Document yrZ37yzvYOYma2p3edBNB4BZ4

PLAINTIFF'S EXHIBIT CF.L-I402 OCCUPATIONAL DISEASES DIAGNOSIS, MEDICOLEGAL ASPECTS and TREATMENT By RUTHERFORD T. JOHNSTONE, A.B., M.D. Director of the Department; of Occupational Diseases, Golden State Hospital, Los Angeles, California-, Formerly Assistant Professor of Medicine, University of Pittsburgh School of Medicine ILLUSTRATED PHILADELPHIA AND LONDON W. B. SAUNDERS COMPANY I `14 I Copyright. HIM. l>y W. B. Saunders Company* Copyright under tlio International Copyright Union All Rights Reserved This book is protected by copyright. No part of it may be duplicated or reproduced in any manner without written permission from the publisher VIAOS I N A. PRSS OP v H, SAUNDERS CSV?*1.' SH'LAOEUPH' A To Orpha WHO WAS NOT JEALOUS OB THE TIME AND LOVE DENOTED TO THIS TASK FOREWORD Tiik recognition of diseases assoeialed with eerlaiu occupations is almost, as old as the beginnings of medicine. It was not. however, until comparatively recent limes that any large-scale altem[)t has been made to prevent and control the conditions which give rise to such health hazards. Now. every industrial country Inis enacted laws and regulations for the protection of workers, with which employers are required to comply. This has given rise to a large corps of special ists in the fields of law, engineering, medicine, and related subjects. For the doctor who wishes to practice industrial medicine successfully, it is practically obligatory for him to have not only an intimate knowl edge of the old. as well as the many new. diseases arising from the manufacture of products, but also extensive legal knowledge that will enable him to testify as an expert and to present evidence in accordance with court procedures. The objective of medical service in industry is to give prompt emergency relief to the injured as well as to those who become ill while at work. But an even more important goal is to prevent both injury and disease arising from or aggravated by occupation. It is therefore imperative that the doctor should have a good working knowledge of occupational diseases and accident prevention, as well as familiarity with production processes, if he is to render that greater service toward which industry is always striving. Through research and experience, industry has made important contributions to the promotion of health and in recent years has put into practice many hygienic measures that are far in advance of those required by law. These activities contribute to industrial and social advancement. The industrial physician and the medical department' of industry have come to be recognized as important factors for the attainment, of industrial efficiency and social well being. The changes in this special field arc so rapid that books on indus trial medicine seldom cover the entire subject. There has been a loua- felt need for answers to the. questions arising almost daily in the prac tice of industrial medicine, and (his book meets that objective, in llu- fields of both relief and prevention, and from the standpoint of com pensation law and other legal aspects. The author of this volume ha- collected and brought up to the minute an enormous amount of in formation that is presented clearly and comprehensively, ba<cd largely on his own practice and supported by the expericner in this count r> and abroad. Vktou G. Ifi:isi:u. M.I). PREFACE Until recently tlic physician was concerned primarily with diseases caused by infection, degenerative changes, or metabolic dysfunction. But almost overnight the industrial chemist created an occupational environment which offered a variety of hazards to normal health. To the diseases of commonalty have therefore been added those which find their origin in dusts, fumes, solvents, metals, and noxious gases. The rapidity with which such occupational hazards have been evolved finds the physician uninformed and the undergraduate untaught. The occasional article in medical periodicals has called attention to some of the existing hazards, but false conceptions have frequently been provoked. Certain occupational hazards have escaped attention; some have been too greatly minimized, while others have been overemphasized. It is obligatory, therefore, that knowledge be disseminated to the profession as to what constitutes a harmful ex posure, what exposures are invariably innocent, and what effects are to be expected from exposure to certain substances. In addition, the information to be found regarding some of the older industrial poison ings needs revision, especially as to diagnostic laboratory findings. This changing aspect of medicine not only has challenged the pro fession to recognize these diseases of occupation, but has charged it with a medicolegal responsibility. Originally, the Workmen's Compen sation Act was designed to compensate for injuries "by accident" and excluded disability not traumatic in origin. For this reason industrial service and treatment were largely surgical in nature, being adminis tered by a comparatively few men who were employed by large plants or industries. But gradually the laws in many states have been amended to include all, or at least a specified number of. diseases of occupation. The indications are that all of the remaining states will soon make similar provision. Following such enactments, the medical responsibility shifts from a few surgeons to all -physicians in every community. The workman with insidious disease of possible occupa tional origin will consult his family physician upon whom will be imposed the duty of determining its compensability. The foundation for the equitable fixation of liability, therefore, rests upon diagnosis. The fundamental aim of this book is to outline a basis for the vii VIII l*KKKAC,E iliat/noxix and treatment of llie more common occupational diseases, to interpret the medicolegal phase, and to offer from experience the expected disability. The last two functions approach the first in im portance. since the physician is expected to slate whether or not the alleged exposure could cause lhe disability claimed and. if so, how long the disability period will be. The presentation of the problem and tlie arrangement of the material have been designed to meet the needs of the general practitioner, but the medical student has not been lost sight of in this design. In addition, the book should be of occa sional value to the legal profession whenever the fixation of liability in the compensation ease offers a problem. The author offers no apology for the simplicity of this presentation. He is not a scientific investigator or toxicologist, but rather a prac titioner in the field of occupational diseases. He has had to work out his own salvation in many instances unaided by books of reference. To him has come the realization that thousands like him need to know more about the common earmarks of these diseases and how to con sider their medicolegal aspects. Invariably, the occasional discussion of these conditions is likely to appear in periodicals to which the ordinary physician does not subscribe. If he has access to such a source, the sub ject is usually discussed in a manner too scientific for practical applica tion. In this connection, many of the illustrations utilized herein present no intricate problem to the experienced physician, but they have been purposely chosen because they represent the common run of cases wherein errors most frequently occur in estimating their status of compensability. In order that the medicolegal phase of industrial medicine, as it is discussed in subsequent chapters, may be thoroughly understood, the author urges a thorough reading of the first three chapters. In them are discussed certain aspects of industrial medicine not always under stood or appreciated by the beginner, or even by men who have Iona been engaged in this type of practice. Of those substances which offer a hazard to health, the hydro carbons. which comprise most of the solvents, have been roughly grouped as solvents rather than into the aliphatic or aromatic series. Those substances which are most prevalent or most injurious to health, such as benzene, lead, carbon monoxide, carbon tetrachloride, or silica, have received comprehensive consideration. Treatment is given in detail. Tt is a lamentable fault of most textbooks to refer to a certain drug or method of treatment without specifying the amount of the drug that should be used, or the procedure to be carried out. For instance, "treat the existing acidosis" is a statement made in most textbooks without detailing the manner of treating it. This text ha> SEKKtir l'HKK.VCK ix not assumed that every reader is acquainted with every phase of treatment or the dosage of every drug prescribed. Tile material and experience which form tile background for 111 is book have been provided by a clinic which for twenty-live years has been devoted to a surgical and medical industrial service. It had its inception shortly after the adoption of the Workmen's Compensation Act by the stale of California--which, it is important to add. was one of the first states not only to adopt this act but to include occupa tional diseases within the meaning of the act. Thus the tradition of this institution is linked closely with the beginning and progress of workmen's compensa tion. The annual admissions to this clinic exceed 11,000 patients, repre senting multiple and varied occupational diseases and conditions such as arc found in the chemical, mechanical, and general manufacturing industries: in milling, agriculture, cattle-raising, and meatpacking; in citrus- and walnut-growing: in fishing and canning; in shipbuilding and airplane construction; and in many other occupations. Of par ticular value in tile author's experience has been the fact that a goodly percentage of these admissions were referred cases from all over Southern California which had been previously diagnosed and their medicolegal status adjudged elsewhere before being studied at this clinic. This referred group has afforded an opportunity to observe a cross-section of the existing viewpoint among industrial physicians regarding the purpose of compensation; to note what phases of indus trial medicine were not understood by the profession at large; and to be impressed with the fact that a scientific basis for diagnosis of the more frequent occupational diseases is not adhered to by the majority of physicians. By way of illustration, it is surprising how many prac titioners look upon the basophilic stippling as the sole laboratory procedure to be resorted to in cases of alleged lead poisoning. Very few search for the. lead in blood or urine: nor can many give the normal figures of such tests, either for lead of for other industrial intoxications. This book was therefore initiated because of the foregoing observation. Owing to this peculiar type of experience, which is not afforded to many, certain Exhortations are reiterated many times in the following pages. They are not to be construed as unjust criticism, but as helpful guideposts to those who as yet may be groping their way in this, as yet too-little-understood, field of medicine. It is impossible to give credit to all those who have played a paid in this effort. With humble admiration the author salutes those pioneers in this field whose efforts have advanced industrial medicine and raised it to the level of other branches of medical practice. Unfor tunately. a complete individual citation of this group of leaders in X I'HEFACK industrial medicine cannot lie inside, lest ill the* enumeration a few deserving name's lie omitted. Whenever the writer's experience has. in his judgment, been inadequale in Ihe presentation of'this subject, he has been aided by personal correspondence or by reference to the publications of these investigators, which aid is duly acknowledged. More intimately, the various members of the staff of this clinic have been most helpful. To I)r. C. E. Early. I feel a deep sense of gratitude difficult to express. As the Director and Chief of Staff of the clinic, he has permitted me a free rein in the management of my department and in. the pursuit of this work. Ilis line sense of justice and his adherence to the highest ethical ideals in their application to industrial medicine have been a source of inspiration to all his associates. Special credit must go to my associate in this department. Dr. Clifford B. Cherry, for the indispensable aid he gave in preparing the detailed treatment. Tn a clinic devoted to industrial medicine, the incidence of skin lesions is exceedingly high. Whenever tile diagnosis or occupational relationship is obscure, these cases arc referred to our consultant. Dr. Nelson Paul Anderson, who has so kindly contributed the chapter on "The Occupational Dermatoses." The author feels that the drawings which illustrate certain portions of the text and some of the .i-rav films, especially those in the chapter on "The Industrial Back," are an important contribution to the book. For these he is sincerely grateful to Florence Sugden Pierce. I am gratefully indebted also to Margaret Lee. who typed the first draft and cheeked the bibliography, and to Bertha Taylor Griffin for the many hours she spent in the correction, revision, and editing of this manuscript. Ri'thekfoki) T. Joii.vstoxk. Los Axoklks. California, October. 1941. CONTENTS PART I CHAPTER I The Pciipose op Workmen's Compensation- , . PACK I CHAPTER II The Admixistrvtion ok Workmen's Compensation and Methods op Evu.catino Disability 7 CHAPTER III The I'Yxctio.k of the Physician as Rebated to Workmen's Compensation t? PART II GASES. SOLVENTS, AND FUMES JJenzexe (Rk.nzol) CHAPTER IV .. ... ............. ..................................................... (J7 CHAPTER V Tub Petroleum Hydrocarbons .. ............................................................. 88 Carbon Tetrachloride CHAPTER VI . . ........................loo Carbon Disclpide CHAPTER VII llo CHAPTER VIII The Chi.orinatei) Naphthalenes and Diphenyls; ............. , 127 CHAPTER IX TkTKACHI.ORKTHANF. AXIS THlelll.OltKTHYI.KNE ... l."U CHAPTER X Nitrobenzene. Dichloroiiiku'cirometham:. ami Ethylene Dichi.oride ih En;<shine axis Ciii.okini: CHAPTER XI . | IlYDROt.EN SlLlTDE CHAPTER XII I jfi XII CONTKXTS CUAITKR XIII (`\uhu\ Oioxiim; ami Si i.n it Diomuk ( IIAITKH XIV Mirrim, Ciii.oiodk and Mcrim. Alcohol Ammonia and Piienoi. CHAPTER XV Carbon Monoxide CHAPTER XVI .. CHAPTER XVIr Tin-: Cyanides and Nmir< 1*Y\iks chapter xvnr Mktai.TV.mf. Eever. Wei.din'o. and Cases eiioai Carbon Arcs PART III THE METALS Lead CHAPTER XIX .. . Mercery CHAPTER XX ................................................ Manganese and CniioMii'xr CHAPTER XXI .. .... Cadmic.m CHAPTER XXII Selenilwi and N anadu ni CHAPTER XXIII ............... Arsenic CHAPTER XXIV ...................... CHAPTER XXV Zi.vc. Antimony. Coddek. and Tin . Simlicosis PART IV THE DUSTS CHAPTER XXVI r.\< k Uio KM1 71 17.7 I HO -20H `.'I >.71 -'<10 -'77 -2SK -291 *21)9 900 AVTIIIMCCiSIl.H OM*. Asbestoses The Inert Dusts CONTEXTS CHAPTER XXVII CHAPTER XXVIII CHAPTER XXIX Thk Industrial Back Hernia PART V CHAPTER XXX CHAPTER XXXr PART VI The Dermatoses CHAPTER XXXII PART VIr OCCUPATIONAL Canckh chapter xxxirr CHAPTER XXXIV Heat and Climatic Affections .. Electrical Injuries Caisson Disease CHAPTER XXXV CHAPTER XXXVI .. .. ... ... , xiii pale 310 ' 3,5.5 S$S1 I-'l 43.5 450 4G5 478 483 PART viri CHAPTER XXXVII The Medicoleoal Relationship of Trauma to Disease CHAPTER XXXVIH Xeuhosis Associated with Trauma--M vunokhixi; CHAPTER XXXIX The Preemploymext Examination ... APPENDIX Tarle of Toxic Thresholds of Common Industrial Substances , 48.5 .500 . .514 .523 Index .52.5 OCCUPATIONAL DISEASES RUST I CHAPTER r THE PURPOSE OF WORKMEN'S COMPENSATION The practice ot' industrial medicine cannot be carried out wills equity to all concerned without an understanding of the fundamental purpose of workmen's compensation. Thirty years have passed since the enactment of this law, which has done more to affect the trend of medicine than possibly any other legislative act. Vet a considerable number of practicing physicians have no knowledge of its meaning or of the manner in which it should function. Time was when such ignorance could be excused, since the administration of the act did not affect the majority of the profession. That day is past. The geo graphical extension of workmen's compensation, combined with the nationwide expansion of its wording to include the occupational dis eases, renders it imperative that all physicians comprehend its pur pose. intention, and philosophy. The physician may correctly diagnose a disea.'C independent of Ills knowledge of the law. but he cannot correctly allocate responsibility if ignorant of this law. Employer-Employee Relationship.--From the earliest limes the relationship between master and servant was unsatisfactory. On farms or estates, or in small-scale industries, the personal relationship be tween the employer and employee was much closer, and care of an injured workman did occur voluntarily. But with the development of large industries this close interrelationship was lost. Accidents were on the increase. Mangled limbs, crushed skulls, or broken backs were the responsibilities only of the recipients. Recourse to the common law by the injured was usually futile because two defen-es. namely, "assumption of risk" and "contributory negligence." were u-ed (o de feat the claim. Employer's Liability Act.--The* courts and legi-lalure-. -onghl to meet the condition by enactment of the Employer'' Liability Ad. This gave rise to the practice of transferring the a'Sinuption of ri.-k 1l > oecri'ATIOXAI, IMSKASKS mi llie purl of tlio employer lo the insurance carrier. who in turn evaded tin- law through many looplmlcs. From the standpoint of llitworkman, the chief inadequacy of llie Fmployer's Liability Act waI lie facl tliiil il was necessary for the claimant to prove fault or negli gence on the pari of the employer. Hvcn when f;iult was admilled or acknowledge ly Ihe court, the compensation return was not well standardized and was usually inadequate. For example, in Allegheny County. Pennsylvania. '2d;> nuirried men were killed by industrial accidents in one year. In per cent of these industrial fatalities, (he widows and children bore the entire income loss: and in only .`!(l pol ecat of the cases did they receive over $500. even if one assumes that all unknown amounts were large and all suits pending would be de cided in favor of the plaint iff. Of the fatal accidents which occurred in Cuyahoga County. Ohio, over a ten-year period, only .`Iti per cent were compensated under the existing laws, and the average amount received by the dependents was $K,`>S.(iI. Abuses of the rights of the workman under the common law or the Fmployer's Liability Act incited action bv the social and legis lative forces of that day. resulting in certain recommendations by those who studied the problem. First Real Compensation Acts.--From this study were evolved the first real workmen's compensation laws adopted by the slate of Xew York in 1010. to be followed the next year by leu more -late-, until today all but two stales have these laws. The cardinal principle of the new act was that liability for an industrial accident must rest upon the employer even without fault. An exhaustive treatise on the law to explain its countless vari ations would be of no value lo persons other than lawyers. Il is tiol necessary that the physician lie informed on all the technicalities of the law. but he should be familiar with that portion of the law which deals with the placement of the liability. Ignorance in this matter is primarily not the physician's fault. His legal course in medical school detailed only information regarding narcotics, illegal abortion, quaran tine. and the like, t'pon entering an industrial practice, lie receives no instructions concerning the meaning of the Workmen's Compensa tion Act. nor has he ready access to any interpretation. For these rea sons the author feels it L appropriate at the beginning of this book to "break down the main portion of the act so that the reader may gain a working knowledge of its intent. Purpose of Workmen's Compensation. Act.--The Workmen's Com pensation Act. or Law. proposes to compensate a workman to a lim ited extent for an injury, or in certain slates a disease, caused by hi' employment. I his benefit is not restricted to lho~e who perform Tim-: i'I'ui'osk or wiihkmkn s comckxsatiox manual labor. 1ml includes any workman-artist. teacher. musician, actor, nurse. physician. and llic like, who is employed lo work Tor others. The law confers benefits of money and medical care for llitperiod of disability, as well as benefits to dependents of the deceased workman when and if his death is due to an industrial exposure. This net is an exercise of the police power of the government designed to protect the workman and to insure a measure of rehabilitation in ease of injury. It was not designed to confer damage benefits, or lo give the injured full compensation for the harm done. Furthermore, and most important of all. the law cannot legally charge the employer with every ill lo which men are heirs. Before workmen's compensation became effective, the workman could rarely obtain relief for a dis abling industrial injury. Flagrant abuses by the employer and increas ing industrial injuries paved the way for a reform. As a result of agitation by certain forces, this act was adopted as a compromise. To the employer it promised protection against damage suits which-might mean financial ruin if in turn he would assume a prescribed limited liability. To the workman it guaranteed certain limited benefits in all eases of injury, even though he could not prove any negligence on the part of the employer. Administration of the Act.--The administration of the act varies somewhat with the different states, but as a whole there is marked uniformity. The industrial com mission-':. or board.',-, or bureau-':, as they may be called, have exclusive jurisdiction in all controversies arising under this law. The claimant must obtain his rights through this com mission and cannot bring suit in other courts lo enforce any right conferred by these statute's, except in certain instances by appeal. Any workman who feels that his ease has not been fairly dealt with by the employer or insurance carrier, can file a formal application for hearing before the rndustrial Accident Commission. Liability under the Workmen's Compensation Act is created by a standardized phrase, taken bodily from the English act and incorpo rated in the majority of the state laws. Condensed it reads. "A ease is compensable when it is a personal injury by accident' arising out of and in the course of employment." Certain states have altered the wording "arising out of and in the course of": for instance. Wyoming compensates for injury to employees "as a result of their employ ment." but the wording used intends that a causal relationship Inshown between injury and employment. In order to understand lliibasic phrase, each part shall be considered. '`Personal Injury."--"Personal injury" means physical harm only. The purpose of compensation is not to reimburse one for ,-i financial loss or wrongs committed against the reputation, social position, or 4 (K'C'l'l'ATIONAL DISKASKS other *cnsihilities of tin1 employee. The lenn has been enlarged in scope in many stales to mean that it is not necessary that a blow, fall, or actual violence occur to classify the ease as compensable. Through the door of this revised interpretation have entered the occu pational diseases in some states. Injury to the body can be sustained from noxious gases, dusts, metals, and tile like. Many stales having no schedule fur occupational diseases have on occasion accepted a ease as compensable upon this basis. "By Accident."--Here again is an attempt to differentiate between a diseased condition and trauma resulting from work. This term places emphasis upon the time interval between the alleged injury and the onset of disability. Obviously a laceration or fracture or severe contusion is apparent to all. and medical aid is immediately sought. In contrast exists the occupational illness, which usually develops in sidiously and which is not immediately apparent. The effects of an accident may lie far-reaching, and the ultimate result foreign to Un expected one. For example, compensation was granted by the Supreme Court of Pennsylvania in a case in which a workman was thrown violently against an object, fracturing a rib. Pleurisy developed, and in the course of this complication the patient became delirious and committed suicide. It was held that each subsequent event was the result of the original injury. The eventual results from an accident may also be influenced by unusual factors requiring an opinion as to whether the end-result is compensable. In Wisconsin a claimant in the course of his employment cut his hand. He was given medical attention, and the wound was practically healed when he engaged in a boxing-match. As a result his injury became infected and ended in the loss of the hand. The Supreme Court sustained the decision of the Industrial Commission that the accident was not the cause of the ultimate disability. "Arising Out of and in the Course of Employment."--This refers to the time, place, and circumstance under which the accident, or disease, takes place. The first, portion of this phrase connotes or im plies the danger peculiar to the work, and under this portion of the phrase must be considered most of the occupational disease*. It rules out conditions common to the neighborhood or district, or conditions which may occur at home as well as at work. Employees spend the greater part of each day at their work, and illness of any type may have its onset while they are at their employment. But. the fact that it arises while one is at work does not mean that it arises out of lie work. This fact is too often lost sight of in regard to backache or hernia, especially. This term "arising out of' implies that it must be incidental lo the work and not independent of the relation of ma-ler TUB lUHPOSB OF WORKMEN'S COMPENSATION 5 to .servant. It need not have been foreseen or expected, but after the event it must appear to have had its origin in the employment. Such an understanding enables one to render a just opinion regarding sun stroke or heat exhaustion or frostbite. "In the Course of Employment."--An injury can occur in the course of employment only while the workman is engaged in render ing service to his employer under agreement of hire. If, after his day's work is done, an employee of his own volition remains to visit others on another shift and suffers an injury, it is not compensable. Should a truck-driver go out of his regular route for reasons personal to him self and not in the pursuit of his work, he would not be compensated for any injury lie sustains while deviating from the. work he was hired to do. Importance of a Detailed History.--It is apparent from the above discussion that a detailed history is of fundamental importance in each case. Before treatment, the physician should go carefully into the allegation professed by the patient. Before the physician expends time and material on treatment he should ascertain whether or not the case is apt to be acceptable to the employer or insurance carrier. Horseplay, intoxication, awkwardness, arguments, or fights resulting in injury should all be reported to the carrier for action before pro ceeding with treatment upon a compensation basis. In rendering emergency treatment the doctor should inform his patient of the basis of his action. Types of Cases.--Having broadly considered the gist of the law, it is evident that cases for consideration resolve themselves into three main groups: t. Those obviously compensable i. Those obviously not compensable 3. Those where compensability is obscure, doubtful, or not readily discernible It is within this third group that most of the occupational diseases find classification. Differentiation of Xon-occupational and Occupational Diseases.-- An analysis of the reports, diagnoses, and testimonies of a large crosssection of physicians relative to their allocation of a case into one of the above three classifications reveals the following facts:l. l. Claims for an illness due to occupational environment run the gamut from Bell's palsy !o athlete's foot. Any disease man is heir to is apt to be alleged as arising from occupation. Since this is so. there is frequently a failure to discriminate between a nun-occupational disease and an occupational one. (i OcrriWTIONAI. IMSKASKS :i. There exists frequently ;i failure Id differentiate mere exposure from an onvironmcnl constituting an aolnal hazard. 4. Tlio moiv accurate diagnose' oomo from lhose- physicians en gaged onliroly in indn.slrial modioino. The inaoonralo aro morr apt lo oomo from physicians engaged part timo. or only raroly. in thi> phase of modioino. .j. A largo percentage of lho errors in diagnosis can bo traced to irresponsibility or disinterest on the part of the physician. He lias failed to visualize the philosophy of compensation. Many fool it is easier to accept or deny a ease automatically than to ferret out the actual cause of the illness. Rejection of Claims.--Lost the reader think that the doctrine preached here and elsewhere in these pages indicates that the indus trial physician or the insurance doctor has combined with the insur ance carrier to defeat the employee in his claim for disability, let him consider the following statistics, '[`lie percentat/e of rejection,v by the various privately owned insurance companies and the self-insured employers is not available, but it is comparable to the figures issued by the Stale Compensation Insurance Fund of California. During the calendar year they accepted voluntarily. withouL any litigation. !Hi.(i per cent of all claims made upon them, thereby rejecting only .4.4 tier cent. In 19.87 the rejections were .8.2 per cent: in 19.88. 2.8 per cent, and in the first ten months of 19.89. 2.5 per cent. It has been pointed out by the Director of the State Department of Industrial Relations of California that certain of the cases that, form the per centage of 2.5 per cent actually file for hearing and a certain number of them are awarded compensation, so that the figure for the number of rejections is nearer 1 per cent. Evidence that the Industrial Acci dent Commission is functioning justly is to be found in the fact that it was upheld in 89 per cent of the cases appealed after its decision. Certainly these statistics offer proof that, from the standpoint of the workman, the philosophy of compensation as it was originally intended is rigidly adhered to in this slate. Deviation from the original purpose should never be indulged in by either the lawmakers or the medical profession. The physician will best maintain this purpose by giving careful consideration to the analysis of the component parts of the basic phrase as they have been interpreted in this chapter. CIIAl'TKR [I THE ADMINISTRATION OF WORKMEN'S COMPENSATION AND METHODS OF EVALUATING DISABILITY Wouk.mkx's compensation laws were enacted to mt*ol thi* economic need.- of a large body of people. They are effective in each stale only to tin' extent to which each slate lias endeavored to adopt the prin ciples and enforce the intentions of the act. It is an acknowledged fact that many evils that crept into the administration of the act could have been avoided had the medical profession early entered into a full participation with the lawmakers. 'Today it is practically obliga tory that the general practitioner and certain of the specialists become familiar with the essential features of the legal aspect of workmen's compensation. To this end the following brief discussion is directed. And also, although this book has dealt consistently with the occupa tional diseases themselves, and has not concerned itself with the traumata which occur in industry, the author appreciates the fact that many of his readers are engaged in a general industrial practice and it was. therefore, thought appropriate to discuss the method of estimating disability and to include tables illustrating the require ments and benefits of compensation as they are in effect throughout the United Stales. 'The tables herein ((noted are authoritative, since they were obtained from the United States Department of Labor. Bu reau of Labor Statistics. Bulletin No. (>7,-2. 1!)40. Financing Payment of Benefits to Injured Workmen.--Financing the payment of benefits to injured workmen is accomplished through insuring the employer's liability. This may be effected through in surance with private companies, in a state fund, or by "self-insur ance.'' A state fund or state insurance system exists in nineteen stale-, in eight of which only the state fund operates, while in the other eleven private companies enter into competition. In the majority of stale- where a competitive basis exists, an employer may become -ell'iusured if he satisfies the requirements specified by that state. Workmen's Compensation Not Compulsory in All States.--It will be noticed from the table on pagcS that while all but one state {Missis sippi) have some form of workmen's compensation, it i- not com pulsory in all of them. There are thirty-two states which have elec tive compcii-alion. but in twenty-three of these election i- pre-ium d s OCCUPATIONAL DISEASES Tviii.k 1 --Ixsi.n.vsr K RnqrmK.vii.'.yrs or Workmiss's Comim:xsvtu>s~ I,avvs Sl;itc- Insurance Required in Compensation ---------- ;---- ---------------- orEk-cthn- ` KxrlS^vor ! Private Companies ('ompolitivc i or by Self-insurance Ala bum; Arizona..................... Arkansas................. California................ Colorado.................. Connecticut.............. Delaware........... District of Columbia Florida...................... Georgia.............. Hawaii .................. Idaho........................ Illinois..................... Indiana..................... I owa.......................... Kentucky........................................ Louisiana........................................ Maine............................................ Maryland........................................ Massachusetts ........ ................... Michigan......................................... Minnesota ................................. Missouri..................... ............... Montana......................................... Nebraska........................................ Nevada........................................... New Hampshire ................... New Jersey.................................... New Mexico................................ New York..................................... North Carolina.............................. North Dakota ............................. Ohio................................................. Oklahoma....................................... Oregon.................................... Pennsylvania................................. Philippine Islands ................... Puerto Rico.................................. Rhode Island............................. South Carolina ................. South Dakota Tennessee....................................... Texas..................................... I tali, . .. Vermont .. .. Virginia ......................... Washington ......................... West Virginia ............................... Wisconsin.......................................... Wyoming...................................... Lnited Slates; Longshoremen's A< t Civil employees Elective Elective Compulsory1 Competitive Either Compulsory Either Compulsorv j Competitive Either Elective , Competitive Either Elective Eit her Elective Either | Compulsory Either ! Elective Either ; Elective Either Compulsory Either Compulsory Competitive Either Compulsory Either Elective Either Elective Either Elective Either Elective Either Elective Either Elective Either Compulsorv Competitive Either Elective Private companies Elective Competitive Either Compulsory Either Elective Either ('ompulsorv Competitive Either Elective1 Either Elective Exclusive Elective Self-insurance Elective Either Elective Either Compulsory Competitive Either Elective Either Compulsory I Exclusive Compulsory i Exclusive Either Compulsory ; Competitive Either Elective ' Exclusive Elective Compulsory i Competitive Either Either Compulsorv I Exclusive ! Elective Either Elective Either Elective Either Elective Either Elective Private comp; ('ompulsorv Competitive Either Elective Either Elective Either ('ompulsorv' Exclusive Elective Excltlsiv e Self-insurain C 'ompulsory Either Compulsorv Exclusive ('ompulsorv Either ('ompulsorv ' No security is required. Insurance is optional. - No security is required, but in case beneficiary filos dolin'ol` doutli rlaim. may deposit KMJUO with dork of (.li^lricl court or >ivc boiul for Hint .tiihhiuI. In otlu-r him*** THE ADMINISTRATION OE WORKMEN S COMPENSATION 9 lo obtain in the absence of positive rejection. this presumption affect inu both the employer and employee. They are: Alabama Alaska Colorado Connecticut Delaware Florida Georgia Indiana Iowa Kansas Louisiana Missouri Nebraska New Jersey New Mexico North Carolina Oregon Pennsylvania South Carolina South Dakota Tennessee Vermont Virginia In other elective slates the employer must take positive action, and if he acts, the employee's acceptance is presumed, except in Ken tucky, where he must sign an acceptance. In Arizona the law is com pulsory for the employer, but the employee may elect not lo be covered. States Compensating for Occupational Disease.--While all but one of the states have some type of workmen's compensation, it is to be appreciated that not all of them have coverage for the occu pational diseases. Originally in all states, compensation was paid for a disability resulting from injury, injury being construed to mean a single trauma to the body. Gradually the injustice of this was realized by a number of the states, and coverage for all or some of the occu pational diseases was included in the meaning of the act. At the pres ent time there exist three groups of states: those which cover all occupational diseases, those which exclude any occupational disease, and the last group which specifies the diseases covered by the act. I have attempted to list these accordingly, but this list cannot be con sidered accurate, since it was difficult to interpret the meaning in several of the acts. Injury in certain states is considered as resulting from a sudden, violent, or traumatic force and excludes "'injury to the tissues" by insidious or slow accumulative effect. Other acts state directly, or infer, that injury is to be construed as any harmful effect upon the body structure, whether the cause is accidental trauma or exposure to harmful substances. The third group of states recognizes only certain specified hazards, and compensates for any disability arising from such. To us of the medical profession it is manifestly unfair that discrimination or total denial should exist in any state. Surely the man who is disabled from constant exposure to lead or claimant may have writ of attachment issued unless employer tiles an undertaking in an amount double that sued for. ; As (o employers. * the state compensation court, has ruled that all public employees are subject to the act, without light of election by either the employer or the employee. ' By direct appropriation of Congress. 10 (K'Cri'ATIO.VAI. IMSKASKS benzol is just a.. deserving of medical care and compensation as one who lacerates hi.', linger or break' his lea:. There is no (|iiestiou in this writer's mind that this inconsistency in the law will rapidly be changed. Governmental bodies which eompelisate for all occupational dixeaxe are: California District of Columbia Illinois Indiana Wisconsin Cuilcd Stales Government (for its own employees) Tlmsc which dcxiynate flic onrupationx or make alloiranccx in the interpretation of the act arc: Arkansas Connecticut Delaware Kentucky Maryland Massachusetts Michigan Minnesota Missouri (?) Nebraska New .Jersey New York North Carolina .North Dakola (?) Ohio Pennsylvania Khode Island Washington West Virginia (silicosis only) Those .'(ales which specifically exclude occupational dixeaxex are: Alabama Arizona Colorado Florida (?) Georgia Idaho Kansas Louisiana Maine Montana Nevada New Hampshire New Mexico Oklahoma Oregon South Carolina ( ?) South Dakota Tennessee Texas Utah Vermont Virginia Wyoming The following tables are self-explanatory and need no comment. Tuii.k - -Status Makivc N'cmkhicai. Ivxkmiwioss1 Kmployer--Are Kxempf Who Ha\e Fewer Than ~ pliuKMm-c*s t p,*l{uKycmc*s J Kiuploytvs .1 Kiiiphove*. :( Km. ' n i-.in- II Km- |llo\ CCS l.i Km* [|lV ecv Id K plou-. * iM.iInnti.i ' Arizona j FloridaI Kentucky * Tc.va> Hah , WKcoimii Colorado ' Alaska New Mexico1 Aikaiisiiv* . Maine j (lent gu New Yotk" ('ounce! [ctil Puerto Uieo Delaware Ulmde Island Kansas New IlainjJsfiuc* TNcournthesCs'c.t( nilnia' Missouri' Vermont Virginia 'south Cam- Uah. hna l hv following states do not make miuieiK.il exemption*.: Cahlornia, Distitel ot Columbia. llaa.ui. Idaho. Illinois. Indiana. Iowa. Louisiana. Maiylaiid. Massaclui'etls. Michigan. Minnesota. Montana. Vehiaska. Nevada. New Jersey. Noith Dakota. Hreitoiu PcmisvKama. Plnli|>pities. South Dakota. Washington, West Virginia. Wyoming. and l nited States Civil Kiupiovees' .md LoiigshoiomenN Aetsi. In some of these slates, however, coverage is limited to certain enumerated industries. -Al option of Workmen's Compensation Cnimmvdon. immorieal exemption does not applx in him* ni kn/aidmis employment s. I raelor saw units and other saw mills emplov mg !< or less are excluded. Nmiimoal exemption does not apple j) mjtirv occurs when at work ii[iou anv delink. <a pole, or such structure 10 led or more sihove giound. Contract for budding nr budding lepair wuk ' eov eied it oiiii.u tor emplov s or itmie emphn re. . anv one time. Nnmeneal exemption applies only in ea*e nl imu-ha/mdoU'* eiuptoymeiits. However the It gunips .,t idoii' industries aie so <-oiupieheii*avc lh.il the immencal exemption seldom apphc'. Numerical exetn(>iion doe* not apply in euiplov iiieul m mines and in building < oust i u< t ton. ' Numerical exemption applies oidv in <ase ot nondia/anlmi' eiuptoymeiits. * "mw nulls and logging opei ators vv it h less l hau |. employees are exehlded. Tun.i: : W\itim; Timi: lti;<piui:i> i:v Kun Srxri: No Waiting Time I In (i l);!>* 7 Da\s .Compensation Paid for IU or 11 l )ays j Waiting Period if Disability Lasts Specified Time Oregon Vlaska 1 Florida f> Arizona Arkansas Alahuma (ltd j Aluhama l weeks* ( olorado MO* t Arizona (-2 weeksi Illinois (C. (`ulifomia' Iowa < | t- ; Arkansas t weeks? Maryland *.'b Connecticut i Connecticut < I- weeks * Missouri <!>' Delaware | Dela ware < V weeksi Oklahoma Distriel of Co t District ofCoiumhia *7 . Mhodc Island *:L i lumbia ' weeks * ' SoMthCaroliunCl <\ (ieorgia I Hawaii (7 weeksi . I'tali Cb ' Hawaii''1 | Idaho 11- weeks A Washington (.'if Idaho Wisconsin Indiana Illinois VIO duvsi* Movi-i.r I I Slates: j Kansas j Kentucky \ t weeksi Civil Fmploy- * Kentucky | Louisiana ((5 weeks! ees Cif Louisiana * Massachusetts (*2 wks Maine0 , Massachusetts i Michigan *0 weeks, Minnesota 11 weeks* ! Michigan* | Missouri (t weeks! Minnesota1 Montana VS weeksi Moniana' j Nebraska ;fi weeks- Nebraska 1 Nevada (1 week* \ Nevada 1 New Hampshire * l | week l New Hampshire j New Jersey *7 weeks' New Jersey j New York (.> weeks? I New Mexico Nortli Carolina weeksf ; New York North Carolina \ Nortli Dakota (1 week Khode Island Il2 weeks? North Dakota I South Carolina (*2 weeksi Ohio1* South Dakota Hi w eeks- i Pennsylvania*" j Tennessee ((> weeks? j Philippines' \ Texas (t weeksi \ Puerto Kiro11 Virginia (fi weeksi ( South Dakota West Virginia (J weeks! Tennessee Wisconsin 110 days* " Texas' Wyoming (1.7 days- | Vermont 1 l'nited Slides: Long ! Virginia shoremen *7 weeks West Virginia Wyoming*1 ('nited Stales: ! Longshoremen i 1 A[)plies only to temporary disability. * In east* of (k'al li, eompen.sation is payable from dale of death 1 Compensation begins on dale of injury in ease of permanent partial disability. 4 If disability period exceeds 4 weeks, waiting period is to be reduced by f days, and by 1 additional day for each week the total disability exceeds \ weeks. 'Total disability, bid compensation payable from first day of disability in ease of partial disability. *'Applies only to temporary total incapacity. If compensation extends beyond stieli number of weeks after injury, compeusalion for fifth, sixth, and se\euth week is increased by two-thirds. In ease employee has beneficiary or dependent residing in ( nited States. If there is no such beneficiary or dependent, waiting period is `2 weeks, but if disability continues <; weeks, compensation payable from date of injury. ` Abo. no compensation allowed for the first week of total disability, whenever it ma\ 1 No compensation to injured "work-relief employee^" during first *2( weeks of dis ability. except in eases of permanent injuries- in specific schedule or death. !S Applies- (o temporary disability only. No compensation i" allowed for first 7 da\' following dale on which employee presents himself to physician for treatment. II 12 OCCO'ATIO.VAn DISEASES Table 4- Minimum a mb Maximim Hji.vkitt.s l'.vuku Woiikmex's Compensation Laws, bv Kvtent oe Disability \mi bv Stati:, Ji i.v 1, 1!)K) Death l.unil >f P> ments Stale Percentage of Wages i Mavimum Period Per Week ' Total J maxi- Mavi- jmiiui1 1 Minimum mum , 1 Alabama Alaska . | Arizona.... , 25-05 300 weeks i $5 *or actual wage, if less* lo-OO'^l Widow-flood, or specified minority | aia.mij j $51,000 age of children Arkan.sjis 1.5 0.5 4.50 weeks $7 20.00t -7,000 California. 0.5 ' $0.50 '.i.nn* -.-`t.'i Colorado > .5(1 31-2 weeks- *55 14.00; 4.375 Connectieut. 50 , 31-2 weeks *7 25.00; 7.SOO Delaware < 15- 0(1 i 285 weeks', thereafter, to children till i Weekly wage deemed not 18.00* 5.130 j .specified age under $10 District of * Columbia 15-00'-,,e Widowhood or specified minorily '' Weekly wane doomed 2.5.001 7..500 ' age of children ,, under $1*2 Floiidu. .. 35-00 3.50 weeks $0 lor actual wage, if lev IS.OOj ,5.000 Georgia.... ; i3iI 300 weeks _ ............................ Hawaii 25-00 { 31*2 weeks; thereafter to children to < Weekly wage deemed i 30.0U; .5.000 age tU dor 104 weeks more, if nn* under $.5 married and iucapsddcl Idaho . 10 .5.5 400 weeks (in case of incapacitated, $0 (or actual wage. If lev 1-2.00 unmarried child. 400 weeks more I after reaching 18 yea rat i Illinois, . , 417 weeks t $7..30 <20.00} 5..500 Indiana.. . fowa. 300 weeks 00 300 weeks iI $$80k.v80> lor actual wage, 10.50, .5.000 1.3.00* 4,500 Kansas {Total minimum not i IS.(H)t 4.000 Kentucky... 05 400 weeks \1 8.)than $`2000 W.00 4.800 I/Ouisiana... Maine... Maryland. . Massachu setts. . - 3212-05 300 weeks 00 7 a 300 weeks 00--, 410 weeks $3 (or actual wage, if less I $({ | $8 (or actual wage, if lev. I ! $4400 weeks; thereafter to children till 2(1.00' ti.OOO IS.00 4,000 IK.00} ,5.000 <10.00 , specified age; other dependent-. 0G"n percent--mavimum period. i .500 weeks Michigan 002:d 300 weeks 18.00 5.400 Minnesota 30-00J3 StW weeks; thereafter, if dependent j $S for actual wage, if lev 20.00- 7..500 Missouri.. Montana. Nebraska, wife and cluldien to total of $7500 8000 -,-jj 002'-4 weeks 5 $8OO-OO^! MW weeks 00-rj 3-2.5 weeks ; $0 for actual wage, if le- 20.00 13.815 21.00 s. 400 1.5.00 4,875 Nevada.... !I New Hamp I0-00'^| Widowhood, or specified minority age of children ; IS. 40. shire .. . New Jersey ,, 35-00 300 weeks; thereafter lu children till j $10 for actual wage, if le New Mevii-o specified ace 20-00 300 weeks 1 1 85 is.no 5.4nn New York . l.-0(r a Widowhood, or specified minorily 23.US age of children unless blind or crippled Noilh Caro lina do 350 weeks is.oo, o.ooo North Da kot.i !U (!i>- ; Widow hood, or -pec iiicd minorit \ Weekly wage deemed 20.00 15.000 age of child i en under $18 \ : 'Potal mavimum payments computed by Ihticau of Labor Statistics, where not stipulated by law. l In ca>e of uueompIieato<I silicosis or nshc-'to'is, maximum is $.500 if death or disablement occurs m first month act becomes effective and maximum Increases 850 each month untd limits piovidcd for accidents .ire reached. * For injuries occurring alter July 1, 10351. the installment rale, but not the aggregate amount, shall t.o in creased 10 jicr cent. ` For wi*Iou-, phis $2 for each child under 18. or over 18 and incapacitated. - 150 times average weekly earnings. I THE ADMINISTRATION OF WORKMEN S COMFKNSATION 18 Tuti-ii 4-- Mixiuiwr and Maximum Bkxkitis i .sdkh \Vuhk.\iex"-; Compensation 1,u\s. BY K.vn-.NT OK 1>1<AU1UTY AND BY STATE, JlT.V 1, 1!) HI (\>n Lilli le<l Di'tilh --( "imlimivit Uiii>t of Payment aliitc Percent- . age of W.ll'Os i Maximum Period Per Week Minimum ______ , Total ma\*i- Mimaixuit- . mum Ohio. . (>(*( Period between denib and 8 .veal- 8IS.7.5! $(1,500 after dale of injury t Oklahoma Oregon..*. , , , Widowhood. or .specified mmonly } ............................ '\`10.0U. * am* of children r ? Pennsylvania. 15 (5(5-;; OHO weeks; tJicreallrr. reduced pay- Weekly wage deemed nut 1S.O0, ment- to children to .mv It* under $15 ` Philippine Islands.- -25~<*0 *2()K weeks Weekly wage dcorneal not *l$.QU -THOU under 4 nor over 80 pgsOs Puerto Rico. .... ................. ...... ... 4 .'J.out) Rhode Island., 50 500 weeks $8 Itf.uol H.000 f'oulli Carolinn.............. 00 0.30 weeks $5 > >5.00f <1,000 South Da- i i - koto.,. .1 Tennessee. . .. j .............................. ... . .30 i 400 weeks - i ............................ .. 1 >>.3 {or ac,|iul wage, if lessi * 0.000 I0,00| .3.000 Texas. . 00 ' MOwecks ' $7 _ ->0.nt>j 7,*>0t ['(ah. 00 Period between death and 0 years Total minimum nut undei <l0.00* 7,.300 a after date of injury * $*2000 Vermont., , I.3-.30 i `2G0 weeks ! Weekly wage deemed not 10. RM 0.500 ;< ' under $.3 Virginia .35 f 000 weeks ` .'SO * 10.00! .3,000 Washington..) . j Widowhood, or specified minority) ............... ,, . . '.3.3.00{ 1 \ age of children West Virginiaj , . . f Widowhood, or specified minority j ............................................. > ;;00.00, | | age of children ! Wisconsin30.. j Wyoming. 11 ` ..................... . ... ................. '$10 ... j ........................................................... | $180 per year lo I child 15.00j n30.(MJl 8,500 I'nitedSlatesd j ' Civil cm-j 10~<i0-.ij Widowhood, or specified minority j Monthly pay deemed not -20.02. ,, ployees. age of children { muler $87.50 Ixiiigshore-; l5-(5(!-'ij Widowhood, or specified minority Weekly wage deemed not *2.3.00 7..30O men. age of children * under $1*2 Permanent Total Disability Alabama ,. Alaska Awona .. . * Aikaiisiis < alifurnia. t.olorado . . ( oimeeticnt.. 55-05 l* 05 <1.3 (55 .50 .30 .350 weeks 8.5 or actual wage, if less* Life } 450 weeks ` 87 j *211 weeks; thereafter to tier cent of 80.50 ! wages for life ' Life ` 85 5-20 weeks 87 :$IS.UU 80.000 20.110r -7,000 -25.00- .. It.OO !-'-25.oOfi:i.oim * In ease of uncomplicated -ilieosis or nshe-to-is. uuuimini is $500 if death or disablement occurs in fir-i month act becomes effective ami maximum inerea-e-. 850 each month until limits provided lor accidents are leached. LW.` Per month, for widow, phis $$ for each dependent child. ' Plus 10 per cent for each dependent child .not lo exceed 5.* under Id years. Henelits mar be extended indefinitely in meiitorious ea-os. ` Per inoiilh for widow with -2 children, pin- .3 for m*|| additional child under 10 year*. `J Amounts are increased or decreased up to 1.3 per cent for employers or employees violating -afety tegulaltoiis; triple compensation for minors illegally emplovcil. } Compensation ecpi.ils i limes average annual wage, payable in installments of .30 per cent of average weekly rale, but total for death, plus dtsabiHlv compensation, may not exceed 70 per cent of weekly wage for liom -280 to 1000 weeks, depending on age. Additional compensation allowed lo dependent -pouse with de pendent children, according to age. 'Per month, to widow, plus 85 for each ehdd under 10* v**ars. s*' Per month, for widow or invalid widower total ssWOO-, plus $IS0 per year per child total $5000/. 5| $5 (or actual wage, if less) sifter RlO week-. Plus additional allowance for constant attendant if necessary. llJ Additional compensation at -aim* rale tor maximum of Kit week-* for -eriou.s and jwrm.iiwnl disfigure, mmit of face, nock. head, or hand-, hut combined *-ouipen-a(ion not to exceed 5*20 weeks. 14 OCCUWTIOXAI/ DISKASKS I'mjij: 4 Minimi m wd.Mwimtm Hiaiht-s i ndkk Wokkmia's Comimasvtion Ia\\s. k'v Kvii.vi ui- Di's.vmu r\ v\n in Siwti:. Jn.\ I. into (`nnlimicil I'cntmut nl Total Disability- (`onlimtrd l.uilii <<i l\i\ meats Male IVreciit- .U'C of Warov 1 Ma\iiiriim 1'i-riod IVr Week Mimmuni _ M,.\imum Total :na\i' ilium Delawaic .30 17.1 weeks 8.3 or aetnal waye. if less* sl.i.im X (.11(1(1 District of ('olutiil >1.1 Florida. Heoiyia o<* Wlu\U* |>*)iod ol *|wd>dtS\ .3o-nn .`(.10 weeks .30 :(.10 week' XX or aetnal waye. it lew* 1 $0 <or aefnal waye. it less ` St (or actual way.*, if less; 2.1,01 7..ion |s,m .1.000 2o.no 7.000 Hawaii Idaho . ch til*2 weeks S3 '.3.3 (id (00 week'*. (lioicaller SO ueckh xs. v *o 2.1.00 .1.000 10,00 Illinois j It dependent eliiMieu .10 -(1*1 H7 weeks XT..10 811 if 1 elidd under -ip.uo < , 10. .s|2 it -2. s|.`( >1 ;i. ami . Indiana .*1.1 .100 weeks X| 1 if 1 or more XS.H0 or aetuai waye. it less! Ms .10 .1.000 Iowa, Kansas, Kentucky. lamisiana . Maim* Maryland. I , 1 (HI 100 weeks 00 11C weeks <1.1 ,, .3-20 weeks (5.1 11 100 weeks (If!*'. .100 weeks Whole period ol di-abdily SO *or aetnal waye. it lew. *0 8.3 | On* actual wane, if less* 1 *0 x8 ior actual waye. it less* 1.1.00 ls.00 1.1.01) 20.00 IK.OU 20.00 it.000 7. IhS 7..100 s.ono 0.000 0.000 Mawarlm- vl'ltv , (Hi-;. .100 weeks I SO <or act mil waye. if less; Is.uo M.aOO l>u( not under *7 for nor- ntiil wecklv limns of 1.3 or over/ Miehiyau i 00 - .100 weeks *7 |s (10 0.0(10 Minnesota * MDsotin, . ; <h;-' ;<i Whole period of disability j *8 (or , id mil waye. if K*ss( 00 -' 000 weeks; thereafter -2.1 per cent of i $0 20.00 MMHI0 20.00 1 wnyes for life 1 Montana j .10 00 ' :j .100 weeks . jJS 21.00 10..100 Nebraska 00 {j .`500 weeks; Ihereal'lei. for life t.3 jkt i Xt (or actual waye. f h*ss. I 3.00 *ent of wanes dnd not umler $4,50 j oiraetual XMH wauo. if h'ssi.tud not o\er 1i Nevada 00 Life X`i.0-2 I,:.v3 New ilamp' , sliiie .10 2100 weeks XX ls.00 1.(00 New .lci-cy 00- (00 weeks; llieiealler at (educed rail* , AMI -or aetuai waye. si lcss *iu proportion to cat nine capacity 1 20.00 if siihmittiiu' to reliahiliialion New Mexico. 00 .1.10 weeks -SKI (oi- a< Inal waye. if lessi ls.00 i.tnjo New Vork . 00- : Lite Sl.3 or actual waye. u less. > -2.3.00 N'oitli Cam* lina 00 (00 weeks S7 ls.00 0.000 North Da- . i kota * 00 - ; Whole iieriod ol disuhditv ( $0 (or ;;lelual waye. if less. 20.00 (.1.000 Ohio Oklahoma * ; on-' { Life 00 .; .300 weeks SK ior , let mil waye. if less XX or ;iclual waye, if lessi ls.7.3 |S.OO 0.000 Oieyon Whole |K*rnd f disability 80.0*2 -- s.(}S Pennsylvania.! 00- . .300 weeks ! 82) 'or actual waye. m>t under s.3 ls.00 7..100 Philippine Is lamic , 00 208 weeks 1 pCsOs ls.00 .1.000 Puerto Rico .10 ;ft(l weeks SO 10.00 .(.000 Rhode Island, .10 1.000 week- x7 20.00 10.000 "Ninth Cam- liua 00 .300 weeks s.3 2.1.00 0.00(1 ''mill Dakota .7.1 X7..30 1.1.00 ,:.ooo |*t* sOs, - Flos iuMilion.il allowance for onl.uit attendant if necessary. i: III addition to tnmpousaliou. oinphnce ililderyuiny vocational lelfahdilaliuu is paid m.t m.tinieliallri1, mavimum 810 ueeklw ' Ward tv inoiea-ed .3 per cent for each dependent child. III l.'lse of illjuiles oreurriliy alter .Jillv I, I<nui|cUsUt|oli |s uicie.i'CiI Ml Jn-I <ciil. Hcllefils are paid unlit amount equals death benefit. There tiler annual lilt* pension ol s ji. i- < cut I-.' |i**r rent of total pievioii' payments. 1 Thereafter .5U per <**1 it ot wnyes <|iii my dl-abditv. " I'liiv 111< 111 (111 \ for e.irli !<*( u'lK fen I ehdd. TICK AD.MIMSTHATIO.V OK W'OUK.MKX S COMPENSATION' I.) Tu<m-: t -.Mimmi m wd Mwimi'm r\i>t:i< Wokmiv\\ (`omi'iasviiun Lwv" jn K\tim <ii I)s>vmi.m wn in St*\n:. Ji I. !!40 (onl Pmmnintt Total I)i,sahifiti/ Ccmlimicd l.liilll of Payments **tate Percent age ol WagCs MaMiiiilUi Period ____ - Tennessee.. Texas Hah Vermont. Virginia Washington West Virginia Wisconsin*1'* Wyoming , K. Civil `MU* ployees I.o0}slioremen .. . , V ........................... .50 .5.50 weeks (>o KM weeks (SO Whole peiiod o( dis.dnhlv 50 2(W week< .5.5 .500 weeks Whole |H'i'Soil of disabliilv (S( - < Life 70 Life (SO-} Whole period ol disability (!(i ' | Whole period of divuhditc Per Week Minimum Maxiiiniiti Pul d maxi mum . -- *5 <or actual warn*, if less. *7 *7 *7 (or actual wane. 0 less* *< MM'l sx* *11 *.50 per mouth: additional benefit for disfigmemeul _ `SIO.OO 20.00 10.00 1.1.00 Hi.00 Xi.orjo S.0-2O 1.000 0.000 liO.OO Id.no 21.00 70.00 ' fu.ijun $10. Mi (or actual wage, if * 20.0-2 lesst *S (or actual warn*, if le%si *2 5.00 7..500 Permanent Partial Dixatrilit// [Maximum period fur specdle itijurif> is mx-en. followed bv maximum priind (If jp-onlerl for disabilities not listed hi solu'tluli1 of specific injuries there referred to ax "mm-lisled disabilities'* Alabaimi Alaska Arizona .. Arkansas. . California... Colorado . Connecticut. , Dcl.iwaic . Dish id Ot Ciilumhia ii Florida (Ynrgia Hawaii Idaho .5.5 0.5 *' .5.5 0.5 0.5 .50 .50 .50 < *00 weeks *5 tor actual wa^c. if lessi ` '200 week's: din mg disability, for non* ( listed disaliiliiy j -200 wtx'ks; 4.50 weeks for inm-hsled ' $7 { disability { *240 weeks ; *0. .50 ` -20K weeks .? . *22.5 weeks; .5*20 weeks for u<*u-iisled $7 disability |!I4 weeks; -2S.5 weeks for (um-listed , *5 or actual wajre. if lessi disability (i(S - i* 2HS weeks; diumi; disnhifit w for non- *S (or actual wa^e. if less* listed disability' : .50 (SO i 200 weeks; 0.50 weeks for non-listed | *0 <tir actual w,ij.'e. tf less! disability ; .50 1 *200 weeks; :SU0 weeks lor lum-hsled ' -X4 'or actual w:ue. if less disabililv (SO , .`M2 weeks .5.5 20S weeks SIS.O0 i *?,-2UU I> !' i ( xMt.OO'-'c.OOO l * -25.00* o U.Otlj ` 2.1M2 t *2.5.00! HUmo 1.5.00* 4.27.7 < 1 2.>.00;SN7..>OU IK.OO-'M.UOO 2ti.no * .i.tmo w.00`:'5.nnu lO.OOPDkSOS Amounts are increased ur decreased up to 15 per cent for employers or employees \ minimi' safelv u*i*ulahoiis; triple (ompousalum for minors illecally employed. ' $5 tor actual wajre, if lessi after MW weeks. * Phis, additional allowanee for constant attendant if iieeessaiy. l-Additional <ompeiisatiou for total disability, ami 104 xxeeks for serums ami permanent disiimuciueul of face, neck, head, or hands, hut eomhined (omprusatiou not |o exceed .5-20 weeks. In addition to compensation, employee uiidernuim: vocational rehabilitation is pail cost ot uinmie. nance, maxiiimm *10 weekly. ' f oint>eiisa(ton for 2(50 weeks, then K5 per cent of average weekly wanes for life. In addition, .mam * iiicieuvcd .5 per cent for e.irh dependent *fn|<{ not lo e\red .If under IH years. ;i Per month if wife and *2 eluldieu. phis x*> p,r cub additional elnld. phis *25 for constant aMend-mi it neeo.ssary. '* In addition empl<vee ivceivim* icliabUitation instruction is paid ro%l (lf maintenance, maximum *lu weekly, foj maximum of 20 weeks. .*6 |Vr month, phis AIKO per year lor eaeh eUild. Additional benefit for disfiuiireuieiit. '"`In addition to eomjietisattnu for tempoiaiv lulal disability. Theie is ,m additional .imomii !* dideuiemeut. M Phis life pension ut fiom HI to to per cent for \er 70 pel cent disability. '' I addition to compensation for Icmpcu.uy lol.il disability. For mui-lt'led permanent p ii li.d di* iL.htx m.ixinmm is stUiKI. I heic i- an additional amount for di*fii!ii<cincnt. '* In ad lil'on lo compensation for temporal-* total disability. 10 OCCUPATIO.\'AL DISEASES Tama: l--Mivimi.m and Maximum lii:.vi;i rr.s i-vi>i:it Wohkmi-.x's Commas itiov fail's, in" K.vriAr op Disamlitv wn nv Sruu, Ji i.v I, 10to Coiitinm-il I'rrmaitciil I'arthtl l)i*tibilH// - CuMlinuuil Limit (if Payments Mate Percent* aire of Wages M.(\irmiiii Period Per Week Minimum Maximum Total Maximum Illinois 50 05 225 weeks; 117 weeks Ini' iiundisted $7..50 >$ll if I <*JiiJ<f under 20.00-'5.500 disability 10. $12 if 2, $18 if 8. and Indiana. . . . $14 if 1 or morel 55 ( *2.5U0 swaebeilkitsy; .700 weeks for linn-listed ,j $8le.8ss0i for net uni wage, if 10.50) 5.000 Iowa ! k'an.sas, , 00 ' 2*2.5 weeks $0 <or actual wage. if lessi 00 210 weeks; 115 weeks foi mm-lisled ` 15.00 8.875 1.8.00 -'7.170 Kentucky..,. disability 0.5 , 200 weeks; 885 weeks lor nun*hs(cd $5 f2.no t.iJdi) disability Louisiana.... ! Maine .. .. , 05 100 weeks , $8 mr actual wane, if less) 00- Lit) weeks; .`500 weeks tm mm-h'led , $0 20.00i 8,000 I8.00j 5.100 disability Maryland.. Ma.ssachusetts..... i1 oloi-O` 200 weeks I 175 weeks $8 for actual wane, if lessi | ............................ 15.00 J'8,750 "10.001 1.750 Michigan .. 1! 00 :j! 200 weeks; 500 weeks for noil-listed ! $7 18,00* 0,000 .* disability Minnesota . 00 a 150 weeks including 25 weeks eaoli f $8 'or.ictual wane, if less! 20.00'-'JI.000 Missouri.... .j for healing and relial)ili(atioii) | 00 sj 2.02 week; 400 weeks fur non-listed J $0 20,0(I|*`8.000 disability Montana... ,1 50-00- i[ 200 weeks; 500 weeks for mm-listed I $8 21.001 10,500 disability j Nebraska. . ,j 00--:ij 225 weeks; 800 weeks for mm-listed { SO for actual wane, it less) 158)0 1.50(1 Nevada........ j New Hump- t disability 50 .200 weeks J $0.02 18.H5P8.000 shire........ 50 ! :mo ivct-k., , .$8 18.00 5.100 New Jersey.. 1 00 3 a:ji 200 weeks; eunittlalive for 2 or more ( $10 lor actual wane, if lessj 20.00i!'l0.s specified injuries, to maximum of ` non 500 weeks New Mexico.. 00 . ISO weeks $10 "or actual wane, if less) 18.00 'St.10 New York.. ,, 00-;;jd 812 weeks; during disability, for non- j -S8 tor actual wane, if less/ - 25.00 North Caro- listed disability iina . . 00 ' 200 weeks; 800 weeks for noli-listed * $7 18.00 --0.000 North Da- j " disability kola ..... 00-3.2.81 weeks; 150 weeks for non-h-(ed $0 208)0 *8.000 disability Ohio ...... Oil-}, 215 weeks .......................... ... ... IS.75--' 1.000 Oklahoma ., OO-3I 250 weeks; 000 weeks for mm-lisled $8 (or actualwane, if levs) 18.00: '1,500 disability Orenon ... | .. . 1 208 weck.s for married workman j $8.08 ' H.51 " 2.100 Pentisylyaiiia. 003,{| 215 weeks; 800 weeks for mm-lisled 8!), or fullwane, but not 18.00 1.500 disability, weekly maximum $15 muler $5 Philippine Is lands..,.. 50 208 weeks in addition to mm|otwi* ....... *8.000 I (ion tor Icmpoiary total disability: Pueito Ktco. Ithode Island. benefit for certain disligmetnenl 50 800 weeks $1.50 50 150 weeks; 7*10 weeks. |r non-listed $8 1200..00(01,,5-1'8'8.1)0000 disability, weekly maximum, $18 ' Pesos. :;in addition to compensation, employee undcrkoiug locational lelinbihlatmn is (Mid os{ u| mam'enance, maximum $10 weekly, * In case of injuries oceurriun alter July l. 1080, compensation is increased 10 p**r <cut. ;r Additional benefit for disfigurement. mcitl. In addition to compensation for (cntporaiy total disability. There is an additional benclil for di-lieerc* 3 In addition to compensation for temporary total disability, la addition to payments for Iota! disability, not to e\ceed 01 weeks. There is an additional amount, nut to exceed death benefit / if disfigured w here no -peeilir los*. * In all fiK-s. in addition to all other t-mupen-ntioii. Pur inm-li-li-d di'.ibdi*. . 00-*, (a....... .. o( wn-klv aaircs durum disability. inaMunun .-MS, total maximum sl.jdU. THE ADMIXIriTKATIOX Of WOKKMEX S OOMI'F.XSATrOX 17 Table t--Mi.vi.ml'm and Maxi.\ic.u Bexi.iti's i-xdkk Woiikmex's Comi'D.vs.ation I,aa\-s, by Extent op Disability and by .State, July 1, 1910 --Continued IWmaiwul Partial Disability--Continued l,unit ot Payments State Percentam* of Wages ` Period IVr Week Minimum . ____ MToatxai*l M ixi> mum mum South Caro- j linn........... < south Da- j kota..... 1 ! Tennessee.. t Texas.... ; Utah.. - . Vermont.... f \ irguiia.... Washington. ,t West Virgimaj Wisconsin10., .j ; Wyoming..,. { L\ S.: J Civil cm- ( ploycc-j. .| Longshore- \ men.... j j (it) ' 200 weeks; 300 weeks for mm-li\tcd - 3.5 disability X2.5.0U s-30.000 < .5.5 * 200 weeks; 312 weeks for uon-lis(e<l i 37.,50 (or actual wage, it lossi ! disability .50 400 weeks 35 <or actual wage, if less* (it) 200 weeks; 800 weeks for iinn-listcd 37 disability *w 200 weeks; 312 weeks for non-listcd disability .50 r 170 weeks; 200 weeks for mm-lisU'd 37 <or actual wage, it lessi disability Jd 200 weeks; 300 weeks for mm-hsted 80 > disability |! , h\ 240 weeks; 340 weeks for non-listcd | 38 disability 70 i 500 weeks, plus 70 per cent of earn- 814 mg> for jiealiug period. .Maximum ! for non-listcd disability, 1000 weeks \ ..... ...... . . * 830 per mouth I.5.00*-1* 4,080 10.00' (U00 >0.00 U.000 ' K5.00 Ni.2.50 1.5.00*15 3.000 10.00*-'* o.ooo "'3.t 000 10.00' .5.140 2I.UO;i'2l,000 - 7iUI(l*:'2,.5UO t Whole period of disability . ............................ . . *(i.0v\ .. <)(>*;* -88 weeks; during disability. fm- mm- I 88 (or actual wage, if lessi : listed disability s ' 2..U0T'<7,.500 ; Tentpantry 'fatal Disability Alabama. .. Alaska. , ' Arizona..... Arkansas .. California....! Colorado.. . Connecticut., Delaware District of Columbia .. Morula.,. , Georgia...., Hawaii,.., Idaho .. .5.5 -0.5 0.5 -7 (i.5 0.5 0.5 .50 .50 .50 , 300 weeks ; Whole period ot disability v433 weeks } 4.50 weeks *23!) weeks [ Whole period ol disability * 5*20 weeks 47.5 weeks 85 (or actual wage, if less) x7 80.50 85 87 33 Cor actual wage, if lessi 00-' in Whole pciiod of disability 88 for actual wage, if lessi .50 -00 * 350 weeks ' 30 (or uctu.d wage, if less/ JO 3.50 weeks ' 34 (or actual wage, if less/ 00 ! 31-2 weeks 35 (or actual wage, if less) .5.5-00 1 400 weeks; thereafter 30 w <ytl.v OSS. SB . if dependent children > 818.00 * . -20.00 4*7.000 25.00 .5,075 1 4.00. 25.no 13.000 1.5.00 4.000 i -'2 5.00. 7,500 ' IS.00 .5.000 *11.00 7.000 2 5.00 .5,000 10.00 lu caisc ot uncomplicated silicosis or a.sl>e.stosiv, maximum is 8,500 if death or disablement occurs m first month act becomes effective and maximum increases 850 each monlli until limiU provided for accident' are readied. 10 AmpuuU are incieannl or decreased up lo 1.5 per cent for employers or employees violating safety regu lations; triple compensation tor minors illegally ompfoved. In addition to compensation, employee undergoing vocational rehabilitation is- paid cost of in.unlenam e. maximum 310 weekly. u I*his 5 jkir cent for cadi dependent child. -Jln addition employee receiving rehabilitation instruction is p.tid cost of maintenance, maximum AlO weekly, for maximum of -20 weeks. -'Additional benefit for disfigurement. 5<iIn addition to compensation for temporary total disability. There is an additional amount lor dis(iguicmcnt. In addition to romiMUisation lor temporary total dDabilily. * Tor nou-li.sted disability, .50 per <vnt of wages. *s Hus J per cent for each dependent, child -not i exceed 7; under IS years. **a W heie there ai e 2 or more injunc', au employee may receive compensation in excess ot m ixinmin ei\*u 3 Per month. Plus 310 per monlli for total dependent*. leadmg in the t'nited stales IS occriwrioXAi. di.ska.sks Tuii.i, 1 Mimmi m \\d .M.wimi'm Hi;xi:rns r.x'DKii \Yoiik\ii:v'- ('uiiimv\svtio,\ I.aw>. in Kxtkvt cik Disaiiiutv \\i> iiv Statk, Jri.r I, 1IIMl Continued Ti nrpnrarif i'-iial Dixaliilili/ Continued l.iinit c|' f'.iviiK'iil' Htalr Peiecnlage of Wages Maximum J'eimd Illinois,.... j .>() <5 Whole period of disability Indiana.. . IKoawnsaa.s...., , . j> Kentucky... .] Louisiana.. Maim*... . Maryland... Mavvoutiue_hu_- ; 55 ( 500 Mook> 0<(1J jj 840If0) wweeeekkss 65 5-20 weeks 65 800 weeks 500 week* 81*2 week* 6(i2;(j .100 weeks Michigan ! Minnesota j Missouri........ | Montana... [ Nebraska. , I .Vevada... j New^ Damp- . shire,.. } New Jersey . New Mexico.. New* York.. North Caro lina ... North Da kota ..... Ohio..., Oklahoma... Oregon.. Pennsylvania. (10 -3 .500 weeks 60 -.j 800 weeks a3 400 weeks 50-6(i^;, 800 weeks 60*3 800 wcek.s 00 488 weeks 50 800 weeks (Hi2 > 800 weeks 60 ' 550 weeks 66 ^ Whole period of disability 60 400 weeks 66 23 Whole period of disability 66 2 3 81* weeks 800 weeks 40-662-,' Whole period of disability 500 weeks Philippine Is lands... . ) i Puerto Uieo.. Rhode Island.! South Caro- ( Him.... I South Da- r kota , 1 Tennessee . ; Texas... Hah.... . * Vermont___ I Virginia____ | Washington. West Virginia! Wisconsin10 ' Wyoming.. 00 *08 weeks 50 104 weeks 50 1000 weeks (H) 500 weeks 55 50 800 weeks 60 401 weeks (SO 81* weeks 50 *60 weeks 55 500 weeks Whole period of disability 002i 78 weeks 70 Whole period of disability Whole iieriod of disability Civil ein- ' ployers. * Longshore* . men 00*3 Whole period of disability 6(S-' ( Whole period of dUahiiilv IVr Week Minimum Maxi mum Total Maxi mum ,$7.01) i$U if I ehiid under 8-20.- i $j,.)i) Hi. $1* if -2, mil if :k and 00 $14 if 4 or more) $8.80 tor actual wage, if less) 10.50 5,0011 Si) (or actual wage, if less! SO 1.1.00 L500 18.00 7,488 $.5 j SO$8 (or actual wage, if less) 15.00 7,500 ,-20.00 0 00(1 0,00018.00 $S for actual wage, if less) 20.00 .8,750 1 $9 (oractual wage if less; hut l not under $7 for normal I w eoklv hours of 15 or over) j vl18.00! 1,500 | i $7 | $8 (or actual wage, if less) 18.00 *0.00 90..000000 $8' $6 (or actual wage, if loss) 20.00 8.000 *1.00 0,800 $0 (or actual wage, if less* 15.00; 4.500 $0.9-2 I6.6*i};*7,-200 $8 $10 for actual wage, if less) $10 (or actual wage, if less) $8 (or actual wage, if less) 18.00 *108..0000 50.,100000 9,900 -25.00 5.000 $7 18.00 0,000 $0 (or actual wage, if less) $8 (or actual wage, if less) $8 (or actual wage, if less) $6.9* (or actual wage, if less) $9 (or actual wage, hut not under $5) less)4 pesos (or actual wage, if $1.50 $7 $5 20.00 1188..7050 **.88 18.00 8.750 5,400 7.500 ) 18.001:8,000 lO.Ooj 1,0411 i0.00| 10,0011 .00 6.000 $7.50 for actual wage, if less) $5 (or actual wage, if less) $7 $7 foractual wage, if less) $7 (or actual wage. i( less) $6 $8 ""................................................. $7.85 $50 {Mir month 15.00 8,000 *106.0.0001! 84,.800*00 '5 16.00) 6,*50 )5.00i 8,9<)( 16.00' 6.000 ! *116.0.0001' |,*ts w 90.00' * $18.46 (or actual wage, if j loss') , $8 (or actual wage, if less) *6.9*,' * *5.00 7.500 1 Pesos. - Amounts are increased or decreased up to 15 per cent for employers or employee* violating safety regu lations; triple compensation for minors illegally employed. In addition to compensation, employee undergoing vocational reliahiiitation is paid rest of mainte nance. maximum $10 weekly. 59 In ease of injuries occurring after July 1. 1989, compensation is increased 10 per rent. Plus 5 |k.t cent for each dependent child nol to exceed 5) under 18 years. ,r Plus $10 per month for tol.il dependents residing in Cnited States. r* Same as for iwrmam-nt total disability; .special schedule of monthly payments for tirst 6 mouths of dis ability. for married or widowed employee. '* Per mouth; additional benefit for disfigm eim-iil. TIIK AD.MIMS'I'KATIOX OK WOKIi.MKX S COM I'KNSATIOX I!) Tvm.K .'i N't much in- Wr.i-.KM mu Wiik 11 ('umimix-satihx 1m I'u'uii.k i-oh Si'wii h-.ii Kjchiks. hv Status tir I.oxk of Cvo Of M-m* Arm Lshmil-i i der) *Uml , -Mid- , leg i numpi|.*lnw,r *, die `Finger d-'iugerFingor j ! tat hip) [ Foot Alabama1.. Arizona12... California6. Colorado2.*. 200 /32*(i0 \`217 200 *3240 1*220 208 225 Delaware1. 194 District of 2S0 200 200 312 210 225 250 225 210 Kentucky1. 200 Louisiana1. 200 150 Maryland2. 200 Massa 0 75 chusetts10 11\* 50 Michigan1. 200 Minnesota2 200 Missouri1.. M2 \212 Montana1.. 200 Nebraska2, 225 Nevada2... F260 (*217 New Hamj>- shire11.., 170 New Jersey5,. 230 New Mexico2. 180 New York12 13 312 North Carolina1 200 North Dakota1 234 Ohio2.,.. 215 Oklahoma1. 250 Oregon11... 208 Pennsyl- vania1,. 215 i:> 5217 `173 150 tjso MOO 104 j ! ' : k 175 15S 212 150 150 244 200 170 200 150 (50 150 150 125 150 3 75 * 50 150 175 3175 MOO 150 175 '217 *173 > '- 140 175 110 244 150 1 105 105 , 200 165 : 175 lid t > 00 M0 l `30 "{ f 00 00 45 *1 :is ! *32 '2X 20 3S :i-5 30 i 30 1 :lo 5 *24 ; >20 IS 30 30 -** - ~ 20 `>4 . *20 25 20 15 175 17 i 217 15 175 '16 *240 M2 13 20S 20 208 13 194 51 2s' IS 17 ' -48 -TOlid 35 30 30 IS 175 35 30 20 IS 175 00 40 30 25 IS 288 70 40 40 30 20 180 70 40 35 25 20 1110 00 40 35 30 20 200 40 30 25 20 15 200 60 37j 30 30 IS 200 ' 00 s45 v30 *20 * 15 200 50 30 20 20 20 175 50 30 25 IS 15 150 50 30 25 20 15 175 3 40 3 20 12 12 12 50 60 35 30 20 15 175 00 35 30 20 15 200 3 60 3 45 3 35 3 35 122 J207 `55 `40 * 30 30 *16 60 30 30 20 12 200 60 35 30 20 15 215 85 30 30 22 17 217 40 25 20 15 10 170 65 40 30 20 15 175 50 25 20 lo 12 180 46 30 25 15 288 00 35 30 20 15 175 45 201 24, 15} 13! 234 >60 '35 t '30 >20 '15 190 tiO 35 30 20 15 175 M 35 20 17 13 191 00 35 30 2ft * 15 215 125 173 125 100 104 156 135 173 125 125 205 125 J35 150 125 125 125 125 125 150 50 125 150 150 125 150 173 120 125 100 205 125 1385 140 150 139 150 > Hear i Sight (fear- ing. Too j 1 Toe 1 of an ! Ky 5 mg. 1 Far ) , Both I'ar.x 3ft j 30 j 30 32 26 10 | 100 u : *M30 10 100 s .SO 11 U139 [ 87 | 40 40 35 150 260 150 160 no 3X 1.1 208 52 15li 30 10 11s ' 26 X 140 52 20(1 so 10 100 40 150 30 10 100 15(1 38 16 128 60 312 30 12 **140 35 150 35 12 120 50 125 60 150 201) 25 15 100 50 150 30 10 110 25 too 30 10 100 20 10 100 25 10 100 25 10 100 50 100 12 12 50 30 10 100 30 10 100 52 i.Hi 40 14 ul\S 44 16X 30 12 `M20 20 120 30 10 125 50 100 30 11 1 *130 87 26ft 20 30 30 3.8 30 195 30 30 22 i 8 100 42 10 100 40 12 "125 16 160 35 60 10 100 70 71 100 1 29} j 10 125 10 100 t) 87 78 ' 125 17(1 Uid 135 15ft 150 156 2(is 150 1 Payments under this schedule are exclusive of or in lieu of all other payments. 2 Payments under this schedule arc in addition to p.i> merits for temporary total disability (luring the healing period. 3 For major memiwr. * Kor minor member. " By enucleation. 3 Payments under this schedule are exclusive of or in lii-u of all other payments. Am mnts depend on age and occu pation of employee. Figures given are for unskilled workman illl years old. fi Payments under this schedule are in addition to pajments for temporary total disability during healing period: !JlJ per cent of -specific schedule to be paid employee. Kmployer must p*y 2 per cent additional to special iudemuiu fund. For IojvS of second to . 30 weeks: third toe, 20 weeks; fourth toe, 15 weeks: and fifth toe. 10 weeks. 3 For loss of a metacarpal bone for corresponding thumb, finger, or fingers, 10 weeks are added. v Payments cover total disability for period specified. Partial disability based upon wage, loss may be compen-ih-d at end of period given for not over .`100 weeks tn all. 50 Payments under this schedule are in addition to all other compensation. 11 Plus compensation for actual healing period not m eyes-i of specified number of weeks, e\eept in case of loss .j hearing. 13 In lieu of other payments unle.-* perio<l of temporary total disability exceeds fixed periods for each class of injury. "Computation based on compensation payable to a married man or a man with dependent child. Pajmerit' are m addition to payments for temporary total disability during healing period. '20 occri'.vno.v.YL disk.ysks Tuiu: o--Xijmiikii of Weeks ion Wmai Compensation Is Payable for Specified In.iikiks, iiy Status--(.'ontinuoil I.o.-s nr r.ov* of l\-o (1 - i1 1 r \ SUIr Arm , <ut * 'hutii- Hand dvr* 1 humli lwlc\ urncr Mid He 1 inner ttl.K 1 Kitwer' l.itlh* 1 ;`iiu'cr< ,-t ,'{lt hl|c , , Circuit5 Other not Toe Toe .Siiiht of an ICyo Hearinn, I Fur HearIv.iis Philippine ' * / 1 V- -- " Wundts- i 20K . I (>0 to i ::0 25 20 ( 10 j 1(10 ` i;m 25 J 10 100 10 204 \ hiurto Rico .100 *200 |s<| 50 , 33 25 25 1) ' 250 < I (id 25 15 13 too 25 5 200 s' Rhode island? i0 ; AO 50 ' 20 20 . IS [ too so :io 10 SO South Carolina , 200 loO 00 .15 .10 20 . 15 - 175 * 125 .10 10 100 0 150 [ South \ Dakota- * *2(10 no 50 .15 M 20 l.i ' Hill 125 :;o *M0 100 '200 130 00 *15 .0 20 13 ? 175 . 125 :;o 10 100 l.Vl Texas*1 . 200; 150 ' 00 ' 45 ' :;o ' 21 *15 i 200 i 123 *10 10 100 150 ' 200 . 150 00 ` 30 ` 30 20 12 5 ISO 1 125 ` 30 12 13 120 ( * Vermont?,, 170 . M0 Vinrima1 . > 200 ISO O) , 25 20 15 . 10 l 170 | 120 20 s' 100 W2*. 170 <J0 *15 .10 20 * 15 175 125 00 HI too 50 \ West ij VirRinia1 240 i 200 so . 40 2S * 20 20 240 1 MU } 40 Id 132 \\ iscoiuJn*. 300 t Cnited l"i "1 , 30 j 500 ; 250 "*25 50 * States: i ' long- *` i* shoremen5.... JS0 1 212 * 51 ; 2x; is . i; ; 7 | IMS ! 173 20 S HO ; 52 200 11 For additional lo;>.s of 1 or more toes other than the great toe, an additional period of 10 weeks. lu lieu of all other benefits except medical and hospital. v> For loss of second toe, *10 weeks. Table G--States Limiting the Period and Amocnt op Medical Benefits Neither Time nor i No Limitation on Amount Limited j Amount No Limitation on , Both Amount and Time . Time Limited Arizona Alaska ; Florida , Alabama California * Arkansas Iowa 1 Colorado Connecticut i Indiana Louisiana Delaware1 District of Columbia Massachusetts Hawaii M ichigan . Maryland New Jersev (leorgia1 tCansas1 Idaho ; Nevada , Now Mexico Kentucky1 Illinois J New Hampshire | Ohio Maine1 Minnesota ; North Carolina- Oregon Missouri1 Nebraska ! Oklahoma a Rhode Island Montana New YorkJ ' South Carolina Utah Pennsylvania f North Dakota * Texas West Virginia South Dakot; i Philippines Virginia Wyoming Tennessee i Puerto Hico > Washington^ Vermont Wisconsin1 l Cnited States: ` Civil employees Longshoremen I i 1 Additionul .services in .special cases or in discretion ot commission. - Except in case of treatment for silicosis or asbestosis. 