcoaln among roekworkers who had been ex|*o*ed to dust, of which about 35 i>ercent wns free stllen, vnrled from 10 percent among those who liiid workeil In coticentrntlons of less than 200 million particles per eiililr fisit for less than 15 y ears to irj iiereent among llmse roekworkers who hurt hcen employeil for more lim n 25 years In d u st concent rut Ions exceeding 300 million particles per cuhlc foot. 10. Age per se apt reared to play a m inor n d e la the development of nnthrnro- sl lie. ids. 11. Analysis of the d a ta for the purpose of determ ining snfo lim its of dust ex posure Indicated th a t employm ent In an atm osphere containing less than 50 million dust particles per cuhlc foot would produce a negligible num ber >f cases of nnthrncnslltivisls when the q u arts content of the dust wns less than R percent. In (lie gangways w here the slllcn content of the dost was nlsmt 13 lereent a safe lim it apiienrod to lie 10 to in million particles |ier cuhlc foot. Tlie lim it of tolera tion far roekworkers w as set tentatively at 5 to 10 ni'!U>>n dust particle per cubic foot of nlr. 12. riilm onary Infection Incron sod w ith length of service more rapidly among Ihe men In Ihe hnutngewnys than in the control group ami much more rapidly among the regular miners. The highest rates of imlmonnry Infection, however, were found among Ihe rnckworkom of more than 15 yenra' service. 13. The prevalence of pulm nnnry tuberculosis among the hard-conl-mlnlng em ployees a t ages liolow 3R was slightly less than th a t found through studies of tubereulosla among mnlo ad u lts In the general pnpulntlon of the country. In the a go group 35 to -44, however, the prevalence o f tuberculosis was a bout tw ice, a t ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 37 ages 45 to 54 about 5 times, and for th e ages above 55 it was about 10 tim es the ra te found In the general population. 14. The highest prevalence of clinicnt tuberculosis occurred among the rockworkers. A fter 20 years' service .`17 percent of these workers presented evidence o: pulmonary tuberculosis 15. Pulmonary infection (tutw rculosls and nontuberculosis) was found among 58 ercent of the men having early anthracoslllcosls and in 92 percent of those in the more advanced stages. 10. Clinical tuberculosis was dlngnosed in 15 percent of those w ith early antlirnco8llicosi* and in 45 percent of those In the more advanced stages. 17. In the control group 1.7 percent w ere found w ith m oderate or marked physical impairment causing decrease! capacity for work ns eompnied with 9.ft percent among the regular m iners and w ith 12.0 ercent among the rockworkers. W ith the exception of the rockworkers, no group showinl nuHlernie or marked Impairment In excess of that found among the controls when the period of employment was less than 20 years. However, an excess In th e prevalence of slight impairment was found among the regular m iners and among others In group A who had worked from 10 to 20 years in atm ospheres containing more than 1(M) million dut articles or cnhlc foot. 18. In a group of 155 completely disabled form er anth racite w orkers which did not Include any known oases of tuberculosis 10 percent proved positive for pulmonary tntierculnsK 19 M ortality front respiratory dlscj <es w as found to be much g reater among an thracite workers than In the general adult m ale population of the country. The data indicated that underground w ork In the absence of dust did not pre dispose to fatal attacks of respiratory disease. 20. The term *'jinihrncosiiir<osi't(* Is used in this report ns a descriptive title for the form of pneumoconiosis romnionlj called m iners' asthma. 21. The correlations between exposure to dust and the evidence of constitu tional changes left little doubt as to the etiological significance of the dust In the n lr breathed, hike correlation* w ere found tetween the silica exposure and the extent of pulmonary changes. Kibhcy (10ft) reported in 1931 that virtually 100 percent of the miners who worked in the several coal mines operated hy his company in Alabama had nnthracosis nnd that they had a higher mortality rate from tuberculosis than any other wnfre-earninp proup. From a study of industrial morbidity statistics for the period 1924-27 Rloondield ( /M) found t lint 38 cases of pneumonia had devel oped tiinonp the 1,037 hituminous-conl miners employed during tho same period in the mines operated in connection with an iron and steel plant. Occupational analysis disclosed that 33 of the 38 pneumonia cases were a^ociated with only 2 of the 09 different occupations in the mines--pick mining and loading coni. The pneumonia rate per 1,000 for mil uns and loaders was HI. whereas tho rnte for nil other mine workers was only H.fi per 1,000. In an investigation carried out in IMS mul 19.`19 in Utah, tho United Stales I'uhlic Health Service (107) found tho incidence of nnthrncosilicosis u n io n ) '10 underground bituminous-coal miners to he 4.0 per cent ; nmung 727 nonferrotts metnl miners, 9.1 percent had silicosis; and among ,.'191 smelter workers, 2.7 percent had tho disenso. I'ulmonfiry tuberculosis was found in 0.2 percent of the coal miners who had silicosis; in l.'Ui percent of the metnl miners who had silicosis; and in 10.2 percent of the smelter woi kers who hnd silicosis. 'I'llis is in contrast to the 2.1 percent, 1.0 percent, and 4.9 percent of the nonsilicotie workers in these respective groups. The incidence of tuber culosis among the workers with no silicosis in the coal nnd metal mines was nbout that of the general population, whereas tho incidence of 38 REVIEW OF LITERATURE ON DUSTS tuberculosis among the nonsilicotic smelter workers was about twice as high as among tne general population. Jones (108) discovered 80 cases of silicosis during 4 years of medicnl practice among coal miners in West Virginia. These cases were de termined by careful fluoroscopic and roentgcnographic study of the chest nnd routine snutum and blood analyses. These cases included only those in which exposure to dust had been in bituminous-coal mines alone. The nppnrent similarity of the risk in mining and the risk in the processes involved in excavating and tunneling, so far ns the silicosis hnznrd is concerned, led to an investigation of such processes in New York City by Smith nnd Fehnel in 1929 (OS'). O f the 208 drillers, blasters, nnd exenvators examined 42 percent snowed early and 15 per cent showed well-developed silicosis. Evidence of tuberculosis, in cluding both active and inactive cases, was found in 9 percent ot the totnl number. Although rock drilling where injurious amounts of d r cf are produced may require only a brief period on many contract jobs, io importance of dust-control menstires is indicated by the following statement in the Connecticut Health Ilulletin (109) : It muni he reineml>oro(l th a t drlllliiK la an occupation c n lllrs for experleecetl men and th a t the duration of exposure of the d rille rs Is not lim ited to any one Job but Is continued over n period of years as the d rille r (toes fro-n Job to Job. It Is nccordlncly fallacious to stnte th a t, because th e d rille r's ex|>osure In any one location Is of n brief duration, adequate protection need not tic p. ovlded Inasmuch ns It requires n considerable period of time for silicosis to develop. Ill 1942 P o r r o , P n t t o n , n n d H o b b s r e p o r t e d (110) 15 c a s e s w i t h 5 p o stm o rtem s o f pneum oconiosis in the tnlc in d u stry in N ew Y o rk State. T hey attributed disability or death directly to pneum oconiosis i n 13 c a s e s ; t h e p n e u m o c o n i o s i s w a s c o n t r i b u t o r y t o d e a t h i n o n e c a s e a n d incid ental to dentil in nnothor. T h e conclusion w as th a t p n eu m o coniosis causing disability and death occurs in tnlc w orkers, the dis a b lin g tissue c h a n g e s l>eing duo p rin c ip a lly to talc itself. Greenburg (111) reported in 1947 a study of the tremolite tnlc mining nnd milling industry in northern New York Stnte. In the initial roentgen-ray survey in 1940 advanced fibrosis was found in 32 of tho 221 men examined, a rate of 14.5 percent. In comparison of talc workers with enrpet workers, Grienburg found thnt fibrosis was present, in only 2.5 percent of nil carpet workers nml in 4.9 percent of those 50 years of ago or older; it was present in 51.5 percent of talc workers in this age group. The fibrosis found in this study wns of a fino, diffuse type, with a roentgeuograpbic appearance of granulation or nodulation in a hazy background. I t tended to lie disabling ntui wns frequently accom panied by dyspnen, cough, nml fat igue. Thero wns also some evidence thnt this fibrosis wns characterized by increased susceptibility to tuiierculosis, ns clinically significant tuberculosis was diagnosed by roentgen examination in 8 of 18 cases of tromolito-talc fibrosis where thero had been no other dust exposure. Annlysis b y the N e w Y o r k S t a t e D i v i s i o n of I n d u s t r i a l H y g i e n e o f si G x a sam rdne p r l e(1s 1f1r o) , m h two t a l owever c , m fo ines und showed 1 p o r c o n t or l e s s o f n m o u n ts of q u a r t z ranging free silica. from 12 to ) mm a PHYSIOLOGICAL EFFECTS OF BREATHING DUST 39 20 percent in mineral samples from two mines in the same area. Greenburg (111) stated that it was difficult to explain this marked difference in findings, except on the supposition that Gardner's samples included some of tlie quartz-bearing stratum overlying the talc deposit proper. GRINDING INDUSTRY According to Hoffman (4), the industrial insurance m ortality sta tistics of the Prudential Insurance Co. from 1897 to 1914 showed that 143 (40.9 nercent) of 305 deaths among Grinders were due to pul monary tuberculosis. In another group of 5,988 grinders, which in cluded cutlers, scissors grinders, anil ax, plow, and other steel grinders, but excluded foremen and superintendents, the actual mortality from all causes was 17 percent over the expected mortality; in other words, for every 100 deaths expected on the basis of normal experience there were 117 deaths in this group. In 1920 Winslow and (ireenburg (//$?) investigated the dust hazard in an ax factory. They quoted Drury's exhaustive statistical study on the incidence of tuberculosis among grinders and polishers as show ing that, from 19(H) to 1918, the death rate in a group including 90 polishers, 85 wet grinders, and about 25 dry grinders was 1,000 percent. Their investigation revealed dust conditions serious enough to cause such nil excessive death rate. To indicate the effect of silica ns a predisposing cause of tuberculosis Hiddell ( / /-j), in a paper published in 1920. quoted the following mortality table prepared by Drury for a Connecticut community (agricultural except for nil ax factory employing 800 men) : D e a th r a te fr o m tuhereuinM i* in a C o n n e c tio n ! c o m m u n it]/ Per 100,000 E ntire population of factory d istric t___________________________________ 200 S ta te ns a whole__________ . ______________________________________ 150 Enolnry p o p u l a t i o n ______________________________________________________ (150 Polishers and g rin d ers_________________________________________________ 1,050 In a review of pulmonnrv tuberculosisdevelo|>ed in a large grindiug- wheel plant, Clark (114) found thnt. from January 1, 1918, to Decem- l>er 31, 1939, there were 42 cases of active pulmotmry tuberculosis, 38 of whom were men and 4 women: 37 of the group were employed at factory work of some kind, while 5 did clerical work. O f the 42 workers who developed tuberculosis 20 were dead nt the time Clark prepared his report, 18 were living, and 4 could not be traced. Of the 18 living, 13 were working, 3 were nt home under enro of a physi cian, and 2 were in hospitals. The nverago numlier of employees d uring A cco the rdin 13-year g to K e spsel erirod(11w~n>s), 2,400. over 1 0 0 enses of silicosis w ere nlleged to have oiVuirred in the ab rasive-pow der in d u stry in one S ta te , in v o lv ing four com panies which pum ped sand by hydraulic pressure to a plant, w here it was w ashed, steam -dried, screened into vnrious sizes, a n d then p ulverized in closed tube m ills. S ix o f th e w o rk e rs h a d died ( l t d ) a n d b e e n a u t o p s i e d , a n d n i n n y o t h e r s w o r e r e p o r t e d t o lin v o d i e d , b u t the results of the autopsies were not known, C lark observed f o r 30 y e a r s e m p l o y e e s w h o h a d lie e n e x p o s e d t o t h e i n h n l n t i o n o f a r t i ficial abrasive d u sts in nm ounts very m uch g re a te r th a n in th e use o f mm m m m m m wm m m 40 REVIEW OF LITERATURE ON DU8TS g r i n d i n g wheels. Several studies supported by continuous observa tion, examinations, and X-rays failed to disclose any definite health hazard to healthy workers. As a further check, Clark (116) reviewed all those (90 in number) who hnd been exposed for 25 years or more; 87 of these were in pood health nnd working, and 9 were pensioned but in pood health. None of these men seemed to have been affected by their many years of exposure to the constituents of artificial-abrasive grinding wheel?,. To check the generally accepted beliefs concerning the harmfulness of exposure to artificial abrasive dusts, Clark (116) wrote to the phy sicians heading the medicnl departments of 22 companies, which were the largest- users of grinding wheels in the United States, for their experience with pneumoconiosis caused by the dust of grinding wheels. Among the 18 replies received, none reported pneumoconiosis as a problem, nnd the incidence of tuberculosis wns low. Clark (116) concluded that artificial abrasives belong to the non toxic mineral dusts mentioned in the following quotation from the Journal of the American Medical Association (117) : Only silica (SIO.) Is capable of Inducing silicosis but any other m ineral dust under conditions of prolonged and gross exposure may cause some Increase In pulmonnry lllirosls. If the relative potential harm of silica Is rnted as 100, these o th er nontoxic m ineral dusts may be rated only on an ord er of 5 or 10. Moreover, the niirosls Itself Is not pnthngnnmle, since m any o th er dusts, alkalies, nclds, or vapors may Induce somewhat sim ilar. If not Identical X-rny markings. GRANITE INDUSTRY In his report of dust phthisis in the granite-stone industry, published in 1922, Iloffmnn ( 116) summarized the results of his investigation as follows: Tile granite-stone Industry Is carried on hy wage e arn e rs who, broadly speak ing, live under sanitary conditions above the average, so tlm t possibly unfavorable environm ental factors srp of decidedly secondary Importance. The housing conditions under which granite workers live are also above the average, so th a t In tills respect the environm ental factors nre favorable to a low m ortality ra th e r than otherwlae. Anthropometric reconls clcnrly establish the fact of n superior physique. Indic ative of a higher degree of disease resistance, an determined hy n relative weight above the overage. From this |mlnt of view, therefore, granite workers should experience a relatively low m ortality from pulm onary tulierculosls Instead of a m ortality decidedly almvc the nvernge normal lo Industrial occupations. G ranite workers, considered hy s|iectflc occupations, show wide variations In tuberculosis frequency, the excess In the death rate living most m arked among (he inon employed In grnnlle-atone cutting, It lielng c-qw'clnll.v severe nmnng men employe! In llie use of pneumatic tools. t 'erinln Mvupntloas, aucli ns isillslilng, i i t sharpening. last selling, etc., do not show a m arked excess, If any, tn the m ortallly from pulmonnry tutierculnsln, clearly Indicating th at the risk Is prac tically proportionate to lust exposure. (hinipare! w ith (lie normal death rnle of ndult m ales of the S ta le of Vermont, or of New England, the mortallly from pulmonnry tulierculosls among granltcatone w orkera hns lncronsel enormously during the Inal 2 years, ns cnntrasusl w ith a dim inishing m ortnllty In the population a t large. Agnlnat n decrenso In the pulm onnry tulierculosla dentil ra te of ndult m ales of the S ta te of Mnssachuselta from 2HR.fi |>cr 100,000 cxixiscd to risk d uring lRIlfi-pn ' i 202.2 during 1015-1H, there had Imen an Increase In (he corresponding dentil t.tle of granite cutlers of Ihe New Rnglnud Slntcs from -1.22.0 |ier 100.000 during 1RH5-90 tn 1,0(10.7 during 1015-IR. The only other occupation for which Inform ation Is available for the mrrespondlng period of time Is th a t of glssn-bottle blowers, PHYSIOLOGICAL EFFECTS OF BREATHING DUST 41 among whom the m ortality from pulmonary tuberculosl* dim inished from 418.6 per 100,000 to 2UH.0. These sta tistics for the New England S ta te s a re confirmed by sim ilar d a ta for every o ther stonecutting center of the U nited S tates, proving with absolute certainty that in every section of the country the tuberculosis m ortality of this group of Industrial workers Is increasing. In c o n tra st to a locally diminishing death rate from this most fatal of all diseases * -. Recalling th at the normnl pulmonary tuberculosis m ortality o f ad u lt males in M assachusetts Is only 203/2 per 100,000, it Is shown th a t the p re sen t d eath r a te from pulm onary tulierculosls among granite cutters Is 5 tim es the norm al experience In the population a t lnrge and probably 6 times w hnt It should be on the basis of strictly nonlnjurlous occupations carried on largely under hygienic conditions and in the open air. The same conclusion applies to nontuberculosis respiratory diseases, for it Is shown th a t the m ortality from bronchitis, pneumonia, and a sth m a Is also on the Increase among granite cutters, In contrast to a dim inishing ra te of fre quency among ndult males of the general population. In the second series of investigations on health of workers in the dusty trades, published in 1020, the United States Public Health Service studied the granite industry at Barre, Vt. (119). The occu pational groups were divided into four general classes based on the amount of dust to which they were exposea: (A) H and pneumntle-tool cutters, 014 persons, exposed to nn average of approxlm ately ftO million particles. (ff) All other occupational groups exposed to more than average plant d u sti ness. T his group contained 1(M persons In occupations w here the dustiness averaged lietwecn 27 and 44 m illion jmrtlcles. (C) Those occupational groups consisting of 14ft persons exposed to average plant dustiness (20 million particles). (/>) Those occupational groups exposed to less than average plant dustiness. T his group contained 10 jiersnns In occupations where the d u stin ess averaged let\veen ft and 0 m illion p articles. T h e results o f the stm lv on prevalence o f silicosis a n d tuberculosis a m o n g these w o rk ers are sum m arized in p a rt as follow s: Having a clear-cut diagnosis of silicosis and complete Inform ation w ith regard to the m agnitude of dust exjN>sure, It wns jnissibie to study the proportion of persons developing silicosis by length of service. In the A group, o r Mint group In which there wns heaviest dust exjosuro, the first case of slilcosls appeared a fte r approxim ately 2 y ears of service, and ly 4 years of service all In th is group seemed to have <leveloi>cd a t least nn early ense of silicosis. In th e sam e dust- count group the first case of more-developed silicosis np|tenred a fte r ft years of service, and by 9 years approxim ately IK) percent had advanced to th is stage. The study of the other dust-count grout* showed th at the development of silicosis was proportionate to the lust exposure. In the case of th e /> group 2 cases of early silicosis occurred a fte r 10 years' exiwsure, and 1 case o f m oder ately developed silicosis a fte r ft years* ex|Hsnre. O cncnit prevairnre o f tu b a eo m p lh 'a tia ff tiU ro tl* .--In plants carrying m orbidity records, w here It was believed eertnln th a t all cases of tul>emiloRl* were diagnosed ns such, the total ra te was ft.7 percent o r O.ft percent If early cases are (w inded. L atent or susN 'Vtcd <uses of tat*or< (lost* (among (host* g h e n physical exam inations) gnve nn additional ft. percent. These figures represent the numlter of cases found over n itcrlod of 2V4 years, and consequently the ra te Is dlfV rent from w hat would 1k obtained on nn o rd in ary cross-section survey. T u b c r r u t o tit b y d u * t g ro u p * a n d p e a r t in g r a n ite .--The association between the high tuberculosis prevalence among granite workers and the dust bar.nrd wns shown by determ ining the rates for th a t disease In the different dust-count groups by length of service In the granite Industry. The com parison between A and it grout* and f* and P grout* was extrem ely significant. No cases were found In the P group, and V group furnished hut ft cases, 1 of w hich occurred under ft years* cxjtnsurc: another, under 1U years. Of p a rticu la r Im portance Is the fact th a t In ftft years of exftosure the ra te did not rise. R a te s for the ) 42 REVIEW OF LITERATURE ON DUSTS A >n<l B itroupa rUe ntondlly w ith Increase of length of service to 15.B percent In tro u p A nn<l 10.1 percent In croup B . Even when th e suspected tuberculosis caees a re added, the ftenernl picture Is not m aterially chanced. In neith er the O or I) croups does there occur any excess of cases after lone exposure, while In the A and R croups the ra te rises with lencth of service In a sim ilar m an n er as for active tuberculosis. A c c o rd in g to Goodrich (120), statistics show that the death rate from tuberculosis among workers exposed to silica dust and, to a smaller extent, other dusts is excessive. The introduction of pneu matic and electric tools in processing stone Iirs caused a tremendous increase of tuberculosis of the lungs in those working with these appliances. In 1890, when stone was cut and polished with compar atively crude tools, the death rate from tuberculosis among tliese workers wns 150 per 100,000. By 1910 it had increased to 1,080 per 100.000 and by 1925 had reached 1,950, an increase to 13 times thnt of the period before high-speed tools caine into use. The explanation, of course, is that modern equipment creates many times the density of dust produced by manual labor. Cases of silicosis also became very numerous, and many of them developed tuberculosis. During this same period, when tuberculosis was increasing so rapidly among these work ers, the death rate from tuberculosis throughout the country was re duced to about half the rnte of 1890. The report of the Special Industrial Disense Commission of Mas sachusetts (21) shows thnt the granite industry presents a severe silicosis hazard. The commission surveyed 314 granite establishments and studied dust conditions in 13; X-rny and physicnl examinations of 951 granite workei-s disclosed thnt 15.2 percent had silicosis and 7.0 percent silicosis with tuberculosis. FOUNDRIES The Special Industrial Disease Commission of Massachusetts sur veyed 225 foundries (121), in which 12 dust studies and 1,014 physical examinations and X-rays were made. In the foundries studied, dust counts were excessive in connection with many of the operations. Tlionccd for immediate, elfectivo control of dust conditions m found ries wns evidenced by Ilie fact that H.H percent of workers examined had silicosis and 2.0 percent silicosis with tuberculosis. In a study of the foundry industry, McConnell and Fehnel (122) found thnt tho death rate for respiratory disenses (including all forms of tulierculosis and influenza) for iron and steel foundry workers was about two and one-third times that, for workers in all industries com bined nnd wns more than twice that for workers in nny of the in dustries selected for comparison. More than a third of all deaths among fo'oidry "'orkers were caused by some respiratory disease, whereas little moro than a fifth of tho donths of workers in industry wore duo to these causes. A striking fact revealed is tho uniformly high death rnte in this industry for each of the respiratory diseases throughout the working |>eriod of life. Another outstanding fact is tiio high rate for pneumonia, bronchitis, etc., the fomulrynien's rnte being nearly three times that for all workers combined Among iron and steel molders, founders, nnd casters, where 12 dentlis from pneu monia might have been ox|>octed, there nct.ually woro 38, a ratio of PHYSIOLOGICAL EFFECTS OF BREATHING DUST 43 nctim! to expected deaths of 315 percent; 24 deaths were recorded for respiratory tuberculosis, where 13 might have been expected, a rntio of 179 percent; the ratio for influenza was 216 percent, based on 23 actual compared with 11 expected deaths. In an analysis of the occu pational mortality of adult, white, male, industrial policyholders of the Metropolitan Life Insurance Co. who died during i 922-24 the proportion of deaths due to any one cause in any one specified occu pation group is compared with the proportion due to the same cause among all occupied white males. Again, pneumonia was the lending cause of death among foundry workers, n condition not true of any of the other 71 occupations included in the analysis. When differences in the age composition of the two groups were taken into account, it. was determined that the proportion of deaths from peuumonia was 120 percent higher for foundrvmen than for occupied males generally. Likewise, the proportion of deaths from influenza was 82 percent higher, that for tuberculosis of the respiratory system 6 percent higher, and that for other respiratory diseases 17 percent higher. McConnell and h'ehnel {122) emphasize the harmful effects on the lungs of ex posure of workers to dust inlmlntion; 67 of 215 X-rays taken were diagnosed as positive for silicosis. Advanced cases of silicosis were not found among those examined, but sufficient evidence of occurrence of the disease was presented. As the result of a health survey in 1931 by the Metropolitan Life In surance Co. {123) of representative foundries in and around Milwau kee, Wis., 67 of 215 employees studied (31 percent) were diagnosed ns having silicosis, but advanced cases were not found. As these re sults indicated a definite hazard, the report recoinnv'nded the selection of workers in foundries by preemployment examinations and chest X-rays, along with jteriodic examinations of those dangerously ex posed. In 1938 Slimier (123) reported a 4-yenr survey which was begun in 1932; 4,035 foundry employees were studied. About 7 percent hud definite silicosis, with half of the totnl group having had fewer than 10 yenrs of foundry exposure. Of the 279 with silicosis, CO (22 per cent) had tuberculosis. In a report issued in 1939, the Division of Industrial Hygiene of the New York State Department of Labor {124) stated that 2.7 percent of the whole group of foundry workers had silicosis, while 10 percent of (lie workers having more tlian 40 years' exposure were affected. In 1931 a survey was made of 21 foundries in Wisconsin {125); 215 roentgen examinations were made. Of 130 men examined, 1 had second-stage silicosis plus tuberculosis; 31 had first-stage silicosis; and 30 were classed as doubtful. Of 62 men from steel foundries, 2 had second-stage silicosis; 25 first-stagp; and 0 were doubtful. Of 18 men from the malleable iron foundries, 7 had first stage anil 2 were doubt fill. In 1939 Sander reported (125) a study of 4,000 foundry workers, 7 percent of whom were silicotic; 2 percent of the 7 percent were also tunercula r. From the time (1937) (lie amended occupational disease law of Ohio (125) added silicosis to the list of compensable diseases to Dceeml>er ) ) 44 REVIEW OF LITERATURE ON DUSTS 31,1940, 579 silirosis claims were filed; 194 of these claims were allowed, 100 of which (r>l percent) originated in foundries, 52 in iron foundries, 27 in steel foundries, and 21 in nonferrous foundries. Tho following summary by Williams (127) of the range, average, and average deviation of the free silica content of vnrious raw ma terials anu dusts present, in foundry operations indicates the possi bilities of contracting silicosis in the foundry industry: Sum m ary Table N um ber of ample Average fliOt (percent) Range of 810 (percent) A era* deviation (percent) 1 . Foundry a a n d s ................................ ................................ 5. Purlin* compound*--carbonai* .................. ............... 3. Psrtlng compound--phoaphat* ................................. 6 Molding............................................................................... e. d m n ln g ........................................................................... 7. Bund m d ltlo n ln * ........................................................... 8. Bh*k-out........................................... ........ 10 2ft l 17-40 6 5 \ 6 53 tr-d *1 6 19 3.1 tr-9 1.7 6 no 12 1 6-49 7 4 IS 12 S tr-61 10 2 13 13.2 4-27 3 8 12 8.4 2-22 4 1 * K id u d tn f lilt* partings. CEMENT INDUSTRY A 3-year study of the cement industry by tho United Stntes Public Health Service (128) revealed the following: X-rny nims were otitnlneit of ttie cheats of 53 employees In several different oc cupational g ro u p s , length of service vnrylng from 0 m onths to 15 yenrs. On the tmsla of the finding* these employees were rliiaalflcd Into live groups, ns follows: (1) Those showing evidence of pneumoconiosis, (It) those showing evidence of tuberculosis nnd pneumoconiosis. Cl) those ncgsllve for pneumoconiosis, (4) those showing evidence of tuberculosis w ithout pneumoconiosis, nnd (5) doubtful esses. The enrllest ense of pneumoconiosis np|>onrod a fte r .1 yenrs' ex|osuro to cement. O f the 53 men selected, 37 had been In the Industry more than 3 yeara and are therefore uaed na a basis of comparison. Among these 37 inen 15 showed evlclpnce of imcunioeonlosls, 8 of the 15 also having tuberculosis. In the group of 22 who showed no evidence of pnemnoconloals 8 gave evidence of arrested tuberculosis, 4 showed no evidence of either pneumoconiosis or tuberculosis while 10 were considered doubtful. In none of the enses showing pneumoconiosis were there any ellnlrnl symptoms of the condition, although the gonornl fibrosis present nnd Its distribution through the longs were Indicative of the condition. Cement workers appeared to have more than a normal moonlit of cnlclded nodes In th e InngR. Of the 57(1 workers examined 21. or 3.7 |>erreiit, were dlngnoaed as either posi tiv e or suspected cnaes of pnlmomiry tiibcrciiloRln. In only two cases, however, w as the disease active nl the lime of the Amt series of special chest cxnmlnnllon*. nnd neither np|ienred to progress na the result of ex|sisure to the dusts. In the history of Isdh eases It wns evident thnt the dlsense hnd dcvrlo|>ed be fore the men entered Ilie cement Industry, One of them died nlsmt a year after the study closed, while w ith the oilier (he dlsense npix-nred to li m e become quiescent when the study was closed. All the re st of the enses, with the excep tion of three, which were doubtful ns to diagnosis, appeared to Imve ilevrln|>ed their lesions lioforo they entered lhe Industry and were eontlm dtig In tlictr occiip.itlons without any evidence Hint the lesion* were progressing. Itussell (128) cnlculntetl (lint tho frequency of disability due to respirntory diseases among cement workers was twice as grant ns the average rosnirntory rate among employees of 11 manufacturing plants in relatively nondusty industries. Tho highest rate for all ) PHY8IOLOGICAL EFFECTS OF BREATHING DUST 45 respiratory diseases in any one of these establishments was 30 percent below the rate for cement workers. In 1935 the Portland Cement Association requested the Snranac Laboratory to survey a representative group or its member plants and examine a lame number of employees to determine whether there was a dust hazard in the cement industry. In the report issued in 1939 (130), it was stnted that the survey of 17 cement plants and ex amination of 2,278 workers revealed that the incidence of tuberculosis and other chronic infections of the lungs was less than that in the general population. It was concluded tnat prolonged inhalation of cement dust has no unfavorable influence upon susceptibility to tuber culous infection. The results of this survey seem to contradict the conclusions reached by Russell ( ISO). POTTERY INDUSTRY A physical examination of nil but nbout 1 percent of the workers in nine West Virginia potteries was given between July 1930 and July 1937 by the United States Public Henlth Service (131). Of the 1,027 men and 889 women examined, 106 men and 17 women were in the first stage of silicosis; 55 men and 5 women were in the second stage; and 6 men were in the third stage. In Ohio (/t'6') in the four divisions of the ceramic industry which form the whiteware group--china, tableware, floor nnd wnll tile, and insulators and sanitary ware-- 42 silicosis claims were allowed in the period August 1, 1937-October 1, 1940; 21 of tho claims originated in china nnd tableware plants, 17 in floor and wall-tile plants, and 4 in electric porcelain plnnts. SILICA AND FIRE-BRICK INDUSTRIES Pennsylvania is tho largest producer of silica brick in tho Unitod States. Four representative plnnts engaged in this industry were investigated l>v the Ihireau of Industrial Hygiene of tho Stnto De partment. of Health. Tho results of this investigation were pub lished in 1941 (132). Physical examinations of 1,035 silica brick workers revealed that 538 (51.9 percent) had silicosis. Tuberculous infection wns found in 123 (11.9 percent) of tho 1,035 examined. A study, reported in 1945, was made by Stalker (133) in the re fract ory-brick industry in Kentucky, which ranks fourth among the States in production and in number of people employed in the industry. The manufacturing processes employed in these plants are of the conventional type and nro basically similar to those described in the Pennsylvania silica-brick study (132). Tho raw materials and m atur ing temperntures, however, are quite different from silica brick. Tho raw plastic d a y contains 17.7 percent SiO, nnd tho raw flint clay 7.1 percent SiO,. 