1 In case of disability resulting from inhalation of harmful dust, period of treatment is limited. Virtually unlimited under administrative practice. THE ADMINISTRATION' OF WORKMEN*S COMPENSATION 21 Table 7--Maximum Periods and Amounts op Medical Service, by States Stale Maximum j Maximum Period ! Amount State Maximum ! Maximum I Period Amount Alabama.................. I 90 dav*1 $200. New Hampshire i 30 davs i Unlimited. Alaska...................... | 1 vear Unlimited.'-' New Jersey............ j Unlimited $100.3 Arizona................... j Unlimited Unlimited.12 New Mexico.......... j Unlimited $400. Arkansas8................ j 60 davs3 Unlimited. New York"....... 1 Unlimited Unlimited. California................ j Unlimited Unlimited. North Carolinas i 10 weeks' Unlimited. Colorado................. | 4 months1 $500. North Dakota. . . j Unlimited i Unlimited. Connecticut............ Unlimited Unlimited. Ohio........................ Unlimited | $200.3 Delaware................. 30 days3 $150.3 Oklahoma.............. 60 days3 1 Unlimited. Districtof Columbia Unlimited Unlimited. Oregon................. . Unlimited !$2503 Florida..................... Unlimited $250. Pennsylvania........ 60 days $150.5 6 7 Georgia.................... 10 weeks3 $500. Philippines............. Unlimited Unlimited. Hawaii..................... Unlimited Unlimited. Puerto Rico........... Unlimited Unlimited. Idaho8................... Unlimited Unlimited. Rhode Island........ Unlimited $200.' Illinois8.................... Unlimited Unlimited. South Carolina . .. 10 weeks3 Unlimited. Indiana8.................. 90 days1 Unlimited. South Dakota.. .. 20 weeks $300. Iowa......................... Unlimited $600. Tennessee........ 30 days' $200. Kansas..................... 60 days $I00.3 Texas..................... 4 weeks12 13 Unlimited. Kentucky................ 90 days3 $200.3 Utah....................... Unlimited $500.3 Louisiana................ Unlimited $250. Vermont................. 2 weeks $50." Maine...................... 30 davs1 $100.3 Maryland................ Unlimited $500. Virginia............ .. 60 days12 Unlimited. Washington........... 13 Unlimited. Massachusetts........ 2 weeks3 Unlimited. West Virginia8... . Unlimited $800. Michigan................. 90 days Unlimited. Wisconsin.............. Unlimited Unlimited. Minnesota.............. Unlimited Unlimited. Wyoming............... Unlimited $150." Missouri.................. 90 days3 $750. United States: Montana................. 6 months $500. Civil employees.. Unlimited Unlimited. Nebraska................. Unlimited Unlimited. Longshoremen... Unlimited Unlimited. Nevada.................... 6 months3 Unlimited.2 1 Additional service may be given at option of employer. 2 Employees centribute. 5 Additional service in special cases or at discretion of commission. 33 Additional service may be authorized, not to exceed 91 days. I In case of hernia, if employee requires operation he is entitled to service without limitation of time. 5 In surgical cases maximum may be increased by order of commission to $500. 6 A special operating fee of $100 allowed in case of hernia. 7 In case of disability resulting from inhalation of harmful dust, period of treatment is limited to 90 days, but may be extended for an additional 360 days by the Industrial Board. 8 Special limitations upon medical benefits in case of certain occupational diseases. 8 Exclusive of hospital treatment. 10In case of employee receiving hospital treatment for more than 14 days, the maxi mum is $250. II Also hospital first 30 days, maximum $150. 12 Extended in unusual cases. Not to exceed 180 days. 13 In case of temporary disability, continues not longer than period of compensation, and in case of permanent disability not beyond the date of award. Employees contribute. u Additional expenditure of not more than $200 for medical service and $300 for hospital treatment may be authorized by court. DIGEST OF WORKMEN'S COMPENSATION ACT (CALIFORNIA) The following is a digest of the Workmen's Compensation Act as it is administered in California. Naturally, the act in certain of the other states will vary from the California law, but this digest will jj orrri'.mox.u, diseases serve to present a survey of the basic phases of workmen's compen sation in general Excluded Employments.--Tin- law does not give eoiiipeiisatiou to employees engaged in household domestic service (household domes tic servants who work For one employer For fifty-two or more hours per week are not excluded from the provisions of the workmen's compensation laws and the employer of such household domestic servants must carry workmen's compensation insurance). The law does not give compensation to employees engaged in labor that is both casual and not in the course of the trade, business, profession, or occupation of the employer unless the employer carries compensation insurance or has filed an acceptance of the law with the commission, nor to employees engaged in farm or agricultural labor of any description, if the employer has rejected the compensa tion act and posted notices of rejection on his premises; or if the employer's payroll does not exceed $;>()() in the year preceding the injury. Employees working on board vessels in navigable waters and railroad employees engaged in interstate commerce, at the time of the injury, are also excluded as there are federal laws governing such employments and the state law cannot be made applicable. Questions as to whether employment is excluded should be sub mitted to the commission for advice. Employer's Security.--Every employer, except the state and all of its political subdivisions or institutions, who has one or more persons employed, even part time, in occupations not specifically ex cluded. is required to secure the payment of compensation in either of the following ways;1 1. By insuring and keeping insured for full coverage with an au thorized compensation insurance carrier 2. By obtaining a certificate of consent to self-insure from the Industrial Accident Commission To obtain the commission's certificate of consent to self-insure, the employer will be required to furnish security in the form of a surety company bond or approved collaterals that are legal investments for savings banks in this state. The minimum amount of security re quired in this respect is now $;><),()()() but is always subject In regula tion by the members of the commission. Tf the employer complies with this provision, all of his liability to his injured employee or the dependents of the deceased employee is fixed by and limited to the provisions of this law. If the employer does not secure the payment of compensation in either of the two ways mentioned, he is not only liable for eompen- T1IK ADMI.\rSTKATIOX OK WOKK.MB.N ri CO.M I'KX.SATIOX 43 sat ion lull, subject to a suit for damages in the superior courts. In case of the wilful failure by an employer to secure the payment of compensation, the amount of compensation otherwise recoverable shall be increased 10 per cent, such increase in no event to exceed $1000. The law makes it a misdemeanor to fail to secure the payment of compensation, and the penalty for this misdemeanor is a fine of not more than $500. or imprisonment for not more than six months, or by both fine and imprisonment. Tf an employer is continuously uninsured for thirty days or more, the tribunal before whom his ease comes must at least fine such employer $300. The commission also has the power through court proceedings to abate or close up any business in which the employer fails or refuses to carry workmeifs-compensation insurance on his employees. Every employer subject to compensation laws and not self-insured must keep posted at his headquarters, or at one or more of his places of employment, a notice that shall state the name of the employer's current compensation-insurance carrier. It is a misdemeanor not to keep such notice posted. Information concerning the failure of any employer of labor, other than those excluded, to secure the payment of compensation in either of the two ways mentioned above or information concerning the failure to post such notices of current insurance carriers should immediately be forwarded to the Industrial Accident Commission. Liability of Employer.--When an employee sustains an injury "arising out of and in the course of the employment" (and the em ployment is not one of the excluded classes), the law requires the employer to furnish the injured with certain measures of relief. The term "injury," as used in this law, includes any injury or disease arising out of the employment, including injuries to artificial members. The obligation to furnish the measures of relief becomes the liability of the employer immediately after knowledge or notice, and must be furnished or tendered without demand. Disability indemnity is paid by the employer or his insurance carrier. The Industrial Accident Commission does not pay such in demnity. Such insurance carrier may be the State Compensation In surance Fund or any private insurance carrier authorized to write workmen's compensation insurance. Insured Employers.--If the employer carries compensation in surance, the insurance carrier assumes the obligations of the em ployer. but the employer must understand that his contract (policy) of insurance requires him to notify the insurance carrier promptly `24 oeerp.vnowu, diseases of any injury to his employee. The necessity for such notice cannot be too strongly urged. Serious results sometimes grow out of ap parently slight injuries, and the employer may become involved for failure to comply with his contract. Insurance carriers furnish forms for report and will inform where injured are to be sent for medical and surgical treatment. An employer in addition to posting and keeping posted the no tice. of his current compensation-insurance carrier should immedi ately notify any injured employee of the name and address of such insurance carrier. Notice to Employer.--An injured employee should promptly no tify the employer, his employer's superintendent, foreman, or other person in authority, of the fact of injury if the employer or those mentioned do not have actual knowledge of such injury, in order that the employer may have opportunity to furnish the measures of relief. Failure to give such notice may prejudice and defeat a claim for compensation. Compensation.--The measure of relief which the law provides is termed "compensation." This term, therefore, includes both treatment and indemnity payment, and is to be furnished to the following extent: l. All the medical, surgical, and hospital treatment, inchitling medicines, medical and surgical supplies, crutches and ap paratus, including artificial members, that may be reason ably required to cure and relieve from the effects of the injury. If the employer or insurance carrier does not furnish such treat ment after due notice or knowledge of injury, and within a reasonable time, the injured employee has a right to obtain it elsewhere and the employer or insurance carrier will be held liable, for the reason able cost. If treatment is obtained elsewhere, the injured must select a practitioner who is licensed to practice in medicine or surgery in order to recover the reasonable cost of treatment. If the injured prefers to select bis own doctor and treatment hr may do so. but it will then be at bis own cost unless tile employer or insurance carrier consents and agrees to pay for such service. Where treatment is not furnished by the employer or insurance carrier, the injured must nevertheless submit to examination by a physician or surgeon selected by the employer or insurance carrier when so requested. Failure or refusal to submit to such examination will prejudice the right of the injured to disability indemnity. THE ADMINISTRATION' OF WORKMENS COMPENSATION "2. If the injury causes disability of more than seven days, ex clusive of the day of injury, then the employer or insurance carrier shall thereafter (jay the injured (15 per cent of his loss of average weekly wanes during the remaining period of disability. .Vo indemnity is payable for the first seven days of disability, and disability commences the day after the injured cpdts work as a result of the injury. This indemnity is payable on the employer's regular payday, but not less frequently than twice in each calendar month. The disability indemnity is not 05 per cent of the actual wage. The law provides that the disability indemnity shall be 05 per cent of the average wage, and that the average is 95 per cent of the actual. Wages in excess of $40.48 per week, or $175.43 per month, are not taken into account, as the law provides that the average weekly wage shall not be taken at more than $3S.40, nor less than $10. For these reasons the weekly indemnity for tcmixirary total disability is never more than $25. nor less than $0.50 a week. In arriving at the actual earnings, overtime is included, and also the market value of board, lodging, or other advantages if they are furnished as a part of the remuneration. To figure the disability indemnity correctly, where the earnings are between the minimum and maximum, mul tiply the daily wage by the number of days employed per week: add the overtime and value of other considerations, if any; deduct 5 per cent from this sum, and multiply the remainder by 05 per cent. 3. If the injury causes the loss of any member, or impairs the normal use of any member of the body, such as amputation of bone, permanent stiffness of joints, loss of sight, hearing, etc., the result is what is termed a "permanent partial disa bility." Where such injury occurs, or results, the commission should be applied to for a rating when the medical and surgical treatment has been completed or the condition no longer yields to treatment. For each 1 per cent of loss that the rating tables adopted by the com mission give, for such injury, the injured will be entitled to four weeks of disability indemnity. The indemnity for permanent partial disability i* not in addition to what may have been paid during the period of treatment and recovery. The rating will show the total number of weekly payments to be made, beginning the eighth day after the injury, and any payments made during the period of treat ment and recovery are a credit on the total to be paid under (lie -20 (X'Cl'l'ATIONAL DISKASKS rating. Tin1 remaining payment*. if any. an- l<> he paiil as they be come due and without regard to when the injured return* to work or what his earnings may lie after lie does return. If the disability i* rated at 70 per cent or over, the injured will be entitled to the weekly indemnity of f>5 per cent of his average weekly wage* for 2MI weeks, and thereafter a weekly life pension of 1 per cent of llio.-e wage* for every 1 per cent of disability in excess of 00 per cent t. If the injury cause* death, the employer or insurance carrier is obligated to pay burial expense to the extent of $150. and a death benefit to those who were dependent upon the deceased for support at the time of the injury. A person or persons totally dependent will be entitled to a death benefit of three and one-half Limes the average annual earnings of the deceased but not to exceed $(>000, and not to be less than $2000. A person partially dependent will be entitled to a death benefit of three and one-half times the annual amount devoted by the de ceased to the support of such person, this amount not to be. more than three and one-half times the average annual earnings of the deceased nor to exeeeil $0000. Death benefits are payable in installments of 05 per cent of the average weekly wage of the deceased until the total death benefit has been thus paid. The commission will determine who are dependents, ami the extent of their dependency, upon the request of any party in interest. Penalties and Forfeitures.--The law provides that if the injury is caused by the serious and wilful misconduct of the employer, in demnity is increased one-half. The employer cannot carry insurance against this penalty, which is chargeable to, and payable by. the employer only. The law further provides that if the injury is caused by the serious and wilful misconduct of the employee, indemnity is reduced one-half. The last-mentioned provision does not apply when the injury causes death, or results in a permanent disability rated at 70 per cent or over, or where the employee is under sixteen years of age. The fact of wilful misconduct must be established and *o held by the commission in formal proceedings before indemnity can be increased or reduced. Xo compensation is recoverable where injury is caused by the intoxication of the employee or where the injury is intentionally selfinflicted. TUB ADMlNISTU.VnON Of WOKKMKX S COM IM'.NS.vnOX 'll Limit of Time to Enforce Compensation.--Proceedings k> com pel tlic payment of any of the benefits provided l>y this law are brought' before this eommission. but lhe legal right to maintain such proceedings is barred after a certain length of lime. Where no medical treatment has been furnished or disability payment made, proceedings must be commenced within six" months from the dale of injury. Any payment of compensation or agreement therefor, or furnish ing of medical treatment, will extend the time six months from the date of the agreement or the last payment or last medical treatment. Proceedings for the collection of the death benefit must be com menced within one year from the date of death, subject to certain restrictions. These limits of time do not begin to run against an employee or dependent' under the age of twenty-one until he has reached that age. or an incompetent person, unless a legal guardian has been ap pointed for such person. The commission has weeks' continuing jurisdiction over its formal orders and awards, and any amendment must be made within that time. Application for Adjustment of Claim.--Proceedings for the ad justment of any claim are instituted when an application for such adjustment is filed with the Industrial Accident Commission. Blank forms of application will be furnished on request or will be prepared for signature at cither office of the commission. Tt should be distinctly understood that no report of injury, cor respondence. or application for permanent disability rating will be considered the commencement of proceedings. A formal application is headed in bold type Application for Adjustment of Claim. When an application for adjustment of claim is filed, due notice will be given interested parties of the time and place of hearing. A referee will conduct the hearing, and opportunity will be afforded parties to present competent evidence in support and defense of claims, and all parties should be prepared to present their evidence at such time. Agents or Attorneys.--If claimants desire to be represented by an agent or attorney, the commission will fix the fee to be paid the agent or attorney out of any award, and no agreement to pay a greater sum is valid or binding upon claimants. Indemnity cannot be assigned before payment, and it is only subject to liens fixed by the eommission. Miscellaneous Provisions.--The law provides that the term casual, as applied to excluded employments, shall be taken to refer 28 OCCUPATIONAL DISEASES only to employment, where the work contemplated is to be completed in not exceeding ten working days, without icgard to the number of persons employed, and where the total labor cost is less than one hundred dollars. An injured employee is cutilled to one change of physicians. When so requested, the employer or insurance carrier shall nominate three practicing physicians competent to treat the particular ease, from whom the employee may select. Medical and surgical treatment includes nursing, medicines, medi cal and surgical supplies, crutches and apparatus, and artificial members. A permanent disability rating is not the commission's award. The issuance of a rating docs not protect the injured against the limit of time to enforce payment. ESTIMATION OF DISABILITY Trial by Jury versus Expert Opinion.--Estimation of the extent of disability and the amount of the award is made in most states by the industrial commission, which is a fact-finding body. In a few states, however, trial by jury is the method used to determine the extent of injury, and appeal is permitted as in other civil conten tions. This latter system is obviously unfair. Juries are too often influenced by sentiment, emotional suggestions, and a desire to see the claimant secure personal retaliation. These conditions have no place in the just administration of compensation. Much better is the system which entails two separate opinions; one is from a licensed medical doctor, who indicates the extent of physical disability or functional loss; and the other is from the lawmaking body, which bases its award upon a rating schedule as adopted by the state. Most states have fashioned their schedules upon a plan of fiat rating of disability benefits. In California the benefits paid for permanent dis ability vary with age and occupation. The philosophy of this varia tion will be explained subsequently. Estimating Temporary Disability.--The term "temporary disa bility" implies that the condition is one not apt to be permanent. In the legal sense it is the healing period, but from the medical viewpoint it is the prognosis. On first thought, estimating temporary disability should not be difficult, hi the ordinary practice of medi cine it is not. for recovery is estimated purely from the scientific factors entailed in the illness or injury. But in industrial eases re covery is often contingent upon other factors. The workman may have been fired; or the job may have been about finished at the time of injury; or he may be aware of a strike's being imminent; or he may lie overly cautious about returning to the >ame hazard. I'hy- THE ADMINISTRATION OK WORKMEN S COMPENSATION 29 sicians often prolong temporary disability or create a claim for per manent disability by tactless statements or erroneous diagnoses. A salesman, following' an automobile accident, was hospitalized in a nearby town, an upper body cast was applied, and he was informed that he had a fracture of a thoracic vertebra. He developed marked tremor of the head and right arm. which persisted until a compro mise and release was effected after the payment of considerable money. Actually, he had a failure of fusion of a thoracic vertebra, but no pathological injury (Fig. 91). Estimating Permanent Disability.--Estimating permanent dis ability is a complex procedure, and as yet the method is devoid of uni formity. It most frequently involves the loss or use of a member such as a finger, hand. arm. or leg. Variations in the amount of disability as expressed by several examining physicians will often exceed from 25 per cent to 40 per cent. No two physicians employ the same type of implement for measuring motion, or include identical factors in their estimation of the patient's chance of rehabilitation. McBride,2 who has given considerable thought to this problem, includes functional, vocational, and cosmetic loss, earning-capacity, and adverse influence in securing employment. Scudder's Method.--Scuddcr3 does not rate his fracture cases until the end of one year, and employs the following method: {Anatomic result Functional result Economic result The use of the figures 1, 2, 3. 4 (A^Ityty) after each letter gives the percentage value to the final estimation, allowing a range of 25 per cent for each figure. 1 = 25 per cent 2 = 50 per cent 4 = 100 per cent 3 = 75 per cent Accurate Rating.--There are four factors which make up the total of an anatomic result: 1. Length 2. Alignment (total) by inspection and measurement 3. Apposition: judged by roentgenograms taken in two planes 4. Angulation Suppose Suppose Suppose Suppose apatient has normal length .............. apatient has poor alignment............ apatient has half apposition ............ apatient has 10 to 15' angulation . 100 per cent 75 per cent 50 per cent 50 per cent 4)275 084- per cent :>(i <)(vr i*ati (> \a i. i)isi:asks 'I'hi> patient would receive A" because 08--- per cent is nearer 75 per cent in (lie gross rating. There are four factors which make up the total of a iuuctioind result: 1. Total functional result, subjective (asking the patient) 4. Total functional result, objective (by observation) muscle strength and staying power 8. Joint movement above the fracture, as compared to the other side 4. Joint movement below the fracture, as compared to the other side Suppose the patient says lie is as good as before. . 100 per cent Suppose on observation, he has less power and movement on fractured side: can move the part (walk, or use his arms) about 1 of that which he did before .................................................... 75 per cent Suppose his joint above has limited motion, esti mated at V;, off normal..................................... 00 per cent Suppose his joint below is normal ....................... 100 per cent 4)541 This patient would be rated as F:1. 85 per cent There are four factors which make up the total of an economic result: 1. Same work as before, lighter, or heavier work 4. Same pay as before, more, or less 8. Same hours of work. more, or less 4. Same volume of work. more, or less Suppose a patient has a lighter job...................... 50 per cent Suppose a patient gets :j;j former pay................... 75 per cent Suppose a patient works half as long each day.. 50 per cent Suppose a patient turns out 1the volume of work................................................................... 88 per cent 4)408 This patient would receive lv. 54 per cent Addeil up. that patient would receive A:iP::lv. McBride's Method.--McBride believes that it b not enough to measure extension, flexion, pronation, supination, rotation, and the like. lie considers also the ability of the injured one to perform tin- acts of pointing, reaching, pinching, grasping, holding, pushing, pull- THE ADMINISTRATION OK WORKMEN S COM I'KNSATION :il ini'', catching. throwing, pressing, kicking, turning, and lifting. These fiinetions. in addition to the estimated anatomical and physiological limitations, .should permit the trained physician to arrive at. a fair computation of percentage of disability. The elements of motion as listed above are considered under the functional factors of: I. Quickness of action `2. Coordination of movements :i. Strength 4. Security 5. Endurance (i. Safety as a workman 7. Prestige of normal physique McBride gives the relative value of each of the functional fac tors in respect to 100 per cent incapacity in a general way as follows: 1. Delayed action .................................................. 10 per cent 2. Awkwardness .................................................... 20 per cent .`5. Weakness ............................................................ 20 per cent 4. Insecurity .......................................................... 10 per cent 5. Diminished endurance....................................... 20 per cent (>. Lowered safety factor ....................................... 10 per cent 7. Adverse influence of conspicuous impairment.. 10 per cent The total of these respective percentages of loss incurred will repre sent the partial loss of the part as a whole, and is to be estimated as a jKTcentage of the loss in respect to physiological and anatomical limitations. Permanent Disability in California In California, when the physician determines his patient is ready for a permanent rating, a standard form, furnished by the Industrial Accident Commission, is filled out and mailed directly to that body (Form 9). Upon the information furnished, the rating committee of the commission bases its award. It is apparent that this form doe-not furnish as complete a basis for determination of disability a> that suggested by McBride. It has the advantage, however, of secur ing more standardized information from a large group of physician.', many of whom are ill-trained in this phase of medicine, than the method advised by McBride. Possibly our medical schools of the future will graduate men trained in a uniform method of estimating disability. For a broader and more general consideration of the method of estimating permanent disability. I am indebted to Douginas A. OCCU P AT [<) N XIJ DISKASKS Form No. j) NOTICE.--This original report must bo sent by (he examining surgeon direct to lIn* Industrial Accident Commission of the State* of California and not to any other parly. DO NOT write in here .VO. state of California DEPARTMENT OF INDUSTRIAL RELATION'S INDUSTRIAL ACCIDENT COMMISSION PERMANENT DISABILITY RATING DEPARTMENT Statk Rrn.niNG, Civic Ckstkh, Sin* Kkascisco <i(H State Hni.nivc. ('me Ckvtbk, Ix>s Anoklks SITtOICON'S .SPECIAL REPORT--UPPER EXTREMITIES This Blank to Be Filed Only When Maximum Restoration of Function Has Been Attained Name of patient, ,,. . Age OtTiijMlion. Date of accident .. Address..,.. Name of employer .... Insurance company I. (Jive description of injury, staling the condition of the patient when first called to your attention i. Give description of treatment employed in this cae in full, slating what operations have been performed and with what results.. ... ...... .................................................. .`I. Name anti address of surgeon who operated ami assistant. Surgeon .. ....................................... .. Assistant. ......... 4. Ha.s repair been delayed from any cause?......... ......... If so, what?'... ... .5. \Na.s there any previous permanent disability or deformity?.................... If '>, what?.............. U. Is there evidence of luetic, gonorrheal or tubercular infection or alcoholism?. . ,, .If so, what? 7. leinperament of patient, any evidence of hysteria, neurasthenia, or hypochondria?. If .so, what?.., .... ............. .. ............................. ,,...................,,...................... S. Date of last treatment. .. . Is pre.senl condition permanent? ... Mh.it is the PERMANENT D1SAHILITY in this case, if auv? Discuss fully from the following stand points: a. AMPUTATION ... .. ... .............................................................. b. DEFORMITY................................... .. ... . ...... . , . c. ANKYLOSIS or LIMITED MOTION ......................................... ................... d. ANESTHESIA or PARESTHESIA . LOSS OK FUNCTION. Note.---Record as far as possible the loss of function in degrees and in the form of -i fraction in compauson with the corresponding uninjured member. Example: Injury to linger, index, major, proximal joint. Motion is found to be 60. Motion iti the index*, minor, proximal joint is found to lx* tm0. The fraction found then is 60/90, which represents existing function. Estimates will be made on VOLUNTARY, NOT PASSIVE, motion. In finger immobilities* give distance by which finger tips fail to reach pdra of hand ou active flexion ami to what part of palm. Signed this........................... lav of surgeon executing blank sojn here "'I reel ami Vo. . . HI .City or Fort it TIIlv ADM IX1STUATION or WOKK.MKX S COM l'KNSATIOX oo Campbell.' a referee of (lie California Indii.slrial Ac'c-i<k-nL Commisdon. a l law Angelo.-: Permanent Disability Defined.--While the aid dm'' nol define this term. a disability is generally regarded a' "permanent" where further change--for belter or --i>woi'm nol reasonably lo be an ticipated under usual medical standards. 1L may be lhal no further treatment is possible, or lhal (lie only treatment suggested is so problematical of success as to warrant the employee's refusal lo undergo it. In such an event, it is permanent within the meaning of the act. In practical legal results, the healing period is over, and a permanent aftermath of disability exists. In connection with this re sult of injury, disability primarily means impairment of function in whole or part of a member or of the entire body. Ordinarily the term "permanent." when applied to a personal injury means "lasting during the future life of the injured parly." But, under certain insurance policies, it has been interpreted as meaning "lasting or continuous,'' as distinguished from transitory or temporary. Under United States War Bisk Insurance. ". . . if it be reasonably probable that this status will long continue, . . ." it is permanent in legal contemplation. Influenced by the requirement of liberality in interpretation, under some compensation acts a dis ability is regarded as permanent when it is shown that the injured employee will suffer such disability for an indefinite period. Because of the absence of a statutory definition, the California standard has been a literal interpretation of the term. This makes it a question of medical fact and involves an occasional insoluble problem of proof, complicated by the limitation upon the period of temporary disability. As a matter of substantial justice, any disa bility which lasts beyond the statutory period of temporary disabil ity should, ipso facto, be regarded as permanent. Permanent Disability in General.--Where an employee, aged sixty, has been totally disabled for several years, the condition is permanent. The mere possibility of slight improvement is insufficient to change the character of the disability. Loss of use of a part, a* reduction of vision to merely light- and dark-perception, is total los> of the part. Loss of Finycrs and Toes.--In eases involving but one finger, for most occupations, there is a smaller rating for the amputation at the middle joint than for immobility at that joint. This is based on the theory that a finger which is stiff at the middle joint is in the way of the full use of the remaining fingers, and that one is actually better off without such a finger than to have it stiff and protruding. In general, there is no rating given for the loss of terminal phalanges :>4 OC ('l I'ATIOX AI. DISKASKS of flic minor middle, ring. or liftle finder for most occupations. Ccrlain occupations in mechanical lines do gel a rating for loss of ter minal phalanges of the major middle, ring', or little lingers, but most occupations do not get a ralinsr for these phalanges, even on the major hand. There is no rating given for the loss of the distal phalanx of the second toe, for a laborer; the distal phalanges of the sec ond, third, fourth, or fifth toes for most occupations; or the little toes for most occupations. Where the permanent disability rating has been exhausted by the temporary-disability payments, the mak ing of the rating releases the carrier from further payment to the injured. A hernia remediable by operation is not regarded as a per manent disability. Lon* of Sight.--The loss of the sight of a single eye. the other re maining normal, is not so severe a handicap as the loss of an arm or leg. since the ordinary working-man or mechanic will teach his re maining eye to do the work of both eyes with an efficiency compar able to that of a two-eyed man. Consequently, the disablement inflicted by the loss of one eye cannot usually be rated as high as the loss of an arm or leg. However, the loss of both eyes is as severe a handicap as the loss of both arms or legs. Co.s'.s- of Teeth.--The loss of teeth is usually not rated, because it is possible to reconstruct such loss and provide a man with a satis factory substitute. It is only when the jaw is so badly injured that artificial teeth cannot be supplied, in which the loss of teeth is both permanent and of such an extent that it interferes with the employee's ability to eat to maintain his strength, that a rating is given for the loss of teeth. Loss of sexual power does not constitute a ratable permanent disability under most acts. Actuarial Background of Permanent Disability.--hi California il is believed that permanent total disability is worse than death. In Un case of permanent tola I disability the injured man not only is as un productive as he would be if dead, but, in addition, is a burden upon his family to the extent that they must hear the cost of his personal expense. By a study of average expenses among wage-earners, it was determined that 40 per cent of a worker's wage could fairly be said to represent the cost of his own upkeep. On this basis, the worker idead so far as his contribution to the support of his family is con cerned when he becomes permanently disabled lo the extent of (SO per cent and is thus, theoretically at least, just able to earn enough for his own support. Life Pension* anti Death Benefit*.--The California schedule, there fore. provides the same compensation for a (it) per cent permanent disability as for death. From this point to 100 per cent, or total im- Till-; ADM IXISTUATIOX OK WOUKMKN S COM L'KXSATIO.X |miniici11. the act provides ;i life pension of the difference between what is left of the employee's cartiiim capacity and 40 per cent. Tims, in ease of an SO per cent impairment, tile employee can theoretically earn only -20 per cent of his former wage. and the act therefore pro vides him with a pension of 20 per cent. In ease of a 90 per cent impairment, the pension is .'SO per cent, and where the disability is total the pension is 40 per cent. The compensation for permanent partial disability thus grades gradually into that for permanent total disability. The full death benefit is payable in all eases where the disability is rated 00 per cent or over in addition to the life pension, which does not start until the death benefits have been exhausted. 240 weeks from the date of the injury. Basis of Permanent Disability.--If the injury results in permanent disability, the indemnity begins on the eighth day after the injury and is payable in llie same manner as prescribed for temporary dis ability. The permanent disability rating is based upon the age and occupation of the injured man at the time of injury, and also upon the nature of the physical impairment or disfigurement at the time of rating, with due consideration being given to It is diminished ability to compete in an open labor market. This is then worked out under the provisions of the Permanent Disability Hating Schedule, which results in a percentage of disability, entitling the employee to four weeks of indemnity for each 1 per cent of permanent disability. For all ratings in excess of 70 per cent the employee receives 24(1 weeks of indemnity at 05 per cent, of his average earnings within the limits provided, and thereafter, during the remainder of his life. 1 per cent of such average weekly earnings for each 1 per cent of perma nent disability in excess of 00 per cent. If the rating does not exceed 09.75 per cent, it is paid at the usual weekly rate until received in full. The employee is entitled to and must be rated upon his handicap in the occupation in which he was engaged at the lime of his injury, irrespective of his previous work. Where two forms of occupation are combined under the same employer and under the same general engagement of hire, the rating is based upon the occupation for which the greater disability exists. Effect of Age Differences.--The permanent-disability ratings re flect age differences, since adaptability to a changed condition is de pendent upon age. A boy of fifteen is believed to possess full powers of rehabilitation from an injury. He has not yet learned his life's work. If he receives an injury, he can change his life's work with reference to that injury and therefore be considered but little handi capped. When an employee reaches the age of seventy-five, he is regarded as possessing no power of rehabilitation. Tf the injury dis- :>(> Of'C'l'PATIOXAIj UISKASKS ablcs him and requires a change of work, lie is industrially barred for the rest of his life. The different ratings for age are. therefore, appor tioned through a range of from 7 to 7.7 per eent between the age.-' of fifteen and seventy-five, the greatest being for a man of seventy-five and the smallest for a boy of fifteen. The fact that there may be exceptions to this principle is ignored. The average man of that age. occupation, and disability is the necessary basis. Schedule on Statutory Ratings.--In some of the slates, typified by the Longshoremen's Act. and the schedules of Missouri. Colorado, and New York, there is a .statutory schedule of indemnity for spe cific permanent disabilities. Under such a .scheme, no distinction is made on account of the age of the employee, his intelligence, efficiency, strength, health, condition in life, or the like. The act bases the in demnity solely upon disability due to the loss either of a member, part of a member, or its function. Such a plan is comparatively simple in operation, since it takes no cognizance of .situations which may reflect a loss of earningcapacity greater than the average to employees engaged in specific operations. Where the average loss to workmen generally is the basis of indemnity, it can truly be said that there is little necessity for the receipt of testimony on the extent of such loss of earning or of functional capacity. The trained personnel of the compensation authorities is as well qualified to pass upon such matter as any other persons. The better practice, however, requires that the record con tain either lay or expert, testimony on the degree of disability. The compensation provided by such a schedule is exclusive for the named disabilities. However, injuries resulting in partial incapacity not among the named disabilities are not controlled by the schedule. "The Legislature evidently believed the loss of a specific member or organ deserved the compensation staled, whatever else occurred. If. however, additional injury should increase the workman's partial disability, cither permanently or temporarily, he should receive addi tional compensation.11 . . . "If there is an additional or independent injury which produces disability, it is compensable, even though it is a consequence of the (scheduled disability). It is an independent injury that produce-, its own disability, separate and distinct from that resulting from the loss of the member. . . . "Where, in consequence of amputation, injuries result which are distinguishable from those immediate results of the amputated limb, for example, if a nervous disorder ensue, or blood poisoning sets in, or a phlebitis develops, affections such as these were not intended by the . . . Act to be compensated in the loss of this member."-"' TUB ADMINISTRATION OB WORKMENS COMPENSATION ;!? Permanent-Disability Rating Schedule in California.--The degree of permanent disability is determined by reference to the rating sched ule. It is based on the law of averages and is the result of intensive actuarial investigation and analysis of bodily functions particularized to the various occupational activities. The present schedule is that adopted in 1914 and has been modified but little since its adoption. Provision for its use was made in the ael. which did not include the schedule, however, since it was desired that the latter remain flexible and be subject to whatever change experience should indi cate. The schedule is but printa facie evidence of the actual disability present. The schedule can be changed at any time by the commission and be effective for all pending claims, even though they wore filed before the schedule had been amended. Theory of Permanent-Disability Rating.--The theory of perma nent-disability rating is that an employee of any stated age, occu pation, and disability will be able to rehabilitate and readjust himself to his new earning-capacity within an average period. The rating-; are so computed as to provide disability indemnity during that esti mated period. A former commissioner" has outlined the controlling principles in corporated into the schedule: "The California schedule is based upon two theories: (1) that permanent injuries should be compensated for, not upon the basis of loss of future earnings, but upon the loss of earning capacity; and (i) upon the necessity of providing an adequate period of rehabili tation. . . . "The underlying theory of the schedule is that there is a certain standard occupation and . . . age which can be used as a basis in determining the percentage of disability caused by various injuries: that all other occupations can be rated in accordance with the stand ard occupation, depending upon the physical requirement and skill: and that the ago of the injured person can be made a function of the standard age, based upon the diminished ability to rehabilitate himself as lie becomes older. . . . "The standard occupation is taken as that of an ordinary unskilled workman and the standard age as :>9. The occupation chosen makes an admirable standard because of the simple nature of the physical requirements placed upon the different parts of the body. Age 9!) was taken as the standard age because statistical records at that lime showed this age to be the approximate average age of persons injured in California." Concurrent Indemnity for Temporary and Permanent Disability.-- Due to the fact that the same injury may cause a series of grades of `>8 OCCUPATIONAL DISKASKS disability. and each may haw a statutory provision relating lo il. fn'"'iimitif*- witli temporary total, which morses into temporary partial anti terminates with a permanent partial or total disability, some problem arises as lo the amount of indemnity to be paid. This is pri marily. of course, a matter to be determined by the particular act involved. liven so, confusion arises because of the declaration in some of the statutes (hat the schedule1 allowance for a staled permanent disability is "in lieu" of all other compensation. The acts fall into two definite croups on this subject, liilher be cause of the absence of the "in lieu" clause, or because of the liberal interpretation of the section by the courts, a largo number of juris dictions allow both temporary and permanent indemnity for the same injury. The statutes of this type vary from full payment for each grade of disability to but partial recognition of each within prescribed limits. The other group makes the schedule award exclusive. A pro vision for specific* injuries does not necessarily provide for a combina tion of specific, injuries. How to Use the Schedule.--The California Permanent Disability Rating Schedule is divided into groups under roman numerals, each referring lo some portion of the body, starting with the head and ending with the toes. For example. I refers to disabilities resulting from skull injuries: II pertains to eye injuries: IH to ear injuries. The degree of disability is a subdivision under the respective headings, complete loss of both eyes is II-l; complete loss of one eye is 11-3. 1. A carpenter, aged forty-one. with amputation of the right, major hand at the wrist is to be rated. Under Table I (nature of the injury), page (i. heading "VIIT--Hands," loss of the major hand is given as "VIII-1, line 41." Under '1'able II (occupation), page 13, carpenters arc listed as "Form 20." Referring to Table II. Second Division, under the disability number "VIII-1" and under Form 120. we find the letter "I),'' which is the table to which the case belongs. At page 42 we drop to line 41 of Table IX and along line 4L lo the proper age. forty-one years. This gives "52:0" or 52 per cent as the rating-. In formula, the rating reads: "VIII-l-41-20-l)-52:0." Other wise stated: Disability VIII-I Line 41 Occupation 20 Table D Per Cent 52 I he percentages are staled 28:1. 12:2. These figures are not deci mals, but quarters. Thai rating would be 28.25 per cent and 12.5 per cent. Only odd ages are given. The rating is taken at the nearest odd age. At age thirty years and four months, the man is nearer age thirty-one than twenty-nine, requiring a rating at age thirty-one. THE AD.MINISTKATIOX OF WOKK.MUX S COMPENSATION Hit 2. A laborer. im'cd forty, lias lost one half of the gripping power of the left, minor hand, with the thumb normal. In Table I. under disability heading. "XVI--All fingers not ineluding thumb." we find "KVT-8, line -id." covering immobility of the minor hand. Proceeding as before, we develop the following formula: Disability Line Occupation Tabic Per Coil XVI-8 ->-f 'i A AO: I Disability in Silicosis and Allied Conditions Estimating a disability resulting from an occupational disease, such as silicosis, has to be done without the use of concrete measure ments and figures which serve as a basis of estimation in traumatic injuries. As has been many times intimated, permanent disability from occupational diseases is rare. However, silicosis and the allied conditions of anthracosilicosis and asbestosis constitute a problem of disability determination which remains unsolved. For a review of this phase of the problem, the reader is referred to the author's discussion under the medicolegal aspect of silicosis. It is apparent from the general nature of silicosis that a subsequent disability may never be anticipated by the victim, and yet years after having removed himself from the hazard he may break down as a result of his previous ex posure and remain unrewarded. One thing is certain, that the num erous problems presented by the dust diseases can best be handled by the industrial accident commission or a specially appointed board in each state, rather than by lay juries. Fixing Responsibility.--One of the chief problems has been the placing of responsibility for the disease, which involves fixing the date of disability. In many states the general rule both in workmen's compensation eases and in common-law eases is that the date of the accident is the dale the disability commenced. This tends to place full responsibility upon the last employer. Tn California liability is prorated upon the carious employers, according to the length of ex posure with each. By a sort of general agreement among the insurance carriers, little emphasis is placed upon dust counts and the working conditions at the various places of employment. Formerly a defendant carrier would present dust counts and descriptions of the workingconditions at the place of his insured in order to prove his liability was minimal, or none. But it was often contended that a dust count today or the working conditions today cannot be assumed a> exactly representing those of some years previously at the same place of employment. Today, in California, liability is estimated largely upon the basis of length of exposure in each employment. To illii-- 40 OCCUPATIONAL DISK ASKS trail. a claimant lias worked in a -alien hazard for .5000 day-.. -2000 of which were spent in another slate. Since this stale has no power to secure action or decision from another slate, these 2000 days are de ducted. In this state, the claimant worked for .`>000 days and for lima' different employers, for employer A. 1000 days: for B. 1500 days: and for C, 500 days. Each employer is, therefore, held for his propor tionate amount. To the writer this method appears fair. First of all. it dispenses with the cost of liability in eases where the exposure occurred in other states. If a coalminer from the anthracite district of Pennsylvania drifts into goldminiug in California, a California employer should not be held liable for the days spent in Pennsyl vania. It dispenses with quibbling regarding the extent or manner of exposure. Disability Prior to Enactment of Laws.--A problem which con fronts the states recently assuming liability for disability from sili cosis is the matter of easement of payment for a total disability which has accrued prior to the enactment of provisions for compensation in that particular state. Xew York. Ohio. Pennsylvania. Michigan, and West Virginia, to mention only a few. have had to face this situ ation. The intention and attitude of the Bureau of Workmen's Com pensation of the state of Pennsylvania illustrate this phase. The following is based on Challener's discussion7: The claimant must have had an aggregate employment of at least two years in the Commonwealth of Pennsylvania in an occupation having a silica or asbestos hazard, during a period of eight years next preceding the date of disability. . Under the Rules of Procedure of the Workmen's Compensation Board (Rule 41) the two-year period may be calculated in any one of three ways: 1. When during any two calendar years in the preceding eight years he has been employed in such an occupation: or 2. When he is employed in such an occupation during the eightyear period for a total number of working days equal to twice the number of days the men employed in that indiutry work during an average year: or !>. YS hen he has been employed in such an occupation during any twenty-four calendar months during the eight-year period. Compensation by Employer.--Section 56 of the Occupational Dis ease Act provides that. "The total liability of the employer unto (he employee or his dependents under this section shall not exceed llnsum of $.<h(>00.<)()." TIIB ADMIX ISTItATIOX OF WOHK.MKXS COM I'KXSATIOX 41 Tlic Chairman of the Board of lIn- Pennsylvania Bar Association, in discussing' llic -ilieosis section, calculated that a man 44.0 years old. who became totally disabled, had a maximum life expectancy of 25 years, and if lie lived his full expectation of `25 years, he would receive $14,400. A reverse calculation indicates that his theoretical man received $18 per week for 500 weeks, or $9000 plus $00 per month for the balance of his expectancy (15 years) or $5400 or a total of $14,400. This method of calculation is apparently based upon Section 4 of the act. which provided: When an employer and employee shall be subject to the provisions of Article 3 of the Workmens Compensation Act as therein provided, compensation for occupational disease shall be paid in all cases by the employer according to the schedule provided in such Act. subject however, to the special terms and conditions relative thereto, as set forth in this act. Compensation by State.--In determining whether the employer'liability is $.`5000 or greatly in excess of that amount, as intimated by the Chairman of the Board, it is also necessary to consider Section 7 of the act. This is the section that provides for part payment by the Com monwealth, starting at nine tenths the first year and decreasing one tenth each year until in ten years the employer will have paid the compensation in full. To take a concrete illustration, let us assume that a man is totally disabled on January 1. 1938. from silicosis. The Occupational Disease Compensation Act does not specify his weekly rate of compensation, and it is necessary to refer to the Workmen's Compensation Act which fixes it at $18 per week, assuming that his earning-power justi fies the maximum rate. We would then have this situation. Ilis com pensation at $18 per week would amount to $930 a year: under Sec tion 7a the stale in the first year would pay nine tenths of that amount or $843 and the employer would pay one tenth of that amount or $93 a total of $930. First year . . Second year Third year . Fourth Year Slate . $843 750 (>;>? 470 Employer $ 93 180 `279 310 Total $930 930 930 79`2 $`2 7`20 $8?4 $3000 42 oecnwno.N'Ai. diskasks My the end of the third voar ho has rocoivod $2808. so that if $0000 is (lie maximum compensation lo which lie is entitled, the payments would run out in the fourth year. But while tile employee has received $8000 the employer lias paid only $874. Does the employer owe any thing more? Tt should he noted that Section 5/; does not create a lia bility of $.`5000. hut on the contrary slates that the liability of the employer shall not exceed $.3000. The language seems to be significant, and the result is. therefore, in accordance with the terms of the act. Any other interpretation would produce an anomalous result. Tf this were not so and it should be held that an employer must pay $.3000 in all eases, then our theoretical man who became disabled in January, 1938. would continue to receive compensation for nine voars as follows: First year................... ............. Second year ............... ............. Third vear................................ Fourth year ................. Fifth vear.................... ........... Sixth year.................... ............. Seventh vear ............... ........... Eighth vear ................. ........... Xinth vear................... ........... State $848 750 057 471 878 285 192 20 Em ftloyer $ 98 180 279 872 405 558 051 744 252 Total $980 980 9.80 980 980 9.80 93(5 9.80 272 $7700 '1'he net result would then be lo give an employee who became totally disabled in 19.38 a payment of $7700. but another employee who sustained the same disability ten years later would receive only $`{000. as in his ease there would be no contribution from the stale. In a personal communication from Challeners regarding his dis cussion of the above phase of tile Workmen's Compensation Act in Pennsylvania, he writes. "At the time I wrote this paper, there had been no decisions determining the amount of liability." Implying that a recent interpretation had been handed down. Challener says further in his letter that the Workmen's Compensation Board has interpreted the act ". . . as restricting the liability of an employer and the Commonwealth of Pennsylvania to the total payments of $3000.00 in all eases of silicosis, anthraeo-silicosis and asbestosis. Under tile Board's decision, the liability of an employer to pay compensation, where the silicosis results in total disability during the first year, is restricted to one-tenth of $.3000.00 or $.300.00 for his entire disability. The Commonwealth's obligation, where the silicosis results in total THK ADM I.VISTUATIO.V OK U'OIIK.MEN' S COM FKNSATIO.X 4.`i disability during llie first year is $:>v24().0(). . . . However, llicre have been no appellate eourl decisions deciding Ibis matter." Similar restrict ions are found in lhe- statutes of oilier states: Ohio (Laws of 19:17. Section 14(>5. (>S) A'nr York (article 4. Chap. 887. Laws of 19:5(i. Section (Hi. effective June (i. 19.`i(i). and Michigan- (0.1). Amendment, 19:57. Section 4) restrict the liability of the employer by fixing a maximum benefit of $:500(>. with a limitation of 500 for disability occurring during the first month after the act became effective plus $50 additional for each month thereafter until the maximum of $:!()()() is reached. The West Virginia act. following the precedent set in South Africa, divides silicosis into three parts and awards $.>()() for the first stage. $1000 for the second, and the full benefits of the Workmen's Com pensation Act for the third. OPERATION OF INDUSTRIAL ACCIDENT COMMISSION To this point, the discussion in this chapter has considered the manner in which the intentions of the Workmen's Compensation Act are fulfilled. A brief further discussion is necessary of that body which has the power to enforce the act. This body in California is known as the Industrial Accident Commission, as it is in most stales, and it.duties in this state closely parallel those of the other states. "The Act creates a board of three members known as the Indus trial Accident Commission. Claims for compensation are filed with the Commission: hearings are held and awards are made. "The Commission may make and enforce safety rules and pre scribe safety devices. Its procedure is largely judicial. It has powers to administer oaths, issue subpoenas, lake testimony and punish for contempt. Its proceedings commence by application in writing fol lowed by notice of hearing. The statutory rules of evidence and pro cedure do not govern. The Act gives the Commission a. continuing jurisdiction over its awards for 245 weeks, and it may during this period alter or amend them for good cause. Appeal lies to the Supreme Court or District Court of Appeal by a writ of review. The findings and conclusions of the Commission on questions of fact are conclu sive and final and not subject to review. The Appellate Court is lim ited in the appeal to questions of whether the Commission acted without or in excess of its powers, or the order, decision or award was procured by fraud or was unreasonable: or that, the findings of fact did not support the order, decision or award under review. "The Industrial Accident Commission is a division of the Depart ment of Industrial Relations. Its functions are performed by various departments within this division. 44 OCCVI'.mO.VUy DISKASKS "Tin* judicial division of the Industrial Accident Commission is called its `(.'om[)cnsalion Department.' Headquarters are at San Fran cisco, with a substantial branch at Los Angeles. A staff of more than twenty judicial officers known as referees decide the claims brought before the Commission by employees, with all decisions subject to confirmation or approval by the Commission itself. "Referees travel in various parts of the State eaeli week to hold the hearings necessary to permit the presentation of claims by injured men or women in all of the State's 5S counties. With a relatively small staff of officials and employees, the Compensation Department thus covers the State, hearing and passing upon the amazing total of 10,000 original claims of compensation each year. Supplemental matters usually requiring an equal amount of procedural work account for about 4,000 more decisions per year. '`This extremely busy department awards annually an estimated total of nearly $7,000,000 in compensation in addition to medical benefits. Its decisions form the basis for disposition of thousands of unlitigated claims totaling many millions more. ``Hearings are conducted by referees and juries are dispensed with. Medical evidence is nearly all submitted in writing and points of dispute are reduced to a minimum by stipulation. Parties need not be represented by an attorney unless they so desire, since the referee will examine all parties and witnesses regarding the facts of each case. These procedural short-cuts greatly reduce the time needed for the presentation of a controversy. The average ease is pending less than eight weeks, as compared with former periods of from six months to six years in civil courts. "Medical Department.--In the consideration of cases, the Com pensation Department is assisted by two related bureaus, the Medical Department and the Permanent Disability Rating Department. The Medical Department examines thousands of applicants annually with out charge to the injured person, and the medical files of thousands of other cases arc reviewed and expert medical opinions are given orally or in writing to the referees. "Bills for medical services to injured men are approved or revised. Cases of an especially difficult nature are referred to independent medical experts chosen by the Medical Department. The entire work of this department is directed primarily toward assisting the Com pensation Department to decide eases before the Commission. "The Permanent Disability Rating Department is also of great assistance in formal matters before the Compensation Department, as well as in many cases where no claims have been filed. The de termining of the extent to which an employee has been permanently TUB ADM IX1STKATION OF \\ OHK.MK.V S COM l'F.A'SATIOX 4.5 crippled b,v an injury is frequently an involved problem. These prob lem.''. however, have been greatly simplified by means of a schedule which lakes into consideration Ihe workman's age, occupation and (he nature of Ihe injury. The adjudication of the amount of compen sation as determined by the schedule for flic disability suffered is the work of (he Permanent Disability Hating Department. "Legal Department.--The Legal Department, through its attor neys. represents and appears for the Industrial Accident Commission in all actions and proceedings arising under Lhe provisions of any of the law administered by the Commission. The decisions of the Com mission are defended by the Legal Department in all appellate pro ceedings. This involves preparing briefs and making oral arguments in the Stale District Court of Appeal, the Slate Supreme Court, and the T.'niled States Supreme Court. "It is also the duly of the Legal Department, through a specially appointed law enforcement officer, to enforce the compulsory fea tures of the Workmen's Compensation Law. Employers who are re ported as not carrying compensation under the present practice are at first warned that they are committing a criminal act. and if the warning is disregarded and violation continued, or if evidence of previous violation is found, prosecution proceedings against the em ployer are instituted. A permanent file of all employers reported as uninsured is kept by this department and a program of enforcement through cooperation with local law enforcement agencies throughout the State is maintained. "The law also gives the Commission, through its Legal Depart ment. the right to file injunction proceedings against any employer failing to abide by the provisions of the law requiring compensation insurance. "In addition to the foregoing, the Legal Department has the duty of bringing criminal proceedings for violation of the safety laws and orders concerning air tanks and boilers, elevators and motor boats. It acts as legal counsel to the Commission, rendering legal opinions when required, and represents it in all litigation involving the Com mission. "Accident Prevention.--The Commission has the power and super vision over any employment and place of employment in this Stale for enforcing its safety orders. This function lies with the Bureau of Industrial Accident Prevention. "The Commission may require and prescribe what safety device.-., safeguards or other means of protection are adapted toward the safely of employees. It may fix reasonable '-taiulards and enforce reasonable orders for adoption of reasonably uniform safeguards." a -Mi ()('('['I`ATIO.\AI, DISEASES Finally, after consideration of all that lias boon previously writ leu in this chapter, it can be summed up by stating that the purpose of workmen's compensation is adhered to by the physician who renders his opinions after a complete study upon an unbiased basis. He prac tices this phase of medicine best who disregards the insurance carrier, the patient, the court, and the social or economic consequences of his decision. Fpon his integrity and sanity rests the structure of one of the finest laws ever to be promulgated. REFERENCES (. Information Heyardiny the California Workmen's Corn/mutation and Mulch/ f.au\ Indus!ml Accident Commission. San Francisco. *2. McBride, Karl I).: Disability Evaluation. .1. B. Lippincoll Co,. FliHudclphia. 1930, p. 41. :i. Ibid. 1. Campbell. I). A.: Workmen's Compensation. Barker. Slone, and Baird Cm. Los Angeles. Vol. F. pp. 719-7JW, ~>. Kranko vs. "Wm. Sehollhorn Co.. 93 Conn. 13. 104 All. 4X7. 1918. (i. Xa fixer. A. If.: L\ -S. Labor Bulletin \o. *281. pp. 01-00. 11)31. 7. ('balleuer. 4Yin. A.: Lecture on Compensation Lairs, Depl. of lud. Hyiriene, School of Medicine. Cniversily of PHUburjih. 1039. S. Personal eonmumieation from Win. A. Challener lu author. May `2. 1911. 9. California Safety Xcics, -?-}.* 4 (June). 1910. CHAPTER HI THE FUNCTION OF THE PHYSICIAN AS RELATED TO WORKMEN'S COMPENSATION The recognition and prevention of disea.se. or the proper applica tion of a remedy when disease presents itself, has traditionally con stituted the duly of a physician. Hut the practice of medicine under Ihc administration of the Workmen's Compensation Act imposes ad ditional obligations. In addition to a knowledge of the law then: exist certain other requirements necessary for the adecpiate dispo sition of this work. The employee, employer, insurance carrier, and the court assume that the physician understands his relationship to them. Hut since physicians generally have received little or no in struction on this relationship, there exists a lamentable stale of misunderstanding. Where shall the doctor or student obtain the funda mentals sufficient to render him competent in this work!-1 In this chapter the intention is to enumerate these fundamental requirements anil to suggest acceptable methods of meeting them. Scope of Act in One's Own State.--The first duty of the doctor is to acquaint himself with the scope of the act as adopted in the state in which he practices. It behooves him to secure a copy of the act from the State Department of Labor, or the Industrial Accident Commission. In the previous chapter it was intimated that it is not necessary that a physician be informed on all the technicalities of Un law. Tl is not expected that he be a quasi-attorney. Many points of the law do not concern him. nor should they affect his conclusions on the medical aspects of the case; but on the other hand there are certain sections of the act which involve both medical and- legal inter ests and which should be understood by the physician if he is to avoid errors in the conduct of an industrial practice. For instance, the patient who enters a claim for the first time nine or ten months aft el an alleged injury supposedly occurred is barred, in most states, by the statute of limitations. This is primarily a point for legal decision, but a physician should be cognizant of if so that he will deny treat ment until properly authorized. It is not infrequent to find this factor of time interval ignored. It should be understood what eonstituleIrcatment. As an example, a patient who desires to reopen his case, which has been closed some months before, is sent to a doctor for examination only. The examiner should offer no advice, suggestions. 48 OrcTl'ATlOXAI, IMSKASKS nor give ;i |irc*'*c,ri[lion. for in most dale-' this i> considered l>y the court as "treatment." The statute of limitations is thereby waived, and lolling of flu* statute by lIn* doctor ha-> Iwn indulged in. Groups Excluded from the Act.--Tlu- industrial physician should know what groups of people, if any. are excluded from the benefits of the act. In some stales, farmers and domestics are not covered by the act. In California, a domestic is covered if she works lifty-lwo hours a week. Some stales specify what disease will be compensated, thereby excluding all others, while certain slates have unlimited cov erage. In some of the commonwealths there exists a limitation in time and cost of medical and hospital benefits in compensable occupational diseases; in others it is unlimited. Special provision is made relative to the status of hernia in twenty-five dales. "Aggravation of a pre existing condition" receives a varied interpretation, and in Connecticut and Florida disability or death due to the aggravation or acceleration of venereal disease is not compensable. These are but a few of the peculiarities of which the doclor should be informed. Advantages in Knowing the Law.--An understanding of the law not only aids the physician in protecting himself but permits him to be of greater service to the workman. To illustrate, instituting pro ceedings for compromise and release settlements is a function ordi narily confined to the legal interests or the claim department. Most states require the approval of the court before this can be entered into. A few permit this practice without interference. Not often, but occasionally, the physician who appreciates the benefits of this alternative may suggest it for the good of the patient, especially when he has studied the ability, character, and capabilities of the disabled one. A branch manager for a camera concern on the West Coast re ceived a compensable skull fracture which entitled him to a weekly compensation of $25. While not physically disabled it was apparent he could never resume his executive work. It was suggested to him that he accept a lump sum of money, release, the carrier of all further responsibility, and invest this money in a small photographic supply store, a business in which he had had experience, and one in which the responsibilities could be shared by his wife. This he did. and today at a lake resort he has a business which yields a greater return than his compensation. Furthermore, he is useful and happy. Similar examples could be cited. Many times a good industrial physician who is aware of this existing possibility in the law can serve in re habilitating the working-man. However, he should discriminate be tween the responsible and the irresponsible. Some might dissipate a lump sum of money, as did the dissolute soldier with his bonus. TUB FUNCTION OF THE PHYSICIAN 49 References.--A discussion of many oilier aspect.- of the compen sation act cannot he indulged in at this time. For those interested, it is recommended that they obtain for reference a hook entitled Workmen'.': Compensation Act.'; in the Cnited State.':, published by the National Industrial Conference Board. New York: also. Adminis tration of Workmen's Compensation by Waller F. Dodd, the Com monwealth Fund, New York. Another excellent reference is an article by E. Ransom Koontz, M.D., in the. Journal of the American Medical Association, lit/: 5(i.`> (Feb. 17), 1940, entitled "Compensation for In dustrial Injuries and Occupational Diseases." An intelligent compre hension of the law constitutes the first step in becoming' an efficient industrial physician and often demarcates one from the routine lir-taid man. Importance of Keeping Records.--The next important step is the establishment of a well-systematized office. "Paper work" is abhor rent to most doctors, but the handling of compensation eases requires meticulous adherence to details. First reports must be followed by periodic progress reports. Records must be kept in a manner accept able to the courts and accessible months or years later. Case histories and especially ,r-ray films should not be destroyed for at least five years. Such a, procedure not only is important from a legal stand point, but is of value to him who, at intervals, wishes to read a paper based upon a series of cases. The office should be run much as a hospital record room with emphasis upon the. nomenclature used anil the methods of filing adopted. As this is being written, the Coun cil on Industrial Health is preparing a recommendation on standard terminology for industrial medicine. A universal conformity to this would seem advisable. The Doctor's Fee.--A doctor's bills are often disputed by insurance companies, therefore charges for service, -'applies, or physiotherapy should conform to the accepted fee schedule of the district, and extra charges should be explained. The author knows of a young physician who for more than a year made long trips to see patients, charging only the accepted fee for calls, not knowing that he was entitled to additional remuneration for mileage beyond a certain zone. It is recommended that the young physician or beginner in this field in spect the methods of service and office management used by men long experienced in this work. In addition he should visit the claim departments of several insurance companies in the nearest metro politan area in order to learn their methods of handling the claim and to ascertain what is expected of him. Tin* old family doctor managed to live in spite of his indifference to bookkeeping through contribu tions of eggs, butter, and chickens, but Mich procedure i- not avail 50 occri'ATiox.vr, mskasks able In l lie- industrial physician. 11 is financial .success is not alone dependent upon lii.s professional ability. The installation of a good system and the employment of a good bookkeeper an' factors of competence in the service rendered and the returns gained. Court Testimony.--A despised but required function of an indus trial physician is his testimony in court or before an industrial referee. The writer wishes to enlarge upon this duty. Competent testimony in the compensation case is rare, fn general medicine, the knowledge of the disease in question is fairly well understood by every physician. The etiology, symptoms, complications, and treatment of pneumonia, pernicious anemia, syphilis, etc., form a part of the experience of all practitioners of medicine. This cannot be said of silicosis, benzene, carbon tetrachloride, diehlorclhylene. or other poisons. It is not infre quent to find divergent opinion offered by physicians who have had no experience with the causative agent involved. Honest mistakes arc bound to arise in any medical testimony at times, due to confusion or emotional imbalance of the witness: or to the failure to be properly prepared; or to being unwittingly led into erroneous commitment by a lawyer. The great majority of errors made by the medical witness in an industrial court arc the result of ignorance and of inadequate information regarding occupational diseases. For example, a youngphysician made certain misstatements regarding the effects of sulfur dioxide, during a trial and when cross-examined, he admitted his state ments were guesses, since he. had had no experience with this gas. Another physician stated on the witness stand that the bronchiectasis shown in tile films of a pottery worker's chest was due to silicosis which had resulted from the patient's exposure to silica. The facts were that tile patient had worked six months in a "wet process." and tile films showed no evidence of silicosis. Off the stand and off the record the physician later admitted that lie had read of silicosis but had never seen an .u-ray film depicting this disease. Testimony of (his type is damaging to the true facts of the ease, bill unfortunately the referee or courts do not always recognize the inexperience or lack of authority behind such testimony. Difference between Possibilities and Probabilities.