'lo determine tho hazard of silicosis to which tho workers were ex posed, 870 men were examined, representing 87 percent of tho em ployees. The term "pneumoconiosis'' is used by tho investigntors (134) for the characteristic pulmonary change noted in 11 percent 86321$ -- BO------- < 46 REVIEW OF LITERATURE ON DUSTS of Ilie moil examined. This change was not of the typo or magnitude usually ncocptcd in compensation courts as the discrete, liodulnr fihrosis of silicosis. The report of this study concludes that continuous employment in the lirehrick industry, without dust controls, leads to the development of characteristic diffuse, finely granular, pulmonary fibrosis. Con glomerate silicosis may develop after long employment in dry pan mills without adequate dust controls. AUSTRALIA In 19(12, while a system of sewers was being dug in Sydney, Aus tralia. the Sewer-Works Ventilation Board (J.%0) was appointed to inquire info the working conditions and to recommend means of im provement. whereby the work could be rendered less hazardous. The l\oard found that-- For many years pina minera employed In this clnaa of work (tunneling) sufforcil acutely from a illaeaae which waa for a long lim e known by the ra th e r mlalradim: lorm "aewer <lleaae," hut na the com plaint liecnme more widely known It wna alrnngly auaja'cted (hat duat waa the chief cauae of the mlachlef. The hoard gave the fumes of explosives and the expired air from Ihe lungs of Ilie miners in imperfectly ventilated tunnels as causes contributory to (lie high mortality but stated that the dust fiom ham mering. drilling, and use of the pickax was probably the solo cause of the disease once known as "sewer disease." In 1912 Armstrong (ISO) investigated a reported epidemic of pneumonia at Broken Hill and found that the death rate from pneu monia among underground mind's in that locality during 1910-12 wns C.5 per 1.000, or nearly 4 times as great as that for all mnles in New South Wales. In 1914 a royal commission was appointed to inquire into the mining industry at Broken Hill. With regard to in dustrial diseases, this commission stated that pneumoconiosis and phirnbism were among the risks of a miner's calling, while other dis eases--for cxnmple, pneumonia--were added risks hut not strictly industrial because they affected other than miners. From unanimous medical testimony the commission concluded (130) that pneumonia was more prevalent, severe, and fnlal nniong minis in Broken Hill than among any other class in the State. Although attributing the disease primarily to sudden changes in temperature, the commission advanced the opinion that dust inhalation in. any form would pre dispose to disease, ll also stnted that pneumoconiosis was virtually unknown at Broken Hill and blamed mining in other States for such casos as had been noted. Tuberculosis, however, was a disease to w h ich the minors nt Broken Hill, us elsewhere, were peculiarly sub ject, and work in a mine was considered particularly dangerous for nny tuberculous patients. In 1919 the Technical Commission (130), constituted to examine (ho miners at Broken Ilill, for (lie first time in Australia used X-rays in diagnosing silicosis as an occupational disease. Of 4,.1,17 mine employees examined, 193 were diagnosed ns having pneumo coniosis--90 in the first stage, 44 in the second, and 59 complicated with tulieivulosis; 39 cases were definitely diagnosed as suffering from PHYSIOLOGICAL EFFECTS OF BREATHING DUST 47 pulmonnry tuberculosis only, and 26 others were thought to be suf fering from uncomplicated pulmonary tuberculosis. Of 2,018 under ground men examined in 1!>22, 2G6 showed pneumoconiosis--lid in the first stage, 51 in the second stage, and 102 complicated by tubercu losis; 107 additional men were diagnosed as suffering from tulierculosis only. In 1922 the New South Wales Board of Trade, in conjunction with the Commonwealth Department of Health U36) investigated clini cally and radiologicnlly the prevalence of pulmonary diseases among workers in sandstone and other siliceous rocks in the metropolitan district of Sydney; of 716 men examined, 123 were suffering from silicosis. Under the standards set by the Broken Hill Commission, 47 of these were diagnosed ns having first-stage silicosis, 38 secondstage silicosis, and 38 pneumoconiosis complicated by tuberculosis; 16 were diagnosed ns hnving pulmonnry tuberculosis only. The Workers'Compensation Commission of New South Wales (1ST) reported on 1,300 of 1.500 workmen examined up to August 23, 1929, ns follows: Of 107 stonemasons examined, 9 had tuberculosis, 17 had silicosis of various stages, and 26 had silicosis with tuberculosis. Theso men had worked in the industry 10 to 55 years. Of 29 monu mental mnsons examined 2 bail tuberculosis, 1 class A silicosis, and 5 silicosis with tuberculosis. Of 37 ballast qunrrymeti, 1 had tuberculosis and 2 marked silicosis. Of 80 dimension quarrymcn, 6 had tubercolosis, 3 early silicosis, 2 marked silicosis, ntid 16 silicosis with tuber culosis. Of 377 rock choppers examined, 12 had tuberculosis, 25 silico sis, and 10 silicosis with tuberculosis. lu 1931 Moore ( 137) reported nil investigation in New South Wales to determine the incidence of fibrous pneumoconiosis among coal miners; 471 volunteers who had worked n least 10 years underground were examined by the Division of Industrial Hygiene; 199 came from 1 mine, several employees of which had had pulmonary fibrosis; the remaining 277 volunteers were employed in 8 other mines of the district. The percentage of cases of fibrosis for all men examined was 25.!). The percentage of fibrosis among men with coal-mining history only ranged from 22.5 to 25.7 percent; the |H>rcentage incidence among men who bad worked nlso in metal mines or quarries as well as in c o a l mines was 39.7. In Tasmania in 1928 ( /,7/J), tho various mining centers were visited in turn and men examined clinically end radiologicnlly virtually at tho mine bead; 65 percent of the" mine employees available were examined. Of 134 underground workers, 5.9 percent were suffering from uncomplicated silicosis and 2.1 percent from silicosis with tuliorculosis. Of all the workers examined, 1.1 percent were suffering from 1iibcti uiosi.-, only--1.2 prn'oiit of the underground and 1 percent of the surface workers. In 1911) a royal commission appointed to report on pulmonary diseases among the miners in the Western Australia gold-mining industry ( ) concluded that-- Tho minor U limro llnhlo to lutm ill so irononitly thnn tho iitoru^o nmlo <>vr IT* your of iijjo. Tin* m inor 1 Jos hmii-llvotl tlmti tho iivonmo nmlo m o r 1.\ l*nrlly on nenumf of grontrr llnhlllty to Inn Ul*on*o. ) 48 REVIEW OF LITERATURE ON DUSTS Tuberculosis of the limes Is on the Increase among m iners and Is twice as prevalent a s among m ales over Jl>. I'nf'lm onln among the nente, ami bronchitis, asthm a, emphysem a, and fibrosis of the lungs among the chronic lung diseases are more prevalent among miners than mong m ales over lfi. The following principle was laid down: Any m an suffers from fibrosis to the extent to which be Is exposed to the con tinued Inhalation of m ineral dnt. If there Is no dust, there will be no fibrosis, and conversely, the continued Inhalation of dust certainly produces fibrosis. During an investigation (AM) of pulmonary conditions of mine employees in Western Austrnlia in 1925-26, 3,039 men were examined at Knlgoorlie and 1,028 at. 9 other mining centers throughout the State. Of the 4,067 men examined, 798 (19.6 percent) presented definite evidenreof pulmonary silicosis, and 155 (3.8 percent) had tuberculosis; 12 of the latter group had tuberculosis without silicosis. Of the 1,759 surface workers, 6.6 percent had silicosis, 1.5 percent silicosis with tuberculosis, and 0.3 percent tuberculosis alone. The surface workers engaged in dry milling without previous underground experience showed the highest incidence of silicosis--9.6 percent were atrected compared witli 2.2 percent of the employees engaged in wet milling without dry-milling experience nnd 2.0 percent of those who hnd had no wet- or dry-milling experience. Of the 2,308 underground workers, 23.3 |K>rcent hnd silicosis, 5 percent, silicosis witli tuberculosis, and 0.3 percent tuberculosis niono. At least 51.6 percent of the workers en gaged in developing and 39.2 percent in stoping were affected with silicosis or tuberculosis, in contrast with 8.4 pcrcei ` of those without stoning or developing experience. Since 1926 the mine employees in Western Australia have been examined annunlly by the Commonwealth Department of Health (138). O f 2,290 men previously classed as normal, 30 (1 3 percent) were found on reexnminntion in 1927 to bo suffering from uncompli cated silicosis and 13 (0.5 percent) hnd tuberculosis only; of 491 diag nosed as silicotic, 86 (17.5 percent.) hnd silicosis with tuberculosis. Of 2,822 men classed as normal in 1927,48 (1.7 percent) had progressed to 1928 to silicosis only, 11 (0.4 percent) had progressed to silicosis plus tuberculosis, and 3 (O.t percent.) had simple pulmonary tubercu losis; 25 (5.9 percent) of 425 silicotics on reexnminntion showed signs of tuberculosis complication. Of 2,293 normals reexamined in 1929, 100 were diagnosed as silicotic. Silicosis was not disclosed in any case under 40 years of age or with less than 5 years of underground work. Bndham (130) reported that, of 477 coal miners working in the same pit, who were examined in 1930, 25 showed evidence of librosis. In New South Wales 116 of nliout 10,000 coal miners employed under ground hnd been eom|>ensi\ted. Tabulation of data resulting from the examinations conducted from 1925 to 1939 revealed a stendy decline in the incidence of advanced nnd enrly silicosis and an increase in the liunilier of normal jicrsons em ployed in the mines from 80 percent of the total to 95.63 in 1939. For example, 11.4 percent of the miners exnminod in 1925-26 had enrly silicosis, nnd in 1939 tho {>ercentngc wns 4.0; comparable figures for ndvnnced silicosis were 4.5 and 0.1 jiorccnt, resi>ectivcly, and for silicosis and tuberculosis 3.3 nnd 0.2 percent, respectively. ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 49 In 1907 n report on miners' phthisis to the Committee of tlie Bendigo Hospital, Victoria, Australia (135) stated that there was undue mor tality among Bendigo miners due to respirntory diseases, notably tuberculosis. The cases examined were classified according to two clinical types--a pure fibrosis of the lungs, nonttiberculosus in origin; silicosis; and a mixed type with a tuberculous infection in a fibroid lung. Of 01 men exnmined in Bendigo in 1928, 9.4 percent of the un derground workers were diagnosed as suffering from uncomplicated silicosis and 7.5 percent from silicosis and tuberculosis; 3.3 percent of all workers had tuberculosis only. CANADA Elliott {11)0) was the first to direc. attention to silicosis in Ontario, Canada; in an article on Silicosis in Ontario Gold Mines, published it; 1921, he reported that 3 of 11 underground workers examined by him presented evidence of silicosis, indicating tlmt the disease was being contracted in this mining area. In 1925 and 1920 n further sur vey was made by the Industrial Hygiene Division of the Ontario Department of Health. Miners witli more than 5 years' experience underground in the individual mining area and with no exposure to silica dust elsewhere (a few of those examined had had some expos ure elsewhere) were given a physical examination. Of 1,220 men ex amined, 74 showed evidence of silicosis--52 in the anteprimary, 11 in the primary, and 11 in the secondary stage. During the period April 1, 1920-April 1, 1927, a survey of silicosis was made in the Porcupine group of mines in northern Ontario under the auspices of the mine operators in compliance with the amendment to the Mi ners* Plitliisis Act of April 8, 1920, bringing silicosis under tlio status of a compensable industrial disease. Approximately 4,000 miners were examined for tuberculosis, silicosis, or Ixith. As a result, 94 silicosis claims were submitted for compensation. According to the South African nomenclature 39 of these 94 cases were diagnosed nsjinteprinmries, 28 as primaries, and 27 ns secondaries; in addition, 247 men showed either positive or probable tuberculosis ( l i t ) . From 1920, when silicosis was included in the list of compensnblo diseases under the Canadian Workmen's Compensation Act, to 1940, 402 claims had been accepted for compensation {142). NETHERLANDS In The Netherlands {1)3) a medical examination of 2.013 stone masons in 18"'.) rcveiiicd lu'.i tuberculous cases and 10.8 percent strongly suspected of having tuberculosis. During the perioil 1891-1900 tho denth rnto niViong stonemasons for all men between 18 and 50 years of ngo wns greater than in any other occupation. Even such injurious occupations ns typesetting, cigarmnking, and diamond cutting showed considerably lower death rates. The denth rate in tho ago group 18-24 yenrs differed little from the average for all occupations; tho highest denth rate was noted between 3(! and 50 yenrs. Of 952 stone masons dying during 1880-98, 87 percent died of diseases of the re spiratory orgnns. '1 he first general examination of adult stonemasons ) 50 REVIEW OF LITERATURE ON DUSTS was conducted in 1929, the second in 1020, and the third in 1929. In 1929 in nearly hnlf the eases the X-ray gave more information than the physical examination. Of 09 cases in 1929, lung affections were not shown clinically in It* hut. were shown in the X-ray examination, and in 98 cases they were shown l>oth clinically and by X-ray. On examining stonemasons who, in the course of their lives, had ownoerkkeidndceorftasitnonKei,ndKsronfn esntobnuergnn(d14o3t)h errespwo rhtoedh athdawt , orrtkf e1d0 msaonrde stthoanne workers, 2 were in the second stage and 5 in the third stage of silicosis nfte'- 20 to 90 years' employment in the occupation; of a total of 74 Belgian limestone masons, only ! were in the, second stage nnd none in the third stage after the same number of years' employment in the occupation. Tsing the third stage for comparison, the proportion was more unfavorable among the 90 stonemasons working various kinds of stone including sandstone than among the Belgian limestone work ers, although relatively favorable in comparison with the sandstone workers. A striking fact was (he large number (77) of Belgian lime stone workers who snowed no affection after 10 to 90 years' employ ment compared with only 4 stonemasons working all kinds of stone. Fewer cases of third-stage silicosis were found among Belgian lime- itone workers after 40 to COyenrs' employment or longer than among sandstone workers. In his general conclusions K rnnenburg (143) mndo the follow ing statement, re g ard in g the effects o f sandstone a n d lim estone : The working of sandstone alone must lie regarded ns more Injurious to the lungs than the working of llinestone alone. The working of sandstone alone doe* not alw ays lend to symptoms of silicosis and. on the other hand, the w ink ing of llinestone alone (lld g la n lim estone, ninrhle) ilia's not prevent silicosis In a serious form. The working of snndstone nnd limestone alternately appears to produce less serious results In the snme period th an the working of sandstone (144) alone. An i n q u i r y b y V o s s p i m n r a n d D o u b r o w into the respiratory affections of 000 men w o rk in g in the coni m ines o f T h e N etherlands f r o m 1929 t o 1999 r e v e a l e d o n l y o n e w o r k e r w i t h nil i m a g e o f m i c r o - nod u ln tio u ; all the others presented a perceptibly norm nl thoracic imnge. S ix ty o f th e 000 w o rk ers Imd been em ployed at rock d rillin g for more th an 20 years, the o th ers fo r m ore th an 10 years. 143). I n 1995 a n i n q u i r y w a s m a d e r e g a r d i n g s i l i c o s i s i n t h e c o a l m i n e s o f B e l g i u m b y 15 p a r t i c u l a r l y c o m p e t e n t i n e d i c n l m e n ( One thou s a n d w o r k i n g m i n e r s w e r e g i v e n X - r a y e x a m i n a t i o n s ; 900 o f t h e s e Imd w orked exclusively in rock (tu n n e le rs ) ; a n d 100, used as controls, b ad been occupied exclusively in w o rk in g the coal seam . N orm al subjects were the exception in all w orkers w ho Imd w orked for at least 10 y ears in th e m ine. A considerable n u m b e r of th em w ere suffering from extensive or highly developed fibrous o r even from nodnlnr nnd pseudotum ornl forms. T he investigators were surprised to discover, in w orkers em ployed on the coni seam nn d n o t in direct contact, w ith rock dust, ns high n p ro p o rtio n nffected ns am o n g rock w orkers. D u r i n g th e 10 y e n rs fro m 1930 to 1940, p e rio d ic r 'iitgenologic exa Col m li i e na rs t(i1o 4n6s ) wer of e w m or n k d e e r s by in the M edical Service of roek in the S ta te m ines T he N etherlands H endrik, Emma, W ilh elm m a, an d M o u n ts, A to tal o f 2,300 w o rk ers in rock w ere ex- PHYSIOLOGICAL EFFECTS OF BREATHING DUST 51 amined. During a period of more than 10 years, 4,977 X-ray pictures were made of the lungs of 2,320 underground hard-coal miners work ing in rock; 10.15 percent of the pictures revealed mild pneumoconiotic changes (reticulation and silicosis type I ) ; 1.45 percent showed mod erate changes (agreeing with silicosis type I I ) ; nnd 0.54 percent indi cated more severe changes (as with silicosis type I I I ) . Although these figures refer to rock workers, Mey (46) states th at: The thmiKlit obtrudes that not only the rook work Rives rise to the api>enrance of p n e u m ( K ` t n |o f i c c h n n g p . DENMARK An X-ray examination of 401 men nnd 337 women employed in 5 Danish porcelain works (147), reported in 1934, showed that 45.2 percent of those examined hnd silicosis nnd 100 percent of those over 50 years of age were ndeeled. This investigation led to the introduction of preventive measures, the efficacy of which was studied in 1941 and 1942. Radiographic examinations were made of 39 workers, 32 of whom had been examined in 1932. This follow-up study revealed that it is most, difficult to he certain of the radiographic diagnosis of early porcelain silicosis. Some of the cases reported ns having mild or be ginning second-stage silicosis at the earlier examination showed "no or no certnin silicosis'' at the examination given in 1942. The authors concluded that great, experience is required to lie faiily sure that an X-ray film indicated incipient silicosis. Gudjonsson and Mdllcr (14~) found silicosis widcspcrnd nmong the 951 porcelain workers they examined in Denmark. V. Stuh-Christensen (14$) examined workers in the foundry, stone cutting, grindstone, cement, scouring-powder, polishing, tile, and sand-blasting industries of Denmark. All of the 90 foundry workers except 5 were nble to work at the time of the examination, 'l'lie author observed that, with these workers, silicosis ap|>enred lietwecn 10 and 19 years of work; tieyoud this period all the workers became affected. 1*ifty percent of the molders in a lnrgo foundry examined by Koitiissnreck ( 14S) presented rather serious pulmonary affect ions, the typical disease imnges appearing only after 30 yenrs of exposure. Of 23 grindstone cutters examined 17 hnd silicosis. In the cement industry Stub-('hristensen found slight silicotic les ions nfter 10 to 20 yenrs" work; after 40 years' work the lesions were present in almost 100 percent of the workers; CO percent of his eases nnd lesions of the first stage, 8 percent of the second stage, nnd 5.5 percent of the third stage. The nutlior stntes thnt, in the cement in dustry, vigorous physique does not, nppenr to protect the workers against, pulmonary lesions. In tho pohsliing industry, of 40 workers examined 12.5 percent hnd silicosis in tho second stage; none wns in the third stage, nnd none had silicotiiherculosis., FRANCE On October 1G, 18G0, the Medical Gazette of Lyon ( 149) stated : It h n s lHon P sIiililN io d by rpoont s t n f h t l o s Hint ninonx the1 w o rk ers om p lo yts l In th e in Inos o f ('oriiounlllos (51 In m 100 11list o f IIsomho o f th o chont, \\ hlh* In t hr n ,s>! o f rho j*>|>ulHflon Ml hi n 100 iIIim! o f tliN enus-v ) ) 52 REVIEW OF LITERATURE ON DUSTS Between April 1042 Rnd May 1943, Martin and Roche (ISO) exam ined G09 rock miners. Six of tliese had ordinary tuberculosis. Radio- logic deviations were observed in 102 or 16.0 percent of the remaining 003 miners. Coal dust was incriminated by the authors in the genesis of 14 cases of pneumoconiosis in rock workers who had been employed in coal previously. Experience for 12 months preceding August 1943 of the chief physi cian (161) of the new Society of Coal Mines of Bouches-du-Rhone did not reveal a single case of pneumoconiosis of silicotic appearance among lignite miners. Little dust is produced in the extraction of the lignite, but a hazard exists in working the lignite. Fifty-five workers, some of whom were the oldest and some of whom had worked for a long time drilling in the rock encasing the lignite veins, were considered n.s suspects. They were examined clinically and radiologically ; 47 of these workers showed no innrked pneumoconiosis and no trnce, past or present, of tuberculosis. Eight of the 55 workers were clearly patho logic, but only 2 had spent all their occupational life in the exploitation of lignite; both of these revealed important pulmonary fibroses but did not have the classical signs of silicotic pneumoconioses. INDIA In the many discussions on the incidence of silicosis among quartz miners in various parts of the world, the Kolar field in India hns been cited repeatedly as an exception to the general experience that sili cosis is an occupational disease among such minors, as is seen, for instance, among miners on the Rami (162). The Rege Committee (16.1), however, reported in 1046 th at silicosis is an occupational--indeed the only occupt ional--disease prevalent in the Kolar. Tt is now so recognized, and in 1942-43 compensation was awarded in 778 cases. According to Barenhrng (164), although classical silicosis docs not occur in the Kolar gold field, it. is not denied that pneumoconiosis (which means dust disease of the lung) does occur. A lter many yenrs of exposure to dust, this disease enn 1 incapacitating. The condit ion is characterized by a heavy dust deposition in tlio lung with an absence or a minimal degree of fibrosis. lVisability is alisont for many yenrs, l>ut. susceptibility to tuliercnlosis is increased. Apparently the reason for the difference in the disense as it occurs in the Kolar gold field and the Witwatersrand is due to the lower silica content of the mine dust, which is about 10 percent, and the IColnr dust is coarser tlinn the Rand dust. The position as given by Bnrenhrug ( 164) is th at Kolar miners inhale large quantities of a relat ively coarse dust (tlio number of particles above 20 microns in miners' lungs is most striking) composed mainly of silicates of aluminum, magnesium, iron, calcium, sodium, and jmtassiuin and about 10 percent free silica. The Rand miners inhale relatively small quantities of a very tine dust with a free silica content of 70 percent. Barenhrng estimates that tho lvolnr miner inhales almost as much free silica as tho Rand miner. If this is accepted, the low toxicity of tho Kolar dust, must lie due to dilution of quartz by tho silicates and/or the relatively large sizo of the dust PHYSIOLOGICAL EFFECTS OF BREATHING DUST 53 particles. It is even possible that the silicates modify or inhibit the action of quartz. Barenbrug (1-54) concluded his article with the following statement: All this la conjecture hut one thing Is certain. If R and m iners worked In d u st concentrations com parable w ith those existing on the K olar gold field, silicosis would be as serious a menace on the Hand aa It was at the beginning of this century. If the Hand reverted to dry m ining the silicosis haznnl would lie the most form idable problem to be faced and unless there Is a revolutionary develop m ent In m ethods of dust control It Is dlfllcult to foresee how It could be overcome. The problem of the nblllty of Rnnd m iners to work efficiently In the altered con ditions of higher dry-bulb tem peratures Is of secondary Importance. Acclima tization to high tem peratures kept a t a m oderate level with the nld of air cooling plants and Improved ventilation Is possible but a s fnr as we know acclim atization to Inhaled silica particles Is not possible. ITALY 111 Italy the first clinical and aiiatomicnl observations {155) prob ably were made by Kniiinzziui. Biontli (15ft) in l!>0(i noted that the greatest damage to the miners in the mines of Sardinia was due to the action of dusts from gangtie rot. tabling silicates. lie also noticed that virtually all coal miners were addicted to coughing and continued to expectorate black sputum even some time nfter (hey had quit thei" occupation. lie found minor dust injuries among the Ilergnmo miners in 1007, perlmps because they labored intermittently in mines and on farms. However, in n few miners, especially the older men, Bioiuli found pharyngitis and bronchial catarrh, with dark sputum due largely to the black smoke of the candles used; lie observed that acute affections of the respirntory apparatus were more serious and more obstinate in these workers. In 20 post mortem examinations of Sardinian miners, Frongia {157) in 1008 noted that the cause of death was in most cases an acute infec tion (pneumonia); lie also found among these workers many cases of serious and diffused arteriosclerosis, emphysema, and nnthrncotic foci, with more or less diffused softening of the tissues and gangrenous foci containing a black brothlike matter--the characteristic finding of black phthisis. On the other hand, he found foci of bronchiectasis due to tuberculosis infection in only five enses. Eighty-five percent, of the fatal eases ninong these miners, therefore, were not caused by tulierculosis infection. I'esenti, Kota, and Finzi {158) in 1006 reported on health conditions of workers in lime, cement, and plnster. l 'cseiiti affirmed the high incidence of pneumoconiosis among workers in cement and plaster but did not include proportionnl statistics. lie believed flint inhala tion of cement dust neither produced tuberculosis nor favored the progress of the disease. Rota and Finzi found that, of 6.1 deaths among the permanent workers engaged entirely in lime and cement work, 28 died under the nge of 40 nnd 11 umler 50. The cause of deatli in 20 of the 03 cases wns pulinonnry diseases--0 actito pneu monia, 2 pleiiromediastiiiitis, and 0 tuberculosis. Rota and Finzi stated that there wns no truth ill tho statement that workers in lime kilns enjoyed a certain immunity from tuberculosis. On the contrnry, they claimed thnt the greatest toll to this disense wns paid by kiln workers. For example, 5 of 35 deaths of such workers were duo to 54 REVIEW OF LITERATURE ON DUSTS tulicrculosis. Physical examination of 218 factory workers revealed 122 cases of harsh respiration in the upper respiratory passages, owing certainly, they asserted, to an incipient pneumoconiosis or infiltration of dust into the peribronchial lymphatic channels. Harsh respira tion was more common in those employed for a long time, especially those who had worked 10 to 12 years; it was evident in 52 of 128 kiln workers, 18 of 20 workers transporting stone, and 43 of 50 crushingmnchinc operators, baggers, and porters of sacks. Many workers were also emphysematous. Itinnchi (7.W) made a careful clinical and radiological examination of 250 workers employed in more or less closed workrooms, as sculp tors, rough hewers, modelers, and workers in grinding rooms. After excluding all en-.e of suspected syphilis and other chronic lesions, lie studied 73 workers in marble who had no inherited disease or previous dsense history nnd were free from definite or suspected symptoms of affections of the respiratory passages that might come under the category of common infections. X-ray examination revealed diffuse nodes of thickened tissue spread over almost the entire, respiratory surface. In these cases he could determine only a slight percentage (20 percent) of functional alterations with symptoms of chronic bron chi! is a id pulmonnry emphysema. As the result of n radiographic and clinical examination of 105 C arrara ma,bleworkers employed in mnrble grinding nnd of such workers ns sculptors, rough hewers, sawyers, nnd polishers Turano ( 100) concluded: T he change* met with among C nrrnrn mnrhlownrker may t>e classed In the Initial stafre of pneumoconiosis, (lint Is to sn.v, com prising the least serious form s of the disease, such as the very mnrkeil reinforcem ent of the pulmonary outline, due as dem onstrated by personnl observations, to the processes of arte ritis and lym phangitis, and In certain easi>s e<|ually to conditions of emphysenin lisnnlly present among those workers. I hnve also found frequent pleuritic changes which enn he relnted to Inhalntlon of mnrble dust, hut never lesions of the pulmonnry parenchyma. The raillologlcnl ns|>ect of pulm onary tuberculosis among workers examined Is, on the other hand, highly Im portant, since It shows an atypical picture on wlilch are noted lesions with unusual sites nnd apical nnd suhclnvlcular regions unaffected. It Is this fact which has led me to adm it the probability of a com bination of pneumoconiosis nnd tulierculosls. Finally, statistical ns well ns radiological d a ta Justify absolute exclusion of the theory of a particular Ismlgn or mnllgnnnt course of tuls-rculosls among m nrbleworkers, ns likewise of any kind of predts|Hisltlon to the said specific disease. According to Parincgginni (101), social consideration of silicosis, which before compulsory insurance wns almost nonexistent, suddenly was pressed on the attention of doctors, industrialists, and magistrates between 1937 and 1943. In 1941, 1.773 appeals wero forwnrded to tho section on labor con troversies ot the Tribunal of Milan; 883 (or 47 percent) were for physical injuries of persons duo to work. This group was divided broadly into accidents and diseases whilo nt work. Tito diseases in cluded 954 cases of silicosis (98 percent) nnd 11 cases (2 jmreent) of other diseases; 002 of the ensos of silicosis wore examined by I'arnicggiani (101). Of the 002 trinls for silicosis 319 (58 jiercent) were conducted io the end; of those, 342 were promoted by tho workers who ) ) PHYSIOLOGICAL EFFECTS OF BREATHING DUST 55 ) had worked in dusty industries limited to the Province of Milan. The judgment of the cases was ns follows: Favorable to tho workers (silicosis ascertained) 201 (,r>8 percent), unfavorable to workers (silicosis nonexistent) 148 (42 percent). R U SS IA In Russia an extensive field study wns made in 1930-35 (162) at one anthracite and two bituminous-coal mines in the Donetz B asin; it was carried out under the Ukrainian Central Tuberculosis Institute and I the Donetz Institute for Industrial Hygiene and Occupational t Diseases. iI} In the Khrustalnv (anthracite) colliery, pneumoconiosis was found in 11.1 percent of the 298 men'--5.7 percent in stage I, 2.3 percent in l stage II, and 3.0 percent in stage II I. In the Vetku (bituminous) colliery, the incidence of pneumoconiosis was lower, being found in t 3.3 percent of the 1,32!) men ; 2.3 percent in stage I, 0.9 percent in stage II, and 0.1 percent in stage III. In the Gorlovka (bituminous) col liery, the incidence wns also comparatively low, being found in 2.3 percent of the 987 men: 1.5 percent in stage I, 0.5 percent in stnge II, nnd 0.3 percent in stnge III. SOUTH AM ERICA BRAZIL The high temperatures found in the lowest depths of tho Morro Velho. the deepest mine in the world, do not permit wet drilling. In 1939 a commission of thr ee doctors (166) examined 2,197 of the miners, 908 of whom wore X-rayed; 304 were found to be definitely silicotic-- th at is, 33.48 percent of those X-rayed nnd 13.83 percent of those exnmincd. CHILE During the period 1942-45, more than 1,200 persons suspected of having pulmonary silicosis entered the Institute Medicine del Trnhnjo de la Coja lie Segno Obligatorio (Medical Institute of the Compulsory Insurance Fund) (164) m Chile. Two hundred verified cases of sili cosis were analyzed; 172 were pure pulmonary silicosis and 28 silicotuberculosis. All of those examined worked in tho copper mines, except 20 who were employed in industries manipulating quartz, as glasswnre, and in ceramic factories. As a resultof his recent studies in South America, Bloomfield (165) found it is well-known that in Chile many workers with silicosis are still employed in industrial establishments ill which silica ill the form of quartz is handled. For example, 15 percent of 1,000 copper miners exnminedi/in 1940 were found to have silicosis with varying degrees of disability. The company indemnified 02 cases that year. In tho same mine, nearly 500 silicos'iscases had boon settled during the preced ing 12-year period. Although lust hazards are now being controlled in this establishment, (her' arc still approximately 150 men employed by the company who will eventually 1 compensation cases liecnuso of previous dust exposure. 56 R EVIEW OF LITERATURE ON DUSTS mv According to Bloomfield (1GG)^ although Peru has had an occupa tional disease compensation law since January 12,1935, it is virtually impossible to obtain nation-wide statistics on the incidence of occupa tional diseases. One firm that employs nearly 12,000 workers reported that 271 cases of silicosis were certified by its medical department for payment in 1946. Other examples of occupational diseases in Peruvian industry are at hand. In one mine, which employed nearly 1,500 workers at its various installations, some 1,900 applicants for work were examined in 1946. Three |>ercent of these were rejected because of silicosis, ap parently acquired elsewhere. Another mine employing some 500 men examined 890 applicants for work during the first 0 months of 1947. Nine percent of these men were rejected because of silicosis and 14 percent because of tuberculosis. Still another mine, employing about 450 men, reported that 8 percent of its workers had silicosis and tuber culosis. Another mine employing 500 workers reported 20.1 percent illness among its workers. The causes were pneumonia, ,rippc, bron chial pneumonia, and silicosis. There were 84 cases of lilicosis at this establishment. At this same mine, 19 percent of 815 persons exam ined for employment in 1940 were rejected because of silicosis and tuberculosis. O f tho 150 men rejected for these 2 causes, 128 had sili cosis. And finally, the experience of still another mine was available for tlie period 1935 through 1942. During those 8 years, if some 0,499 men examined, 14.3 percent were found to have silicosis. During the same period, only 1.9 percent of those examined were found to have tuberculosis. I t is obvious from the abovo data, even though thoy are from scat tered sources, that high rates of silicosis and tuberculosis exist throughout. Peruvian mines and mills. Unquestionably these rates are an underestimate, since it is known that a high labor turn-over tends to mask true conditions. Labor turn-over in the factories is slight., with the exception of one factory where it was reported to bo 50 percent, nnnually; but in most of the mines it is extremely high, running from 35 nnd 50 percent yearly to more than 100 percent., espe cially lor unskilled labor. sra iN A very high illness frequency of pneumoconiosis was reported (1GG) in 1937 among the Itodaquilar coal miners. Of 110 workers employed in the mine, 40 exhibited more or less advanced disease, al though tho mine hail lieen opened only 0 years. Suspected or detect able changes appeared on the radiograms of these 40 miners, 22 of whom showed silicotic nnd tnlieirnlous chnnges. There were 12 cases of silicosis I, 2 cases of silicosis 11, nnd 9 enses of silicosis III. It was also determined that 10 workers had died of silicotuberculosis during 1935. SWEDEN In 1942 Bruce (M) issued a report of a clinicnl and industrial medi cal study on silicosis ns nn occupational disease in Sweden. The study 1 PHYSIOLOGICAL EFFECTS OF BREATHING DUST 57 ; included porcelain factories, iron works, sand blasting, smelters, sand stone and quartz crushing, quartz mills, sandstone grinding shops, and mining. Among the 2,631 workers examined by the investigator in the in dustries mentioned 99 were suspected of having silicosis, 025 (23.7 percent) had silicosis, of whom 408 were in the first stage, 141 in the second stage, and 76 in the third stage. The highest percentage (45.0 percent) of silicosis cases was found among sandstone grinders; however, only 20 were examined. The next highest percentage (35.4 percent) of silicosis cases appeared among the 229 casting cleaners, followed in order by the furnace ma sons, with 31.2 percent of 80 workers examined; the iron-ore miners, with 27.3 percent of 959 workers examined; the sandblasters, with 26.7 percent of 15 workers examined; the quartz-mill workers, with 24.6 percent of 65 workers examined; the porcelain workers, with 23.5 percent of 614 workers examined; the founders, with 19.0 percent of 259 workers examined; those employed in shaking out, with 12.5 percent of 24 workers examined; employees other than casting cleaners of casting cleaning plnnts, with 10.5 percent of 86 workers examined; furnace workers in silicon alloy plants, with 8.2 percent of 170 workers exam ined; and zinc and lead miners, with 4.9 percent of 81 workers . exnmined. The Swedish coal mines appear in a much more favorable light than those in Germany, owing to the natural humidity of the mines which prevents formation of much dust. Since 1931, when the rock-dust lung came under the general law compensating industrial diseases, no case of silicosis has been reported in the Swedish coni mines. Of 543 underground drillers in the metal mines of Lapland ex nmined, 215, or 39.6 percent, hnd silicosis. K W n7.FR I.AN I) ^According to the reports received by the Swiss Nntional Cnsunlty Fund (107), the number of cases of silicosis reported for miners had increased from 2 in 1935 to 94 in 1944. The total of all reported cnses of silicosis was 850, of which 367 were miners and 483 workers in other occupations. From January 1 to December 31, 1945, the medical service of the Central Administration (108) has been required to pronounce defi nitely on about 2,500 reports of exnminntions nnd X-rays of insured persons exposed to silicosis and exnmined according to the require ments of the Federnl Council and about 300 reports of registered in sured according to article 65 LAMA (occupations exposed to quartz | dust, excluding working in galleries, tunnels, and in mines), i Of those examined, 112 were declnred disabled by silicosis or sili- i cotuberculosis, nnd 66 were declnred able for siliceous dust-producing ; occupations. ' Up to 1947 nbont 1,400 cnses of silicosis have been determined in I > Switzerland (10!)). \ \ 58 R EVIEW OF LITERATURE ON D U STS TYPES OF DUST INJURIOUS TO HEALTH The relation between dust inhalation and lung disenses was recog nized very enrly, ns indicated by the liternture cited, but it wns also recognized flint certain dusts caused severer symptoms with quicker fatal issue than others. As the symptoms caused by inhalation of cer tain dusts were long delnyed or were nttributed to other causes, such dusts were considered harmless and some even beneficial in the pre vention of lung diseases when inhnled with the more harmful ones. Ancient writers seldom distinguished between the various forms of respiratory diseases but rather referred to a general relntion between lungnlTections nnd dust inhnlntion (34), and no really scientific inves tigations of the workers or the dust were undertaken. Ramazzini, how ever. described the effects on workers of various types of dust produced in such industries ns the hemp and flax industry, silk combing, nnd corn sifting, in addition to mining and similar industries. According to Collis (34), the distinctions, implied or definitely stated, in Rnmnzzini's excellent clinicnl description of the types of respiratory trouble which follow inhalation of different dusts are-- the more notable. I>ecniise even todny pneumoconioses a re pigeonholed In clinicnl touching ns a single entity, ascrllied to exposure to any and every form of Injurious dunl, of wlileli pulmonary fibrosis auras up th e pathological findings and phthisis ttie morbid result. In the decode preceding 1802, when the study of public health wns organized in England (5-i), Groenhow made nn clnbornte statistical inquiry into the influence of occupation on health in connection with lectures on public, health at. St. Thmnns Hospital. Simon, then medical officer to the General Hoard of Health, considered Greenhow's inves tigation so important, that liis report was published by the Hoard, and shortly after when Simon became medical officer to the. Privy Council lie entrusted Groenhow with the dutv of further investigations in the great, industrial centers. The resulting roports were, according to Collis (34), the first example of State medical inspection of factories, and he made the following statement regarding them : Throughout those reports runs ns n them e the Influence of d u st Inhntntlnn In causing pulnmnnry dlsonso, whether among lead minors In Yorkshire, tin miners In Cornwall, needle |Hilnlers In Aloester, cotton operatives In Lancashire, flnx hecklers In Pntely Itrldge. metnl grinders In Birm ingham nnd In Sheffield, oont miners In South Stiiffurdsldre and In South W ales, or stone dresser* In Stroud. Why work so well started was then nllowed to lie dorm ant for so tong, while oilier astiecls of piddle health were being strenuously developed hy medloal offloers of lienlth with Inspectors of nulsnncca appointed for every town and district, reinforced now hy a halallen of tuberculosis officers Is astonishing. As a result of investigations in South African mines and in other mining districts of tlic world so much attontion wns focused on one particular dust--silien--ns the most, harmful encountered in industry (lint most investigators had accepted other dusts as harmless or of n e g lig ib le importance ns health hazards in industry nnd the disease silicosis resulting from breathing silica dust as the only important dust disense. Other dusts, such ns the silicates (asbestos, for ex ample). linve been found nlmost as lmnuful as silica ust, but. the effect on the lungs is somewhat different from that of silica, and the hazard not so widespread. TYPES OF DUST INJURIOUS TO HEALTH f>9 From general underground experience for more than 25 years in coal and metal mines and from an intensive study of dust for 8 years, Harrington (170) concluded that-- Any dust Insoluble In tbe fluids of the respiratory passages ami In sufficiently finely divided form to float In the nlr and be breathed by underground w orkers will ultim ately be harm ful to health If the lust Is In the a ir In large q u a n titie s and la breathed by w orkers for considerable pcrhxls of time. T h is applies to insoluble nonm lnernl as well ns m ineral dusts or m ixtures of them and Includes onl dust or m ixtures of coal and other lusts. T here a re nlso some definitely harm ful mine dusts which are soluble, nnl some dust experts appear to believe th a t the so-called insoluble lusts under certain com lltlons become soluble and are harm ful only when soluble. An outstanding impression gained by Ballantyne (171) from the reports of the International Conference on Silicosis was that silicosis constitutes only one facet of a very Inrge question--the prejudicial effect of dusts in general upon the human subject. Ho concluded that-- It (silicosis) Is only one of several close-related pulm onary affections due to dusts of different kinds. It Is the most im portant of these, but only because It Is the most definitely known and so many workpeople are exposed to the risk. In the case of asbestos lust knowledge regarding the Injurious effects of Inhaling It him advanced so fa r ns to Justify the adoption of legislative m easures analogous to those relating to silicosis. There are many other kinds of dust, however, as to the effects of which, when Inhaled, we have little or no knowledge, and the investigation of which calls fr early attention. Tho report of the Silicosis (Medicnl-Arrancements) Committee is sued in London in 1029 (172) contains the following statem ent: We a re convinced th a t silicosis Is more wltlesprea! than Is generally Indleved and th a t It occurs t> some extent In n number of Industries and occupations where Its presence has not h*en suspected. In 1930 Kettle (12) called attention to the harmfulness of breathing dust: D usts of various klntls occur In the atm osphere In nil p a rts of the w orhl, and the inhalation of tin's* dusts over jierlods <*f years Incvltntdy pnaluces changes In the lungs. Everyone Is fam iliar with the pigmented lung of the city dweller, an exam ple of n pathological change produced by the Inhalation of dust which Is of no clinical im portam e whatever, hut an exaggeration of this condition In the onl m iner causes definite symptoms, and when the Inhaled (lust Is not the relatively harm less carbon, hut me of the much more sin ister posslhtllttei, serious pulm onary changes develop The pneumoconioses h a re receive! less a tten tio n th an they deserve, even In textbooks of medicine and pathology. Ilut to the loctors whose p atients are excised to lusty trades, to those resixmslblc for the conduct of these truth's, ami (o the fn*tory ln s|sv to r pneuitMWnnlosIs Is of great moment In tho report of u study of dust conditions in Germnn industries, published in 19112, Ivochtkcmper and Teleky (*W) stated in tho vipumn w * T he breathing of any died leads t<>Injury of the lungs, If It Is Intensive enough anil contlnuKl long enough. W ith intensive and long-cuntInued Inhalation of dust, entirely q uartz free dust hauls to lung chmigt*s eh arly recognizable In the X-ray picture. The blood vessels apisMir more clearly defined; there are also more num erous and thicker honey comb form ations, hIro lufiltinteil m ottling whleh, however, never shows the very sh a rp delineation and density m usts! by <|tmrU. The subjective sym ptom s re fe ra ble to tin' changes a re slight; then* Is none of tin* lung rigidity c h ara cte ristic of silicosis hut a complication of diseases, eaiHM'lally liroitchhvtnsl* and emphysema. 60 REVIEW OF LITERATURE ON DUSTS I t 1 theoretically poaatble from the report th a t m any of the occnpntlonal dust breathed In Immenae amount* over a very long time lead to change* not recognized by us today. In a discussion of etiology, pathology, and physical signs of silicosis Levey {173) stated : However, a lung filled with dust la a wounded lung and should be considered as subnorm al In It* vital resistance tow ard the onset of dlsense. A lung con taining silica dust hH* a strong predilection toward the onset of tuberculosis. T his susceptibility Is unusual. TERMINOLOGY OF DUST DISEASES The following terminology of dust diseases of the lungs (17i) is now used by most writers on the subject: Pneumoconiosis.--A general term covering all dust diseases of the lungs, fibrous or nonfibrotiR (from Greek pnewnon, lung, and konia, dust). Silicosis.--A fibrosis caused by free silica (or quartz) nnd the bestknown scientifically of the dust diseases of the lungs. Silicatosis.--A type of fibrosis found after exposure to certain min eral dusts and assumed to lie caused by various silicates. I t is distinct from the sharply defined, coarse, nodular fibrosis caused by silica dust. Anthracosis.--A duRt disease of the lungs found in coal m iners; it is ill-defined and is presumed to depend on inorganic dust in coal. The lungs are black. Siderosis.--A term npplied to a fibrosis of the lungs found in metal workers. The condition is ill-delincd. The lungs arc yellow or red from metallic oxides, generally of iron. Asbestosis.--A fibrosis of the lungs with characteristic microscopical stigmata due to breathing asbestos dust, a silicate of magnesium. In his bibliography on silicosis, Caiw.zi ( / / ) called attention to the arbitrary nomenclature that has been applied to dust diseases for centuries. These diseases have been named at various times and by various authors, according to (1) the lesions observed, as fibroid phthisis, lung fibrosis, cirrhosis of the lung, and chronic interstitial pneumonia; according to (S>) the cause, ns dust phthisis, dust fibrosis, dust lung, and dust disease; nnd according to (1) occupation, ns miner's imthisis, collier's lung or phthisiR, miner's lung, g rit fibrosis, gritty phthisis, grinder's rot or lung, grinder's disense, cutter's lung, stonemason's lung of phthisis, millstone maker's phthisis or disease, knnpper's rot., stone hewer's dust lung, rpinrtz lung, nnd phthisis of miters. Some authors instead of phthisis used the term "chalicosU" or "asthma," accompanied hy the occupation. PNEUMOCONIOSIS Tho diseases resulting from inhalation of dus's generated in in dustry during tho progress of certnin processes are now known generically ns pneumoconiosis, having been so named by Zenker, ns men tioned previously. In a brief summary of information regarding certnin of the pneumoconioses other thnn silicosis, Collis (/77i) PN EU M O CO N IO SIS 61 called attention in 1931 to some of the respiratory diseases that may be caused by dust but seldom are recognized ns dust disenses. He clnssed the inorganic dusts ns insoluble, soluble and harmful, and mixed. Under insoluble dusts he mentions that those from certnin materials, such ns bnsic slag and emery, nn oxide of aluminum, are insoluble in the tissues. Inhaled particles fall on the walls of the bronchi and bron chioles, where they are entnngled in secreted mucus and then swept back by ciliary action to be expelled finally in sputum. If the ex posure to dust is excessive over a period of time, nn inflammatory hyperemia of the walls results, with excessive exudation of mucus; finally the process extends beyond physiological elasticity: then de generation and destruction of the ciiinted mucosa occur; microbic invasion follows: and chronic bronchitis is established. T h e process described by C'ollis is a reaction to th e in h a la tio n o f all dusts not ra p id ly nbsorlied; hence, bronchitis stands out ns ch ie f of the dust diseases and d u rin g m iddle life causes m uch recurrent invalidity and incapacity an d , a fte r m iddle life, high death rates. D ust bronchitis cannot be distinguished clinically from b ronchitis due to exposure at hot furnaces, fum es in industry, or severe clim atic conditions; its association w ith d u st inhalation, therefore, lacks recognition. If the dust particles are small enough (5 microns or less) to be drawn into the finer bronchioles and alveoli, which are the seat of attack for pneumoooccij a similar reaction is stimulated, the resist ance of these parts to infection is lowered, and pneumonia results, l 'neumonia is even less recognized ns a dust disease than bronchitis; nevertheless, mortality records of those employed in dusty occupa tions are high. However when fine, particles of insoluble lusts are carried by plmgocyted dust cells from the alveoli into the lymph stream nnd lymph nodes of the lungs they tend to remain there as foreign bodies nnd do not provoke any particular tissue reaction. C 'o llis (75) s a i d t h a t t h e m o s t - s t u d i e d d u s t o f t h e s o l u b l e n n d h n rm fu l d u sts in th is g r o u p is th a t o f silica. T h e d u sts o f silicates follow ; nltlm ugli m an y silicates, such ns fire clay n n d p o tte ry clays, a p p ear to exert little if an y h n rm fu l influence upon the lungs, recent w ork lias show n th a t certnin o th e r silicates, such ns bnsalt an d asbestos, react injuriously on the p u lm o n a ry tissues. T h e reason fo r these differences is not c le ar: but p ro b ab ly it lies in the c o n stitu tio n o f various silicates, the S it) , rad ical being less firmly atta ch e d to the molecule in some instances th an in others. Collis (175) defined nsl>ostosis as n pneumoconiosis that advances to a fatal end without the supervention of any characteristic infection. It is n s im p le d o s t c o n d itio n , just ns is sim plN s ilic o s is ; but it is more distressing in life and more rapid in its progress than silicosis. It c o n tra ^ even more strongly with pulmonary mycosis, which is due to a living infection upon otherwise hen Why lungs. Regarding mixed dusts, C'ollis (175) said tlint, ns long ns any dust, consists of only one sulistmice, its influence can be isolated and studied; but the case is different when more than one substance is present in the dust. Coal dust, which recently 1ms been carefully investigated (/TV?), is taken as nn instance in point. No undue mortality from respiratory sn.vjia m i. 6 ) 62 REVIEW OF LITERATURE ON DU8TS diseases was ncted among coal miners when the coal worked con tained little or no mineral m atter and the miners were not exposed to other dusts, such as those arising from rocks intervening in the coal measures. The miners in the Nottinghamshire coal fields furnish a good example; tho lungs of these mert may be as black as the coal they work, but they remain resilient and free from fibrosis . Gooding (177) stated tuberculosis which accompanies pneumoco niosis often Incks its usual features, and it is probable that more de tailed investigation would revenl tuberculosis m a much greater pro portion of silicotic miners. In discussing the nomenclature of dust diseases Pancoast and Pen dergrass (27) stated that, although silica (SiO) seems to be the active fibrosing agent in most conditions recognized as essentially a pul monary fibrosis, adherence to the general term "pneumoconiosis" still seems advisable. Some other dusts undoubtedly cause a fibrosis directly, and still others may either tend to retard the action of silica, as coal dust and clay, or enhance its action, as alknlies in the mixtures of silica and powdered soap in scouring powders. "Silicosis" is the term much more frequently used, mainly becntiso it is not so un wieldy and usually describes accurately the particular phase of the condition under discussion. "Miners' phthisis" appears in the laws of South Africa but is otherwise an obsolete term generally recognized as implying silicosis or pneumoconiosis. There is now reason to l>elievo that silicates nlso produce considerable fibrosis through their silica content or through a specific action of their own. Pnnconst nnd Pendergrnss (27) stated that the occupational terms are advisable because, certain peculiarities have been attributed to the dusts of those industries^ even though the condition still remains silicosis or pneumoconiosis. For example, in anthracosis (he action of silica seems to tie modified by the coni dust mixed with i t ; more over, coni dust alone may produce a mild fibrosis. Collis and Gilchrist (176), in an investigation of coal trimmers working at the Cardiff docks, discovered tlint inhnlation of large nmounts of coal dust nlone over a period of years produced evidences of mild pneumoconiosis which presented tho same roonlgpiiogrnphic appearances ns silica. I t has been suggested thnt. clay lias a sim ilar effect in protecting the workers in some of the operations in the pottery industry hut not all of them. The term "chalicosis" has been applied in the past to pneumoconiosis of potters. In recent, years certain very unusual features in connection with pneumoconiosis among nsliestos workers have brought the term "pul monary nsliestosis" into active use. According to Ilnldane_(/7.9), evidenco is accumulating constantly that scattered librosis, giving essent inly the same X-ray picture ns early silicosis, is comparatively common as a result of excessive dust inlinla- tion but without accompanying liability to tuberculous infection. However, he stated that this condition should not tie called silicosis; sinco it seems to nrise from excess of any kind of dust, not merely siliento dust, pneumoconiosis seems the most suitable ''nine for it. Silicosis nnd nsbestosis are forms of pneumoconioMs that have Ipen clearly defined clinically; the other forms of pneumoconiosis, such ns anthracosis, siderosis, and many otliors, still luck complete definition. SILICO SIS 63 Although considerable radiographic evidence has been accumulated on these latter types of occupational-dust exposures, corroboratory evidence has not oeen deduced on all of them from correlations of Xray findings with pathological anatomy, chemical examination of tissues, anci studies of the industrial environment {179). The condition of the lungs giving a roentgen appearance similar to that of silicosis but caused oy inhaling certain nonsiliceous dusts has been called (180) "benign''pneumoconiosis. Pendergrass and Leopold (180) found it impossible to differentiate the roentgen appearnnce of nodulation of silicosis or the pseudonodulntion of benign pneumoconio sis from the shadows cast by many pulmonnry diseases unassociated with the inhalation of dust. The diagnosis.of the pulmonary lesions in such circumstances depends upon the collaboration of the internist-the roentgenologist and the laboratory technician. Pendergrass and Leo pold (180) conclude that-- To differentiate Ivetween silicosis and benign pneumoconiosis one m ust h a re a detailed knowledge of the occupational history, the environm ental conditions of the worker nnd the precise Information regarding the nature, concentration and particle Rlze of the dust to which he Is exposed. A dvanc'd silicosis Is usually disabling and, when complicated w ith tuberculosis, It In fatal. Advanced nsbestosls produces disability nnd ultim ately may Induce death from cardiac failure. llenlgu pneumoconiosis produces nothing hut shadows cast on a roentgenogram. IVe owe to (lie worker, to tatair nnd to Industry our utm ost efforts to distinguish between these conditions. Tho first case of lung cavity due to necrosis in n caso of graphite imenmoconiosis was observed m 1940 by Dtmner and n 1939 a worker aged 04. who bad been working with Hagnnll graphite (181). for 17 years, was pronounced tuoerculnr and sent, to a sanatorium. His spu tum was alwnys free of tulierclo bacilli. lie did not return to work with graphite but was able to do light work for 6 years. When first seen by the authors in 1944, the radiologic aspects of his chest were unchanged from those revealed on the films taken in and since 1939; they showed massive opacity in the right upper zone, similar, but fninter. opacity in the left upjier zone, nnd a rounded opneity the size of a golf lmll superimposed on the lower p art of the left root shadow. In April 1945 lie suddenly brought up large amounts of black material containing about 0.07 percent carbon. The size of most of tho particles was 5 microns or less, with only a few over 10 microns. Silica was not detected. SILICOSIS DEFINITION Rovida (1844-77), the first to mention silicosis in a publication (IS~), used the term in 1871 in describing "a ense of silicosis of the lungs with chemical analysis." According to Onrozzi (11), however, Rovida stated in his article that-- The nnme comes promised for (tie first tim e by Achilles Vlseontl, prosector In the OnimhIiiIc Mngglore of Milan. (A "prosector" Is an an ato m ist wlio imikes dissections for nnntomlral demonstration.) ) ) 64 REVIEW OF LITERATURE ON DUSTS At one time it wns believed thnt several substnnees could produce the lung condition called "silicosis," but, it is now agreed rather gen erally that all types of dust fibrosis of the lungs are due to some form of the clement silicon (183). The recognition that silicon was the important element in pneumoconiosis was a great step forward but, according to a statement by Kettle (183), the teaching that only one form of silicon--the oxide silica--can produce the disease was accepted too readily. The realization in recent years thnt asbestos can produce serious pulmonary fibrosis should have been a warning th at this view wns too restricted, ns borne out by the work of Jones on seriate. However, the following definition adopted at the International Sili cosis Conference in South Africa in 1930 (184) 3 still accepted: Silicosis Is a patlioloRlcnl condition of the lungs due to Inhalation of silicon dioxide. It enn tie produced experim entally In animals. SYMPTOMS Inhalation of silica dust is seldom accompanied by evidences of irritation and if free, from other irritating dusts may be breathed without arousing suspicion of its dangerous character (119). The following discussion of symptoms of silicosis is based on the findings of 9,CCS! examinations of 7,722 mine employoes at the Picher Clinic of the Ilureau of Mines in 1928 (99). Dyspnea.--Shortness of breath has been generally recognized as the cardinal symptom of silicosis. Dyspnea accompanies exertion in the earlier stages of silicosis ami increases progressively until, in the later stages, it often prevents any labor. The apparent distress on exertion, frequently noted in silicot ics who deny shortness of breath, seems out of proportion to the very slight rise in pulse rate taken 2 minutes after exertion. Pain in chest.--Chest pains were admitted frequently, generally anteriorly, and more often on one side only. In many instances the pains seemed of a redox character. In nearly all cases they were vague and flitting and did not seem to interfere with manual labor. Pains in the shoulder and possibly in the posterior part of the chest probably are considered by many of the men as "rneumntic" ; such pains seem partly responsible for the largo number of complaints of rheumntism. Cough.--This symptom is frequently admitted in silicosis and gen erally is unproductive. Expectoration.--This symptom was admitted infi-equontly. When present in uncomplicated silicosis the sputum usunlly is clear or has a bluish tinge and is of a viscid, tenacious consistence, very difficult to cough up. The color of expectoration may be due to the color of rock mined. Hemoptysis.--Hemoptysis appeared to be more common among sili cot ics than was cx|>octed. In some instances, particularly in seeondns well os in third-stage silicosis, fibrotic areas may mask n tuliereulous lesion which remains unrecognized until it becomes an open lesion, when tho sputum will show the tubercle bacilli or '. >morrliage will call attention to the true condition. ) SILICOSIS 65 Night sweat.--I t seems probable that some of the admitted night sweats were not true pathological night sweats, but tl.e relative^' high incidence in the silicotic groups appears difficult to explain except on the assumption that at the time of the sweats, some active infectious process wns in progress. This could be due to tuberculosis; it may have been due to a pyogenic infection or malaria, as 33 percent of the silicotics examined gave a history of previous attacks of malaria. Los of strength.--The loss of strength admitted by silicotics in most instances probably was connected with their dyspnea on exertion and was due. to respiratory insufficiency. This probability is strengthened by the small number of silicotics with poor physical development (4 of a total of l,0f>2). Gastrointestinal symptoms.