--What the medical witness needs to appreciate, and what the referee or judge should be careful to discriminate, is the difference between possibili ties and probabilities. Too often possibilities exist lml the probabili ties are remote, and yet an inexperienced physician will permit a clever attorney to secure an admission of unlikely probabilities. An example of such an incidence is the ease of a truck-driver who picked up the end of a narrow, light piece of pipe and staled that at the lime lie noticed a mild twinge in his right lower abdomen. The incident TUB Kl NtTION OK TUB lMIYSKTAX 51 was forgotten. Three nights later he was awakened with pain, nausea, and vomiting'. He was operated upon for appendicitis, and following the operation he recalled the occasion of lifting the pipe and subse quently filed a claim for appendicitis resulting from lifting. ILis physi cian testified that the act. could have produced the pathology which necessitated an operation. The author was asked upon the stand by the claimant's attorney, if it were not possible to produce or aggravate appendicitis by the act described. IIis answer was that he personally might become president of the United States, but that it was vastly improbable. It is imperative in these medicolegal disputes that the physician adhere to the likely and more reasonable elements rather than those extremely unlikely and improbable. What is needed is a more uniform basis for evaluating the relationship between the hazard and the disease. Undergraduate and postgraduate training will par tially fulfil this need, but it can never be fully obtained unless the doctor ignores his affiliation with the employer, or carrier, or divorces his tendency to s.vnqtathize with the patient. It is obvious that there is a great national urge to care for the unfortunate. Such a trend is inevitable and cannot be associated with, or attributed to. any particular political group. Unemployment in surance. old-age pension, and other legislative acts are born of eco nomic necessity. Their provisions must not be confused with the benefits of workmen's compensation. To fulfil faithfully the require ment of court testimony, the physician should be prepared with data relative to the history of the case, the physical and laboratory find ings. a knowledge of the disease and of the. accepted postulates con cerning that disease. Fallacious assumptions are repeatedly cited in the following pages. The Medical Report.--All employers or insurance carriers have a standardized form, "The Surgeon's First Report." which they ask to be filled out immediately and forwarded to the nearest office of the company. Such a succinct report is sufficient only when a minor injury is sustained, such as cuts, burns, or minor fractures. It is insuf ficient in severe degrees of trauma and never satisfactory in a case of occupational disease. The occupational diseases are rarely acute, seldom immediately apparent, and usually require detailed study and investigation. Obviously it is impossible to imparl the result of such endeavor on a stereotyped, one-page printed form. These case- re quire letters of some length. The reason a letter is essential is ex plained in the following paragraphs. Regardless, however, of the type of report submitted, it should be done with as little delay as possible. This sets into motion the machinery relative to the ease, enabling the workman to receive his compensation when due if the ease is 5-i OCCl'I'ATIOXAL DISKASKS compensable: or permitting llu` carrier lo investigate the taels .sur rounding (lie claim before accepting or denying their responsibility. In a well-written letter the occupational environment will be deeribeil, the non-occupalional factors cited, the symptom.-., physical and laboratory findings listed, and the entire mass of information evaluated in the conclusion or discussion. If the disability is tlue to occupation, then the extent is estimated. These important parts of such it letter deserve further description. The History.--The art of case-history taking cannot be imparted lo others. The student may be instructed upon forms, methods, or outlines to follow, but the ability lo ferret out the essential facts either resides in him or doesn't. It is the idiograph of a good clinician. Much of the importance in the narrative of the patient may be read between the lines. To follow the trail as it wends its way without losing it by deflecting questions elicits a clear-cut story. During ten years of teaching physical diagnosis, the author constantly empha sized that the patient should be permitted to recite liis history before the historian writes down, a word. The habit of beginning the inter view by immediately setting down on paper the statements of the patient and having him wait until the historian catches up with him results in a stultified, incoherent story. This practice is to be espe cially condemned in industrial medicine for the following reason. Fre quently the patient has been previously interviewed by a claimsman. investigator, or insurance representative. To these he has given a statement which has been written down word for word and then signed by the patient. If then the doctor to whom he has been subsequently referred immediately starts Lo record every statement made, the patient is most apt to assume that the history he is giving is further legal information, not medical, and therefore he "freezes" or guards his every utterance. IIow much better it would be if the physician sat back and listened to the story, guided it as he saw fit. and then recorded it at its conclusion, going back if necessary lo clarify certain points! The history should be written in the words of the patient and not in the third person. It should ordinarily classify the case as obviously compensable, obviously not compensable, or one where compensability can be determined only after a complete study. In the writer's opinion this history should not be too short. An alleged occupational illness demands the recording of seemingly irrelevant facts. It not only must include the customary details concerning the onset as would be of interest in any illness, but must delve into factors of occupation -ueh as the materials handled, their composition, their noxious or inert form, the content of the atmosphere, the length of time of an acute or chronic exposure, the use or non-use of respirators or other protec tive devices, the adequacy or inadequacy of ventilation, the previous occupation of the patient, his previous medical and family history. Some of this information cannot always he obtained from the patient, nor always from his employer. Solvents vary in their chemical com position, and the concentration of metals or dust in the air may not he known to the workman or to his employer. In such instances, reli ance must be placed upon the hygienist, engineer, or chemist. It is inadvisable to assume the correctness of the patient's statement re garding the environment of his work or the composition of the mate rials he handles. The Physical Examination.--It would seem impertinent to suggest that this be most complete, yet frequently if is not complete. This negligence occurs more often in industrial medicine than in general medicine, apparently because of faulty assumption. In general prac tice the patient presents his symptoms to the doctor, seeking an ex planation of the cause. In industrial medicine the patient tells the physician that his symptoms are the result of a certain exposure or incident. There exists, therefore, a tendency to accept the patient's theory without an investigation or complete physical examination. The alleged back sprain is an excellent example of this type of assump tion. In the chapter on "The Industrial Hack." the author cites his study which reveals that nearly 70 per cent of the eases previously accepted by physicians as back sprain were, upon investigation, due to conditions not of industrial origin. In most instances pain was due to obvious but overlooked focal infection. Cancer of the spine was treated as a back sprain; a patient with well-marked pyonephrosis received physiotherapy for a sacro-iliac slip; the pain of aortic aneu rysm was attributed to an inhalation of formaldehyde, and the pa tient received many weeks of compensation. Malingering has been at tributed to patients with fractured vertebrae, or nucleus pulposus without benefit of a roentgenological or neurological examination. Additional instances would further serve to emphasize the urgency of a complete physical examination upon the presentation of even a trivial complaint. The Laboratory Investigation.--There is a prevailing opinion among the members of the profession that insurance companies will not pay for special laboratory procedures. This is not true. The failure to investigate the ease properly from a laboratory standpoint, com bined with inadequate histories, incomplete physical examination, and indifferent cooperation, constitutes the chief reason for the tendency of insurance companies to centralize the examination and treatment of their patients in the hands of a few doctors upon whom they can rely. 54 OCCrl'ATroXAL IMSKASES Any physician wlm attempts to establish his diagnosis by the aid of special tests will receive favorable recognition from these companies and will find them willing to permit the case to remain in his hands. The reason is obvious. In any alleged case if the laboratory investi gation substantiates the physical examination in establishing the authenticity of the claim, money is saved to the carrier and litigation is avoided by instituting treatment to hasten the patient's return to normal health. As an illustration, consider the following two methods of reporting a ease of alleged lead poisoning, hi a small town, one hundred miles from a metropolitan area, a workman develops an ill ness which he believes is the result of exposure to lead. I)r. A. examines him. does a blood smear for stippled cells, and reports his diagnosis accompanied by a bill for $7.50 or $10. In this same town. Dr. B. examines the same type of case. In addition to the blood smear In dues a complete blood count, collects by accepted methods a twentyfour-hour urine specimen, and in a proper container mails it to a testing laboratory in the city for evidence of normal or abnormal amounts of lead in the urine. Upon receiving the report, he forwards his diagnosis accompanied by a bill for blood count, blood smear, special examination of urine, postage, and his examination fee. His bill may be $2.5 or more. The second and more comprehensive report is the more valuable, for it saves further consultation or repetition of tests if litigation arises. Charges for needless laboratory study are soon recognized as padding the bill, but procedures carried out to establish the diagnosis, and accompanied by an explanation of their expediency, arc rarely questioned. Conclusions or Discussion.--All letters to the carrier pertaining to an occupational-disease claim should end with a discussion of the positive and negative findings. In it the physician evaluates the fac tors which have led him to his decision or diagnosis. In a medical report from one physician to another, the physical examination and laboratory reports are of predominant importance. But in a letter which is to be read and understood by a claimsman or the. court, the .final discussion receives the greatest attention. This discussion should be devoid of scientific terms, or if they must be used, they should be immediately explained in lay term'-. In the recital of findings in the physical examination or special investigation it may be impossible to avoid scientific nomenclature, Mich as Hoffman's sign, Babinski's sign, or that 0.08 mg. of lead was found in the urine. Tn the discus sion. these must be explained as to their significance in establishing or denying the patient's claim. Findings and tests have value to the layman only when they arc understood. That portion of the medical report devoted to discussion is similar to the rebuttal in a debate. In TIIH ITNCTIOX OK TIIK PHYSICIAN OO it the clinching statements to all that has been related previously are made. Il .should be well organized and endowed with reason, judgment, and truth. Estimation of Disability.--It i- incumbent on the industrial phy sician that he. stale in a ease that is proved to be non-compensable that there "exists no disability arising out of the occupation." If a case is acceptable he should estimate the length of temporary (Us ability and the possibility of permanent disability. Il should be appreciated that the employer or insurance carrier is required by law to set up a reserve for all eases in his files. This reserve is similar to that carried by life-insurance companies and signifies the stability of the company to meet the claims that might be made. The selfinsured or insurance carrier is subject to an examination of his books at any time and without notice by the state auditors. lie is dependent therefore upon the medical reports to set up this reserve. In addition to estimating the length of time for a temporary disability and the probability, or improbability, of permanent disability, the period of treatment should be predicted. The Attitude of the Industrial Physician.--In a day of radical ism, communism, and altered beliefs in all walks of life, an exhorta tion to hew to the line is not amiss. Medicine long ago emancipated itself from the, shackles of priestcraft. While various schools of thought and philosophy have come and gone, medicine has maintained its unbroken continuity of methods and ideals. Industrial medicine liasfreed itself of the unwarranted stigma of charlatanism. Never has its future been so bright, and no branch of the profession offers the young medico a more brilliant career. The development of new in dustrial hazards offers a problem for solution not paralleled in any other type of medical practice. The field is new. not crowded, and the call is urgent for the right type. But he who answers must be quali fied. It is not given to every physician to be a surgeon, or to every one to have research ability. Just so it should not be expected that everyone can practice industrial medicine successfully. Toward the Patient.--Among the important attributes is hi.attitude toward the patient. His demeanor toward the injured work man should be no different from that of the general practitioner toward his private patient. If anything, it should be more indul gent. solicitous, and sympathetic. While there are individual cases of malingering or falsification of claims, these are not frequent. When present, they must be denied. The majority of injured or ill work men are desirous of obtaining relief and being rehabilitated. Fre quently they misunderstand the relationship of their illness to their occupation, or they misunderstand the purpose of compensation. The ;>U (X Cl'I'ATIOXAL DISEASES examining physician. through kindliness and indulgent explanation of tile conditions., may win the patient'- gratitude and understand ing. so that he offers no problem in the equitable disposition of his ease. One outstanding fault existing' among industrial physicians is the tendency to consider the patient a "ease number" and hurry him through in order that the next one may lie quickly served. This re sults in errors in diagnosis and. as previously intimated, a too fre quent acceptance of a case as compensable when in reality it is not. Again let it be emphasized that the occupational-disease claim re quires laborious effort and is rarely ever to be hurried through as an emergency. blindly, in regard to the altitude toward the patient, it must be remembered that the intention of the law is that in doubtful eases the benefit of the doubt is to be given to the patient. The least one can do in these eases where uncertainty exists is to slate honestly that the diagnosis is not certain and a definite fixation of liability can not be made. In such instances the court or Industrial Accident Com mission will recognize the honesty of the report and will decide as the findings warrant. Toward the Employer or Insurance Carrier.--The attitude of the physician toward the employer or insurance carrier is one which, at the present time, causes grave concern. The philosophy of this era has tended to make compensation insurance, health insurance. It is not infrequent to find a physician who will say, "The poor devil has no money, and the insurance company can well afford to care for him even if the condition isn't due to his work." This is altruistic and commendable from a standpoint of humanitarianism. but it is not honest. It is unwittingly an insidious undermining of the basic structure of compensation. This thought is repeatedly stressed throughout this book. In the previous paragraph it was urged that the virtues of sympathy and understanding be extended to the pa tient, but this sympathy should not alter one's judgment. The in dustrial physician must constantly guard against favoritism. Once the condition is apparent as being of non-oecupational origin, the opinion must be so expressed. The idea for rigid adherence to the honest acceptance or denial of a ease is not made in order that the insurance companies may be favored, but that the purpose of the compensation act may be observed and preserved. The industrial physician should respect the right.- of the general practitioner or the family physician. If the ease is determined to be of communal origin, the patient should be referred to the family doctor. It can not be too -trongly emphasized that there be no competition belwc.-u the.-e two pha-cs of medicine. Tilt; FUNCTION OF THE PHYSICIAN 57 Toward Industrial Practice.--Finally, the physician should never consider an industrial practice a side issue in his professional duties. He should not feel aloof to this type of work. Most of the gross errors in this field come from the doctor who conducts a general practice and. for pecuniary reasons, indulges in a partial industrial practice. H he cannot gain the full vision of the purpose of industrial medicine that is so necessary to the successful pursuit of this type of practice, lie would better refrain from any participation in it. The first step toward success in any occupation is to become interested in it. This requires of the industrial physician not only a knowledge of the diseases common to industry, but in addition an understand ing of the law under which these diseases are compensated. The disciple of Ohauviu can find no harmonious niche in industrial medi cine. The requirements demand practical adherence to a simple, workable legal enactment evolved for the good of the workingman. ACCEPTABLE METHOD OF REPORTING AN OCCUPATIONAL DISEASE The following case history may serve as a mod.-l to those un familiar with an accepted method of reporting an alleged occupa tional disease. Gentlemen: At your request. Mr. Jack X------- reported to this clinic January 2, 1940. for an examination. He is fifty years old, and gave his address as Mojave, California. He had previously been examined May 17. 1939, and certain facts in the history and certain physical and labora tory findings of that time will be incorporated in this letter. The patient relates the following history: History.--``About one year ago I was exposed to fumes as a re sult of some dynamiting. They blasted in the mine at 2.45 in the afternoon but the men did not return to work until 7.00 a.m'. the following day. In the meantime they had used the blowers to draw out the fumes, but when we returned to work the gas was still pres ent. I and my partner were sent down to this particular level where they had been dynamiting, and while in there niv partner dropped dead. I don't remember exactly how I felt. but. it did not seem to bother me much just at that time for I went up to the surface un aided and made my report to the boss. I stayed away from work for about one week following this accident and then returned to work. After that, however. I was off a number of times because* I felt sick. ' In the past year I have lost a good deal of weight, have become very short of breath, have pains in both shoulders, and I cough a great deal. Xo: I don t spit up with this cough very much. As far as I know T have never had any lever, f seem to be getlunr worse. .58 OCC't'PATION'AL DISKASKS and I think it is due to that gas and also due to the dust. 1 think both of them have affected my lungs." Past Medical History.--Usual childhood diseases. Influenza. 1918. Denies any other serious illness since reaching adult life. Family History.--Father died at the age of eighty-six from gen eral senility. Mother died at the age of seventy; cause unknown. Three brothers living and well: two brothers dead, both because of accidents. Four sisters living and well; two sisters dead; cause unknown. Wife and four children, living and well. Occupational History.--The patient's first employment was with the Iron Blossom Mining Company in Utah at the age of eighteen, at which time he was engaged in laying a pipe line. lie also worked for the Chief Consolidated Mine in Utah, being engaged in mining silver and lead. lie was engaged in mining gold and copper for a short period with a company called, he thinks, the Keystone Mine. His mining experience in Utah was from 1907 to 1997. This was not all underground, for at times he was employed above the surface dumping cars, repairing tracks, mucking, caring for mules, etc. He came, to California in 1937 and began working for the Golden Queen Mine in August, 1937. With this company he has worked as a tram operator, as a mucker, and as a stopper and liner. He states that the operations for this company are conducted under conditions of wet mining. Physical Examination.--The patient is a poorly nourished adult male, whose present weight is 127 pounds. Two years ago his weight, he alleges, was 155. His temperature was 98.3 degrees. The pupils reacted normally lo light and accommodation. The eye grounds were negative. The ear canals and drums were normal. No nasal obstruction. No cervical adenopathy. Teeth.--Marked pyorrhea involving the gums of the incisors and bicuspids. Many teeth missing. Tonsils atrophied. Chest.--Inspection revealed emaciation of the intercostal spaces. The inspiratory excursion appeared normal anteriorly, but poste riorly there was a definite lag at the right base. In the upper loft chest anteriorly there was a high-pitched percussion note which was markedly in contrast to that of the opposite chest space. The breath sounds on the left showed a harsh type of breathing throughout. Over the left base, both anteriorly and posteriorly, could be heard a coarse friction rub. Over the right base posteriorly the breath sounds were absent. Heart rate of 88, regular: no murmurs heard. Blood pressure 130/8-1. No apparent enlargement of the heart. Tin- re-l of the physical examination was negative. OFTHK Kl'.VCnON THK 1'IIYSICIAN 5!) Laboratory. Blood Count.--Erythrocytes 4.,200,0()0: hemoglobin, .S4 per cent; leukocytes. 11.150: polymorphonuclears. per cent; lymphocytes. i'i per cent: mononuclears. :> per cent; l ransitionals, i ]>er cent. Vrinalyxi.s.--Specific gravity l.(W4; alkaline reaction: albumin- ancl sugar-negative. Microscopic: negative. v-Ray Examination.--May 18, 1!).`J9. An .r-ray film of the chest reveals a deviation of the trachea to the right in the lower third, and a large elongated area of increased density in the left upper, extending laterally from the mediastinal area. The edges are smoothly rounded. The area of increased density is !) cm. long and approxi mately 5 cm. wide, centrally. There is no apparent increase of den sity in the lulnm below this area. There are two areas of increased density on the right, one centrally located in the base. 4 by (i cm. The edges arc feathered. There is a small elongated area of increased penetrability centrally located. There is another area of increased penetrability, irregular in contour, extending laterally from the su perior aspect of the right hilum, with no apparent increase in hilum density. The diaphragm is tented, bilaterally, with sharp costo- phrenie angles. The heart is small. The right apex is clear. There is pleura! thickening in the left. There is an accentuation of linear markings on the left, particularly in the downward axis. .r-Hay pictures taken at this most recent examination, January `2. 1040. show the previously mentioned mass in the upper left lung lo be considerably enlarged but still well defined and well demar cated. Pleural adhesions not noted in the former films are now pres ent in both bases. The. mass in the right Lung and the one adjacent to the hilus are likewise enlarged. In neither the pictures taken in May, 10:5!). nor these most recent pictures is there any evidence of undulation or emphysema. Discussion.--It was learned that the explosive used was that of dynamite containing nitroglycerine lo approximately 4.0 per cent. The toxic effects of gases liberated by such explosives in confined spaces arc naturally greater than the effects of these same gases in the open air. The two chief gases resulting from such explosions are carbon mon oxide and nitrogen dioxide. These deserve momentary consideration. Xitroycn Dioxide.--Exposure to this type of fume may result in one of three types of reaction. There may be immediate death, or de layed reaction, or no effects whatever. It is not uncommon for a person who has been exposed lo nitrogen dioxide to notice no particular effect other than a mild upper respiratory irritation for an hour or two. or even longer. Following this interval of from an hour to ten or twelve hours, there may set in a violent reaction or death. At this time the patient coughs violently, has a sensation of suffocating, and has short ness of breath. The cough is often markedly productive and the spu- CO OCCUPATIONAL UISKASES turn may be blood--freaked. If the patient survives this episode, lie may recover within a day or two. or pneumonia may eomplieale the picture. There is rarely any permanent sequela from such an exposure. Carbon Monoxide.--Carbon monoxide gas is absorbed through the lungs into the blood and affects the hemoglobin of the red blood cells. It thus affects the ability of these cells to carry oxygen from the lungs to the tissues which demand it. Here again death may be instanta neous, or the patient may suffer severe headache, nausea and vomiting, shortness of breath, a feeling of constriction in the chest, and may lose consciousness. If the gassing has been severe, edema of the lungs may be present, and within a few hours or a day or two. pneumonia may develop. However, if the patient does not die. recovery is usually complete. If any permanent sequelae develop, they are usually of the nervous system and appear within a week or two following the acci dent. From this discussion of these two gases it is apparent that exposure to neither carbon monoxide nor nitrous dioxide would cause permanent pathological changes within the lung. While this patient had a definite exposure to a combination of noxious gases he. by his very own state ments. was only slightly affected by them, and his recovery from this minimal affection was complete. Silicosis.--In the patient's claim of ill health he believes that in addition to exposure to gases, dusts from mining have affected his lungs. This belief is easily understood, since most laymen have the idea that the dusts from any mining process permanently affect the lung tissue. However, in the occupational history it will be noted that he had very little exposure to silica dust, and that, at no time did the .r-ray pictures reveal the presence of silicosis in the lungs. Therefore, this cause of illness can be definitely ruled out. On the other hand, the .r-rav pictures, the history of existing ill health, and the symptoms and signs present indicate a malignancy of the lung tissue. The signs and symptoms resulting from this disease were first noted in the patient at or about the time of his exposure to the fumes from dynamite. Therefore, the onset and development of the cancer must have antedated the period of gas exposure by many months. Conclusion.--Investigation of this case would rule out any of the occupational factors and would indicate that the patient's disability is due to cancer and that this cancer is lion-occupational in origin. There exists. Iheretore. no temporary disability and no permanent disability arising out of the patient's occupation. Very truly yours. Comment on the Presentation of the Above Case.--The above ca.-e was chosen from the files of this clinic to illustrate the presentation of THE FIWCTIOX OF THE PHYSICIAN 01 facts, especially llio discussion as it was treated by the author. It should be noted that the claim of the patient, his history of exposure, his past ami mo.-l recent occupational history, the physical examina tion. and the laboratory findings are all detailed in a manner that the lay or the legal mind can readily understand. Then, the substances alleged to be the cause of this patient's illness are considered in the discussion. The known effects from exposure to these substances are set forth in contrast to the pathology actually found. From all of the pre sented facts a conclusion of non-occupalional origin of the man's dis ease is made. Such a presentation, with the weighing of all facts, better enables the court to arrive at an equitable decision. PART II (IASKS, SOLVENTS. AM) Fl'MKS A< uoss (ho pathway to normal health of the industrial worker lies the mysterious shadow of the Rases, solvents, and fumes. A criminal may he fingerprinted and photographed so that he is known to the police, hut he may easily escape recognition by the general public. Similarly, the danger from exposure to certain substances is known to the toxicologist but the profession as a whole has not as yet. learned to distinguish the characteristics of such conditions. The lethal effect of carbon monoxide or cyanide has been well publicized, but the insidious damage done by lesser known substances receives little consideration. General Effects.--It is important that we know which of these substances may be acutely fatal, which produce only temporary effects, and which may produce permanent damage. The very term "gas'' conjures up false impressions of the noxiousness of various gases in the minds of most people. In this respect a lesson can be drawn from the first World War. War gases were designed to kill or cripple. How effective were they? The Surgeon General's office reports 70,552 gas casualties with only 1221 deaths, or a rate of 1.73 per cent (Amer ican troops). What about the secpielae? In the immediate years fol lowing the cessation of fighting, asthma, hay fever, bronchitis, and especially tuberculosis were alleged as resulting from "being gassed." The Veterans' Bureau was deluged with claims. Investigation revealed the vast majority of these cases to be neuroses, malingering, or incor rect diagnosis. Colonel Adelno Gibson,1 of the Chemical Warfare Serv ice. in a study eighteen years later, states. "These gases produced rela tively little after effects." The consensus both here and abroad is that gassing left no large aftermath of tuberculosis, nor did it predispose to tuberculosis. Effect on the Blood.--Since the solvents and gases have an effect in many instances upon the blood cells, and since anemia of some type is invariably present, do these anemias become chronic and do these noxious substances produce leukemia? Overwhelming evidence points to complete recovery from secondary anemia with few excep tions. Regarding leukemia, only fragmentary evidence exists. Falconerreports a case of lymphatic leukemia four years after an acute ex posure to benzene. IIe .suggests that leukemia may have developed as an overcompensatory measure for previous destruction of leukopoielic (i:s ()4 <><((. I'ATIONAI, OISKASKS tissues. Alice Hamilton" refers to a re|)ort of Martland who noted a blood pieture characteristic of myelogenous leukemia in a patient with benzene poisoning. She states that she has seen two such eases herself. It would appear as sane reasoning to deny compensation on any of the anemias if they occur after an interim of non-exposure or if they occur many months or several years after an acute exposure. However, as noted in the chapter on benzol, the recent work of Hunter. Mal lory, and others indicates the possibility of latent effects from benzol poisoning. If they are alleged to have resulted from chronic exposure, the only criterion to accept would be the proof of the exposure. The case mistaken for idiopathic aplastic anemia, reported by Askey and re ferred to in the section on petroleum distillates, illustrates this point. Effect on the Liver.--In addition to the disturbed blood pieture. the acute or chronic assault to the body metabolism by toxic sub stances vitally affects the liver. Xot only does this organ metabolize the carbohydrates, fats, and proteins, maintain a normal blood-sugar level, carry on the diaminization of the amino acids, excrete bile and perform other duties, but it serves to detoxify toxic substances. These may be endogenous or exogenous. It is responsible for the handling of these by-products so that they are to be excreted from the body in a non-toxic or less toxic form. For instance, benzol may be conjugated by the liver with the formation of the organic sulfates, aromatic acids, and alcohol, which are converted into glyeuronates. Other noxious agents are detoxified by the liver and passetl off in the excreta in a manner as yet not fully understood. However, there is a limit to its capacity to handle enormous amounts or a tolerance to constant, re peated injury. Certain substances in particular appear to have destruc tive or damaging effects upon the liver. In industry the halogenated compounds such as carbon tetrachloride, the chlorinated naphthalenes, trinitrotoluene, tetracldorcthane. and also cadmium, manganese, ar sine, anti others arc known to affect this organ. It should be realized that the ability of the liver to detoxify these poisons varies with indi viduals and that some have marked susceptibility to these noxious substances. This variation in susceptibility is seen every day in the routine use of chloroform or avertin. Effect on the Kidney.--The kidney is often damaged when acute poisoning occurs from certain solvents, ft is not uncommon to see uremia in workmen overcome from carbon tetrachloride. Nature and Concentration of the Contaminant.--In predicting the outcome of a case of industrial poisoning, the nature and concentration of the contaminant, as well as the usual pathology produced, must be taken into consideration. While each of the gases or solvents has itown peculiar reaction, certain general facts may be accepted: (I) Any OASES. SOLVENTS. AND FCA1ES 65 substance introduced into the body in excess is harmful. (2) Few, if any, of the gases or solvents are stored in the body. Living in uncon taminated atmospheres for sixteen out of every twenty-four hours re sults in an interchange with oxygen that ordinarily maintains the blood free from saturation. (3) Short, severe exposures usually result in but short, temporary disability, (-t) Constant daily exposure to amounts slightly in excess of the recognized limit, may, and often does, result in chronic illness. (5) Odor as well as irritation to the eyes, nose, throat, or lungs should be ordinarily construed as an atmosphere that is unsafe for continuous exposure. There arc a few exceptions to these axioms; but if they are constantly kept in mind, better medicolegal decisions will result. A stumbling-block to honest diagnosis is the subterfuge that often exists in the manufacturing of these products. Trade names conceal the properties, and frequently the formula is not on the label. Re quested information from the manufacturers does not always meet with cooperation. Therefore, if the suspected offending ingredient can not be determined because of any one of these conditions, it behooves the physician to submit a sample to a testing laboratory. A further difficulty is the fecundity of carbon compounds. They appear to repro duce with ease. Individual Susceptibility.--In the final estimation of any case, consideration must be given to the individual's make-up. Obesity, al coholism, endocrine imbalance, and personal and home hygienic fac tors may play a part in susceptibility. In this present period of the practice of medicine, allergy is being greatly emphasized. Enthusiastic proponents account for any reaction not specific in its etiology upon this basis. To the author, this is a dangerous procedure. Until allergic reactions to gases or solvents are more definitely established, a physi cian should be wary of accepting a case on such a basis. Observation during the next few years should clarify the situation. Classification.-- A. Aliphatic solvents 1. Sources () Petroleum () Wood distillation (c) Fermentation (d) Fats (e) Synthesis 2. Toxic effect (a) Less than aromatic solvents (b) Hydrocarbon derivatives more toxic (i(i ocrri'.vnoN.u. diskasks B. Aromatic solvents 1. Sources () Distillation of coal tar (b) Distillation of pine lar (<) Fat (</) Synthesis 2. Toxic effect (a) Greater than ali|)hatie solvents (b) Hydrocarbon derivatives more toxic Symptoms Produced Dependent Upon.-- A. Nature of solvents 1. Toxic effect greater as their power of solution in fat- is greater 2. Toxic effect less as their solubility in water is greater .'J. Solvent mixtures B. Severity of exposure ('. Length of exposure D. Susceptibility of individual 1. Preexisting organic disease 2. Nervous instability :>. Alcohol K. Specific action of solvent 1. Action on fats and lipoids, particularly of the central nervous system 2. Action on specific organs (a) Methyl alcohol on the optic nerve (b) Chlorohydrocarbons on the liver (e) Carbon disulfide on central and peripheral nervous systems (</) Benzene on the blood-forming organs (c) Action of certain solvents on the skin, removing fats The following pages do not attempt a complete discussion of all the solvents. By and large the newer preparations present problems similar to the ones studied. Before this ink is dry. other substances will find their way into industrial use. but it can be expected that they will be evolved from the hydrocarbon compounds and that the reaction in general will be similar to the ones now understood. REFERENCES J. (liitMin. A.: **( liemical Warfare a< Developed (lurin'* flu* World War and IVihuhle Future Development." Bull. .V. I\ Arad. Med., series. Id: .`JD7-W1 iJuIy*, V.VM. i. Falconer. 1C. II.; "ItinUmoe of Lymphatic Leukemia Following Hen/ol i'ui'-onina." Am. J. M. Sr.. ISC: (Sept./. I<m. Hamilton. A.: Industrial Tajrirolagt/. Harper and Hrothers. Xew York. IWH. p. UW. CHAPTER IV BENZENE (Benzol) Tins coal-lnr derivative should be referred lo as benzol lo dis tinguish it from the petroleum distillate, benzine. Rarely coming in contact with pure benzol, the workman when exposed is subjected to a commercial variety containing also tuolcnc. xylene, olefins, paraffins, and carbon disulfide. Because of the long-recognized dangers of benzol, efforts and legislation have been in effect to suppress its use or lo have if properly labeled for easy recognition. Yet. like crime, it continuously reappears under a new guise. Frequently solvents will be labeled "nonhazardous" because they are non-inflammable, or non-explosive, yet they may contain a high percentage of benzol. The demand for this substance as a solvent of gums, resins, fats, rubber, and alkaloids, and as a fuel creates a field of wide exposure. The dangers of benzol decrease when men are informed of the ex posure and adopt proper precautions. Occupational Hazards.--Workers with airplane dope, makers of aniline dyes, artificial leather, and batteries (dry), bronzers. rubbercement mixers, compounders of rubber, degreasers. drycleaners. electroplaters. cnamelcrs. engravers, extractors of oil and fats, laequerers. lithographers and rotogravers. painters, rubber-tire builders, shellackers. varnishers. vtilcanizers. welders, and so on, are liable to this hazard. Pathology.--An extensive review of the literature reveals a general agreement that chronic benzol exposure produces a disturbed hema topoiesis. but there appears no uniformity of opinion regarding the pattern the blood picture assumes. There exists no definite laboratory basis for a diagnosis of tliis poisoning, but not because there has been a lack of clinical reports: for since Santesson's description in 18!)7 of nine cases of purpura haemorrhagica in girls working with benzol-rub ber cement, the literature has been replete with various clinical find ings in persons exposed to this solvent. Likewise much animal experi mentation has been engaged in. Such experimentation tends largely lo reduplicate the conditions of acute exposure rather than the chronic. What has been needed is a controlled investigation of a large series of eases in which the degree and length of exposure were known and which entailed a hematological, pathological, and postmortem study. Wry recently this has been done by several investigators, and there (is OirU'ATIOX.VI, 1MSBASKS is every rea-on to believe lli.it from this work, and a further study of tins type, a more accurate basis lor diagnosis will be derived. Rone-Marrotr Reaction.-- Before considering the hematological phase, sonic attention should be given to the actual pathology. The most marked lesions occur in the bone marrow. For years it has been assumed that a medullary aplasia occurred. Cases arc on record in which patients with a known exposure to benzol have been denied compensation because they demonstrated hyperplastic marrow, which was considered not typical of benzol poisoning. Some years ago Ham ilton,1 realizing the variations in the pathology of all blood diseases, predicted that further study woidd alter the viewpoint then held. Her prophecy has been substantiated in the work of Mallory-: Thompson. Richter, and EdsaiF; and Rhoades and Miller.1 Recently, Mallory and his co-workers have studied nineteen canes, fourteen of which were completely auLopsicd. and histological material was obtained from each of the nineteen. In the aulopsied cases, ma terial was obtained from several specimens of bone marrow, including the long and flat bones, as well as from the thoracic and abdominal viscera, liver, and spleen. None of these patients had been exposed for less than six months, four being exposed for less than a year: eight from one to four years; and seven from four to twelve, years. Exclud ing two cases of possible leukemia, the remaining number could be divided into two groups--six showing marrows less cellular than nor mal. and nine revealing hyperplasia. In comparing his findings with the history of each case, Mallory was of the opinion that intensity of exposure was not a determining factor in the bone-marrow reaction, hut that duration of exposure was. Cases of less than a year's ex posure showed a hypoplasia, whereas those with prolonged exposure evidenced a hyperplasia, indicating that the initial effects of benzene upon the bone marrow were to depress it but that the prolonged effect was to stimulate it. On the other hand, from these observations it might be reasoned that since persons react differently to benzene exposure, the occurrence of a hyperplasia enables the worker to continue for many years, where as the development of an aplasia results in rapid disability or fatality unless the patient is removed from the exposure. Effect o>i the Liver.--The chief findings in the liver were the prom inence of the Kupffer cells, which were loaded with hemosiderin, and central necrosis, possibly due to terminal infection rather than to the benzene assault. In Mallory's fourteen aulopsied eases, the spleen wa> rarely noted to be enlarged clinically, but was frequently found en larged at the autopsy table. Increased cellular activity was usually present. Well-defined foci of hematopoiesis were seen even in eases of BKXZEXE (BKXZ.OI.) (it) ininim;i 1 general changes. These became more marked and numerous with increasing severity of the k`>i<m. These investigators noted a f>;ciicral pa nil Id ism between bone-marrow and splenic hematopoietic' ac tivity. In spile of fi-ci|Uont purpura of the skin, mucous membranes, and serous surfaces, they noted no gross brain changes except in one ease showing several subarachnoid hemorrhages. Latent or Delayed Effects.--Since one of the primary functions of this book is to show the medieoleyal relationship of the disease, the latent or delayed effects of benzol poisoning deserve special considera tion. This phase of the disease concerns itself with the leukemias and certain neoplastic changes. There appears to be increasing evidence that this solvent may initiate a pathological alteration of the bone marrow which can slowly progress for months or years after exposure. The sequence of events in the anemias due to benzol is comparable in many ways to the changes which occur following exposure to .i-ra,vs or radium, as reported by Martland'' in 19:11. He observed in a benzol worker marrow typical of pernicious anemia, and in another the blood picture was characteristic of myeloid leukemia. Penati and Vigliani collected ten eases from the literature of leukemia in workers with verified histories of exposure to benzol. Mallory and his co-workers had two cases of leukemia in their series; Erf and Rhoades" had one in their group. It is not unreasonable to believe that many more such cases have not been reported. Regarding neoplastic changes. Mallory- states: Also suggestive to anyone who has studied even superficially cases of the hyperplastic type, are the evidences of what for a better term may be called a neoplastic tendency. The degree of anaplasia, the rapidity of growth as judged by the number of mitotic figures, the development of cells having no counterpart in normal tissue but com mon to a variety of malignant tumors are phenomena characteristic of neoplasia which the authors have never met heretofore in such a marked degree in non-neoplastie states. Complications in Establishment of Compensation.--These two pos sible sequelae just mentioned offer complications in the establishment of compensation. Hunter7 following a study of eighty-seven cases, staled that the most unexpected observation made in his series was that the first clinical symptoms and signs of chronic exposure may appear long after exposure has ceased. Assuming that these observations are accurate, one can visualize for the future tiro types of cases: One is the person with leukemia or neoplasm who has had adequate benzol exposure, but because of the interval of lime existing between exposure and illness, no claim is 70 OCCl'I'ATIOXAI. DISKASKS mailt1 or relationship recognized. The oilier is lhe worker with a blood dvserasia who. months or years after a varying degree of benzol ex posure, alleges his condition to be due to that solvent but whose de gree of exposure was probably insufficient, and a coincidence is very likely. Most claims for an occupational illness are made during the period of exposure or shortly afterward. This observation regarding the latent effects of benzol promises to confuse the administration of compen sation. Time and adequate evidence from abundant material will be necessary before acceptance or denial of this possibility can be made. Blood Picture. Leukopenia Xot Diaynoxtic.--It has been accepted that the earliest evidence of the effect of benzol exposure is leuko penia. Largely this has been the only lest relied upon, and in many plants a routine white-cell count constitutes the basis for permitting the workman to continue his work or removing him from the exposure. From the recent investigations such a practice is questionable and probably unreliable. It seems odd to this writer that although Ham ilton warned a number of years ago that dependence should not be placed upon leukopenia for diagnosis and cited a ease in which the white cells were 0800 but the red cells only 1,500,000, yet textbooks continue to cite leukopenia as the characteristic finding in benzol poisoning. Recent investigations by Hunter, at the Massachusetts General Hospital; Greenburg. Mayers, Goldwalcr. and Smith, of the New York Department of Labor; and Erf and Rhoades, of the Rockefeller Insti tute. indicate that leukopenia is not a prevalent isolated finding. In Hunter's series, leukopenia was not found without other abnormali ties in one of his eighty-nine cases. Greenburg'* and his co-workers found a deviation of the while count in only 14.5 per cent of T>2 work ers examined. Of his patients who were daily exposed to benzene vapors, 85 per cent showed a normal white-cell count. Furthermore, there appears no basis for assuming that leukopenia is produced in the presence of a severe anemia and purpura. In Hunter's series a switchboard operator developed a fatal ease of anemia, the cause of which was not evident at first. Tt later developed that she daily cleaned her board with a solvent containing 50 per cent benzene. At the time Hunter saw her. she had marked pallor, generalized ecchymosis. and questionable enlargement of the spleen. The rest of the physical examination was negative. Her blood count was: hemoglobin. -2*2 per cent; red blood cells. 1.800.000; white blood cells, 7400; poly nuclear cells. 48 per cent; lymphocytes, 40 per cent: mononuclears. 7 per cent; ba.sophilcs. 1 per cent; and unclassified cells. 4 per eeid. Biopsy of the bone marrow showed marked hypoplasia. HKXZKXK (I5KXZOI.) 71 Of Ifuiitt-r's eighty-nine cases, fifty-seven showed multiple devia tions from lIn- nonmd as noted in Talde >S. lie particularly stresses the fact that, omitting' a ease of leukemia, the leukocyte count was normal in two and the polynuclear percentage was normal in two. but in every single instance of fatal poisoning. the absolute number of polynuclear leukocytes was decreased. Hunter also [mints out that a decrease of the polynuclear percentage is a better index of early poi soning than either a leukopenia or an absolute polynuclear decrease. Tw.i.k S Mn.TiiM.i-: I)i:vi mows I'umi tiik .\oiimvi.> Kry I limey I os l.oiikocvU-s Nil. of Case'- _____ ___ I'olvmielear 'Cells l'orooiUas:e> Ali.solille I'olvmieleai' Cells (LVrcenUao' X -t- - X - - X - - > Inei-easC'd...................... ' 7 Normal.............................. -21 Decreased........................... -2!) Total.............................. .77 ' .'I ' .`I ! I ` 1 ` 0 I ;J | t ! I j -2 ' C .7 , 1.3 . 1 11 10 } 7 ; 1-2 U -2 S !) ! 1(1 ' -2 (I 1.3 ; i j (i J 1!) 0. 7; IS -2.3 ! U -2!) -2 -2(1 17 ' 17 2.`1 ` -20 (I t 1.3 Id* * Hunter, I'. J.:./. Iiiilnsl. llt/ij. unit Toxicol., It-, .`ill!) (Oct.I, 1!)!!!). Macrocytosis.--What appears to be a valuable contribution to the study of benzene not noted in other investigations is the finding of Grecnburg and his workers regarding the mean corpuscular volume, mean .corpuscular hemoglobin, and the mean corpuscular hemoglobin concentration. In their series of cases they found a distinct tendency towards maeroeytosis. The average cell size was greater than 94 cu. //. in 9.9 per cent of the control group, as compared to 40.7 per cent over !)4 cu. p among those exposed to benzene. The average size was less than 90 cu. p in 79.4 per cent of the control group, as compared to 90.1 per cent of the benzene-exposed group. They had fifty-five eases in one of the plants inspected which showed a white-cell count above .5000. Upon the basis that benzene causes leukopenia, these eases might have been classified as negative for benzene poisoning. Vet 41.K per cent of them were found to have red corpuscles larger than 04 cu. p. In only three of the sixteen eases in this plant, with less than 5000 leukocytes, were the erythrocytes normal in number. This indi cated to them that with benzene absorption the mean corpuscular volume is definitely increased in a large proportion of eases. Regarding the mean corpuscular hemoglobin, they estimated the hemoglobin concentration by the constant method of Wintrobe rather OCCCl'ATIO.XAI. IHSKASKS Ilian by the usual method calculated in terms of color index. They found that the erythrocytes of benzene workers are likely to contain more than normal amounts of hemoglobin. Calculation of the mean corpuscular hemoglobin concentration shows that, in addition to the greater content of hemoglobin, there is also an increased concentration. Significant Hematologic Abnormalities.--The incidence of signifi cant blood abnormalities found in the series studied by (irecnliurg and his co-workers is somewhat differently classified as revealed in Table f). Tahu-: 9- -I\cii)K\('i-: op Seomkkwvt Blood Aiivohmai.itiics i\ Mi:v Kveosun to Hkszi-.vk Tc.nI Criteria of Alinoniiiilily 1 Total Texl.N Made ! Abnormal So. ! Pcrcfnfdf/r Krvthrocvles, ,. I Less than 4..> million i 1.59 j 7<i | 47, K Mean corp. vol.. .. i More than 94 cu. ju Platelets........... 5 l,c.vi Umn ioo.owi 103 1 +K bi.d 107 i 3.5 ;.? Hemoglobin. , n ,,t Less than L`L0 #m. per 100 re. 1 '>3.5 i 39 ; 1.5.3 Leukocytes., ,* Less than .>,000 |. .'i.`l`> ! 't +H i * (rrcenhiirg., L., Mavers, M. K., (ioldwater, L., and Smith, A. It.: ./. hnhi.il. Ih/ii. and Toxicol., dl: +13 (Get.), 1939. Erf and Rhoades investigated benzene poisoning in six rotogravure printers, one chemist, oue beauty-parlor worker and one rubber-ce ment worker. Concerning the leukocyte.v, they noted that early, when the bone marrow was hyperplastic, the presence of myelocytes and irritated leukocytes was noted, but later, when the marrow became aplastic, there was a decrease in the white cells. Til fifty-two patients tested for bleeding time by Erf and Rhoades, they noted an excessively long bleeding time in only two eases and moderately prolonged bleeding time in only three, although the blood platelets were below 100.000 in thirty-five eases and below 50,(100 in twelve others. 'I'his group noted no significance in the sedimentation Hite of men exposed to benzene. Erf and Rhoades made a noteworthy observation when they studied the free hydrochloric acid conical of the stomach of their nine patients and found it to be present in every one. This finding should have some value in flic differential diagnosis of pernicious anemia from benzol poisoning. Urine-Sulfate Ratio.--Tt is held by some that a valuable lest for the evidence of benzene absorption is to determine the urine--nlfatr ratio. This is chine by dividing the amount of inorganic sulfates present in the urine by the total sulfates. The specimen should be obtained HENZKXK (BKN/.OI.) it'liilc' the worker is e.vpoxeJ and not aftc-r lie has been absent for m'v(t;iI days. 'Flius. if the test is to be of value, it must lie done only on those actively engaged: it lias no [dace in the diagnosis of those once removed from the exposure. One senses from the opinions in various reports that the present status of this test is that it has a confirmatory value but cannot be relied upon specifically as a diagnostic one. Summary.--A review of the investigations previously mentioned, as well as the work of others not cited in these paragraphs, leads to this conclusion: that chronic benzol exposure brings about a varied clinical and hematological picture, and that anemia, leukopenia, throm bocytopenia. retieulocytosis. high color index, increased fragility of erythrocytes, ttrobilinuria. and prolonged coagulation lime may or may not be present. The bone marrow may be normal, aplastic, hyper plastic. or leukemic. The variation of the findings is due probably to the degree of exposure, length of exposure, and individual suscepti bility. In spite of the varied picture two facts remain evident: (l) that anemia invariably results from exposure and (2) that leukopenia is not a common early finding. Furthermore, if leukopenia is present, other abnormalities of the blood picture are also seen. Such observa tions should discourage the confinement of diagnosis to a white-cell count alone. DIAGNOSIS Signs and Symptoms.--In acute benzol poisoning, the symptoms are due to an irritant and possible destructive effect upon the central nervous system, whereas chronic exposure affects the hematopoietic system. Fatigue, lethargy, and dryness of the mucosa are the most common findings. These are accompanied eventually by some or all of the following: loss of weight, headache, anorexia, dizziness, insomnia. cpistaxis, bleeding gums, nervousness, palpitation, and intestinal colie. Basis for Diagnosis. Differential Diagnosis.--Obviously benzol poisoning must be differentiated from the various anemias, chiefly pernicious anemia. This is extremely difficult at limes when it is real ized that not only does benzol poisoning assume frequently atypical forms, but likewise do the various blood dyscrasias. One cannot place definite reliance upon the high color index of pernicious anemia, for if will occur in benzol poisoning. Until recently it was not known whether achylia was present in benzol poisoning, but the work of Frf and Rhoades would indicate that there is no achylia in this chemical poisoning. j 4 OCC'l'I'ATIO.VAI. IMSKASES The c-l;iblisliMienl of a diagnosis depends upon lhe following points: I. History of Exposure. () Concentration. (/;) Duration.--A short. abrupt. severe concentration is apt to produce immediate in toxication from which the patient ordinarily recovers quickly. Pro longed exposure to insidious amounts has the more damaging effect, but the actual exposure should be proved. i. Analysis of the Atmosphere.--This must be done under the exact conditions of the alleged exposure. ). Analysis of the Exact Solvent and the Conditions of Concentra tion in- Which It ll',v Allegedly Used.--It has been previously inti mated that solvents change their benzene content from lime to lime as well as their trade names. In an effort to substantiate or deny exposure, the analysis for the benzene content should be of the sub stance in use at the time of the alleged exposure, not at the time of the trial. Many employers assume that the chemical content of a solvent they buy is standardized and constant, whereas in reality it frequently is not. 4. .1 Complete Blood Count.--A white blood count alone is in sufficient proof for or against the diagnosis of this poisoning. Diminu tion of the red- cells and increase in their size are better criteria than dependence upon the reduction of the leukocytes, particularly early in the disease. Regarding the change in the size of the red blood cells, one must be sure to rule out pernicious anemia, since they show this phenomenon in that condition as well as in certain other toxic poison ings, as has lately been realized in the blood picture of those exposed to methyl cellulose in the "fused collar" industry. The mean corpuscle volume and the concentrated hemoglobin content are additional con firmatory findings. 5- Signs and Symptoms.--The average case should show the vari ations of these as enumerated. The atypical case will show a clinical picture with no significant laboratory findings, nor will it reveal an abnormal and indicative blood picture without signs or symptoms. Here again the history of exposure is all-important. fi. Biopsy.--Biopsy may be resorted to in medicolegal contro versy. It must be evaluated with the blood study and the history of exposure. This may likewise be said of autopsy findings. MEDICOLEGAL ASPECTS Temporary Disability.--Most patients lend to recover upon re moval from exposure. No set lime can be given, for this depends upon the recuperative powers of the patient and the severity of his ex- HEX ZION E (BENZOL) to l'lic majority of patients recover after Irom a lew mon111> Iti a year. Permanent Disability.--If l lie it has liecn unresolved hemorrhage into the brain or involvement of the nervous system, the disability may be total or partial and should be so rated. 'Phis should not be done for at least two years after the initiation of the disability. Rarely does there occur a complete permanent disability, but occasionally there is a partially permanent one. The possibility of delayed or latent disability or fatality has already been discussed. Illustrative Cases.--The first three of the following eases are taken from an investigation of chronic benzene poisoning by the labor de partment of Xcw York, the Massachusetts General Hospital, and the Rockefeller Institute for Medical Research. Case I.--Fatal, exposed for twelve years. Blood picture suggesting aleukemic leukemia: marrow hyperplastic: no necropsy. Male, aged forty-eight, first seen November I. 1900. Had worked as a matcher of colors for twelve years in a factory producing artificial leather. Doing the same work during the whole period, he had been heavily exposed to benzene fumes. He was referred for an opinion because a recent blood examination had shown an anemia, a white-cell count of 000(1 per cu. mm.. 51 per cent of polynuclear cells, and a moderate number of myelocytes and normoblasts. Three years previously, how ever. his blood had been reported as normal. Present Illness.--The patient had tired easily for the past year. He complained of numbness and cramps in the legs on getting out of bed in the morning. There had been dyspnea on exertion for the past year, but his symptoms were not getting worse. For some years he had occasionally noticed blood on his toothbrush. There was no his tory of bruises, petechiac. or blood loss. The past history was noncontributory. Physical Examination.--Patient well developed and nourished but definitely pale. Pupils slightly irregular. There was slight edema of both shins. The knee jerks were active, the vibration sense well fell. The. rest of the examination was entirely negative. Laboratory Examination.--Urine, normal. Hemoglobin. 55 per cent: red blood cells. 4.420.000 per cu. mm.; while blood cells. 450(1 per cu. mm.: polynuclears, l.`> per cent: lymphocytes. -24 per cent: mononuclears. -2 per cent; cosinophiies. 5 per cent: basophiles. 1 pol ecat: normoblasts, (i per cent: young and late myelocytes. -20 per cent: young polynuclears. 10 per cent; unclassified cells. 0 per cent: eosino philic myelocytes. 1 per cent. There was marked anisoeylosis and poikilocyto-is. many microcytes, macrocyte.-., and tailed forms, occa sional stippliuu. and a rare myeloblast; platelets, normal. Biccdim; 70 OCcri'ATIOXAL I) IS MASKS time, thin.' and one-quarter minutes: tourniquet test, negative: icteric index-. 8; cell volume, ? /<,. Coarse.--A week after this examination the patient entered the hospital for study and. at litis lime, the blood was essentially the same except that the white count was 1,`i.oOO per cu. mm. It was thought that the patient had early myelogenous leukemia. .r-Rays of the pelvis and lumbar spine and a blood Ifinlon test were negative. A bonemarrow biopsy was performed. A diagnosis of benzene poisoning with hyperplastic marrow was made. The patient was sent home to recu perate. A short time later, however, he developed influenza and an abscess of the car. lie entered his local hospital, and anemia became marked (red blood cells. 1.900.000 per cu. mm. with many normo blasts in the blood smear). He became rapidly worse and died on January 14. 1980. six weeks after having been first seen. Xo autopsy was performed.7 In this ease there is no question of a history of exposure or of the probable relationship between benzene and the eventual anemia. The important suggestion to be pondered is that benzene has been the provocative agent in the production of a leukemia. The three eases in this series, added to the ten already reported in the literature, are sufficient to cause a reconsideration of the toxic effects of benzene. Case II.--W. D. S.. fifty-four. male, a factory worker, entered the hospital complaining of bleeding from the gums. For seven years the patient had operated a spreading-machine in an artificial-leather fac tory. in the process of which he was constantly exposed to benzene fumes. About a year before entry he first noted occasional bleeding from the gums and a slightly productive cough. Present Illness.--For about two months there was slight swelling of the ankles and puffiness of the eyelids, associated with polyuria and polydipsia. For six weeks there was constant bloody oozing from the gums. Physical Examination.--Examination on admission showed pallor, marked hemorrhagic oozing from the gums, and numerous purpuric spots on the skin. The tip of the spleen was barely palpable, and the liver edge extended (i cm. beneath the costal margin. Laboratory Examination.--Urine was normal. Red blood count was 1.900.0(H). with 4;5 per cent hemoglobin. The white cells num bered 800 with 10 per cent polymorphonuelears. .5 per cent lympho cytes. 8 per cent monocytes. 4 per cent eosinophilcs. and 14 per cent basophiles. There was marked stippling of red cells, occasional nucle ated red cells, and rare myeloblasts. Platelets were markedly reduced in numbers. Reticulocyte', were per cent. Bleeding lime was over twenty minutes, and there was no clot retraction in forty-eight hour-. The icterus index was 8 units. 9 BENZENE (BENZOL) 7? The patient was given five transfusions without improvement. He died on the twenty-eighth hospital day. Xecropsy. (a) Skin.--leterie. multiple petechial hemorrhages. Edema of both lower extremities, (b) Lnnt/s.--Pulmonary edema and hemorrhagic bronchopneumonia with red blood cells and fibrin but relatively few polymorphonuclears. (c) IJcer.--`2095 gm. Kupffer cells markedly prominent and filled with hemosiderin. Islets, normal. Within the sinusoids are scattered immature blood cells and moderate numbers of clasmalocytcs. (d) Spleen.--480 gin. Corpuscles in normal numbers but compressed by surrounding collars consisting of dense aggregations of indeterminate stem cells accompanied by a few normoblasts and phagocytes. Splenic cords are widened and contain hemorrhagic extravasation and hemosiderin-laden phagocytes. Lining cells of sinusoids are prominent. Many of the sinusoids are filled with stem cells, crythroblasts. and occasional normoblasts. There are also some clasmalocytcs with both red and white cells ingested. Archi tecture is generally preserved save for a few foci in which masses of stem cells obscure the structure, {e) Bone Marrow.--Markedly in creased cellularity in both rib and femoral marrow. No fat remains, and there is no evidence of fibrosis. Architecture is obliterated by large clusters of stem cells, erythroblasts, and normoblasts, although mod erate numbers of myelocytes and polymorphonuclears may also be observed. Megakaryocytes are rare, mitotic figures abundant, and occasional giant cells with monstrous nuclei may be seen. Phagocytes with hemosiderin arc abundant.- It is rare that autopsy is performed in alleged benzene poisoning, and, therefore, this case has that significance. Particular attention is called to the findings in the bone marrow of abundant mitotic figures and the occasional giant cells with monstrous nuclei, which serve to support Mallory's contention of neoplastic tendencies in certain in stances of benzol poisoning. Case III.--Male, aged forty-seven. Admitted May 19, 1998, com plaining of weakness and ecehymosis. The patient had worked for a rotogravure printing company for three years, and only during the month preceding admission had he noticed increasing weakness and fatigability. He had used solvents containing benzene and was con stantly exposed to the fumes. Ten days before admission, subcu taneous ccchymoses appeared on the extremities. Physical Examination.--The patient was a well-developed and well-nourished male, showing no evidence of recent ccchymoses or purpura. The oral mucous membranes appeared normal, and the liver extended two fingerbreadths below the right costal margin. There were no other pertinent findings. 78 (K ( r I'AT I () X A1. 1)1 SKASKS Laboratory Examination.--Krylhroeytcs. -2,70(),()0(>: hemoglobin. 7-2 per cent; leukocytes. -2450: platelet'. .>0.1)00; reticulocytes. 0.-2 per cent. Differential count: polymorphonuelcars. 70 per cent: cosinophiles. -2 ]>er cent: lymphocytes. -20 per cent: monocytes. S per cent. Fragility, norinal. reterus index. <S. Fasting gastric contents contained free hydrochloric acid. Urea clearance 1:55 1-20 per cent of normal. Urobilinogen excretion: fecal, 410 mg. and :5.`50 mg. excreted daily dur ing two periods: urine. .`5.8 mg. and 1.1 mg. daily for Uvo periods. A sternal bone-marrow puncture was done, and the marrow was found to be normal. Supravital differential count of the living marrow cells: neutrophilic myelocytes. -2-2 per cent: myeloblasts. -2 per cent: polymorphonuelcars, `21 per cent: normoblasts, 4.5 per cent: erythroblasts. 10 per cent. Wasscrmann test, negative. ('onr.se.--Uneventful. The patient received liver extract and thi amine intramuscularly for three weeks in the hospital and three months in the Out-Patient Department. Laboratory Examination (four mouths after admission).--Frylhroc.vtcs, :>.8:50.()00; hemoglobin. 9.5 per cent: leukocytes, 7700: plate lets. -2.50.000: reticulocytes. 4.8 per cent. Differential count: polymorphonuclears, ,5-2 per cent: eosinophiles. 4 per cent: lymphocytes, :J8 per cent; and monocytes. 0 per cent. Serum bilirubin, 0.85 mg. per cent. Urobilinogen excretion: fecal. 191 mg. and 19`2 mg. excreted daily during two periods; urine. 0.8 mg. and ().(> mg. daily during two periods. The patient recovered fully and was followed over a period of one year with no recurrence of symptoms.1* This ease illustrates the complete manner of investigation from the laboratory standpoint, the treatment, and the eventual recovery. Case IV.--After working in a benzene tank for about twenty min utes a workman joined his fellow workers at lunch, complaining of dizziness and severe headache. One hour after returning to his work, he was found unconscious. lie died two hours after being removed. This tank had but recently contained a composition of 80 per cent benzene and 15 per cent toluene. The patient's history of previous good health was established. The autopsy showed scattered hemor rhages in the brain, pleura, and intestinal mucosa. The blood was very dark and fluid. The death was adjudged compensable. Case V.--A migrant to California had been engaged for two weeks in an airplane plant spraying a solution containing :>() per cent ben zene. One morning he suddenly fell to the floor in convulsive seizures, frothed at the mouth, and was taken to a nearby physician. The pa tient denied ever having had similar attacks. The physician diagnosed the ease as epilepsy and stated that probably the exposure to benzene BENZENE (BENZOL) 7!) had provoked the attack. The workman then filed for compensation for a disease resulting from his employment. It was only after some weeks of difficult investigation that the workman's former family physician in Texas was contacted. He pro vided proof that this man had been subject to epilepsy for years. The case illustrates: (1) the idle remark of a physician without due con sideration for the import of his statement, and (2) the fact that epi lepsy is common to all walks of life and is not the result of an occu pation. While a single attack may be precipitated by a complementary factor arising out of a physical or chemical exposure, it would be absurd to assume that such exposure initiated the syndrome. If, in this case, the occupational exposure brought about the attack, the temporary disability was about one hour. Case VI.--A twenty-eight-year-old Xegro had been employed for three years in a paint and lacquer plant where there existed a mod erate exposure to both lead and benzene. He presented symptoms of nausea and vomiting, abdominal cramps, pains in the back of the legs, and weakness. The community physician diagnosed his condition as due to benzene, and he was on compensation for eight weeks. Subse quent examination ruled out any evidence of abnormal lead in the ex creta; the blood examination showed 3,100,000 red blood cells, 55 per cent hemoglobin, 9200 white blood cells (with 82 per cent polynuclears). The Wassermann test was negative. In view of the then current opinion that leukopenia had to be present to substantiate a diagnosis of benzene poisoning, he had been subjected, fortunately, to other tests. Examination of a slide after it had been sealed for twenty-four hours revealed sickle cells. Only persistent effort revealed the actual cause of this patient's condition. The patient was denied further disability compensation. Many more cases could be cited where physicians have accepted cases as compensable due to benzene poisoning simply upon the pa tient's history of exposure, without laboratory investigation. Dyspnea in a fifty-five-year-old electroplater who actually had cardiac failure, or chlorosis in a young girl, is an instance of this. TREATMENT Prophylaxis. Frequent Physical and Laboratory Examinations.-- Constant vigilance by blood examinations and air analysis should be the established order wherever benzene constitutes a hazard. The routine white-cell count commonly resorted to should be supplanted by a complete blood count, for reasons emphasized in the preceding paragraphs. Only those in fine physical condition should be placed OC(Vl'.VrlOXAL D1SKA.SKS BENZENE (BENZOL) 81 where a benzene hazard may arise, and frequently physical, as well as laboratory, examinations are indicated. Men should be rotated, and upon perceiving the least variation from the normal, the worker should be removed from his exposure. Likewise, workers should be instructed to report for examination upon noting bleeding from the nose or gums or other mucous mem branes, or if unaccountable subcutaneous hemorrhages or discolora tions are noted. Safety engineers have done an excellent job of pre venting accidents by educating the employees regarding the dangers which exist in certain types of employment. It is high time for a similar educational campaign to be conducted in the various occu pational diseases. Many serious cases of poisoning from benzene and other noxious agents could be prevented if the employees themselves knew, or were informed, of certain early signs or symptoms. To find a case of far-advanced anemia in one who had for sonic time noted bleeding and certain symptoms of general malaise, denotes not igno rance on his or her part, but a failure of education or instruction. Proper Ventilation.--Obviously, proper ventilation is extremely important. Since benzene fumes tend to form pockets and are very diffusible and heavier than air, the ventilation should be general and from the floor by means of suction. Dermatitis.--Dermatitis is prevented by the rubbing into the skin of olive oil or other animal or vegetable fat, or by the use of a wax ointment prior to handling the substance. Rubber gloves may be used but do not ordinarily withstand the action of benzene, so synthetic rubber, which resists the solvent action much better, should be sub stituted. Anemia. Blood Transfusions.--In those workers who have de veloped anemias of varying degrees together with other symptoms of benzene poisoning, the most valuable form of therapy is blood trans fusions repeated frequently if necessary. In attempting to carry out this type of therapy, Gray. Greenfield. Fig. 1.--Bone Marrow (Vertebral): There is pronounced hypoplasia with re placement of, marrow substance by fat. Most of Die sinusoids are collapsed. Those which remain patent contain only small clusters of hematopoietic cells, the predomi nant elements being non-uucleated erythrocytes. (COO X) (Mallory: Iniiu.it. Hyg. and Toxicol., St: (Oct.] 1939.) Fig. 2.--Bone Marrow (Vertebral): A higher power view from the same section as Figure l. A. group of sinusoids distended with erythrocytes is seen. Comparatively few nucleated elements are evident, and these are almost all normoblasts, (500 X) (Mallory: J. Indust. Ilyg. and Toxicol., St: [Oct.], 1939.) Fig. 3.--Bone Marrow (Vertebral): The sinusoids are all widely dilated and tilled with hematopoietic elements with normoblasts, erythroblasts, and stem cells predomi nating. Only a few giant cells are seen. The marrow fat has completely disappeared. (300 X) (Mallory: J. Indusf. Ilyg. and Toxicol., It: fOet-1. 1939.) 0 OCCCPATIO.VAI. IHSKASES UKXZKNK ( ISKN/.OI.) S.`> ami Lederer' weir confronted with ;i com- of aulohcimigglulimilioii. although this patient had had tliree previous transfusions. They point out that autohoniaggliitiiialion is the inleraelioa of the agglutinin of tile seruiu will) the agglutinogen of the red blood eell and ean ocelli' only at a tempera lure below that of the body. They eliminated the difficulty by heating the patient's serum and cells to body tempera ture. Liver Extract amt Iran.--Since the anemia is frequently of the macrocytic hyperehromie type, liver extract intramuscularly in large dosages (1.5 to tit) unit's daily for four days, then every two or three (lays), or venlrieulin orally (15 to till gin. daily), sometimes both, should be tried. If the anemia appears to be of a secondary type, the use of iron in the form of ferrous sulfate (5 grains: O.IM gm.). two or three times a day. is advised. Leukopenia indicates the trial of poll(nucleotides intramuscularly (10 to 40 ee. daily), although marked im provement under this form of therapy has not usually been demon strated in these cases. Roentgen Rays.--For further stimulation of the blood-forming organs, the use of roentgen therapy to the long bones and spleen and bone-marrow extracts has been suggested. Others have used ascorbic acid in moderately large doses with reported success. Diet.--The diet should contain nourishing food with an excess of animal fats and a high calcium content. Calcium preparations may be given orally as supplements to the diet. Intravenous infusions of from 1000 to 0000 cc. daily of from .5 to 10 per cent dextrose in saline are of value. Good results from the use of ascorbic acid in daily doses of from 200 to 400 mg. intravenously and orally, until a normal vi tamin C level is attained, have been claimed.1" Mouth, Nose, Throat, and Skin Hygiene.--Because these patients frequently die of a terminal infection, particular attention should be paid to mouth, nose, throat, and skin hygiene. Fig. -t.--Hone Marion' (Vertebral): Fat is no lonyer present. Then* is early in- liltration with thin strands of fibrous tissue. The sinusoids are all dilated hut some are filled with normoblasts and rent lewd stem eells and others only will] non-mielealed erythrocytes. The large dark-staining elements are hemosiderin-laden phagocytes. 0100 X) (Mallory: J. lmln.il. Ili/ij. and Toxicol., lOel.K 1!)3D.) Fijf. .).--Hone Marrow (I'ertebral): The marrow dious dense whorl-like lihrosis with no lat and only a few persistent distorted sinusoids. These are filled with small islands of regenerative hematopoiesis amona` which normoblasts predominate, etuil '/ {Arch. Hath., 3->->. I'l.'tS.j 1`ijr. (i.--Hone Marwic (Tcinorali: Fat is completely replaced by cellular marrow. 'the wide range of polyeellularily ami the resemblance to Hodgkin's sarcoma are ap parent. '1 here is an admixture of stem cells, phagocytes, normoblasts, and mullinucleated jdant cells. Only a rare <iranuloeyle can be delected. A background of thin fibrous stroma may be observed. (7.70 Xt iMallorr: .1. Indn.it. ft iff/, and Toxicol., 1 Oft. |. 11)3!)./ S4 occupational mskasks Fig. 7.--Spleen: Pulp lymphocytes have almosl completely disappeared. Billroth's cords exhibit marked hemorrhagic extravasation and contain only a few scattered lymphoid elements. Sinusoids are small, but littoral cells protrude prominently into their lumens. (500 XI (Mallory. ./. /adust. IImi. and Toxicol., II: (Oct.1. 1030.) Fig. 8.--Spleen: A nmlliuuclealed giant cell is shown almost completely filling a splenic sinusoid. Stem cells and normoblasts may be seen in immediate propinquity. UOOO X) (.Arch. Path.. 15: 3-H. 1038.) Fig. 0.--Spleen: A section demonstrating the resemblance to Hodgkin's disease. There is dense fibrosis and apparenl loss of architecture although a few distorted sinusoids filled with stem cells may he seen. Two arterioles are evident ils the sole remnants of sclerosed malpighinn corpuscles. In the scarred stroma are a variety of cells among which mullinuolealed giant cells are particularly noteworthy. The small dark-staining round cells which simulate lymphocytes at this magnification are. actually normoblasts. 1300 X) (Mallory: ./. Imlu.tt. Ihjij. ami Toxical.. It: |()cl.|. 1!I3!)./ HKX7.KXK (UKXZOI.) So mmm K+-.: ' -1 $$ `J1^ &4&..-SMS *: ' x . iU vfv**^ ,, jB^ge^iS ii;. II ..** -- v; $ *? v > r j \**rvC. i Fiji. 10.--Lymph Xodc: Lymphoid cords arc shrunken and irregular in appear ance. The total lymphoeylic conleid is diminished. Sinuses are widely dilated and filled with interlacing strands of spindle-shaped phagocytes. (*>.)() X) (Mallorv: ./. Indu.sf. Ihjif. and Toxicol,, JJ: i()ct.|. Fiji. ii.--Lymph Xode: A section through the rorles: shows apparent obliteration of the subeupsular sinus and invasion of the capsule. Radial sinuses are compressed and distorted as the result of hyperplasia of the pulp. The latter contains, in addition to densely packed Iymphocyle>. large numbers of ;dl varieties of hematopoietic cells. Mullimiclealed giant. cells may be readily identified. (JUKI X/ (Reproduced through the courtesy of I)r. Ellis Kellerl. Ellis Hospital Laboratory. Schenectady, New ^ork.) so OCCTPATIOXAL D1SKASES Pig. 1*2.--t.irer: The illustration represents* Hie edge of (lie 4 cm. tumor nodule noted in the gross. Broad sheets of leukemic cells may be seen invading and destroy ing liver parenchyma. (I.>0 Y.) (Mallory: J. Imluxt. Hifg. am! Toxicalit: lOel.5. I`K1!U Fig. lit.--hirer: A higher power view of the section shown in Pig. 1*2. Invasion beyond the coniines of the liver sinusoids by leukemic cells may be observed. These cells are almost all myelocytes although identification is not possible in the illustra tion. Among them, however, small numbers of normoblasts may be identified. Paren chymatous cords show obvious disruption. (000 X) (Mallory: J. Indusi. fft/y. and Toxicol.. Jl: [Oct.j. Fig. It. : Fig. 1.5. 1 Fig. It.--lion? Marrow (Femoral): Simisoidnl margins :uv obscured. There is marked eellularilv with ervllirogenie elemenl.s preilimiinaling. Normoblasls and crvtliroblasls an* readily identified. There are abo moderate numbers of phagocytes and megakaryocyte-like cells, one of which contains a mitotic figure. (300 X ) (Mallory: J. Itiditxl. Ilyrj. tiud Toxicol.t il; lOcl.J. I939j f Pig. !>.--Spleen: Architecture K partially obscured by a marked accumulation of | sic*in cells and normoblasls. These appear to lie (for the most part) within barely j visible distorted sinusoids. A large multipolar mitotic figure is evident. (000 X) (Mallory: J. Intlusi. 11 yg. and Tcxicnf.. IT. [Oct.I. 1039.) I'ijs. 10. Kip. 17. Fig. 10.--Spleen: Large numbers of stem cells fill the simmtiids ami appear also in the intervening pulp. The cells are arranged in irregular clusters. Nuclear vesieulurity ami relative lack of differentiation are apparent. (1000 XJ (Mallory: J. Iuduxt. U>nj. and TorieoL. !l: <0e|.}. 1030.; Kip. 17.--Spleen: A .selerolie malpighian corpuscle is demonstrated. Only the central arteriole is recognizable, the lymphoid substance of both corpuscle and pau-nchynni having been replaced by fibrous (issue. In the region of the arteriole, the collagen is concentrically arranged, and a few polymorphonuclear* and residual lympho cytes are seen. KUewherc there are scattered mnmoblasts. stem cells, ehi'-matoeyles ami mullinucleated giant cells. (100 X) (Mallory: J. Indu.st. Ihjg. and Tax'coL, l\; lOet.j. 1039.; Fig. 18. 1 i ' Fig. 19. Fig. IS.--Liver: The sinusoids ermtaiu elu-lers of hematopoietic colls. A group of stem cells and a multinucleated cell indistinguishable from a megakaryocyte are seen. (7.50 X) (Mallory: J. Indusl. Ilyg. and Toxicol., II: iOcl.]. 1939, Williams and Wilkins Co.) Fig. 19.--Lymph S'ode: A higher power view from the section shown in Fig. II. Large numbers of multinucleated giant cells may be seen in the midst of a relatively fibrous stroma. Some of these cells are indistinguishable from megakaryocytes. One ' contains a large mitotic figure. (.500 X) (Reproduced through the courtesy of I)r. : Ellis Kellert, Ellis Hospital Laboratory. Schenectady, Xcw York.)I I i BENZENE (BENZOL) S? REFERENCES I. Hamilton. A.: Industrial Toxicahujy, Harper and Brothers. New York. 1931. >. Mallon. T. B.. (v:tll. K. A., and Bricklcy. W. "Chronic Exposure to Bcn/cnc (Benzol t HI. The Pathologic ResulK" J Indus!. ////</. and ToricuL. II: 3.m-377 (OeU. 1039. Thompson. W. I'., Richter. M. X.. and Edsall. K. S.: "Anal\Ms of So-Calleii Aplastic Anemia/' Am. J. M. *SY., /.s7; 77-KH (Jan.). I L Ulmades. C. I*., and Miller. I). K.: "II etiology of Hone Marrow in Apla>tic Vue- inia." Arch. I*(i/h.. Hi: 6*LS-(i(i3 (Sept./. 1933. J, .Maitland. If. S.: "Occurrence of Malignancy in Radioactive Persons: General review of data gathered in study of radium dial painters, with special reference to occurrence of osteogenic sarcoma and inter-relationship of certain blood diseases." .1///. J. Cancer. 1~>: I (i (Oct.). 1931. (i. Erf. L. A., and Rhoades. (\ P.: "The Hematological Effects of Benzene (Benzol) Poisoning."./. Indus!. lhj(j. and Toxical.. II: kl-43.) (OetJ. 1939. 7. Hunter. E. T.: "Chronic Exposure to Benzene (Benzol; II, The Clinical KlVerk." ./. ludust. linn. {U,{t Toxicol., II: 331-3.7 I (Oet.J. 1939. 8. Greenhurg. L.. Mayers. M. R.. Goldwater. E.. and Smith. A. R.: "Benzene (Ben zol) Poisoning in the Rotogravure Printing Industry in New York City." J. Indus!. Ih/ff. and Toxicol., II: 39.7-kO (OcL). 1930. 9. Gray. 1., Greenfield. I., and Lederer. M.: "Benzene Poisoning." J.A.M.A.. //J (April (5). 10 H). 10. Meyer. A.: Communication to the Editor under "Queries and Minor Xoles." J.A.M.A.. IOS: !)1I (March 13), 1037. L CHAPTER V THE PETROLEUM HYDROCARBONS Thk petroleum distillates are chiefly gasoline. naphtha, petroleum ether, and benzine. Those whose boiling points range from ;><P to !)()' C. arc- used as motor fuels, while the solvents range from 70J to 150 C. Above '270 C. occur heavy oils, vaseline, and paraffin. Occupational Hazards.--Automobile mechanics, chauffeurs, dcgreasers. dryeleaners. buffers, and housewives are liable to this hazard. DIAGNOSIS Signs and Symptoms.--Headache, vertigo, nausea, vomiting, drowsiness, apathy, mild intoxication indicated by unsteady gait and giddiness (naphtha jag), irritation of the skin, visual disturb ances, and sometimes twitching of the muscles arc symptoms in less severe cases. In the severely acute cases, clonic spasm, convulsions, and death have ensued. Entering the body, usually through the lungs, the fumes from these substances have an anesthetic action affecting the central ner vous system. Instances of ingestion of gasoline or kerosene have been reported by Xumi and Martin and others. St. Leger,1 Schneider.'" Battlcy,3 and Johnstone1 have reported instances of gasoline entering the lungs in liquid form. Chronic exposure may cause a loss in weight, tachycardia, and secondary anemia. A slight leukocytosis is not un usual. Considerations in Diagnosis. Differential Diai/noxiti.--Disease of the heart, lungs, liver, kidneys, and the blood-forming organs have been attributed to the toxic effects of the petroleum pinducts without, as yet. adequate proof. While any of the' symptoms mentioned above may occur, there is a need for more abundant correlation between the manner of exposure, the nature of the substance, and the result ing pathology. When an employee working with these distillates de velops primary or secondary anemia or leukemia, it does not follow that the cause resides in his work. E.vptixure to Combination of Proi/nets.--Most petroleums are relatively noil-poisonous. Straight-run gasolines are relatively safe. Cracking of gasoline as done commonly in California results in unsaturaled compounds which are more toxic than the saturated. Furthermore, other solvents are sometimes added to what appears to THE L'KTHOUJl'M UYUKOCAHHOXS Hi) be a straight distillate. This suggests tlit- possibility llial whenever disease does arise from exposure to these petroleum products it is because of an unrecognized combination existin'!;. This is illustrated by tile case Askey'' reports. When seen (he man had purpura haeutorrhagica and profound anemia with leukopenia. Believing it to be an idiopathic aplastic anemia at first, Askey subsequently considered the possibility of benzene poisoning. The patient was a painter occu pied in washing paint off metal plates in a bath of gasoline. This discovery did not solve the problem, but Askey later was informed that California gasoline may contain from H per cent to `20 per cent benzene (benzol). Variety of Findinyx.--Experimental work has not arrived at a con clusive unanimous opinion. Papers from Russia stale that it is pos sible to produce leukopenia in animals with petroleum benzine if enormous doses are used. Granulopenia was not marked. They report a decrease in the red blood cells and hemoglobin early in the exposure, but. with subsequent return to the normal occurring. Their work would indicate an increase of nervous diseases and secondary anemia, but no nutritional disturbance in those exposed to these substances. On the other hand. Hayhursl'1 conducted observations on a series of patients subjected to chronic exposure. He states that disability began from three weeks to several years after exposure began. He lists the symptoms as headache, dizziness, loss of appetite, dyspepsia, restless ness. insomnia, paresthesias, pains in the back, legs, and heart region, weakness and dyspnea. Objectively they revealed from a 10 to 50 per cent loss of weight, tachycardia, secondary anemia with leukocytosis, mental depression, stupor, twitching, and tremors. Gasoline as Hazard. Antony Gasoline-Station Attendants'.--Fre quently gasoline-station attendants confront the industrial physician alleging an illness due to daily contact with the fumes. The weight of evidence is against the validity of their claims. Few such cases are reported in the literature, and when they occur analysis of the facts leads one to suspect carbon niono.ride (from within the garage) and not the gasoline as the noxious agent. Furthermore, the paucity of these claims in comparison with the thousands of gasoline-pumpers throughout the country who work at this trade tor years argues against its likelihood. Any existing illness is probably coincidental. On the other hand, men exposed to large amounts of the concentrated fumes, especially with an admixture of oxygen, have been overcome or have died. Antony Workers with Gasoline Fnyines.--)uhns<m` reports the eases of forty-two men working with gasoline engines in a tunnel who were overcome by these fumes. Two were completely asphyxiated. !)() OCCl'CATIOXAL DISKASKS remaining unconscious for twenty minutes. On regaining conscious ness. they could move their limbs but could not speak. They com plained later of frontal headaches, but no nausea or vomiting. The following day they showed no effects. The day following the exposure, -ixteeu of the other workers were affected. On another day. eighteen were affected. The blood contained no CO, and the air in the tunnel contained no CO. Among Those Using Gasoline for Cleaning.--The l nited Stales Public Health Service-' examined a group of twenty-two workers oper ating coupon-canceling machines who were exposed constantly to fumes of gasoline used in cleaning stamps and belts. Their dispensaryattendance rale for sickness was higher than a controlled group. When perfumed kerosene was substituted, the sickness rale was lowered and their output increased. It is to be suspected that the ventilation wapoor. Tetraethyl Lead as Hazard. Toxicity.--The addition of tetraethyl lead to gasoline results in a noxious substance, the hazard of which is confined chiefly to those engaged in blending or producing this type of motor fuel. In 1924 a number of deaths occurred among workmen at plants where this fuel is manufactured. As a result, a special com mittee investigated the toxicology of tetraethyl lead and concluded that: 1. Tetraethyl lead constitutes no undue hazard to the garage worker, gasoline-pumper, or the general public. 2. A relatively small industrial group is actually exposed to the hazard. Of this group, the chief ones are those who produce or blend this substance or those who come in contact with its products of decomposition, such as cleaners of storage tanks or railroad tank cars. .`i. Minute amounts spilled upon the skin in handling the liquid produce no ill effects since the quantity of this substance per gallon of gasoline is so low as to be lexicologically in significant. 4. The preventive problem can be reduced to the minimum by requiring tetraethyl lead to be colored by a dye to distin guish it from other types of gasoline and by having it prop erly labeled wherever it is sold, pumped, or stored. If is not likely that any of us will ever be confronted with a ea>e of tetraethyl lead intoxication occurring in one engaged in its pro duction. But it is not unlikely that any physician may have occasion to diagnose and treat a patient who has been exposed to the decom position products of tetraethyl lead, and therefore a brief description of the pathology and symptoms is justified. tiik pktuoi.kim immocAUisoxs 91 Patholoyy.--Tin- pathological changes which occur arc widespread hut are not specific of this poisoning, Congestion of all the viscera is common. a.-> well as hemorrhage into all parts of the body, although hemorrhage into the gaslro-inlestinal tract, has not been noted in man. In the white matter of the brain occurs the greatest amount of hemorrhage, together with engorgement of the cerebral vessels. The next site to be most affected is the lung, where hemorrhage', conges tion. and edema are found. Degenerative changes in the liver, kidneys, heart, -plecn. and pancreas have been reported. Syhiytoms and Signs.--Those ''ary with the degree of exposure. They appear within a short lime in one severely exposed, while in the one who has received a small dose symptoms are usually delayed. This, according to Madder' is the result of two factors: (1) "The decomposition of lead within the body with the liberation of watersoluble lead compounds; and U2) the delayed absorption from either the pulmonary epithelium or the skin." () Prodromal Period.--Investigators of this type of intoxication state that there is a prodromal period of from eighteen hours to eight days prior to the onset of real symptoms, varying inversely with the magnitude of the exposure and the severity of the poisoning. The victim appears to become increasingly nervous; sleep is difficult and disturbed by terrifying dreams. Apprehension and anxiety progress; into slates of excitement accompanied by headaches and vertigo. Occasionally the patient becomes depressed and evidences delusions of various types. Generalized weakness and fatigue arc common com plaints. Physical Examination.--Upon examination the reflexes are hyper active. although those reflexes not normally present are not seen. The eyegrounds reveal no abnormal finding'-, although visual weakness may be complained of because of weakness of the extrinsic muscles of the eye. Tremor, especially of the upper extremities, is noted in the majority of the severely exposed. The heart rate is slow and the systolic and diastolic blood pressure is lowered. Laboratory studies yield little diagnostic significance. Complieaiion.s\ Sequelae, and Convalescence.--What is the endresult of the non-fatal eases of tetraethyl lead intoxication? Maehle" studied a series of cases over a long period of time, lie stales: In mild and moderately severe cases in which there were brief periods of delirium no complications developed. As a consequence of circulatory weakness and exhaustion in severe or fulminating cases a variety of complications may conceivably develop, such as acute cardiac dilatations, cerebral edema, pulmonary edema or similar !)`2 OCT rPATIOXAL DISEASES lesions associated with temiinal stales. No complications occurred in tile present series, however. Sequelae have not been seen. Convalescenee may lie protracted with .symptoms persisting as long as from eight to ten weeks, hut no residual symptoms or evidences of damage have been observed. A group of fourteen patients not included in this series have been under medical observation at monthly intervals continuously since the time of intoxication in Libia and have not given any evidence of subnormality, physical alteration or increased susceptibility to intoxication. They have been continuously at work in the manufacturing operation, the majority of them having been in supervisory positions during the past two years where the exposure is often greater than that experi enced by day workmen. Such evidence, plus the absence of focal brain lesions at necropsy, indicates the reversible nature of the injury from tetraethyl lead and reduces the likelihood of damage from cumulative subclinical exposures. MEDICOLEGAL ASPECTS Acute cases are not common in industry. Housewives, cleaning with naphtha have become dizzy, drowsy, or have fainted. Dorner reports a case where the patient fell into a lank of crude benzine and remained comatose for three days before regaining consciousness. A motor paralysis was the sequela. Temporary Disability.--In mild cases, temporary disability may exist from a few hours to several days. Complications may prolong the temporary disability to several weeks. Permanent Disability.--If a severe, acute exposure leaves a perma nent defect, it is usually a disability of the nervous system. Epilepsy has been reported as occurring several months after the acute ex posure. Indictment of the exposure in such instances must be ques tioned. Retrobulbar neuritis has followed acute exposure, and ner vousness over a period of months is frequently alleged. Chronic exposure may result in a temporary total disability in which the workman requires months to several years to regain normal health. Permanent changes in personality, mental confusion, generalized weakness and muscular twitching have been accepted as results of chronic exposure. Such statements are to be critically questioned. Illustrative Cases: Case I.--This ease was reported by the author1 in May. 1!):58. I'p to the present writing it is the only one found in the American literature. Present Illness.--A white male, aged thirty-one. was brought to the Golden Stale Hospital complaining of severe chest pain, and with dyspnea and cyanosis. His employer who accompanied him staled that T1IK I'KTKOLKIWl IIYDUOCAKHONS !):> M-veral hours previoudy the palit-nl wa^ engaged in buffing an aulo fender. Desiring' some gasoline lo remove llie fine dust particles, he attempted to siphon gasoline from the lank of the ear. Inserting one end of the "airline hose" into the lank, he stretched out on the floor below and started to draw. Due to the diameter of the hose, the fel low had difficulty in removing the hose from lps mouth when the gasoline gushed Ihrough. This time-interval and the patient's position enabled a large quantity of gasoline lo cuter the patient's mouth. By the time the victim got to his feel he was strangling violently. He stated. "All I spit out was fumes." Ifis mouth and throat were Fig. SO.-- (May SO. l<):S7.) Films taken lifly-lwo hours after exposure show fluid level in right chest with some clouding of lel'L lung. (Author's article in hulnst. Met!.. 7: 243-`>.)l |May|, 1038.) burned, and within a half hour lie experienced pain in the right chest, especially around the nipple area. This became so distressing that he was taken first lo the Georgia Street Receiving Hospital and then to our clinic. Physical Examination.--Examination revealed ashen gray facies with general cyanosis. lie assumed a sitting position, leaning to the right, and refused to lie down, claiming that his breath would be cut off. Respirations were .'!`2 and shallow; pulse. 90 with fair volume: temperature, 100; blood pressure, 10-2 (>G. Examination of the chest revealed a pronounced lag on the right; percussion sounds on the left were slightly less resonant than normal; on the right they were 1)4 OCCtl'ATlOXAl. DISK ASKS Kijt. ->1.-- (May '24. Films taken four (lavs later show partial recv-Mon of fluid level with eloudiness exist iiifi above fluid level. (Author's article in linl.iml. Med.. 7: |May|. ItKiKJ nil-: I'ETHOLF.r.M hydhocakho.vs 9.3 Fin. S3.-- ('June 3. U)3?.l Disappearance of evidence of fluid. Evidence of pleurodiaphmgmalic adhesion. (Author's article in Indust. Med.. 7: S4S-eJ.il [May). 1!)3S,; Hr. '14.-- (June II. IUS7.) Lung livid* in accord with the normal, well-aerated ImiRs. Adhesion now reduced to a verv small area. (Author's article iu Indust. Med., 7: 113-2.il I.Mayl. 1D3S.J `Hi Orrei'ATIO.VAI. DISKASKS noticeably diminished. There wen- scattered rale-' llu'oniilioiit both lungs. The rest of the physical examination and the details of the progress of the ease will not he given at this lime. lie developed a hacking, harassing cough which was productive of a brown sputum. Within thirty hours, evidence of a pleural effusion existed. Roent genograms confirmed this suspicion. Further confirmation was ob tained by the aspiration of 10 ec. of amber-colored fluid. The patient made an uneventful recovery, and was discharged on the sixth day (Figs. 20. `21. 22. 2.`5. 24). Laboratory Examination.--The laboratory study on this patient was entirely negative. The urine showed a trace of albumin, the blood chemistry was normal, the sputa revealed no evidence of tubercle bacilli and only a few scattered pneumococci. Examination of the sample of effusion showed it to be reddish yellow and slightly cloudy. Microscopic examination revealed numerous lymphoid and blood cells. Inoculation of various media revealed no growth, and the guinea-pig inoculation produced no pathology in two months. Testimony of the employer and a fellow-employee as eyewitnesses of the accident was obtained. The gas was a cheap grade of cracked gasoline. The patient had been in good health, had lost no time from his work for years, and personal and family history denied the pres ence of tuberculosis. A sterile effusion argued against the possible eti ology of acute infection. The sudden onset and the rapid return to normalcy were in favor of the alleged cause. While no eases had been reported in our own medical literature, several instances of similar disturbances occur in foreign publications. He returned to work within ten days of the accident. The ease was considered occupational in origin. Case II.--A movie director engaged three men to renovate a yacht lie had just purchased. One man was assigned to clean and polish the engine-room, which was a rather small confined space. An unidenti fied gasoline was employed in removing the grease. Failing to appear for lunch, one of the men was found on the floor of the engine-room in a stupor. The glass bottle which contained the gasoline was broken, and the room reeked of gasoline. Brought to the deck, the patient regained consciousness but complained of severe frontal headache and -marting of his eyes. Medical examination two hours later found no objective disturbance, and the laboratory findings were negative. lie alleged headache and dizziness for a period of five weeks, at which time he was denied further compensation. No physical or pathological cause could be found for the man's sudden abnormal condition. The circumstances appeared sufficiently typical to permit a diagnosis of gas intoxication, ft was found (hat TIIK I'KTKOI-Kl'M il YDKOCAlfHOXS !)7 Lhi' man had not boon oin|>loyod for several months, and this parlienhir job was for only throe days. The question of the actual exist ence of his symptoms for a period of live weeks entered into the ease. Compensation for that period was granted. Upon discharge he main tained that lie could not work because of his headache, but four days later he secured a job and worked uninterruptedly. Case III.--A white male, aged fifty-eight, was employed by a garage as a handyman. One day he was found slumped over in a ear he had.just parked within the garage. lie was taken home and put to lied by order of his family physician. The patient complained of weakness of the right arm, headache, and the doctor noticed a thickness of speech. After four days in bed, lie arose one night to go to the bathroom, stumbled, and was found in a stuporous condi tion. Ilis physician found him to be semi-comatose: the right arm was paralyzed and the left arm fractured. A diagnosis of gasoline poison ing was made, and the claim was received by the insurance company. The insurance carrier dispatched a physician who noted the following: a blood pressure of 240''120, marked peripheral sclerosis, vascular engorgement of the fundi, albumin and casts in the urine. Subsequent study revealed (JO mg. of non-protein nitrogen per 100 ce. of blood. The blood count was not significant. Inquiry into the man's occupa tion showed that lie, had had no exposure to gasoline. For the past year he had complained of occipital headaches and tinnitus. lie had stopped reading because his glasses "did not fit." It was established that no undue exposure existed. The physical examination definitely indicated hypertension. Compensation was denied. Case IV.--A maid employed' in a home was asked on numerous occasions to clean wearing apparel with naphtha. One cold day she cleaned several articles in the kitchen. The doors and windows were closed. The patient was found on the door bleeding from a laceration of the posterior scalp. A garment was soaking in the dishpau of naphtha, and the patient was removed from the kitchen to her bed room where she regained consciousness, but was unable to account for her accident. Physical examination and laboratory studies were nega tive. She recovered and resumed her work in three weeks. In the absence of any other cause, the fact that the patient was leaning over naphtha in a confined room was accepted as sufficient evidence of naphtha intoxication. The resulting head injury di-abled her for three weeks. The case was accepted as occupational. Case V.--A sixty-year-old male was employed in a drycleanins* establishment. lie reported a loss of weight, increasing fatigue, less ened appetite, and obstipation, to his family physician. The blood 98 (K ('ITATK).VAI. DISEASES count .allowed ;i marked secondary anemia. lie was advised to dis continue work, and a diagnosis of "anemia due to a solvent" was made. The diagnosis was accepted, and compensation was paid for the first five months. Subsequent examination showed marked anemia, increased loss of weight, abdominal pain, a mass in the abdomen and blood in the stools. Gasiro-inicstinal examination revealed evidence of cancer of the large bowel. Investigation of the man's occupation established the fact that he was a checker of goods as they were loaded onto trucks. Ife had worked at that occupation for only six months and was never exposed to fumes or gas. Carcinoma accounted for all of his symptoms. Further compensation was denied. TREATMENT Acute Cases.--Invariably these cases are acute, and if the patient survives the exposure no specific treatment is necessary. The Unconscious Patient.--If the patient is seen while uncon scious, removal to the fresh air and inhalations of from 5 to 7 per cent carbon dioxide in oxygen are indicated. Saturated clothing should be removed and the skin cleansed of any of the material. The patient should be wrapped in blankets and kept warm. At this time circu latory failure, if present, should be treated by any of the following drugs: coramine (1.5 cc.). caffeine sodium benzoate (7U> grains; 0.5 gm.), metrazol (1U to 4's. grains; 0.1 to 0.3 gin.) or camphor in oil (1 to 2 cc.) intramuscularly. The coramine and metrazol may be used intravenously and will also act as respiratory stimulants. Artificial respiration usually is fell to be contraindicated because of the exist ing lung damage, and adrenalin administration has been found to give poor results. Prevention of Pulmonary Complications.--The lungs especially need to be watched for complications, such as bronchopneumonia. After the first portion of the acute stage where respiratory stimulation chiefly is needed, oxygen therapy may be substituted for the carbon dioxide and oxygen inhalations. For cough, codeine phosphate or sulfate (!m to 1 grain; 0.0325 to 0.005 gm.). perhaps in a cough-syrup vehicle, is useful. Nervousness and Restlessness.--These conditions may require sedation by any of the following drugs: chloral hydrate (10 to 30 grains: 0.05 to 1.95 gm.). phenobarbital (1 grains; 0.1 gm.). sodium bromide (10 to 30 grains: 0.05 to 1.95 gm.). or paraldehyde (2 to 4 drachms; <3 to 10 ce.). The paraldehyde may be mixed with elixir lactate pepsin, poured over crushed ice. and administered by mouth, or it may be given rectally in olive oil with 1.5 ce. benzyl alcohol. Epsom salts (1 ounce; 30 gm.) should be given. THE I'KTKOLEC.M 11 Vt)HO( AKIiOXS !)!) Venesection, followed by blood transfusions, to rid the body of methemoglobin. has been advocated.'" When ingestion of the sub stance has occurred, lavage with epsmn salt.- solution is of value. Conjuncfiritis.--Due to irritation from petroleum distillate fumes, conjunctivitis may be treated by dropping 1:1000 adrenalin solution into the eyes four times a day. followed by the use of cold applica tions for from ten to fifteen minutes. Bland boric acid ophthalmic ointment should also be used. Chronic Cases.--Patients in chronic eases chiefly need removal from their exposure. The diet should lie high in caloric's with added vitamin preparations. For the secondary anemia, ferrous sulfate (5 grains: 0..T2 gin.), two tablets three times a day. may be used. The ferrous sulfate preparations seem effective in relatively small doses, and they also seem to cause less gastro-intestina) discomfort than other iron compounds. REFERENCES 1. St. Ledger. A. \\\: "hihiilalion of Petrol." Med. J. Australia, 1: Mi) (March IS). 1922. 2. Schneider. It.: "('her akute. Benziu-vergiftuug." Med. Klin., it): 1108-1169 (Aug. *2.5). 1933. 3. Baltlev. J. C. S.: "Effect of Liquid Ga.solino on Pulmonary Tissue"." J.A.M.A., 1.570-1.571 (May 17). 1930. 4. Johnstone. It. T\: "Pleural Effusion from Gasoline Inhalation." Indust. Med., ?: 213-2.11 (May). 1938. .5. Askcy. J. M.: "Aplastic Anemia Due to Benzol Poisoning. Report of Two Cases." California and West. Med.. Jfl; 262-203 (Oel.). 1928. 0. llayhurst, E. It.: "Poisoning by Petroleum Distillates." Indust. Med., A: ,53-03 ' (Feb.). 1930. 7. Johnson, J. G. \Y.: "Toxic Effects of Gasoline Fumes." Canad. M. .1. .(., d: 118. 1913. 8. Hamilton. A.: Industrial Poisons in the United States. The Macmillan Co.. New York, 1929. p. -104. 9. Maehle. \Y. F.: "Tetra-ethyl Lead Intoxication and Poisoning by Related Com pounds of Lead." J.A.M.A.. Klo: .578-.58.1 (Aug. 2.5), 193.5. 10. Barbour. O.: "Kerosene Poisoning." J.A.M.A.. S7: 48S (Aug. 14). 1926. ('II APT HR V[ CARBON TETRACHLORIDE Carbon tetrachloride is a clear, colorless liquid, having an odor resembling that of chloroform. It is insoluble in water but mixes with alcohol, chloroform, ether, benzene, benzine, and dissolves most of the oils. The fumes are heavy, being o.ti times heavier than air. Occupational Hazards.--Carbon tetrachloride is used widely as a degreasing agent for metals, textiles. and in drycleaning: as a solvent Pii, 'l~>.--Liver of Hal IJ77. diowinji advanced cirrhosis; color, yellow; 110 exposures to 400 part's per million. (Smylli and Siuylli: J.A.M.A., Nov. MKiO.f for rubber, lacquers, resin, and animal fats: in the doping of airplane wings: in the manufacture of (ire-extinguishers; as a delousing agent: and is commonly found in the home as an agent to remove grease spots. Pathology.--Intentional ingestion of this substance for medicinal purposes (hookworm) does not concern Us. loo r.YKIiOX T IvT li A ('111.0 HIDK 101 Fig. 28.--Liver of Rat 395, showing regenerated cirrhosis; color, normal; 08 ex posures to +00 parts per million, and 1.50 days without exposure; section resembles Fig. 27. (Smyth and Smyth: J.A.M.A., Nov. 21. 1930.) Fig'. 27.--Liver of Hal 393. showing regeneration from cirrhosis, with contracted Scplums: magnification. 2.10; 70 exposures to 100 parts per million: 03 days without exposure. (Sm\th and Smyth: JA.il.A.. Nov. 21. 1930.; 102 OCCl'l'ATION.U. DISEASES (lencral Ejects.--Industrially. inliahition of the* fimu's through tho respiratory tract produces changes in tin1 tissue of various organs, alteration of metabolism and disturbances of Lbe blood ebemislry. The gas. like chloroform, exhibits powerful anesthetic properties. Sud den severe exposure results in a depressive action upon the heart. Sudden death is due to failure of the heart or ventricular fibrillation, rather than respiratory failure. Specific Effects.--Animal experimentation reveals a necrosis of the liver (Figs. 2;3. 20, -27). This undoubtedly occurs in human exposure but it would appear that the kidneys in the human are more involved than the liver. There is an increase in the protein metabolism, the by-products of this increase being sulphuric acid, phosphoric acid, oxalic acid, bcta-oxybutyric acid and others, leading to a condition of acidosis. Poindexter and Greene1 report an autopsy of a ease of long-standing exposure which showed cirrhosis of the liver with ascites, infarction of the right kidney, and compensatory hypertrophy of the left. DIAGNOSIS Signs and Symptoms.--Nausea, vomiting, weakness, vertigo, burn ing sensation in the epigastrium, headache, excitement, cough, and narcosis arc present in the early stages, followed by oliguria, albumin and casts in the urine, symptoms of uremia, convulsions, deep coma, and death. Chronic exposure will cause headache, vertigo, decreased appetite, gastric distress, and allegedly jaundice without ascites. Some investigators believe that an individual susceptibility exists resulting from lowered nutritional states, alcoholism, and deficient intake of calcium. They maintain that carbon tetrachloride combined with alcohol exerts a synergistic action upon the liver. Test. For Concentration in Air.--Examination of the air where the patient works may be necessary as well as expedient. For a working day, 100 parts per million parts of air is considered a safe level; for short exposure, a concentration of below ,500 parts per million. For Presence in Body.--In cases of death, chemical analysis of the various tissue will affirm or deny the presence of carbon tetrachloride. While there exist no simple, specific tests to prove the presence of this substance in the body, certain examinations will serve as a reliable aid when considered with all other factors in a given case, [t has been shown that long exposure or severely acute exposure may produce amblyopia characterized by concentric restriction of the visual field', damage to the liver, and alteration of the calcium metabolism; and therefore measurements oj the visual fields, the icteric index, and the ran den lleryh reaction should be made. Tests of the blood calcium CARBON TETRACHLORIDE 103 1'X should further aid in the diagnosis of suspected cases. Smythe- be M lieves that repeated examinations of this nature at intervals, in those working in known exposures, would serve to detect early injury. MEDICOLEGAL ASPECTS Exposure outside Industry.--Because of the cheapness of this solvent and the fact that it is non-inflammable, its frequency of use is mounting daily. Its increased use is bound to produce numerous claims for disability. It is of utmost importance, therefore, that em phasis be stressed at this time upon several points. Today, acute or chronic reactions to carbon tetrachloride are actually rare. The ma jority of cases happen outside industry where, ignorant use of the substance has occurred. Likewise, many of the cases referred to in medical literature took place before the present-day knowledge of the solvent induced proper ventilation as well as proper precautions. During the first World War, production was at a premium, and both precaution and ventilation were neglected. Much of the present-day impression regarding its dangers is a result of that period of unsuper vised use. Fatalities in Industry.--The almost negligible effect of this agent can best be illustrated by referring to the work of Smythe.3 His re view of the literature up to 1935 showed only twenty-seven fatal cases of acute poisoning. Fourteen were the result of the administra tion of this substance as an anthelmintic. Of the remaining thirteen cases, only six occurred in the United States. He found only thirtythree non-fatal, acute, or subacute industrial cases in this country, but not all were typical, since thirteen patients were exposed to mixed preparations. Ninety-six patients working in a carbon tetra chloride hazard were studied by him. Correlating his animal experi mentation, men working for a long period of time in this exposure developed a resistance showing fewer abnormalities than the men just starting to work in such a hazard. No man considered materially or appreciably weakened by the exposure was found, nor was there found among them pallor or jaundice. One enlarged liver was seen in a man in this group who was admittedly a chronic alcoholic. The men uni formly reported that the subjective symptoms of headache, nausea, vomiting, and fatigue were present only during brief periods when the ventilation was bad, or when machine-cleaning, spilling, or other intermittent exposures were present. Contrary to common belief, anemia was not ascribed to. This investigation is reviewed here to offset prevailing misconception of the action of this solvent in indus try. The symptoms previously outlined do occur in persons exposed j { 104 OCCUI'ATIOXAL DISEASES to carbon tetrachloride, but they usually occur in non-industrial exposures. Temporary Disability.--This is short, a few days at the most. Acute, severe exposure may produce symptoms lasting for from sev eral weeks to several months, although complications such as neph ritis may prolong this period. Permanent Disability.--This is extremely rare. Removal from ex posure results in recovery. When liver cells are damaged, regeneration usually occurs. Impaired vision usually returns to normal. Illustrative Cases: Case I.--A workman dropped a container of the carbon tetra chloride in the basement of a drycleaning establishment. While at tempting to improvise a cork for the neck of the container he was overcome. His employer awaiting him upstairs became, impatient and went down to this small, dank basement to find the employee com pletely unconscious. The employer first shook the patient, then dragged him to the stairway, where he too collapsed. The office girl, wishing to inform her employer that he was wanted on the telephone, found them and summoned help. The employer revived in the ambu lance, and the employee shortly after he arrived at the hospital. Both patients made uneventful recoveries. The exposure was definite and the reaction typical. Recovery was in keeping with the usual run of cases. Case II. Present Illness.--A fifty-two-year-old janitor noticed an increasing fatigue, generalized weakness, dyspnea, palpitation, and edema of the ankles. After he had complained for some weeks, his wife noticed that he seemed quite pale. During this time one of his helpers became ill one night while handling a cleaning solution. It occurred to the janitor that possibly this substance which he used on the brass fixtures almost daily was bothering him. He consulted his physician who, following a physical examination, "felt inclined" to believe that the patient's suspicions were correct. He was ordered to stop work, rest, and to get plenty of fresh air. Several weeks later, a claim for compensation was made. One month later he was examined at our hospital. Physical Examination.--Upon examination it was noted that his color was slightly lemon-tinged. The tongue was smooth and sore. Extreme weakness was evident, and exertion in getting on and off the examination table produced marked shortness of breath. He had a bilateral reading of 20 on the gripping machine. Pulse was 88, heart tones weak, blood pressure, 110/80. Abdominal examination was nega tive. Prostate normal. Neurological examination essentially negative. No particular numbness of the limbs was complained of. CAIIBOX TETRACHLORIDE 105 Laboratory Examination.--Urine. 2 plus albumin, with many granular casts, no sugar: red blood cells, 2,200,000; hemoglobin, 72 per cent: color index. 1.68: marked distortion of the red cells. The gastric contents were not examined. Xo blood investigation was made at the time the patient was first seen. The rather universal opinion that solvents produce anemia was accepted by the family physician, and he assumed that the man had been affected by a solvent. Investigation of the cleaner showed that it did not contain tetrachloride. Its purpose was to polish, not to clean or act as a degreaser. The patient had pernicious anemia. Placed upon the proper therapy the man regained his health. The case was not compensable. Case III.--Butch reports a case where a fifty-four-vear-old man used a solution of 60 per cent carbon tetrachloride and 40 per cent gasoline to clean old telephones. Following a six months' exposure it was necessary to hospitalize him, at which time it was found that he had cirrhosis of the liver. After four months of treatment and ab sence from work he recovered. From the history of this case, the illness was occupational in origin, and compensation should be allowed for a temporary disability of four months. The case illustrates the point that liver regeneration occurs in carbon tetrachloride intoxication and that permanent dys function of the liver is not to be expected. Case IV.--Gonzales4 reports the case of a housemaid, aged forty, who contrary to directions on the gallon container of "Quick as a Wink" cleaning-fluid, poured almost the entire contents in a basin and dipped the garments in the liquid. She immediately became dizzy and faint, staggered out of the small room in which the operations were performed, and collapsed. A physician after reviving her ex pressed the opinion that she had suffered a "heart attack." A few days thereafter, at the behest of her mistress, she proceeded to clean dresses in a similar manner and was found dead beside the basin con taining the fluid. Necropsy.--The necropsy was negative except for a moderate grade of chronic diffuse nephritis, pial edema, and injection of the laryngeal and bronchial mucosa. A chemical examination of the organs revealed the presence of carbon tetrachloride and dichloropropane. The analysis showed 18 mg. in 500 gm. of lung and 14.5 gm. in 500 gm. of liver, of chlorinated hydrocarbons of low boiling point. The amounts were loo small to isolate the substances in pure form. These results were determined colorimetrically. Analysis of the color 10(5 OCCUPATIONAL DISEASES less fluid remaining in the container indicated approximately (50 per cent carbon tetrachloride and 40 per cent dichloropropane. No comment is needed other than to slate that this is an example of exposure occurring outside of industry where ignorance of the solvent, its dangers and the proper methods of usage exist. Case V.--Iiauscman and Ilelly' tell of a forty-six-vear-old disin fector who inhaled the fumes of carbon tetrachloride. He died on the twenty-sixth day after his intoxication. Death was hastened by a pre existing nephritis. It has been previously stated that this substance affects the kid neys. In this instance, the already insufficient kidneys were further damaged. Death was compensable since it is held that even though a workman has a disease existing at the time of injury, the employer has accepted him as he is; therefore, the aggravation of the disease resulting in death is compensable. Case VI.--A thirty-eight-year-old Negro male was first seen by the writer on March 6, 1940. His usual occupation was that of a yard man engaged in handling scrap tin. On March 1 he was assigned the task of cleaning long felt bags which had contained lead dust. He did this by immersing these bags into a large vat which contained a clean ing solution. He could not estimate how many bags he had washed but states that he stood over this solution for seven and one-half hours. Present Illness.--As he was finishing his day's work he felt sick to his stomach, and on his way home he vomited several times. This vomiting continued, and a severe headache ensued. Along with this headache the patient noted a bubbling sensation in his ears and a ``waxy haze" over his eyes. Later that evening he noted several blebs or blisters on the dorsum of both hands and described these as ``water blisters." The following day he reported to the office of the commu nity physician, who opened these blisters and applied ointment. At this time the hands were quite swollen, nausea was still present but no vomiting, and headache was severe. The patient complained of an exceedingly dry throat, and the "waxy haze" over his eyes persisted. Past Medical History.--Pneumonia at the age of seven; otherwise negative. Denies venereal disease. Physical Examination.--The patient was a tall, well-built adult Negro. His pupils were small, and the reaction to light was question able. The eyegrounds were normal in appearance. The teeth were stained, and there was some recession of the lower gums. The throat was injected and inflamed. The tonsils were large and cryptic. (a) Lungs.--No adventitious sounds were noted. The heart rale was 80, regular; no murmurs were heard. Blood pressure was 140/90. CAKBOX TETRACHLORIDE 107 (b) Abdomen.--No organa or masses wore palpated. There was alleged tenderness over the upper mid-quadrant. (c) Extremities.--The skin over the dorsum of both hands was wrinkled, and there were numerous denuded areas. The surfaees of both hands including the fingers and palmar surfaces were greatly swollen. The denuded areas constituted second-degree burns. Laboratory Investigation. Tests on March 7. 1940 Urinalysis Blood Count Voided specimen: Straw color Clear appearance Specific gravity, 1.022 Acid reaction No sugar, albumin, oracetone Microscopic: 3-4 pus cells. Mucous threads present Hemoglobin 88percent Erythrocytes 5,520,000 per cu. mm. Leukocytes..............7550 per cu. mm. Polynuclear neutrophiles ................55 per cent Lymphocytes.................... 39 per cent Large mononuclears ... .3 per cent Eosinophiles.......................-.3 per cent Blood Tests Wassermann ........................negative Kahn ....................................... negative Laughlcn .............................. negative Tests on March 11. 1940 Urinalysis Voided specimen: Straw color Hazy appearance Specific gravity, 1.018 Acid reaction No sugar, albumin, or acetone Microscopic: 0-1 pus cells Blood Count Hemoglobin ..................... 92 per cent Erythrocytes 5,300,000 per cu. mm. Leukocytes............8100 per cu. mm. Polynuclear neutrophiles .................45 per cent Lymphocytes................... 43 per cent Large mononuclears .... 6 per cent Eosinophiles ..................... 6 per cent This patient improved slowly, and ten days after his initial ex posure the headache had disappeared, there was no nausea or disturb ance of hearing, and there was no complaint of disturbed vision. He was annoyed by an exceedingly dry throat. The burned hands im proved gradually and were completely well twenty-six days after the initial burn. Inquiry revealed the fact that the solution used contained 25 per cent carbon tetrachloride and 75 per cent ethylene dichloride. Among 108 OCCUPATIONAL DISEASES other effects from the latter substance there has been reported a smoking of the cornea due to an infiltration by the lymphocytes and connective tissue cells. When such a disturbance occurs, it usually clears up within several months. This reaction was not actually noted in the case just reported, but from his complaints there must have ex isted a mild but unrecognized alteration. His general systemic com plaints were compatible with carbon tetrachloride intoxication. The reaction to the hands is not common. Ordinarily these solvents do not cause burns to the skin to this degree. It is thought, however, in this instance that the continual submergence of the hands in the solution for over seven and one-half hours did produce the burns noted. It is interesting to note that the patient was not warned against the character of the solution, and the employer did not know the con sistency of the substance used. The case was compensable, the tem porary disability being one month. There was no permanent dis ability. Case VII.--On March 29, a night janitor employed by a movie theater was assigned to clean a carpet in a restroom, which had only a small opening in the ceiling for ventilation. He worked on his hands and knees over a bucket of cleaning fluid, constantly wringing out the cloth and re-dipping it in the cleaning solution. He worked at this for hours with one short intermission in the fresh air. He went home and slept from 6 A.M. until 1 P.M. Present Illness.--Upon awakening he felt rather dizzy and had a severe headache. Thirty hours after the exposure he became nauseated and vomited several times. He felt feverish and chilly, and his eyelids, hands, and feet became swollen and felt stiff. Frontotemporal head ache continued. Vomiting also continued at intervals for the next five days. He developed a cough, expectorated blood-streaked sputum, and the swelling of his hands and feet grew gradually worse. On April 5, he voided practically no urine and had extreme burn ing on attempts at urination. He stated that he could void only a few drops of urine at a time. It was on April 5 that he was brought to the Golden State Hospital. The patient's complaints on admission were headache, dizziness, recurring nausea and vomiting, loss of appetite, burning on urination, oliguria, stiffness of the fingers, and swelling of the hands, feet and eyelids. Past Medical History.--Entirely negative for any previous injury or serious illness. The patient is married; has no children. His habits are temperate. His only alcoholic indulgence is that of a light wine. Physical Examination.--The patient was a robust, while male of about forty-five years, appearing to be acutely ill. Temperature, CARBON TETRACHLORIDE 109 97.4 F.: pulse, 04: respiration, 20; blood pressure: systolic. 156; dia stolic, 90. The skin was free from eruption and presented slight gen eralized pitting edema. (a) Ilcad.--There, was a diffuse subconjunctival hermorrhage of both eyes. The fundi appeared to be clear on the first ophthalmoscopic examination. (b) Lungs.--A few large, rhonchus rales were heard. Otherwise normal. (c) Abdomen.--Tenderness existed across the upper abdomen, particularly over the liver area. Upper border of liver dulncss at sixth rib: lower border at the costal margin. Liver palpable and quite tender. There was no rigidity of the abdominal muscles. Laborafory Examination. Urinalysis Blood Count Straw color Clear appearance Acid reaction Heavy albumin content Numerous epithelial and cells No blood, casts, sugar, or tone present pus ace- Hemoglobin ...................... 80 per cent Color index ......................................89 Erythrocytes 4,570,000 per cu. mm. Leukocytes .... 11,050 per cu. mm. Small lymphocytes.......... 22 per cent Large lymphocytes.............0 per cent Large mononuclears... .1 percent Polynuclear neutrophiles 71 per cent N.P.X................... 128 mg. per 100 cc. The urinary output during the first twenty-four hours after ad mission was only 40 cc. On the second day it was 60 cc.; third, 33 cc.; fourth. 60 cc. The fifth day, or the eleventh day after exposure, it was 250 cc. From this period there was a gradual increase in the urinary output. Blood chemistry on the second day after admission, or the eighth day of the disease, was as follows: N.P.N., 77.5 mg. per 100 cc.; urea nitrogen, 56.2 mg. per 100 cc.; creatinine. 5.5 mg. per 100 cc.; uric acid, 20 mg. per 100 cc. Subsequent urine examination continued to show heavy amounts of albumin, and microscopic blood appeared. The blood chemistry re peated on April 11, or the thirteenth day, was as follows: N.P.X.. 100 mg.; urea nitrogen, 68.5 mg.; creatinine. 4.5 mg.; uric acid. 8.4 mg. Two days following admission, the blood-pressure reading was 170/100. This gradually receded until at the time of discharge it was 116/76. On April 12, examination of the right and left eyes showed the media clear. Retina, disc, macula essentiallv normal. Ill) OCCUPATIONAL DISEASES On April 24. the blood count in contrast to the previous one re vealed: hemoglobin. 111) per cent: color index, 1.1: erythrocytes, 5.010.000; leukocytes. 0100; polynuclear neutrophilcs. 74 per cent. Shortly after the patient entered the hospital in addition to the liver dulness and the tender liver, he developed an icteric tinge to the skin and sclera. This was very light. On April 24, approximately twenty-six days after the onset, the van den Bergh tests, both direct and indirect, were negative, and the icteric index was 2.5. On May 15, a repeated Wasscrmann was negative. The renal func tion tests, including the phcuolsulfonphthalein and Mosenthal. indi cated satisfactory kidney function, and the N.P.N. on that date was 37.5 mg. per 100 cc. The patient was discharged from the hospital on the third day of May. He was examined at periodic intervals; on June 15. for instance, he had gained weight; blood pressure was 110/06; pulse, 72. There was still slight residual puffiness of the eyelids. The urinalysis on that date was negative. Concerning the injury to the eyes, the following report of the case by the ophthalmologist is of interest: Examination of the eyes was first done about the second day of hospitalization. At that time the patient complained of "blurred vision." He stated that he could recognize people but that the image was "blurred." A detailed examination of the visual acuity was not done at this time since the patient was extremely ill and it was diffi cult to get his full cooperation. Examination showed the presence of subconjunctival hemorrhages involving the bulbar conjunctivae and external canthi of both eyes. The ocular tension as estimated by palpa tion was found to be within normal limits. The conjunctivae were pale. The corneas were clear and iris of each eye negative. After dilatation the pupils were found to be round. The media was clear. The fundi were clear. No variation from the normal was seen in the macula, nerve head, or retina of cither eye. After the patient was discharged from the hospital further exami nation of the eyes was done. The patient complained that he could not see as well as formerly for distance or near. Examination of bulbs showed them to be essentially negative. No changes were seen in the fundi. Uncorrected vision was found to be H.E., 20/30; L.E., 20/40; near, Jaeger 111, K.E.; Jaeger 111, L.E. After the use of homatropine, vision was found to be 20/50-2 in the right eye and corrected to 20/20-3 with a plus 75 sphere combined with a plus 25 cylinder axis 90 degrees. Left eye 20/70 corrected to 20/20-2 with a plus 1 sphere. Postcycloplegic examination of near vision showed correction to Jaeger 1 with a plus 75 sphere addition in each eye. Perimetric examination of the visual fields showed a contraction for form and color in both eyes and within 30 degrees when using a CARBON TETRACHLORIDE 111 5 mill, diameter test object on a 30 cm. radius perimeter. The central and blind spots were explored with one degree, test object at 1 meter distance. No change was found in these areas. The patient had diffi culty distinguishing green and blue in all areas within the field of vision. A further check-up examination on October 28. showed no essen tial changes in visual fields other than that noted in the previous examination. Visual acuity, however, had improved to lt.E., 20/20-3 and L.E.. 20/20-4 uncorrccted; and corrected to R.E., 20/20-1; L.E., 20; 20-2. At the time this patient was admitted to the hospital the exposure was established by the testimony of a fellow-worker and by his em ployer who assigned him to this job and gave him the cleaning-fluid that was used. The manufacturer of this fluid first maintained that this solution contained no harmful substances and specifically claimed that it contained no carbon tetrachloride. However, analysis revealed it to be a very light naphtha containing 25 per cent carbon tetra chloride. The findings of acute toxic nephritis, a hepatitis, bronchitis, and a disturbance of vision were in keeping with the known effects of undue exposure to this solvent. Temporary disability lasted from March until December of the same year, and during this time the insurance carrier assumed all liability. On December 11, the patient brought suit against the manufacturer and recovered his claim. He was then lost sight of, and no further statement can be made as to whether there remained any permanent disturbance of his visual field. Other than this possibility, there remained no permanent disability. TREATMENT The severe case of carbon tetrachloride poisoning will require a rigid regimen, the purpose of which is twofold: to treat the liver and renal damage, and to restore a normal blood chemistry. The patient should be removed from all contact with the substance. He should be supplied with an abundance of fresh air and with inhalations of from 5 to 7 per cent carbon dioxide in oxygen, if necessary, for respiratory stimulation. Increasing Blood Calcium Level.--These patients have a low blood calcium level. Therefore, a high calcium intake should be provided to bring their blood calcium to the high or normal level, which it has been shown experimentally prevents liver and renal damage to some de gree. This can be accomplished by giving 10 cc. of a 10 per cent solu tion of calcium gluconate intravenously two or three times daily*, with 12 gm. calcium gluconate, or 8 gm. of calcium lactose by mouth. 112 OCCO'ATIOXAL DISEASES Proteins in Diet.--The diet itself should contain a high proportion of carbohydrates. "200 to `250 gm. or more per day, together with a low fat and a low meat protein ratio. The meat protein is limited because of the evidence that increased retention of guanidine prolongs and in creases the symptoms of carbon tetrachloride poisoning. However, in view of the demonstrated value of protein in liver regeneration, a high level of other forms of protein should be maintained. Actually, follow ing the early acute symptoms, a still higher protein level would prob ably be of value. Bread, milk, sugar, and Karo syrup are obviously of much value in the diet, to which may also be added extra vitamins. Dextrose Solutions.--The intravenous administration of from 2000 to 3000 cc. daily of 10 per cent dextrose in physiological saline is indicated. In renal disease or when circulatory collapse induces defec tive renal function, the injection of physiologic solution of sodium chloride may occasionally produce or aggravate acidosis. This effect is brought about chiefly by diluting the bicarbonate already in the body at a time when the kidneys are not excreting the excess of chloride. In some instances, then, the use of 10 per cent dextrose in distilled water, rather than in 0.9 per cent sodium chloride may be indicated. However, in most instances the 0.9 per cent sodium chloride solution may be used since even abnormal kidneys excrete salt solu tion well if serum proteins are not reduced or cardiac failure is not present. Dextrose solutions, by providing food and aiding the circula tion, help the kidneys to adjust extracellular volume and concentra tion when sufficient sodium chloride is available. The administration of from 50 to 200 cc. of 50 per cent dextrose intravenously per day is also of value, but where cardiac involvement is present, not more than 50 cc. should be given at one time. It has been suggested that some of the fluids may be given per rectum, rather than intravenously; 120 cc. of 10 per cent dextrose every four hours may be used rectally. Insulin.--From five to ten units of insulin three times per day may aid in the oxidation of the intermediate products of protein, fat. and carbohydrate. There have been a few reports of the satisfactory use of Hartmann's buffer solution and of methylene blue, but neither of these agents has been used extensively in these cases. Digitalis.--This has been advised routinely for the treatment of myocardial involvement but would seem to be of questionable value in most cases. When used, regular digitalizing dosages of 1'/_> grains (0.1 gm.) per 4.5 kg. of body weight should be employed. Epinephrine should not be used, particularly if myocardial involvement is pres ent.0 CARBON TETRACIU.OKIDE 113 Diuretics.--Diuretics, other than the mercurial ones, are indicated. In treating oliguria or anuria the use of papaverine hydrochloride or sulfate, V. grain (0.03-25 gm.) intravenously or by mouth, is said to be of value on the basis that these drugs relax the arteriolar spasm asso ciated with the toxic nephritis. There are claims of success for the use of hexylresoreinol for treatment of kidney irritations. Other Medication.--Free catharsis is of value, but oily prepara tions are contraindicated. Transfusions arc sometimes necessary. If anemia of the secondary type is present, ferrous sulfate in enteric coated tablets. 5 grains (0.32 gm.) to two tablets, three times per day should be prescribed, and if a macrocytic type of anemia accompanies the liver damage, the use of liver extract is indicated. If any bronchial conditions develop, inhalations of compound tincture of benzoin and pineneedle oil, followed by a cough syrup with codeine phosphate or sulfate added should be used. Sedation may be necessary for the restless or for the excited. When the eyes are involved, their treat ment should be consigned to the ophthalmologist. Experimental work with a purified concentrated hog's liver ex tract" has demonstrated an accelerated healing of liver tissue in rats after carbon tetrachloride poisoning, in addition to protecting the liver from damage. The active ingredient appeared to be sodium xan thine. Its clinical use in carbon tetrachloride poisoning is not yet re ported. Prophylaxis.--From the standpoint of prophylaxis, proper ven tilation is essential. In addition, closed systems should be used, or, if these are not possible, positive-pressure helmets may be necessary when the concentrations arc very high. Exhaust systems should be provided with intakes at the floor level rather than near the ceiling. The possibility of skin contact with the substance should be elimi nated. There should be frequent examination of workers, and careful selection of those who are to work with this hazard. Rotation of work ers should be frequent. The diet of carbon tetrachloride workers should be high in calcium, including at least one quart of milk daily. Alco holic beverages should be avoided. REFERENCES 1. Poindexter. C. A., and Greene, C. H.: "Toxic Cirrhosis of the Liver. Report of a Case Due to Long Continued Exposure to Carbon Tetrachloride,"' J.A.M.A., 102: 201.3-2017 (June 10). 1931. 2. Smylhe, II. F., Sinythe. II. F., Jr., and Carpenter. C. P.: "Chronic Toxicity of Carbon Tetrachloride; Animat Exposures and Field Studies," J. Indust. Hyg. and Toxical., IS: 277-298 (Mav), 1930. 3. Ibid. S 114 OCXU PAT]OXAL I)ISICASES 4. Gonzales. 'J'. A.: "Needs for Improvement in Medico-Legal Investigation." Xcm England J. Med., 21~>: 38--390 (Aug. 271. 1030. 5. McNally. Will. I).: Toxicology. Industrial Medicine Publishing Co.. Chicago. 1037. 0. Davis, P. A.: "Carbon Tetrachloride as an Industrial Hazard," 962 (Sept. 20). 1934. 7. Barrett. II. M.. MacLeau. I). L., and McHenry, K. E.: J. Pharmacol, and Expcr. Thcrap.. 131 (Ool.), 1038. CHAPTER VII CARBON DISULFIDE Investigators iu most every industrial country have called atten tion to the harmful effects of this gas, but in America it has received scant notice. As far back as 18(15 Delpeeh, in France, recognizing its devastating effects upon human tissue, remarked, "He who works in sulfur (CS2) is no longer a man." Occupational Hazards.--Carbon disulfide once found widespread use as a solvent. Because of its deleterious effects it was later largely replaced by less noxious substances. Industry, however, still finds it indispensable in certain processes, the chief of which are these: as a solvent in the extraction of fats, oils, rubber, sulfur, iodine, the oils from seeds and bones; in the preparation of some lacquers and var nishes; as an insecticide and disinfectant; and finally and most espe cially in the manufacture of rayon (viscose rayon). It is mistakenly thought that this fast-growing industry is located only in the Pennsylvania-Delaware area. Actually there are fifteen or sixteen plants en gaged in the manufacturing of artificial silk scattered elsewhere in the United States. Survey of Literature.--The average industrial physician rarely comes in contact with illness resulting from chronic carbon disulfide poisoning; the medical literature is devoid of articles concerning it; textbooks of medicine ignore it, and even recent publications dealing with occupational diseases fail to describe it. Until Gordy and Trumper made their report1 in 1938, no papers dealing with this subject had been published in America since 1905, although Dr. Alice Hamilton had urged an investigation of the rayon industry in 1937. In 1938, with the cooperation of the United States Department of Labor,2 the medical staff of the University of Pennsylvania, under Lewy, the American Chemical Society, and the Pennsylvania Depart ment of Labor and Industry, the first coordinated group study of this gas ever to be conducted, either in America or in foreign countries, was made. Owing to the inexperience of the profession with this sub stance, and to the fact that a better understanding will become obli gatory on all industrial physicians, a resume of the aforementioned survey is presented. Resume of Group Study.--Carbon disulfide belongs to the anes thetic group of noxious gases. It is a colorless, transparent fluid which 115 no OC'Cl'lWTIOXAL DISEASES is inflammable ami highly explosive, an additional reason why il. was largely discarded as a solvent. It enters the body through the lungs and is immediately carried by the bloodstream to all the organs, in cluding the brain. It is eliminated through the. urine, skin, and lungs. Lehmann- concluded, following his experiments, that from 80 to 85 per cent of the inhaled carbon disulfide is again exhaled, leaving from 10 to 15 per cent to be retained. If poor ventilation is present, ex haled fumes may be returned to the workman in the atmosphere to be again inhaled. Thus intoxication is dependent upon the relationship Fig. 28.--Longitudinal section through the sciatic nerve of a dog with experi mental CSa poisoning. The axis cylinders are distorted, swollen, and fragmented while the myelin sheaths still stain fairly well. (Lewy.) between the intake and the exhalation of CS2. Dissipation of the fumes at the same pace as the intake will prevent the appearance of symptoms. Artificial silk, or rayon, is made by a viscose process, which is the converting of cellulose into a gelatinous mass by the addition of sodium hydroxide and carbon disulfide. During this process, hydro gen sulfide is evolved. This by-product is less noxious and damaging than carbon disulfide. Carbon disulfide has a specific gravity of 2.62 as compared with air, and hydrogen sulfide 1.17 as compared with air. Being heavier than air, both of these substances hang in the CAUBOX DISULFIDE 117 breathing zone of llie workers. Followin';: llieir investigation, the Penn sylvania Department of Labor and Industry- set the following stand ard of the permissible limits of CS2 and Ib.S in the breathing zone of the, workers: 10 parts per million for CS2. when existing alone, and 10 parts per million for IDS, when alone. If combined, then 5 parts per million of each. Pathology.--Primarily this gas produces severe neural poisoning. This can be understood when it is realized that CS2 is a strong solvent for fat and that the neural tissue function is dependent upon the lipoid set-up in the nerve fibers, myelin sheaths, and cytoplasm (Figs. Fig. 2!).--Cross-section of the sciatic nerve of a dog with experimental CS2 poisoning. The myelin is swollen and fragmented. The axis cylinders are unequal in diameter, some swollen while others are extremely thin. (Lewy.) 28, 29). Any portion of the nervous system may be affected, thus accounting for involvement of the sensory (Figs. 30. 31), motor, mental, or psychical functions. Blood changes following disulfide ex posure and intoxication arc for the most part consistent with a sec ondary anemia, but no typical picture can be adhered to except for a more or less uniform abnormality of the monocytes. These show a relative and absolute increase in numbers, as well as characteristic alteration in the morphology and staining properties. They contain multiple minute neutrophilic granules and often numerous vacuoles. Creskoff2 termed them "toxic monocytes" and felt that their presence in the blood picture was indicative of a pathological state. 118 OCCUPATIONAL DISEASES Fig. 30.--Dog IGo. After six-weeks exposure to 400 parts per million CSg. eight hours daily, five days a week. The animal is unable to stand on its forelegs with the back legs supported. The (log is in partial flaccid paralysis. (Dewy.) Fig. 31.--Same dog unable to stand on hind legs with the forelegs supported. (Lewy.) DIAGNOSIS Signs and Symptoms. Acute intoxication is rare in industry. In the mild to moderately severe eases the picture is that of alcoholic intoxication, with headache, nausea, reeling, giddiness, talkativeness, laughing, crying, or stupor. More severe cases may continue through this initial stage into coma and death. CAIIBO.Y BISULFIDE 119 Chronic Intoxication.--The following table is reproduced from the study of 159 viscose rayon workers and taken from the aforemen tioned Pennsylvania study. Table 10--1 ndiuated Symptoms or ('arson' Disulphide and Sulphuretted IIydrookn Poisonino Totaled from (Questionnaires of 1.5!) Viscose IIayon Workers (8i I. Itrain: Restlessness................................................................................. Talkativeness....................... ............ .. Easy excitability............................................. .... . .. Irritability................................................................................. Change of character.................................................. Apathy..................................... ............................................. Withdrawal................................................................................. Chronic fatigue................................... .................................... Depression................................................................................. Listlessness.................................................................................. Difficulty of concentration................................................... Forgetfulness.............................................................................. Partial loss of memory................................... .......................... Headache...................................................................................... Vertigo.......................................................................................... Insomnia................................................................ ..................... Day drowsiness.......................................................................... Hallucinations: sight, hearing..................................... Ideas of persecution.................................................................. II. .Verves: Hands heavy............................................................................... Hands numb and tingling................................................ Weakness of muscles; legs, arms. . .................... ................ Loss of sensation....................................................................... Difficulty going upstairs.......................................................... Muscular pain............................................................................ III. Disturbance of Vision: Dimness of vision...................................................................... Cloudiness of vision.................................................................. Narrowing of field of vision................................................... Change in color perception..................................................... Double vision............................................................................. IV. Digestive System: Loss of appetite......................................................................... Loss of weight............................................................................ Indigestion................................................................................... Pain in stomach........................................................................ Nausea.......................................................................................... Constipation............................................................................... Diarrhea...................................................................................... Vomiting............................. ........................................................ Shortness of breath................................................................... Pain behind breast bone......................................................... Abdominal pain..................................................................... Palpitation................................................................................... Ulcer of stomach (reported)..................................... ............. V. Characteristic Color of ('omplexiou.......................................... VI. Reported I.oss of Libido............................................................. VII. Significant Symptoms of Sulphuretted Hydrogen Poisoning: Irritation of eyelids.............................................................. .. Inflammations of eyelids......................................................... Pain in eyes................................................................................. Feeling of sand in eyes............................................................ Photophobia................................................................................ Tearing or burning of eyes ................................................... Haloes around lights................................................................ . 11.5 . -27 . 100 . 120 . 00 . SO . 78 . 118 82 . 81 . 81 . 87 . 2!) . !)!) . !>7 . 10!) . 99 -l!) . 1.5 . 50 57 91 18 05 98 0.5 01 7 7 12 08 70 92 03 59 91 12 10 34 31 21 23 0 38 50 .50 72 .54 08 01 31 34 120 OCCUPATIONAL DISEASES () Disturbance of Vision.--Of this vast and varied symptoma tology just outlined, one of the most frequent and earliest disturb ances noted is altered vision. Objects become indistinct and appear to be veiled in a color fog. Failure of vision is fairly rapid. In a report of his phase of the investigation llobb McDonald states-: The failure of vision or amblyopia is known to be produced by several exogenous toxins, such as lead, carbon disulphide, tobacco, and alcohol. Fortunately, a. differential diagnosis between these poi sons by means of special examinations as the determination of the fields of vision, especially the central holds, is usually possible. Carbon disulphide causes a scotoma (a blind area) in the center of the visual field where the vision is most acute. This is called a central scotoma and it has several characteristics that distinguish it from the scotomas due to lead, nicotine, or alcohol. Some of these toxins also cause a con traction of the peripheral field of vision. The. loss of vision comes on more rapidly in carbon disulphide intoxication than in any of the other intoxications and also shows more rapid improvement if the source of intoxication is removed. These changes in the visual acuity are due to carbon disulphide affecting the optic nerve or the visual cells of the retina. Chronic mild inflammation of the optic nerve may cause an enlargement of the blind spot. (This is a small blind area in the field of vision denoting the area where the optic nerve enters the back of the eve. It is present in every eye and must not be confused with a central scotoma which was mentioned above.) In some affections of the optic nerve, an en largement of the blind spot precedes the development of a central scotoma. In the observations during the viscose rayon survey, approxi mately' one-half of the workers gave a history of some ocular trouble. However, no one was seen in whom diminution of vision could be objectively proven to be due to a central scotoma. Two gave a history very suggestive of having had a central scotoma at some previous time and one was found to have poor central color vision. Enlargement of the blind spot was found in slightly less than onequarter of those examined and was found with greater frequency in those employed in the churn room than elsewhere. This phenomenon has not previously been noted in the literature on carbon disulphide intoxication, and may be of significance, when present, in establishing an early diagnosis. (6) Disturbance of Hearing.