--These symptoms were pronounced in the inore-advnnced cases, and loss of appetite wns admitted. Other pronounced symptoms in advanced cases of silicosis were constipation, epigastric discomfort, and other vague complnints which the men termed "indigestion." The causes of the gastrointestinal symptoms were not ascertained. Sayers (JS.5) summarizes the clinical findings in silicosis as follows : The practically constant clinical signs a re: A certain lack of elasticity of the chest wnll during the movement* of respiration, together with a somewhat re duced air entry, anil a i lm rncterlstlc alteration of the Inspiratory m urm ur from the normal "vealculnr" clinractor to a higher-pitched or "harahened", "thinned", ami commonly somewhat shortened typo, the expiratory murmur, although some what prolonged, remaining fa in ter than the Inspiratory. Tlila type of hreath sound Is very characteristic with some modifications, of silicosis In all Ita stages and, th is clinical sign has also the significant clm rncter of more or less complete rogenernll7.ntlon. i t Is first noticeable a t the anterior, lateral, and liasal regions. In the m inority of enses, however, the hreath sounds may he sim ply diminished, hut hreath sounds which a rc aimpl.v dim inished or which, on the other linnd, are merely somewhat loader or m ore "pronounced-' than norm al a re not spoolnlly characteristic of silicosis. Usually there nre no nccnmpaidnients, but n stray rhorehus may be henrd here and there. T his complex of physical signs Is alm ost constantly preaent In enses of a alight degree of "sim ple" silicosis. T lie cough mtiy lie put down to the coincident bronchitis and hronchlolltla, the recurrent jmlua to slight lntcrcurrent local pleurisies. PATHOLOGY According to l'anconst (7) the pathological features of pneu moconiosis are: (a) Enl rnnee of dust; (b) "dust cell" or inncropnago; (r) entrance of the dust cell into the lymphatic system of the lungs as a carrier of silica or other particles; (</) influence of the deposited silica in the production of fibrous tissue; (e) action of silica; (f) elim ination of dust; and (<7) predisposition of tho fibrotic aim silicasaturated lung to respiratory infections, especially tuberculosis. The hWg, as descriiied by Gardner (JUS) is an organ that permits interchange of gas between the blood and tho external air. As it is in free communication with the exterior, it is more or less exposed to tho action of atmospheric impurities, both particulate and gaseous. Certain mechanisms protect the lungs from the accumulation of such foreign particles. The nose, through which tho respiratory tract opens to tho surface of tho body, is guarded by a coarse filter of hair. 66 R EVIEW OF LIT ER A T U R E ON D USTS Behind this is a series of tortuous passages with moist walls which trnp many smaller particles. In addition, the nasal cavities nnd the remaining portions of the upper respiratory tract, the pharynx, the trachea, and the bronchi are lined by cells covered with minute vibra tory hairs, and cilia. Wavelike vibrations of these hairs tend to carry particles lodging on their surface away from the lungs nnd back to ward the surface. Particles that succeed in pnssing these barriers nnd penetrate to the terminal air spaces of the lungs are ingested by wandering scavenger cells or phagocytes, which come from the partitions between the spaces for the purpose. These cells move independently nnd tend to carry the foreign particles out of the air spaces into a si>ecinl drainage system known ns the lymphatics. The lymphatics are minute vessels which drain into sedimenting basins known ns lymph nodes. They are situated nlong the course of the vessels nnd bronchi and at the root of the lungs where the trachea divides into the two main bronchi. I'or ordinary amounts of atmospheric pollution, these protective mechnnisms nre adequate to prevent significant accumulation of foreign par ticles in the functional part of the lungs. If a person continues to work in a very dusty atmosphere for long periods his protective devices cannot cope with the situation, the mechanisms themselves ere dam aged, and the dust particles collect where the air should be (18(1). BcltRnd King (187) visunliz.ethe sequence of events as phagocytosis, inflammatory clvan^e, organization, nnd rethulin fibrosis. Each is characterized by a distinctive morphological feature: (a) Phagocytosis by the konioplmge; (b) inflammation by fibrin; (c) orgnnizntion by the fibrocyto or dictyocytc; and (d ) fibrosis by rcticulin. One im portant cellulnr element, the foreign-liody giant cell, is often present throughout all four stnges. All dust cells are phagoc.ytoscd in the parenchyma of the lung. The principal cell involved in this activity is a large wandering, amebic, mononuclear cell which Bolt and King (187) have designated as the koniophage but. which is also known ns dust cell, endothelial cell, macrophage, or histiocyte. Particles up to 10 microns in size are dealt with almost entirely by this type of cell. The foreign-body giant cell usually takes care of the lnrgor particles. According to Kasten (188), coal dust is phagocytized more quickly and more completely than stone dust. Qunrtz causes violent changes, nnd vacuoles dovelop. Mature vacuoles unite to form one largo one, filling tho complete cell at Inst. The smaller the quartz pnrticles, the more quickly nnd completely tho process develops. In contrast to this, colls tlint have taken up coal dust do not show vacuole formation in such a degree but do show fatty degeneration. Kasten (188) con cluded that tho malignity of qunrtz is caused by its clicmicophysical effects on the tissues ("surfneo effect" !. Definite inflammatory change is indicated bv tho presence of extrn- vnsaled fibrin. Commonly, it is mingled with tho dust-lnden konio- phnges in small shreddy deposits and nccomjiunied by a little fluid exudate nnd occnsionnl granulocytes. This initial inflammation plays nn important, pnrt in determining subsequent changes. It is somewhat unpredictable nnd capricious in incidence. The quality of tlie dust hns something to do with it. Tho incidence of initial inflammatory SILICO SIS 67 change is roughly proportional to the silica content of the dust nnd roughly inversely proportional to the coal content. Exceptions to both these rules are frequent (AW). According to Sinison (AS.9), if the first line of defense is passed and particulate matter reaches the nlveoli, the cells lining the alveoli are stimulated to activity. They swell, become detached from the walls, and develop an active phagocvtic function. The particles are phngocyted and are then carried in one of two directions; some of the phngocites, now laden with dust, pass to terminnl bronchioles, whence they may be removed in the sputum; others pass into the walls of the vestibules nnd terminal bronchioles. In time, large numbers of dust laden cells accumulate and onuse condensation of the tissues about the entrance to the primary unit. During the period of excessive dust inhalation and possibly for n short-time afterward, dust cells are con tinually reaching and entering the areas of condensed tissue nt the entrance to the primary unit; others lenve the condensed areas and enter the regional lymphatic vessels, along which they pass to the minute masses of lymphoid tissue which lie between branches of the pulmonary artery and the adjacent bronchioles, vestibules, ami atria. Dust cells stimulate the lymphoid tissue and cause it to become hyper plastic. With continued arrival nnd accumulation of dust cells in the lymphoid masses, more or less well-defined aggregations are formed. The site of an aggregation can retnin oidy a limited number of dust cells, so that with new arrivals an overflow results. The cells com prising the overflow and those thnt have escaped arrest pass onward in the peribronchial and perivascular lymphatic vessels, finally being trapped in the lymph nodes nt the root of the lung. In silicosis these lymph nodes are the first sites to show fibrosis. As late ns 15)47, l 'olicard (190) stnted thnt the exnct mechanism of this accumulation nnd its pliysiopnthologic consequences are not well known, although the phenomenon of the accumulation of dusts in the connective tissues of the pulmonary arteries and the bronchi is constant and indisputable. lie claims that, in a normal lung, the dust cells are rapidly and easily carried away by the lymphatics during the periods of oeginning pneumoconiosis. There is never any permanent accumulation of dust in the arterial or bronchial tissues. There is an accumulation of dust only when conditions have become abnormal, especially if thero is stasis of the lymph--for example, ns a result of ganglion lesions down stream. Tho lymphatic current is then slowed nnd the dust cells im mobilized. l!y accumulating in tho lymphatics of the tissues, the dust cells obstruct their o|ienings, ns vast, ns they are. The course of tho lymph, already slowed before the accumulation, is impeded still more, j>or- hnps arrested completely. From this arises an important cotiseouence--edema of the tissues. Edema favors fibrosis. It disturbs tlie functioning of the tissues of the pulmonary lobes by making them rigid nnd abolishing their elasticity, ro lica ra {190) thinks that this edematious process is not well-known nnd deserves more attention. At certain points the tissues are fibrosed. Thero is r u increase in their collagenous and reticulnr deposits (precollagenous). This fi brosis is irregular. A segment of about 1 to 3 mm. npponrs fibrosed, 68 REVIEW OF LITERATURE ON D U STS with two apparently normal segments of tissue interposed between. This irregular disposition of the fibrosis in a tissue where the accumu lation of dust on the contrary seems regular speaks against a direct librosing action of mineral particles. I f tliey intervene in the processes it is in indirect fashion,still notspecified. I'olicard (100) refers to the British statement that fibrosis of the pneumoconioses is due to fibrils of the reticulum. In fact, the large fillers show the reactions of the collagens and the finer ones those of the reticulum. The latter are always abundant but appear to be simply collagenous fibrils in the process of formation?that is; "precollagenous'' fibrils. In nil the cases it cannot be a question of fibrosis exclusively due to the fibrils of the reticulum. Another fact to which Policnrd (190) calls attention as little known is the calcareous (and probably plioeplio-ealcareous) impregnation of the tissues hnving accumulated mineral dusts. This impregnation is revealed by micro-incineration. This is not a calcification. In par ticular, it does not increase the hardness of the tissue. The lime is on this level, not in the solid and crystalline form, consequently rigid and hard, but in the moleculnr form combined in protein complexes. The dist met ion is essential. Policnrd (190) states that one consequence of this impregnation is important for medicine, that a normr' ---- '------ ` ~ ' or silica dust also is transparent. docs not give any image on the ra lecn impregnate! by lime, the radio-opaque lime causes the tissue to become opaque, which leads to radiographic images. In particular, the aspect called "reticulation" seems to have to be connected with calcnreons impregnation of sclerosed and hypertrophed tissues. The mechanism of this impregnation has not bwn determined but it un doubtedly exists. I f inhalation of injurious dust other than silica--for example, asbestos dust-- is continued over a long period or over a shorter period when the concentration of dust is great, a diffuse, cellular fibrosis develops in the walls of the bronchioles, vestibules, and atria. The fibrosis tends to extend locally, involving the supporting connective tissue of the ndjacent blood vessels and to some extent the walls of tlie alveoli in the immediate neighborhood. There is usually desqua mation of the epithelial lining of bronchioles and vestibles, ofton with out evidenoo of a definite exiulnte. In very advanced cases the fibrosis may extend to tho septa, to the supporting tissues of the bronchi and larger blo<xl v>ssels, and to the atveolnr walls. Even in these coses fibrosis is localized to tho supporting tissue about the entrance to the primary unit. I t may ndvnnco to such an extent that tho bronchioles bccomo'constrictc!, some! imes retaining tlioir circular outline in cross section and sometimes being reduced to mere slitlike openings. Rounded nodules of cellular character occasionally are seen, but the dense hyaline typo of nodule usunlly is absent. Dust containing only a smnll percentage of silica also may produco tlieso changes, and the liability to generalized fibrosis is greater when a low-grado type of infection (not necessarily of tuberculous origin) complicates tho dust offoct. SILICO SIS G9 Simson (189) said these changes appeared to be primary lesions caused by inhalation of any injurious dust, but when most of the inhaled particles are composed of or contain silica a specific and localized type of fibrosis--the silicotic islet--also develops. The first evidence o f the specific and localized lesion, which Simson (189) termed the "silicotic islet", is seen in the aggregation of dust cells that probably represents the site of the lymphoid mass. A smnll. round area of fibroblasts appears in the center of an aggregation: on fu rth er development a central core of dense, fibrous tissue is formed. I t often becomes hyaline in character and in larger and older nodules takes on a whorled arrangement. A fully formed, single silicotic islet consists of a central mnss of dense, hyaline fibrosis arranged in whorls and surrounded by a comparatively nnrrow zone of cellular fibrosis in concentric laminae. Scattered through this mass, lying between connective tissue cells and fibrils, are scanty, large and small round cells and a little particulate matter. A deposit of fat may be seen also in suitably stained sections, the degree varying with the age of the nodule. The early fibrotic nodule thus formed is surrounded by numerous dust cells. The growth of the silicotic islet, continues by successive new nrrivuls of dust cells and subsequent extension of tlie fibrosis at the periphery of the fibrotic nodule. Apart from the individual single or composite palpable islet, nonin feet ivo silicosis may appear as a "massive" type of fibrosis. Seen microscopically, such lesions comprise numerous contiguous single and composite islets. The fibrosis is of the same character ns that of the single islet.; there is no evidenco of brenking down. The intervening nlveolnr tissue is much compressed and collapsed, but there is no evidence of inflammatory infiltration or of definite m atting together of the indi vidual islets. As a rule, the larger blood vessels are not constricted. These changes, according to Goodrich (120), mnke the lungs less elastic, increase their hulk, mnke nerntioti of the blood less efficient, nnd decrease circulation through the lungs. As a result, a more vigor ous respiratory elTort is necessary to supply the blood with nil adequate amount of oxygen nnd to remove the accumulated carbon dioxide in the blood. An increase in inspiratory effect is needed to create greater negative p rassure within the chest in order to draw the same nmount of air into the less elnstic lungs, and an incrense in the normal tidnl volume is needed because of the decreased aeration of the damaged alveolar structures and the impaired circulation through these alveoli. As the volume of the lungs increases from the continuing deposit of silica anil the increasing amount, of fibrous tissue, the chest gradually is hold and later fixed in a position of partial inspiration, and breath ing heroines more and more diaphragmatic. Even diaphragmatic breathing eventually becomes less efficient because of the usual develop ment qf a basal pleurisy which causes the inelastic lungs to adhere to the upper surface of the diaphragm. Secondary infection with bac teria may cause still greater lung damage. Chronic bronchitis or bronchiectasis may bo caused by streptococcus, staphylococcus, pneu mococcus, or other pyogenic organisms, ns evidenced by investigations of file United States I'uhlie Health Service (191) oil the development of pulmonary infect ions in pneumoconiosis. The results of the bactri ologie nnd experimental study show that-- ) ) 70 r ev iew of liter a tu r e on dusts In general, the slllrotle lung Ir more susceptible to bacterial Infection than the nvernge lung. T his In probably due to the Irritatio n of tbe reaplrntory tissues by the Inhaled diiRt pnrtleles which weakens the mucous m em branes nnd renders them susceptible to Infection. The toxic Influence of certain in organic diista upon tbe tissues may be a contributing factor. The relation of tuberculosis to pneumoconiosis has been studied to a consider able extent, but com paratively IIl He w ork has been done in connection w ith other Infectious processes of the lung, for example, pneumonia, lung abscess, bronchlectnals, nnd Influenza. An Investigation was made of these conditions, both bacteriologlcally ami experim entally, w ith the view of obtaining a better understanding of the predisposition to, and the mechanism of. Infection of the lung In certain dusty trades. BroncblectnslR, lung abscess, and gnngrene occur frequently In hard-rock miners. It has been definitely established th at aerobic, pathogenic bncterla, nnd certain fungi are responsible for these conditions, but the lilgh percentage of cnees in which the anaerobic mlcrulies of the mouth and throat have been reported would suggest thnt they nt least particip ate In tbe etiology of the diseases. According to Tillson (192), many of the phagocytes of the hings, when carrying mineral particles, become trapped in the lymph chan nels and nodes nnd therefore nre not eliminated. Those free in the blood stream are charged positively at the hydrogen-ion concenfration of the blood nnd move to the enthode in an electric field. Bacteria carry a negative chnrgo and therefore are attracted to the phagocytes, are ndsorbed, nnd then ultimately absorbed. The agglomeration of bacteria increases the efficiency of this process, as the largo phagocyte cell can dispose of mnny bncteria in one contact. This clumping of bacteria depends upon the plasma salts being at a high enough con centration; otherwise, bacterial absorption becomes a slow process. Silicosis is a progressive disense. I f enough silica has been in haled to initiate nodule formation ench focus continues to enlarge until a stnto of equilibrium is established. Nodules not visible by X-ray when a man leaves the silica industry may incrcnso enough in size to lie rendily delectable some years Inter. Tho pr< gression of tbe process is favored nnd accelerated by the development of pulmonary Infection (186). In fact, many pathologists doubt whether the fibrosis of the lungs that constitutes the essential pathological nature of silicosis ever arises independently of a primary infections process (193). Rist, Mnyel, nnd Donbrow (19/t), after studying the question from the medicolegal point of view, wore convinced that silicosis can not dovelopother than in persons alrcndy infected with the tuberculous virus and hence refuse to regard silicosis ns a true occupational disease. Attentive and long-pursued clinical observation of ensos of pul monary fibrosis led Croizior, Martin, and Polieard (196) to doubt the practical existence of an essentially pure silicosis. They cited as clinical anatomopathologic proof the fact that, almost, alwavs tuber cular infection intervenes in cases of silicosis. They considered the term "silicotuberculosis" very oxnct for expressing the combination of tiilierculosis nnd silicosis. Their position on this subject was as follows: The question hns Iveen posed ns to w hether in this Instance It I" the slllcn thnt lx*Ktua or Indeed Ihe tuberrwlosla. In our opinion the prim ary Intervention of tho tuberculosis appears probable, The fibroses thnt we hnve observed represent ImclUosIs modified by tbe allien more th an tubercubirlred silicoses. T he fact thnt m iners have pnaaetl 10, 20, nnd moro years In Die siliceous dust a n d havo ) SILICO SIS 71 rem ain ed free of pulmonary silicosis la proof th a t silica alone cannot create these fibroses In a norm al lung-. According to Gardner [196), only a limited number of individuals ever contract pure silicosis. Most of the hazardous occupations in volve exposure to mixed dusts, and the pulmonary process that de velops consequently is a silicosis modified by other less-active constituents. 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 silicotic reaction with n more or less typical localization in the upper part of the lungs. Such cnses may exhibit none of the characteristic symptoms of tuberculous intoxication for many years and often are discovered only in routine roentgenogranhic examinations of large groups of active employees. Ultimately these men develop symptoms, expectorate tubercle bacilli, and finally die of tuberculosis, but the course of their disease is protracted. There are still others whose roentgenograms show so much evidence of tuberculosis that the char acteristic features of silicosis are obscured. Nevertheless, they have long been exposed to dust, and p< st mortem examination will reveal the nodular fibrosis produced by silica. Like those of the preceding group, these cases run a definitely chronic course and may not die of their infection until the fifth or sixth decade. Finally, there is an other group, with well-developed nodular silicosis, whose members apparently have never had a tuoerculous infection. Such men become infected, develop a rapidly progressive tuberculosis, and die within 0 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 nt autopsy (166). Gardner claimed (166) there is no difficulty in demonstrating that silica produces n reaction in the body specifically favoring m ultipli cation of tubercle bacilli. Kettle infected a'definite quantity of lino silicn particles beneath tho skin of one flank of a white inouso and in the opposite flank the same quantity of nlmninum oxide particles. A large dose of tubercle bncilli 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 days large masses of them will bo found at the site of the injected silica. Tlie bacilli are no more numerous whore the alumina particles have localized than in any other part of the body. Apparently the reaction induced by the silicn produces a favorable medium for the growth of these bacteria, but they disappear later and may be very hard to find. The snino seems to be true of the sputa of men with silicosis and tulierculosis. Gardner (1S6) reiterntod that only silica and a limited number of the silicates nre known to produce definite and serious pulmonary damage. In the enso of silicn, this is associated with specific indispo sition to tulierculosis and pneumonia. O f the silicates, asbestos is definitely recognized ns a cause of pulmonary fibrosis. Its importance in predisposing to tuberculosis is not yet settled. Apparently the "specific indisposition to tuberculosis" mentioned by Gardner is not always present in silicotics; Gudjonsson (197) found ) ) 72 REVIEW OF LITERATURE ON D USTS tlmt tuberculosis was rather rare nmong granite and sandstone workers in Denmark; of c>0 workers with silicosis, 4 had old calcareous foci, ami none had active tuberculosis as far as could be determined by X-ray; 1C of 218 workers without silicosis showed old tuberculous processes, indicating that tuberculosis is equally frequent in both groups. He stated: Tills result Is In accordance w ith results from e a rlie r Investigations regarding silicosis In this country, thnt Is, tlm t tuberculosis Is no m ore frequent nmong those stifTcrlng from silicosis than among those not so nlTIIcted ; according to this, tuber culosis m ight scorn to hnvo no direct relation to silicosis. T h is finding Is ill contradiction with many Investigations from other countries, but It is none the less n fact. A tthe International Conference on Silicosis (181/) it was agreed that the microscopic pnthologicnl changes that may be produced by the prolonged inhalation of silica dust are: (a ) The development of n condition designated In South A frica ns a dry bronchiolitis, characterized by nn accum ulation of dust-filled phagocytes In or In relation to the tcrinlnnl bronchioles, w ith possibly some desquam ation of tlielr epithelium. (ft) The ncciumilnthm of diist-contnlnlng phagocytes about nnd In the Intrnpulmonnry lymphoid tissue nnd their transportation through the lymphatics Into tlm t r n c h e o h r o i i c h 'nl lymph nodes. (T he conditions described above under (n) nnd (ft) do not constitute tbe disease silicosis.) (c) The gradual dcvcloisncnt of fibrous tissue within such accum ulations of p h a g o c y te s and the formation of clmrncterlsHc nodules of hyaline fibrous tissue (d) Iregenerative chnnges In these foci. (c) The hynllne nodules Increase In sire by extension of tlielr jicrlplicry. Coalescence of ndjacent nodules takes place and brings about Involvement of fu rth e r area s of the lung. (The conditions described under (c ), (<!), niul (c) constitute ttie disease silicosis.) Microscopically, the changes observed in silicosis nro : ( ) I n fftc n u l l / nfiiffc.--A variable numlicr of palpable pearly.w hite nodules up to 2 o r 3 mm. In diam eter on the pleural surface of the lung. On sisdlon, the cut surface of the lung Is stgdded with pigmented foci, widely scattered, a mod e rate pro|sirtlnn of which nrc only Just pnlpablc. T he tracheobronchial lymph nodes are slightly enlarged nnd deeply pigmented and may exhibit foci of fibrous Induration. (ft) h i t l e r utt ip r .--T he fllirotlc nodules a re Increased In num ber, sire, nnd density, and conlcscence of these inny lie found. T he iMirtlon of the lung lietwpen the fllirotlc nodule* may lie cinphysoiantmis. The tracheobronchial lymph nodes may tie sm aller In sire than those seen In the early stage nnd a re fibrosed. It was also agreed that the presence of tuberculous infection usually modifies the pnthologicnl nppearnnee, and special attention wns drawn to the following three types: (a ) In which the picture of silicosis above described m ay Is* little. If a t nil, modified, hut In which only a biological test can dem onstrate th e present of II tubcrrutOMls. (ft) la which the coexistence of silicosis nnd typlcnl tulierculosls lesions Is Cosily m -o g n lrn b b '. (c) In which the presence of tulierculosls Is easily recognizable, hut the ex istence of slllcosl 1 la more difficult to determine. Ill m asslre silicosis cardiac hypertrophy and subsequent dilatation may oceur. In silicosis with Infecllrc processes cardiac changes may also occur. No evidence waa adduced In regard to Involvement of kidney or liver. licit nnd King {187) presented, ns n result of their experimental studies on chronic pulmonnry disease in South Wnlcs coal tniners; the following criteria ns n basis for judging the dust effect in the animal ) SILICO SIS 73 lung: (1) Initial inflammatory results; (2) effective retention of dust; (3) connective tissue reaction ; (4) density of reticulin fibrosis; and (5) distribution of lesions. A summary of their detailed explanation of these criteria follows: (1) Excluding: complicating factors, initial inflammation is indica tive of an immediate irritant action on the part, of the dust. It is im portant also ns the determinant of the type of organization to follow and therefore has n considerable influence on the end result, Except in a few cases, probably complicated by infection, the initial reaction showed no great fluctuations in intensity. No accurate means were available for assessing the extent or severity of inflammation in the animals surviving the initial reaction (and this includes the great majority). (2) Effective retention is defined arbitrarily ns permanent storage of dust in the fixed tissues of the lung, in contradistinction to casual retention, in which the dust is lodged in potentially mobile, loose-lying cells without engaging the fixed tissues. Effective retention is brought about only when (lust deposits are overrun and secured by connective tissue, a process which is conveniently referred to ns organization of tho dust. (3) Connective tissue reaction. Organization of dust deposits pro ceeds in one of two ways, or sometimes ns n mixture of both : (a) As a foreign-body reaction, or (b) ns an organization of intlammatory exu date hereafter referred to by tho authors ns ucarnification". Accord ing to which of these characterizes tho reaction, a dust is classified ns of less or greater pathogenicity. (4) Reticulin fibrosis, as opposed to collagen fibrosis, measured in terms of reticulin fibrils, constitutes the most important single cri terion of pnthogenicity. Reticulnr tissue is the histological basis of coni mineis' pneumoconiosis and it assumes a similarly fundamental role in experimental pneumoconiosis, thereby affording a significant basis of comparison between the two. Whether in iiiiinmls or in man, the density of reticulin reaction pro duced by any given mineral dust is tho liest available histological index of its chronic liarinfulness. (b) Distribution of lesions provides a further guide to patho genicity. The less noxious dusts, producing only the simplest of foreign-body reactions, tend to be dispersed into smaller and smaller aggregations, which become more and more widespread as time goes on. This process may be regarded as n form of resolution, by virtue of which the foreign material is lilted into tho structure of (lie lung, presumably in such n wa v as to produce a minimum of embarrassment to respiratory function. More, harmful dusts, on the other hand, tend to retain a nodular distribution, and sometimes coalescence is carried to the point of producing large continent lesions. Coalescence mny be evidenc<vof an inflninmntory complication--for example, pneumonia. Fisher (/OS) has outlined rnther clearly tho process of acquiring pneumoconiosis as follows: Wlien brentlilnc tnkes place In an atm osphere rotitnlnliiK an abnorm al iptnntlty of lust, a certain amount of this (lust Is filtered off by the nose; much of tbo o s nmlndor, ns the a ir pnssis down the wlmlpliie nnd bronchial tula's. settles on them, while some may reach the term inal nlr-saes. The laoncldut luls's. In ttoprocess of hranchlna. become more ant. more narrow so (hat It Is only the finest ) ) 74 REVIEW OF LITERATURE ON DUSTS dust which reaches the air-sacs (alveoli) of the lung. The Inner p a rt of the bronchial tubes Is provided with a lining of tiny flngerllke projections (ciliated epithelium) which bend over with rapid whlpllke movements, the whole layer acting like nn ever-moving conveyor to help to carry the dust cells mixed with mucus upw ards tow ards the throat. By "dust cells" Is m eant scavenger cells or "phagocytes" as they a re called. These scavenger -ells take up the dust which Impinges on the w alls of the air-sacs (alveoli). The dust laden cells may either (a) return to the bronchial tubes, (6) m igrate along the supporting fibrous frnmework of the lung and lymphatic channels, or (c) stay In the lohulesor air-sacs. In ord er to avoid dust accum ulation In the lung, the rnte of ridding the lung of dust must be grenter than the rnte of dust entry. In the ordinary conditions of life this Is so ; It Is only when working conditions expose the Individual to abnormal concentrations of dust over prolonged periods that the rate of elim ina tion falls behind the rnte of entry and pneumoconiosis develops. It Is generally nccepted that the lungs cannot rid themselves of all kinds of dust with (spinl ease. In the case of silica, a larg e r proportion of the dust which Is breathed Into the lungs seems to stay there than ap|ears to be the case with other dusts. Thus a com paratively sm all dally exposure may, In time, accum ulate sufficiently to bring about the condition of sim ple silicosis. The silica du st tends to be held up In the lobules and a l'e o ll, probably In relntlon to the lymphntlc system of the lung, and this Is evidenced as small hard lumps symmetrically dotted about the lung T his condition Is known ns nodulntlon and the nodules, ns they a re called, show, when cut across, n concentric formation. These flbrotlc nodules, with nn Increase lii the fibrous tissue In th eir neighborhood, destroy the elastic quality of the lung, and this, together with other factors, accounts for the breathlessness which Is the m ost prom inent and constant symptom of the disease. At this point I m ust bring In the w ord emphysema. When spenklng of slllcosla or pneumoconiosis tills term nienns the unnnturnl distention and rupture of nlr-sncs of the lungs. The nlr-sncs. having lost th eir elasticity, do not expand and contract normally. They Increase In size and the dividing w alls rupture, forming larger distended areas and lung ventilation Is lessened. T he form ation of hard sm all nodules Is characteristic of simple silicosis, but before the nodules are clearly formed there usunlly develops a general Incrense of fibrous tissue In the lung and to this Is given the name "nrliortsntlon." As one w riter put It, "first you hnve the tree with nnked brnnches, then berries nppenr on the branches." This brings up to the condition of pneumoconiosis among coni m iners cnlled " rotlculntlon." Retlculntlon Is the term given to an X-ray appearance which usunlly shows a line nncl evenly distributed network of shadows. The network Is finer than th a t of nrborlsntlnn. T he question often discussed Is w hether "retlculntlon" In the coal m iner In sim ply n precursor of a nodular condition ns In nrhorlsntlon In the Itnnd m iner or nn en tity III Itself. We need not pursue the m atter here except to note the Important fact that before the coming Into operation of the Coal M ining In d u stry (rnenniocnnlosls) Compensation Scheme, UMtl, com|>ensatlon would not lie paid If retlculntlon only existed and the nodules were absent. STAGES Tlio Miners' Phthisis Act of 1925 of the Union of South Africn {]!)