--Batson- concluded that the endorgan of hearing was not ordinarily disturbed, but the inability to fix attention by those intoxicated resulted in a pseudo loss of hearing. (c) Blood Chemistry.--A study of the blood chemistry of these patients revealed an increased serum cholesterol above the average CAIiliOX MSUI-FIDE 121 and a decreased percentage of esterified cholcslerol, no matter what the severity of their intoxication. For a variable period after exposure the blood and urine contained a significant and determinable amount of CSo. (d) Composite Symptomatology.--As this book goes to press, Gordy and Trumper,:i who deserve much credit for their constant con tributions to knowledge of this solvent, augment their previous re ports with twenty-one additional cases. The symptomatology noted by them in these cases is as follows: 90 per cent showed cncephalopathic features varying from lethargy, anxiety states, and irritability to vertigo. One of these was frankly psychotic; practically 75 per cent showed diminution or loss of libido; 70 per cent revealed varying de grees of neuropathy; and 07 per cent had subjective eye symptoms; more than two-thirds had gastro-intcstinal disturbances; more than half, varying degrees of asthenia, headache, muscular stiffness, and dyspnea; and a few had a picture simulating angina pectoris; 55 per cent of these victims had symptoms which pointed to localized lesions of the central nervous system, including parkinsonism; 30 per cent had vasomotor symptoms, and a similar percentage showed blurring of the optic disc. Differential Diagnosis.--One should be very reticent about ac cepting a case as one of carbon disulfide poisoning because of its rare use. Alleged cases demand immediate contact with the plant or in dustry to certify its presence or absence in the patient's working con ditions. Among the aids to differential diagnosis of CSo poisoning, the reaction of corneal and pupillary reflexes ranks first. Corneal. Reflex.--Marked decrease or loss of the corneal reflex, especially if bilateral and not accompanied by sensory disturbances in the distribution of the fifth nerve, is an extremely rare event in dis eases other than CSo poisoning. Pupillary Reflex.--The same consideration holds true in relation to the pupillary reflex in absence of syphilis, epilepsy, or an intra cranial mass lesion. Neuropathy.--Finally, in a polyneuropathy, especially with predi lection for the peroneal nerve, CSo poisoning should be considered when other causes have failed to explain the disease. The combination of polyneuropathy with a Korsakoff psychosis gives a picture almost identical with CSo poisoning. Strangely enough, alcoholism is rare among viscose rayon workers. Syphilis and Tabes.--Diminution or loss of patellar and pupillary reflexes, ataxia, shooting pain in the legs, and loss of libido may raise the question of differential diagnosis between cerebrospinal syphilis H3 OCCUPATIONAL DISEASES or tabes iind ('So poisoning. However, in uncomplicated CS2 poison ing the Argyll ltobcrtson type of pupillary reaction and the charac teristic reactions in blood and spinal fluid are absent, and loss of vibratory or position sense has not been observed. Multiple Sclerosis.--Differentiation between multiple sclerosis and CSo poisoning, though often impossible in the. beginning, is not diffi cult in a fully developed case. So, also, the differential diagnosis against post-encephalitic parkinsonism and senile paralysis agitans is difficult only in the early stages. Various Erroneous Diagnoses.--It may best serve the purpose of pointing out how to avoid a wrong diagnosis to enumerate some erro neous diagnoses recorded in various hospitals on histories of patients who were actually suffering from chronic CS2 poisoning: ovarian de ficiency because of loss of menstrual period and vicarious severe head ache; pituitary tumor because of loss of vision, pallor of disks, loss of libido, temporal headache; mastoid disease or tumor of the auditory nerve because of ringing in the ears, subjective deafness, and vertigo; thyroid gland disease because of tremor, profuse sweating, and loss of weight; tuberculosis because of loss of appetite, cough, shortness of breath, and night sweats; blood disease because of increased number and pathological forms of monocytes. Importance of Questioning Patients.--It may be difficult to diag nose chronic CS2 intoxication if the physician does not ash for and the patient does not mention the hazards of his occupation. The oc currence of CS2 poisoning and the opportunity for frequent contact with persons suffering from the effect of this poison are obviously linked with a comparatively small number of industrial centers. Many an experienced practitioner and specialist will never actually see a case of CS2 intoxication. Nevertheless, carbon disulfide is now a recognized industrial poison in this country. It is, therefore, important that every physician question his patients about their past and pres ent occupation and keep himself fully acquainted with industrial haz ards and occupational diseases. This cannot be overemphasized. MEDICOLEGAL ASPECTS Temporary Disability.--Effects from mild exposure tend to dis appear soon after removal from the exposure. Permanent Disability.--This is not to be expected in the majority of cases. No conclusions have been drawn regarding the psychiatric stigmata of carbon disulfide intoxication. Concerning the peripheral neuropathies, weakness and paralysis of the muscles return to normal gradually when exposure is no longer encountered. Advanced paralysis may take from nine months to two years for recovery. The expectancy & CABBOX DfSULFIDK 123 for full recovery from most of the neurological disturbances is good, although from months to several years may be required. This may also be said for visual damage. Illustrative Cases.--Several patients have presented themselves presumably suffering from exposure to carbon disulfide. In most in stances this has been erroneous assumption, as illustrated by Case I. Case I.--A fifty-six-year-old refrigerator repairman was suddenly seized with severe chest pain, became cyanotic and extremely short of breath. He was taken to a nearby physician by two fellow-workmen who informed the physician that the patient had been exposed to carbon disulfide. The physician administered artificial respiration and then transferred the patient to this clinic. While the patient was being examined, an associate immediately contacted the employer by phone to learn that carbon disulfide was never used in that plant, although sulfur dioxide was, but that this particular patient had not been ex posed even to this latter gas. The clinical picture was typical of coronary thrombosis, and the electrocardiogram was confirmatory. Death occurred twenty-two hours later, and the autopsy revealed a fresh thrombosis. According to the physician, either the fellow-workmen of the pa tient told him of exposure to carbon disulfide, or he misunderstood what the workmen said. Obviously his treatment was contraindicated in coronary thrombosis. A moment expended to call the plant to ascer tain the type of exposure would have been expedient. The case was not compensable. It is used here to emphasize the need for immediate investigation of the hazard and thus avoid faulty assumption. Case II.--A twenty-four-ycar-old woman was employed in the printing of "decap" paper. This paper is covered with a gelatinous coating which protects the printing underneath, but which upon wet ting reveals the letters or configurations underneath, and the process enables the printing to be transferred to other substances, especially glass. They are designed to transfer printing or figures to windows, windshields, and the like. In the formation of the gelatinous mass, carbon disulfide was used. In order for the process to function prop erly, a dry room free from air currents was necessary. It appears that this company was newly formed and inexperienced in the process. The girl had been with the organization since its inception, which was five weeks. Present Illness.--For several weeks she had noticed a loss of appe tite, and on several occasions, particularly at the noon hour, she noticed when she went outside to eat her lunch that she seemed light headed, was inclined to be giddy, which was noticed by her fellow- 124 OCCUPATIONAL. DISEASES employees. One day at the noon hour she appeared to be unsteady on her feet and "felt drunk." Upon returning to her afternoon work she became slightly hysterical, first laughing and then crying. She was sent home, and upon arrival felt numb, and her limbs seemed heavy. Numerous aspirin tablets were taken to relieve a pronounced head ache and pains over both kidney areas. On the following morning she felt greatly improved, the improvement continuing throughout the day. On the second day following the onset, she felt "practically normal," but reported to a physician because she had not urinated since the afternoon or her leaving work. Further inquiry brought out that she had dull pains in both flanks and was depressed mentally. Past History.--Negative for illness except an appendectomy in 1924; divorced, no pregnancies. Physical examination revealed a well-built, healthy appearing fe male. There were no objective findings in the physical examination. Laboratory Examination.--Kidneys, ureter, and bladder, negative for pathology. A trace of albumin in the urine; no casts or red blood cells. Hemoglobin, 85 per cent; red blood cells, 4,500,000; white blood cells, 8600, with 63 per cent polymorphonuclears. The author was too little versed in the knowledge of carbon disul fide at the time this patient was seen to subject her to certain other tests. A non-protein nitrogen test was not done, and the eyes were not examined by an ophthalmologist. Exposure was verified, and the symptoms were classical enough as we then knew them, to accept this case as one due to occupation. The patient made an uneventful recovery within a week and returned to work, but not at the same place of employment. Case III.--This case was reported by Gordy and Trumper.1 Present Illness.--A man, aged forty-nine, foreman in a viscose fac tory who worked principally in the reeling room,, first became ill in April, 1935. Headache, vertigo, rapid loss of weight, and paresthesia in his hands and feet developed. With this there was also insomnia, causeless weeping, and night terrors. He had had aching in his bones for months. For some time he felt that his mind was not working properly. Both his wife and his son had noticed that his actions had not been normal and had told him about his crying and screamingwhile sleeping and that his body shook all over. His memory was unreliable. He described episodes resembling fugues in which he would find himself at some place and could not remember how he got there. He was unable to drive a car because he was uncertain of himself. He complained of dyspnea and a sense of oppression in the chest. He also had episodes of blindness lasting for a few minutes and also double vision. He was unable to retain a position because of his memory faults. He had a marked diminution of libido. CARBON DISULFIDE 125 Examination.--The patient was fairly well built and gave evidence of having lost weight, his weight at that time being 15C pounds (71 kg.). The pupils were regular and reacted to light and to accommoda tion. The eycgrounds showed slight pallor of the temporal discs and slight atherosclerosis. The cranial nerves were normal except for mild tremor of the tongue. No ataxia or other evidence of cerebellar dysfunction was present. The biceps, triceps, knee, and ankle jerks were present and equal; there were no pathological reflexes and no dis turbances in any of the modalities of sensation. Blood 'pressure, 150 systolic; 100 diastolic. Mental Status.--The patient tended to lie morose, apathetic, somewhat indifferent, and his thought processes were retarded. He was oriented in all spheres, but his memory was definitely dulled. He found it difficult to place various occurrences in the past in any sort of proper sequence. He had formerly had the reputation of being a firstclass worker, with an ability to handle other employees. At the time of examination he had a marked lack of initiative and a sort of child like dependence on others. A man who worked with viscose and was subject to chronic ex posure to carbon disulfide fumes suffered headaches, vertigo, loss of weight, paresthesias, insomnia, causeless weeping, night terrors, fugues, petit mal episodes, depression, impairment of memory, loss of initiative, and impairment of libido. The neurological examination was negative. The case was compensable. TREATMENT Prophylaxis.--The most important point is prevention of such poisoning. Preventive measures consist primarily of rigid examina tion of the plants, to insure modern, safe equipment and the presence of adequate ventilation. The storage and pipe conveyance of carbon disulfide must be satisfactory, and explosions should be guarded against. Medical examination of those exposed to this hazard should be at intervals not greater than one month. Men should be taught to report the first intimation of any unusual symptom; and if this solvent is the suspected cause of the complaints, the employee should be at once removed from the hazard. The drinking of alcoholic bev erages by those apt to be exposed to carbon disulfide should be dis couraged. Diet.--To date no adequate or specific treatment for cases of chronic carbon disulfide poisoning is known. It would seem likely in view of the similarity of many of these cases to Korsakoff's syn drome, that a diet high in vitamin content with the vitamin B com 126 OCCl'PATIOXAL DISEASES plex as ail adjunct would bo of value. If vitamin B complex is to be used, tile dosages should be relatively large, <?.</., from 50 to 60 mg', of thiamine chloride parenterally daily; 200 mg. of nicotinic acid daily; riboflavin. 1 mg. three times per day; vitamin B, 20 mg. twice daily parenterally, and so on. Liver extract, in dosages similar to those advised in the chapter on "Manganese" might be tried. Psychiatric and Ophthalmological Attention.--The aid of a psychi atrist will be needed for most of these patients, since a program of mental hygiene will need to be instituted. The ophthalmologist should be consulted on problems related to the eyes. Exercises for existing muscular weakness, sedation and tonics may be of value. If parkinsonian-like symptoms are present, a trial of those drugs mentioned in the chapter on "Mercury" for control of these manifestations might be made. The acute case will rarely be seen. When such a case does occur, artificial respiration, from 5 to 7 per cent carbon dioxide in oxygen inhalations, and the respiratory and circulatory stimulants mentioned in the chapter on "Petroleum Hydrocarbons" are used. REFERENCES 1. Gordy, S. T., and Trumper, M.: "Carbon Disulphide Poisoning, with Report of Six Cases," J.A.M.A., 110: 1543-1549 (May 7), 1938. 2. Group Study: "Survey of the Carbon Disulphide and Hydrogen Sulphide Hazards in the Viscose Rayon Industry," Bull. 46, Department of Labor and Industry, Pennsylvania, 1938. 3. Gordy. S. T., and Trumper. M.: "Carbon Disulphide Poisoning. Report of TwentyOne Cases," Inilust.. Med., !): (May), 1940. CHAPTER VIII THE CHLORINATED NAPHTHALENES AND DIPHENYLS The chlorinated naphthalenes are naphthalenes in which one or more of the hydrogen atoms has been replaced by chlorine. Occupational Hazards.--In industry they usually occur in mix tures in which more than one chlorinated product is present. In the manufacture of the chlorinated diphenyls, C(iH(i is converted into Ci 2H1 o, which in turn is chlorinated into Cl2Cl, (). The higher the chlorination, the higher the toxicity. These substances are non-in flammable and are resistant to a high degree to heat, moisture, and electricity. Because of this they are used extensively in wire insula tion and electrical condensers. DIAGNOSIS Signs and Symptoms.--A common reaction to exposure to these chlorinated naphthalenes and diphenyls is an acneform, skin eruption which is rather characteristic. Systemic reactions are not frequently reported and are not well understood by the general profession. Ani mal experimentation would indicate damage to the liver, especially if there had been previous liver damage. Drinker, Warren, and Ben nett1 showed that their animals revealed no significant liver changes until extremely high concentrations were used. Prolonged exposure to high concentrations brought about death with severe jaundice in evidence. The liver at autopsy showed central fatty degeneration with necrosis of the liver cells. In these rats which showed the marked liver changes, no other organs were involved, apparently. Exposure in Presence of Liver Dysfunction.--Greenburg2 and his associates had the good fortune to study three fatal cases with acute, yellow atrophy in which this exposure existed and was considered the etiological factor. They emphasize the lack of knowledge concerning these substances and note the infrequency of case reports. They pointedly cite the case of a young woman who had been exposed to the chlorinated naphthalenes and had developed a jaundice. After a long, serious illness, the girl, according to her physician, was on her way to recovery and within a few weeks would be able to return to her former work. They intimate that the physician had never in quired into her employment and was unaware of the especial danger of exposure to the chlorinated naphthalenes in one who had had liver 127 1-28 OCCUPATIONAL DISEASES dysfunction. Tn their three cases they were unable to locate any previous predisposing cause for the liver atrophy. In two of the three cases there had existed previous hepatitis from this exposure. They concluded their investigation with the following recommendations: 1. Persons suffering from typical acneform eruptions should be removed from further exposure. 2. Persons who have had. at any time in the past, jaundice of even a mild type should not work with these substances. They urge that workers who have, had typhoid fever, malaria, gall stones, or other diseases known to affect the liver, be forbid- S den to work in this exposure. 3. Persons receiving arsphenamine or other drugs known to affect i the liver should not be further allowed to work with poten tial liver poisons. (Certainly this is a worthwhile recommen dation which might be applied to all workmen engaged in handling the solvents but one which has escaped any emphasis.) 4. Persons working with the chlorinated naphthalenes and di phenyls should not be subjected to chloroform or avertin anesthetics; or persons who have been subjected to such anesthetics should not be immediately returned to their exposure. 5. Pregnant women should be immediately removed from this type of work. MEDICOLEGAL ASPECTS Illustrative Case.--The following case3 illustrates the toxicity of the chlorinated naphthalenes. Case I.--A seventeen-year-old white girl was admitted to the hos pital deeply jaundiced and in a semi-comatose condition. Other than a tonsillectomy, her past medical history was negative. Following one year of high school, she obtained a job, her only one, with a concern manufacturing electrical condensers for radios. Her work consisted in soldering condensers where she was exposed to fumes of trichloronaphthalcne and tetrachloronaphthalene. She was also subjected to fumes of the higher chlorinated naphthalenes from the scaling opera tion conducted in close proximity to her bench. Present Illness.--This began about five months before admission to the hospital, or approximately two months after beginning work in this plant, at which time she noticed several pigmented areas on her l face. These continued to increase in severity and extent, and caused ! her to visit the Out-Patient Department of the Lincoln Hospital. | where sugar was found in her urine. Upon being referred to the skin j clinic, a diagnosis of acute catarrhal jaundice was made. Her rectal THE CHLORINATED NAPHTHALENES AND DIPHENYLS 12!) temperature at that Lime was 100 F.. and there was a diffuse papulopusfular eruption on her face. From then on she suffered from in creasing weakness and nausea: the appetite was poor, and the skin became more jaundiced. Headaches developed, but she continued working until seven days before admission to the hospital. Physical Examination..--The patient gave the impression of being a colored girl. The temperature was 100 F.; pulse, 114: respirations, 2(1. Careful examination of the face and neck revealed a negroid type of pigmentation beginning in the hair line and extending down to and including the neck. The eyes revealed deep jaundice of the sclerae and the conjunctivae. The skin of the thorax and lower part of the body was a dark brown with a yellowish sub-tinge. Over the abdomen there was a girdlelike area of deeper pigmentation begin ning at the level of the umbilicus and extending down to the pelvis. Other positive physical findings were a slight injection of the throat, apical systolic murmur, slight edema of the hands and feet, abdomen distended and tympanitic, liver on percussion small, with tympany extended to the very costal edge. Laboratory Examination, (a) Blood Count on Admission.-- White cells, 9100; red cells, 4,200,000: hemoglobin, 87 per cent: lympho cytes. 20 per cent; polymorphonuclears, 80 per cent; bleeding time, 4.5 minutes: clotting time, 2.5 minutes; platelets, 220.000. (6) Blood Chemistry.--Non-protein nitrogen. 35 mg. (later 45 mg'.) per 100 cc.; protein, 0.9 mg. per 100 cc.; urea nitrogen, 20.8 mg. per 100 cc.; creatinine, 2 mg. per 100 cc.; glucose. 88 mg. per 100 cc.; cholesterol, 145 mg. per 100 cc.; calcium, 8 mg. per 100 cc.; C02 com bining power, 52 vol. per cent; icteric index. 230. Van den Bergh reaction, immediate direct reaction; Wassermann test, negative. (c) Stools.--Urobilin present, (d.) Urine.--Specific gravity. 1.008: alkaline; albumin, negative; sugar, a trace; acetone, 1 plus; bile pig ment present; urobilin, a trace; a few red and white cells. (e) Spinal Fluid.--Pressure normal; cells, 10; lymphocytes, clear; glucose present; globulin absent. (/) x-Ray examination of the heart, lungs, and bony framework, negative. (g) Gastric Contents.--Antemortem and postmortem examination revealed no arsenic, lead, tin, or antimony. A trace of phosphates was reported, probably from inorganic phosphates ingested before ad mission. Clinical Course.--This was steadily downhill. On the evening fol lowing admission the patient went into a deep coma with CheyneStokes breathing, pupils immobile to light, deep reflexes greatly de pressed, and the liver dulness appeared diminished. The patient died two days after hospital admission. Diagnosis.--The patient presented a picture which was distinctly puzzling to all who saw her. Consideration was given to: 130 OCCUPATIONAL DISEASES 1. Obstruction to the common bile duct 2. Toxic jaundice possibly due to some dye 3. Obstruction to the inferior vena cava 4. Blood dyscrasia 5. Addison's diabetes (>. Hcmachromatosis, and finally 7. Acute yellow atrophy of liver and pancreas possibly due to an unknown industrial poisoning. Autopsy Findings.--An autopsy was performed at the Medical Examiner's office by Dr. Charles H. Iiochman, Assistant Medical Examiner. The report in full was as follows: Body is that of a white, adult female, well developed and nour ished. Cyanosis of lips, ears, and fingernails. Marked pigmentation about eyes, lower lips, neck, and abdomen. General icteric tinge to entire body. No evidence of violence. Some edema about the ankles. Hair is black. Eyebrows black. Brown iris. Conjunctivae and sclerae icteric. Rigor mortis present. Postmorten lividity of dependent parts. Scalp incised and reflected, calvarium removed. Brain found con gested. Meninges bile-tinged. On section, no evidence of intracranial injury or hemorrhage. Dura stripped and reveals no evidence of frac ture. Body opened in usual midline incision. Sternum removed. Some remnants of thymus still present. Lungs are free. Bronchi contain a bloody mucus. Mucosa injected, has yellowish tinge. Hemorrhagic infarct about the size of a hen's egg in left lower lobe. This is airless and dark red in color, and firm. There are also similar smaller areas in other lobes. Heart is small and shows some sub-epicardial hemor rhages. Some hypertrophy of left ventricle. Valves thinned. Arteries natural. All are bile-stained. No significant findings in myocardium or coronary arteries. Esophagus is natural. Stomach is distended, contains some dark material. The rugae are somewhat hypertrophied. The duodenum con tains green chyme. The ampulla is patent. The jejunum, ileum, and large gut are natural. Many petechial hemorrhagic areas noted in the mesentery with some enlargement of mesenteric lymph nodes. Liver is small, weight 720 gm. Capsule, wrinkled. Right lobe on section shows areas of yellow surrounded by red areas. Left lobe much firmer although liver cuts firmly throughout. All ducts patent. Gallbladder small. Wall thickened throughout. Pancreas is natural in size, somewhat congested. Spleen is natural in size. On section, firm, dark red in color. Follicles are somewhat in distinct. Kidneys show swollen cortex. Evidence of parenchymatous degeneration of epithelial cells. Capsule strips easily. No granulation. Degenerative changes in cells of glomeruli only. No glomerulitis. Uterus is small. Endometrium bile-stained. Ovaries are natural in THE CHLORINATED NAPHTHALENES AND DIPHENYLS 131 size: right contains corpus luteum cyst. Bladder wall is somewhat thickened. Mucosa is injected. Microscopic Examination, (a) Liver.--From the size of a throughand-through transverse section one suspects that the entire liver was about one-half normal size. Liver segment is very firm and composed of two distinct and peculiar types of tissue: (1) that constituting major portion of parenchyma is red in color, firm and elastic in consistency; (2) other areas are light yellow and are scattered indiscriminately throughout reddish areas. Yellow areas from one-half inch to two inches in diameter. External surface of liver, judging from this por tion, was smooth. A typical picture of clear sub-acute, yellow atrophy is revealed. Slides show that red area is composed of so-called "red atrophy" in which all the liver cells have disappeared, their place being occupied by their normal supporting stroma, which seems to have been spared, great numbers of blood cells, early fibroblastic proliferation and older scar tissue. Tn these red areas, numerous bile ducts are seen. These also seem to have been spared destruction. The yellow areas are com posed of actively regenerating islands of liver cells. The toxin evidently has destroyed most of the liver cells, leaving intact their supporting stroma, blood vessels, and bile ducts. The latter seem to be regenerated. Those liver cells spared destruction have regenerated and have formed yellow islands seen in the gross picture. There evidently has been one or more attacks of hepatitis judging from the different ages of the pathological process in various parts of the liver. (6) Skin.--Shows an increased density of corium which stains deeply with eosin. Some of the epidermal cells arc slightly deeper in corium than normal. (c) Heart.--Shows mild parenchymatous myocardial degenera tion. (d) Kidneys.--Show severe epithelial degeneration involving ep ithelium of tubules and glomeruli. No inflammatory reaction of glomeruli. (e) Adrenals.--Show severe parenchymatous degeneration of cells. (/) Pancreas.--Shows intense degeneration of cells of acini and of islets. Summary.--An unknown toxin has evidently caused a severe dif fuse cytolysis involving most of the organs, predominantly the liver. The latter has evidently undergone and recovered from previous at tacks of a similar nature. Too few cases of this type find their way into the literature in such a completely studied manner. It serves not only as a study of the effects of the chlorinated naphthalenes but to reiterate the effect the solvents have upon the body, especially the liver. 132 OCCriWl'IOXAL DISEASES TREATMENT Prophylaxis.--It should bo constantly reiterated that the primary Ireatment is prevention. Ventilation should be proper. As indicated in the foregoing chapter, the recommendations of Greenburg and his associates concerning the type of person to be employed where this hazard exists should be followed. The knowledge of an existing hazard by both the employer and the employee, and the recognition of cer tain early symptoms by the workman, will greatly reduce actual in toxication. Obviously this is an educational program. No specific therapy has been evolved for these cases. The acneform skin, lesions and the liver damage are the two symptoms toward which treatment is chiefly directed. Skin Lesions.--Prevention of the papulopustular skin eruption may frequently be accomplished by installation of showers, and by the formulating of rules requiring a change from street clothing to work clothing at beginning of the day's work, and, following a shower, a change back to street clothing at the end of the work period. The most satisfactory treatment of the skin eruption, once it has occurred, consists of quartz light and rr-ray therapy, together with mechanical removal of the comedones. The worst cases are treated with quartz light each day for from fifteen to twenty minutes, the less serious ones three times per week, and the mild ones once per week. ar-Ray therapy should be directed by the radiologist or dermatologist. The pustules should be opened, and these might respond well to the use of sulfathiazole powder or ointment locally. Extreme body cleanliness should be practiced. Cases of very resistant exfoliative dermatitis have been described in which the use of sodium thiosulfate, splenic extract, cal cium gluconate, autohemothcrapy. roentgen therapy, and numerous baths, powder, and ointments were of little avail. Liver Disorder.--This may be treated much as described under "Tetrachlorethane," the chief points being a high carbohydrate, high protein diet with adequate fluid intake, and particularly intravenous infusions of 5 to 10 per cent glucose in saline in amounts of from 2000 to 3000 cc. or more daily. The use of calcium and of sodium xanthine experimentally has been of no value in prevention or treat ment of the liver damage due to the chloronaphthalenes 4 This differs, for example, from the treatment of carbon tetrachloride poisoning in which calcium products are of much value. REFERENCES I. Drinker. C. TC.. Warren. M. F.. and Bennett. G. A.: "Problem of Possible Sys temic Effects from Certain Chlorinated Hydrocarbons." ./. Iinlusl. ling, mid Toxicol.. 19: 2S3-31V (Sept.). 1927. THE CHLOItINATED NAPHTHALENES ANI) DIPHENYLS 13.`5 2. Greenbnrf;. L.. Mayers. M. R.. ami Smith. A. R.: "Systemic Effects Resulting from Exposure to Certain Chlorinated Hydrocarbons." J. Indiixl. Ih/ij. and Toxicol., .'I: >!)-:! (Feb.). 1939. !). Ibid.: Taken by Green bur from the services of l)rs. Kenneth Taylor. Edwin Hauser, ami Scott. Johnson of the Lincoln Hospital. New York. L Drinker. Cecil K.: "Possible Systemic Toxicity of Certain of the Chlorinated Hy drocarbons with SufiKestions for Permissible Concentration in Air of Work rooms." J. hidiixt. Ihjr/. and Toxicol.. II: la.) (May). 1939. CHAPTER IX TETRACHLORETHANE AND TRICHLORETHYLENE The vapor from tetrachlorethanc (C-TECE) is six times heavier than air and is industrially prepared by the action of chlorine upon acetylene. Occupational Hazards.--It is an excellent solvent for fats, gums, and especially for cellulose acetate. It is by far one of the most dan gerous of the chlorinated hydrocarbons. It smells like chloroform, is absorbed easily and slowly, with prolonged after-effects. Pathology.--In animal experimentation it produces fatty degenera tion of the liver, kidney, and heart. In the human, its usual effect is the production of acute yellow atrophy. The outstanding lesions found at postmortem examination are those of acute cirrhosis and atrophy of the liver, fatty degeneration in the kidneys and heart, hemorrhage into the lungs and serous membranes, and edema of the brain. Hamilton1 reports a case of a girl making safety frames for goggles with celluloid dissolved in a mixture containing 30 per cent tetra chlorethanc. Almost at once she felt nauseated and after four days was forced to stop work because of gastric distress. Following a few days' rest at home she returned to another job but in the same room. She became jaundiced, but continued to work for two weeks and then became rapidly worse, dying in ten days. The immediate cause of death was hemorrhage into the mucous membranes, especially the stomach, which led to the observation that benzene may have been present in the mixture. Autopsy, however, revealed a marked atrophy of the liver. Diagnosis. Signs and Symptoms.--Excessive concentration gives an initial warning by lacrimation, salivation, and irritation of the nose. Continuation in the exposure will result in restlessness, general ner vousness, dizziness, nausea, or vomiting and coma. I11 the acute stage of the poisoning, the diagnosis is greatly aided by the blood picture, which shows a progressive increase in the mononuclear cells, some times reaching 40 per cent, a slight elevation in the white cells, and a progressive anemia. Experimenters have stated that the narcotic action of tetrachlorethanc is similar to chloroform but the hemolytic effect is seven times that of chloroform. Medicolegal Aspects. Temporary Disability.--If the exposure has not been immediately fatal, the noil-fatal and the eventually fatal i:u TETHACIILOUETHANE AND TlilCIILOHKTIIVLEXE 135 cases run a similar course, according to Zollinger.- This period may he from three days to three months. After this time, in tile non-fatal cases, the symptoms gradually decrease, and recovery takes place. Fatal types enter into a second stage of exacerbation of symptoms and finally pass into a third stage of coma and death. Zollinger calls the first stage of from several days to several months the "early prejaundice.'' The second stage is jaundice without toxemia, whereas the third stage is jaundice with increasingly severe toxemia. He, as well as others, agrees that when jaundice is severe the patient will not recover. Permanent Disability.--If the exposure is not immediately fatal and the victim survives the non-fatal period of several months, there is no permanent disability, for recovery appears to be complete. Treatment.--The chief concern in formulating a therapeutic reg imen is directed toward the improvement of liver function. Diet.--The patient should be given a diet high in carbohydrate, since this food factor aids in the regenerative process of the injured parenchymatous cells. In addition, the inclusion in the diet of foods high in protein is indicated, since recent research3-" indicates a pro tective action to the liver of diets high in protein. The ability of the liver to deaminize and metabolize amino acids appears to be normal up to the very last stages of hepatic insufficiency. The fat content of the diet should be low; from 200 to 250 gm. of carbohydrate and from 1.5 to 2 gm. of protein per kilogram of body weight should thus be included in the diet. Infusions of Dextrose.--It is of particular importance when severe or even moderate liver damage is present to administer by intra venous infusion from 5 to 10 per cent dextrose in physiological saline solution or in distilled water, preferably about 3000 cc. daily. It may. in very acute cases, be necessary to give such infusions by continuous intravenous drip. Vitamin K and Bile Salts.--The use of 2-niethyl-l,4-naphthoquinone (synthetic vitamin K) and of bile salts has been suggested. Vitamin K may be given orally or parenterally in doses of from l to 4 mg. daily, and the bile salts arc administered orally in dosages of from 2 to 3 gm. of desiccated whole fresh bile. Prior to the administra tion of these substances the prothrombin level of the blood should be determined, and a subsequent check on this reading will indicate whether the vitamin K is of value in the individual case. On the question of the value of vitamin K in such cases there is considerable disagreement. There is evidence to indicate that if hepatic injury is severe enough, vitamin Iv is not effective in correcting the prothrombin deficiency.3 Since, however, little toxic reaction to vi- 130 OCCUPATIONAL DISEASES taniin K or to whole fresh bile occurs, their trial use is suggested."- s In eases of hemorrhage, blood transfusion is indicated, and for secon dary anemia, if present, enteric coated tablets of ferrous sulfate. 5 grains (0.32 giu.), two tablets three times daily should be used. The intravenous administration of 10 ec. of a 10 per cent solution of cal cium gluconate twice daily will be of value. The oral use of T2 gm. calcium gluconate or 8 gm. calcium lactate will supply about 1 gm. of calcium daily. Under normal conditions the daily calcium requirement is from 0.5 to 1 gm. REFERENCES 1. Hamilton. A.: Industrial Toxicology, Harper and Brothers, Xew York. 1934. 2. Browning. K.: Toxicity of Industrial Solvents, Medical Research Council of In dustrial Health Research Board. Chemical Publishing Co., Xew York. 1938. 3. Bollman. J. L., Butt. H. It., and Snell, A. M.: "The. Influence of the Liver on Utilization of Vitamin IC" J.A.M.A., llo: 1087 (SepL. 281. 1940. 4. Goldschmidt, S., Yars, H. M.. and Ravdin, I. S.: J, Clin. Investigation, IS: 277 (May), 1939. a. Miller. L. L., and Whipple. G. H.: "Chloroform Liver Injury," Am. J. M. Sc., 199: 204 (Feb.). 1940. G. Messenger, AY. J.. and Hawkins, AY. B.: "Arsphenamine Liver Injury Modified by Diet." Am. J. M. Sc.. 199: 2GG (Feb.), 1940. 7. Townsend, AY. R.. and Mills, F. S.: "Hemorrhagic Tendency Associated with Prothrombin Deficiency and Its Treatment with A'itamin K and Bile." Canad. M. A. J., id: 541 (June), 1940. 8. Butt. II. R., and Snell. A. M.: Vitamin IC, AA\ B. Saunders Co.. Philadelphia, 1941. TRICHLORETHYLENE Trichlorcthylene. belonging to the group of chlorinated hydrocar bons of the aliphatic series, of which chloroform is the best-known representative, is produced from ethylene by the replacement of three hydrogen atoms with chlorine. It is insoluble in water, but mixes freely with alcohol, benzene, acetone, and other organic solvents. It vapor izes easily at room temperatures, is relatively stable in air and noninflammable. but under certain physical and chemical conditions it may decompose, with the formation of hydrochloric acid. In contact with naked flame, phosgene is formed, as will be illustrated later by a specific instance. Trichlorethylenc is fast becoming a popular in dustrial solvent. Occupational Hazards.--In drycleaning it is replacing gasoline, naphtha, or benzene since it is non-inflammable, is readily recov ered, and no excessive loss occurs. It is also replacing carbon disulfide in the extraction of fats and oils. Some common uses are to obtain oil from olives, corn, cottonseed, and linseed: extracting certain properties from wool, silk textiles, and leather; as a solvent for tar. pitch, and resins; as an admixture with rubber cement for adhesive TETRACHLOliETllANE AND TlilCllLOliETUYLENE 137 purposes (crepe soles): as an insecticide: and on a large scale as a solvent for garbage, tankage, and bones. Pathology.--Postmortem examination of a victim to sudden, severe exposure may reveal nothing of note. Several such negative autopsies have been so reported. Animal experimentation and the tissue of a number of humans reveal generalized congestion of all organs. Edema of the lungs and petechial hemorrhages occur. If death is delayed sev eral days, fatty degeneration of the liver, kidneys, and heart is in variably present. Chronic exposure results primarily in affecting the central nervous system. By searching the literature the writer found the following lesions reported by different observers: retrobulbar neuritis, neuromyclitic complex, paralysis of the hyoglossal nerve, polyneuritis of the limbs, amblyopia with central scotoma, paralysis of the sensory fibers of the fifth nerve, partial or complete destruction of vision, and paresthesia of different areas. Atrophy of the liver is not frequently reported. Diagnosis Signs and Symptoms.--The initial effects from small, minute dos ages arc similar to those from chloroform, namely giddiness, excite ment, or confusion, to be followed by narcosis or death if the exposure is intensified or prolonged. Constant exposure of the skin results in extraction of the fat from the skin and subsequent cracking, dry dermatitis. Stuber1 collected 2S4 cases of poisoning by trichlorethylene, 202 being acute and 84 chronic. Of this group 25 were fatal. She lists the feeling of drunkenness, confusion, mental dulness, nausea, and vomiting among the more frequent symptoms. Of the fatal cases one patient supposedly died of phosgene poisoning. General fatigue, loss of appetite, dyspnea, and unexplainable pain in the chest are addi tional complaints. Psychic disturbances with epileptoid seizures have been reported. As mentioned under "Pathology," partial or total blindness is a common sequela. Medicolegal Aspects McCord- established 10.000 parts per million parts of air as defi nitely narcotic to man. Temporary Disability.--From mild exposure, recovery may occur within a few hours or a few days. In severe cases, recovery from symp toms of headaches, dizziness, nausea, paresthesia, and the like, may be expected after a few weeks to several months. Permanent Disability.--Permanent disability is usually the result of an involvement to varying degrees of the optic and trigeminal 188 OCCUPATIONAL DISEASES nerves. Ratings should not be made until the condition shows evidence of being stationary. However, the reader is warned against hastily accepting an eye disability as one resulting from undue exposure to trichlorethvlene until this source has been proved as the cause to the exclusion of all other factors. With the increasing use of this solv ent it can be foreseen that many victims of optic atrophy will assume the cause as occupational anti relate it to some previous exposure to trichlorethylene. An equitable decision on the part of the physician will require careful evaluation of the occupational factors as well as elimination of the common causes of optic atrophy, such as tabes, paresis, atrophy following skull fracture, focal infection, diabetes, hypertension, anti other noil-occupational conditions. Illustrative Cases: Case I.--A young man presented himself at the clinic with an extremely dry dermatitis involving the palmar and dorsal surfaces of both hands, as well as the flexor and extensor surfaces of the lower third of the arms. Numerous fine cracks were in the skin. He had been under treatment for epidermophytosis without success. Inquiry re vealed that for the past several months the involved portion of his body was exposed to trichlorethylene. The skin reaction in this case was typically one where the tissue had lost its normal oil content. It was known that the solvent he used could do this and also that no other cause for the condition was ap parent. The case was, therefore, considered of occupational origin. The condition cleared after he changed his occupation. Case II.--Two Negroes were assigned the task of cleaning machin ery parts in a large tank containing trichlorethylene. One of these was but slightly exposed since he was required to carry and stack the parts after they had been cleaned. The other man worked over a tank of this solvent in the far corner of the plant where ventilation was poor. This was the first day this work was undertaken, and after about two and one-half hours, the Negro engaged in the actual cleaning fell over onto the floor unconscious. Rushed to the hospital, he arrived in a semi-comatose state. He could be aroused but could not answer questions. There was a two-inch gash over the right temporal area. The patient's partner described the work these two had been doing and volunteered the information that the patient complained of being dizzy and "acted drunklike.'' Further examination disclosed profuse perspiration; deep, slow respirations, which were increasing in fre quency as the examination proceeded; heart rate of 86; blood pressure. 102/70. While the examination was being conducted, the plant fore man was reached by phone and after slight delay informed us that TETRACIILORETHAXE AXI) TKICHLORETHYLEXE 139 the .solvent was triehlorethyleno. Oxygen was then administered. The patient became mentally clear within a half hour only to vomit fre quently for the next several hours. During this time he complained of severe headache and epigastric pain. Subsequent laboratory investi gation was not significant. He was discharged from the hospital in three days and returned to work at the end of ten days, free from symptoms. Case III.--McNally3 reports a case of narcosis in a man following five days' exposure to trichlorethylene. On the fifth day of exposure the patient "began to feel sick, went home and slept through the rest of it, all of the following day and until two o'clock in the morning of the third day." Among the various things noted in the physical ex amination were nystagmus, enlargement of the blind spot, injection of the throat, congestion of the lungs, and marked dyspnea. The pa tient made an uneventful recovery. McNally cites this case as one of phosgene poisoning resulting from the decomposition of trichlor ethylene by the gas flames used to heat the solvent. Treatment Prophylaxis.--From the standpoint of prophylaxis, several points are important. Addiction to this solvent has been reported by numer ous investigators, and it is known that men will at times voluntarily inhale it. For this reason, rotation of men should be practiced where this substance is used for long periods. In degreasing plants where heat is used, acid-proof flues are necessary to carry off the fumes to the outside. If such flues are not provided the gas heating process should be condemned. In the general use of trichlorethylene, proper ventilation should be strictly enforced at all times, and the skin should be protected by clothing and gloves as nearly as possible. It is well to apply ointments of oil or fat. for example a mixture of equal parts of vaseline and rose-water ointment, to areas such as the hands and arms, which are liable to be most exposed. Dermatitis.--For patients who present a dry, fissured type of der matitis, the chief therapy is similar to that suggested in those meas ures to be used in prophylaxis. The patient should be removed from exposure to the offending solvent until the dermatitis has cleared, and in quite a few cases it will be best to advise him to change his occupation, although careful protection of exposed parts of the body may prevent recurrence of the dermatitis. For the treatment of the acute dermatitis, simple ointments, such as rose water with l per cent phenol and 0.5 per cent menthol, may be of value. The Acutely 111 Patient. Respiratory Stimulants.--These are needed. Here, the most valuable of all will be inhalations of a mixture of from 5 to 7 per cent carbon dioxide with oxygen. When such in- 140 OCCUPATIONAL DISEASES halations arc not available, artificial respiration by the Schaefer method must be used, anti later if pulmonary edema is pvesent, the administration of oxygen either by a tent or intranasal apparatus will be of value. It should, however, be remembered that oxygen in itself is not a respiratory stimulant, and when used without the addition of carbon dioxide may actually depress rather than stimulate respira tion. The intravenous or intramuscular injections of coramine. 1.5 cc., or the intramuscular injection of metrazol. from VA to 4)4 grains (0.1 to 0.3 gm.), are of questionable value in treatment of the respi ratory failure, although their use has been advised. Shock.--They may, however, be of definite value if shock is pres ent. For treatment of this, from 1 to 2 cc. of camphor in sterile oil, or of caffeine sodium benzoate, 7'{> grains (0.5 gm.), may be used. Of much greater value will be the use of transfusions of citrated serum and the intravenous infusion of 1000 cc. of 10 per cent dextrose in saline. Diet.--Following the very acute period a soft diet and normal fluid intake may be resumed, but if symptoms of nausea and vomit ing persist the use of from 2000 to 3000 cc. daily of 10 per cent dex trose in physiological saline is advisable. The administration of thi amine chloride (vitamin Bt) in dosages of from 30 to 00 mg. daily, at first parenterally, is suggested in treatment of the neurological manifestations. During the convalescence a high caloric diet with vitamin adjuncts should be given. Exposure to Phosgene.--If the acutely ill patient has been ex posed to phosgene resulting from the decomposition of trichlorcthylene by gas flames, he may present a somewhat different picture, with pul monary edema, dyspnea, and cyanosis playing prominent parts in the picture. Here again respiratory and circulatory stimulants are indi cated. In addition, venesection of 500 cc. may be of value in treating the pulmonary edema. During the first World War intratracheal medication of from 1 to 3 drachms of the following mixture two or three times per day was found to be beneficial after the very acute stages had passed: 5 per cent each of guaiacol. camphor, and menthol in liquid petrolatum or olive oil. No instances of lipoid pneumonia from the use of this preparation are mentioned. The Gray Stage.--During the acute phase a syndrome may occur, referred to in the findings of the chemical warfare service as the "gray stage," in which pronounced pulmonary edema, almost utter inability to breathe, and shock arc seen. In such a stage the temperature falls, and there is a marked increase in blood concentration necessitating oral and intravenous administration of physiological saline solution. A fine degree of medical judgment is needed to balance the need for TETKAOHLOKETHANE AXI) TKICHLOHETHYLEXE 141 venesection on the one hand and for decrease in excessive blood con centration by administration of fluids on the other. REFERENCES 1. Stuber, K.: "Gesondheitseluidignngen bci tier gewerblichcn Yervendung lies TrichlorilUiylenes." Arch. f. Gewcrbepath. u. Geirerbcyhyg., 2: 39S. 1931. 2. McCord. C. 1'.: "Toxicity of Tiichlorelliyloiie." J.A.M.A., 0-5: 409, 1932. 3. McNally, IVm. D.: "A Case of Phosgene Poisoning," Indu.it. .1/ed., ft: ;,)39-.)4t. 1937. CHAPTER X NITROBENZENE, DICHLORODIFLUOROMETHANE, AND ETHYLENE DICHLORIDE NITROBENZENE While nitrobenzene (CoH3N02) poisoning is not a frequent in dustrial condition, it occurs often enough to warrant a short discussion in a book of this type. In general, its action is similar to the other nitro and amido compounds. Early in the literature it was pointed out that the amido compounds affected the blood chiefly, but in addition the nitro compounds involved the central nervous system. Occupational Hazards.--Nitrobenzene is used in the manufactur ing of shoe dyes, floor polishes, perfumes, flavoring extracts, explosives, and the anilines. Pathology.--Icteric pigmentation of the skin to deep jaundice, acute yellow atrophy of the liver and necrosis of liver cells, degenera tive changes in the other organs, and ecchymosis of the membranes of the intestinal tract are common findings. Blood Bicture.--Blood studies reveal anemia, with alteration in the size, shape, and staining qualities of the cells, as well as paleness, fragmentation, and polychromatophilia. Early spectroscopic examina tion of the blood will reveal a methemoglobin or lines between a methemoglobin and oxyhemoglobin. Later, if cyanosis is deep, this cannot be demonstrated. In the acute exposure, if death has not occurred, the cells regenerate, and the blood picture is much like that of pernicious anemia. The white cells are usually increased. In chronic poisoning these white cells may decrease below the normal with a relative in crease of the lymphocytes. Malden,1 in his study of the workers in a factory where aniline and benzene were made, noted that in the slower forms of poisoning there was a stimulation of the red blood cells with a decrease in the hemoglobin. He commented on the change in the size of the cells and their stippling qualities and considered stippling as characteristic of aniline poisoning as in lead poisoning. If death is immediate, there are no characteristic pathological changes. Signs and Symptoms.--In a severe exposure death may be pre ceded by fast, irregular breathing, weak, thready pulse, marked cya nosis, convulsions, and coma. In mild poisoning the face is flushed, and there may be severe headache, burning of the throat, tightness in the 142 XITHOBEXZEXE, OICHEOKODrFU'OKOXIETHAXE 143 chest, dizziness, disturbance of gait, and diminished or cloudy vision. Chronic poisoning is said to occur and is marked by languor, drowsi ness, dyspnea, mild cyanosis, and sometimes diminished vision. Medicolegal Aspects.--Temporal')) disability is usually short but, of course, is dependent upon the degree of intoxication and the com plications which have arisen. Permanent disability is rare. When present it is usually due to an altered vision. Bladder tumors may result from exposure to the amido compounds, but they are not attributed to the nitro group. Illustrative Case: Case I.--A chemist's assistant dropped a can of nitrobenzene, spilling it on his lower legs and saturating his trousers. He started to pick up the can, but soon fell forward onto the floor. He was rushed to the hospital without having his clothes removed. Upon arrival he was unconscious. Respirations, at first rapid, became slow and irregular. The pulse was difficult to feel, the heart tones distant and weak. Cyanosis was marked. A sample of blood was of a deep-brown color. Death occurred an hour and a half after the accident. Postmortem ex amination revealed nothing of note. The man had been in good health and two weeks before had passed a preemployment examination. It was definitely established that the substance was nitrobenzene. The symptomatology, sudden death, and character of the demise were in keeping with the known reactions to acute exposure to this agent. The case was compensable. It should be emphasized in cases such as this, or the one cited under "Phenol." or any other type of saturation from a noxious sub stance, that all clothing be removed from the victim immediately. Such a procedure obviates the possibility of further absorption. Treatment. Immediate Measures.--In acute poisoning the con taminated clothing should be at once removed, and areas of the skin on which the substance has been spilled should be cleansed with alcohol. Gastric lavage with water containing epsom salt, which de lays absorption, is performed, although as in phenol, mercury, and arsenic poisoning, the lavage is not of as much value in the industrial case as in that of poisoning by ingestion, which is more apt to be seen in private practice. Oils, milk, and alcohol should not be given by mouth since they tend to favor absorption. Prevention of Respiratory and Circulatory Failure.--Inhalations of carbon dioxide, from 5 to 7 per cent, in oxygen are indicated for respiratory stimulation, and corn mine. 1.5 cc., metrazol, from V/, to 4% grains (0.1 to 0.3 gm.), caffeine sodium benzoate. T1/, grains (0.5 gm.). or camphor in oil, from 1 to 2 cc., may be given intra- 144 OCCl'l'ATIOXAL DISEASES niuscularly for respiratory and circulatory stimulation. Intravenous infusions of from 5 to 10 per cent dextrose in physiological saline solu tion are indicated, and transfusion (1550 to 500 ee.) may he necessary. If acidosis is present, it should he treated as described under "Methyl Alcohol." Epsom salts, from to 1 ounce (15 to .`50 gin.), is usually given orally. Hepatic Inquiry.--Following the acute stage, treatment directed at correction of the liver damage may be necessary, and this should follow pretty closely that outlined under "Tetracldorethane." If a macrocytic type of anemia develops, liver extract, from 15 to :50 units per day for the first three or four days anti then at intervals of from 5 to 10 days, is given. REFERENCES 1. Malden, \V.: Some Observations on the Conditions of the Blood in Men Engaged in Aniline Dyeing and the Manufacture of Nitrobenzene and Its Compounds." J. Uyg.. 7: 072-88.3, 1907. DICHLORODIFLUOROMETHANE This substance is known to the trade as "freon" or "P-1 A" It is the result of experiments conducted by refrigeration engineers to find a less noxious refrigerant. It is a clear, water-white liquid, boiling at --21.6 F. Experiments conducted by the United States Bureau of Mines, with dogs, monkeys, and guinea pigs exposed to this gas. per mitted this body to conclude that injury or ill effects from this re frigerant were remote possibilities. To our clinic has never come a patient alleging any ill effects from this gas, but there were reported to the writer two deaths supposedly resulting from a heavy exposure. Two men entered a fairly small room, which had been kept closed, to test the presence of this gas. They were immediately overcome and died. I was unable to check the veracity of this report. The engineer who reported this instance claimed it was due to a dense, highly con centrated collection of this gas. Its presence is detected by burning a halide light against a copper plate. If freon is present, the blue light turns to green. Brief mention is made of this gas. not because of the likelihood that the reader will see many cases like the above, but rather to inform him of the remote possibility of ill effects. ETHYLENE DICHLORIDE Occupational Hazards.--Ethylene dichloride (CklUCk) finds its usefulness chiefly as a solvent for fats, as a thinner for lacquers, as a degreaser in drycleaning, and as a fumigant for moths, weevils, and the like. It is frequently combined with carbon tetrachloride (see ease XITHOBKN'ZKNE. DICHLOIlODIKLCOKOifETHANE 145 under "Carbon Tetrachloride"). and is of approximately the same order of toxicity as trichlorethylene. Signs and Symptoms.--Following acute exposure, dizziness, nausea, vomiting, weakness, trembling, abdominal cramps, diarrhea, drowsi ness, and slight breathlessness may be noted. In addition, there may be evidence of irritation of the nose and eyes, ataxia, degeneration of the liver, nephritis, and perivascular hemorrhages of the brain. It appears to have a greater selective action upon the kidney than most of the solvents. Opacities of the cornea have occurred due to the infil tration of lymphocytes and connective tissue cells. In animal experi mentation these usually clear within several months. Treatment.--Treatment consists of general supportive measures as indicated with the other solvents and of similar prophylaxis. The use of a high carbohydrate, high calcium diet has been of definite value. The intravenous administration of 10 cc. of 10 per cent calcium gluconate to the patient shortly after his admission to the hospital has relieved markedly the epigastric cramps and vomiting. This pre sumably is because of the relaxing effect on smooth muscle of the cal cium carbonate. As in treatment with the other solvents, it will be valuable to use intravenous infusions of from 5 to 10 per cent dextrose, in physiological solution of saline if chloride loss following vomiting is present, or in distilled water if it is felt that the salt content will increase renal damage, in amounts varying from 2000 to 3000 cc. 10 CHAPTER XI FLUORINE AND CHLORINE FLUORINE Fluorine is not ;i constituent of the human body at birth, but due to its inevitable ingestion and incomplete elimination, it does become present in later life. The substance is widely found in nature, being observed in excess quantities in water in certain portions of the country,1 in ores and minerals, and in soil." Its two chief components arc sodium fluoride and hydrogen fluoride. Occupational Hazards.--Art-glass workers, brewers, bleachers, dyers, etchers, glass-finishers, aluminum-extractors, insecticide-manu facturers, and those engaged in the mining of various ores and min erals are liable to this hazard. Cryolite is a source of aluminum, alum, and caustic soda. It is a fluoride of aluminum and sodium, containing 146 ['LCOKINE .VXD CHLORINE 147 as much as 50 per cent of fluorine. In llie Failed States the phosphate, rock from which superphosphate fertilizers are obtained contains as much as 4 per cent fluorine. Rock phosphate is a source of phosphate for baking-powder. Fluorine forms a part of numerous insecticides and fumigating preparations. Fig. 33.--Normal spine of man. (Bishop: Am. J. Roentgenol., May, 1936.) Signs and Symptoms.--In industry action is usually local, causing degrees of injury varying from slight burns to corrosive, destructive lesions. It may aft'ect the eyes, the upper respiratory tract, the lungs proper, the intestinal tract, liver, spleen, and kidneys. Vomiting, diar rhea, shallow respiration, convulsions, and coma have been reported. Fatal doses diminish the blood calcium and damage the vasomotor and respiratory centers. Chronic poisoning causes mottling of the 148 OCCUPATIONAL DISEASES teeth, gastric and nervous disturbances, and loss of weight. The ;c-rays reveal marked changes in the bones. There is a disappearance of no'rrnal bone structure with a replacement of an almost milky white opacity, the outlines of which lack sharpness. Bone Changes.--Bishop* quite recently reviewed the available literature concerning the roentgenographic study and added a case of his own (Figs. Z1-A1). The first observations were made of a group of cryolite-miners who were being studied for silicosis. It was noted that these men had general ill health, although length of exposure was only Fig. 34.--Bone changes of chronic fluorine poisoning. Note density of ribs and scapulae and the enlargement of the inferior ridges of the ribs, posteriorly. (Bishop: Am. J. Roentgenol,, May, 1936.) ten years. In addition to thirty-nine of the group of seventy-eight showing first- or second-degree silicosis, over half of the group pre sented definite bone changes. The changes varied from a "fleecy thick ening of the bone lamina and an increase in the whiteness of the bone shadows on the roentgenogram to an actual opacity of the bones and calcification of the ligamentous attachments." These bone changes have been mentioned here because they might, at some future time, enable the reader to recognize what otherwise might be passed over as an obscure condition and also to suggest that a roentgenogram of the bones might prove a valuable confirmatory factor in suspected cases. FLUORINE AND CHLORINE 14!) n Fig. 3.7.--.1. Bone changes of chronic fluorine poisoning. Compare with R. Note increased bone density, normal bone Irabeculation. and spicule formation along anterior iliac margins and external pubic borders. 11. Osteoplastic metastasis of carcinoma of prostate. Note mottled appearance due to areas of bone absorption adjacent to areas of sclerosis. Normal bone architecture has been lost. (Bishop: ,4m. J. Roentgenol., May, 19364 150 nccvp.vnos.xl diseases Tests.--There is no simple lest to determine the presence of this substance, in the chronic, case. If an acute case results from ingestion, the stomach contents can be examined for the presence of fluorine. Excessive amounts can be determined [lost mortem by comparing the fluoride present in the bones with the normal known range. ! I l Fig. 30.--Osteoplastic metastasis of carcinoma of prostate, same case. Note mottled appearance of vertebral bodies, the crush fracture, and the absence of dense osteo phytes. (Bishop: Am. J. Roentgenol., May. 1930.) J' Medicolegal Aspects.--There has been too little industrial experij. ence with this substance to form a basis for an estimation of cither }' the expected temporary or permanent disability. Aside from its reac tion on the bones, nothing is known about its effect on other tissue. It appears that the fluorine salts are deposited in bones with other FLUORINE AND CHLORINE 151 calcium salts. In the body metabolism, that part of fluorine which is not combined with calcium is eliminated. An adequate calcium intake prevents toxic symptoms. Hence the reaction in one person may be entirely at variance with that in another. The majority of cases of fatal poisoning have been those of accidental ingestion, or occasionally where taken with suicidal intent. Industrially, there are numerous cases of local injury to the tissue resulting in temporary burns without permanent damage. Fig. 37.--Osteoplastic metastasis of carcinoma of prostate, same case. Compare with Fig. 34. Note mottled appearance and lack of widening of ribs. (Bishop: .4 m.. J. Roentgenol., May, 1036.) Illustrative Cases: Case I.--We have not seen this case duplicated in the literature. The patient was admitted to the surgical service of Dr. Harry Alex ander, with a history of having fallen while carrying a small bottle of hydrogen fluoride. The bottle broke upon the cement floor and splashed the victim on his face, both hands, left arm, and left thigh. One-half hour after the accident the patient was admitted to the hos pital, and it was noted that all involved areas had burns of a second degree, but the fingers of the left hand were blanched. Within two hours, the distal portions of all fingers were dusky. The following- 152 OCCUPATIONAL DISEASES morning they were definitely gangrenous in appearance. In spite of treatment, subsequent amputation of all the distal phalanges of the left hand except the thumb was necessary. The lesions elsewhere healed without complication. The caustic or corrosive action of fluorides upon tissue has been frequently mentioned but there exist no case histories of gangrene following contact with hydrogen fluoride. In this case a destructive endarteritis occurred. There was no question of the occupational origin. Permanent rating for the loss of a portion of the fingers was allowed. Cases of Acute Poisoning.--Hickey1 reports a case of a girl, ten years old, who was given by mistake a teaspoonful of sodium fluoride for potassium and sodium tartrate. She died soon afterwards, Mc Nally5 reports a woman who died soon after eating an omelet in which roach powder had been used instead of starch. This same author cites a case in which a woman took a white powder for a laxative and died four hours later. Her physician ascribed death to carcinoma. Six weeks later the body was exhumed, at which time gross pathological change in keeping with fluorine poisoning was noted and fluorine in excessive amounts was found in the bones. Treatment. Combating Calcium Deprwation.--Since the mech anism of fluorine toxicity consists of a calcium deprivation, treatment should primarily be designed to correct this and thus render the fluorine inert. In the acute case of poisoning, gastric lavage with lime water or a weak solution of calcium chloride, together with from 10 to 20 cc. of 10 per cent calcium gluconate intravenously from once to three times a day is used. Respiratory and Circulatory Complications.--If cyanosis is pres ent the administration of oxygen by an intranasal tube or by a tent is indicated; and respiratory stimulants may be needed, such as cam phor in oil, from 1 to 2 cc., intramuscularly; carbon dioxide. 7 per cent, in oxygen as inhalations; coramine, 1.5 cc.. intramuscularly or intravenously; or metrazol, from V/> to 4% grains (0.1 to 0.0 gm.), intramuscularly or intravenously. The latter two or adrenalin, 1 cc. of a 1:1000 solution, intramuscularly are indicated for circulatory failure. Shock.--The use of 1000 cc. of 10 per cent glucose in saline given slowly intravenously will be of value in combating shock, particularly if pulmonary edema is absent. The patient is, of course, kept warm with blankets and hot-water bottles. Sedatives in Complications.--Codeine, from ]/o to 1 grain (0.0325 to 0.005 gm.) , repeated every four to six hours, is at times needed to allay violent coughing. The codeine may be given in any of a number FLUORINE AND CHLORINE 153 of soothing cough syrups. Dilaudid hydrochloride, from ] '3.2 to ViG grain (0.002 to 0.004 gm.). given hypodermically or by mouth may also help in this regard, as do morphine sulfate, from to % grain (0.011 to 0.016 gm.). and pantopon, from ]v, to grain (0.011 to 0. 022.gm.). These sedatives and one of the barbiturates may be needed to control convulsive seizures. Bronchial Asthma.--If symptoms of bronchial asthma appear, the use of one of the following is indicated: ephedrine sulfate, % grain (0.024 gm.), given every four to six hours; neosynephrin, from 0.25 to 0.5 per cent solution used in a nebulizer; aminophyllin, V/j grains (0.1 gm.), every four to six hours, or 7grains (0.48 gm.) in 20 cc. of distilled water, given intravenously slowly over a five-minute pe riod: or epinephrine, from to 1 cc. of 1:1000 solution hypoder mically, or as inhalations of a 1:1000 solution from a nebulizer. Obstipation and constipation may need attention; and if vomiting is severe, the further administration of from 5 to 10 per cent dextrose in physiological saline solution (1000 to 3000 cc. daily) is used. No established treatment exists for stiffness of the body due to bony and ligamentous changes, but it appears that on gradual elimination of the fluorine considerable reduction takes place in osseous overgrowth. Treatment for Burns.--It is suggested that the burns be treated as described by Jones.1'1 The burned area is thoroughly washed with or immersed in a warm saturated solution of sodium bicarbonate. Then an ointment prepared from thorough mixing of two parts medical paraffin or glycerin with one part of magnesium oxide is massaged into the burned area, and a dressing of the same ointment is applied; 2 cc. of sterile 10 per cent calcium gluconate solution is injected into and under all areas showing whitened skin. The magnesium oxide oint ment dressing is renewed night and morning for five or six days. After this period boroscptic ointment is an efficient and soothing application, and healing can be completed by dressing with ichthvol ointment. The eves, if involved, should be irrigated for at least an hour with normal saline solution, and then the ointment described above should be applied. REFERENCES 1. Smith, >1. C.. T.anlz. E.. and Smith. IL V.: Tech. Bulletin No. 32, Arizona Agri culture Experimental Station. June 10, 1931. 2. Dean. H. T.. Dixon. R. M.. and Cohen, C.: "Mottled Enamel in Texas." Pub. Health Rep.. 50: 4-21-44-2 (March 29). 1935. 3. Bishop. P. A.: "Bone Changes in Chronic Fluorine Intoxication; Roenlgenographic Study, .4in. J. Roentgenol., 35: 577-585 (May), 1930. 4. Hickey. M.: Bull., Massachusetts Board of Health. 341. 1911. 5. McNally. IVin. D.: Toxicology, Industrial Medicine Publishing Co.. Chicago. 1937. G. Jones. T.: "Treatment of Hydrofluoric Acid Burns." .1. Iniluxt. Ilyg. and Toxicol., 21: 205 (June). 1939. 154 OCCUPATIONAL DISEASES CHLORINE Chlorine is a greenish yellow gas. not combustible in oxygen, burns in hydrogen, ami in the sunlight combines to form hydrochloric acid. It is produced largely from common salt by the electrolytic, process and is sold in containers for commercial purposes. Occupational Hazards.--Its greatest use is in those trades where a bleaching process is needed. It is also found in the manufacturing of nitric acid, in the dye industry, in paper (bleaching) and textile works, and is used widely in the making of disinfectants. Signs and Symptoms.--Severe dosing causes suffocation, which may be short, or the gas may affect the nervous system producing uncon sciousness or death. Following the first effects in the more severe exposures, the entire respiratory tract may develop edema with pneu monia developing within a few hours. While serving with an evacua tion hospital during the first World War. the author noted congestion of the nose and throat among patients, with increased redness of the tissue. Scattered moist rales were frequently present. Pneumonia oc casionally ensued, but most of these patients recovered. Sloughing of the tissue has been reported, but a recent communication with one of the officers in charge of our gas ward states that he never saw this occur. Common Findings in. Industrial Use.--In industry, the severe or tragic effects from this gas are rare. The average case is one where a whiff of the gas has produced coughing, and a sensation of an inflamed throat or burning "deep in the chest." These men usually recover within a few hours or a day. Instances are known where persons have been overcome and rendered unconscious only to recover within a short time without any ill effects. Chronic exposure to chlorine has been reported to have produced opacities of the cornea and perfora tions of the nasal septum. Like chlorine, bromine chiefly affects the respiratory system. It is rarely an industrial hazard and needs no further comment. Medicolegal Aspects.--Temporary disability is usually short, a few days at the most. A complication, such as pneumonia, if it arises with in a few days, is compensable, and the entire period of disability due to the complication is compensable. Permanent disability is extremely rare. Treatment. War Use versus Industrial.--The author has had ex perience with two sources of chlorine gassing: one while in the first World War and the other from industry. In the first instance, the vic tims were more severely affected because they could not usually with draw from the hazard. In industry, there occur but few severe, ex posures. Men are warned of the presence of this gas and immediately FLUORINE AND CHLORINE 155 withdraw. If severe afi'eetiou occurs. treatment is directed to the res piratory tract in order to relieve the irritation and the congestion. Immediate Measures.--The patient severely gassed with chlorine should he removed from the toxic atmosphere promptly, and all con stricting clothing about the neck should he loosened. He should be kept quiet in a recumbent position and should be wrapped with warm blankets while hot-water bottles are applied. Oxygen should "be ad ministered in all cases. It is considered best not to wait for cyanosis to develop, since the administration of oxygen will often prevent cyanosis and relieve the pain of deep inspiratory effort. Venesection of from 400 to 000 cc. is an extremely valuable measure and should be performed early on all patients who have been exposed to heavy con centrations; but, as already indicated, such exposures in industry will be very rare. The early use of such phlebotomy often prevents devel opment of edema of the lungs, and if used later often relieves pul monary edema and cardiac embarrassment. The early intravenous ad ministration of 10 per cent dextrose in physiological solution of sodium chloride may be combined with venesection to combat shock and re duce viscosity of the blood. As with phosgene poisoning, venesection is contraindicated if the gray stage of anoxemia with pallor, collapse, and rapid, thready pulse is reached. Relief of Pain and Excitement.--Morphine sulfate is not to be used if pulmonary edema and respiratory embarrassment have ensued. Some advise, however, its use for relief of pain and excitement soon after injury. Atropine, epinephrine, digitalis, and strychnine are not of much benefit. Caffeine sodium benzoate, 7% grains (0.5 gm.), or from 1 to 2 cc. of camphor in oil given intramuscularly sometimes produces beneficial results. Complications.--If pneumonia is a complication, oxygen therapy is continued. If a specific infection superimposed upon the injured lung is demonstrated, the use of the appropriate chemotherapeutic agents, e.g., sulfanilamide, sulfapyridine, or sulfathiazole, and serums is advised. Olive oil in the eyes may be effective. Codeine phosphate or sul fate. l/> to I grain (0.0325 to 0.065 gm.), for cough, or spraying of the nose and throat with a soothing solution, is at times useful, but for this latter use products containing oil should be avoided because of the danger of developing a lipoid pneumonia. The patient should be placated regarding any permanent effects to the lungs. A neurosis may be avoided by the initial attitude of the physician and malingering obviated by the emphatic imparting of existing statistics and knowl edge regarding these cases. CHAPTER XH HYDROGEN SULFIDE Hydrogen sulfide in a concentrated form is deadly and, like hydro cyanic acid, exceedingly rapid in its action. Its characteristic odor, like that of rotten eggs, is familiar to all. It is a transparent gas. readily soluble in water, and is the natural product of putrefaction of animal or vegetable matter. Because of its intense odor it is easily recognized even in minute amounts. Occupational Hazards.--This gas is never used directly in indus try but is formed frequently as a by-product of certain processes. It is to be found in sulfur dye works, tanneries, in the production of carbon disulfide, in the heating of certain rubbers containing sulfur com pounds, and may offer a hazard to those working in sewers, mines, wells, caissons, and tunnels. As reported under "Carbon Disulfide," it exists in the process used for the manufacturing of artificial silk or rayon. It is invariably present to some degree in the refining of oil. Pathology.--This gas is both an asphyxiant and an irritant. When death results, it is from respiratory failure and occurs within a few minutes, although the heart may beat for a short period after respira tion has ceased. It is important that those first on the scene of action remember this and institute artificial respiration. Persons seemingly dead have been resuscitated by such means. Locally it is an irritant; systemically it affects the nervous system. This may range from drowsiness or sleepiness to convulsions, delirium, deep coma, or death. Because of its action upon the vagus nerve, the heart action is slowed. Within the bloodstream hydrogen sulfide is rapidly oxidized without any toxic products resulting from this oxidation. The pathology re sulting from poisoning by this gas is apparently transient, for if death does not occur because of asphyxiation, recovery is usually complete. It is significant that at postmortem examination in those cases where death has been instantaneous, the tissues reveal nothing characteristic. Signs and Symptoms.--These can best be described by listing the reactions as they occur at certain concentrations. At a low concentra tion of between 100 and .200 parts per million there exists a mild irri tation. especially to the eyes. This usually results at the end of a day's exposure. Within a half hour to an hour 500 parts per million will bring about excitement, headache, dizziness and staggering, diarrhea and dysuria. to be followed sometimes by bronchitis or bronchopueu- IIYDROGEX SCLI'IDE 157 monia. Short exposures of fifteen minutes to concentrations of from 800 to 1000 parts intensify the previously mentioned symptoms or may result in death. Above this may mean instant death. Chronic poisoning results in headache, inflammation of the eyes or eyelids, digestive disturbances, loss of weight, and general debility. This constant exposure is confined usually to chemists or testers in oil refineries. MEDICOLEGAL ASPECTS Temporary Disability.--This may be from a few minutes to a few hours or a few days. If a pulmonary complication arises, the disability is for the course of that affection. Permanent Disability.--This is rare, if ever. As in cyanide poison ing. if the dose is not fatal complete recovery occurs. Illustrative Cases: Case I.--While working for an oil company in the. Long Beach refineries, a Cracker Stillman's helper started out at 6.30 A.M. to make his rounds at gauging his tanks. Failing to return, he was found one-half hour later lying in six or seven inches of water, face down. Medical aid did not reach him until one-half hour later. The medical examination at that time revealed a male of apparently twenty-six or twenty-seven years. No cardiac sounds could be heard; the pupils were dilated and fixed. He was deeply cyanotic. The extremities were relaxed and moderately warm. There was a minor abrasion about % inch in diameter over the left temple, with no swelling. The neck did not appear to be out of line, and no crepitation could be heard upon manipulation. He failed to respond to cardiac stimulants, and the pulmotor squad using carbon dioxide-oxygen inhalations obtained no re sults. The autopsy examination showed water in the lungs; otherwise it was entirely negative. No injury to the brain or body was found, and the heart was normal. The top of the tank which this man was gauging was covered with a half foot of water to prevent the escape of gases. At three places around this tank there were escape valves or pipes, and at one place there was a covered gauging hole. This hole is covered by a flap top, which is opened by a mechanical foot pedal. It is so situated and arranged that usually the wind blows the escaping gas away from the workman. On this particular morning the wind was toward the posi tion the workman would have to assume in operating this gauge. It was, therefore, felt that when the victim lifted the lid he received an unusually high concentration of hydrogen sulfide, was overcome, and fell forward into the water. In this particular refining process, they were engaged in "cracking" 158 OCCri'ATIOXAL DISEASES the oil into different fractions. This was being done by lieating this oil to a temperature of 1000 C. At this point the hydrogen sulfide given off is abundant and highly concentrated. The author questioned several petroleum engineers and was told that this concentration is also increased under certain weather conditions. In the absence of any other obvious cause of death or circumsFauces which could account for his death, it was held as compensable. The coroner stated that death had been too sudden for any changes to occur that would aid in the postmortem diagnosis. Case II.--A workman engaged in repairing a tank from which hy drogen sulfide was escaping first became dizzy, noticed a pressure in his head, and then became unconscious. He returned to consciousness in eight or ten minutes and was removed to the hospital. There the examination revealed no cyanosis or dyspnea. The pulse was 60 per minute, and the blood pressure 1 4-78/70. A few scattered moist rales were heard throughout the lung fields. He recovered completely within thirty-six hours and returned to work at the end of four days without any further disability. Case III.--Just prior to this material's going to press a second case of death in a Cracker Stillman came to the writer's attention. In a nearby oil refinery this man was found dead. His body was at the foot of the gauging hole. He was thirty-four years of age; his past medical history was of no significance; and autopsy revealed no organic lesions to account for his death. Death was held compensable. TREATMENT If this substance is apt to be present in an industrial process, masks should be worn which would not only prevent inhalation of the gas but also protect the eves against irritation. Ventilation should be adequate. Combating Respiratory Failure.--In severe poisoning, chief atten tion is directed to the respiratory failure, which appears to be due to depression of the respiratory center. The patient should at once be moved from the point of contact with the gas, and fresh air provided. Artificial respiration is started at once, and as soon as available inhala tions of mixtures of from 5 to 7 per cent carbon dioxide, with oxygen, are commenced. The use of respiratory stimulants--such as caffe ine sodium benzoate, 7% grains (0.5 gm.); coramine, 0.5 cc., intra muscularly or preferably intravenously; camphor in oil, from 1 to cc., intramuscularly; and metrazol. V/> grains (0.1 gm.)--may be of value here because of the central character of the respiratory failure. Bronchitis and bronchopneumonia may appear as complications, and require the ordinary treatments for these conditions. I1YDK0UEX SVLFIDE 159 Care of Eyes.--The eyes may be severely irritated, and the condi tion may even go on U> the development of corneal ulcers. As with other irritants to the eyes, e.y., ammonia, they should at once be thor oughly washed with water. Following this the use of a saturated boric acid solution and of olive oil is advised. Local anesthetic solutions, such as 2 per cent butyn or 0.5 per cent pontoeainc hydrochloride, may be used in relief of pain. Continuous warm boric compresses may be of value in preventing further complications. When available, the advice of an ophthalmologist should be sought. CHAPTER XIII CARBON DIOXIDE AND SULFUR DIOXIDE CARBON DIOXIDE Carbon dioxide is a colorless, odorless, stable heavy gas found even in the purest atmosphere. Considered as a waste product of cell metab olism, it is a vital factor in normal respiration. It is a product of res piration, combustion of coal and wood, decay and fermentation. It is frequently found in small, confined spaces such as caves, wells, cis terns, and crowded halls. It changes arterial blood into venous rapidly. Blood pressure increases following stimulation of the central nervous system. The pulse rate becomes slow, the respirations intensify, and sufficient quantities may produce paralysis. Occupational Hazards.--Employees in blast-furnace shops. large refrigeration plants, boiler-rooms, charcoal burners, caisson workers, divers, coalminers, brewers, vatmen, and submarine workers are liable to this hazard. Signs and Symptoms.--Headache, vertigo, dyspnea, drowsiness, weakness, and ringing of the ears are symptoms, and severe concentra tions may produce giddiness, loss of muscular power, increased res piration, profuse perspiration, and mental excitement. Following the stimulating phenomena, high concentration may produce depression, coma, and death. Dry ice (solid carbon dioxide) produces only local but severe disturbances to the skin. Medicolegal Aspects.--Temporary disability is very short, a few hours to a day or two. Permanent disability docs not occur. Deaths have occurred. Illustrative Case: Case I.--A longshoreman entered a hold of a ship just docked in order to unload fruit from South America. He was overcome in a short time. Two fellow-workers rescued him, but both of them were partially overcome. All three men reported back to work the following day. Examination of the men by a physician was not made until two hours after the incident. Aside from lassitude and headache, no other com plaints existed. The ship had been delayed by storms. The fruit was found to be in a marked state of decay. All of the men exposed reacted to the expo sure. Subsequent physical examination was negative for other causes. 100 O.UiBOX DIOXIDE AND SCLFUR DIOXIDE 1G1 Treatment.--The chief objective is to restore normal respiration either by means of artificial respiration or oxygen therapy. Once suffi cient aeration is obtained, the patient usually recovers without seque lae. The oxygen should be administered by a mask or intranasal apparatus. Artificial respiration should be without dead space or re breathing. Treatment of the acidosis by buffer solutions may be of value, although these are seldom needed if the condition is recognized early. The solutions to be used are those mentioned in the discussion of the treatment of acidosis under ``Jlcthvl Alcohol"; that is, sodium bicarbonate, r-molar sodium lactate, laclalc-Ringer's solution, inter stitial salt solution, and physiological saline solution. SULFUR DIOXIDE Sulfur dioxide is an irritating gas arising from the combustion of sulfur. It is a common component of the atmosphere of industrial communities and can easily be detected in the air. Its concentration is higher in cities subjected to fog, such as Pittsburgh. According to Schade, its presence in the air in Pittsburgh was too slight to cause concern. In industry the maximum amount of concentration allow able for a short time (thirty minutes to an hour) is from 50 to 100 parts of S02 per million parts of air; for prolonged exposure. 10 parts per million parts of air. Occupational Hazards.--Its most frequent use is in the operation of small, home refrigeration units. Exposure may also be found in the occupations of sulfuric acid makers, smelters, foundry workers, blast furnace operators, bleachers, cellulose-workers, workers at coke ovens, disinfectant workers, dye-makers, petroleum-refiners, and vulcanizers. Signs and Symptoms.--Irritation and inflammation to the eyes, nose, throat, and lungs, and occasionally digestive disturbances. It is so irritating to the eyes and throat that man usually withdraws from an exposed atmosphere before further damage is done. Instances where withdrawal was impossible are reported, showing edema of the lungs as well as paralysis of the respiratory center. Chronic exposure ac cording to Kehoe produces a chronic catarrh, a nasopharyngitis and disturbance of the sense of smell or taste, increased lassitude, and fatigue. Other observers have noticed a lessened tendency to colds, bronchitis, or other respiratory infections. Direct contact of the eye balls with this liquid has caused frozen eyeballs, according to Clark. Medicolegal Aspects. Temporary Disability.--Usually there is none, but occasionally one or two days are required. Permanent Disability.--There is no permanent disability. Expo sure does not induce cardiac disease, tuberculosis, or chronic bronchial n 1G2 OCCUPATIONAL DIS(CASES disturbances. Removal from the exposure results in a disappearance of symptoms. Illustrative Cases.--The cases seen at this clinic have invariably been very mild. We have experienced no fatalities. In most every in stance it was not necessary for the patient to withdraw from his work. The following incident is an example of certain symptoms which may present themselves. Case I.--A twenty-eight-year-old male was seen on April 9, 1940. He had previously been seen in February of the same year for a slight exposure to this gas. On the day of this most recent exposure, he and a helper had gone to a home to recharge an electric refrigerator and had taken with them a drum filled with sulfur dioxide. The patient stated that these drums arc filled at the plant when cold, and occa sionally more is put into them than they can stand. As they were about to recharge the refrigerator, the drum exploded, striking the helper on the lower leg and fracturing it. This occurred in a small, en closed room, and both workers were almost overcome. The clothing of both was frozen stiff. The older mechanic managed to get his helper outside, where he removed most of the clothing and then pro ceeded to the hospital. Examination of the helper revealed the fractured leg (tibia), and a few rales within the lung fields. His chief complaint was referable to his right eye, which had been frozen. He was placed under the care of the ophthalmologist for care of the eye and the orthopedic surgeon for the fractured leg. He required no particular medical treatment. The eye slowly returned to normal in four weeks, and the fracture healed without complications. There was a temporary disability of thirteen weeks. No permanent disability. The mechanic complained of pain in the throat and chest and a feeling of constriction. His respirations were embarrassed. Examina tion showed the throat to be red and the eyes injected; the lungs were full of scattered musical rales, best heard at the beginning of expira tion. His picture was typical of bronchial asthma. He was hospitalized for twenty-four hours, given two hypodermics of adrenalin, and thirty hours after exposure the lungs were clear. There were no abnormalities relative to the heart or blood pressure. His temperature was 99 F. on admission and returned to normal by the time of discharge. He re mained away from work four days. He was reexamined two weeks later, at which time he was entirely normal. However, he decided to quit this type of work, owing to fear of a repetition of his recent experience. The temporary disability in this instance was four days, with no permanent disability. Treatment. Irritation of Eyes.--Workers in industrial plants, fire men, or refrigerator repairmen, who are apt to encounter this gas, CARBOX DIOXIDE AXI) .SULFUR DIOXIDE 163 should wear gas-masks. Treatment of an eye injured by this gas is similar to that of the eye injured by ammonia. Copious laving of the eye with water, followed by the introduction of saturated solution of boric acid and by the use of a local anesthetic, such as 0.5 per cent pontocaine hydrochloride, is indicated. These are followed by the application of olive oil or some similar oil. Corneal ulceration should be carefully watched for and treated appropriately if it occurs. Respiratory Disturbances.--For those overcome by the gas, in halations of from 5 to 7 per cent carbon dioxide in oxygen are used over a long or short period, depending on the severity of the case and the individual patient's reaction. If pulmonary edema is present, oxy gen alone is used. In very severe cases artificial respiration is employed coincidentally with the inhalations. In some cases the use of respira tory and circulatory stimulants such as coramine, metrazol, and caffeine sodium benzoate may be of value. A few days of absolute bed rest should be advised for those who have a fairly severe exposure, and this should be. continued until all evidence of respiratory embarrass ment ceases. During this period codeine phosphate or sulfate, from Vi> to 1 grain (0.0325 gm. to 0.065 gm.), every four to six hours, will alleviate the cough and may frequently be combined to advantage with a soothing cough-syrup mixture. Bland oils should be applied to the exposed membranes. For those who display symptoms of acute asthma the subcutaneous administration of % to 1 cc. of 1:1000 solu tion of adrenalin may relieve the symptoms. The use of a nebulizer for inhalation of 1:100 adrenaline might also be of value. In very severe cases pulmonary edema requiring venesection could conceivably occur, although we have not seen such an instance. In such a case, acidosis may accompany the anoxemia and intense air hunger. Treatment of the acidosis, if present, should follow the sug gested outline given under "Methyl Alcohol." Some authors feel that the severely ill patient should not even be asked to move in bed, since any slight exertion may cause the failure of an overworked and as phyxiated heart.1 REFERENCE 1. Henderson, Y.. and Haggard. II. IV.: Noxious Gases and the Principles of Respira tion Influencing Their Action, The Chemical Catalog Company. New York, 1927, p. 120. CHAPTER XIV METHYL CHLORIDE AND METHYL ALCOHOL METHYL CHLORIDE Mbtiiyl chloride as one of the volatile hydrocarbons has the prop erty of producing narcosis or anesthesia if inhaled in sufficiently high concentrations. The chloride, bromide, or iodide compounds of methyl, following absorption, break down into methanol (methyl alcohol) and the halogen acid; the latter combines with the sodium in the blood to form the sodium chloride, bromide, or iodide. Methyl chloride occurs in both gaseous and liquid states. It has a low boiling point, is stable, non-corrosive to metals, non-explosive, and relatively non-inflammable. It is not injurious to foods or textiles and may be used in low-pressure systems of refrigeration. While it does have a sweet odor, it is not sufficiently irritating to serve as a warn ing. Passing through the lungs with little or no irritation, it first acts upon the central nervous system as a mild to severe anesthetic. Enter ing the circulation, methyl chloride has an effect upon the various organs identical to that of the bad whisky of prohibition days, owing to the formation of methyl alcohol. Occupational Hazards.--Methyl chloride is probably the most popular substance used in mechanical refrigeration. Except for chloro form-makers, dye- and color-makers, refrigeration-plant employees constitute the majority of workers exposed to this hazard. Signs and Symptoms.--Progressive drowsiness, vertigo, disturb ance of gait, mental confusion, nausea and vomiting, intestinal cramps, hiccoughs, visual disturbances, tremors, convulsions, coma, and death are the results of exposure to methyl chloride. Prolonged inhalation may injure the heart, liver, and especially the kidneys. Recovery from the initial symptoms may be complete, but a few days later death may result from the degenerative changes in the organs just mentioned. Anuria may result with suppression for from thirty-six to fortyeight hours. Acetone and diacetic acid arc common findings in the urine, along with casts and the presence of the formates. A blood count taken soon after exposure is apt to approach normal, but two or three days later there may be a moderate to profound anemia. Most 16-t METHYL CHLOKIDE AND METHYL ALCOHOL 1(55 of these patients have leukocytosis. Spinal punctures may show an increased pressure, but this is not a constant finding. McNally1 reports a drop in both the systolic and diastolic blood pressure. Weinsteinreports ease histories of two patients in which there was no initial drop in blood pressure. He. docs not report the reading several days later. Tachycardia is common, but cyanosis is not. Tests.--There arc no specific tests. The finding of formates and acetone in the urine, and also the sweet odor of the breath or an "acetone" breath, arc confirmatory aids. Medicolegal Aspects. Temporary Disability.--Patients suffering minor exposures recover within a few hours to a day or two. Severe exposures may require several weeks to a month. These patients usu ally complain of residual headache and nervousness. Neurosis or malingering must be considered beyond that time. Permanent Disability.--If death docs not occur in the severely exposed, eventual return to normal may be expected. Illustrative Cases: Case I.--While repairing a refrigerator located in a small confined passageway of an apartment, a thirty-two-ycar-old repairman noted dizziness and headache. He stepped out on the balcony for fresh air and a rest. After ten minutes he returned and continued working for nearly two hours. The owner found him dazed and stuporous; when aroused, he answered questions incoherently. She thought that the man was drunk and telephoned his employer. Wisely sensing the possibility of exposure to a gas, the employer rushed him to a hos pital. Upon arrival he responded intelligently to questioning. Vomitus was observed on his clothing, and he vomited several times following arrival. The odor to his breath was like that of chloroform. The tem perature was normal; heart rate, 102; blood pressure, 124/80. The general physical examination was negative, and no abnormal neuro logical findings were present. The urine and blood count upon admis sion were normal'. The following morning the urine was mildly positive for acetone and formic acid. He was discharged the third day after admission, at which time the red blood count was 3,400,000; hemo globin, 60 per cent; white blood count, 12,350; polynuclear ncutrophiles, 68 per cent; lymphocytes, 23 per cent; large mononuclears, 5 per cent; eosinophiles, 4 per cent. The urine was normal. Check-up examinations during the next three weeks were negative. On the twenty-first day following exposure his blood count was: red blood count, 4,700,000; hemoglobin, 80 per cent; white blood count. 8200. He had returned to work sixteen days after exposure. A substitute repairman reported finding a leak in the system on which the patient had been working. No alcohol was detected on the 166 OCCUPATIONAL DISEASES breath. No other cause for the illness was found. The physical exami nation and laboratory findings were in keeping with the history and conformed to the usual ease of methyl chloride exposure. The case was considered compensable. Case II.--A fifty-eight-year-old maintenance man, employed for six years by a refrigerator company, developed persistent pain in his chest, which was more severe at night. Some weeks later lie developed a cough and noted dyspnea. Believing his lungs were affected by this gas, he consulted his family physician who informed him it was not his lungs but his heart that had been affected by this gas. He was ordered to slop working and rest in bed. A diagnosis of cardiac en largement due to prolonged exposure to gas was sent to the insurance carrier. Twelve weeks later he was referred to our clinic for exami nation. A palpable pulsation was noted in the upper right sternum. At the second left interspace, both to the right and to the left of the sternum there was a loud, blowing diastolic murmur. A water-hammer pulse with high pulse pressure existed. Blood pressure was 190/100. The fluoroscopy revealed an aneurysm of the ascending aorta. The Wassermann was four plus. Two major errors are apparent in the initial diagnosis. Search was not pushed to determine what kind of heart disease was present, and it was assumed that chronic exposure to methyl chloride could pro duce this heart disease. The case was not compensable upon the basis that the condition was due to syphilis, a disease not caused, irritated, exacerbated, or precipitated by this gas. Treatment. Inhalations and Artificial Respiration.--Severely ex posed workmen should at once be removed from contact with the substance. Inhalations of from 5 to 7 per cent carbon dioxide in oxy gen are certainly indicated, and artificial respiration may be needed. In this phase of the treatment the object is to remove from the lungs all possible methyl chloride. It is felt by some that these inhalations should be continued every three hours over the first twenty-four to forty-eight hours. The respiratory and cardiac stimulants frequently mentioned in other sections, c.g.% the chapter on "Phenol," should be used when respiratory or circulatory failure appears. Treatment as in Methyl Alcohol Poisoning.--As indicated above, the methyl chloride taken into the body is decomposed into methyl alcohol and hydrochloric acid. The latter forms relatively innocuous substances such as potassium and sodium chlorides in the blood. The treatment for the methyl chloride poisoning, then, becomes the same as for methyl alcohol poisoning. The patient is hospitalized imme diately, and energetic treatment of his acidosis is begun. For details of this, "Methyl Alcohol" should be consulted. METHYL CHLORIDE AXD METHYL ALCOHOL 167 Convulsions and Restlessness.--If convulsions occur, they require 4 gm. (one drachm) of potassium bromide in 4 ounces (120 cc.) of water as a retention enema, but under no conditions should chloral or chloroform be given. For the convulsions and resLlessness the use of other sedatives, such as phenobarbital, seconal, nembutal, sodium amytal, and sodium luminal, as well as others of this type, may be of value. Abdominal Pain.--Some cases in which paroxysms of severe ab dominal pain have been a prominent part of the picture are reported. In these morphine sulfate. % grain (0.016 gm.), was used, together with intravenous calcium. It would appear of value in cases presenting such severe cramps to use 10 cc. of 10 per cent calcium gluconate intravenously, repeated as needed. The use of 1 cc. of 1:2000 prostigmine methylsulfate with the morphine may enhance its effectiveness and allow reduction of the amount of morphine.3 Anemia.--If this develops, it is treated with ferrous sulfate, 5 grains (0.32 gm.), two or three times a day, if it is of a secondary type; if it appears to be a macrocytic type, with liver-extract prepa rations. REFERENCES 1. McNally, Wm. D.: Toxicology, Industrial Medicine Publishing Co.. Chicago, 1937. 2. Weinstein, A.: "Methyl Chloride (Refrigerator) Gas Poisoning: Industrial Hazard," JAM.A., 10S: 1903-160;) (May 8), 1937. 3. Slaughter, D., Parsons, J. C.. and Munal, H. D.: "New Clinical Aspects of the Analgesic Action of Morphine," JAM.A., 115: 20.58-60 (Dec. 14), 1940. METHYL ALCOHOL The toxic effects of methyl alcohol would not have to be detailed if this substance were known only by this name. However, it is vari ously labeled as methanol, carbonol. wood naphtha, methyl hydroxide. Columbia, Colonial, or Manhattan spirits, standard wood spirits, green wood spirits, etc. It is obtained by the destructive distillation of wood, and its chemical formula is CH:!OH. It is used with varying degrees of purity. Occupational Hazards.--Some form of methyl alcohol is used by woodworkers, painters, shellackers, linoleum-, leather-, and soapmakers, printers, photographers, dyers, dryclcancrs, rubber workers, cementers of rubber, felt-hat makers, aniline-dye workers, makers of antifreeze mixtures, in the collar-fusing process, and in many other trades. Pathology.--The effect of methyl alcohol on the optic nerve is well known, having been dramatically presented to the profession and layman alike during the period of prohibition. In addition to the visual disturbances, it may affect the liver, kidneys, heart, and brain. 16b OCCUPATIONAL DISEASES Certain investigators have reported anemia after chronic exposure. It is held that its toxic action is the same whether absorbed through the skin, by ingestion, or by inhalation. Ruliny Out Other Substances.--Before attributing deleterious ef fects to methyl alcohol when it is used in certain processes, it is well to consider the possibility of other substances being present and act ing as the causative agent. Greenburg' and his associates studied the use of acetone methanol (methyl alcohol) in the collar-fusing depart ment of a shirt factory. They found a disturbed blood picture in nine of the nineteen subjects studied; in others, an abnormal neurological change; and in some, symptoms of fatigue and drowsiness. A few gave a negative clinical picture. The exposure of these workmen was not only to acetone methanol, but to ethylene glycolmonomethyl ether. They then studied a control series of workers subjected to acetone methanol only and found no abnormalities in the blood picture or the physical examination. They concluded that the ethylene glycolmonomethyl ether was responsible for the altered picture in the first group. Signs and Symptoms.--In contrast to the initial stimulation pro duced by grain alcohol, methyl alcohol causes a depression of the cerebral centers. Headache, temporal pain, nausea, drowsiness, which graduates into stupor, coma, and death; or in some instances, delirium, maniacal actions, then coma and death. Medicolegal Aspects.--One part per million is considered a safe working atmosphere. There would rarely be any danger to the use of this substance if it were properly presented to the consumer. As McNally insists, every container should be labeled in large red letters "Poison--Wood Alcohol." Temporary Disability.--This is usually short, from a few days to a week or two at the most. Permanent Disability.--This is invariably the result of impaired or destroyed vision. Illustrative Cases: Case I.--After working for three days cleaning a vat with a tradename product, a workman became acutely ill, vomited, complained of gastric pains and blurred vision. He quickly recovered from all symptoms except his disturbed vision. He is now subtotally blind. Case II.--Two women worked at pencil-varnishing. They suffered from headache, nausea, and blurred vision. Both claimed that in the open air the symptoms vanished. Constant exposure caused a gradual impairment of their vision.- Treatment. Special Measures in Industrial Case.--The treatment of the case of methyl alcohol poisoning seen in industry will differ METHYL CHLORIDE AXD METHYL ALCOHOL 169 to some extent from that seen in private practice. In industry the toxic action will have usually been produced by absorption through the skin or by inhalation, in contradistinction to the ingestion of the prod uct more commonly seen in private practice. For this reason the use of emetics is not indicated, and the value of gastric lavage with 4 per cent solutions of sodium bicarbonate will not be so great, although this latter procedure may be used and will at least be of value in treating the resulting acidosis. Correction, of Acidosis.--The most important phase of the treat ment is directed at correcting the acidosis which is produced in the body by the formation of formic acid from the methyl alcohol. It has been the writer's experience to find that medical literature frequently advises treatment of acidosis, but fails to give details of such treat ment. For this reason, some detail in the treatment of acidosis is here included. In other sections where treatment of acidosis is suggested, reference to this description has been made. The use of sodium bicar bonate or sodium lactate intravenously is advisable. It is safest to calculate the dose necessary to restore the serum bicarbonate accord ing to the method of Hartmann and Scnir5: (60--CO:.,) 0.7W mM. = 2.24 mM. millimols of sodium bicarbonate or sodium lactate CO., w serum carbon dioxide content in volumes per 100 cc. body weight in kilograms One mM. of sodium bicarbonate is 0.084 gm.; 1 mM. of sodium lactate is contained in 1 cc. of r-molar sodium lactate. In marked acidosis when serum carbon dioxide is not known, 5 mM. of sodium bicar bonate (1.4 gm.) per kilogram of body weight is a safe dose. Hart mann recommends the injection of one-half the calculated close of sodium lactate intravenously and one-half subcutaneously as onesixth molar sodium lactate. R-molar sodium lactate is obtainable in sterilized ampules, which most physicians will find more convenient than sodium bicarbonate. Sodium bicarbonate cannot be boiled or autoclaved in an unsealed vessel without forming the highly toxic sodium carbonate. Sodium bicarbonate may be weighed and added with aseptic precautions to sterile water or dextrose solution and in jected intravenously in a 2 to 5 per cent solution. Both sodium bicar bonate and sodium lactate may be given by mouth when the patient is able to take them by this route. (a) Solutions for Use in Acidosis.--Several very valuable solu tions for use in treatment of acidosis arc on the market. An interstitial salt solution (sodium chloride, 6.5 gm.; sodium bicarbonate, 2.5 gm.; 170 OCCCPATtOXAL DISEASES and potassium chloride, 0.1S gm. per liter) may be prepared by the addition of the contents of a 50 cc. ampule (Sharp and Dolimc Co., Philadelphia) to 500 ce. of sterile water. It may be used in practically all eases of acidosis without additional sodium bicarbonate and may be given subcutaneously or intravenously. Lactate-Ringer's solution (sodium chloride, 6 gm.; sodium lactate, 2.7 gm.; potassium chloride, 0. 4.gm.; and calcium chloride, 0.2 gm. per liter) is equally valuable and is prepared in concentrated form in ampules the contents of which are to be diluted with distilled water (Eli Lilly and Co., India napolis) . Other Measures.--In addition to treatment of the acidosis the patient should be kept warm. Intravenous infusion of 10 per cent dextrose in physiological saline may be of value in supporting him. and for this there has also been advised the intramuscular administra tion of atropine sulfate, %0 grain (0.0015 gm.), not to be repeated; strychnine sulfate, %o grain (0.002 gm.); metrazol. 1% grain (0.1 gm.); camphor in oil, 1 to 2 cc.; coramine, 1.5 cc.; or caffeine sodium benzoate, 7% grains (0.5 gm.). Aromatic spirits of ammonia, from y2 to 1 drachm (2 to 4 ce.) by mouth is said to be of value. If pain is present, the use of morphine sulfate, % grain (0.015 gm.), despite its central depressant effect, or codeine phosphate, 1 grain (0.065 gm.), is frequently used; and if delirium is present from %0o to ^00 grain (0.0002 to 0.0003 gm.) of scopolamine hydrobromide may be combined with the morphine. Use of 50 per cent solutions of sucrose in treatment of cerebral edema if present has been suggested. The oral administration of a large dose of magnesium sulfate is usually part of the routine. With the exception of the eye, most abnormalities from chronic exposure clear up after removal from exposure. REFERENCES 1. Greenburg, L., Mayers, M. R., and Smith. A. R.: Ind. Bull. Div. of Indust. Hyg., New York State Department of Labor. Vol. 18. No. 10. Oct.. 1939. 2. Bull. No. 86. New York State Department of Labor. 3. Hartmann, A. F., and Senn, M. J. E.: "Studies in the Metabolism of Sodium r-Lactale: II. Response of Human Subject with Acidosis to the Intravenous Injection of Sodium r-Lactate," J. Clin. Investigation, 11: 337 (March). 1932. CHAPTER XV AMMONIA AND PHENOL AMMONIA Ammonia is an irritant causing inflammation of the eyes, nose, throat, and lungs. Like many other irritants, it is rarely absorbed into the bloodstream, affecting the surface tissues only, and especially those which are moist, such as the conjunctivae and mucous membranes. Ammonia in liquid form is furnished in steel cylinders, or supplied in water as a hydrate. Liquid ammonia is most extensively used as a refrigerant, but there are at least thirty other occupations or processes which use ammonia. The aqueous solution is widely used in the various arts. Tannery and dye workers, employees working with explosives, fer tilizers, sewers, varnish silk, nitric acid, etc., may be subjected to its effects. Signs and Symptoms.--Conjunctivitis, swelling of the eyelids, burning of the throat, coughing, pulmonary edema, irritation of the skin, especially if it is moist, dyspnea, and respiratory failure are symptoms. Because the gas gives a warning signal, fatal dosing is not common. The maximum concentration allowable for prolonged exposure is 100 parts ammonia per million parts of air. For a short exposure the maximum concentration allowable is from 300 to 500 parts per million of air. Exposure to more than these amounts, or a very short exposure to from 5000 to 10,000 parts per million, has been fatal. Medicolegal Aspects.--This gas offers little in the way of contro versy. The occupation, the facts surrounding the alleged accident, the characteristic odor, and the signs and symptoms presented easily establish the case. Temporary Disability.--This is usually not more than seventy-two hours. If the eyes are severely burned, there may be a temporary disability of several weeks. Pneumonia may occur following pulmonary edema or severe inflammation of the lungs. To be considered com pensable, the patient must present these symptoms within a few hours or days following exposure, and not several weeks or months later. Permanent Disability.--This is exceedingly rare, and if it occurs is most apt to be due to involvement of one or both eyes. A concen- 171 172 OCCUPATIONAL DISEASES tratecl amount of ammonia in contact with the cornea is apt to cause prolonged disturbance of vision or permanent damage. Once perma nent loss of vision is established, the extent should be determined and so rated. Treatment. General Pleasures.--If liquid ammonia is spilled upon the clothing, all clothing should be immediately removed and the body thoroughly drenched with water. The eye injured by ammonia should be immediately and copiously washed with water, and this may be followed by the introduction of a saturated solution of boric acid. If pain is severe, the use of a local anesthetic such as 0.5 per cent solu tion of pontocaine hydrochloride is indicated. Thereafter the applica tion of olive oil or some similar oil is desirable. Continuous warm boric compresses to the eyes may be of value. The usual treatment for corneal ulcers should be instituted if this complication occurs, and an ophthalmologist should be consulted. Respiratory and Circulatory ,Measures.--If the concentration of fumes has been severe and respiration affected, inhalations of from 5 to 7 per cent carbon dioxide in oxygen should be given, and if pul monary edema ensues the use of oxygen by means of a tent or intra nasal apparatus is advised. The administration of such respiratory and cardiac stimulants as the following may be of value: coramine, 1.5 cc.; metrazol, from lJ/4 to 4% grains (0.1 to 0.3 gm.); and caffeine sodium benzoate, 7% grains (0.5 gm.). Some of the respiratory and cardiac effects may be reflex from the pulmonary bed in origin, and because of this the intravenous administration of atropine sulfate, from %o to Vts grain (0.0011 to 0.0009 gm.), and papaverine hydro chloride, % grain (0.032 gm.), might be of value. These should be freshly prepared from the powders just before use. PHENOL Phenol is used widely in industry, but in spite of its severe toxic properties and corrosive action rarely leads to fatalities. The occa sional case, however, is of interest. We are not concerned with the accidental or intentional drinking of carbolic acid, but rather with the effect upon the system by absorp tion. Phenol is readily absorbed through the unbroken skin and is inhaled in the form of vapor. Phenol and the two naphthols, alpha and beta, once absorbed are partly oxidized, partly excreted in the urine in a combination with sulfuric and glycuronic acid, or are ex creted unchanged. The effect is primarily on the central nervous system. Signs and Symptoms.--When phenol is absorbed through the skin, the symptoms develop rapidly (as will be seen in the illustration AMMONIA AND PHENOL 173 below). Dizziness, tinnitus, dyspnea, confusion, muscular twitching, loss of consciousness and death may follow. In mild absorption, head ache, dizziness, irregular rapid respirations, and a weak pulse may be present. When death occurs, it is usually within a few hours of exposure. Illustrative Case: Case I,--A twenty-two-year-old male, employed by a concern manufacturing ink, was crossing the plant when he dropped a bottle of carbolic acid. This saturated the right leg, right side of the ab domen, and the chest. Fellow-employees immediately removed his shirt and threw water over his upper body. The patient then walked across the street to a physician's office without any difficulty'. How ever, within fifteen minutes after arriving at the doctor's office he collapsed and died. Autopsy examination, at this clinic, revealed extensive first- and second-degree burns of the right side of the body, right arm, right leg. and scrotum. There was hyperemia and edema of the lower por tions of the lower lobes of both lungs, marked hyperemia and edema of both kidneys, pancreas, and spleen. There was no change in the heart or liver. Analysis of portions of the pancreas, spleen, and kid ney was positive for carbolic acid, and the chemist reported the quan tity found was increased five times over that usually found in these tissues at autopsy. As in any instance where a patient is saturated with a known noxious solution, all clothing should be removed in order to prevent further absorption. The above case illustrates the rapid absorption through the skin and by inhalation, producing death. Treatment. Principal Steps.--As indicated above, the case of phenol poisoning encountered in industry will usually differ from that seen in private practice in that the mode of poisoning will be by ab sorption through the skin or by inhalation in the form of vapor rather than by drinking of the material. The most important steps, then, in the acute case of industrial phenol poisoning will be: (I) the removal of all clothing to prevent further absorption; (2) washing of all involved areas on the skin with a 25 per cent solution of either alcohol or glycerin; and (3) treatment of shock. Respiratory and Circulatory Measures.--The patient should be kept as warm as possible, and symptoms of circulatory shock and respiratory depression should be treated by use of the various stimu lants mentioned in previous sections. For the respiratory stimulation the most valuable are inhalations of from 5 to 7 per cent carbon dioxide, and solutions such as mctrazol, 1 f t grains (0.1 gm.); camphor in oil. from 1 to 2 cc.; caffeine sodium benzoate. 7*^ grains (0.5 gm.). 174 OCCUPATIONAL DISEASES intramuscularly: or coraininc. 1.5 cc., intravenously or intramuscularly. For the circulatory shock intravenous infusion of 1000 cc. of 10 per cent dextrose in distilled water, and drugs such as the coramine, caffeine, or epinephrine hydrochloride, from l/> to 1 cc. of 1:1000 solu tion, intramuscularly, may be used. However, there is some question concerning the advisability of the use of epinephrine in cases of poison ing, for the reasons indicated in the section on treatment of electrical injuries. The use of digitalis preparations is frequently mentioned in treatment of circulatory shock, but seems of very questionable value in this situation. First-Aid Measures.--As first-aid measures, a quantity of olive oil, cod-liver oil, cottonseed oil, castor oil, or any other available vegetable oil should be given by mouth, as well as egg-white. Mineral oil affords no protection against phenol, since the solubility of phenol in it is quite small, about 1 in 50 parts. Alcohol, previously thought to be of value, should not be given by mouth or used for gastric lavage, since alcohol, although a good solvent for phenol, seems to increase the rate of absorption of phenol from the stomach. Thorough gastric lav age with 10 per cent solution of glycerin, or, if this is not available, with sodium sulfate, 15 gm. (4 drachms), to the pint of water shall be carried out. Nephritis, if it occurs as a complication, should be treated by the standard methods employed for this disease. It has recently been shown by Meyer1 that a high protein diet given to rats increased very definitely their resistance to phenol poi soning. This observation, however, probably has no great practical significance in treatment of the poisoning once it has occurred, other than to suggest the use of a high protein diet. REFERENCE I. Meyer, A. R.: Proc. Soc. Exper. Biol, and Med., Jl: 402 (June), 1939. CHAPTER XVI CARBON MONOXIDE Unlike most of the hazards discussed in this book, that created by carbon monoxide is not confined primarily to industry. Poisoning from this substance is apt to confront men in any walk of life. As a cause of death its incidence closely approaches that due to automobile accidents. The cardinal facts concerning an illness or death following sub-Icthal or lethal exposure are well known to all who practice medi cine. It is said to be the oldest of all poisons, dating back to the time man first made a fire and hovered over the flame. Much has been written about carbon monoxide, and investigation of its action has been profuse. Yet there still remains considerable confusion as to cer tain phases of CO poisoning, which needs to be clarified, especially as it concerns workmen's compensation. It is with that fact in mind that the following paragraphs are written. Properties.--Carbon monoxide is a colorless, tasteless, almost odor less, insidious gas with a density of 0.967 as compared to air. It can be compressed into a liquid and a solid. It burns with a blue flame. When combined with one volume of oxygen, it forms two volumes of carbon dioxide. Carbon monoxide originates from incomplete combus tion of carbonaceous material. Sources of Incomplete Combustion.--There are several: Illuminating Gas.--This in many parts of the country is referred to as "manufactured gas" in contradistinction to natural gas. Illumi nating gas is obtained by forming an admixture of water gas with coal gas, or a petroleum product. It generally contains between 20 and 30 per cent of carbon monoxide. In most cities where this gas is manufactured, the average composition is as follows: Substance Per Cent Carbon dioxide ................................................................. 3.5 to 4 Benzol .................................................................................. 1.0 Olefins .................................................................................. Oxygen ................................................................................ Hydrogen ............................................................................ Methane .............................................................................. 5.0 to 3.0 to 44.0 19.5 6 5 Nitrogen .............................................................................. 4.0 to 5 Carbon monoxide ............................................................. 20.0 to 21 176 OCCVl'ATIOXAL. DISEASES Water Gas.--This is made by passing steam over heated coke and contains about 40 per cent carbon monoxide. Coal Gas.--This is formed from the distillation of coal and contains about 5 per cent carbon monoxide. Natural Gas.--This contains varying proportions of methane, ethane, nitrogen, and carbon dioxide. It contains no carbon monoxide, but if combustion is faulty there may be carbon monoxide present. Occupational Hazards.--Because it is practically ubiquitous, it is impossible to list every hazard. The more common sources arc elec tric furnaces, blast furnaces, manufacturing of gas. distillation of oils, charcoal ovens, refuse plants, kilns, and coal mines. To a lesser extent for acute poisoning, but a common source for chronic exposure, is the occupation of presser in tailor shops, laundry workers, garage me chanics, furnace-tenders, firemen, cooks, and housewives. Broadly, anyone who works where power or heat is being generated by a com bustion process of carbonaceous material may be exposed to carbon monoxide poisoning. Pathology.--As a prelude to the discussion of the pathology of carbon monoxide it would seem appropriate to mention certain physio logical phenomena of this gas. Types of Asphyxia.--CO belongs to the group of gases classified as asphyxiants. Of these there are two division: (1) Those which result in asphyxia due to a cessation of breathing. This may be from a me chanical obstruction to normal respiration or to the action of drugs upon the respiratory center. Strangulation, drowning, or confinement in an oxygenless vault or cave-in of dirt are examples of mechanical asphyxia. Morphine and chloroform, acting upon the respiratory cen ter, are examples of the action of drugs. (2) Asphyxia resulting from a deficiency of oxygen but where breathing is not interfered with. Comparison of Cyanide and Carbon Monoxide Poisoning.--This second type of asphyxia is produced by two chemicals, carbon mon oxide and cyanide, each of which acts differently within the body. As pointed out under ``Cyanides," the cyanides poison the tissue cells in all parts of the body to prevent the entrance of oxygen into the cells. Carbon monoxide on the other hand reacts within the blood stream. While carbon monoxide enters the body only through the lungs, it causes no immediate reaction within those organs. During acute carbon monoxide poisoning there exists no interference with oxygen entering the lungs in sufficient quantities. But after the initial reaction with the CO, the blood can no longer absorb what oxygen the lungs supply. In cyanide poisoning the oxygen enters the body and is transported by the bloodstream, but the gate is closed against its entering the various tissue cells of the body. CARBON MONOXIDE 177 Supplanting of Oxygen in Bloodstream by Carbon Monoxide.-- As carbon monoxide enters the bloodstream, it immediately com bines .with the hemoglobin and replaces the oxygen. The normal oxy hemoglobin is therefore converted into carbon monoxide hemoglobin, as illustrated by the following equation: Hb02:C0: :HbC0:02. This reaction is reversible, for as oxygen is supplied and carbon mon oxide removed the oxygen supplants the carbon monoxide existing in the bloodstream in combination with Hb to again form oxyhemo globin. It should be noted that the red cells which carry this carbon monoxide are not injured in the process. Finally, concerning this inter change of gases, it is important to know that carbon monoxide has a greater affinity for hemoglobin than has oxygen, this affinity being estimated at approximately 300 to 1. General Changes.--The body at the time of death may show cherry-red blotching at various areas. Upon opening the body, one finds the blood bright red. It is usually coagulated but at times fluid. Hemorrhages may be present in the lungs, pleura, pericardium, in testinal tract, uterus, and under the mucous membranes of the body. Regarding the heart, there is a marked lack of sufficient autopsy re ports to enable investigators to formulate a definite conclusion con cerning the cardiac damage which may result from CO poisoning. To date the evidence would indicate that there is no marked damage to the heart or coronary vessels unless the exposure has been of the severest type. The lungs usually reveal no special change unless the period of unconsciousness has been prolonged. Changes in Central Nervous System.--Primarily, the central ner vous system sustains the greatest injury as a result of carbon mon oxide poisoning, although the nerve tissue of any part of the body may be involved. Vascular lesions constitute a prominent part of the pathological alteration, the arteries as well as the veins being involved. In the brain the vascular stasis is pronounced, the vessels being dilated and packed with red blood cells. Petechial hemorrhages are often numerous and scattered. Following the vascular congestion edema ensues. The increased congestion and accumulative edema will cause a rise in the intracranial pressure. Owing to this widespread involve ment of the brain, a victim who survives a sublethal but severe ex posure may show evidence of disseminated encephalitis, bilateral softening of the lenticular nucleus, internal hydrocephalus, or a combi nation of these lesions. DIAGNOSIS Signs and Symptoms.--Following the work of Haldane, Henderson, and Haggard, and Sayers and Yant, of the Public Health Service of 12 178 OCCL'PATIOXAL DISEASES the United States and the Bureau of Mines, Hamilton1 formulated the following table: Percentage of CO in Air 0.02 0.04 0.08 0.16 0.32 0.64 1.28 Effects Possible headache, mild frontal in two to three hours. Headache, frontal, and nausea after one to two hours. Occipital after two and one-half to three and onehalf hours. Headache, dizziness and nausea in three-quarters of an hour; collapse and possible unconsciousness in two hours. Headache, dizziness, and nausea in twenty minutes; collapse, unconsciousness, and possibly death in two hours. Headache and dizziness in five to ten minutes; un consciousness and danger of death in thirty min utes. Headache and dizziness in one to two minutes; un consciousness and danger of death in ten to fifteen minutes. Immediate effect; unconsciousness and danger of death in one to three minutes. The signs and symptoms of carbon monoxide poisoning fall into one of three groups: (1) acute asphyxiation, (2) acute asphyxiation with delayed symptoms, and (3) chronic poisoning. Acute Asphyxiation.--As seen by the above table, this may vary in its extent, being dependent upon the concentration of the gas. the activity or inactivity of the patient, and the individual susceptibility. Headache and dizziness may be noticed with possible nausea if the concentration docs not immediately overcome the patient. Survivors have related a throbbing type of headache with roaring in the ears, confusion, and general weakness preceding their unconsciousness. Un consciousness occurs when nearly half the hemoglobin is bound to the CO. If bodily effort is made during the exposure, unconsciousness comes on more quickly. It is thought that CO is eliminated in from twelve to twenty-four hours. Patients usually recover consciousness at a 50 per cent CO-hemoglobin level if the poisoning occurred sud denly and the patient is not long in the contaminated atmosphere. The duration of exposure is more important than the percentage of CO in the determination of severity and in the production of perma nent sequelae. CARBON MONOXIDE 170 Acute Asphyxiation with Delayed Symptoms.--Symptoms and neurological changes may be noticed immediately, or there may be a delay of from a few days to several weeks. Based upon the recog nized pathology, most authorities contend that signs or symptoms must appear within the first three or four weeks. After that time they are to be considered as coincidental and unrelated. This contention is frequently questioned in medicolegal cases, as seen in Case III. In the unquestioned case, the picture is varied. Headaches and dizziness may ensue and persist. Visual deficiency or blindness may be present. Twitching, choreiform movements, or convulsive seizures occur. The emotional life and willpower may be profoundly altered. Apathy, dis interest, dulled memory, lack of judgment, and in fact the whole gamut of mental changes even to idiocy or imbecilia have been noted. There may be confusion, hallucinations, states of excitement and symptoms suggesting general paresis. Parkinsonism is not unusual. In addition to the effect upon the central nervous system, pneu monia may set in within a few days following the acute exposure. Deglutition pneumonia following vomiting of food has been reported. There are also references in the literature to complications following hemorrhage into the kidneys, spleen or liver. Permanent damage to the heart is highly controversial. Chronic Poisoning.--Carbon monoxide is not cumulative. It is re placed by oxygen. The regulation of the number of working hours is such that man lives in an oxygen-pure air at least twice as long as in a contaminated air every twenty-four hours. Therefore, chronic exposure is not likely to produce pathological changes. But constant assault to normal function may result in dysfunction, such as loss of appetite, digestive disturbances, headaches, diminished vigor, poor color, and apathy. These disappear upon removal of the patient from the exposure. (a) Claims of Disability.--Claims of disability due to chronic carbon monoxide poisoning are difficult to evaluate. There arc usually no objective findings, and the subjective symptoms may well be the result of non-industrial disease and usually are. The basis for accept ance or denial of the case of alleged chronic poisoning is less stable than in the acute cases. (b) Unreliability of Tests.--The blood cannot be depended upon for a diagnosis. While it is sometimes possible to demonstrate carbon monoxide in the blood of the chronically exposed, many factors tend to discredit the test. Testing the air after duplicating the exact con ditions under which the patient works would be a better method when possible. While it has been generally contended that chronic exposure leads to an increased red count and hemoglobin, this cannot be ac 180 OCCUPATIONAL DISEASES cepted as a criterion for a positive diagnosis. Tests showing a poly cythemia may have caught the patient at a time when the cells were responding to the tissue's demand for more oxygen. Later there may be a decline from this primary response to the point where the pic ture may be that of a moderate secondary anemia or even of pernicious anemia. In most instances a rigid investigation will reveal other causes for the symptoms allegedly due to chronic carbon monoxide poisoning. Exposure on. Highway.--Truck-drivers who make long hauls are subjected to an exposure which might bo. termed the "subacute" car bon monoxide poisoning. While that term has never been applied to this hazard by other writers, it is meant to designate those cases which fall short of exposure to a sublethal dose but exceed the minute chronic assault. The following investigation illustrates this contention and is an important contribution to the present status of carbon monoxide poisoning. Survey in California.--In a survey2 conducted in 1938 by the In dustrial Hygiene Service in conjunction with the California Highway Patrol, 1105 commercial motor vehicles of various types were tested during five-minute runs on the highway, under varying weather and road conditions, to determine the amount of carbon monoxide in the air breathed by the driver; 2.9 per cent of these vehicles were found to be in a potentially dangerous condition, due to concentration in the driver's compartment of over 0.01 per cent of carbon monoxide, which may cause headache, sleepiness, weakness, faulty judgment, and impaired driving ability, if inhaled continuously over a period of six hours or longer. The four-mile section of U. S. Highway No. 70, between Blythe, California, and the plant quarantine station at the state line, was selected as the location for the survey. The majority of automobiles entering Blythe from either direction have been run continuously for several hours. It is under such conditions of prolonged exposure that the driver and passengers arc most likely to experience the toxic effects of relatively low concentrations of carbon monoxide in the car. Several instances have been reported in which the occupants of an automobile reaching Blythe, after a continuous three- or four-hour run, have gotten out of the car, walked a short distance, and collapsed, due to partial carbon monoxide asphyxia. Automobiles to be tested were taken at random. The tester entered the car with the carbon monoxide indicator, and rode to the other end of a four-mile test run. making a continuous reading of the carbon monoxide concentration at the driver's breathing level, while the car was driven at a. normal speed. Comparative readings were taken with CAHBOX MOXOXIDE 181 windows open and closed. Cordial cooperation was obtained from drivers and passengers of all cars included in the survey. AVhcn the concentration of carbon monoxide in the car was found to be higher than 0.01 per cent, the source of the trouble was located by checking along the exhaust system with the car at a standstill and the engine idling. Large defects, such as broken mufflers and miss ing tail pipes, were obvious on visual inspection. Small leaks in the exhaust line, unnoticcable. on casual inspection, were immediately apparent when the flexible hose attached to the carbon monoxide indicator was held at these points. Defects were pointed out to the driver, with recommendations for repairs. Summary of Findings.--Of the 1005 automobiles in which determi nations of carbon monoxide concentration were made, 30 cars, or 2.9 per cent, contained concentrations of the gas in excess of the safe limit; 50 per cent of these potentially dangerous cars were ten or more years old. In a majority of ears in which comparative readings could be made with windows both open and closed, the concentration of carbon mon oxide was higher when one or more windows were open than when all windows were tightly closed. This was particularly noticeable in cars with tight floor coverings, and with no large openings in the dash. This illustrates the fallacy of the widespread belief that keeping win dows open while driving is in itself a guarantee of protection against gas. On the contrary, if gases are escaping from the exhaust system, the suction created by open windows may draw into the car larger quantities of gas than would enter with windows closed. In each of the 30 automobiles in which a concentration of carbon monoxide in excess of 0.01 per cent was found, the trouble was traced to defects in the exhaust system. In the absence of exhaust-system leaks, the amount of gas reaching the breathing level of driver and passengers was greater in cars equipped with short exhaust pipes, than in cars with long pipes. Illustrative Accident Due to Poisoning.--During the survey an accident occurred which is an illustration of the accident hazard due to exhaust leaks. A sedan being driven at moderate speed, on a straight, level highway, ran into the ditch and turned over. A sample of the driver's blood, taken one hour after the accident, showed that 18 per cent of the blood hemoglobin was combined with carbon mon oxide. About one half of the carbon monoxide in the blood washes out in the first hour after removal from the exposure. At the time of the accident the driver of the car probably had a carbon monoxide-hemo globin saturation of about 35 per cent. This is sufficient to cause head 182 OCCUPATIOXAL DISEASES ache, weakness, nausea, dizziness, sleepiness, faulty judgment, im paired driving ability, and in some cases unconsciousness. The driver had noticed a hissing sound in the engine, but had continued driving. She noticed a gradually increasing headache and sleepiness before los ing consciousness. Inspection of the wrecked car showed a blown-out exhaust gasket, and several small holes in the dash. Undoubtedly, en gine gases caused partial asphyxiation of the driver. Conclusions.--The following conclusions were reached: 1. Carbon monoxide asphyxiation is responsible for many other wise inexplicable highway accidents. 2. The underlying cause of this hazard is the escape of exhaust gases from leaks in the exhaust system and their entrance into the car in dangerous quantities. Tests.--The hygienist, not the industrial physician, should concern himself with the estimation of the carbon monoxide present in air where man works. References to such tests are of no value, therefore, in this discussion, but the industrial physician should on occasion re quest that such estimates be made in order to establish the authen ticity of the claim. On the other hand, every industrial physician should know and be prepared to test the blood of any patient sup posedly overcome by carbon monoxide. Spectroscopic and microspectroscopic methods are designed for the investigator or one who has immediate access to a laboratory equipped for such tests. But the following test is simple. Tannic Acid Test of Blood.--Sayers and Yant's tannic acid method gives an approximate quantitative estimate of the CO present. In a small test-tube dilute 0.1 cc. of suspected blood with 0.4 cc. of dilute ammonia (1 cc. of strong ammonia per liter). Mix and add 1.5 cc. of freshly prepared 1 per cent tannic acid solution. Let stand over night and compare the color either with permanent standards or with standards prepared simultaneously as follows: Bubble CO or illumi nating gas through 1 cc. of oxalated blood until saturated. Dilute this and also 1 cc. of normal blood with 4 cc. of dilute ammonia. Make up a scries of mixtures of these hiked bloods (in 0.5 cc. volume) corre sponding to 10, 20. 30, 40. 50. and 60 per cent saturation. Add 1.5 cc. of tannic acid solution to each. In none of these tests are the color differences well marked if the CO saturation is under 20 per cent. In acute poisoning the saturation usually ranges from 25 to 60 per cent or more, but it falls quickly after the patient is removed from the source of poisoning (30 to 50 per cent per hour in air, about four times as fast in 95 per cent O and 5 per cent C02). CAHBOX MONOXIDE 183 Another simple test is merely that of boiling some withdrawn blood. Ordinary blood becomes brown-black, while blood rich in CO becomes a brick-red mass. While easy to do. this test is devoid of any estimate of percentages. A handy, quick determination is that of taking 2 cc. of carbon monoxide blood with an equal quantity of water and adding three drops of one-third saturated solution of copper sulfate. This will give a brick-red precipitate, while normal blood will yield a greenish brown one (Zalcski). Differential Diagnosis.--An authentic history of exposure, the ab sence of the odor of alcohol on the breath, and the presence of the symptoms previously outlined will indicate a CO poisoning. Difficulty lies in the variation of degree of intoxication resulting in a simulation of other diseases. Drug poisoning, alcoholism, cerebral and cardiac accident, and coma from diabetes or uremia must be considered. Sui cidal intent must be differentiated from industrial exposure. Finally, a diagnosis of acute carbon monoxide -poisoning is never positive un less determined by an examination of the blood. In instances where carbon monoxide is suspected but where it has disappeared from the bloodstream it may be found hours later in the spinal fluid. Sequelae of Acute Carbon Monoxide Poisoning: 1. When the dose has been sublethal and the exposure short, recovery rapidly takes place within a few hours or a day or two at the most without residual symptoms or signs. 2. If the dose has been sublethal but severe, the patient may: (a) recover within a few days to continue his previous state of health with out ever showing any subsequent evidence of carbon monoxide poison ing; or (6) signs or symptoms may be noted upon the patient's emerg ing from the initial coma; these may persist for several days, several months, or for the duration of the victim's life; or (c) following the unconscious period, the victim may be apparently normal for a few days to several weeks, only subsequently to reveal nervous or mental impairment. Here again the length of this impairment is indefinite. It may be temporary, lasting for several weeks to several months, or be a permanent change. Effect on Liver, Spleen. Kidneys, and Lungs.--There is no volume of evidence that severe acute exposure affects these organs in any permanent manner. The lungs will invariably reveal moisture immedi ately following the gassing. This will immediately disappear, or pneu monia may be a complication, although this is not common. How ever, pneumonia, to be attributed to exposure to this gas, should ensue within a few days to a week following the exposure. Tuberculosis is not a sequela. Glycosuria is frequently present in acute poisoning 184 OCCUPATIONAL DISEASES from this gas. It usually disappears within a few days, and normal liver funetion is resumed. It is held that the mobilization of sugar in such instances results from central nervous system impairment during the phase of asphyxia. Some differ from this view, placing the respon sibility upon the adrenals or the thyroid, or both. While the urine also reveals albumin, this likewise soon clears up and rarely is there permanent damage to the kidneys. The previous paragraph indicates that the. majority of the sys tems of the body escape damage to any appreciable extent from an assault of carbon monoxide. Two systems, not mentioned in that para graph, deserve more detailed consideration; namely, the nervous and circulatory systems. Effect on Nervous System.--From what has been written, it is obvious that the central nervous system exceeds all the others in its frequency of injury. Yet the frequency of permanent damage does not parallel to any extent the incidence of injury. The profession and laity have an erroneous belief that patients who show early mental or nervous changes continue to do so for the rest of their lives. Probably the best concrete rebuttal to such a belief is to be found in the report of Schillito.3 In the New York City area from 1925 to 1935, there were more than 21,000 cases of acute intoxication from carbon monoxide. Schil lito reviewed these records, as well as the records of seven state insti tutions that receive the mental and neurological patients from that city. From his investigation he estimated that only one in every 500 patients with acute carbon monoxide poisoning later showed mental or nervous symptoms. Regarding subsequent psychoses, he found only one case of carbon monoxide psychosis to 2000 other types of psy choses, or a percentage of 0.05. Effect on Heart.--Does acute carbon monoxide poisoning produce cardiac changes of a permanent nature? Concerning the occurrence of nervous system lesions due to CO intoxication there exists no lack of evidence, but regarding permanent heart lesions, dogmatic opinion should be withheld until reasonable scientific deductions can be made from a large scries of autopsied cases and also from a scries of cases in which the state of health was known before exposure and in which these patients have been followed for a long period of time after ex posure. The consensus in the literature is that, aside from the expected imposition placed upon the heart at the time of gassing, there persists no cardiac damage. Invariably, autopsy reports describe profusely the pathological changes in the central nervous system, but only occa sionally refer to findings in the heart, which would suggest a coiuci- CARBON' MOXOXIDK 185 dental relationship rather than a consistent sequela. Paul YUiite.4 in discussing remote causes of heart changes says: Some changes in the heart have been reported, as for example, sub endocardial hemorrhage after CO poisoning, but such changes have been neither extensive nor consistent. Chronic symptoms and signs, such as the inverted T waves in the electrocardiogram resemblingcoronary T waves, should be ascribed to pre-existing heart disease, whether or not accentuated or revealed after CO poisoning, about which especially there has been so much uncertainty. (a) Electrocardiographic Changes.--Stearns, Drinker, and Shaughnessy'* conducted an electrocardiographic study of a series of cases of carbon monoxide asphyxia to find that the most common deviation is an abnormality in the T waves or in the level of the ST segment. They feel that the changes, having been transitory, may be ascribed to carbon monoxide asphyxia, except when coronary disease may have been a contributing cause in some cases. (b) Basis for Diagnosis of Cardiac Injury.--There is no intention in the previous statements to imply that permanent cardiac damage cannot occur following a severe, prolonged exposure. In such instances signs and symptoms referable to the heart should be in evidence, im mediately or soon after the exposure. The condition should be fol lowed by periodic examination; and if it is apparent that the impair ment is of a permanent nature, the workman should be accorded compensation. But the onset of a heart lesion months or years after an exposure to carbon monoxide poisoning deserves no consideration as to their relationship. More will be said upon this point after sev eral recent articles have been reviewed. (c) Opinions on Cardiac Involvement.--That carbon monoxide rarely produces any cardiac damage finds adverse opinion in a report of Beck and Sliter in 1938, and reiterated more recently by Beck, Schulze, and Suter.' Their observations include both the acute and chronic types of exposure. The first article deals with the role of car bon monoxide in the causation of myocardial disease, while the sec ond one considers nervous system lesions as well as the cardiac. They state that carbon monoxide anoxemia does not differ essentially from anoxemia associated with severe forms of anemia, and point out that certain investigators have called attention to the association between angina pectoris and pernicious anemia. The factor responsible in both instances is the diminished oxygen-carrying capacity of the hemo globin. They vest authority for this belief in the papers of Keefer and Resnik, Elliott, Cabot, and Allbutt, wherein it is expressed that the 186 OCCUPATIONAL DISEASES anginal syndrome, as well as coronary disease, may result from anox emia of the myocardium. But Beck and Suler do not emphasize the fact that in severe anemias the anoxemia is a constant factor. It would seem that they refute themselves when they go on to quote Kroetz as stating that: The classic anoxemic lesions in the heart of victims of carbon mon oxide are hemorrhage, necrosis and processes of granulation and re generation, and these lesions coexistent with similar lesions in the brain add to their significance. The lesions undergo rapid regenerative changes, and the processes of repair may be fully developed by the ninth day. This observation of Kroetz is in keeping with the observations of White and also those of Stearns. Drinker, and Shaughnessy, concern ing electrocardiographic changes previously referred to, and in which there is evidence that the changes are transitory. Beck and his workers state that carbon monoxide anoxemia has a predilection in the heart for the left ventricle and the papillary muscle of the mitral valve. These hemorrhagic lesions, they avow, are fre quently found at autopsy. Such a contention is to be challenged. While it cannot be disputed that such hemorrhagic lesions may be found at postmortem examinations, they have not been observed or reported in sufficient frequency to classify them as regular, consistent sequelae. It would appear that Beck and Suter, and Beck, Schulze, and Suter have had opportunity to study a series of cases which presented mul tiple symptoms of ill health. Among these were patients who also had symptoms referable to the circulatory system. In the first of the two papers presented by the above men they considered a series of 136 cases of supposed carbon monoxide anoxemia of a chronic type ex tending over a period of fifteen years. The chief complaints of many of these patients, they state, were referable to the cardiovascular system. They do not state how many of the 136 patients revealed car diac lesions undoubtedly due to chronic exposure to this gas. Nor do they indicate that the percentage of patients having cardiovascular lesions was high enough to exclude any doubt as to the causal rela tionship. Only five histories are detailed; and, of these, two patients had coronary thrombosis; two had angina pectoris; and one myocar dial failure. The first patient cited was thirty-six years of age; the remaining were seventy-four, fifty-nine, sixty, and fifty-five years re spectively. a period when heart disease may be expected irrespective of other causes. The following is a case they report to illustrate their point: CARBON' MONOXIDE 187 B. C. Tv., a lawyer, aged fifty-nine, a resident of Oklahoma, re ferred by Dr. XL L. Lewis, had suffered for two years prior to admis sion from frequent attacks of precordial distress, clinically diagnosed as angina pectoris. Although for several years the patient had had only occasional attacks of angina pectoris, in the late fall of 1934 they increased in frequency, averaging one daily until Jan. 10, 1935, when he went to Dallas for consultation. From there he came to Baltimore for further study and observation. During this period he did not have a single attack, nor did he have any while under our observation, a period of two weeks. On examination Feb. 6, 1935, he was unable to recollect having had a single attack during the summer months when not ex posed to carbon monoxide. This fact led to the assumption that carbon monoxide was a factor in the production of his anginal attacks. Further inquiry revealed a history of exposure to carbon monoxide over a period of twenty-five years. His house was heated by natural gas in open heaters, inadequately ventilated. For the previous five years he had been exposed also in the gas and oil fields; besides, he frequently detected escaping gas in his automobile while driving with the win dows closed. In addition to anginal attacks, he complained of symptoms of anoxemia: dyspnea, palpitation, weakness in the legs, unsteady gait, cramps in the calf muscles, headache, vertigo, cardiospasm and par esthesia. He used alcohol and tobacco moderately, drank coffee to excess and overworked. His blood pressure was 102 systolic and 80 diastolic, his pulse rate 66 and his temperature subnormal. The heart was slightly enlarged, with an occasional dropped beat and reduplication of the second sound. No murmurs were heard. The blood vessels appeared normal for a man of his age. Laboratory studies showed mild glycosuria, a blood sugar content of 174 mg. per hundred cubic centimeters, a basal metabolic rate of minus 21 per cent and a negative Wassermann reaction. A blood count showed hemoglobin content 81 per cent, red cells 4,780,000, and white cells 8,250. Electrocardiographic study by Dr. King revealed an abnormal tracing suggestive of myocardial degeneration, possibly of coronary origin. The diagnosis of angina pectoris was confirmed by Dr. L. F. Barker. By improving the heating conditions and adopting a more hy gienic mode of living, the patient improved and remained free from anginal attacks for some months. He later had symptoms of myocar dial degeneration with congestive heart failure. In the above history, the exposure to carbon monoxide allegedly resulted from living in a house heated by natural gas, from being ex 188 OCCUPATIONAL DISEASES posed in the gas and oil fields, and from his automobile. The ease history does not reveal the extent of the exposure in any of these three phases. Just why these exposures must be accepted as the cause of the man's precordial distress is difficult to understand. Possible ad verse criticism of such reasoning would not be entertained if the ex tent of exposure had been reported. But upon a similar basis of rea soning, the alleged cause cannot be accepted until the actual extent is known. As a counter argument the author's uncle could be used as an illustration. This member of the Johnstone family lived his entire life in homes heated by natural and manufactured gas, worked for over thirty years in the gas and oil fields, and had the usual exposure to automobile exhaust fumes. Yet he died at the age of eighty, free from any cardiac involvement. His case can be reduplicated by millions of others. In the case reprinted from the article of Beck and Suter it is inti mated that the freedom of attacks during the summer was due to the absence of exposure to carbon monoxide from heating sources. Else where in their article they refer to the seasonal incidence of heart attacks and suppose that this increase in the winter is the result of gas stoves. They refer to reports by Wood and Hedley8 and by Mas ter, Dack and Jaffe,n wherein the seasonal incidence of heart attacks is studied. But after reading the two papers they refer to, one can find no inference that carbon monoxide is a factor in the production of heart attacks. These two sources are concerned with the factor of cold as a precipitant of heart attacks. In contrast to these contentions of Beck and Suter, McNally,10 who has had a wide postmortem and pathological experience with carbon monoxide, makes no observation that chronic exposure pro duces cardiac lesions or that cardiac lesions are apt to appear months or years after an acute exposure. Sandall11 found no abnormality of the heart in 85 per cent of cases in which tachycardia had been a definite symptom. Loewy1 reported a case of chronic carbon monoxide poisoning in a furnace-tender after an exposure of ten years in whom the symptoms were referable to irritation of the labyrinth. No cardiac lesion existed. Baader1 reports a case of labyrinthine disturbance in a man who had charge of a gas-generating department of a manufactur ing plant in which there was a four-year exposure. He observed no cardiac condition. Hamilton1 states: The subjective symptoms described by men and women who work continually in air vitiated by carbon monoxide cannot be distinguished from the symptoms of ill health which come from factory work itself, from long hours indoors, making the same movements over and over, plagued by noise and vibration, by excessive heat and humidity, the CARBOX MONOXIDE 189 effects of all of which may be enhanced by poor food, crowded sleep ing quarters, advanced age. or some chronic disease. It may be that the symptoms will disappear if the patient changes to another kind of work; but even that is not evidence of the action of carbon mon oxide, for the new factory may be comfortable, the man may be better adapted to his new job, and his wages may be higher. In her monograph she makes no mention that heart lesions follow chronic exposure or are to be expected; nor does she intimate that, once the patient has recovered from his acute exposure without im mediate evident sequelae, a cardiac disturbance may appear sometime later. (of) Cardiac Resistance to Carbon Monoxide.