!)) defined silicosis ns follows: For the purposes of th is Act . . . the expression '`silicosis'' shall mean silicosis of the lungs. A person shall, for the purposes of this Act, be deemed to have or to hove had silicosis (a ) In the ante-prim ary sfopc, when It Is found by the B ureau th a t the earliest detectable specific physical signs of silicosis are or have been present; w hether or not capacity for work Is or hns lieen Impaired by such silicosis; (b ) In the prim ary tape, when It Ib found by the lturenu th a t definite and specific physical signs of silicosis are or hnve been present, and thnt capacity for work Is or hns been Impaired hy th n t disease, though not seriously and perm anently; (c) In the ccondnry fopc. when It Is found hy the Bureau th n t definite nnd specific physical signs of silicosis are or have been present, nnd thnt cnpnclty SILICO SIS 75 for work Ir or has boon seriously nnd perm anently Im paired by thnt disease, though not seriously, and when It Is found by the B ureau th n t tuberculosis Is or has been present. Later, in view of the greatly altered aspect of the disease in South Africa (200), it became necessary to recognize additional groups of cases. At the meeting of the First International Conference on Sili cosis at Johannesburg in August 1930, the three clinical stages of silicosis recognized locally were nccepted ns follows: First stage.--Respiratory symptoms slight, few or no physical signs and ca pacity for work little Impaired. Roentgenograms show the linear shadows Increased nnd present discrete shadows of nodiilntlon. Second stage.--All physical signs nre Increased. TJie nodular shndows are In creased In number nml size nnd show a tendency tow ard confluence. Third stage.--All signs and sym ptom s nre greatly accentuated, nnd there In a total loss of working enjmcity. When tuberculosis Is present, the stage classifica tion must he bn sod more or less upon n loss of working capacity th an upon phyalcnl a lp ts nnd roontgonogrnphle nppenrnnces. It wns recommended tlint an Internationally comparable roentgenogrnphlc technic nnd terminology be adopted, and th a t a further study he made of the correlation of roentgen nppearancea, pathology, and symptomatology of alllcoals with or without tuberculosis. The Committee on Pneumoconiosis and the Committee on Standard Practices in Compensation of Occupational Diseases of the American Public Health Association in a report on silicosis (201) described the stages of the diseases as follows: The disease is divided arbitrarily into first., second, and third stages for convenience of description and possible compensation purposes. First stage (corresponds to antoprlm ary stage of South Africa).--The symptom of uncomplicated first-stage slllcnsl.a a re few and often Indefinite. The mnu mny npiuirently be (pillo well nml his working capacity not notleenhly Impaired. Slight shortness of In oath on exertion nnd some unproductive cough, often w ith recurrent colds, are the most nsunl symptoms. The man may linve n tittle less ability to expand Ids chest th an form erly, nnd the elasticity of the chest may lie slightly lmpnlri'd. The earliest specific Indication of the presence of silicosis la the radiographic appearance, consisting of generalized arborization throughout both lung fields with mote or loss smnll, discrete mottling. Tltla ch aracteristic m olding Is due to slindowa cast by the discrete Individual nodules of fibrous tissue in the lungs and la essential to the dlngnoala of rIIIcosIs. W ithout tills finding the diagnosis of silicosis Is not sustained except liy autopsy. Second stage (correspond to prlm sry stage of South A frica).--A definite sh o rt ness of lircntli on exertion Is usually found, and pains In the chest are a frequent complaint. A dry morning cough la often present, sometimes with vomiting, nml recurrent colds arc more frequent. Keen then the m an's appearance mny lie healthy, hut lie Is dispnole on exertion, he cannot work hs well ns form erly, tils chest expansion Is noticeably decreased, llie movement liolng sluggish nnd diminished In elasticity. The characteristic radiographic nppenrnnce la a generalized nieillum-slzed mottling throughout both lung fields. The shndows of the Individual nodules are for the most part discrete nml well-defined on n background of fibrous artHirlznllcm, but there inuy Ik here and th ere lnrger but lim ited opacities due to Irregular pleural thickening or to a localized aggregation of nodules. Thlrtl'Stage (corresponds to the secondary stage of Booth A frica).-- tn the th ird stage the shortness of breath Is m arked nnd distressing even on slight exerllon. The rough Is more freq u en t; the expectoration la In most cases alight but m ay he copious. The Individual's cnpnclly for work liernmes seriously nml |Hrnmnently Im paired; Ills expansion la g reatly decreased even with forced In spiration; he may lose flesh ; Ida pulse ra te may be Increased, and Ida heart may become dilated. The radiographic appearances In the th ird stage nre further neeentunted. the m ottling Is more Intense, flu nodules a re larger and take on a conglom erate form so that large shadows nre shown corresiHiudlng to areas of dense fibrosis. 76 R EVIEW OF LIT E R A T U R E ON D USTS Physical exam ination of an Individual m ay reveal changes In percussion And auscultation, mild In the first stage and Increasing with the progress of the disease. These alone a re not sufficient to be of g re at value In diagnosis of silicosis. Pnru'oast and Pendergrass (SOS) questioned the wisdom of designat ing nny appearance of pneumoconiosis by any term denoting numerical stages of progress. 1 hey prefer to designate the appearance by a term which implies itspntnological nature: Now this m>|eitrnn<T of prom inent hllmn shadow s nud Increased prominence of trunk shadows and linear m arkings, w ith o r w ithout the faint haze, has In this country at least Ihnii designated as the f i r a t a t a g e of silicosis or pneumo coniosis. There may be s^me excuse for continuing to call this the first stage, but continued ex|Krlence with cases of pneumoconiosis developing In various Industries 1ms led us to question the wisdom o f designating any appearance of pneumoconiosis by nny term denoting num erical stages of progress. We prefer to designate the np|enrance by a term which Implies Its pnthologlcnl n a tu re and to call It not a stag e b u t th e p e r i v n a n t l a r - p e r l b r o n c h i n l - l y m p h n o d e type of propnitdernnce of the condition. In cases with silicosis which Is m oderately slow In Its progression the m icro scopic nodular lymphoid deposit proliferatio ns tend to Is me conglomerate ami to produce n macroscopic nodular process . i this ap|Karnnce was found as a more advanced stage of silicosis In the e a r11- r cases examined, and espeeinll> among m iners In th is country. It was and Is still called the a ee o n d Minor of the eondlti >n. It Is conspicuous by Its absence or Insignificance, how* ever , In m any Industries, notably the g ra n ite c u tte r, ann '.bluster, sandstone and iiolesfos workers. It Is esj>eclnJly likely to be absent or inconspicuous In those who a re developing silicosis rapidly, such ns lit those working with pulverized sand and without adequate probation. If this npi>enrnnoe Is absent or nearly so as a stag e of pi< gross In ro many Indus tria l silicoses, why designate it as a niiiiierlcnl stage of progress a t nil? Wo have censed to do so nnd have called this appearance th e n o d u l a r tf /p e or prciMmderuncc of sllIn d ie llbrosls, or, more csirrect ly, kIIU*osIs. T here Ib another ty|e of silicotic npiw*nrniee which w as very puzzling to us at find lieenuse of Its exact Identity and our Inability to find the pro|Hr place for It In a numerical classification of progressive stages. * Fortunately a definite pathological place seems to have lnen found for the condition and n roentgenological classification for the appearance. We have designated this ns the i n t c r a t i t l a l t y p e o f p r e d o m i n a n c e and have sulallvlded It Into rapid nnd slow, which suhclnsslflcntlon m ust depend Inrgely uism the physical factors and tim e of ex|>osuro. * T his ty|>e of fibrosis will alm ost Invariably progress to the term inal stage with little or no appreciable nodular npjw'nrnnce. C are m ust h* exercised In differen tiating It from a chronic Interstitial lung change resulting from pneumonia or continued upi>er respiratory Infection ns In the Hlmises. The m udltlon responsible for this npiKuirnnce In advni *cd form nnd of rapid development has Ihmmi term ed "acute silicosis" by Chapman atul some others. There are few, tf nny, argum ents to be recorded la connection with the terminal stages of silicotic llbrosls. Instead of the t h i r d a ta g e , we have preferred to call Ibis ns|sx*t of Ihe dlscnse th e term inal d l f f u a r fl tn o n tn . It Is more or less Incapaci tating In practically nil Instances, and nil too often completely so. With respect to the classification of silicotic appenrnnecs hasetl upon known pathological chnngcs, Pnuconstnnd Pendergrass (SOS) suggest tho following in place of the old numerical stages: 1. Peribronchial-perivascular lymph-node predom inance or typo. This mny be rapid or slow, usually tho Intter. '. Knrly In terstitial predominance. T hta mny Ik extvemely or moderately rapid, ric|Mndlitg on the silica Intake. It may or may not have an associated slight nodular np|ienranee. 3. Advanced Interstitial predominance. 4. Nodulur predominance. Rapidly or slowly progressing. ). silico sis 77 5. Advanced diffuse or term inal fibrosis. Conglomerate nodulnr type. In te r stitial type. Massive flbrotlc type. DIAGNOSIS According to the Silicosis (Medical-Arrangements) Committee of Great Britain {172) silicosis can be dingnosed, even in its early stages, but the diagnosis is not free from difficulty. F or instance, the clinical signs of silicosis resemble to a great extent those of other chronic dis eases of the chest; further, silicosis may be complicated by the presence of tuberculosis in any stage. Irvine (203) says that it is impossible to deduce a practical standard of diagnosis from accounts of the disease furnished separately by the pnthclogist, the radiologist, and the clini cian. Clinical examination is obviously nil essential factor in the deci sion in any individual case, l>ecnuse it provides im portant information otherwse not obtainable regarding the general and local condition of the patient, the degree of incnpncitntion, if any, and the presence or absence of complication by active infection or by disease of other organs; but in a disease like silicosis clinical evidence in ninny cases is inconclusive and mny be misleading. Other menus of diagnosis in the living subject nre radioscopy, radiography, nnd in the Inst resort the pathological condition found after death. Radiography also hns its limitations; on the one hand, not all forms of pulmonary fibrosis re vealed by it, even in miners, nre of silicotic origin; nnd, on the other hnnd. certain types of radiograph which do not show unequivocally "sjiecific" signs of silicosis may under certnin circumstances be re garded legitimately ns affording evidence of the presence of a sili cotic factor in the case. Accurate knowledge from which to formulate a reliable general standard of diagnosis can be obtained only by corre lation of the results of pathological observation in a lnrge number of cases with radiographs taken from the chests of the same individuals shortly before death and with the results of clinical examination made during life. The final adjudication in any individual case must always incorporate Ihe additional evidence supplied liy expert clinical examination, which indeed is frequently the deciding factor, particu- larly in borderline cases. Sayers (135) included under "clinical manifestations" those factors that can l>o ascertained from the individual having the disease--per sonal data, past history of diseases, occupation, present history, physi cal examination, and roentgen and laboratory observations. Levey (173) believed that any diagnostic medium in the early stages of sili cosis should not lie overlooked. The ini|>ortnnce of the serologic ex amination and correlation of the physical examination with the past history is so great as to render all the stops of Use complete examination of almost equal importance. Although nunc claim that no diagnosis of silicosis can be made properly without roentgen-ray examinat ion such examination must not be considered adequate, except in advanced stages. The examinations at the Bureau of Mines Richer Clinic (SO) included collection of data oil race, family history, per sonal history, past history of illness^ occupntior.nl history, nnd physi cal, X-ray, and laboratory examination. A brief summary of sumo of the results of the examinations follows: sos: in--oo--- a 78 REVIEW OF LITERATURE ON DUSTS Family history.--The incidence of silicosis or silicosis complicated with tuberculosis was found to increase as the family histories of the men were classed as good, average, or poor. Personal history.--The use of tea, coffee, or tobacco apparently has no relation to silicosis or tuberculosis. A fter silicosis hns developed, however, the use of alcoholic drinks and patent medicines increased markedly; the men take these to alleviate the symptoms of silicosis so th at they can continue work. A study of age groups in published results of several investigations on silicosis shows that, in the early years of the occupational life of those in dusty occupations, the incidence of silicosis is low; but, with increase in the age group, regardless of length of employment, it increases slightly up to about the Rge of 40 and thereafter markedly. Age, therefore, hns an important bearing on the occurrence of sili cosis and should lie considered in employing men for work in dusty atmospheres. No correlation could lie made between silicosis or tuberculosis nnd overcrowding in sleeping accommodations. The number of hours of sleep bore no apparent relation to silicosis or tuberculosis. Past history oi illness.--The data seem to indicate thnt all infectious diseases of childhood, except diphtheria and scarlet fever, probably docrcaso resistance to tuberculosis and silicosis. Picher is free from malaria, but many of the men reported they had lmd malaria; among these men the incidence of tuberculosis nnd silicosis was compara tively high. Tonsillitis, especially if the attneks are recurrent, seems to be associated with tuberculosis but apparently hns no relation to silicosis. The highest incidence of silicosis or tuberculosis, or both, was among men who reported bronchitis, pleurisy, and asthma. The lowest incidence wns among tlioso who reported influenza, pneumonin, coryza, and liny fever. An unknown and disturbing factor in the attempt, to discover a relationship between silicosis or tuliercnlosis nnd other diseases was the difficulty in determining in many instances whether they occurred before or after silicosis and tuberculosis hnd been contracted. The data show that the incidence of physical de fects increases among men with silicosis nnd tuliercnlosis. Severn! explanations nro ottered for this fact: Men with silicosis or tulicrru- losis usually are somewhat older than tlioso in tho essentially negative group; the silicotics hnvo hnd n much longer jieriod of servico in tho mines than the negntive subjects; certain physical defects may in crease snscepl ihility to silicosis. Nnsnl obstruction nnd chronic cntnrrh, enlarged turbinates, ade noids, or other conditions that, cause month breathing nro associated with, an in Hie incidenco of silicosis. Poisons having a verti cal-hanging heart are more likely to develop tuberculosis or already have i t ; this finding ngrees with South African experience. Occupational history.--A detailed statement of occupation is the most, im portant single item in the history of silicotics. Tho more statement thnt tho nrnn is a miner hns slight vnlne, if any. Many underground occupations expose tho workmen to very little dust, especially in well- opernted mines. The Picker histories included "cupntion before mining, past occupation underground, number of years in present SILICO SIS 79 occupation, kind of mineral mined, and total years in metal mines. All examined were divided into two groups according to duties--those exposed to large amounts of dust (those employed at the face) and those exposed to relatively small amounts (those away from the face). The data indicate that the men in certain positions contract the disease more quickly than those in other positions. With the development of first-stage silicosis, there was a drop in the number of weeks and shifts worked, and with second-stage silicosis there was a marked drop in amount of work performed on each shift. Men with silicosis and tuberculosis worked intermittently during 15 weeks of the year, while third-stage silicotics worked part of only 9 weeks; the number of shifts worked by these two groups, however, was almost the same (54 and 52, respectively). Physical examination.--No marked symptoms of ill health, such as paleness, loss of subcutaneous fnt, or decrease in muscular development, appear until silicosis reaches the third stage or until it is complicated with tuberculosis. Men with first- and second-stage silicosis appeared, on the whole, to be in better health than those in the essentially nega tive group. As silicosis advances, weight shows n slight tendency to increase until the third stage is reached or until tho disease is complicated with tuberculosis. This increase may be due to some extent to tho increase in age. An analysis of systolic blood pressure by age groups shows thnt the blood pressure of the younger men did not cnnnge appreciably but that the average of the older men who had silicosis was slightly higher than of those in the corresponding age group who wcro essentially negative. Clinical observation shows that tho blood pressure of sili cotics tends to remain normal or increase only slightly, hut in tuber culous cases it shows a definite tendency to drop. Any persistent marked drop in the blood pressure of silicotics indicates probablo tuberculous infection. It is generally nccepted that tho cardinal physical finding in sili cosis is diminished chest expansion. Emphasis should be put not upon chest expansion but rnther upon tho importance of comparison with a man's earlier chest expansion. Probably if tho vital capacity of a largo, unselectod series was measured for comparison the decrease in vital capacity of silicotics would be greater than any chest-expansion meas urements, however carefully taken, would indicate. Certain breath sounds rarely noted in the chests of healthy people not working in dusty occupations are often detected in tho chests of miners, particularly those with silicosis. The slight changes revealed by examination of the heart probably could be^attributed to the ages of the groups of silicotics. ROENTGENOLOGICAL ASPECTS OF SILICOSIS It is generally accepted tlint the X-rny offers the best mid most re liable indication of the lung changes that occur in silicosis, particularly in the early stage. Tho value of this method of diagnosis dejiends largely upon the skill of the technician who takes the pictures and tho experience of tho reader who interprets them. 80 R EVIEW OF LITERA TU R E ON DUSTS In fact, according to Croizier, Martin, and Policard (106), radiographic diagnosis often is very delicate. This is due to tlie unceasing movement of the organ; if even for an instant it can be voluntarily immobilized in "its incessant coming and going," nevertheless it is subject to perpetual agitation, determined by the periodic flow of the arterial blood; this is why the posing time for making an impression on the film necessarily must be extremely short (106). Pancoast and Pendergrass (202) believed that the ability to inter pret roentgenograms of cases of pneumoconiosis properly must be based upon Severn! very important factors, which may be enumerated as follows: Knowledge of the anatomy of the chest and many of the physiological problems associated with its anatomical constituents; thorough familiarity with normal roentgenographic and fluoroscopic appearnnccs and permissible variations therefrom within normal limits; knowledge of the histology of the lungs nnd especially of the lymphatic system ; clenr perception of the pathology of the condition of pneumoconiosis and of nil conditions which may simulate it in roentgenographic api>earaiices; exj>erienced intimney with the roentgenographic nppearances of the condition in question nnd of those that resemble it, bnsed upon fundamental knowledge of the pathology represented; knowledge of the physical factors involved in producing the suspected or nlleged pneumoconiosis; and employment of the proj>er technic to show to lull advantage any or all of the abnormali ties present, for technic may fully enlighten, may so modify appear ances ns to be confusing, or may be quite misleading. The fibrotic changes revealed by the X-ray study of the Pichcr Clinic (90) are classified arbitrarily ns definitely negative, more fibrosis than usual, decidedly more fibrosis than usual, three stages of silicosis, nnd silicosis plus tulierculosis. Definitely negative.--In the definitely negative cheat the hllm n shadows are not more than 7Vj cm. In w idth from the m ldline nnd do not cover more than two Interspaces and one rib a t a tnrgi't distance of 48 Inches. The hlluni shadows occasionally mny allow one or m ore fnlrl.v Ia rite ealclflcntlona. The pletnres disclosed little If any evidence of nn nnnannl mnnnnt of jx'rlhm nchlal thlckcnlni; 111 any of the definitely negative chests. The bronchial tree usually cannot lie traced fa rth e r Ilian the Inner edite of the ndd-lhlrd of the lime and never lieyond the Inner section of the outer third of the lime. The a reas lietwecn the shadows llwown by the bronchial tree are clenr nnd show no evidence of nny Inflnmmntory changes. Kora flbrotl than usual.--T he hllm n shadowa a re larger than norm al--thnt Is. more Ilian TYt cm. wide (from m ldline)--nnd cover mere thnn two Inlcrspnees nnd one rib. Most of these cover more than two Interspaces anil two ribs. The caleincatlons within the lillttm shnilowa allow a very definite Increase nnd some times arc icry Inrcc. T he bronchial tree aimwa definite thickening nnd often extends well Into the n|iexes. In the m njorlty of cases its branches can ls> observed radiating to the outer third of the lung. Deoldeflly more flbrotU th an usual.--T his clnss corresponds to th n t sometimes referred In ns preslllentlc. T he hlltini slmilown nre definitely enlarged nnd dense. The X -ray rending allowed Hint 114.4(1 percent of these cases nt lMcher had largo, dense, hllmn shadows. The bronchial tree ahnwa a definite thickening nml extends to the periphery of the lung, Involving the bronchioles nnd possibly the nlr vesicles. F lrst-itage sllloosls.--T he lillnm shadow s nre Increased In density nnd arc Inrgor than normal. In ninny Inslnnces (of ric h e r cases) lnrgcr cnlclftcd s | h i| s were noted In nr around the hllm n shndows. These were nrger than th e s e generally observed as the result of tnltcrrulnsl* In childhood. In aevcrnl Instnnoos ccllectlonn of such cnlclfii alIons Involved the entire hllmn. ) SILICO SIS 81 Following enlargem ent of the Iilltun shadows, the e n tire bronchial tree Increases In density. It Is very noticeable and often can be trac ed to th e o uter m argins of the lungs. Along the thickened bronchial tree near the Idlunis are small shotlike spots, sometimes described as "beads" or bronchial "buds." When the spots liecome noticeable throughout the lower section of the lungs the case Is classified as the beginning of first-stage silicosis. The spots are fairly dense, one-eighth Inch or less In diam eter, discrete, w ith Irregular fuzzy outline. W ith advance In the disease the spots Increase In num ber, density, and sire. The diaphragm was humped In only a sm all num ber of th e ric h e r cases In early silicosis, and no displacement of henrt shadow as a result of the disease In this stage wns observed. Bccond-itage illlcoili.--The htlum shadows are large and dense but generally do not show any more definitely than In flrst-stnge silicosis. T he bends or buds along the hrouchlnl tree become lnrger, more num erous, denser, and clearer In outline; the condition Is best described ns a general "m ottling." T he m ottling Is bilateral, and the density Is about equal on both sides, Indicating th a t the changes sta rte d In Isitli sides at or about the sam e time. T he diaphragm Is often humped or "peaked," and num erous bands of ndhe- slons arc noted at the bases. The henrt shadows usually nre normal. T hird-stage illlcoilt.--The spots descrlt>ed under second-stage silicosis tend to coalesce, forming lnrge nreas of marked density. In some of the cases very large areas of marked density were observed--usttnlly In the m iddle section of the lungs--which were sim ilar to tuberculous consolidation: these areas, however, usually were bilateral and blended so perfectly with the snowstorm nppenrnm-e ns to suggest silicotic nreas, which the physical exam inations and laboratory find ings tend to confirm. 811icosU plus tuberculosis.--T he ordinary silicotic findings described under the different stages of silicosis were noted In the rich e r cases ( 1 0 0 ) . In many of them detection of the Itegimdng of tul>eroulous Infection w as difficult l>ocnuse of the extensive silicotic changes. The hllunt shadows were more likely to show cal cified s|K>ts tlinn In uncomplicated silicosis. In some of the enses the calcified spots or glands were very large and occasionally occurred In large munliers. With the beginning of tulierculosls areas of mnrked density w ere observed, usually nt one or both ajH-xes. These a reas w ere not so dense or opaque ns the flbrollc areas of silicosis and appeared cottony or wooly, Usunll.v they were unilateral hi the beginning but often liecnme b ilateral before denlh. In some Instances these nreas occurred in the mldsoctlon of the lungs opposite the hllunt. Large areas of marked density mny occur In th is region, and it w as difficult to determine by X-ray whether the nren wns a walled-off tuberculous nbscess or a dense flhmtlc nren of silicosis. Pnnconst ami Pendergrass (04) summarize the roentgenological phases of the condition as follows: 1. The |ierlvnsoulnr-lwlbi'onclilu! Iym|di-m>de nsjiect Is due to tlu* relaying of ptingoeyted dust to ttie pulmonary lymph nodes and th eir subsequent enlargement and ultim ate partial fibrosis to"(lie gradual enlargem ent of lymphoid de|islts along the eourso of lymph vessels and the subsequent tlilekeiilng of these vessels and stnsls of contents. This Is rlinrncterlzrd rooiitgenogrnphh'ully by huwensed prominence of the hllum and trunk shadows and llnenr m arkings. This nppenr- nnoo Is by no means elm rncterlslle of pneumoconiosis alone, and oven If It does Indlente the rendition the plinsp Is nlisolutely not Incapacitating. It. together w ith a barely i>erepptlhle appearance of macroscopic nodules, corresponds to the so-cnlled first stage. 2. The Modular nspeet Is due to the gradual enlargem ent of lymphoid deposits and their eoalescem-e Into quite apparent nmerosooplc nodules svm m etrleally scnlfered throughout Isilh lungs. T his i-orresponds to the so-enlli*d second stage. It Is conspicuously absent In many Industries, especially when (lie silica Intake Is rapid. It. The Interstitial l.v|s> of the condition results from n hllum w ard and pleural- w ard bloek III the lympiialles mid the pat-iipt* of dust phagocytes In large numbers Into the Interstitial Interalveolar tissue nud subsequent fibrosis. It npi>enrs ns n faint homogenous hare, first on tlie right side, then on the left. If the silica Intake Is com paratively slow. It mny accompany the perlvascular-perlbronrhlal lymph-node aspect, but If more rapid, It muy be associated w ith the nodular type 82 REVIEW OF LITERATURE ON D USTS or may projcraaa without tha latter directly Into the term inal etnite of the condi tion w ithout liny evidence of nodulatlon. The unprotected or Inadequately pro tected aandblaater, aand pulverizer, and aandatone-Rhraalve w orker or uranlte c u tte r have Iteen among those especially prone to present th is rapid In terstitia l aspect. 4. T erm inal and Incapacitating silicosis Is characterized by three general a p pearances--a term inal diffuse fibrosis of a conglomerate nodular type, one which Is quite sim ilar In appearance to a generalized chronic fibroid tuberculosis, and th e term inal stage characterized by large fihrous consolidated areas, which closely resemble tuberculous consolidations quite frequently, but which we are now learning to differentiate one from the other. According to Gardner (AW), anatomic and roentgenologic studies of the lungs of persons exposed to various types of industrial dusts have demonstrated that all inhaled foreign substances do not produce the same kind of pathologic reaction. He divides the forms produced into three categories--linear, nodular, or diffuse in character. A linear pattern characterizes the general type of response to most inJinled inert foreign materials; nodular lesions apparently are confined to silicosis; and diffuse reaction is exemplified in asbestosis. Mixed patterns are produced by dusts such as granite, which is composed of several different elements. Biihme (77) stated that the hard-rock miners of the Ruhr coal dis tricts are peculiarly suitable for investigations of the development of tuberculosis in the silicotic lung since before beginning work they are examined medically and employed only if they prove to be healthy and free of tuberculosis His description of the process of the development of tuberculosis in the silicotic lung follows: B y X - r s y e x a m i n a t i o n of hnrd-ro ok minor w ith finely m o ttle d rM corIr, we encounter occasionally picture* which. In Addition to fine Rllleotle mottling, e h o unilateral round nodule*, mostly In the Infrnclnvlrulnr region, whitt we o therw lRe d e s i g n a t e hr p rein n tu re Infiltration. How ev er , they tiRimlly cnuRp no cllntcnl sy m p to m * In silicotic* hr p r e m a t u r e InfiltrntionR ro often do---loss o f w eig h t, n i g h t went*, wenkneRR, fever a r e lucking it f i r s t ; Indeed c a t a r r h cannot lie determined a* a result of the ohRtruction of the drainage system by IIIoorI*. L ik ew ise th e Rcttling tim e o f th e red blood co rpuscles a t firRf Ir o f t e n no rm n l. NevertheleRR th ese nodule* do not heal e n tir e ly b u t progrpRR, Although Rlnwly, and often lend to very extensive consolidation which atiafoinlcnlly npt>cnr8 n* nn in t i m a t e m ix tu re o f hIIIcoIIc tiss u e w ith Rntnll tu b ercu lo u s foci (tuberculo-slllrosl*). Finally, however, those Inbemiln-slllootle nodule* under fortnntloti lend to dl*lnlegrnte Into central rnvltle*, often rapidly Increas ing In size an d secreting haclllUNcotitiilnlng Rpututn. From this moment on the tulMrculn*tft domlnnteR th e d ise ase picture. N u m e r o u s tu b e r c u lo u s a s p i ra t i o n no dule* develop, e*|ieelnlly In th e lung nectlon* o f tho*e less affected l*y hIIIcorIr. l a r g e r tulerculo-*llleotlc nodules also may Ik* deveto|ied In th e lung*, which o th e rw is e rIiow only Rtlglit Rlllcotlc chnugOR. It ap|K*nr* a* th o u g h In Micro cases th e r*ck dURt Ir deposit i*d moRtly w h ere a lr e a d y tlRRue chnugoR w ere determ in ed by alight tutierculon* foci. T h e ol*ervntln* of ttlose may lie mentioned here, a c cording to which nn enrichm ent of alllclc acid Iin* been detected In th e tuher- culou* hllum cnvltle* even when no alllcotlc consolidation h a s been formed In th e lung*. In o o n tr n a t to these very chronically progressing form * w i t h tuberculo-Rlllcotlc nodule* a tuberculous focus occn*lonnlly may tend to dlRtIntegrate In Rlllcotlc lung* from the beginning without the formation of the lnrger tubereulo-nllleotlc nodule*. *o tliat ttie occurrence of tnbcrculoRl* w ith all It accom panying sym p tom* npi>cnrR In I he fore ground p rem atu rely. Such form* a r e freque ntl y en- coMderiH! r a p e d Jly when th e rock-dust h a z a r d la ver y Revere a n d t h e rIIIcorIr develops after a few year* (sandblasters, scourlng-iKmdcr worker*). ). silic o sis 83 The Infrao ln rlcu lar consolidation focus Is a frequent form of development of tuberculosis In silicotic* but not the only one. Many times a progressive tubercu losis is develoi>ed In the silicotic lung from form er apex-foci. W ith a nother group of i>ntienis It Is to be assum ed Again th a t an old Inactive dissem inated tut>erculosis flares up under the action of rock dust and th u s In numerous places lends sim ultaneously to the form ation of foci of consolidation with which a silicotic wall is often found around the caseous tuberculous center, or tuberculous and silicotic tissue Is combined In alm ost all foci. We can find, a s m entioned above. In the finely mottled silicotic lung the same form of evolution of tul>erculosls ns form erly and certainly as Infraclavlcular foci from a chronic apex affection or as scattered foci of disease. The course of tuberculosis, however, ts differentiated most from accompanying sili cosis by the form ation of tiilercuto-slllcotlc nodules and the retu rn a fte r years of the clinical symptoms of tuberculosis. If silicosis has already reached the corresponding third stage the moment of the appenrance of tuberculosis and Its extent are often very much more difficult to determine. The more severe Infiltration of the lungs with silicotic nodules makes very difficult the recognition In nn X-rny picture of a beginning tubercu losis, and clinical symptoms, ns already stated, tend to m ake the tulerculosl* first If It has progressed further. My opinion Is based on the tuberculosis becoming m anifest w ith third-stage silicosis often a fte r It has remained completely latent for years and cannot be diagnosed certainly by X-rny. T his Is especially confirmed by the fact th a t inoculation of guinea pigs with sputum from such patients frequently does not show |K>alttve re su lts for years before the nppenrnn<*e of tuberculous symptoms. Often enough tuberculosis inny already be present In the first or second stage. A dem arcation between tulverculous and silicotic occurrence is scarcely ftosslbte during life In ninny advanced cases. In any case tuberculosis Is much more fre quent with third-stage silicosis than Is clinically recognized. Wlltjen found active tuberculosis twice ns frequent by lung autopsy as was determined dlnlcnlty; my ov n experience confirms this. The anatom ical finding, however, also does not alw ays allow a sharp differ entiation between silicosis and tulierculosls In extensive consolidation. Haldane (205) considered the diagnosis of silicosis, apart from a history of serious exposure to dangerous dust, extremely difficult, and the sooner an agreement can l>oreadied ns to the ground for a diagnosis of silieosis the better; hut these grounds must bo consistent with known facts regarding the infrequency or frequency of phthisis in the kind of occupation in which the patient has been actually engaged--for ex ample, ordinary collier's work or work in driving a road through highly siliceous rock without adequnte precautions. Smith (SOG) has pointed out striking discrepancies between symp toms and physical signs and pulmonary filjrosis, as shown by the 2v-ray. In a study of rock drillers in tho vicinity of New York 25 percent of those whose X-rnys showed unmistaknblo silicosis had no symptoms whatever, and in a study of granite workers (207) in the same locality. f> cases of 17 with advance! silicosis had no symptoms. Absence or symptoms does not indicate absence of silicosis. Smith quoted an incident reported by AVatkins-Pitchford; of a group of 541 miners who bad l>een receiving compensation for silicosis on tho bnsis of a physical examination nfone, 41 percent were found not to have it when X-rays wero introduced. She considered a physical examination somewhat of a luxury where lnrgo groups of workers nro being ex amined for silieosis; where economy of time and expense is desirable, it would seem legitimate to limit the examination to a good roentgen ogram supplemented by oorupntionnl history. McNally (SOS) stated lliat. during life, the diagnosis of silieosis dc|>ends on tho history, clinical examination, and roontgonogrnphic 84 R EVIEW OF LITER A T U R E ON DU8TS evidence of the disease. Many times the roentgenograms are not decisive, so the diagnosis of silicosis, silicosis plus tuberculosis, or tuberculosis cannot be made wtih certainty. At autopsy the doubt may still linger; then a chemical examination for the quantitative determination of silicon dioxide aids in reaching the correct diagnosis. The Committee on Pneumoconiosis of the American Public Health Association (209) has prepared the following tabulation of the vari ous lesions of silicosis and has attempted to depict the character of the shadows cast, on an X-ray film by these lesions. The tabulation applies only to silicosis resulting from inhalntion of dust with a high silica content. H ealthy lungi and adnexa Roentgenological appearance: 1. H enlthy lunga, aa defined by the N. T. A. Committee report. 2. Irregular exaggeration of the linear mnrklnga, w ith ponalhly aonio bending confined to the trunks. 8. Increased root shadow. Hlstologlcnl nppenrnnre: 1. Essentially the normnl tissues of the vascular tree, the medi astinum, the bronchi, nnd trachea. 2. C ellular connective tissue pro liferation nltont lymphatic trunks In the wnlls of vessels and bronchi. Reading may be due to various onuses, ns blood vessels seen end on, arterio sclerosis, m inute arena of fi brosis In lymphoid tissues along the trunks. 3. Cellular reaction In the trneheobronchial lymph nodes with extensions along different lym phatic trunks. These changes come within normnl variations when not accompanied by recognised organic disease. d im ple illtcoele Roentgenological appearance: 4. Nodulntlon--discrete shndows exceeding (1 mm. In diam eter, tending to uniform ity In slxe, density, nnd bllnternl distri bution, with well-defined l>orders surrounded by apparently normal lung shadows: The outer nnd lower lung Holds characteristically show fewer nodules. 0. Conglomerate shadows th at np- |tenr to result from a cnmhtnntirtt, r,f c,,n"olldnfI'm of nodu- Inllon usually with associated emphysema manifested by-- ( ) !<ncnllxcd Inerensed tra n s parency of the lung with ioss of tine detail. (6) intensification of tlio trunk shallows hy con trast. (0) Depression of the domes with |NiMslhle tendency toward Indtvldunfixation of the costal cnm|>oncntS of the diaphragm. Histological appearance : 4. Circumscribed nodules of hynllne fibrosis loenteil In the parenchyma of the lung. Oc casionally some of these nod ules may show microscopic foci of central necrosis. 5. The result of the coalescence of discrete nodules ; an area In which the nodules are clnseU packet! and most of the In tervening lung Is replaced by more or less hyaline fibrous tissue. The lung architecture Is pnrtlnlly obscured. No domnuBtrnhle evidence of Infec tion. Emphysema Is a entn|>ciisntnry dilatation of the air spaces with or without thick ening of the septn. SILICOSIS 85 S i m p l e t l l l c o s i t --Continued Roentgenological appernnce--Con. 5. Conglomerate shadows, etc.--Con. (d ) L ateral view : Increase In the prenortlc and retrocardiac space with exag gerated hnckwnrd bow ing of the spine. Widen ing of the spaces lietweea the ribs may or may not be present. Silicosle ictth infection The characteristic nppcnrnnces described under simple silicosis are modified by infection ns follows: Roentgenological nppenrance: 0. I^ocnllzed discrete densities nntl/or strlngllke shadows ac companying those of simple silicosis descrll**d above. 7. M ottling---shadow s varying In size w ith Ill-defined borders and lacking uniform ity in density and distribution, ac companying simple silicosis. 8. Soft nodulntlon--the nodular shadows described under sim ple silicosis (4) have now a s sumed fuzzy borders and/or Irregularities In distribution. The change may or may not accompany the simple mottling <>r (7 ). 9. Massive shadows of homogene ous density not of pleural origin symmetrically or asym m etrically distributed. Histological appearance: 0. S trands of llbroiis tissue, often along trunks and septa, with or without areas of calcifica tion, Indicative of "healed" Infection. 7. (a ) A reas of bronclio-pneutuonln with or without cnseatlon, 1. e,, ncute Infection. (b) Lobular areas of prolifera tive reaction with or without caseation, '. c,, chronic In fection. 8. I'e rln o d u lar cellular reaction either exudative or prolifera tive In character. 9. E xtensive nrens of tlbrosls prob ably duo to organised pneu m onia of tuberculous or nontuberculous origin superim posed uiKin a coexisting silicotic process. Outlines of normal structure may be prac tically destroyed. Croizier, Martin, and Policnrd (105) stated tlint, in spite of their efforts, they found it impossible to use the nomenclature suggested by the 1930 Conference of the International Labor Ofiioe, believing the classification to lie too complicated and absolutely unusable in ordi nary prnctice. These authors (105), as a result of their extensive studies of underground coal miners in the region around Suint- iltiennai' grouped the radiographic images into subnormal, nodular and pseudotumoral ininges and unilateral or bilateral densilieations. HOW FIRROSIS OF THE LTJNOS IS PRODUCED Kettle (183) pointed out that silicosis resents to the pathologist two fundamental biological problems: W nat is tho exact process by which fibrous tissue is formed in tho lungs in response to the presence of dust and how (lex's dust induence the progress of a coincident in fection! IIo considered that these problems lio "at tho very root of 86 REVIEW OF LITERATURE ON DU8T8 (he mntter," and even if the answers were known ho doubted whether the situation ns it exists in industries could be handled much more satisfactorily. He said, Hut If we cannot explain the how of the m atter we m ay atilt hope to speak with some nulhorlty al>out the ichm and the ichere. We can discuss with profit such questions ns the Identification of dangerous d u sts; whether they act chemically or physically; the Influence of their physical sta te on their action; the Influence of associated dusts; and the relationship of dust to Infection. For ninny years it was held thnt fibrosis of the lungs characteristic of silicosis was produced in response to irritation caused by hard, slinrp qunrtz crystals; t lint is, Ilie dust was believed to net mechanically. To Kettle (1S3) this point of view hnd some merit, as it 1s nnturnl to think thnt hard, slinrp quartz particles would wound and tear the soft tissues of the lungs; it is, of course, a commonplnce of pathology thnt. foreign bodies in the tissues excite a certain amount of reaction which is followed by the production of fibrous tissue. This fibrosis, however, is never extreme and is never compnrnble to the extensive fibrous tissue formations recognized ns lesions of silicosis. In point of fact., if a harmless dust is inhaled in large enough quantities some of it remains in the lungs and causes mild fibrosis by the mere me; chnnicnl irritation of its presence. This fibrosis is never severe enough to interfere with the function of the lungs; and in its distribution, particularly in its amount, it bears no comparison to that seen in silicotic lungs {183). Kettle {183) considered solubility a prim ary factor in the harmfulneis of silica, nnd lie believed that, a perfectly insoluble substance is incapable of causing pneumoconiosis. Exactly how the dissolved silica nets in the production of fibrous tissue is not known. Ilis sug gestion thnt it acts chemically ns n cell poison has liemi severely criti cized, probably on Iho grounds (lint, since silica enters into the com position of niiimal and vegetable protoplasm, it cannot bo a protoplas mic poison. Ilis reply to this criticism was that phosphorus enters into the composition of protoplasm, yet people have beer killed by phosphorus and others have lieen hanged for poisoning them. Koppenhdfer {210) suggested two theories to explain the reaction of the body fluids to quartz; (1) The superficial layers of the rpinrtz pnrticles corrode, resulting in a splitting ofT of minute portions; () a colloidnl reaction takes plnco in the weak alkaline medium provided by the tissue fluids, resulting in a gradual solution of the particles, lie thought thnt probably both factors ojiernte but. the presence of silicic acid in colloidal form has the most harm ful efTect.. Peacock (211) in 18(50 was the first to descrilie n microscopic demonstration of silica in Iho lungs. In 18(5(5 Schmidt {213) reported sand in the lungs of all persons--except the newborn--ranging from 4.'2 to 17.3 percent of silicon dioxide in the ash. According to \Voskressensky {213) the lungs of individuals whose occupations do not expose them especially to dust inhalation contain an increasing amount of silica in direct proportion to the nge. This investigntor found'that. 3.5 to 53.7 per cent. of the ash of the lungs was silicon dioxide, and in the peribron chial lymph glands the nmount, was much higher, ranging from 18.3 to 55.(5*percent of the nsh. McNally {208) gave the silicon content of Iho lungs of eight persons working in dusty atmospheres ns follows: ) SILICOSIS 87 Case 44 ... Mm 327.. 420 . 403......................................... 300....................... 440.............................. ................. 010 per Ash. per cram of cent dried tissue, tng. Occupation 10 7 17 14 IZ36 14 58 10 00 8.R4 A 49 150 2 6 Millstone sharpener. 14.0 Alone cutter. 2.4 Machinist. 3.6 Engineering draftsm an. 4.3 Coal m iner, T S year. 6.0 Ptono quarry man, 0 years. 96.0 G ranite cutler. 10.9 7.Inc m iner. McNally (SOS) nlso stated that tho lungs of tuberculous subjects contain somewhat more silicon dioxide than those of normal persons; this may come from inhalation or directly from the blood stream, ns the blood of tub Tculons subjects contains more silicon dioxide than that of normal persons. 1le ((noted Oollis to the etfect that nil clinical observations have shown that a silicotic pntient is particularly liable to tuberculous infection and that the silicotic process continues to ndvnnee after complete withdrawal from exposure. Gardner (Si/,) found flint, witnin limits, silicosis is a progressive disease. A man may leave a dusty industry without, demonstrable evidence of nodular fibrosi? in his roentgenogram: if ho hns alrendy inhnled enough qunrtz, tissno reaction will continue in the absence of further exposuro until its effects become apparent in roontgenopram sof subsequent years. ITowover, equilibrium between the irritnnt m the lungs and the tissues is eventually established. New silicotic nodules cense to form, and the original ones undergo only slight increnso in size. Progression is always self-limited, and most of the pulmonary tissno remains essentially normal. There is no disability ooenuse the pulmonnry reserve greatly exceeds the nmount of lung replaced by small localized nodules of scar tissue. Ill his report. on a comparative study of the solubility of finely di vided rock dust in water, Kerosine, and alcohol Myers (S/f>) mndo the following statement, regarding siliceous dust. I t will lie noted In lest 1 Hint the process of solution (In distilled w a te r) of the B-ing. q u antity of siliceous (lust was gradual throughout the 28-dny iierlod. solution being nearly complete at the end of th is tim e, while the BO-mg. w eight of siliceous dust did not dissolve a fte r the first 24 hours. It Is bellovod th a t the finest particles wont Into solution very rapidly and that there w as enough of them In BO tug. to sa tu ra te the solution In the first 24 hours. T he B-ing. w eight containing m any larger particles and only a tenth as m any of the extrem ely tine p articles as BO mg. went Into solution slowly, nml the solution w as not sa tu ra te d until the en tire am ount wns In solution which took between 21 and 28 days. Hefferimn (SKI) summarized his theory of tho action of silica on tho lungs us follows: 1. Silicosis Is n result of the local action of hydrated silica upon th e pulm onary tissue. T h is action Is of n physicochemical nature, and the speed of Its develo)m ent, other things being equal, delicada upon the rapidity with which fresh si lien hydrosol Is form ed nml brought Into contact w ith pulnm nnry tissue. 2. Substances which fnvor (he form ation of silica hydrosol from silica, when added to the slllcn dust, accelerate the development of silicosis-- for example, the alkalies. Sol.(noces which retard or prevent the form ation of hydrosol from slllen, or which coagulate the liydroaol when formed, re ta rd or prevent silicosis--for example, carbon, coal dust, clays, and probably many other substances. 88 REVIEW OF LITERATURE ON DU8TS 3. T he notion of nlllen In producing the nodular pulm onary fibrosis which we term "silicosis" hns not been paralleled no fnr by any nonslllceous substance. 4. Silicn Is a norm al constituent of plant and anlm nl cells; Us presence seems psscntlnl In certain tissues, and Its absence from the food of the organism dis astrous. 5. The study of th e role of silica In biology suggests th a t m any of th e processes of cell metnlmllsm belong to the realm of colloidal physics. 0. Some ch aracteristic c ellu lar phenomena are explained m ost sim ply by re garding the living pell a s n polyphaae colloidal system. K raut (217) found that the silicic acid content of the blood of vari ous normal persons fluctuates between 1 and 3 percent of the sulfate ash but th at the individual mnintnins his silicic acid content with great constancy. The administration of easily resorbable silicic acid increases the silicic acid content of the blood many times the absorbed amount of silicic acid. Lieb and SclindendorfT (2T8) found the SiO, content of pathological lungs of silicon workers to be 0.3 to 1.40 percent if dried at 120 and 4.0 to 22.8 percent of the ashed tissue. Normal lung tissue showed values of 0.08 to 0.40 percent. The pathological findings corresponded with 1he analytical results. Smith and WikofT (219) noticed a striking correlation between the percentage of SiO, in dried lung substance and the severity of silicosis as determined by an entirely independent method of diagnosis. They reached the following conclusion from their analytical findings cor related with the histological diagnosis and occupational history of nine cases of silicosis in men engaged in the construction of a tunnel through rock rich in silica: If one rompnTe* the percent of nsh In tb e dry lung substance In enoli cnee with hletologlcnl dtngnoeln be will note n very good correction, for tbe SIO. content of the lung Increneen with the nevertty of the enne. tin the other o ther hnnd, If the severity of the ense Is to he determ ined chemically hy the percent of SKI, In the total ash, the correlation fall. We believe, therefore. Mint the |>ereent SIO, In the d ry lung substance In a m uch b e tte r criterion of nlllconla than Is tbe per cent o f SIO. In the total ash. Haldane's (220) explanation of the large percentage of the siliente soricito which Jones found in the lungs he examined is that, sericite is less soluble than free silica in tho alkaline liquids of the lungs. Kottlo mentioned (219) in this connection that, crystalline silica when inoculated in the veins produces lesions but. tlint amorphous silicn does not,; moreover, readily soluble silica and insoluble silica do not. produce lesions, but. lietween these two is a silica that, "turns tho tricK." In 192!) Mnvrogordnto (24 ) gnve ns tho enttso of simplo silicosis the re action of tho rotiotilo-endotholinl system of (he organ concerned to in vasion hy freo silicn; but. dust phthisis, the clinioo-pathological entity met in practice, is superficially n variable disease. Beyond the external factors'and the retioulo-endothclinl system ns an apparatus lies the man. Individuals vary in their ability to resist, tho dust they inhale. The amount, of dust that, can lie recovered from a lung need bear but little relntion to the extent, or character of the lesions found. Travers (221) remarked atiout one or two facts that were brought to his attention following a review of the literature on silicosis but tlint nppnrent.ly bad been unnoticed before. A study by Kay (1923) showed tlint the solubility of mechanically ground silicn was markedly higher than that of crystalline silica; this fact may go far toward accounting G JLICO SIS 89 for the poisonous character of mechanically produced dusts. I t is sug gested (221) that the microcrystnlline material present in the lung, which is probably silica, is separated from the lung fluids nlrencly saturated with mechanically transformed silica. The presence of the microcrystalline material may have no connection with the toxic property of the silica. From a mineralogical standpoint, on the basis of solubility ratio of quartz and the silicates, U dluft (222) presented for explanation of silicosis the following theory: The chemical nn<! mochnnlcnl theories recommended by m edicine a re both pn rtly right. Both methods of operation go along side by aide. The body attem p ts to get rlil of the Infiltrated dust hy m echanical and chemical means. Thereby, those m inerals which a re stable, mmfTeoted, and ns fa r ns posslhle even newly formed under the given conditions, are to be considered as m edianlrnUy harm fu l ; w hile on the other hand the easily a tta ck e d and more or less soluble m inerals In a chemical way are removed nnd thereby cnn be cliemlcnlly active and chemi cally harmful. The remarkably severer hnrm fulness of the free m ineral nclda (silicic acid, titanic acid) and nchl m inerals over the bnslc appears to he ex plicable In th a t between the alkalies of th e blood o r of the body and th e iiorthm s of the Inhnled dust particles passing Into solution there exists nn equilibrium which In the ense of free a d d s nnd a d d m inerals lends to excessive alkali loss, while with the Induration of basic m inerals such nn Injury docs not occur. This alkali Interpretation should lie cnrefully proved. The mnnner in which stone dust exerts its effects on pulmonary tissuo remained a matter of speculation nnd argument for many years (223). The following review of the investigations that led to the modern chemical theory of silicosis is taken from nn article by King (223). I t was lirst thought that, the fine particles of stone dust cut and lacerated the tissues with which they came into contact. As viewed under the microscope the mineral particles certainly showed sharp edges nnd points, but. it was nevertheless difficult to believe that such extremely fine material could traum atize a tissue. As a consequence, doubts were enrly expressed ns to the validity of this "mechunicnl" theory of silicosis. Two crucial experiments turned the attention of investigators to nn alternative hypothesis. The first of these was by Gardner (22), who in 102:1 brought convincing evidence against the "mechanical" theory by demonstrating that the dust of silicon enrbido ("carborundum"), which is extremely hard ami has just as sharp edges ns stone dust, failed to produce the typical fibrous reaction which powdered stone dust (particularly th at of quartz or flint.) would cause when placed in the lungs of nnimnls. Those classic experiments of Gardner's marked the beginning of the modern theories nnd investi gations of silicosis. Tl'e second investigation which made the "mechanical" theory of silicosis obsolete was that of Gyc and Purdy (225) in 1!>22; also Gyo and Kettl^(&5) in 11)22, and Gye nnd Purdy (22(1) in 11)24. These workers produced in mico treated with amorphous silica a lesion char acterized hy acute inflammation nnd necrosis nnd in the liver a condi tion of necrosis by the injection of colloidnl silicic acid. Gardner nnd Cummings (227) in 1033 obtnined sim ilar results by the injection of finely powdered qunrtz. All this work pointed to the jxissibility that stone dust might he harmful to the lungs, not because it was hard and sharp, but because it produced a soluble substance which was toxic to the tissues. Policaru (22S) in 1033 showed that cells poisoned with 90 REVIEW OF LITERA T U R E ON DU8TS dissolved silica (silicic acid) do not disintegrate and disappear as do other cells, but tend to preserve their structure in a fashion which suggests mummification. Kettle (82.9) in 1932 brought the final proof that tho dissolution of a soluble substance from the stone particles was necessary to produce silicosis by demonstrating that the same quartz particles which rendily produced silicosis in animals would no longer do so if they were first coated with a thin layer of iron oxide, which did not niter the sharpness but which effectively prevented any part of their substance from going into solution. The modern "chemical'' theory of silicosis, then, supposes that the fine particles of stone dust which get into tne lungs are pathogenic, not because they produce a sort o f microscopic trauma, but because something of a toxic nature dissolves from their surfaces. This toxic substance is thought to be silicic acid. King (88-1), however, has noted discrepancies between silica solubil ity and disease symptoms. In commenting on the results of his experimentson the solubility of dustscompared with their disease-producing tendency, King (88-1) snid tlint the solubility theory had been too usefid to abandon because of tho discovery of some discrepancies and anom alies, although it is difficult to reconcile these differences. He con cluded that either the noxious dust releases something that is harmful to tho living cell or it hns special surface properties th at enusc ab normal reactions in certain ceil constituents which become adsorbed on its faces. The difficulty of imagining what such reactions could be drove him back to the notion that, a noxious dust, must be toxic because it yields a toxic substance. King (8SiS) suggests the following ns a possible explanation: C ertntn siliceous dusts, a t least, lielinve ns If they relense such a poison Into th e cells which engulf them. O thers, which hnvc the sam e effect tin cells, <h> not lllierate alllele acid so readily la the test tul>o. Still others llt>erntc n little m ore silicic arid lint do not harm cells. May It perhaps lie th a t siliceous dusts release soluble slllra differently In cells than III the test tulip, nml tlint some dusts may lllierate the silicic acid In n different and m ore noxious sta te than o th er duals? Silicic acid la constantly liclng nlisorbed Into the body through th e Intestine and excreted by tho kidney; It dis>s no harm . I t 1 possible tlint th is alllele acid Is different from th a t released from the su rface of a q u a rts p article engulfed In the body of a phagocyte. It would lie d a rin g to speak of n nascent silica," lint som ething of this sort limy actually occur. For the silica released from particles of the pathogenic allleeoiia dusts certainly has special projicrtlcs, and these s|sv ln l properties may tie due to th e form In which It I" released Into (he protoplasm In contact w ith the particles In th e cell. Such a speculation may appear fa r fetched, but It 1 a possible explanation, and It may serve the purpose of lending to furth er cx|M>rliiieiita which may have a useful outcome. It was ngiwil at (bo Intornntioiml Conference on Silicosis in 1930 t that * To produce the pathological condition, silica must reach the lungs: (n) In n chemically nnconililnod condition, nlthough the d u st Inhaled nmy lie cith er a nntnral m ixture of silicon dioxide w ith oilier du sts, such as occur* In granite, or nn nrlldclnl m ixture, such as scouring powder. (6) In fine particles of the order of leas than 10 m icrons. T h ere Is no evidence ns to (he lowest lim it of slue In which the particles m ay be cnpahle of producing the disease. (a) In sufficient amount and ovor a certain period of tim e: these two factor* are reciprocal variants. Tho mnxlmum of these two respective factor* has not yet lieon determined. SILICOSIS 91 Silica dust plays the dom inant role In the production of silicosis, adm ixture of other dusts tending to modify the pictu re In the direction of th a t of o th er pneumoconioses. In some relntlon to the proportion of free silica Inhnled. T here Is ex|>erlmentnl evidence th a t the solubility of silica In the tissues Is an essential factor la the causation of stllcosls. According to Bndlmtn's summary (230) of the information supplied by various members of the International Silicosis Conference, silicosis becomes noticeable after widely differing periods of exposure to silice ous dust, depending apparently upon: 1. The am ount of dust Inhaled. 2. T he percentage of free silica contained therein. 3. The size frequency (or fin en ess) of the particles Inhnled. 4. The n atu re nnd sort of such ottier substances (Including vapors a n d as may be Inhaled sim ultaneously or otherwise. 6. The powers of resistance of the Individual concerned. 0. The presence or absence of a complication hy an infective process. gases) In ft discussion of the sericite theory as n cause of silicosis Irvine (231) stated Hint, although it quite probably will become necessary to revise nnd widen the definition of the essential factors in the causation of silicosis, even so nothing 1ms significantly altered the general con ception of silicosis ns n definite pathological entity, which is readily identifiable by the pathologist after death nnd whieli is adequately dis tinguishable during life hy expert clinical nnd radiological examina tion, or the knowledge that this disease, year by year, produces many cases of incapacity or death. The position, he said, in these respects is not significantly affected by the present luck of complete knowledge re garding the exact constituents of a siliceous dust that may cause sil icosis. In spite of considerable opposition from certain quarters, this view was accepted at the meeting of the International Lnlmr Confer ence at Genova in June 11)34, and the conference accordingly affirmed tlio international recognition of silicosis as an occupational disease nnd described it as "silicosis, with or without pulmonary tuberculosis, pro vided Hint, silicosis is an essential factor in causing the resultant inca pacity or death." In a paper on the etiology of silieosis presented at the Fourth S ar anac Laboratory Symposium on Silicosis, Cummings (2:12) stated that only two important factors are involved in the fnnunln for the causa tion of silieosis--the individual's susceptibility to injury by line pnrticlesof free silica and the degree of harmful exposure offered by the en vironment in which he is employed. The rolo played by individual susceptibility is indicated hy the fact th at some workmen have lmd long periods of uninterrupted service in some of the most dangerous occupations without having been nffected adversely (232). Among the important factors (232') affecting susceptibility to in jury by dust are aimlomical |>eciilianties of tlio respiratory mecha nism, tno physiological response to dust inhalation, previous dust ex posure, tlio presence of pulmonary infections or other pathological processes--particularly tulierculosis--tlio age, nationality, nnd gen eral health. The most important factors comprising the degree of exposure to harmful dusts are composition, sire distribution, nnd physical charac teristics nnd concent ration of dust sus|eiuled in the atmosphere at the 92 R EVIEW OF LITERATURE ON D USTS breathing level, together with the duration of exposure and the gen eral conditions of work (232). In the discussion of Cummings' paper, Lanza (2.12) pointed out th at individual susceptibility had been exaggerated in the lny mind some times to draw attention from the major problem of atmospheric dust concent ration. He expressed doubt of innate variations in the capacity of different individuals to react to silica dust. He admitted that there were variations in the reaction of different individuals apparently ex posed under identical conditions to the same kinds of dust. He was in clined, however, to lielievo that the conditions were not identical as no history could revenl every dctnil of exposure from the time a man left school. Cummings (232) expressed surprise that medical men should ques tion individual susceptibility, which provides the real reason for their participation in tho control of silicosis. Why otherwise should it be necessary to make preemployment examinations before putting men into dusty jobs if it were anticipated thnt nil would react to their en vironment. in the same m anner'( He wns willing i qualify his state ment. to the extent of adm itting thnt individual susceptibility wns not. ns important ns the. degree of exjmsurc to silica. Gnrdner (232) interpreted Cummings' qualifying statement as an admission thnt v..rintinns in susceptibility might be of an acquired nature nnd duo to infection or other causes; nil his experimental ex perience indicated thnt the innate capacity of <he cells of different individuals of the snme species to renct to silica wns essentially the same. In l!).