--An experimental example of the resistance of the normal heart to carbon monoxide is to be found in the experiment of Haggard1- in which he subjected dogs to carbon monoxide, producing death in from twenty-five to forty min utes, during which time he took electrocardiograms. He noted no toxic action of this gas upon the heart, the reaction being due to the anox emia alone. If the anoxemia was relieved, -the effects upon the heart disappeared. Zondek made observations on three young adults who were rendered unconscious by carbon monoxide. In addition to a fall in blood pressure, irregularity of pulse and tachycardia which subse quently became slow, the x-ray study of the heart of these three youths showed dilatation. All three patients made a complete recov ery. To these cases of Zondek's13 may be added an interesting case of Colvin's.11 This patient was rendered unconscious from the fumes of an automobile exhaust. Electrocardiograms taken from twenty-four to seventy-two hours after the poisoning revealed evidence of intra ventricular block. Subsequent electrocardiograms revealed improve ment, and a similar study sixteen days later was normal. He was dis charged as normal. The papers of Beck and his associates have been criticized at some length because of the dangerous implications they make. They would have us draw conclusions upon a basis of reasoning not ordinarily ac ceptable in medicine, certainly not in medicolegal medicine. In indus trial medicine, to assume without accurate knowledge involves an eco nomic injustice. To give credence to Beck's contentions would lead to many false claims and, therefore, to legal entanglements that would parallel the former status of silicosis. To reiterate, the conclusion he and his workers reached is this: In a group of 136 patients who had been intermittently exposed to carbon monoxide over varying periods, they noted that myocardial symptoms were frequently manifested. They propose that the carbon monoxide was the etiology of the car 190 OCCUPATIONAL DISEASES diac disturbance, yet it is not shown that there existed any constant relationship between the anoxemia of CO and heart disability. They do not reveal any figures of the amount of CO in the blood of these patients, or of the amount of CO in the atmosphere. A great deal of their study was with the natural gas of West Virginia, which contains no carbon monoxide; and unless all the allegedly affected persons were using defective appliances, they would not be exposed to carbon mon oxide. It is apparent that every here and there in their scries there was a patient who had heart symptoms and who had been exposed to carbon monoxide at intervals to no known amount. Master13 has estimated that from 500,000 to 1,000,000 Americans sustain a coronary occlusion annually and that this occurs chiefly be tween the ages of thirty-five and sixty. This estimation does not in clude heart lesions due to infection or toxic states. There thus exists a large group of cardiac cases in which carbon monoxide is not enter tained as the etiology. On the other hand, millions of Americans who have had a chronic exposure to carbon monoxide live and die without any evidence of heart lesions. Finally, since this gas is probably the oldest known poison and since its properties are well known, it is most likely that investigators, toxicologists, and pathologists would have long ago recognized a relationship between chronic exposure and heart lesions had one existed. MEDICOLEGAL ASPECTS Criteria for Establishing Compensability of Heart Lesions.--In light of the existing knowledge of the effects of carbon monoxide upon the heart, the following are suggested criteria upon which the indus trial physician could estimate the justice of a claim: Ivimediately after Exposure.--If immediately following, or with in from a few days to a week after a severe exposure to carbon mon oxide fumes, a patient develops a cardiac lesion which was not known to be present prior to the exposure, he is to be accorded the benefit of the doubt and be duly compensated. A non-disabling- valvular lesion recognized as being of long standing and due, for instance, to a luetic or rheumatic cause should receive no consideration. Several Months after Exposure.--If a cardiac lesion is alleged to have had its onset a number of months following an acute exposure of varying intensity, the cause is to be seriously questioned and all factors carefully evaluated before a decision is reached. Several Years after Exposure.--If a cardiac lesion is alleged to have had its onset several years following ail acute exposure of vary ing intensity, the claim is to be denied. I know of no way in which one could reasonably establish the authenticity of the claim. CAHBOX MOXOXrDF, 191 After Prolonged Exposure to Small Amounts.--If a cardiac lesion lias its onset after a prolonged exposure to minimal doses of carbon monoxide, the case must be most carefully investigated. This includes search for evidence of the existence of a lesion in previous medical ex aminations; estimation or measurement of the gas in the alleged haz ard; examination of the blood of the patient if he is still working in the hazard at the time he makes his claim; and consideration of his past medical history concerning rheumatic infections, repeated ton sillitis, quinsy, lues, the thyroid state, evidences of long-standing dys pnea, orthopnea, and the like. Certainly the burden of proof in such an instance is upon the claimant. For instance, it would be unreasonable to assume that a minimal chronic exposure was responsible for arterio sclerosis with hypertension and decompensation in one in his fifties or sixties. Temporary Disability.--This ceases with the termination of the symptoms. It may be from a few days to several months. Prolongation demands consideration of the factors of the original exposure as to degree, length, and severity of the initial symptoms. Permanent Disability.--Almost without exception this occurs when there has been damage to the central nervous system. Such changes should be manifested within from several days to three weeks follow ing exposure. If immediate recovery takes place, a symptom arising months or years later should not be attributed to carbon monoxide without adequate foundation. Search for unrelated pathology should be made. Illustrative Cases: Case I.--A night watchman was found unconscious in "his office," which was only large enough for a bunk, stove, chair, and readinglamp. The light was burning, a detective magazine was by his side, and the gas was escaping from the rubber hose, which had split at the wall connection. Carried outside, he was given artificial respiration. Upon his admission to the hospital, the physical examination was in keeping with the history of exposure and the blood positive for CO poisoning. He remained in a deep coma for ten hours. Following his exit from coma, a complete right-sided paralysis was present with inability to speak. He eventually recovered his speech, the complete use of the right leg and partial use of the arm, but he remained childish, had a dulled memory, failed to differentiate his wife from the rest of the family or friends. He answered all questions by yes or no, but never spoke a completed sentence. Little or no improvement occurred in the following three years. All of the requisites for accepting this case as compensable are satisfied. History, positive evidence in the blood test, and sequelae 192 OCCUPATIONAL DISEASES are in keeping with experience. In this instance, complications were present from the beginning, there being no delay in the onset of symptoms. Case II.--Two truck-drivers, making a long hank pulled into a roadside eating-place. "While the helper entered to procure sandwiches, the driver stretched out in a partially dosed cab with the engine run ning. Interest in a broadcast of the war news in Europe delayed the helper. Upon returning to the truck, he found the driver unconscious. Hushed to a nearby physician, the patient regained consciousness while in the doctor's office and before resuscitation was attempted. No blood examination was made. Headache was complained of for about ten days. He returned to work fifteen days after the incident. The physician's diagnosis was carbon monoxide poisoning. Because the patient was in a cab of a truck, the motor of which was running, indicates that he might have been in a coma from carbon monoxide poisoning, but such an assumption was not established. The proximity of the exhaust to the cab was not stated, no mention of a leak in the exhaust system was inquired into, the patient's blood was not examined for CO, nor was there any attempt to find any other cause for the coma. Compensation for temporary disability was paid by the insurance company. The circumstances and the "doctor's diagnosis'' precluded any other course. If subsequent mental sequelae of an indefinite nature had arisen, the questionable role played by carbon monoxide could never have been established equitably. Case III.--A fifty-nine-year-old night mechanic was found uncon scious in a garage nearby the running motor of a truck. He was appar ently normal two hours previously when he dispatched a truck and driver from the place. After preliminary attempt at resuscitation he was taken to a Long Beach hospital, where a diagnosis of carbon mon oxide poisoning was made. After remaining in the hospital for one week, he went home, but continued to report thrice weekly to his physician for treatment to a leg burn suffered at the time of his at tack. After seven weeks lie returned to work and continued at that for two months at which time he was discharged by his employer. Following his discharge, his wife filed claim for permanent total disability, stating that her husband had undergone a change in per sonality as a result of the carbon monoxide poisoning. This change, she alleged, consisted of loss of memory, apathy, and disinterest, in ability to concentrate sufficiently to finish any project he attempted, and other conditions. Six months after the alleged poisoning and just prior to the trial, the patient was referred to the writer. CARBON' MONOXIDE 193 History.--The past medical history was irrelevant. With the excep tion of poor oral hygiene and slight bilateral edema of the ankles, the general examination was negative. The heart action and cardiac his tory did not account for the edema. The neurological examination was entirely negative. The patient had a stolid, quiet, reticent manner, but his expression did not impress the examiner as being typical of the mask-like countenance of parkinsonism. lie readily answered all questions, was well oriented as to time, place, and events and smiled when humorous remarks were made. The laboratory investigation was entirely normal. Testimony.--The following facts were brought out at the trial. Sometime before he lost consciousness (the patient does not know how long), he had a severe pain around his heart while outside the garage. When he was taken to the hospital no blood test was made for the presence of CO. The wife stated that she noticed definite men tal changes in her husband two or three days after his accident. The physician who first cared for him had recorded no such changes in the progress notes or in his office record. The employer testified that he had noted changes in the character of the patient's work prior to his accident. The psychiatrist who testified for the claimant believed the man had parkinsonism as a result of carbon monoxide exposure. A second psychiatrist who examined the patient, but did not testify, reported by letter that he believed the man did not have parkinson ism and was able to work. The author testified that while the circum stantial evidence strongly indicated a carbon monoxide poisoning, this diagnosis could not be established in the absence of any blood test, and such a diagnosis, while likely, was clouded by the patient's statement that some hours previously he had had a severe heart pain. Furthermore, the author felt that it was impossible for him to evalu ate any alleged change in this man since he did not observe him prior to this accident, and other than the wife's statement there was no evi dence that such a change had occurred. Certainly to him the case was not a definite parkinsonism. The commission found that no evidence had been produced to show that the claimant was either mentally or physically unfit to work as a mechanic. The case is presented not because it adds any thing to the knowledge of carbon monoxide poisoning, but for certain lessons which can be drawn from it. These lessons are to be found in errors of omission committed by the physician in attendance. Had the patient been overcome in his own home, these omissions would not have been so significant. First, while the circumstances strongly indi cated a carbon monoxide poisoning, the diagnosis was never estab lished owing to the failure to examine the blood. It subsequently de veloped that a possibility of a cardiac episode clouded the issue. 13 194 OCCUPATIONAL DISEASES Second, the wife's contention that mental changes set in shortly after the accident could not be denied or substantiated by the physician's hospital record or office file. He failed to appreciate the possibility of the development of latent effects. It should be apparent to the reader, then, that a case of carbon monoxide poisoning arising out of occupa tion should first be established by blood investigation for CO and then observations for sequelae recorded over a period of time. Case IV.--A presser in a tailoring establishment claimed loss of weight, fatigue, and two attacks of coma due to chronic exposure to gas fumes. His physician, upon the basis of history, diagnosed the case as chronic carbon monoxide poisoning. He was given from three to six months' temporary disability and advised not to return to work. The insurance carrier desiring to determine the authenticity of the claim was unable to locate him for three months, but at the end of this time found him visiting relatives in Arizona. An investigation re vealed that he was a Russian Jew; his mother had diabetes: he had been refused insurance because of sugar in the urine eight years pre viously; he had polyuria, polydipsia, excessive appetite, glycosuria, and a blood sugar of 280 mg. Investigation of his working conditions re vealed that he pressed but rarely, usually being engaged in repairing and mending. The machine he did operate when pressing was located by an open window. The case was not compensable. Preponderant evidence pointed to diabetes mcllitus, and the occupational conditions indicated the im probability of exposure. Case V.--The patient, aged thirty-nine, was brought to the clinic by a female physician, who believed that her patient had acute CO poisoning. The history was that the patient was found semi-conscious near a large coffee urn in the hotel where he was a cook. Upon admis sion he was cold and clammy but conscious. He complained of pain in the left chest; lips, ear lobes, and fingertips were cyanotic. Heart tones were distant, the pulse weak, and fibrillation was noted. Blood pressure was 90 systolic, with the sounds immediately disappearing. Electrocardiogram was not taken. The patient died in three hours. The blood was negative for evidence of CO. Autopsy revealed no evi dence of CO in the blood or cavity fluids, but did show a fresh coro nary thrombosis. The case presents no difficulty in diagnosis. Had the patient died at home some days or weeks following exposure without blood deter minations, there might have been legal controversy. Case VI.--An unmarried professional man, aged twenty-seven, was found unconscious with a companion in a parked automobile on CARBON MONOXIDE 195 the morning of February 18, 1984. The estimated duration of expo sure to carbon monoxide, was about six hours, and another three hours elapsed before he was brought to the hospital. The companion was dead when found, which indicated the severity of the exposure. The windows of the car were closed, the engine had been left running, and later investigation revealed a leak in the gas heater with which the car was equipped. On his admission to the hospital, physical examination showed the patient to be in profound coma; he was cold and clammy; there was extreme cyanosis of the face and extremities; and the lips were cherryred. The heart tones were of good quality. The lungs showed moist rales, and breathing was greatly labored. The abdomen was distended and tympanitic. There had been a profuse spontaneous diuresis before the patient was moved from the car. The pupils were widely dilated and reacted only slightly to light; corneal reflexes were absent. The only other neurological feature of import was a bilateral Babinski sign. For the first thirty-six hours after his admission to the hospital the patient remained in a profound coma. For the next thirty-six hours the coma was apparently less profound, and the patient began to show some involuntary movements, moving his head and hands aimlessly. At this time he was also able to take fluids orally. On the following day a more noticeable restlessness developed; the patient opened and closed his eyes, snapped his fingers, and thrashed about in his bed. This behavior continued for nearly two weeks with but little change. Sixteen days after admission the patient rather abruptly regained con sciousness and recovered his power of speech. Neuropsychiatric ex amination at this time showed a marked clouding of the sensorium. Attempts to converse with him elicited only brief, but not entirely pointless remarks. Asked, "What is your name?" he replied, "Puttentain," a response suggestive of a childhood game which the patient had known. To other questions relative to his background he gave abusive retorts, as, "Who the hell wants to know?" He showed no evi dence of recognizing his mother or sister with whom he had been liv ing at the time of the accident, or other close relatives or friends. Questions relative to his physical condition brought a more adequate response, and he complained of pains in his legs and feet. During the days immediately following he was ovcrtalkalive and showed a marked flight of ideas. He was irritable, profane, ob scene, combative, argumentative, and extremely uncooperative. He showed an almost complete loss of memory for recent and remote events. He demonstrated some of the components of the parkinsonian syndrome in a marked degree. These consisted of pill-rolling, drool ing from his mouth, and, to a lesser extent, the masklike facies. This condition was evident on the sixteenth day after exposure lo carbon monoxide and persisted for over a month, disappearing gradually. 190 OCCUPATIONAL DISEASES After lie had regained consciousness the patient suffered severe pains in tile arms and legs and was very voluble in his complaints about this condition. The toe drop on the right was noticed on exami nation of the limbs. The peripheral neuritis responded rather slowly to baking and massage, and except for mild paralysis of the muscles of the right foot, which was aided by a support, the patient made a com plete recovery. lie became oriented in all spheres, regained his mem ory for remote and recent past events, and returned to his normal mental level by the sixtieth day after admission. He was discharged seventy-seven days after admission, but he was unaware of the nature of his illness before this time. On being informed of the circumstances of the accident resulting in his illness, he showed a normal concern for his dead companion and for the possible consequences to himself and his relatives. About a year after the accident the patient was able to resume his professional activities in a limited way, and a year after this (two years after the accident) he had so far recovered that he discharged his full duties without any noticeable impairment.10 This case illustrates the severity of exposure, the onset of neuro logical signs and symptoms within the expected two- or three-week period, and the eventual recovery after a temporary disability of two years. Case VII.--A fortv-two-year-old auto mechanic was found uncon scious in a private garage where he had been dispatched to repair a car. From a subsequent history it was believed the door had been closed by the wind, without the victim's knowledge. The lips, ear lobes, nails, and face were cyanotic, and the body was cold. The respiration was very shallow. Artificial respiration was given until a doctor from a nearby emergency hospital arrived with an oxygen-carbon dioxide apparatus. After fortv-five minutes of this treatment, the patient was removed to the hospital. Immediate examination of his blood showed a 35 per cent saturation of carbon monoxide. The blood pressure was 130, systolic; 85, diastolic. Pulse upon arrival was 130 and regular: temperature, 97.2 F. The heart sounds were distant and feeble; the lungs were normal. The oxygen-carbon dioxide administration was continued for two hours after admission. About one-half hour after ad mission the electrocardiogram showed the S-T segment depressed in Leads I, II, and III, and elevated in IV. The T wave in Lead IV was upright and abnormally high. The patient thrashed about the bed for nearly six hours. The following day he complained of headache, was not clear about the events of the preceding day, and acted indifferently to relatives. At this time there was moisture in both bases of the lungs, the pulse was regular with a rate of 90. The blood pressure was 118, systolic; 80, diastolic. There were no signs of central nervous system in CARBON MONOXIDE 197 volvement at this time. Against his wishes lie was retained in the hos pital for five clays. Upon discharge his general physical condition was normal, as was the electrocardiogram. Two years later this patient was seen because of a fractured rib; and a re-check examination proved him to be normal in all other respects. The factors surrounding the onset of coma indicated carbon mon oxide poisoning. This was soon established by the finding of an abnor mal amount of carbon monoxide in the blood. He returned to his work sixteen days after exposure. The case was compensable. It is used here to illustrate the effect upon the heart of CO poisoning, with the subsequent and rapid clearing of these signs. TREATMENT Prophylaxis.--The prevention of carbon monoxide poisoning in industry is not ordinarily a difficult problem. In the larger industries where combustion of various types is a part of the process, the hazard is well recognized, and, therefore, precautions arc taken. Small plants and garages constitute a more likely source of this poisoning. Ade quate ventilation is all that is necessary to insure against poisoning from this gas, but men need to be warned about closing windows and doors, which they are prone to do in the winter months. Acute Anoxemia.--When this occurs, the victim should be im mediately removed from his exposure and artificial respiration begun. There is no point in delaying this in order to obtain a pulmotor. as is so frequently done. This machine has not sufficient advantage over human manipulation to warrant the delay. It is extremely important, however, that inhalations of from 5 to 7 per cent carbon dioxide in oxygen be started as soon as possible. The inhalations should be in creased to the point where full, deep inspirations are obtained from the patient. AH emergency squads which are frequently called to at tend such cases should be equipped with this carbon dioxide and oxygen mixture with inhalation apparatus for its administration. If such apparatus is immediately available, the patient should be kept warm with blankets and hot-water bottles and treated at the spot, rather than be moved to the hospital with attendant delay in the ad ministration of the inhalations. It should be remembered that prob ably half of the carbon monoxide is eliminated from the body during the first hour after removal from the exposure, and consequently longcontinued administration of the carbon dioxide and oxygen may not be required. If such inhalations are not available, the patient should be transported to a hospital where they can be obtained, and en route it is necessary to continue the artificial respiration. 198 OCCUPATIONAL DISEASES Koch1' recommended blood transfusions preceded by venesection in severely acute cases. lie pointed out that the chief effect of carbon monoxide poisoning was the anoxemia and, therefore, the hemoglobin introduced by means of the blood transfusion will act at once as an oxygen vehicle. Methylene blue, once thought to be an antidote, is not of value and is now thought to be harmful. With the possible exception of caffeine, it is felt that the use of drugs is ineffectual if not actually harmful. Strychnine, camphorated oil, digitalis, pituitary extract, adrenalin, alpha-lobcline, and morphine fall into this category. The use of 12 ounces (850 cc.) of physiological solution of sodium chloride given by rectum every four hours during the first few days has been suggested, as has the rectal administration of a 4 per cent sodium bicarbonate solution. REFERENCES 1. Hamilton, A.: Industrial Toxicology, Harper and Brothers, New York, 1934, pp. 122. 141. 2. Russell, J. P.: "Carbon Monoxide on Highways," California Safety News, 23 (June), 1939. 3. Schillito, F. II., Drinker, C. K., and Shaughnessy, T. J.: J.A.M.A., 106: 669, 193G. 4. Brahdy, L,, and Kahn. S.: Trauma and Disease, Lea and Febiger, Philadelphia, 1937, p. 26. 5. Stearns, Win. H., Drinker, C. K., and Shaughnessy, T. J.: "The Electrocardio graph Changes in 22 Cases of Carbon Monoxide Poisoning," Am. J. Heart Disease (April), 1938. 6. Beck, H. G., and Suter, G. M.: "Role of Carbon Monoxide in the Causation of Myocardial Disease." J.A.M.A., 110 (June 11). 1938. 7. Beck, H. J.. Schulze, W. H., and Suter, G. M.: "Carbon Monoxide, A Domestic Hazard," J.A.M.A., 115 (June 6), 1940. S. Wood, F. C., Hedley, 0. F.: "The Seasonal Incidence of Acute Coronary Occlu sion in Philadelphia," M. Clin. North America, 19: 151 (July), 1935. 9. Master, A. M., Dack, S., and Jaffe. II. L.: "Facts and Events Associated with Coronary Artery Thrombosis," J.A.M.A., 109: 541-549 (August 21), 1937. 10. McNally, Wm. D.: Toxicology, Industrial Medicine Publishing Co., Chicago, 1937. 11. Sandall, T. E.: "Later Effects of Gas Poisoning." Lancet, 2: 857-859 (Oct. 21), 1922. 12. Haggard, H. W.: "Studies in Carbon Monoxide Asphyxia, I. The Behavior of the Heart," Am. J. Physiol., 56: 390. 1921. 13. Drinker. C. K.: Carbon Monoxide Asphyxia. Oxford University Press, New York, 1938. 14. Colvin, L. T\: "Electrocardiographic Changes in a Case of Severe Carbon Mon oxide Poisoning." Am. Heart J., 3: 484, 1927-28. 15. Master, A. M., Dock. S,, and Jaffe, II. L.: "The Relation of Effort and Trauma," lndust. Med., 9: 399 (July), 1940. 16. Sanger. E. B., and Gilliland, Wm. L.: "Severe Carbon Monoxide Poisoning with Prolonged Coma Followed by Transitory Psychosis, Peripheral Polyneuritis and Recovery," J.A.M.A., llh: 324 (Jan. 27), 1940. 17. Koch, K. G.: "Blood Transfusion in Treatment of Acute Severe Carbon Monoxide Poisoning," Miinchen. med. Wchnschr., S6: 126 (Jan. 27), 1939. CHAPTER XVII THE CYANIDES AND NITROUS FUMES THE CYANIDES The cyanides arc dramatized as suicide agents, and the wide use of these compounds in industry is not appreciated. Like carbon mon oxide, they act as an asphyxiant, but instead of combining with hemo globin within the bloodstream the cyanides attack the tissue cells, retarding or stopping oxidation. This protoplasmic action results in the arrest of internal respiration with paralysis of the respiratory center. Since this action within the tissue cells takes place even in an atmosphere of pure oxygen, oxygen therapy is of little use in cyanide poisoning. The chief cyanogen compounds are hydrocyanic acid, cyanogen, acetonitrile, propionitrile. methyl isonitrile, ethyl isonitrile, benzonitrile, and cyanogen chloride. Of these the most toxic is hydrocyanic acid. It is used chiefly for the effect the gas has upon vermin. Sodium cyanide has a wide use in industry as a bath in dipping- or treatingprocesses. Henderson and Haggard cite the following psysiological re sponses to various concentrations of hydrocyanic acid as reported by Robert. Slight symptoms appear after several hours' exposure with from 20 to 40 parts of HCN per million parts of air. The maximum amount for one hour without serious disturbance is from 50 to 60 parts; dangerous after thirty minutes, 120 to 150 parts; rapidly fatal. 3000 parts. The rule of the Public Health Service is that an experi enced workman may enter a room after fumigation if the air con tains no more than 0.1 part per 1000 parts of air. Occupational Hazards.--Fumigation of ships, dwellings, hotels, and apartment houses; the hardening of steel, iron, cutlery, and ma chine parts; cleaning or coating silver; electroplating; metallurgy; tan ning; dehairing and dyeing; and in use as a fertilizer (calcium cyanamide). DIAGNOSIS Signs and Symptoms. Acute Poisoning.--In fatal cases there are rarely any witnesses to the demise. Certain patients who narrowly escaped death report their preliminary symptoms as constriction of the throat, dizziness, fulness of the head, nausea, and vomiting. Some of these patients have then gone into convulsions. Examination of these patients has revealed the eyes to be glassy, staring, and the lfl9 200 OCXTI'ATIOXAL DISKASKS pupils dilated. The body is covered with a cold sweat, and frothing' at the mouth occurs, with the frothing often blood-stained. Respiration is slow and shallow. Involuntary defecation or urination is common. For a lime there may be complete paralysis. If recovery occurs there is usually headache, drowsiness, and difficulty in speaking. As with all asphyxiants, a transient glycosuria is not uncommon. A rosy red color of the skin is usually present, although varying degrees of cyanosis have been observed. To all these cited findings, an almond odor to the breath is confirmatory. Cyanide asphyxia has been considered the quickest acting mode of death, yet McNally cites several interesting instances where the suicide performed an act before death ensued. For example, a man took a drink of cyanide in a hotel, then walked to the window and tossed the bottle out. Chronic, Poisoning.--Cases of chronic poisoning are extremely rare. Gastrointestinal symptoms predominate, characterized by flatulence, cramps, vomiting, and obstipation. The patient becomes increasingly nervous, and headache and dizziness exist. Irritation of the skin, with conjunctivitis, edema of the eyelids, and lacrimation, frequently ap pears in those continuously exposed, especially if exposed to cyanogen chloride. A cyanogen rash is characterized by itching, papules, and vesicles, with frequent secondary infection. Certain observers think the reaction is more the result of lime and other caustic agents than cyanogen. The writer has observed this rash in men doing electro plating. but was unable to ascribe it to the cyanogen primarily. Poly cythemia is the occasional blood picture of the chronically exposed. Tests.--Reagents are: (I) Ferrous sulfate, 1.5 per cent; ferric chloride, hydrochloric acid, and sodium hydroxide, each 10 per cent. To about 10 cc. of the suspected fluid (blood or gastric contents, etc.) two drops of the sodium hydroxide are added. Then, following the addition of 2 cc. of ferrous sulfate and 1 cc. of ferric chloride, the mix ture is warmed, and hydrochloric acid is cautiously added, avoiding any excess. A blue precipitate shows the presence of hydrocyanic acid. (2) Dissolve 10 mg. of ferrous ammonia sulfate and 10 cc. of ammonium acetate (5 to 10 per cent) in 50 cc. of water. If 1 cc. of this solution is added to a small amount of blood containing cyanide, a purplish precipitate occurs. MEDICOLEGAL ASPECTS The author has seen but one industrial death due to cyanide. Of the cases reported in literature, they have occurred most often among fumigators. THE CVAXIDEK AXI) XITROl'S KI'MKS 201 Temporary Disability.--In the acute surviving cases, disability ceases with the disappearance of the symptoms which ordinarily do not last longer than one week and possibly two. In less severe cases, symptoms cease within a few days. In chronic cases, recovery occurs usually within a week or so following the removal of the patient from the hazard. However, cachexia, gastrointestinal disturbances, or psy choses may result in a longer disability. Permanent Disability.--There are no cases following survival re ported. Illustrative Cases: Case I.--A fifty-eight-ycar-old citrus-grove sprayer fell from a ladder as he was ascending it to spray fruit. lie was rushed to a small community hospital, where the attending resident physician was in cited into immediate specific treatment for cyanide poisoning because the employer stated that the man was possibly overcome by the spray, which contained cyanide. Failing to react to the first injection of sodium nitrate and sodium thiosulfate, a second one was admin istered. The patient remained in a deep coma for a number of hours, with a blood pressure of 240/130. Upon regaining consciousness, he was unable to talk: had a complete paralysis of the right side; albumin, easts, and red blood cells in the urine; and N.P.N. of 75 mg. Six weeks later the patient died, and suit was filed by a dependent, claiming death was due to apoplexy precipitated by exposure to cyanide. It was brought out at the trial that the deceased had been refused insurance five years previously because examination revealed hyper tension. Two weeks prior to the accident he had complained to a fel low-employee of weakness of the right arm. which lasted for two days. For several months he had frequented a local drugstore for headache medicine. Ilis attack occurred immediately after lunch. He had not sprayed for one hour and was just about to resume spraying when he fell unconscious. Xo test of the blood was made for the presence or absence of cyanide. The evidence pointed to an ordinary cerebral hemorrhage, preexisting causes for which were known. The effects of cyanide do not occur one hour after exposure as alleged in this case. There is no evidence that small doses would increase the blood pres sure. The claim was denied. Case II.--A male, aged thirty-seven, worked for twelve years for a magazine publisher as an "art painter." During that time his work exposed him to cyanide baths. The methods had been changed at in tervals, but the cyanide element was constantly present. He first no ticed a loss of weight, then marked constipation. Four or five months after the onset of the original symptoms, he had flatulence accom- 202 OCCUPATIONAL DISEASES panicd by abdominal cramps. One week prior to being examined at the clinic, vomiting had set in. Physical examination was essentially negative. Apparent focal in fection was absent. Heart and lungs were normal. The abdomen disclosed no palpable organs or masses and no specific point of tender ness. Neurological examination was negative. Laboratory investiga tion revealed the urine and stools normal; Wassermann, negative; gas trointestinal series, negative; red blood cells, 6,500,000; hemoglobin, 110 per cent; white blood cells, 9200. The patient was removed from his occupation. Within three days vomiting ceased; within two weeks his appetite improved, and a gain in weight was registered; abdominal cramps were less severe and disappeared entirely within a month. Specific laboratory work was not possible, but the mild polycy themia was suggestive. In view of the case history that an exposure existed, that the length of exposure was adequate, and that no other cause for the man's condition could be found, it was considered com pensable. There was no permanent disability. Case III.--Three men were fumigating grapevines to kill "leafhopper," a vine parasite. The material used was calcium cyanide pow der, applied by dusting machines mounted on a truck chassis. The ma chines throwr the cyanide powder through the air to a height of about six feet and a distance of about twenty-four feet on each side of the truck, dusting two rows of vines at each trip. When calcium cyanide comes in contact with moisture, it is decomposed, giving off hydro cyanic acid gas, which is extremely poisonous. Dusting is usually done at night, when air conditions are quieter than in the daytime. The men work in pairs and are instructed to work upwind from the sec tion already dusted. Details of this accident are not known, but a crew of three men was missed one night at about midnight. When found, one of the men was dead, and the other two were unconscious. First aid was given to all the men until they were removed to the hospital. The two who were still alive later developed pneumonia but recovered, with no disability. Gas-masks have now been ordered for all men on this ranch who handle, or are exposed to, cyanide, but it is a question how satisfac tory the use of such masks will be. Gas-masks are essential equipment for use in emergencies. Special canisters, designed to give protection against hydrocyanic acid gas, are good for concentrations of the gas up to 2 per cent in air, but are rapidly exhausted at such a concen tration. In addition, hydrocyanic acid gas is readily absorbed through the skin, so a gas-mask does not give full protection. A man working THE CYANIDES AND NITROUS FUMES 203 in a concentration of the gas as low as 0.5 per cent may absorb enough of the poison through his skin to produce symptoms after a half hour's exposure. In any case, if gas-masks are used, the canisters should be replaced at least every shift, and oftener if the exposure is at all severe; and men should keep out of the gas as much as pos sible. In this accident, it seems probable that sudden air currents car ried the gas back into the men's faces and they were overcome before they could escape. Gas-masks would probably have enabled them to get away. The death of the one workman was compensable. The other two had a short temporary disability. Treatment Death is frequently so immediate that treatment is futile. Oxygen has no value, as mentioned in the opening paragraph. Many patients, however, survive for three or four hours, and hence adequate time for treatment is available. Methylene-Blue Treatment.--Hanzlik and Richardson1 outlined the most effective measures for treatment in cases of acute cyanide poisoning. Fifty cc. of 1 per cent methylene-blue solution (containing 1.8 per cent sodium sulfate) is injected intravenously, and is repeated if necessary until 200 cc. are injected. Frequently, consciousness and reflexes arc restored before the first 50 cc. are completely injected; but if the patient lapses into unconsciousness, or manifests respiratory depression, resume the methylene-blue treatment. As quickly as pos sible, proceed with gastric lavage, using 5 per cent sodium thiosulfate; this oxidizes any unabsorbed poison. For lavage 3 per cent hydrogen peroxide or 0.2 per cent potassium permanganate solution may also be used if sodium thiosulfate is not at hand. Artificial respiration or carbon dioxide, from 5 to 7 per cent, with oxygen may be needed. Circulatory and Respiratory Stimulants.--Caffeine sodium ben zoate, 7grains (0.5 gm.), coramine. 1.5 cc., or metrazol, from 1)4 to 4% grains (0.1 to 0.3 gm.), intramuscularly may be needed for circulatory and respiratory stimulation. Sodium Nitrite Treatment.--An alternative treatment is as fol lows: Give at once a slow and careful intravenous injection of 1 per cent sodium nitrite solution, in five divided injections, until 50 cc. are injected in about one hour. If improvement is manifested, but prognosis is still unfavorable, the injection may be cautiously con tinued, but is to be stopped at once in case of sudden collapse. Epi nephrine, 1 cc- of 1:1000 solution, should be ready at hand to combat nitrite shock, if necessary. Fortify the nitrite treatment at once with the intravenous injection of 20 cc. of a freshly prepared 5 per cent 204 OCCUPATIONAL DISEASES aqueous solution of sodium thiosulfate (filtered), and if necessary continue the injection up to a total of 500 cc., if possible. Treatment directed at further circulatory and respiratory stimulation is used as indicated in the first outline. The solutions used in these treat ments can be readily sterilized by boiling for fifteen minutes. The methylene blue should not be dissolved in physiological solution of sodium chloride since precipitation occurs owing to a common ion (chloride) action. Both the methylene blue and the sodium nitrite appear to act by producing methemoglobin, which in turn combines with the cyanides to decrease the poisonous effects of the latter. Actually, sodium nitrite forms more methemoglobin, but this probably does not contribute to physiological recovery from poisoning, and there is danger of sus tained circulatory collapse to add to the already precarious state of the patient. Sodium Nitrite and Sodium Thiosulfate Treatment.--Ingegno and Franco- treated two patients with 0.3 gm. sodium nitrite in 10 cc. given intravenously at the rate of 2.5 to 5 cc. per minute, and fol lowed this by 25 to 50 cc. of a 50 per cent solution of sodium thio sulfate. given through the same needle and at the same rate. They warned that the sodium nitrite and thiosulfate must not be mixed before administration. If signs reappeared or persisted, one-half the dose of antidotes was repeated one hour later. They also used amyl nitrite inhalations for from fifteen to thirty seconds every two or three minutes. Diet.--A high fat diet has experimentally been shown to reduce the mortality from sodium cyanide poisoning.3 In the rare case of chronic cyanide poisoning such a diet possibly would be of use in addition to symptomatic treatment. The use of sodium thiosulfate, 10 cc. of a 10 per cent solution intravenously, two or three times per week might be of value. Removal from exposure is. of course, at once necessary. REFERENCES 1. Hanzlik:. P. J.. and Richardson. A. P.: "Cyanide Antidotes." J.A.M.A.. 102: 17404.5 (May 36). 1934. 2. Ingepno. A. P.. and Franco. S.: "Cyanide Poisoning." Indust. Med., 0 (Nov.). 1937. 3. Meyer, A. R.: Proe. Sor. Exper. Biol, and Med., it: 402 (.Tune). 1939. Cited in editorial. J.A.M.A., Hi: 49 (Feb. 10). 1940. NITROUS FUMES The exposure of nitric acid to air liberates its oxides, the chief ones being nitrous oxide, nitric oxide, and nitrogen dioxide. The profession is well acquainted with the use of nitrous oxide as an anesthetic. This oxide as well as nitric oxide needs no consideration at this time. THE CYANIDES AND XITKOUS FEMES 205 Nitrogen dioxide (peroxide, NCk) is evolved when nitric acid con tacts organic matter. It is an essential part of many industrial processes. Occupational Hazards.--Nitrous fumes are present in the manu facturing of certain explosives (not gunpowder). certain lacquers, photographic films, metal etching and photo-engraving, metal dip ping, such as the "bright dipping" of brass and copper, or wherever nitric acid or materials composed of nitrocellulose are handled. Car bon-arc booths arc a hazard but arc usually well protected by design and ventilation. These fumes may also offer a hazard to tunnel work ers or miners. Pathology.--As a result of exposure to nitrous fumes, arterial blood is rapidly turned into venous and becomes thick, tarry, and coagulates quickly. Hemorrhages into the various organs occur, espe cially into the gastro-intestinal tract. Marked edema of the lungs is found. The kidneys and liver have revealed lesions in those exposed. The most severe reactions, however, occur with the arterial blood and in the lungs. In the rapidly fatal case there may be no pathology other than congestion of the lungs. Signs and Symptoms.--It should be emphasized that the symp toms are tisually delayed. This latent period may be from a few hours to twenty-four or thirty hours. Unquestionably this offers difficulty in some instances in diagnosis, and unless the facts are known the etiology may be overlooked. No doubt, many cases of nitrogen dioxide poisoning have gone uncompensated. A physician friend of the author's, who was exposed to the fumes resulting from the Cleveland Clinic disaster, drove six miles to his home, felt exhausted, sat upon his front steps for nearly an hour, and then died. Acute Exposure.--In the acute non-fatal cases, headache, dizzi ness, cough, palpitation of the heart, sometimes cyanosis, restlessness, and inability to sleep, are common. In certain concentrations, the workman may feel dopey. This narcotic or depressive action some times retards the cough reflex, and the patient is not warned of his danger. In contrast to the narcosis that may develop, Ebright1 reports a case where the man became wild, irrational, and ran around butting against walls and trees. Pneumonia is a common sequela. Chronic Exposure.--This leads to headache, sleeplessness, loss of appetite and weight, dyspepsia, constipation, and ulcers of the mucous membranes; Laws2 reports a complete loss of vision in some. No proof exists that exposure may lead to chronic pulmonary disease, although certain clinicians have so stated. Medicolegal Aspects.--It is felt that above 0.2 mg. per liter of air constitutes a dangerous atmosphere. 206 OCCUPATIONAX. DISEASES Temporary Disability.--This is indefinite and entirely dependent upon the severity of the dosing, as well as the presence of sequelae. Permanent Disability.--This is not common, hut may occur. Illustrative Case: Case I.--While working on a California aqueduct, a workman was caught in the smoke from a dynamite discharge. He continued work ing that day but that night was awakened by extreme dyspnea and coughing. Three days later he was transferred from the field first-aid hospital to Los Angeles. At this time lie appeared to be in great distress and was apprehensive and restless. His temperature was 104.2 F.; pulse, 136; moist rales throughout both lung fields, with signs of bronchopneumonia in the light lung; and a continuous wracking cough, which was productive of a rather foul sputum. The urine was not abnormal, and the blood count was normal other than 22,600 white blood cells, with 95 per cent neutrophiles. Subsequently albumin and casts were present in the urine. During a period of three weeks, all signs and symptoms cleared, and the patient returned to work in one month after exposure. The physician who first saw this patient out at the aqueduct was acquainted with the effects of nitrogen fumes. When he received a history of the exposure to the "smoke'' from the dynamite, he was immediately suspicious of the cause of the man's illness. Temporary disability lasted one month. There was no permanent disability. A check-up two years later revealed that the patient was working and healthy. Treatment. Correction of Pulmonary Effects.--Oxygen, which has been passed through a bottle containing 2 grn. ammonium carbonate to 1.5 ounces of water, should be administered to patients in acute eases by means of an intranasal tube. (McNally recommends a tube in each naris.) For relief of the pulmonary edema, intravenous 50 per cent glucose in amounts of from 50 to 100 cc., up to 200 cc., daily, is used; salyrgan, from 0.5 to 2 cc. intravenously, at intervals of three days, is also of much value in treating the pulmonary edema. Seda tion for restlessness will be needed in many cases. If pneumonia appeal-s as a complication, the use of specific chemotherapy, i.e., sulfa nilamide, sulfapyridine, or sulfathiazole, may be instituted if a pre dominant organism can be demonstrated in the sputum. In case the carbon dioxide combining power is low, the treatment should be that described for acidosis under "Methyl Alcohol.'' Chronic Exposure.--Persons affected by chronic exposure may also be benefited by intravenous salyrgan. It is said that these patients often find sleeping in a rocking-chair easier than in bed. They will fre- THE CYAN'IDES AND NTTliOUS FUMES 207 queutly need acetylsalieylic acid or phenacetin. 10 grains (0.05 gin.). every four to six hours for headache, or if this symptom is more severe, codeine sulfate or phosphate, from (4 to 1 grain (0.032 to 0.005 gin.), every four to six hours. Sedation with drugs such as sodium bromide, from 10 to 30 grains (0.05 to 1.3 gm.), phenobarbital, 1(4 grains (0.1 gm.), or sodium pentobarbital, 1(4 grains (0.1 gm.), three times a day, is needed at times for restlessness. Constipation may need attention. The mouth washes described under "Mercury" may be of benefit in ulcers of the mucous membranes. The addition of extra vitamins to the diet should be of value. REFERENCES 1. Ebright. G. E.: "Tile Effects of Nitroglycerin on Those Engaged in Its Manu facture," JAM.A.. 62: 201, 1914. 2. Laws. C. E.: "Nitroglycerin Head." JAM.A., .51: 793 (March ;>), 1910. CHAPTER XV1H METAL-FUME FEVER, WELDING, AND GASES FROM CARBON ARCS METAL-FUME FEVER Metal-Fume fever is purely au industrial disease. It is character ized by a febrile reaction following the inhalation of finely divided particles of the metallic oxides. Among the working-men it is known as brass chills, brass-founder's ague, metal ague, zinc chills, speller shakes, and by other names. It is an old disease referred to frequently in the literature and needs but brief description. It is most important that its brief duration and absence of after-effects be emphasized. Pathology.--Actually there is no pathology resulting from this exposure, the reaction being physiological. It baffled the early experi menters as to just why the fumes produced an illness but the dry powder of these metals did not. Injecting soluble zinc oxide, Leh mann1 was unable to produce noticeable symptoms. It was suggested that the inhalation of fumes killed bacteria in the respiratory tract which, when absorbed, caused symptoms. Lehmann thought it might be that the inhalation killed off the epithelial cells, the proteids of which when absorbed produced the symptoms. Drinker- held that it was a physical difference; that the particles of ordinary oxides are large, settle quickly, and rapidly collect in clumps to adhere to the sides of the trachea. The fumes on the other hand are so fine that they pass rapidly through the upper respiratory tract into the lungs. Immunity.--Immunity to these fumes may be developed, but when it occurs there is leukocytosis, functioning as a defense mechanism. It is noticed that if a workman absents himself from his exposure for a few days, he will lose this immunity. Many workers report a state of well-being during the week, but after a week-end they will notice various grades of reaction upon a return to work. Certain workers have reported disturbance of liver function, glyco suria, and increased blood pressure and pulse rate. Signs and Symptoms.--These are closely comparable to influenza or la grippe. Chills come on usually after the patient has left work and last for one or two hours, rarely longer. The body aches all over; nausea and not infrequently vomiting may occur; fever sets in and may reach 102 P., seldom higher; the throat is dry, and there may 208 METAL-FUME FEVER. WELDING. GASES FROM CARBON ARCS 50!) be a dry cough. Weakness. lassitude, or exhaustion are complained of. The leukocyte count, may range from between 15,000 and 10,000 and may persist after all other symptoms disappear. A mild leuko cytosis is present as previously noted in those without symptoms. Chronic symptoms are rarely present other than in some instances when a complaint of generalized lassitude is made. Metal-fume fever is acute in onset and short in duration, the patient usually making a complete recovery within twenty-four or thirty-six hours. Pronounced chronic symptoms should arouse suspicion of lead's being the etio logical factor. Medicolegal Aspects. Temporary Disability.--This rarely lasts more than one or two weeks. In mild instances the patient loses no time from work, merely changing his job or receiving better protec tion. Patients in more acute cases usually return to work in several days. Permanent disability as a result of metal-fume fever is unknown. Cases of death have been reported, but no instances of recovery with permanent sequelae arc reported. Illustrative Cases.--A Negro, employed by a metal company, noticed a back-pain late one afternoon. He went home, changed his clothes, and reported to the clinic alleging back-sprain. While in the clinic he developed marked chills, began to ache all over, vomited on four occasions, had a temperature of 102.5 F. and a white count of 13,200. His headache became pronounced. During the early hours of the next morning a second Negro who had been working with this first patient was admitted with comparable symptoms. These two men had engaged for the first time to dump old bat teries and other scraps of metal into a reclaiming furnace which had a defective door, permitting the escape of fumes. Both recovered within two days. Their physical examinations were negative for focal infection or systemic disease. Treatment. La Grippe Regimen.--No specific therapy is indicated in these cases. Patients may be treated as though they had la grippe. The administration of acetylsalicylic acid, 10 grains (0.65 gm.), every four to six hours combined at times with codeine phosphate, from to 1 grain (0.0325 to 0.065 gm.), will afford relief. The forcing of fluids (water and fruit juices), the use of hot drinks, and rest in bed are of value. These patients will become symptom-free without treatment after absence from exposure for a short time, but for their composure the above regimen is prescribed. Prophylaxis.--The most valuable point, however, is to adopt an adequate medical and engineering program for prevention of the metal-fume fever. The toxic fumes should be controlled at their source 14 `210 OCCT L> AT I OX A I, DISEASES by having operations which give rise to metal fumes carried on, if possible, in a closed process. It will usually be. more practical to em ploy exhaust ventilation with hoods over the process producing the fume. The ventilating system should be designed so that a current of clean air is drawn past the operator and away from him toward the work. Masks and respirators may be provided for protection under unusual circumstances. REFERENCES 1. Hamilton, A.: Industrial Toxicology, Harper ami Brothers, New York, 1984, p. 82. 2. Drinker, P,, Thomson, R. M,, ami Finn, .1. T..: "Metal Fume Fever; Effects of Inhaling Magnesium Oxide Fumes." J, Indust. Ilyg., 0: 187, 1027. WELDING The process of welding is an important, necessary step in the struc tural-steel business, in repair shops, construction plants, and wherever solid metals are in use. Such operations are not without a hazard. Too frequently men arc employed in small, non-supervised shops or in confined areas such as ill-ventilated rooms, vaults, or tunnels. Forced ventilation is frequently absent and respirators ignored. Occupational Hazards.--The hazards of welding are from; (1) fumes, smoke, and gases; (2) radiation from the arc; (3) fire; and (4) electric shock. It is the first of these exposures that concerns us chiefly. In passing, it should be mentioned that protection from radiation is essential. This radiation is often a mixture of ultraviolet light, infra-red rays, and visible light. Exposed parts of the body should be well protected, but the eyes especially should be covered with glasses fulfilling the requirements of the federal specifications. Occasionally, claim is made that sexual impotence has resulted from the exposure to radiation. These claims and their remote possibility induced investigation along these lines. Today there exists no proof that this impotence occurs. Respiratory Hazards from Welding.--These may be divided into three general classes: (1) poisonous substances which may be gene rated by the arc; or by (2) faulty combustion; and (3) exhaustion of oxygen in air. Lead Poisoning.--This is the principal and typical hazard in the class of poisonous substances volatilized by heat. It occurs very fre quently when metals covered with lead paint are cut by either the electric arc or the oxy-acetylene flame. The heat volatilizes the lead, forming lead fume, which results in rapid and severe lead poisoning to the unprotected welder. Metal-Fume Fever.--Welding or cutting brass or zinc (galvanized sheets) frequently results in metal-fume fever, commonly called "zinc chills" or "zinc ague" (discussed earlier in this chapter). Even though METAL-Fl'ME FEVER. WELDIXC. OASES FROM GARBOX ARCS 211 this illness is temporary, it is far from pleasant. Other substances to be found as a coating on certain widely used rods include silicon di oxide. aluminum oxide, titanium dioxide, calcium, magnesium and sodium oxide, iron, manganese, calcium fluoride, and carbon dioxide. It has been suggested that these coatings are toxic when volatilized, but there is as vet little information on this point. Gas Poisoning.--Poisonous gases, of which nitrogen peroxide (dis cussed elsewhere in this book) is probably the most important, are generated by an electric arc. Only recently the death of a welder was attributed to this gas. In this instance, the worker was electrically welding together two halves of a hot-water tank in a room of about 4000 cubic foot capacity. All welding was on the outside of the water tank. The man became unconscious while welding and died six days later in a hospital. There are cases on record of fatal gassing due to nitrous fumes generated by oxy-acetylene torches. A. D. Brandt1 tells of a case in which several men were working with large oxy-acetylene burners on a heavy steel crosshead in a ship compartment. The compartment had a capacity of approximately 5000 cubic feet and was being venti lated at the rate of about 240 cubic feet per minute by means of a fan. After about forty minutes' work, several men collapsed, and one died in a hospital thirty-two hours later. The symptoms were typical of poisoning by nitrous fumes, and tests of the air showed nitrous fumes to be present in large amounts. Mr. Brandt also states that if welding, particularly with oxy-acetylene torches, is done in closely confined spaces, the oxygen of the air may be reduced to a dangerous level. Fortunately, cases of illness or death due to this cause are rare. Other Pulmonary Disturbances.--Cadmium fumes following the welding of cadmium plates may produce severe pulmonary congestion. Chrome plating often irritates the skin. Carbon monoxide may arise from welding. The writer is frequently confronted by welders who claim that their exposure over a period of time has affected their lungs. They complain of an irritating cough and that at intervals their lungs "hurt." In no instance have we noted any characteristic lung changes, except in one man who not only was a welder but had been exposed over a considerable period of time to iron dust. Britton and Walsh- studied a group of 1000 welders and concluded that changes in the chest films may be present in those exposed for many years. However, these changes were not accompanied by any disability. Treatment. Prophylaxis.--Preventive measures include protection of the eyes from flashes, glare, and radiant energy; respirators for pro tection against inhalation; and protective coverings of the exposed `212 OCCUPATIONAL DISEASES parts of the body. Indoor welding should be done where the walls are painted black to reduce the reflection, or booths should be provided. Outdoor welding should be done in portable canvas booths. The treatment of metal-fume fever, and nitrogen peroxide, lead, carbon monoxide, or cadmium poisoning, when they occur as a result of welding, is indicated under those subjects. Electric Ophthalmia.--When this occurs, a superficial injury to the corneal epithelium with exposure of superficial nerve terminals will have occurred. The pain is frequently very severe and may require one of the following for relief: morphine sulfate, % grain (0.01(5 gin.); dilaudid hydrochloride, grain (0.004 gm.); or pantopon, }/> grain (0.022 gm.). Both eyes should be completely bandaged, and locally anesthetic ophthalmic ointments, e.g., 2 per cent holocaine hydro chloride. 2 per cent butvn, or 4 per cent metycaine, are used. REFERENCES 1. Bnuidl. A. D.: "Decreasing the Respiratory Hazard in Welding,'' The Welding Engineer, 21: 21 (Aug.), 1930. 2. Britton, J. A., and Walsh. E. L.: "Health Hazards of Electric and Gas Welding."' J.Indttsf. llyg. und Toxicol., 22 (April). 1940. GASES FROM CARBON ARCS Occupational Hazards.--The commercial use of the electric arc was formerly largely confined to outdoor illumination. Therefore, any prod uct of combustion of the electrodes presented no problem or hazard to health. In the last few years, however, the carbon arc has been used for radiation or as a light source for projection purposes within rooms and small booths. Frequently the question arises as to the harmful effects, if any, from this source. Types of Carbon Arcs.--Carbon arcs may be divided broadly into three types,1 the plain or low-intensity carbon arc, the flame arc, and the high-intensity arc. In the flame arc the primary source of radi ation is the arc stream or flame between the electrodes. The carbons from flame arcs have large cores containing a relatively high per centage of "flaming material." This material may be metal, a mixture of metals, metallic oxides, or other compounds, depending upon the specific type of radiation desired. The high-intensity arc is always operated on direct current at high current densities, and the source of light, which has the highest in trinsic brilliancy of any commercial illuminant, is a cup-shaped crater in the positive carbon. The carbons for this type of arc have large cores containing relatively large quantities of compounds of the metal of the serium group of so-called "rare earth." Carbons of these types of arcs are made in a variety of sizes according to the power input METAL-FUME FEVER. WELDIXCi. (EASES FROM CARBON AIK'S `21.`5 and currents, and in certain eases it is customary to plate the carbons with copper. Gaseous Products.--The burning of carbons in any type of lamp gives rise to a variety of products, part of which are solid, originating from the volatilization of the impurities or substances added to the carbon to imparl specific properties to the arc, and part of which are gaseous. Carbon Dioxide.--Of these gaseous products carbon dioxide is the chief substance, with a small amount of carbon monoxide, and a fix ation of atmospheric nitrogen. These amounts are far below the hazard level. When high-intensity carbons contain relatively large amounts of rare-earth fluorides there is no evidence of the presence of gaseous fluorine compounds. Tests fail to show the presence of any gas react ing with silver nitrate such as hydrogen sulfide, phosphin, arsine, or halogens. Investigators have concluded that the only toxic gaseous products that might be present from this type of combustion are the oxides of nitrogen. These gases are considered in a separate chapter. Ozone.--It has been questioned whether or not ozone is present in this type of combustion. This question is not definitely proved one way or the other, owing to the reactions common to it and to the oxides of nitrogen. It would seem from the work of various investi gators that the presence of ozone is not probable. It would also seem that its intense odor in exceedingly small concentrations would over power any faint odor of nitrogen compounds and thus betray its pres ence. Hill and Flack2 state that there are no respiratory effects if the concentration is so low that it cannot be detected by the sense of smell. Oxide oj Nitrogen.--Of the oxides of nitrogen only nitrous oxide can be classed as a non-irritant to the upper respiratory tract. The others, nitrogen trioxide and nitrogen pentoxide. react with alkali and moisture in the respiratory tract, causing an irritation. When nitrate is formed, there is a definite systemic action, if absorbed. If niti'ic oxide (NO) is given off from the arc, it will react with atmos pheric oxygen to form N02, and with water, then forming nitrous and nitric acids. These are more commonly known as "nitrous" fumes and are insidious, due to the fact that they cause little irritation and little discomfort when inhaled in small concentrations. Moving-Picture Projection Booths.--With the advent of the mov ing-picture booth the question arose regarding the health hazard to the operators in these booths. The question was thoroughly investi gated by MacQuiddv.2 After laboratory tests on guinea-pigs exposed to the undiluted fumes arising from an electric arc there was revealed the spectrum of methemoglobin in their blood samples. It was felt 214 OCCUPATIONAL DISEASES from this guinea-pig test that the arc fumes might be toxic. It was MacQuiddy's conclusion that undiluted gross fumes from the electric carbon arc are toxic to mice, rats, guinea-pigs, rabbits, and cats when inhaled. The pathological changes indicated that the oxides of nitrogen produce these changes. Tollman.* La Towsky, and Bayliss further in vestigated the action of these combustion products. They concluded that the concentrations of the oxides of nitrogen arc high enough to be toxic if exposures to the undiluted gases occur, but such conditions cannot occur with properly installed arc lamps. They further con cluded that any hazard from these gases is easily overcome by ade quate ventilation. Since the operation of a movie machine is an employment of a widespread nature and not confined to region or country, it was deemed necessary to discuss this misunderstood hazard briefly and to point out that actually there exists little or no hazard. Treatment.--The chief hazard here, when it does occur, is from the oxides of nitrogen. The prevention and treatment of such poison ing have been discussed under "Nitrous Fumes.''' Prophylaxis.--The important point here again is prevention. The major portion of such prevention consists of adequate ventilation. It has been suggested that each projector lamp should be connected to a flue in which fumes from arc combustion are exhausted by means of motor-driven fans to the out-of-doors. This fan should turn on automatically as the arc is struck, and the exhaust should run at a minimum of 12 cubic feet a minute, with a rate nearer 100 being pref erable. REFERENCES 1. Collman. U. \\\: "Gases from Carbon Arcs.'' J. Indust. Ilyg. and Tax.. 20 (April), 1938. 2. Hill. L., and Flack, M.: "The Physiological Influence of Ozone." Proc. Royal Son., 81: 404, 1911. 3. MacQuiddy, E. L.. Tollman, J. P., La Towsky, L. IV., and Bayliss. M.: "The Com bustion Products of the Carbon Are." J. Indust. Ilyg. and Toxicol., 20: 312 (April), 1938. PART IIL THE METALS Until recently, metal poisoning was considered as confined to lead, mercury, and arsenic, but with the development of specific alloys, the toxic properties of all metals demand inquiry. Frequently a new process is established without prior knowledge of its effects upon the body having been determined. Facts about Metals.--The following fundamental facts are impor tant in the evaluation of any one of the metals: 1. Certain pure metals are harmless, but a compound of them or their acid salts may be poisonous. 2. The hazard offered by industry is seldom that of a single metal but rather a combination of metals. Frequently fumes from gases or solvents are present with the metal fumes. 3. Deleterious effects usually result from accumulation of minimal amounts, rather than a single exposure to massive amounts. 4. While many metals are irritating to the skin and mucous mem branes, bodily damage is by way of the. respiratory tract. 5. It is well to remember that when a workman in a metal hazard becomes ill, the clinical picture may not conform to the known syn drome of a single metal, but may be altered by the toxic effect of several metals. 6. Injurious exposure is frequently limited to a specific occupa tion or process within an industry; and, therefore, simply because a person is employed where metal is processed, it does not follow that he is experiencing metal absorption. 7. The clinical picture produced by the metal poisonings may be simulated by disease of non-occupational origin. In industrial medi cine it is obligatory that the examination be complete and a thorough laboratory investigation be instituted. 2 if. CHAPTER XIX LEAD Few, if any, of the occupational diseases are so consistently errone ously diagnosed as lead poisoning. It is a sad commentary upon medical education that a disease known to the ancient Greeks, Latins. Arabians, and studied by physicians throughout the subsequent cen turies, inciting profuse material in medical literature, and having such well-defined laboratory findings, should remain an enigma to the pro fession at large. At our clinic, fully 00 per cent of the referred cases have been previously diagnosed as ``lead poisoning" upon a single symptom or a combination of symptoms, without sufficient laboratory study. Similar inadequate presentations are made frequently before the In dustrial Accident Commission. By the same process of reasoning, one might well contend that a person with unequal pupils has syphilis. Like syphilis, this disease is protean in its manifestations. Concerning syphilis, one assumes that with positive serology and clinical symp toms, the diagnosis is correct even though no history of exposure or contact is obtained. However, in lead poisoning, the history of ex posure is all-important. It, combined with the clinical picture and the laboratory findings, forms the triad for diagnosis. Occupational Hazards.--Lead is ubiquitous in industry. The United States Department of Labor lists well over 150 occupations offering this exposure. Thus'is its widespread prevalence indicated. Some of these, however, present no perceptible danger even over a period of many years, as, for instance and in spite of traditional be lief. the printing trade. Smelting, refining, burning, and processes where scrap is melted offer the greatest hazard. Two local companies which melt old storage batteries had a high incidence of lead poison ing until hetter supervision was instituted. Other dangerous sources are in using litharge, in making glaze for pottery and tile, in the manufacturing of batteries, and in the making of varnish. Enameling of bathtubs, stoves, sinks, fixtures, and metalware should also be men tioned. The addition of lead to motor fuel (tetraethyl lead) received consideration under "The Petroleum Hydrocarbons." Modes of Entrance.--Lead enters the body through the lungs, by ingestion, or through the broken skin. The last mode of entrance has -21G LKAI) 'in no significance industrially. The greater portion of ingested lead, if not all of it, passes through the intestinal tract without absorption anil is evacuated. An equivalent amount of lead is 100 times as toxic when inhaled as when swallowed. These facts should readily discount claims made that one has contracted lead poisoning from contamina tion of the hands. However, while this chapter was being written, Raulston informed the author that he was investigating lead poison ing among roofers in Los Angeles County. Subsequently, Magnuson and Raulston1 reported eight cases of lead poisoning among roofers who were in the habit of holding galvanized roofing nails in their mouths. The patients cited had been using fourteen-gauge "hot dip" galvanized nails of various sizes. Adherence to the requirements of the Federal Housing Administration had not been conformed to, and analysis revealed these nails to contain lead from 0.9 to 4.7 per cent in the zinc coating. Most of these patients presented symptoms which simulated appendicitis. At or about the same time the author received a letter from J. P. Russell. M.D.. Chief of the State Industrial Hygiene Service of California, detailing an investigation among shinglers in the area around San Francisco. The urine and blood of these men were found to contain abnormal amounts of lead. The nails were examined and found to contain an abnormal or prohibited amount of lead. Pathology. Effects of Ingestion.--In 1930, Kehoe2 reported his ex perimental study on the effects of the ingestion of lead. Two human subjects were placed on a prolonged regimen of increased oral lead in take of soluble lead, one of them receiving 2 mg. daily for a period of six months, the other a daily dose of 1 mg. for thirty months. Complete clinical observations were recorded, as well as laboratory data of the microscopic blood picture, the excretory response, and the changes in the levels of lead concentration in the urine and blood. Most of the lead passed through the intestines unabsorbed. Kehoe stated that neither of his subjects had had any symptoms of plumbism, not even the vague type seen sometimes in borderline cases. Furthermore, the lead metabolism had not been disturbed in cither one following acute upper-respiratory infections. This study of Kehoe is introduced, not to refute the work of Magnuson and Raulston, and Russell just pre viously mentioned, but rather to serve this warning: any case in which industrial plumbism from ingestion is alleged deserves a most thorough investigation from all angles before it can be accepted. In fact, any illness, occupational or non-occupational, attributed to small amounts of ingested lead.should be seriously doubted until all other possible agents have been ruled out. Aub3 emphasized this last point emphatically in a letter to the editor of the Journal of the American Medical Association: 218 OC'CUPATIOXAL DISEASES Two months ago, in the January 20 issue of The Journal, you published an article by Drs. RaUiinell and Smith to which I must take exception, particularly as it followed so soon after a paper by Dr. II. B. Williams in which also many experts doubt the diagnosis. In this article the child is supposed to have had acute lead poisoning due to only an infinitesimal quantity of lead obtained from orange juice put into an aluminum container. It seems to me unwise to give great pub licity to a so-called established case of lead poisoning in a child who is said to have ingested less than 0.02 mg', of lead. Most persons ingest more than that every day in their drinking water, with absolutely no known deleterious effects. An analysis of the dishes was mentioned but no report on this was made, and it is obvious that no accusation can be made without that, particularly as aluminum dishes should contain practically no lead. Besides, lead does not usually give the acute symptoms ascribed to it in this article. One substance that I know of, namely antimony, may give gastrointestinal symptoms such as vomiting, but to incriminate an infinitesimal amount of lead with out knowing whether antimony was present in the juice is distinctly unscientific. I write this vigorous letter because too much publicity is beinggiven to minor exposures to lead these days. This is particularly true with regard to lead taken by mouth, which is so much less toxic than inhaled lead. That lead may produce deleterious effects there can be no question, but there is no evidence that a small fraction of a millig ram can produce the effects ascribed to it in this article. Fate of Lead in Body.