`18 Croizier, Martin, nnd Policard (/.*W) presented two fnctors ns predominating in the etiology of silicosis--mineral dust nnd tuber culosis. They found in every enso a certain extension of tulierculosis nnd n very sjtceinl frequency of the fibrous forms of this disense wher ever siliceous dusts were present. They then brought up the question ns to which of these fnctors comes first; does the siliceous dust deter mine the fibrosis first nnd thus favor a localization nnd n secondary development of the Koch bacillus or is tho tuberculosis tho first phe nomenon nnd under the nction of siliceous dust takes, from the lieginning of its evolution, a sclerous course? The authors presented arguments for both fnctors but stntcdthnt On the whole. It I only with occurrence of tubercular Infection, lint under very p articu lar conditions, th a t form ation of iuhnrIvc pulmnnnry flhrosls can lie dclcrmlncd. They also stated that : If rock dust aids pulmonary tulicrcularir.iitiou In a innnncr clenrly more pro nounced than coal dual. It linn on tlie contrary tho privilege of determ ining on the surface of ihc affected porta n more marked acteroua reactIna. To remain In (lie diimnln of practical atntenienta we uniat any thnt If the denae, tttiroua phthlaea of coal m iners anmetlmea a re Identical In appenrnnee with (lump of rock miners they nre, nt the nine time, Inllidtely rarer. To stimiiinrlap the determ ining cnaaea of these pnliiimmry ntiroaea of mlnera appears to un to tie : 1. Isles seven' tnlicrcnlnr Infection favored hy the Inhaled dusts which reduce thccfllenry of the natural menus of defense of the organ. 2. An exnggernted sclerous rrn rtlo n of the lung connected with the presence of mineral particles endowed w ith s|>eclfll qualities. REVIEW OF LITERATURE ON DUSTS 93 PREVENTION OF DUST DISEASES As no cure is known for silicosis after it has developed, prevention is the only effective remedy. There are two main lines of approach to the problem of dust-disense prevention in industry--the engineering, through control of dust production and dissemination, and the medical, through selection and control of health of workers by exnminntion; success probably depends upon a combination of the two. Hntch (2-9.?) considered the following measures essential to a com plete, well-bnlanced program of control of the dust hazard in industry: 1. Selection of workers by m eans of physical exam inations In ord er especially to elim inate those w ith tnbe'rculosls and o th er disorders of the respiratory system. 2. Reduction of the dust concentration below the stan d ard of perm issible d u sti ness through adequate means of d u st control and Rood housekeeping. 3. Limiting the frequency ami d u ra tio n of employment In th e dnsty occupa tions. thus reducing the ra te of de|>ositlon of dust In the lungs. 4. Routine m easurem ent of the effectiveness of th e dust-control progrnm by means of periodic medical exam inations and (Inst surveys. Of these, reduction in dustiness is the most direct in its effect and is fundamental to any program of control. Hntch (33) emphnsized, however, that present-day standards of safety are only est mated values and reduction in dust exposure below the estimated threshold value does not give absolute assurance of complete control of the disease. Moreover, a potential hazard always exists in basically dustv indus tries, and a constant guard therefore must be maintained. Workers should be selected by physical examination to insure maximum re sistance against the action of dust in the lungs. The employment of workers already injured by previous dust exposure thus would he Inrgolv eliminated. Routine determination of dust concentrations provides a measure of operation of the dust-control system, hut the efficacy of the control program must be measured by periodic medical examination, as only by this menus can the presence or absence of silicosis be determined.* An inadequate control program thus can l>e strengthened in time to arrest the widespread development of the disease. PRINCIPAL DUST FACTORS PRODUCING PULMONARY PATHOLOGY The principal factors now thought to determine whether exposure to dust will produce pulmonary pathology are nature of the dust, particle size, quantity of the dust dispersed in the atmosphere, nnd length of exposure. (inrdnor (3/,) concluded from his Held studies in some of the dusty industries that the evidence makes it seem improbable that a silica hazard is dclined solely by the number nnd size of the silica pnrtieles m an industrial atmosphere. 1iie other comjjonents of n dust modify its action. Some may inhibit, others retard, and perhaps some will lie foumMo prevent its injurious effects. Every mineral hnscertnin characteristic properties that separate it from other minerals of similar appenmneo when viewed under the polnrizing microscope. These diagnostic characteristics arc supposed to persist even to (lie smallest grains; with patience, therefore, the |>ercentnge of the various mineral constituents of a dust, can |>e determined. (33). S lu m s no -- 7 ) BIBLIOGRAPHY* 1. Richtabdsow, D. W. U nhealthy T rades. (Quoted by Hoffman, t e e ref. 4.) 2. D rinker, P h iu p . D ust, Fumes, and Smoke. In tern e t. Labor Office, Occupation and Ilenlth, vol 1, 11130, p. 003. 8. B askoivu.ix , C harles. Air Im p u rities: D ust, Fumes, anil O ases. (Q uoted by noffm an, t e e ref. 4.) 4. HorrkA N , F. L. M ortality from R espiratory Diseases In D usty T rades. U. 8. Dept, of Labor, Rur. of Labor S tatistics Bull. 231,1918, 458 pp. 6. T hompson, \V. O ilman. 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GOO.--------- . R ep o rt o f P en n sy lv a n ia <'oinm D slon on C om pensation for O ccupa tio n al D iseases. Vol. 4. 1035, pp. 82-87. 001. Atu I I yuikNf Fo i'n iim io n ok A m huca, I nc. F o u rth F a ll M eeting o f M em bers. P itts b u rg h . P a.. Nov. I I 15. 1030. pp. 5-0. 002. U. S. D n 'Aiu \ m:nt of L aiior, D ivision of Lanon Standards. D iscussion of In d u stria l A ccidents an d Diseases. C onvention of th e InlernnM omil Assoo, of Industrial Accident Hoards and Connnlsslons, Toronto, O ntario, Canada, Hull. 01. 1047. pp 70-70. 003 \\ knt Viitut n i Coai. Asrocia'i ion. S ilico sis C ases D ism issed. H ull. GOO, 1035, Pp. 2-3. 0i*4 M in im i W on1 1 ). Id a h o M ine L e g isla tu re A ction Is Ail N eg ativ e In Char* u ctcr. Vol. 3. i m i , p. 20. 005. U. S. D kcari \ t r \ r ok liVnoii, D ivision ok L aiio S tandvudm P rin c ip a l F e a tu re o f W o rk m en 's C om pensation L aw s ns o f J u tv 1011. Hull. <*2 Rev,, ii> 1-4. 21 pp. 000. I nocrtihal H yoiknf F oununhon. T ra n s a c tio n s , 1^`gnl S ection, 10th Ann. M eeting. T rn n s . S er. Mall. 7. jt. IV o f P roe., Nov, 14-15, 1045, p, 4. 007. CnFKiMiFHHY' (Dj *uok l . T lie New O ccu p a tio n al D ise ase M erit R a tin g P la n E x p la in e d . O hio Ind. <'oinndsshin M onitor, vol. Jit, Ml III, |p. 115 11*5 008. L ador Standards. M o n tan a Law P ro v id e* W e lfa re In ste a d of W o rk m en 's Coni|HiisHtlon H eiiehts for D isabled Silicotic*, U nder S afety , H ealth , an d W o rk m en 's Com|HMisation. Vol. 1041, p. 4. 000. W attjls. T ilm u o u a C. Annl.vsls of O ccu p a tio n al D ise ase C om pensation S t a t u te s nm l I>cvc|o|mieit.s In 1017 S essions o f S la te lA'glsinHires P re p a re d for FntimhithVf'i M em bers In d u s. Ilyg. F ound.. 1047, p. 10. 010. (Mk.vfr, P aid. M. S i l i c o s i s C osts R ise |n M ontana. Iml. Ilvg, N ew sletter, vol. 7, 1047. p 3. 011. St Ain of Nfw J kkrkt. W o rk m en 's C om pensation L aw -- Revised S ta tu te * , 11145, 78 pp. 012. D avis, (!.<}., S ai monrkn, Ki i.a M., and E ari y w in f , J . L . T h e Pnoum ooonloses (S ilic o sis) B ib lio g rap h y an d Lnws. Clilcngo, 1034, |>p. 340-475. 013. C u n n in o ti\ m. .1. (I. Silli*os|s In C a n a d a . Record o f [n teiia t. Conf, held a t lohnnneshurg, Aug. 13-27, 1030. In te rn a l. L abor Office, G eneva, 1030, pp. 310-337. ) 324 REVIEW OF LITERATURE ON DUSTS 014. 11atk.(A1T. (I. C. SIHcoals from th e O p erflto r'H S ta n d p o in t. OHnndlan Min. Jour., vol. 50, pp. 21-22. 015. IVorjch apt*a CoMrr.NSATioN Board. T h e W o rk m en 's C om pensation Act of O ntnrlo w ith AmentlmentR lo 1034 anil R egulations of lio n rd Synopsis. T o ronto. C an ad a, 11135, pp. 50-53. 010. SA H trr K niiinfkhino. Som e R e c e n t C h a n g es In W o rk m en 's C om pensation Laws. Vol. 47, 1034, p. 272. 017. A mkrican Pura.ic llr.At.Tn A aaoctA now. O ccupational D isease le g isla tio n . Itept. of Com m ittee on S ta n d a rd P ra ctices In th e Problem of O ccupational D iseases of the Ind. II} g. Sec., Am. Pub. H ealth . Assoc., 1031, 124 pp. OIK. S uioijrin, Iv in . C a n ad a a n d Oom|>enRntlon. T ra n s ., I,egnl Sec., 10th Ann. Meet In?. T ra n s . S eries, Mull. 7. In d . Ily g . F o u n d a tio n , pt. IV. 1034, pp. R-13. 010. C o u .il, K. L. lA*Rlslidlon In V ario u s C o u n trie s R e g ard in g S ilicosis w ith Siieclnl Iti'ference to Com |ionsntlon. Itept. of 4th M eeting, Perm anent Interm it. Commission for S tudy of O ccupational Diseases. Lyon, Apr. 8-6, 102. rip. 133-160. 020. CRiisitiNO-OaiNDimi-M taiNO-QuARRnwo. T h is S ilico sis Q uestion. Vol. 3, 1035. pp. 110-120. 021. Mown O r n e r . W orkm en's C om pensation A ct, 1025. T h e S n n d sto n e -In d u stry (Silicosis) Schem e, 1020. W orker'R R eR lster (la in d o n ), 1020, 24 pp. 022. Co ij.ikry Ol'ABiitAa. P a r lia m e n ta ry In tellliren ce. S ilico sis A m ongst C oal M iners. Vol. 14M. 1034, p. 140; vol. 140, 1034, p. 205. 023 --------- . Ijiw Intellig en ce. W o rk m en 's C o m rsm satlon ; S ilico sis C laim D is m issed. Vol. t40, 1034. p. 322. 024 I ron a n ii Coai. T kaiifw R rv irw . I-egnl In te llig e n c e . S lllco sla A ppeals In th e H ouse of la ird s. Vol. 131, 1035, p. 58. 025 Coi.i .ifrt Ot'ARiilAR. Law In te llig e n c e . W o rk m e n '* C o m p e n sa tio n : Silicosis. Vol. 1.51, 1035. pp. 203-204. 020. ------- . O rd e rs an d A nnouncem ents. S ilico sis (M edical A rra n g e m e n ts). Vo'. 14. 10?4, p. 348. 027. D avis, (3. (!., S ai.monrfh, Ki.rjt M,, a n p E ari.t w in k , J . I,. T h e P neum oconioses (S llleo sla). L ite r a tu r e an d L aw s o f 1034, 1035, p. 419. 028. I utkrnationai. L abor O r n e r . ( 'oinpo n sn lIo n fo r S lllcosla In (Iro n t B rita in B eginning M arch 1. 1035. Ind. m id L nlm r In f., vol. 53, 1035, p. 202. Alia. Jo u r. Ind. 1I)K., vol. 17, 1035, p. 114. 020 SotiTtfaatANn, C. L. W o rk m en 's C om p en satio n In P u ln n m n ry D isease. Jo u r. S ta le Med., vol. 40, 1032, |>p. 709-710. 030 L amcft. S outh A frlen n M ine D u st. .Ian. 31, 1925, p. 243. 31. Wokkvicn' b CoMrr.aaATtoN Co m m issio n o r N rw South W a i w . T lilril A nnual lte|K>rt n u d S ln tlstlc a fo r th e Y e a r J u ly 1, 1028, to J u n e 30, 1020. 78 np. 032. M inino AVI) Miri'Ai.uniiiv. M in e rs' llc n llli. Vol. 10, 1035, pp. 200-201. 033. CroRnr, W. K. M edical E x a m in a tio n a n d C oinis-iisntlon o f M inera fo r In d u s tr ia l In ju ry . O ccupational M edlelno, vol. 4, 1047, pp. 08-85. 034. M aonin. J ican. S u r la p ro p h y la x ie do In silico se d a n s It m ines. (P ro p h y la x is of S ilico sis In M ines.] A rch. M alad. P ro f. Moil. T rn v n tl e t Sec. Soe,, vol. 7, 1010. 475-488. 035. SnttnWAN, I'. T K i'i'M srit. H isto ry of W o rk m en 's Coin|>ensntlon fo r O ccupa tio n al D isease. Hull. Assoc. C a su a lty nail S u re ty Bxec., Ju ly 1035. (Q uoted by 1ml. Misl., vol. 4. 1035, pp. 453-457.) (130. S w iss FrorRAi. C o n s in .. P re v en tio n de In sllleose d n n s le c o n stru ctio n de tu nnels, d e g a le rie s el d a n s leR m ines. 1. A r r te d u conseil federal du 4 dcem bre 1014. II. O rd o n n n n ce 1 d u d e p a rtm e n t fedornl le l'conom ie piiblb|iic o f 23 dcem bre 1014. [P re v e n tio n o f S lllcosla In the C on stru ctio n of T unnels. 0011001. and In M ines 1 D intco o f th e F e d e ra l C ouncil of Dec. 4, 1044. II. O rd er o f th e F e d e ra l D e p a rtm e n t o f P ublic Econom y of Dec. 23, 1041.] (137. I.ano, Vai-rx. S llleose e t n ssu rn n ee. [S ilico sis a n d A ssu ran ce.] Jo u r. Medical do l-eyslii, no. 2, M nrrli-A prll 1045, 10 pp. (138 I 's n n s t i.vania Commirrion on Ciiu itn r a tio n for Occupational DlRFASr.. O crnptlm nl DIrs'Rsc C om pensai bm . C om m onw enlth of P e n n sy lv a n ia , 1033, pp. 58-7.0. 030 S afktv E noinffrino. 'D ie Coat of In d u s tr ia l D isease. Vol. 00, 1085, pp. - 8 1 --282. BIBLIO GR A PH Y 325 (HO. W r a r c tt, V. W orkmen's Compensation L egislation In R elation to Oivupntlonal Diseases. U. S. Dept, of Labor, Bull. 4, Dlv. of L abor S tandards, 1930, r . 40. 041. InnusTRiAt. C o m m is s io n o f W is c o n s in . Disenses of Occupation and O ther N onarcldental Injury Cases Settled In 1940. Stnt. R elease 3214 (M lin.), Dec. 19, 1940, 24 pp. 642. B a r t i.r t t , T. N. (See ref. 040, p. 325). 043. J ones, F. It. Occupational-Disease Com pensation. In d . M ed, vol. 5, 1930, up. 179-183. 644. R o c k P ro duc ts. C alifornia Compensation R ates Increased to Cover Silicosis. Vol. 30,1930, p. 70. 645. K n o in e e r ik o a n d M in in o J o u r n a i- Silicosis S urcharge In C alifornia. Vol. 137,1930, p. 442. 640. G r a f t . W. M. The Resjionslblllty of th e H ealth D epnrtm ent fo r Occupa tional-D isease Control. Safety Kng, vol. 08, 11134, pp. 123-120. 047. West V ir o in ia C o a i, A s s o c ia t io n . Silicosis-Compensation Fund. Bull. 012 1935, pp. 1-2. 048. So u t h A f r ic a n M in in o a n d E n o in f .k r in o J o u r n a i, Employees' Provident Fund. Vol. 40, 1935, p. 787. WO- -------- M iners' Phthisis Hoard. Vol. 40, 1935. p. 7X7. 050. ---------. Phthisis Liability. Vol. 58. pt. I. 1947, p. 391. 051. (lot.urRY G u a r d ia n . W orkmen's Cnimicnsntion In 11*33-- In d u strial Diseases. Vol. 150, 1935, p. 212. 052. R o c k P ro duc ts. Various Rock-Products SuliJiH'ts Discussed b y Mining Engi neers. Sym|isiuni on Silicosis Adds Much Helpful L ite ratu re. Vol. 37, 1934, pp 50-58. 053. A m e r ic a n J o u r n a t . of P u iu j c I I e a i.t h . Conuiensatlon fo r Silicosis. Abs. vol. 23, 1033, p. 1084. 054. W r io h t , G forok W. Industrial Pulm onary Dlsenses nnd C apacity for Work. Occupational Medicine, vol. 2, 1940, pp. 540-550. 05:5. Gfohoe, W. E. Proceedings of (lie Inlerm itiom il Conference Held In Geneva, Aug. 29 to Sept. 9, 1938. Item 7, D eterm ination of D isability nnd Assessment of Hie D ogreeof Stieh Disability In Pnennioeonlosls, 11*40, p. 05. 050. Com. a m i C o i i .if r t Nfavr. Now Fnetorles fo r Disabled Miners. 1IM5, p. 573. 057. Coi.i.ifr y Guardian. Kni|doynient of Silicotic nnd Pneum oconlotlc Persons. Vol. 172, 11*40, p. 09. 328 TNDEX OF AUTHORS Page MorcK F. J . . . . . . . Moahkowky, 1 !.. Mow, K. N ......... MMyurr*a,y.wA.. J ....... Naca), 8 ..................... N., -- ............... Nelderheumer, M . fl N chnn, A .................. N ehon, W. T __ ____ N esbitt, C. T ............. Nicholson, B. 8 . . ___ N lm tytkn, L ..__ . . . . Ogden.--. .... Oler, A .............. Oliver. T h u m . O lir , K. T ... O rmatelo. A. J . O 'hry, U. I . .... Owens, J. fl Owlngs, O. IV.. ........... 130.313 ............. A3 307 ........... 100,316 .............34. 304 ............ 7. .WO ........... 240.321 .............30. 3m ............... 31.304 163.164.170, 316 .............4A 3no ........... 1.10 313 ........... 238.330 ........... 238. 310 ........... 216.318 .............AA. .107 ........... 227.310 . . . 20A.WA.3I* ........... I 316 ........... 144.315 128,133.111.114 . . . 172.17.1. .116 Fulmer. O . T .................................................... 131.11.1 Pancoast, FTmry K ...........................................1W. 02. p e n a n , -- ...... 10 Pap|trnhelm , --................................................... 30.304 p aracehus............................................................. 10.224 Parmegglanl, Luigi ........................................... 54.307 ra ttrreo n , II. fl.................................................. 150.310 P atton, i . K . . . . . . . . . . .................... 38.305 Payne, A K ...................................................... 32.304 Peacock. T. O ...................................................... W. > r r r . . 6 . 1 ......................................................... 1*7. SU Pender*TM . Kugen* P ..................v _ , . f o f o * * 1! 81. 221,3011. 300.310 Traenti, R ota... ............................................ M . 241.2 4 1 3 0 7 pafT. 1 ............. ................................................ 10.302 Plrow, H a n s .. . ............... 32.11 IOA.lAA.lAO.3fM.3ll P in to ____.___ PUny................ . Pollm rd, A___ Porro, F. W.._, roje, A. fl. . . .. Potter, N. M ... Prier. F. i l ___ Proake, FI. O .. Purdy, W. J ... ..................................................... 300 .....................................................18.303 ........... A2. 07.08. 70.80,80.80,02,104, 19. 248. 307.308. 300. 310, 311, 317,321 ................................................. 38,305 .......................................... 104.121.122 ................................................... 140.315 .......................................... 180. 181,317 ............................................................. 00.308 ............................................ 80k 240, 310, 322 Qualntanoe, P . A. 130,312 Ran, fl. fl.............................................................. 101,310 Riddell, A. R ........................................................ 70,308 Kamacvlnl, H .................................................. 10.20.303 lU uschenbach, O. W ........................................ 255,322 R aynor, II. K. O ................................................ 100.311 H erkteh, P .......................................................... 238.320 K ey, A. T ................................................... 5A. 124.307 Hire, 0 . 8 ................................................ SA, 131,306.313 Rlehnrdaon, B .W ............................................ 12.13,302 Riddell, A. R ................................. 30. 25* 353, 305,322 Rlembauli, A ......................................................... 307 Riley, F.. O ...... ...................................................... 300 Rlat. --.................................................................... 70 Rotierte, F. 0 ............................................... 01.304.310 Koleon, W. 1>............................................ 249.2A2 322 Roche, LotiU.......................................... Z 123.307,317 Rockwood, N. O .............................................. 230.3 Rosen, G eorge...................................................... 22/303 ROrale, R ........................................................... 318.3 R othm an, 8 . 0 ...................................................... .100 A F 44,44, IDI, 118,100, 242 300.310, 312 317 ................. ............ WO flabotirln, Irvin -- ..............................................278.324 flnlmonaen. Filo M ............................................ 323.324 flamjwon, llo m er.. Phrrm an. I*......................................................... 287.324 Sander, O ............... ............................................. 43 306 Panders, -- ........... ............................................... 710 .............................. 20 flapplngton, O. O ............................... JM. *8.312 322 Sargent, O. K........ ............................................ 130.313 Sarp. II. M ............. ............................................ 184.317 flaurAat, M . . . . . . . . ............................................ 182317 flayer, IT. 1>........... ........................................... 302 .123 Severa, R. R ------- . . 15. 302 305.300.308.300.318,321 Srnefller, ----------- Schloekow, --________________________ Pag 30. 304 S chm idt,--......................................................... 88.300 8Chrenk, II. H ........ 130.144. 187,312314.815.316,317 Schuller, H. P ........................................................ 307 flrhflrmann, 8 ................................................. 14,30.303 Sehadendorff, F .....................................................88.309 Scrutator................................................................. 316 Seide,...--..................................................................... 218 Selkirk. W . / . B ...................................................338.320 Selby, 0 . D ........................................................ 210,318 S harer, C ed i Oordon........................................ 252 323 Signer, M . I .......................... 184.317 Slmaon, F . W .............. 7.00,308 S kinner,--. . . ........................................................ 128 Pladden, --..................................................... 24 Smith. Adelaide, R ....... 38.83. 04.05,305.300.310.313 fSlm millth h.. OCI...O.B...................................................... 8--8.1-22 300 Smith, O .W .......................................................... 317 Smith, J. M ............................................................ 319 Pmlth, W. 8 ........................................................ 244,321 Paper, O. A ........................................................... 10 .103 Sparka. J. V .......................................................... 28 303 S to ry ,--................................................................ 120.313 Stalker, William W ........................................... 45.306 Steerart, J. Logan................................................ 24,303 Stachheueet, -- ................................................... 20.303 Stoke. R. fl. G ................................. 135,174.180.314 Stratton. Reuel O .............................................. 152.316 Stracban. A . f l .................................................. 248.321 Btub-Chrlstensen, V ............................................ 51.307 St fiber, K a th e rin e ............................................ 140,316 flummerflold, --........................................................ 238 Sutherland, O. L ............... 25.26, 116, 252 303.312 324 Taberahaw, Tiding R ........................................ 183.317 Tebhlrw, Bernard 1)......................................... 183,317 Teltelra, Carlo M artin s.................................... 55.307 Teleky, L ................................... 31.60,114.130.304.312 Thackrah, C . T .............................................. 21,302. Thiele, A ............................................................... 30.304 Thom pson, K. W .............................................. 138.314 Thom pson, L. R ............................... 41,44.64.118.306 Thom pson, R . M .............................................. 135,314 Thom pson, W. O ilm an....................... 13,238.2.320 Tlllaon, n . F ............. 70.110,111,l 0 ,248,308.311,323 Tlsaandler, O ..................................................... 131,314 T lsw l, -- .............................................................. 20.304 T o d d .J .V .......................................................... 110.313 Travers, M . W ............................................... 88.80.300 Trm ldder, Ieone C ........................................... 146,316 T ru tler, R. M ...................................................... 00,310 Tucker, O. R...................................................... 230.320 Ttirano, L ............................................................. M.307 Tweddell, P ........................................................ 239,320 Udluft, fla n s........................................................ 80,310 Uminus, --............................................................ 20. 0 van Dlemerbroek, Isb ran d ................................ 10,30.1 van Mechelen, Victor......................................... 67,107 van Rielen. M ...................................................... 17.302 Vane. R. J ............................................................ 18.302 von LlnnA, --......................................................... 21 W arren, H .......................................................... 303.318 Wateta, Theodore C ......................................... 200.333 W atklna-Pltchfonl, W ..................................... 112.311 Walann, II. K..................................................... 248.321 W atson, 11. I I .................................................... 141,315 Weber, - ................................................................ 238 Welder, --............................................................... 21 W hipple, 0 . 0 ........................... 121. .2 0 7 ,314.318 Whipple, M . 0 .................................................. 133.314 \V|kon, Helen 1........................................... 88.122.30B Wllcoi. P M 201.323 William*, Charles R .................................... 44,126, * Willson, P ................................................. IM. 103.315 Winslow, C..R. A ................................. 30.101,305,317 Wlthera, --............................................................. 12 Wood, W. n ...........................................................25.3U.1 Wnskressensky, --............................................... 8A,>0 Wralwtc, V ................................... 217,218,200.310.325 W right. George W ............................................ 207, 3 X enophon............................................................. 200 Y ant, William P ............................................... 130.314 Yurdako*. fl. M ................................................. IM.317 Zangger, I I ......................................................... 207.318 Zenker. P. A ........................................................ W. W4 Zunlgra, M ..................... i ............................ 55.307,134 ) ) INDEX OF SUBJECTS Pane F are Abrasives, artificial............................................. 101.193 Abrasives Industry, dust-control m ethous.- 191-194 grinding wheels............................................. 191 silicosis, fatalities, ta b le............................... 119 Air, dust content, m ethods of determ ining . 135-150 safe lim its........................................................ 3 under different conditions, table................ 16 silica content harm ful to health..................... 11 Air-dust standards, advisability of establish* I n * ............................................................ 11 Atfken dust counter, description....................... 127 disadvantages ................................................... 127 modified, description ........................... 127-12* dismD Milage* ..................................... 12* Altken konlseope. description...................... 127 Alabama, dust diseases, In coal mines. Inci dence......................................... . . . . 37 Alberta, silicosis com pensation, legislation.... 27ft Alkalies, action on silica in the lungs...............63,<M Alkali m ethod, of treating silicosis, discussion. 248 Alkaline-soap dust, effect on health.................. 118 Aluminum hydroxide, action on lungs, tests.. 244 use In nrutrnllrlng harm ful effects of silica d u s t...................................................... 244 Aluminum sodium fluoride. St* Cryolite. Aluminum therapy, prophylaxis treatm ent. 249-285 Amerlran autom atic d u st niter, deficiencies.. 129 description.......................................................... 129 Anatomy, pathologic..............................................ftft-74 Anderson and Arniapach dust detem dnator. description.............................................. 135-138 disadvantages............................................... 138 Anthracosls, definition, diagnosis, differential. 3, 4.80.231,235.238 Argentina, silicosis compensation, legislation. 287 Asbestos lust............................................ 3,28,58 Aabeetosls, definition, effect on health, Inci dence, and relation to tuberculosis, investigations... 80, 81,82,98,283 Atmospheric dusts, fiee D ust, In air. Australia, llureau of M edical Inspection, work .. 288 d u st diseases. Incidence, by Industries and o c c u p a tio n s....................................... 48-49 New Soutf Wales, Broken Hill, Industrial- disease Investigation ............................. 47 pneumoconiosis. Incidence................. 109 silica content of ore.............................. 100 silicosis com pensation, cost.................. 288-287 pulmonary-disease In v estig atio n s......... 47 Workmen's Cotniwnsatlon Commission, work cited........................................ 47,288,298 lllcoels com|eniiatlon, cost....................... 298 legislation.................................................. 288 Tasm ania, silicosis in v e stig atio n s.......... 47 Western, pulmonary-disease Investigation . 47-48 " B arkston" dust trap, description............. 178 Calspar du st, action on lungs, tests................ 244 Canada, dust diseases. In mine, Incidence-- 49 M anitoba, silicosis compensation, statu .. 278 Nova Scotia, occupational-disease compen sation, legislation.................................. 27* Ontario, gold mines, silicosis. Incidence . 230-231 Mines Act, application............................. 272-278 Porcupine mines silicosis survey . . . . 49 Quebec, silicosis compensation, legislation, ret**nl........................................................ 278 Saskatchewan, silicosis compensation, legis lation, provision.................................... 375 silicosis coiuitcnsation, cost........................ 298 leglslition ....................................... 772-778 Toronto, rlliemls Investigations................ 297 Capacity for o rk ............................................ 797-301 Carbon dioxide theory, as an explanation of s il i c o s i s ............................ 103 Carborundum dust, action on lungs, tests . . 244 Carrier dry-filter api*aralus, for determining dust content of air.................................. 139 Cells, dust counting............................................. 147 Cem ent dust, action on lungs......................... 240-241 effect on h e a lth ___--............. 44,48, M, 54.119, 215 Cem ent Industry, dust dlscr-ses, Incidence . 44.43 Cem ent workers, disability frequency due to respiratory diseases.................. 238,239,242 liability to tnl*reulosls .................................. 238 m ortality ra te ................................................. 241-242 sym ptom s due to dust Inhalation.............. 241-247 Chalk dust, action on lungs.................... 238,240-242 *csts.......................................................... Chile, sUlroals comj>ensatlon, legislation......... 7HA C hina clay, effect on health ............................ Clay dust, action on silica In the lungs........ 82,83 effect on h e a lth ....................................... 82,743-744 us in treating silicosis................................ 8 Cloth method, of determining du st content of air, description...................................... 129-130 dL'advatil'iges................................................ 139 Coal dust, action on silica In the lu n g s........... 82.83 anthracite, effect on health............................. 731 control................................... 185 effect on h e a lth ............................................. 227-738 sources............................................................ 158-185 Coal miners. Srt Miners, " <'oiller" dust trap, description ................... 175-176 Compensation laws, state workmen's, prin cipal features......................................... 281 Condensation methods, of determining dust content of air, description.................... 127 Cotton-wool method, of determining dust content of air, value ............................. 129 Cryolite dust, as a cause of sillcoels.............. >14 investigations .............................................. 1*7 Ctechoslovakla, sllleoals compensation, legis lation........................................................ W7 ! Basalt dust, effect on health ............................... 60-61 Debye-flchener X-ray diffraction method Blood, silicic acid content ................................. 87 efficiency................................................. 1 Bolivia, silicosis rumi>ensat1on, legislation . 3*5-288 Denmark, silicosis, among cryolite workers. . 24 Bratll, slltcoet* com |*ns*U on, legislation.................. 2H7 compensation, legislation............................ W7 British Colum bia, occupational disease com D istrict of Columbia, ooeti|tlona1-dLsms* 1 pensatlon, legislation....................... 278 compensation, legislation.................... 283 Broken Util. Australia, New South Drill dust, control, m ethods.............................. 179 Wales, v Drill-Vac. for controlling dust, teeU ............. 177-178 Bulgaria, silicosis com pensation, Dglslatlon .. 287 Dusts, allaying w ith water In bituminous* Calcium-mineral dusts, use, In treating sili coal m in e s ............................................. 172-173 cosis .......................................................... 8 alum inum . In treatm ent of silicosis........... 249 255 In treating tuberculosis, sum m ary......... 238-242 chemical action on lunga, theory................ 4,11-12 v a lu e .......................... ZW classification ................................... 121149,228-255 California, Inspection Haling Bureau, w ork.. 292 definition ..................................................... 1.12 insurance, rates, fttllrneLs surcharge ........... 2W effect on h e a lth ............................................. 10-12 leatrial Ion...................................................... 283 Jin sfee d in ts named. slUoasU Investigations................................. 383 factors affecting transportation by wind . 109-110 329 ) 330 INDEX OF SUBJECT8 Pint -('ontlnoed Page Page harmful 68 D ust traps for controlling d ust. In abrasives etposttr* r|ulred to produce <IHw K . . 116-1ZI ana grinding In d u strie s.................... 174 quantity required to produce silicosis .. 107-116 In mines, description .................................. 171 list 244 D usty Industries, alarming position of em methods of detecting 144 ployer.............................................. 153-164 l*arth*li s|re Injurious to health......... 104 outline of program to check Industrial In air. filtration methods of determ ining. diseases ............................................... 106-197 frrnn I2M 30 precautions to protect employees . . . . 150-154 tdrol instrum ent for determining, require Earthenw are, ground, effect on health ........... 226 m ents. ........................................... 128 F.lfet grindstone, as a dust producer ........... 191 lm|>ortnnce of determining ...................... 5 KJeetrlfnl precipitation of dust, success........ 169-199 safe lim its .. 1,6,35-36 test plant ....................................................... 135 sampling methods, description........ 124,1) F.lectroslatlc methods, of determining (lust selective...................................................... 144 content of air, description and effi recent developm ents......................133-138 ciency........................................................ i u t\jes .................................................... utt'W different conditions, t a b l e ............... 125 16 Emory dust, action on lungs, te s t s .................. 244 In mol mine, sources . . . 6 Em ploym ent, of silicotic and pnoumoconlotlo rsons.................................................. 297-301 in Industries oilirr limn mining, meth<l of ndtistrlnl health studies, resu lts... . A8 n e l im in a tin g 7 Exhaust hoods, fur controlling dust .................. 2nt In metal mines, sources.................................... 6 in min*, control .................................. 7,158-100 Feldspar dust, effect on health ....................... 230 'ndiiMrlnl, control lock of Information . . . . 6 Flbrrnl* t>f lungs, p ro c e s s ........................ 65-93 estimated num ber of worker* exposed, Filter-paper methods, of dtermlntng dust t a b l e ........................... .... 17 content of air. description..................... 130 mechanical action on lungs, theory............... 4 disad v a n tag e ............................................... 131 methods lor controlling In mechnnlted min- Filtration methods, of determining d u st con hut . . . 165 tent of air, description........................... 129 nilncruloclcnl composition. Importance of Fire-clay dust. Set fla y dust. d e te rm in in g ........................................... 4M Flint d u st, effect on health.......... 3-4.20.229,230,244 particle Ire harmful to health 4-6,11-12 Foam , use In allaying dust ............................. 178 srf lr|e.|re measurements. |inj>rtunre 136 Foundry dust, effoct on workers....................... 122 protector*', use In treating |mlmonnry oiirces...................................................................42-44 r <1(eases 6-9,226-285 Foundry Industry, d ust^nntrol method........42-44 divergence of opinion regarding.................. 285 d u st diseases, In cid en ce................ 30-31.42-44. 122 ivjirs Injuria'-to health ........................... Z&8 Free (He* Set fllllca. D ust-edlerUng devices, value .......................... 201 O snister mines, silicosis among workers ........ 23 Dust-control equipment, engineering dealgn, Ontiley Bridge, W est Virginia ........................ i j j sta tu s ....................................................... 150-155 G erm any, D ortm und mining district, silicosis D a*t diseases. contributing factor.............. 4,94,103 compensation, oust................................. 290 oontml, aim . . 151 d u s t diseases. Incidence, by Industries and attlhnle of employees and operator__________ 162 occupations ........................................... 29-32 engineering 150-165 mining Industry, methods of controlling drill lack of Information..........................101,160,155 d u s t................................................ 162,170 fsetors Involved.................. 66, 101,145. 267 occupational-disease compensation, legisla Importance of nhvsleal e*amltmt|on 2tK> 224 tion ............................................... 287 in sh m sp e ano grinding Industries. . . Itit-HM R uhr district, pneumoconiosis and tuU 'r- substitution of le*s harmful m a in lui . Itm-IUI eulosls among co lliers....................... 2?9 in foundry Industry ................................. IUt-196 silicosis compensation, legislation 296-297 In granite in d u stry ....................................... 196-201 Hold Const, prevalence of M tleeh ami tulier- In mlnlntt Industry.......................................155-158 Hues of approach............................................ 93 medlcnl ....................................7-8.917-209.257 laek of inform ation...................... . 206-209 necessity for eoo|*eratlon between dodors an! en g in eers......................................... 207 remedies ........................................................ 6 c u h n l s ............................................ 32-04 Oooch criiclhlo. for determ ining dust content of air, description ...................... 130 G ranite dost, affect on health . . 116-117.121 q u an tity required to produce silicosis . . . Hm-IUV O rantle Industry, allowable dust counts ___ III dust-control systems .................................. im requirem ents.................................................. 152 s u m m a ry ........................................................ 255 d e fin itio n ........................................................... Z 12 diagnosis, difficulties Involved ...................... 216 S tt afte Rllleosl, diagnosis. economic menace to Industry ...................... 287 historical rAsmtiA ........................................... 18 Incidence, by countries............................ 22-58 ly Industries and occupations............... 22-58 Investigations. Set United Hlates Bureau of Mines; (Inftrwt Htntes U rnnrtm rnt of tabor; United Plates Public Health Hcrvlre; ('nuntrlea and Plates name!. menace t m in e r ....................... . . . . . . . . 261 te rm in o lo g y ................................. 60 Set */a Hlllrosts. abuses .........................................1 4 \ 144.19 197 efficiency.................................................... 196 197 d u s t diseases In cid en t ................................ 39-42 silicosis, in flu e n c e ......................................... 2.122 G ranite workers, liability to tuberculosis 40 42,216 G reat Rrllntn, Advisory Committee on Atnnwpherle Pollution, meteorological office work ......................................... 113 coalm ining Industry, slUcosU, compensrw lion, C o st................................................. 295 Incidence .............................................. 24 26 Investigations ...................................... 234-235 precautions a g a in s t.................................. tuterrulosls, Incidence ............................. Cornish tin miners, phtlilslnlnvestlgntlons IH4 22 . . 22 l>erhyshtre silica brick makers, relative tin- l>o*l e*|*ostire, general discussion.............. 16 D ust Alters, as a means of controlling dust hatard, description.............................188, 201 d i s c u s s io n ................................................ 166 efficiency................................................... 201 develo|wvl In Pouth Africa, elllcleneles.. .. 7 D ust particle, ptrographie Identification. 146-147 D ust respirators, 6ppro\l schedule, llureau of Mine 7 construction ami efficiency........................ 165 value ..................................... 166-187 |>n*l sampling Instruments, Set Instrum ents inimtty toslltoosls ...................... 243,244 dust diseases. Incidence, by Industries and (tccuimtlorM ........................................... 22 Investigation . ............................. 22 57 dust-respirator studies ..... IHfi-PW M etal Orlndbig-lndn.tiles(PIUnsh)Hobrnn>, iwocesses h o v e re d .................... 277-278 N orth HUtTonUhlr pottery Industry, tiealth hatard .................................................. 29 flefractorles-lndustrles Scheme (8IUts), processes h o v ered ............................... 277-276 Pandstone-lndustry (Mlllcnals) Brbame, two- cesses eovered...................................... 777 276 provision.................................................. 277-278 IN D EX OF SU B JE C T S 331 G reat n ritain --Continued P ar silicosis, oornp^n.iftiior, cost............................ 295 insurance rates, ta b le................................... 295 fatalities, by industries, ta b le .................... 119 Incidence by Industries andoccupations.. 72 legislation anti history.. . . . . 275-2*3 Silicosis and Ashestosfs (M edicd-Arrante- ments) Amendm ent Schetne, provi sions .............................. 2*2 South Wales, silicosis, among colliers 21. *4, 27 2H. 21. 277. 2 . 233 V arious-Industries (PIHendsi Scheme, In surance rate*, t a b l e ............................... 295 practical application .................................. 2*b processes covered ......................................... 277 provisions ............................................ 2t Greenburg-SmPh Implnger, elTlclency and lc*ts. results 111. H3 G rinding Industry, dust-control methods 191 -lU d u st disenacs incidence . . 2i -2'*. 29-10, 39 health haraM s... 191 sUiemls among workers ...............................2.19-40 fatalities, table............................................... 119 G ypsum du st, efTcct on health .................. 239-212 H ah n's method of determltdng hist content of air. description . PI Haw aii, occii|*ntiona1-disene romicnsntb>n, legislation ........... . . . 253 H aw k's Nest tu m id (W. V a \ silicosis con gressional investigation ................. 172 H ealth, of a orkers in dust y trades . . . . 3.5-37 H em atite dust, action on tungs and test*. results ................ 214-243 H cm atlre miniTs <ee Miners H ill dltfractosm pr, description ...................... 125 Hill hist counters, description ...................... 137 Illinois. oerupUional diseases, compensation, hyisltUon 253 Impinging methods, of determining dut con tent of air, description, dls-vdv milages, cllleiency. and value 135-14ft 'Improved H ay '1dust trap, description 173 India, Kolar Gold fields, sllimsls, iucMrnre and in\esttgations 9ft. 07 In d u strie h)plenn`. constructive program, renulrements 233 Instrum ents, for determining dust content of air, description .........................12V 140 etlleleney II re<|tiirenicnts .................................. 3 rt rev le v |1t-t.13 Insurum - rotes, for occupational dleaso and lllcusls com | tens it ion 299-297 Internal lonal Silicosis Conference (Johannes burg) nasmunen i ittons ............... 1(W Iron dual, effect on health . . . . 2V use In treating silh*mls ... 9 Italy, lust diseases, incidence, hy industries and occupd ions . (11-33 Jaimit, silicosis, among foundry workers . . . . 122 Jet dust counting apparatus, description .. 128-129 Kadcn dust control system, ailvnntnges, description. and ctUeicney Knnstis, silicosis Investigations . . I7A-177 . . . . 33 Knotiiv, action on lungs . . . 243 Kelley dust trnp. desertpt ion and tests, results 2UJ Kind in ky . slilistsls coiniiensivt Ion. iegi-1 it Ion . 253 Kolar gold fields, silicosis, Incidence and om ir- renoe 95 97.08-102 Konlrneter, for determining dust content of air description, eftlclenry, and tests . 135-117 Kotra kotunieter, cdieienry ......................... 143 Lignite, pneuinoooplosea f r o m ......................... 32 Lima dust, effect mi health 53-34 Lime workers, liability to tut*ercu!n.s|s .. . 23H-242 Limestone dust, cihsd on healih 31, .31, 243 245 Limestone worker*. liability to in1*rculi*ds 2 Lungs, Action of silica on 83 91.214 defensive reactions against silicosis . . . 714 healtiiy, roentgenological and iilstotoglcnl apjwnranre, table ......................... 54 protective mechanisms 3,53 illlcsm content alllcotlc. fihrnftr changes prociis . . . 55,57 . 4.53,79.87 revealed hy X tay, classification . . . . 3,79 I c i n g s --C o n ti n u e d Page roentgenological and histological appear ance, ta b le ................................................ ^ Lung diseases, Interrelation .......................... 23* M agnesium carbonate, action on lungs, tests . 244 use In neutraliting harmful effects of silica dust ........................................................ 214 M anitoba. sillewsl compensation. s t a t a s ........ 275 M arhle d u st, effect on h e a lth .......................... 33.241 M arbleworkcrs, liability to tul*crculos!s....... 3.1-33, 235-242 M assachusetts, foundry Industry, silicosis. In cidence .................................................... 194 granite Industry, slllccel.s. in c id en ce............. 104 ocrupntlnn.d disease ctunpcusatlou. Insur ance rates .......................................... 3-4 slllmsfs, comiicnaalloii, lusumnce legislation 2U1, 2i7. 2SS. 2VTI Medical e lim in atio n and compensation of workers for Industrial Injury...............252-297 Mellon In stitu te of Industrial Kcsenrch, dti<t investigations......................................... H I M etal tlusis. effect on henlth ...................... to-22. 29 Met:! mines, dust, rn iin v i............................... 5. 138 dust-control methods........................................ 153 M etropolitan Life lusumnce Co., silicosis Investigations.. ................................. 33 Mexico, silicosis compensation, legislation M ica dust, action on lungs ............................. . . 2S7 HU M icron, definition................................................. 12 M lcronrojector, midget, for dust determ ina tio n ................................................. H9 140 Microscopic s\stotns, lust particles revealed h y ........................................................... 14-H7 M ine air. filtering. dlsciissU n ........................... 1*8 sources of d u s t.................................................... 13* M ine dusts See Dusts. M iners, anthraelte, mortality from respiratory diseases ................................................. 3ft-37 coal, ap fn ren t Im m unity toslllcusls, theory. 232- pneumoconlosls am ong........................ 47,234-243 hem atite. sym ptom s euused by breathing dust .. 244-245 M iners' phthisis. See Pneumoconiosis. M lncm l dusts, nut um, luck of Inform ation.. . 131 M ining and allied Industries, dust, effect on workers .................................... 119. 152 15 exiwm rc. discussion................................. 1' relative punlltles produced hy various alterations................................................ 153 M ining Industry, lust-control methods . . 133-190 dust disc isos, luP idcnce............................... 72 37 Investigations ............................................... *' menace .................................- ....................... 2,1J m ethods of prevention.................................. IN' health harards .......................................... 134-133 silicosis. rom pensatlon, estim ated coat 2*8-20 Incldonce ........................................... 2,22.23,37, 93-95. 04, 207, 21S. 727. 229. 244. 2l3 precautions against ................................187-1*8 M innesota. oecn|*nlloml disease com |*nsa- tlon, le g is la tio n ............................. 251 M issouri, Joplin district, silicosis investiga tions ......................................... 33 oecumtlnimldlsea.se compensation, legisla tion ................................................. 2M silicosis law suits, m e n a c e ............................... 187 M ontana, U ntie mining Industry, dust InvestI- g vtlons . . . . . 33 .15 M other of-|carl dust, action on lungs . . 210 24 "N . A." d in t Imp, description. . . ......... 173 ,|i|t illm iis'i ioHdetieiv 49 M N evada, silicosis Investigations 33 New Jersey, crupnlUiiialsllsen.su com | tens* tlon. legislation. . . . 351 New Rmil4 Wales. See Australia. Now York, dus| diseases, estimated num ber of workers et|Mrsod . . .291 granite Industry, sdicv*U Investigations... t97-19* occupational-disease coin|*eusatU>n, Insur- auee rates............................................... 291 t a b l e ............................................................ 2 legislation .................................. 2A1 254 p in ts ............... 291 Uoehester, Industrial survey, results . 21 University of, slllnwls Investigations . . 133 332 INDEX OF SUBJECTS New Yo k --O ont n u H p*ge Pegs silicons Investigations........................................ 37 S andstone d u s t, effect on h e a lth ................. 31,63, I IJ illcosls law suits................................................... 154 S andstone in d u s try , silicosis, fatalities, ta b le .. l l j subw av, lust, a n a ly ri* ...................................... 16 S an d sto n e w orkers, liab ility to tuberculosis 238-242 N orth ('arollna, occujmtlonal diseases, com Saskatchew an, slltcnals-compenaation legisla pensation, Insurance ra te s ..................... 293 tion, p rovisions......................................... 77$ illcons com |>ensallonpInsurance rates..................... 293Scouring pow d er. See A brasives In d u stry . legislation....................................................... 263,266 S edim entatio n m eth o d s, of determ in in g d u st N orth Dakota, occnisitlonnl-dlsense compen c o n te n t of air. description ................ 133-136 sation, legislation..................................... 263 Serlclte, a s a cau se of silicosis, su m m a ry of in f l w , d u * tflltrrin g elllclenev.............................. 213 vestigations .......................................... 4,96-102 N oth Scotia. oectipatlnnal-dlsrn.se comiwnsn- Serlclte, th eo ry , criticism o f .............................. 99-102 tion, legislation......................................... 276 Bgnonlna d u s t tra p , d escrip tio n ........................ 176 Ohio, omipnt!onnl-dlrnse compensation, legis latio n .......................................................... 263.2W O klahom a. Plcher Clinic, tlHrosjs investiga tions ......................... ft, 6,33, 64, 77, 79-80, 119-12*7. 159. MO, 212-213, 214. 219, 277 tech n icu sed In radiographic w ork..........219-220 O n tario , See C an a d a. Owen Jet du st counter, description, disad vantages, efficiency, testa................... 138-139 Talm cr dual apim m tus, description................... 132 Pennsylvania, Allegheny (leneral Hospital, d u st Im c sU g alio n s............ 143 anthracite m tn rs, prevalence of sllico-il* am ong colliers............................................. .38-39 Pittsburgh, Iturrrm of Smoke Regulation, d u st Investigations.................................. 143 U niversity of. d u s t Investigations.............. 143 silicosis coni | ten wit ion, cost and legislation. 264,265 P erm lssiiilcdiistluess,standards,necessity for. 150 rf n lt grindifonc, as n d u s t ; rodneer................. 191 Philippine Islands, occupational-disease, oom- |K>nsn(ion, legislation.............................. 26.1 photom etric met hod, of estim ating konlmeter dust sam ples, advantages...................... 148 Thyslm l exam ination, as a m eans of control ling d u s t diseases ................................209-218 rhyrioloRicnl m ethods, of deteeting dangerous dusts ....................................................... 148 rich er Clinic See Oklahom a. Pneumoconiosis, m u ses..................................... 112-113 d e f i n iti o n ..............................................................2,2 9 .0 0 developm ent......................................................... 6*1 pathological features........................................... 65 relation to p u lm o n ary Infection....................... 70 respiratory diseases classed a s .......................... 60 .See b o D u st diseases; Silicosis, TollshlnR l*owder factory, d u s t, effect on w orkers........................................................ 121 Porcelain factories, silicosis and tuberculosis am ong w o rk ers........................... 29 porcupine mtnea, aUlcnals s u rv e y ......................... 46-49 p o tte rs, m ortality from consum ption, ta b le .. 241 pottery-clay d u st. ."See C lay d u st. P o tte ry Industry, d u s t, effect on w orkers---- 119-120 d a s t diseases. I n c id e n c e ........................ 24-26,29-30 slllcoals, fatalities, ta b le ..................................... 119 In c ld e n e a ........................................................... 116 labia ............................................................... 116 ''P ro te c to r" d u sts, use In treating silicosis, discussion............................................... 236-256 Tnerto lllco, ocrupalkmal-dlaeasa compensa tion, le g is la tio n ....................................... 363 pulm onary pathology, d u s t faetora producing. 93 P yrene fnem, for tra p p in g du st, d e sc rip tio n ... 178 Quart* dust Set Silk's dust Q uart* rocks, varieties ....................................... 94 Quel*er. slUroats-romponsnllon legislation, re- Shale d u s t, effect on h ea lth ............................... 236-242 8ldero*ls, definition ........................................ 2,30,60 Silica, am orph o u s, effect on h o ailb ................. 228-229 chem ical p ro p e r tU e ............................................ 94 form s........................................................................ 94 occurrence.............................................................. 4.94 u rin a ry excretion, stu d ies, s u m m a r y ............ 246 uses. In d u s tria l........................................................94-96 Silica brlckm akers, silicosis, relative Im m unity t o ............................................................... 243-344 Incidence............................................................. 22-23 8!!lca d u s t, a rtlo n on lu n g s................................. 70-7J, 86-93, 104-107, 238, 244 as a predisposing cause of tu b e rc u lo s is ___ 39-40 Silica d u s t, effect on h e a lth ....................................10- 12, 22, 35-39, 58-60, 93-116, 155. 191. 236-256 estim ated n u m b e r of m en exjtosed to In the U nited S la te s ............................................ 16 exposure req u ired to produce silicosis............ 6 In 1tottery I n d u s t r y ............................................ 46 n a tu re ...................................................................... 103 n e u tra llia tlo n of harm ful effects on h e a lth . . 244 Silica-soap n o w d er. effect on w orkers............... U 9 Pillcatea. effect on h ealth .................................... 3 Slllcatoals, d e fin itio n .............................................. 2.60 Silicon dioxide. See Silica. Silicosis, cause..................... 63.86-93,190,209. 227,244 Rlllcoste, com p en satio n . Costs an d legislation 262-297 (Bolivia, Canada, Chile, Oroat Britain, Peru. South Africa, South America, and Unltod Stales) control. See D ual diseases, control. co n trib u tin g f a c to r s .............................. 4.93.103,126 d e f in itio n ................................. 2,60,63.232-233 developm ent, relation of am ount of dust b reath ed an d length of rx|>ostira. table 116 diagnosis, by physical oxandnatlon, alWcul- ties Involved ........................................ 220-223 b y X -ray , eq u ip m en t an d technic . . 79,220-223 clinical m an ifestatio n s.................................... 78 difficulties.......................................................... 77-79 m eans................................................................... 77-79 radiological asp e c t........................................ 219-220 fatatltlea, b y Industries, ta b le .......................... 119 Incidence ........................................................... 2,23-68 pathological asp ects...........................................3,65-74 prevention , m e th o d s................................. 93,190.194 relation, to pu lm o n ary Infection....................... 65-74 to tu b e rcu lo sis.................................................. 85-93 roentgenological asp ects....................................... 79-86 stages, d escrip tio n ............................................... 74-77 sy m p to m s................................................................ 64-65 tre atm en t, b y alk ali m e th o d ............................ hy alu m in u m m e th o d .................................... 249 with coal dust and other "protector" d u s t s ....................................................... 226-266 vagueness regarding .......................................... |-y .Sr b e I>ust diseases; Pneumoconiosis, |MSt ............................................................. 376 filllootlo lung*. Srt Lungs. Rmintance m ethods of determ ining dust Con te n t of air, d escrip tio n ............................ 136 R espirators, d u s t. .Hr* l>ust respirator. R espirator filters, ty p e s ................................ 186-190 R espiratory dLsmrnw. caused hy d u s t s ............. 60 Rm plratory protective devices, selection and u s e .............................................................. 167 Rocks, w ith high silica c o n l e n t ......................... IH Ronk drilling, dust-eollectkm m e th o d s.. 174, 186-190 silicosis hazard ................................................... 174 Rock dusting, effect on h e a lth ............................ 273 Hubntw process, of determ ining du al content of BUIootlcs, em p lo y ab ility .................................... 297-301 S late d u s t, action on lungs, t e s t s ................... 244-246 South Afrlea. See U nion of South Africa South Wales. See (treat Britain Steel d u s t, effect on h e a lth ................................... 29-31 Stone In d u stry , d u s t diseases, Incidence. . . . 26-27, 29-32.46,49.63 Sugar-tuba m ethod, of determ ining dust con tent of air, description, disadvantages, a n d etH chm cy,..................................... 131-132 Sweden, occupational disease, legislation . . . 287 S w itzerland, occupational-diseaselegislation . 387 air. d escrip tio n ......................................... 130 T alc m ining, d u s t h a t a r d ...................................... 38 Russia, silicosis com pensation, legislation . . . 2R7 T h e rm al precip itato r, for determ ining dust Pandhlastlng, d u s t diseases, Incidence ............ 22.29 content of air. description Ml AiiK'oeis, fiUAUU!, t a t n e ................................... H9 efficiency............................................................. U t IN D EX OF SU B JE C T S 333 Pare P age T hom as sla t, effect on health ....................... 24tv-241 i U nited S tates In stru m e n t, for determ ining Threshold limit*, allowable concentration U3 dust content of air. tests, results 113-134 T o d d m ethod, of determ ining dt*t content of U nited Slates Public Health Scrviie, dust- air, description . 130 disease Investigations . . . 35. 40, 44, JA1 T o ro n to , silicosis Investigation* ................... 102 tests on u rin a ry excretion of silica, result* 2 r, T re m o llte ta lc m ining, du*t h a ra rd ............... T rew ill du*t tra p , description ........................ 33 U tah, h ealth of w orkers In bitum inous-coal 175 mines, nonferrous m etal mines, non- T ri-S tate lead an d tin e d istrict. silicosis Inves* ferrous m etal sm elters 37 titration* 35, V acuum p ro d u c e r, use in rock d rillin g to con <V4, 77*79,120. l<\2.212-2U. 218, 220.22* Tuberculosis: trol d u s t ....................................................... 2fW developm ent In the silicotic lung ..................gO-Rl V entilation In d u s t Control ........................ 155-158 Vermont, granite Industry, du st diseases. In tre a tm e n t, w ith calcium eom |vm uds ____ 238-242 cidence ................................... 1 . . . . 4! w ith coal du*t an d other "|>rotertor" Vlsco d u s t collector, for grtn<llng m achines. d u s t s ......................................................... 220-237 d e s c r i p tio n ..................... 201 te*ta ............................................................ 23fl T u n n elln g o p crn tlo n s, du st diseases, Incidence 29 W ashing metho<ls. o f determ in in g d u s t co n slUeo*lx Investigations..........................................35-3(1 te n t of air, d `'scrip tlo n , disadvantages, Union of South Africa, allowable dust content an d value ........................................ 132 W ator, use. In controlling drill d u st, disad of air. lim its ............................................... 5 d u s t disc isos, incidence............................. 32 vantages .............................................. 173-174 preventive m ethods ................................. 155-158 e ffic ie n c y ........................................................ 173-171 In controlling m in e d u s t ................... ifig-wu du*t Alter*, efficien c ies..................................... 7-8 W est V irginia, U atdey B ridge, silicosis fatali m ining In d u stry , dust-control metho<l*.. . I55-(/W ties, congressional Investigation . . silicosis, com pensation, cost amt legisla silicosis, com pensation, legislation .......... 2A3.2VI tio n ............................................ W -2 . 204-2 W estern A ustralia, pulm onary-disease Inves M iner's P hthisis Medical Burr functions. 211-212 tigations ................................................ 48 organ ita t Ion...................................................... 32 ; W et drilling eq u ip m en t, stan d ard * , testing 156-158 work .............................................32, MO. 234-233 W hltew are in d u stry , occu p atio n al harard* 17, silicosis Investigations .................................... 32 24.29.45 U nited Stale*, d u s t diseases. Incidence, In Wisconsin, occupational disease com pensation, cem ent In d u s try ..................................... - 44 In foundry in d u stry ................................ 42 legislation ............................................2(13.288 In g ran ite in d u s try .................................... 4*1 Wood chnrvnal, action on lungs, tests . . . . Workmen*.* com pensation laws, classifica 244 in grinding Imlustrv .................................. 39 tion . 1-262 in mining industry ................................ 35 m ining practice, comparison with South X -ray, value in diagnosingsilicosis ................. 4 African practice .............................. 103 X -ray diffraction m e th o d , of determ in in g d u st silicosis, coni|MMiSAtion, et|H*rlence Incidence c o n te n t of air, efficiency......................... 143 an d legislation__ . . . 202 272 X -ray exam inations, as a m eans of control U nited Statas Bureau of M ines, dust-disease ling dust disease*, equipm ent and investigations . . . . . 35, 1 t e c h n i c ......................................................... 720-224 54.77-78.79-80. lit. 158, 15, 212.214,21ft, 217 I Zeiss K oniincter, m odified, description an d d u st-respirator Investigations, sum m ary . 185-IH6 I efficiency.................................................. 144-145 O \/