--As in the case of all dusts, inhaled lead dust is resisted in part by the expulsive action of the cilia. Once past this line of defense, it enters the bronchioles and alveoli to be eventu ally absorbed into the general circulation. Little or no reaction within the lung tissue occurs, although fine metallic lead has been thought to cause some proliferation of fibrous tissue in contrast to the non irritating action of the more easily phagocytized lead compounds. The fate of lead in the blood is today a controversial point. For years many have held to the original opinion of Aub4 and his co-workers that lead is transported as a finely divided colloidal lead phosphate to be deposited as a tertiary lead phosphate in the bones. Once de posited, it is held that lead metabolism closely parallels the action of calcium. Kehoe questions this action of lead. Storage in Bone.--Following his original work, Aub, along with Robb and Rossmeisl.-' found that most of the lead in bone was located in the trabeculae, not in the cortex. Since the trabeculae act as a storehouse for available calcium, it was assumed that lead stored here was available and more easily mobilized. As calcium is disturbed by LEAD 219 bodily functions, so is stored lead. Disturbance of this calcium re pository by acute infections or toxic states also sets lead free into the circulating system. From this accepted principle has arisen the. axiom that "once leaded, always leaded." While this may be true in prin ciple, it is not always true in fact. The author had a patient who was treated two years previously for proved lead intoxication and who subsequently developed pneumonia with no apparent exacerbation from action of the stored load. Nevertheless, it is thought that in the treatment of acute lead intoxication and in the treatment of leaded patients subsequently ill from some infectious process, lead metabolism parallels that of calcium. Opposed to this viewpoint is the opinion of Kehoe. In November, 1939, the author had a case in which the urinary findings and the blood findings were not according to the accepted ratio. By correspondence, the case was discussed with Dr. Kehoe. In no uncertain terms he disclaimed the views mentioned in the preceding paragraph as follows: I would say in relation to this whole question of fixation of lead in the body, that our experience and observations will not permit us to accept the hypothesis that lead can be bound in stable form in any part of the body, with the possible exception of the nerve tissues. The idea that lead is fixed in stable form in the skeleton either normally or through any kind of therapy is, in our opinion, untenable. In fact, all of our evidence tends to show that if the lead content of the body is elevated above the normal, the excretion of lead in the urine will be more or less correspondingly elevated. The role of calcium and phosphorus in relation to lead metabolism has not been worked out. We have never found any evidence that such therapy produces more than minor changes in the distribution of lead in the body and in the rate of excretion from the body. We do not on this account, condemn the use of calcium or phosphorus,-or both, in the treatment of lead poisoning, but we do, however, believe that whatever benefit is achieved is not the result of mobilization or demobilization of lead in relation to depots of deposit. Opinions on Deleading.--In contrast to the opinion and investi gation of Kehoe, Gray and Greenfield" cite two cases illustrating the dangers of deleading in acute lead poisoning and four cases illustrating the increased lead stream with a high calcium diet. In addition to calcium they urge an adequate phosphorus intake. They believe that deleading may be of aid in a differential diagnosis in isolated instances. The importance of dcleading in the differential diagnosis is the finding of lead in biological materials below that which may be considered normal. Again they state: "Deleading may be of value occasionally in continued litigation to determine whether an abnormal storage `2`20 OOC'l'I'ATIONAL DISKASKS of lead exists and is responsible for the continued subjective symptoms in the absence of objective finding's." Also, "if after deleading' for a suitable period the amount of lead excreted in the biologic materials is within normal limits, the symptoms may be due to the toxic effects of lead absorbed during the previous exposure and not to the waves of liberation." Symptoms Only in Presence of Circulating Lead.--These conclu sions reached by Gray and Greenfield arc difficult to understand. Regardless of the opinion on whether lead is stored or not and whether calcium or phosphorus aid in that housing, it is universally believed that symptoms occur only in the presence of .circulating lead. Cer tainly there exists ample evidence of this, and if symptoms continue after lead is absent from the excreta, the patient must be considered a malingerer or a neurotic, with the exception, of course, of patients in whom the nervous system has been involved. Effect on Red Blood Cells.--Abnormal or excessive absorption of lead disturbs the hematopoietic function. The resulting anemia is not because of diminished production of blood, but is due to the destruc tive changes to the red blood cells in circulation. The investigations of Aub, Reznikoff, and Smith7 show that the surface of the red blood cells is affected by lead, causing them to shrink, lose their stickiness and agglutination reaction, and become increasingly brittle, heinolyzing on the slightest trauma. But while these surface changes occur, the interior of the cells is not affected, and the physiological properties of the hemoglobin remain normal. The important point, however, is that this loss in circulating red cells is compensated for by a regenera tion of the erythrocytes. As these young cells enter the bloodstream they are affected by the action of the lead so that their basophilic substance is coagulated, and thus they arc recognized microscopically as stippled cells. This finding of stippling, while it has its confirmatory value, is a prevalent stumbling-block in accepting or denying cases of lead intoxication. This point will be discussed under "Diagnosis." Effect on White Blood Cells.--Regarding the effect of lead upon the white cells, there appears to be no definite uniformity of opinion. Some cases have been characterized by leukocytosis; others by leuko penia. An increase in the monocytes was reported by Brookfield, who thinks it is due to the stimulation of the reticulo-endothelium sys tem by lead. But others, particularly Lenzi, look upon this mono cytosis as being common to all forms of heavily cationcd poisonings. The relation of large to small lymphocytes was considered an early diagnostic sign by Ferguson and Ferguson.'' They believe that the ratio between the large mononuclear lymphoid cells to the small lymphocytes has a closer relationship to the clinical condition than LEAD 221 the stippled-cell count. Stippled-cell counts depend much upon the stain used, the technic of staining', and the visual acuity of the ob server, whereas the determination of the ratio of the large to the small lymphocytes is much less dependent upon personal factors or technic. The Fergusons pointed out that the precise differentiation between the monocytes and the large lymphocytes may be difficult, and they, therefore, included both types in the classification of the large mono nuclear lymphoid cells. Shiels,1' in his investigation of this opinion, found that absorption of lead causes an increase in the ratio of large lymphocytes and monocytes to the small lymphocytes. A fall in this ratio below 2:1 while the patient is exposed to the hazard is associ ated with definite symptoms of lead poisoning. Generally speaking, the more severe the case, the lower the ratio. He concluded that the magnitude of this ratio is more closely associated with the clinical conditions than is the stippled-cell count, and it is a simple and use ful indication by which to judge the imminence or otherwise of lead poisoning and is an aid in diagnosis. Smith, Hathmell and Marcil10 offered a study of shiftograms and hemograms for the early diagnosis of plumbism but concluded that the hemographic indication was not pathognomonic of lead poisoning. The action of lead upon blood platelets offers no diagnostic import. Blackman11 found intranuclear acidolphic inclusion bodies in the tubular epithelium of the kidneys and in liver cells in twenty-one cases of lead poisoning occurring in children, and similar inclusion was reproduced in the kidneys of guinea-pigs, mice, and rats by add ing lead to the diets of these animals. Like the intranuclear inclusions of virus diseases, the majority are stained by dyes. Effect on Nervous System.--In addition to the effect lead has upon the blood system, it also affects the nervous system in varying de grees. The first, and usually the most pronounced, effect is that it appears to have a selective action upon the smooth muscle of the intestine, producing increased tone with loss of motility. The colic of lead poisoning is probably due to the. constriction of the intestines and the loss of mobility, similar to obstruction. Paroxysmal spasms with intense hyperacidity, similar to ulcer states, have been held as the cause by some. Many investigators emphasize the prevalence of gastric ulcers among victims of chronic plumbism. Lead encephalitis has been reported in older literature, although it is rare today. Lesions of the cranial nerves have also been reported, and paralysis of the muscles due to nerve involvement, of which the wrist drop is a wellknown example, is known but rarely seen. It is apparent that when palsy occurs, it is in those muscles most in use or fatigued and. there fore, need not be confined to the wrist, as is so classically claimed. 222 OCCUPATIONAL. DISEASES DIAGNOSIS Signs and Symptoms. Acute.--When it occurs, the acute phase is usually iu the form of luctal-fuinc fever as a result of inhalation of massive doses. There is general malaise, often fever, mild to intense abdominal pain, nausea, and possible vomiting, diarrhea (rarely, early constipation), headache, numbness of the limbs, occasional stupor, and in severe cases, vomiting. Hamilton states that myalgia belongs to chronic plumbism, but we have seen it in three acute cases within the past two years. The urine may be scanty with albumin and casts. Chronic.--The symptoms found iu acute poisoning are usually present in the chronic form but to a less degree. Abdominal pain, for instance, is almost constantly noted, but it is usually not of the severe, colicky type. Increasing fatigue, listlcssness, and mild loss of weight characterize the chronic case. The appetite is poor and constipation common. The value in Table 11 is that it makes a nice distinction between the very early and mild lead absorption and the more advanced but inactive stages, as well as the advanced active stage, with the proper allocation of the corresponding symptoms. From these multiple pos sible symptoms, it might be well to have fixed a typical average case. The patient is usually pale, easily fatigued, lacks interest in ex traneous activities, complains of more or less constant headache, has no appetite; frequently he complains of restlessness and insomnia, and constipation becomes pronounced. To this point he may still not seek medical advice unless he is employed in a hazard where super vision is adequate and men are informed. With the onset of intes tinal pain, however, he presents himself for relief. Rarely does the workman continue in an exposure to the point of having the nervous system severely damaged, or rarely is he permitted to because of the hygienic principles ordinarily instituted in industrial plants. General Principles of Diagnosis.--"Lead poisoning" is an inaccu rate term which fails to distinguish the actual state of one presumed to be affected by lead. Lead is a natural constituent of the soil, water, vegetation, and air; and. because of this, human beings the world over have lead, to a slight extent, in the body tissues. If this were kept in mind, erroneous assumptions would not be so frequent. A patient should be classified as having: 1. Normal lead absorption 2. Abnormal lead absorption, or 3. Lead intoxication For example, one may show lead absorption in the excreta or blood in excess of the recognized normal amounts, and yet have no LEAD Taisi.i: 11--Clinical Skins and Symptoms op Pli'mimsm* 223 Gitori" I 1 Giui> 11 Gitori' 111 Suggestive Evidence of Lead | Suggestive Evidence of In- Absorption : cipienl Intoxication and Inactive or Arrested Plmn- bism Suggestive Evidence of Defi nite, Advanced, and Active Plumbism with Acute Manifestations General Symptomx Patient becomes easily flus tered, moody, restless and excitable General feeling of malaise Pallor Jaundice Slight lead line Arthralgia Slight inanition Fatigued easily Hypotension to normal Slight pyrexia Anemia Inanition Lead line Arthralgia Jaundice General weakness Hypertension Pain in chest Wrist drop Foot drop Persistent metallic taste Slight anorexia Slight constipation Digestive System Metallic taste Coated tongue Anorexia Constipation Slight abdominal eolic Metallic baste Coated tongue Anorexia Marked constipation Paroxysmal colic Nausea and emesis Rigid abdomen Blood in stool Irritability U ncooperativeness XervotM System Slight frontal headache Slight tremors to parkin sonian syndrome Slight ataxia Insomnia Palpitation Increased reflexes Increased irritability E.vegrounds may show chok ing of optic disks Severe frontal headache Tremors Confusion Insomnia Convulsions Fibrillary twitehings Neuritis Visual disturbances Encephalitis Hallucinations Coma Paralysis Cerebral palsy Renal Symptom* Lead which fluctuates be tween normal limits and a very slight rise Trace of albumin and few granular easts in urine Lead which fluctuates be tween normal limits and a positive rise Toxic nephrosis Albuminuria Casts in urine Ilematoporphyrinuria Hematuria Positive but fluctuating lead findings * Smith, F. L., Rathmcll, T. K., and Marcil, G. E.: "Earlv Diagnosis of I'lumbism," Am. J. Clin. Path., S: 471, 1938. 224 CK'Cl'CATION AI, DISEASES toxic symploms. If the meaning of (lie word i.s to he adhered to, then one has load poisoning only when one is intoxicated from lead. The Blue or So-Called "Lead" Line.--One is tempted to state that it would improve diagnosis if this phenomenon had never been described. Its color is not blue but rather a grayish black: it is not actually a line but a series of dots or markings along the free margin of the gums. These deposits may also be found on occasion on the anal margins. A hand lens may aid in bringing out the specks. Defec tive hygiene, pyorrhea, and staining of the teeth may all be mistaken Fig. 38.--Section of fixed unluked portion of blood smear used for the determination of total erythrocyte count and cellular abnormality. Photomicrograph with 10 X ocular and oil immersion objection. Straight lines shown arc from Whipple grid user! as a guide for quantitation. (H.vler and Bradley.) for a lead line. When present this line is no indication of the amount of lead in the body. Stippling or Basophilia.--It has previously been mentioned that when the red cells meet the destructive influence of lead in the circu lating blood, young cells are called forth, and their basophilic sub stance becomes coagulated. When stained, this granulation has a stippled appearance. If found in a suspected case, the conclusion is often erroneously made that "lead poisoning" exists. Unfortunately, there exists a general impression that stippled cells are pathognomonic of plumbism. Thin is not true. These stippled cells may often appear J,EAI> -I'-io in pernicious anemia, secondary anemia, leukemia, hemolytic jaundice, neoplasms, poisoning from benzene, aniline, or any of the chlorinated hydrocarbons, and many other diseases. Furthermore, stippling is not present at all stages of lead poisoning. It is usually present during the acute stage or as held by some, during the stage of exacerbation, as in deleading. It is conspicuously absent in the chronic stage. Tests for Lead Poisoning. Stippled-Cell Count.--The average physician resorts to a stippled-cell count for his laboratory investi gation of a "lead" ease. The finding of five or more stippled cells per Fig. 39.--Luketl portion of blood smear from the same slide as Fig. 38. showing four typical basophilic aggregations and faint outlines of non-basophilie containing erythrocytes. (Hyler and Bradley.) field lias frequently been accepted as an indication of lead poisoning (Figs. 38, 39). Plant physicians, however, will often permit men to continue to work with a count as high as 15. The ordinary stipple count doubtless is of value in plant routine where men are under constant observation and where frequent comparisons are obtained. (a) Staining Method /or Stippled Cells.--The usual staining methods for demonstrating basophilic granules are well known to all. Ruth A. McKinney and Saul llosenzweig, of the North End Clinic in Detroit, suggest the following method and enumerate the advan tages: is 22G OCCUPATIONAL DISEASES The three reagents required are kept for convenience in covered Coplin jars. The technic is as follows: Fix dried smear in acetone-free methyl alcohol for from three to five minutes and transfer directly to Wright's stain (staining time predetermined for each lot of slain used); wash in tap water and transfer to dilute ammonia water (2.5 cc. of stronger ammonia water in 1000 cc. of distilled water); dip up and down rapidly until blue color runs from slide; wash in tap water, dry and examine. The finely stippled or coarsely dispersed "basophilic aggregations" in the red blood cells appear distinctly black against the gray or pink of the stained cell (Fig. 40). The white blood cells retain the usual nuclear stain. The ratio of lead-affected cells to the normal red cells is determined by an adaptation of the Fonio platelet counting technic. A minute opening in a paper disk dropped into the ocular diaphragm gives a suitable counting field. The stipple cells and the normal red cells in each field are counted, but tabulated in separate columns, until 250 normal red cells have been counted. The number of stipple cells is then multiplied by 4, giving the ratio of such cells to 1,000 normal cells. The number of thousands of red blood cells per cubic millimeter multiplied by the number of stipple cells per thousand cells gives the approximate number of lead stipple cells per cubic millimeter of blood. This staining method offers nothing fundamentally new; its chief advantage lies in the fact that a simplification and combination of two previous technics makes possible: 1. A rapid detection and enumeration of stipple cells in a spread which is also adequately stained for a differential count of the white blood cells 2. The utilization of reagents usually found in any physician's office or clinical laboratory 3. A technic which stains dried smears two months old as satis factorily as fresh dried smears McCord,'- as early as 1924, questioned the value of the ordinary stipple-cell count. Basophilic Aggregation Test.--McCord1* and his co-workers as sert that in the 1934-35 epidemic of lead poisoning in the automobile industry, (1900 basophilic aggregation examinations of the blood were made. In addition, during this period 1100 tests were made in other industries. This number includes approximately 500 control exami nations made on workers who were not exposed to lead. Positive baso philic aggregation tests have served as an index for lead absorption prior to the appearance of clinical manifestations of lead poisoning. This test has proved to be of value in the diagnosis of early cases of lead poisoning. Fig. 40.--A schematic drawing to show the presence of basophilic substance creating a "stippled" appearance. LEAD 227 () Principles.--The procedure is suited to application by any physician or laboratory carrying out any blood examinations. The basic principle in the basophilic aggregation test is the enumeration of red blood cells containing basophilic substance, in contrast to the cus tomary procedure of qualitative or quantitative examination for stip ple or polychromalophilic cells. The native state of basophilic ma terial in unaltered red blood cells is not known, but in the process of Fig. 41.--Typical pre-formed punctate stippling in non-liemolyzed erythrocyte (semidiagrammatic) . (McCord.) laking and staining red cells this substance may be artificially aggre gated into readily visible masses (Figs. 41. 42, and 43). In normal human adults, these aggregates rarely exceed 1 per cent of the total number of erythrocytes, but in persons exposed to lead the per centages ordinarily lie above this normal maximum, when consider able lead is being absorbed or when clinical lead poisoning is immi nent. Finding more than from 1 to 1.5 per cent and especially more Z"1S XLOCCl'I'ATIO.N DISEASES Fig. 4`2.--Typical basophilic aggregation in erythrocyte, showing heavy deposit of basophilic material (semi-diagrammatic). (McCord.) Fig. 43.--Typical basophilic aggregation in hemolyzed erythrocyte, showing scanty basophilic material and thus more difficult to recognize than in Fig. 4-. (McCord.) LEAD 22!) than 2 per cent in persons exposed to lead at once suggests lead ab sorption and the possibility of approaching lead poisoning, or the ac tuality of early lead poisoning. In chronic lead poisoning this test usually is not, but may be. positive. As lead poisoning progresses to extended ehronicity, the reliability of the procedure diminishes. The test has been utilized in industries using lead to determine the num ber of exposed workers absorbing lead, as some proof of existing lead hazards; as a guide for the transfer of workers absorbing lead to leadfree departments; as a measure of the efficacy of preventive devices and practices; and as a means for the detection of malingerers. There arc varied types of diseases leading to positive basophilic aggregation tests, but in groups of workers in lead industries, presumably normal except for the possible effects of lead exposures, the positive basophilic aggregation test stands in some relation to lead absorption and its subsequent action. (6) Technique.--The preparation of the smears for the aggrega tion test is best described by Hyler and Bradley,1'1 who adopted the best features of McCord's original technique: Only the best quality of microscopic slides should be employed, and preferably these should be used only once. Trior to use, slides should be thoroughly washed, followed by submersion in acid and alcohol. The blood smear should be such as to obtain an even distribution with such thinness as is represented by ISO to 200 cells to the micro scopic field under an oil immersion objective. These smears, after air drying, may be fixed as later discussed, and stained almost immedi ately, but standing up to sixty hours appears to make little difference in the counts later obtained. In one instance, smears were made on fifty individuals in duplicate. One-half were fixed and stained in six hours, while the second half were so treated at the end of sixty hours. Heading of these slides indicated a variation in the basophilic aggre gation counts of 0.1 per cent. The fixing of one-half of the slide on a longitudinal basis affords some opportunity for error in that vapors from the methyl alcohol used for fixation purposes of one-half the slide may, in the absence of precaution, tend to fix the remaining half to some degree. Three pro cedures have been utilized, the first two of which are far more prac tical. Jones devised a fixation method whereby a longitudinal half of the blood smear is covered with a strip of filter paper and is cau tiously wetted with a minimum of methyl alcohol (acetone free). This is allowed to dry until the filter paper becomes loose. The remaining half of the slide is unfixed in order that laking may take place during the process of staining. In the second method, a shallow utensil, such as a petri dish, is filled with alcohol to such depth that one-third of the slide is submerged by dipping to the bottom of this utensil. After 200 OCOCPATIOXAL DISEASES instantaneous dipping, the slide is allowed to dry horizontally on mus lin or gauze in such fashion as not to permit any drainage onto that portion of the slide for which fixation is unwanted. In either case, a narrow hand of partially fixed cells will exist at the junction of the fixed and unfixed portion of the slide, hut this offers no practical problem, in the performance of this test. This transition zone is ordi narily less than the width of a microscopic field. For precise purposes, it is possible to score the underside of an annealed glass slide with a good diamond, to make a smear in the usual fashion, and thereafter, prior to fixation, to break the slide into two pieces for fixation pur poses. After staining, these halves may be brought into apposition for microscopic examination. For staining purposes, a variety of vital stains might be utilized provided the solutions used are such that permit of cell hiking. In this work, two stains have been utilized with formulae modification from time to lime. Jones has expressed a preference for the Sussmann-Weindcl slain, about which he states: All factors considered, the Sussmann-Weindel solution of toluidine blue, methylene blue, and borax furnished the most uniform results in examination of both fixed and noil-fixed films. The formula is as follows: Toluidine blue ..................................................................... Borax...................................................................................... Methylene blue solution (Loeffler's) ........................... Distilled water..................................................................... 0.5 gm. 0.05 gm. 5 cc. 100 cc. The borax is added to the water, which is heated to dissolve if necessary. The toluidine blue is added and allowed to stand for a few minutes: occasional stirring may hasten solution. Next is added the methylene blue. The solution is then filtered through a single No. 30 filter paper. Our own preference is for a modified Manson methylene blue stain, prepared as follows: Sodium borate C. P............................................................ 0.3 gm. Methylene blue chloride.................................................. 2.0 gm. Distilled water, to ............................................................. 100.0 cc. The sodium borate is added to distilled water which is brought to the boiling point. After cooling, the methylene blue chloride is added with vigorous stirring. Filtration may be desirable prior to the addition of methylene blue, and certainly is desirable after the methylene blue addition and thereafter at intervals. The life of the stain is longer if kept in a tightly-stoppered bottle. . . . LEAD 231 Actual .staining with this modified Manson stain may lie carried out in series of Copin jars, the time being about ten minutes, but it is almost impossible to over- or under-stain. After staining, the slides should be rinsed in three washing's of distilled water and air-dried. Staining the unfixed portion of the slide is in effect a hiking process which removes the hemoglobin, clumps the basophilic material, and brings this into greater visibility. The preliminary examination of the stained slides in making the basophilic aggregation count is done under high power to locale areas of even cell distribution. Final examination is made with the oil immersion objective without the use of a cover slip. Microscopic examination is first made in the hiked portion of the smear. It is observed that the normal erythrocytes are very nearly faded from the picture. These cells appear as a faint shadow with an indistinct periphery. The white cells stain deeply and their various forms may be differentiated. The basophilic material in the red cells of this portion of the slide stands out sharply as coarse granules or as combined granules and network, or as reticulation. The counting technique is facilitated by the use of a Whipple grid and hand counter. All cells in each field containing basophilic sub stance are counted. If any of these cells are divided by the outside margins of the grid, they are counted as belonging in that field. Those cells displaying basophilic aggregations in twenty consecutive fields are counted or in the case of an uneven smear, two rows of ten con secutive. fields each are enumerated. The total number of basophilic cells is recorded. Examination is next made in the fixed portion of the slide opposite and approximating the area that was examined in the laked portion. All of the red cells within the grid are counted, including those touched by the four margins of the grid. Five fields are examined in the fixed area. If the examination of the laked portion was made of twenty consecutive fields, then all of the red cells should be counted in evei'y fourth field for a total of five fields. But if the cells containing basophilic material were counted in two rows of ten fields each, then the cells should be counted in each alternate field for a total of five fields. The result should be expressed in percentage. Hence, if there were a total of (id cells with basophilic aggregations found, this result would be: (53 divided by 4 equals 15.75. and again divided by 78(i. the total number of unlaked red cells counted in five fields, equals 2.0 per cent of the total erythrocytes as basophilic aggregation cells. This technique is such that one sufficiently experienced technician may fix and stain 400 blood smears in one day. or may examine from 60 to 100 stained slides in a working day. In many cases, when readingslides made by the proper methods, three technicians have arrived at an agreement within 0.1 per cent of the basophilic aggregation count. '23`2 occupational diseases Prcparations made approximately in the maimer described in this section have been kept for a period of thirteen years without signifi cant deterioration. In arriving at the approximate number of stippled cells per mil lion red blood cells, the following technique was utilized. A blood smear slightly thicker than the smear for a basophilic aggregation count, was made, usually 200 red blood cells to the field under oil im mersion objective. This was then stained with Wright's dye in the usual way. Examination was made with the oil immersion objective of fifty fields or approximately 10,000 red blood cells. The total num ber of stippled cells found is multiplied by 100 which indicates the approximate number per million red blood cells. At best, the examination for stippling is difficult, entailing much eye strain. Since much of the stippling is of very fine nature, it re quires close scrutiny to avoid missing these cells. The result is that the average technician can examine only 25 to 30 slides per day. Ex aminations of large numbers of employees exposed to lead hazards in certain industries obviously would require considerably more time than for the basophilic aggregation test. Possibly because of the work involved in the above described method it has not been generally adopted. From McCord's experience it would appear that, clinically, patients with early lead poisoning regularly exhibit this high basophilic aggregation content of the blood. Certainly it has a confirmatory value especially in routine plant ex aminations, where the procedure is all set up for a large number of examinations. For the isolated case with a medicolegal aspect, exami nation of the blood, smear for excessive stippling, excreta, and the whole blood, appears simpler. Routine Blood Count.--There exists no distinct picture, but the following changes are noted with exceeding regularity. 1. A reduction in the number of red blood cells i. Changes in the size and shape of the cells out of proportion to the reduction of the red-cell count or hemoglobin 3. A reduction of the hemoglobin usually greater than that of the red blood cells. The color index usually less than 1 4. A fairly frequent leukocytosis. The relationship of the large to the small lymphocyte has already been mentioned Lead in the Urine, (a) Twenty-Four-Hour Specimen.--Using pre cautionary measures, a complete twenty-four-hour specimen of urine is collected in Pvrcx containers and the entire volume submitted to a chemist. A modified dithizone litrimclric extraction is usually em ployed. Most authorities accept a reading as high as ().!<) mg. per liter LEAD 233 as being within a normal range. Kehoe estimates 0.04 as a mean nor mal. This test should be run in every case in which there is suspicion of lead poisoning. If the test is conducted accurately, amounts in ex cess of the normal serve as confirmatory evidence. Diseases of the kidney, dehydration, imbibition, edema, and errors in collection, etc., are factors which may influence the value of the test. (b) Short-Time or Instantaneous Specimen.--In large plants or where a great number of men are to be constantly observed, it is difficult to obtain twenty-four-hour specimens without having them become contaminated or having inaccurate amounts collected. Real ization of this difficulty with the workmen at the Westinghouse Elec tric and Manufacturing Company, at East Pittsburgh, led Barnes to investigate the possibility of correlation between short-time or instan taneous specimen and average twenty-four-hour excretions. It was felt that some correlation might be obtained if factors such as time of day, acidity, specific gravity, or total nitrogen were taken into ac count. After experimenting with exposed, as well as unexposed per sons, Barnes13 concluded that a determination of the lead excreta per hour, as found by analyzing a specimen representing two or three hours' excretion during the working-day, gives a fairly reliable meas ure of the average excretion for that day. It impresses the author that this procedure suggested by Barnes can serve the plant physician where all the factors can be controlled, but that for a single examina tion of a patient suspected of lead poisoning the twenty-four-hour specimen should be obtained. The instructions that are to be adhered to in obtaining these spot or instantaneous specimens are as follows: 1. Have the patient empty his bladder. This first specimen is ob tained for the purpose of starting at a definite time with an empty bladder and is not to be used in the lead analysis. The first specimen should not be placed in the special container. It may be used for the 'wy. determination of sugar, albumin, specific gravity, etc., if desired. Re cord on a data sheet the time that the employee emptied his bladder. The date and the employer's name and occupation should also be recorded. 2. Instruct the employee to return to the medical department at least two hours later (preferably three or four hours later). He should not void his urine until he has returned to the medical department, where the specimen will be taken. 3. When the employee returns, mark the time on the data sheet and have him void directly into the special container. Special care should be exercised to be certain that no dust or dirt is dropped into the container. These containers have been specially cleaned at the c -........ 2134 OCCUPATIONAL DISEASES laboratories and should not be rinsed or cleaned in any way. Do not add any preservative. Do not remove any of this sample from the special container, and do not use any of it for other tests. 4. The results of the test are reported in micrograms of lead ex; creted per hour. Lead in the Blood.--The normal amount of lead in the blood has been well established in recent years. The reliability depends upon . adherence to a most rigid technique to avoid contamination. | (a) Special Uses for Determination.--According to Smith10 and 1 his associates, a differential diagnosis of lead poisoning can be accom| plished by an accurate determination of lead in the serum, cells, and i fibrin fraction of the blood when taken into consideration with the i: total amount of lead in the whole blood. It is possible by this pro cedure to make a differentiation between acute, chronic, and mild lead poisoning, as well as to differentiate between mild lead toxemia and such pathological conditions as gastro-enteritis, hypercalcemia, food poisoning, or colic from other causes. The therapeutic use of lead can be controlled by this procedure, since deleading treatment may be in stigated before an acute lead crisis develops. Results of 0.001 mg. of lead or less in 10 mg. of serum, cells, and fibrin, or whole blood, may be in error and should be considered qualitatively rather than quan titatively. Such a consideration does not change the interpretations, since the important factor is the appearance and disappearance of pathological lead in the serum fraction of the blood. (b) Serum Fraction versus Whole-Blood Content.--The essential difference in the manner in which the analysis of the blood of healthy persons differs from definite clinical cases of acute lead poisoning and periods of exacerbation in chronic lead poisoning lies in the appear ance of lead in the serum fraction of the blood, since approximately 34 per cent of these patients show a whole-blood content of less than 0.01 mg. of lead in 10 gm. of blood, and 18 per cent have a whole-blood content bordering on the normal range of healthy persons. In thirtyfour cases of latent and early acute phases of chronic plumbism there was a definite appearance of lead in the serum fraction of the blood in all the cases, although the lead content of the whole blood in 58 per cent was less than 0.01 mg. in 10 gm., and 44 per cent fell within the limits of the range established by healthy normal persons and pa tients with disorders other than plumbism. In inactive chronic plum bism the serum is normal, but there is usually a definite increase in the lead content of the whole blood over that of the control group. (c) Analysis in Differentiation.--Smith and his co-workers state that a definite diagnosis may be established in borderline cases by placing the patient on acid therapy as practiced in deleading, when an LEAD 235 increase in the scrum fraction and generally in the whole blood will occur. The clinical and physiological course of lead intoxication through its quiescent periods, as well as those of acute and subacute exacerbation, may be followed by means of the analysis of the serum fraction and the whole blood for lead, and a prognosis established. Since it required 10 gm. of blood to make a determination for lead by the diphenylthiocarbazone method, the clinical procedure followed in cases complicated by the presence of malignant growths or blood dyscrasia is first to make an analysis of the lead content of the serum, cells, and fibrin fraction, and whole blood, then follow the trend of the intoxication by means of daily shiftograms and hemograms, and make additional blood analyses when they are hemographically or clinically indicated. However, in uncomplicated cases an analysis is made every second or third day. By such a procedure it is found possible to differ entiate between symptoms caused by mild lead poisoning and those which result from pathological conditions. A range of lead values for the healthy normal person is found to be nil in 10 gm. of blood serum, and from 0.002 to 0.011 mg. in 10 gm. of whole blood. This range is independent of sex, age, climatic changes, daily fatigue, violent exer cise, meals, menstruation, and ovulation. Lead Levels, (a) Of Blood and Urine.--Concerning the evaluation of lead in blood, Kehoe has a different viewpoint. The following quo tation is from the letter to the author previously mentioned: In a study of a rather large number of normal persons, as well as a considerable number of persons with varying degrees of lead absorp tion and lead intoxication, we have confirmed the observations of Willoughby and his associates. I believe that the lead of the blood is carried almost entirely by the cellular elements. Willoughby examined serum and clot and found most of the lead in the clot. We have sepa rated the plasma and cells by the use of sodium citrate and also hepa rin, and have found that the cells under these conditions contain practically all of the lead. Where higher concentrations of lead are present in the blood, there is some tendency for the plasma to contain larger proportions of the lead than in the normal case. However, this proportion is never large and in our experience has not exceeded 10 to 15 per cent. It is usually under 10. It appears that lead so trans ported in the body, is not bound in the sense that it cannot be ex creted, for in general there is approximately a 10 to l relationship in the concentration of the lead in the blood and urine. That is to say, the concentration of the lead in the blood per 100 grams is approxi mately the same as the concentration in the urine per liter. This does not hold absolutely, there being variations both up and down. Gen erally speaking, however, where lead absorption to abnormal degrees 236 OCCUPATIONAL DISEASES has taken place, the urine changes more proportionately than does the blood lead. It seems probable that the equilibrium relationships be tween the cells and the plasma, with reference to lead, are as unstable as those relationships in the case of certain other ions. The material of the erythrocytes is especially liable with respect to its chemical combinations. So far as I know, no one has studied arterial blood with reference to its lead distribution. We expect to do this, for we suspect that there may be considerable difference in the arterial as compared to the venous blood. In any case, lead is normally carried mainly in the erythrocytes, but is excreted by way of the kidneys. From the foregoing paragraphs it can be seen that there is as yet no unanimity of opinion regarding the relationship of lead found in the serum to the total blood-lead level, nor upon the relationship of the urinary lead findings with blood-lead determinations. ICehoe be lieves the urinary-lead findings are of diagnostic value, but less re liance is placed upon this test by Scott and McMillan, Litzner and Weyrauch, or Smith, Rathmell, and Marcil. Tompsett and Ander son10 recently reported a series of twenty-nine cases in which the lead content of the blood and the excreta was examined. In the cases of plumbism they concluded that the total daily excretion of lead in the urine and feces did not run parallel to the level of the lead in the blood. (b) After Removal from Exposure.--Concerning the question of long-continued high blood levels, after the patient has been removed from his exposure, Kehoe believes this is unlikely. This has also been the author's experience. Yet Chaney, of the Los Angeles County Hos pital, informs me that continued high blood levels have been in accord with his experience. Also, Blumberg, Scott, and McNair found blood levels very slow in dropping to normal, from six to twelve months be ing required in some cases. They also state that clinical improvement occurs long before any appreciable drop in the blood level takes place. If this is true, then the commonly accepted viewpoint that symptoms are due to circulating lead will have to be revised. Oddly enough, most of these controversial points were brought out in a single case of ours, which is to be discussed in detail (Case V). While it may appear that the above discussion is too controversial for the purposes of this book, it has been indulged in to emphasize the fact that the diagnosis of lead poisoning is not so simple a procedure as the average medical textbook would lead one to believe. Conclu i; sions can only be drawn after careful consideration of the history, investigation of the exposure, evaluation of the symptoms, and labora I: tory study. In the average case dependence upon the history, symp j* toms, and a blood smear for stippling, is to be deprecated. Accuracy r i' i LEAD 237 can better be obtained by the additional total daily urine test, or the determination of the lead in blood, or both. In this clinic we examine the twenty-four-hour specimen of urine routinely and frequently check it with an examination of whole blood for lead. Collecting Blood for Analysis.--Blood samples must be taken in a space which is free of dust. Despite this precaution, it is necessary to use the most meticulous care against the contamination of samples with surface or atmospheric dusts. The patient must remove any dust-laden clothing before entering the room in which the sample is to be taken, and must wash hands and face or any other parts of the body that may be dusty. The cork should be removed from the tube in which the blood is to be drawn only during the withdrawal of the blood, and should not be permitted to come in contact with the tabletop or any other poten tially unclean surface, but should be held by its topmost part or laid down within its filter-paper wrapping, and replaced as soon as the blood has been obtained. The filter-paper cover should be replaced and secured around the neck of the tube by means of a rubber band. The sterile lead-free needle provided in a second tube should be used to withdraw approximately 10 cc. of blood directly into the blood tube. Under no circumstances may any anticoagulant or other sub stance be added or any intermediate container be used, nor may the needle be sterilized by boiling in water. If the latter should be ren dered non-sterile accidentally, it should be flamed gently before use. After use it may be rinsed out with cold water and returned to the tube. The blood sample should be labeled with the name of the patient and the date and hour at which the sample was taken. Two 10 cc. samples are taken at the same time so that parallel analyses can be made by two different methods. Sampling Lead Dust in Air.--There are times when a claim can be the better substantiated or denied by sampling the air at the place of employment. A safe atmosphere is considered, at the present time, to be 1.5 mg. per 10 cm. of air. To be of any value in medicolegal contro versy, faithful adherence to all the details is necessary in reduplicating the working conditions. x-Ray Examination.--rc-Ravs to determine the effect of lead poi soning on bones are of no value in adult life. They are of value in chil dren only before the epiphyses unite. Summary of Diagnosis.--There are more cases accepted as lead poisoning than are justifiable because a distinction between lead ab sorption and lead intoxication is not made and because the laboratory criteria for diagnosis are not employed. One should not depend upon 238 OCCUPATIONAL DISEASES the "cardinal symptoms." It has been shown that lead is normally present in urine and feces. What the profession needs to know today is the difference between normal and abnormal amounts. An equitable opinion in Workmen's Compensation must be based upon the history, the clinical findings, and the laboratory results. For the sake of em phasis and reference they are reiterated as follows: Urine (24-hour specimen): Normal, 0.01 to .1 mg. of lead per liter Basophilic aggregation test: Normal, 1 to 1.5 per cent Blood: The range of lead value in the normal person is as follows: () Nil for 10 gm. of blood serum () .002 - .011 mg. per 10 gm. of cells and fibrin fraction (c) .001 - .005 mg. per 10 gm. of whole blood MEDICOLEGAL ASPECTS Alleged Complications.--A neglected discussion in literature, and one which certainly deserves careful consideration in a book of this type, concerns the complications frequently alleged to follow lead poi soning. Chief among these are: arteriosclerosis, nephritis, hyperten sion, ulcers of the stomach, neuritis, neuroretinitis, and the effect upon germ cells and fetal life. With the exception of the last-named effect, proof has never been established that any of the other alleged compli cations can result from lead intoxication or lead assault. Recent opinion is that they are coincidental findings. Why then do we find fre quent reference in literature to some of these questionable complica tions? It is not difficult to explain since it is a well-recognized fact that textbooks and medical articles frequently incorporate the opinions of predecessors, assuming their scientific accuracy even though patho logical evidence may be lacking. Arteriosclerosis.--Years ago in the industrial centers of Europe, it was noted that the "old stagers" when they died and were autopsied revealed arteriosclerosis. Writers of that time, in describing the effects of lead, included in their writings the arterial findings. Thus, there drifted into the literature the observation that "lead caused arteriosclerosis." These observations were made before the study of arterial disease was as thorough and scientific as it is today. They were made in the days when a death certificate of "acute indigestion" was acceptable. Mayers examined 381 cases of lead workers for the New York State Department of Labor. She found that while arteriosclerosis oc curred earlier in all types of industrial workers than it did in office workers and professional men, there was no evidence that lead played any part. The Metropolitan Life Insurance Company's study of ar- LEAD 239 teriosclerosis concluded that while this condition is more common in industrial than in non-industrial workers, lead itself was not shown to be an exciting cause. McNally,17 after a study of a large group, con cluded, "It can no longer be contended in the American practice of manufacturing of lead products that lead causes high blood pressure." According to Aub, there is a lack of correlation between the clinical picture and the pathological findings. Patients who present many symptoms suggestive of pathological changes usually show little of interest at autopsy. Regarding compensation, it is obvious that ar teriosclerosis or hypertension in a worker over fifty years of age should not be attributed to lead any more than should the appearance of gray hair or baldness. Sterility and Abortion.--The observations of numerous investi gators leave little doubt that lead in excessive amounts affects the germ cells of both sexes, and as a result, sterility and abortion are fairly common among lead workers. The transmission of lead and ar senic from the mother to the fetus was shown recently in the experi mental work of Calvery.is Gastric Ulcers, Nephritis, and Cirrhosis of Liver.--Claims have been made that lead produces these conditions. Statistics are not avail able to prove or disprove such statements. A review of the literature indicates that such incidence is no higher in laborers subject to plumbism than in any other class of laborer. Such contentions undoubtedly got into print in the day when alcoholism was prevalent among work ing-men. Recent studies show that there is no adequate proof for, and ample evidence against, the theory that lead is an etiologic agent in cases of multiple sclerosis. Neuroses.--The neuroses which follow lead poisoning are frequent and accompany the weekly compensation stipend in a manner similar to the traumatic neurosis. They rarely appear in younger patients or those treated early and thoroughly. It behooves the industrial physi cian to weigh carefully the probability of other causes before assigning to lead the provocative etiology of the so-called complication. " Temporary Disability.--Temporary disability ceases with the dis appearance of the symptoms. The period may be from several weeks to several months. Forty-two days was the average temporary dis ability of sixty-two patients treated at the clinic during 1937 and 1938. Permanent Disability.--Permanent disability is rare. A review of our records for the past five years reveals not a single instance of ac tual permanent disability. When severe cases of encephalopathy re sult, permanent disability (100 per cent) should be allowed. Isolated muscular weakness or nerve paralysis must be estimated for rating v;i .i Wf ! ft' 40 OCCUPATIONAL DISEASES upon the same basis of functional loss as is done in traumatic lesions. Since elimination of lead varies in people, and since persons with func tional weaknesses tend to recover, there should be no rating made in these cases for at least two or three years. In 1931, Kessler suggested that after a period of two or three years, compensability of the claim for permanent disability might better be established by a provocative test. Following this, if the blood and excreta are positive for lead, the possibility of reduction of longevity should be considered. In view of recent investigations one should question whether this procedure would be satisfactory. Illustrative Cases.--Those patients who have been referred to this clinic having been previously diagnosed as having lead poisoning fall into the following groups: 1. The majority have been diagnosed upon the patient's statement that he has lead poisoning because he works "where they han dle lead." They have been subjected to no laboratory inves tigation. 2. A small group with a history of lead exposure has been diag nosed upon the finding of stippled cells in the blood smear. 3. Others upon the presence of a lead line of the gums. Invariably this is not actually present in these patients. 4. A very small number who have been subjected to blood smears. and twenty-four-hour specimens of urine for lead. 5. Rarely has any case been accompanied by a study of the lead in the air at the place of employment. 6. One patient had a whole blood study for lead. Case I.--A man, aged fifty-eight, had been a Linotype operator for twenty-two years. In the summer of 1935 he developed vague pains in the area of the "stomach." These appeared usually at night and were conspicuously absent during the day. He consulted several phy sicians, having gastro-intestinal series, gastric analyses, and other tests performed. He continued working but constantly sought medical advice. In 1937, one physician inquiring about his occupation, had a twenty-four-hour specimen of urine run which revealed 0.08 mg. of lead per liter. The patient was told that he had lead poisoning. He stopped working and filed a suit before the Industrial Accident Com mission of California for compensation. Following the hearing, his claim was allowed. The award was for total, indefinite, temporary dis ability. In the spring of 1938, he developed attacks which signified coronary involvement. Upon being informed of this condition, the pa tient filed a suit for permanent disability due to coronary sclerosis resulting from lead poisoning. The commission again allowed his claim. Two months after this award the patient was sent to the writer for an opinion. LEAD 241 History.--The patient's father died at the age of fifty-eight years of heart disease. The patient denied serious illness or any venereal disease. Physical Examination.--Complete details of the examination will not be related. The heart rate was 80. No murmurs or apparent en largement. Blood pressure 158/90. The electrocardiogram revealed no evidence of coronary involvement but did show low amplitude of the QRS interval with notching. There was moderate peripheral arterio sclerosis. The urine showed a good trace of albumin with numerous granular casts. Blood chemistry was normal. The lead content of the twenty-four-hour specimen was normal. Blood lead was not deter mined. The blood count was normal, and the basophilic aggregation tests were negative. It was not expected that abnormal lead would be found in any of these tests, but they were run because of the medicolegal dispute. The conditions of employment were studied. The claimant ad mitted that they were identical at the time they were studied and tested as they had been during the years he had been employed. Main taining a faithfulness to detail in order to reduplicate the exact work ing conditions under which this man served, the Smith-Emery Test ing Laboratories obtained a percentage of lead in air less than the accepted standard for safety. During the trial, it was shown that the patient had orthopnea, dyspnea, and substernal pain on effort. Several physicians testified that these were signs of heart disease common to men in his age bracket regardless of occupation. It was brought out that no one had been able to produce evidence that this man had ever had excessive amounts of lead in his system. It was shown that the diagnosis of lead poisoning had been made upon one finding, coupled with an assump tion; namely, the finding of 0.08 mg. per liter of lead in the blood, which is within normal limits, and that he had been employed in a trade at one time considered to have a marked lead hazard. This is an example of the prevailing misconception of what con stitutes lead poisoning. It is an example of attributing to employment a disability not substantiated by findings, instead of attributing the disability to a disease syndrome common to the age of the patient. There existed no evidence that the man ever had lead poisoning, but there was preponderant evidence that his condition found multiple duplication in all walks of life. The case illustrates the urgency for a better informed profession. The former decisions were reversed in favor of the defendant. Case II.--A woman, aged thirty-two, presented herself to the clinic complaining of lassitude, weakness, aching all over her body, dry throat, and marked constipation. Four days previously she had 16 242 OCCUPATIONAL DISEASES become aware of abdominal cramps, which were increasing in severity. History.--Occupational history revealed that for six month each year she worked for a tinsel-manufacturing company which made, among other things, Christmas ornaments. Four weeks prior to the onset of her illness, she had been transferred to a small, partitioned room where she dipped ornaments in a hot solution of lead. Ventila tion was inadequate, and no respirator was provided. Past medical history revealed that the patient had had an appendectomy in 1920, and a gallbladder drainage in 1926. Physical Examination.--The gums showed small, spotty deposits along the margins adjacent to the teeth. Blood pressure, 128/70; pulse, 82; temperature, normal. Abdomen: Generalized soreness but no rigid ity. No masses or organs palpated. Scars of former operations. Mus cles of the extremities were tender to the touch. Neurological exami nation was negative. Laboratory Examination.--This revealed red blood cells, 3,100,000; hemoglobin, 68 per cent; white blood cells, 9800. Basophilic aggrega tion test, 1.8 per cent. Routine urine, negative; twenty-four-hour speci men of urine for lead, 0.52 mg. per liter. No blood lead was determined. This history was definite, the urine showed excretion above the normal, and the symptoms were sufficient. The patient did not recover for three months, experiencing an acute reversal during the course of deleading. The case was compensable. Temporary disability of thirteen weeks awarded. No permanent disability. Case III.--A tire and battery repairman, aged forty-two, consulted his physician regarding abdominal cramps, lassitude, headache, and loss of weight. The workman contended that his illness was due to the acid fumes from the batteries that were constantly being recharged or repaired. The physician found a secondary anemia. The patient was in structed to refrain from work and was given calcium tablets. The in surance carrier was informed that the man had lead poisoning. Seven weeks after stopping work, a gastric hemorrhage occurred, and an operation ensued, which disclosed a perforated gastric ulcer. No attempt was made in this case to prove the presence of any disease. No lead was looked for in the excreta or blood. A differential diagnosis for pains in the stomach was not made. Seven weeks of absence from the alleged hazard, along with calcium therapy had not improved the condition. The only effect the fumes from these bat teries might have had would have been a mild irritation to the upper respiratory tract from the sulfuric acid fumes. In the department where batteries are charged in the largest stor age-battery manufacturing plants, lead poisoning is unknown. This LEAD 243 patient worked in a large, well-ventilated room where, at no time, were there more than four or five batteries being recharged. The point in this illustration is that the evidence for lead was never investigated. Case IV.--Bartleman and Dukes report the case of a young ac tress who developed the classic symptoms of lead poisoning. Blood examination revealed anemia and stippled red cells. The diagnosis was confirmed by the finding of large quantities of lead in the urine and feces. The source of the lead poisoning was traced to the use of a greasepaint containing approximately 40 per cent of lead. There is a great variability in susceptibility to lead poisoning. The greasepaint used by the patient was the same brand as that used by several other members of the cast, but so far as was known, no other case of lead poisoning occurred. There was, however, a good deal of ill health and also some complaints of tiredness and headaches among those of the cast who had used this greasepaint previously. This case is cited because it is unusual. It is not an example of in dustrial exposure in the true sense of the word. The possibility of constantly cracked, parched, dry, broken skin in those using cosmetics daily is apparent, although the authors do not record that. They indi cate that they ruled out any other cause. No question of compensation is introduced by the investigators. If the patient bought and furnished her own cream, the liability should be her own, but if the cream was furnished by the owner, then the liability is his, and compensation would be in order. Case V.-- (Because the essential interest in this case is to be found in the laboratory findings, the physical examination and other nonessential factors will be omitted.). A twenty-one-year-old foundry worker presented himself to the author on September 13, 1939, complaining of severe abdominal cramps, together with nausea and vomiting, which he believed were due to exposure to lead. He had worked for the Berg Metal Company for three months, but investigation showed he had been exposed to lead for only three weeks prior to the onset of symptoms. One week before reporting to this clinic he had been seen by his neighborhood physician, who had instituted twice-daily injections of calcium, and calcium gluconate was given orally. The clinical picture was typical for lead intoxication. The patient was immediately hospitalized and eu a search for lead begun. The blood count revealed a secondary anemia of moderate degree and the basophilic aggregation test showed 1.8 per cent of basophiles. The patient had pyorrhea, and the lead line was questionable. The twenty-four-hour specimen for lead in urine fe# showed 0.01 mg. of lead per liter. t' k;. jk >-'f 244 OCCUPATIONAL DISEASES In view of the normal amount of lead in urine, the case incited further search. A hygienist was dispatched to the plant to investigate the conditions of exposure and reported them to be minimal. In spite of calcium therapy and high calcium diet, the patient obtained no re lief from his symptoms. Ten days after he was seen by us, a blood test for lead was reported as showing 0.23 mg. per 100 cc. of blood and 0.12 mg. per 100 cc. of serum. The patient sought his family physician who continued calcium therapy and on November 20, 1939--over two months following our first investigation--he showed in the twentyfour-hour specimen of urine 0.03 mg. per liter, but his blood showed 0.2 mg. per 100 cc. of blood, and 0.1 mg. per 100 cc. of serum. At this point it should be admitted that faulty clinical procedure was followed, in that the laboratory investigating the urine was not equipped to do the spectrographic method of blood examination, and therefore two different laboratories were employed. Thus, after two months of in tense accepted therapy and the absence from exposure, the lead con tent in the blood revealed practically no change. Because of the many peculiarities, the facts in the case were submitted to Dr. Robert A. Kehoe of the University of Cincinnati, and to Dr. V. A. Gant in Chicago, for their opinion. It is to be appreciated that they are com menting upon a case they did not see and of one over which they had no laboratory control. Dr. Kehoe wrote to me in part as follows: In a period of 15 years' experience, we have never seen an adult with lead intoxication without a definitely elevated urinary lead ex cretion. I know of no renal condition which will interfere with the elimination and, in fact, it is our experience that when water can be excreted, lead is also adequately excreted by way of the kidneys. Rela tive to the lead content of the blood in which 0.23 mg. per 100 cc. of blood and 0.12 mg. per 100 cc. of scrum were supposedly found, I am disposed to believe that these results are grossly in error. First, the result of 0.23 mg. per 100 cc. of blood in an adult is entirely incom patible with the urinary concentration of 0.01 mg. per liter. Second, the distribution of lead between cells in serum is not of a type indi cated by these analyses. I have never found less than 85 per cent of the total lead content of the blood in the cells. The plasma, or serum, in our experience has never contained more than five to ten per cent of the lead content. This distribution as reported by you is so un usual, therefore, as to be almost prima facie evidence against its own accuracy. It is also indicated in your report that on November 20, the blood still contained 0.2 mg. of lead per 100 cc. with 0.1 mg. or 50 per cent in the serum. My same criticism holds here. It seems quite obvious to me that if one of these results is correct the other is incorrect. I repeat that we have studied blood containing lead up to almost twice that which you have given here and have never succeeded in finding LEAD 245 anything like 0.1 mg. of lead per 100 cc. of blood plasma or serum. There is the additional reason for skepticism here in that more than two months elapsed since the cessation of exposure, yet the blood lead had not materially diminished. This is against all experience. Blood leads do not remain at such concentrations, in our experience, for more than a short time unless the exposure and absorption have been so massive as to involve very large quantities of lead in the tissues of the body. Dr. Gant in his reply stated: With reference to your letter of December 11, concerning the sus pected case of lead poisoning, I must say that the findings are not in agreement with any case which has been called to my attention. In every instance in the past 11 years it has been my experience always to find an abnormal amount of lead in the urine when an abnormal quantity was found in the blood. As a general rule when it is found that the blood contains about 0.2 mg. per 100 cc. the concentration in the urine will be about one-tenth of that, or 0.2 mg. per 1000 cc. Following the urinary findings and the report of the hygienist who investigated the hazard, the writer was at first in doubt as to the cause of the boy's complaints. But after the report of the lead in blood, he was recommended for compensation. Certain discrepancies existed which cannot be explained. It is pos sible that the hygienist who investigated the circumstances of employ ment was at fault and the patient received a massive exposure which was not recognized. It was established that his exposure had been short and that he wore a respirator. Furthermore, the lead in the urine was determined by a reputable and highly efficient laboratory upon which great reliance has always been placed. Both urine specimens were collected under strict adherence to technique. The lead in blood was examined by Dr. Chaney, of the Los Angeles County Hospital, a man experienced and qualified in this method. Just where the error occurred will never be known. But it is well that it did, for the case has served to bring out the various phases of the controversy and has permitted a discussion of the relationship of lead in blood to that of lead in urine, the relationship of lead in red blood cells to that of lead in serum, and the question of how long lead in blood may persist. The patient was granted temporary disability for three months, and no permanent disability occurred. Case VI.--A twenty-eight-year-old painter was taken to the County Hospital by a neighbor because he had been acting queerly. He complained of abdominal pains, vomiting, headache, and dizziness. Upon alleging that he thought his illness was due to lead poisoning 246 OCCUPATIONAL DISEASES from the paint he worked with, he was considered a "compensation case" and refused admission. He was then admitted to a small sani tarium. Following a cursory examination, a diagnosis of lead poison ing was made. He remained in this institution for five days. Following discharge, he was employed by a new contractor. He worked two weeks, when one day he was observed acting very queerly while painting the woodwork of a room. The foreman discharged him. The patient started home but did not arrive for two days and could not account for the interval of time. At this time he was brought to our clinic. He appeared lucid and claimed constipation, abdominal cramps, and weakness of his wrists. He told the resident that he had lead poisoning and that no one could fool him, for he knew the symp toms. Following a complete study in which there was no evidence of abnormal lead absorption as evidenced by the normal blood and urine, the patient was discharged. One week later he appeared before the Industrial Accident Com mission where he filed a claim for lead poisoning. At the time of trial he submitted a medical report from a physician which stated that this man had "clinical evidence of lead poisoning." No laboratory reports accompanied this diagnosis. It was brought out at the trial that investigation of this patient's claim revealed the fact that he had been committed to an institution for dementia praecox three years previously. He had since married but had deserted his wife. He had not worked as a painter for more than two weeks at a time and then only about six weeks within the past sixteen months. No abnormal amount of lead had been found in any of the tests run by us, and the physician who contended that the patient had lead poisoning had never investigated it from the laboratory standpoint. The patient was denied compensation by the commission. Ob viously the case presented no basis for claim. It exemplifies the type of case that needlessly crowds the calendar of hearings before the com mission. TREATMENT The treatment of lead intoxication is at this time not clearly de fined. A short time ago a definite regimen could have been outlined for use, but recent experimental work has thrown considerable doubt on the value of the older methods. Deleading by High Calcium Diet.--Following the work of Aub, Fairhall, Minot, and Reznikoff,4 which indicated that lead could be either stored or excreted by distorting the calcium metabolism, therapy was directed along these lines. The conclusions drawn from their work were that a negative calcium balance increases the rate LEAD 247 of lead excretion, while a positive calcium balance favors the storage of lead. To this end, then, the treatment for the acute episode in the past has consisted of the following: 1. A high calcium diet, which includes much milk, green vege tables, and potatoes 2. The administration of calcium products and vitamin D orally, e.g., calcium lactate, 1 drachm (4 gm.), once every two hours; or calcium gluconate, 7% grains (0.5 gm.), in milk at threehour intervals, so that the patient obtains five or six doses daily 3. Calcium gluconate, 10 cc. of 10 per cent solution, intravenously daily for five days 4. Magnesium sulfate, % ounce every morning, to sweep out the relaxed bowel 5. As substitutes for the intravenous calcium gluconate in the relieving of abdominal pain, hypodermic injections of mor phine sulfate, y4 grain (0.015 gm.), and atropine sulfate, Hoo grain (0.0006 gm.); nitroglycerin, from one to two '%oo grain (0.0006 gm.) tablets dissolved under the tongue; or the inhalation of the contents of a 5-minim (0.32 cc.) amyl nitrite pearl Disadvantages of Method.--Recently much doubt has been thrown on this method of treatment by the work of Lederer and Bing.19 Their work indicated that the deposition of lead in the bones of growing animals is retarded by increasing the calcium content of the diet and that the phosphorus content of the diet had no significant effect on the amount of lead deposited in the bones. This would indicate, then, that a high calcium diet would be the optimum diet for deleading, rather than for the deposition of lead in the bones. The use of the high calcium diet, then, according to this view might actually be dangerous by mobilizing lead for possible storage in the central ner vous system in the acutely ill patient. Taeger20 arrives at such a con clusion and advises against large doses as well as against the intra venous administration of calcium. Shelling and Hopper21 believed the use of calcium did not induce superior calcification, but rather had the opposite effect, especially when the phosphorus intake was inade quate. Kehoe and Thamann22 were of the opinion that the use of agents to promote the quick release of lead from the tissues was hazardous. Shelling23 demonstrated experimentally that the addition of calcium carbonate to an optimal stock diet containing lead car bonate fed to rats resulted in an increased toxicity. These rats evi denced toxicity and died sooner than the rats fed on the same stock diet to which sodium phosphate had been added. Gray and Green- r!'/ w. 248 OCCUPATIONAL DISEASES field 11 reported a small series of eases where prolonged administration of high calcium diet therapy was responsible for permanent, irre parable damage to the nervous sj'stem. They-4 concluded that a high calcium regimen was the best means of deleading. In view of this evidence, the advisability of the use of a high calcium diet alone is open to question. The frequently dramatic relief of abdominal pain obtained from the intravenous administration of calcium may repre sent, then, only a general depressant action of calcium on smooth muscle rather than a specific reaction as regards the lead in the blood stream. With High Phosphorus and High Vitamin.--Gray and Greenfield24 found the use of an optimal calcium diet, with a high phosphorus and high vitamin diet (D particularly), the best treatment in these cases. With this regimen an essential element was the administration of sodium phosphate, two drachms three times daily. Shelling23 indi cated that in order to deposit lead in the skeleton as an insoluble lead phosphate, a certain amount of phosphate was required, and thus when phosphate was inadequate, free lead might remain in circulation. He stated that the addition of sodium phosphate "provides sufficient phosphate for the deposition of both calcium and lead phosphate in the skeleton, for the excretion of lead as the relatively non-toxic lead phosphate, and also for the formation of colloidal lead phosphate in the blood." As indicated, the work of Lederer and Bing directly op poses this statement and seems to indicate that the addition of phos phate had no significant effect. The work of Lederer and Bing further indicated that the beneficial effect of calcium in the diet in retarding the retention of lead by the body was due to reactions which occurred in the intestinal tract and that calcium carbonate orally was the most valuable preparation. Deleading by Low Calcium Diet. With High Phosphorus.--In the past a regimen of a low calcium, high phosphorus diet, phosphoric acid, and magnesium sulfate had been used successfully by Gray2,1 in deleading treatment. He used the diet in Table 12 with claims of success. He also elaborated a similar diet with a calcium to phosphorus ratio of 1:4. To these were added 20 minims of viosterol (250 D) daily, since vitamin D was deficient in the diet. Previously he had used a low calcium diet consisting of meat, liver, potato, rice, tomatoes (cooked without milk), canned corn, bananas, apples (peeled), tea, coffee (without milk), butterfat, bread (prepared without milk, such as salt-free nephritic bread or sodium bicarbonate biscuits or crack ers), sugar, salt, and pepper. Phosphoric acid in amounts of from 10 cc. every two hours for six doses daily to 10 cc. once every hour for LEAD 249 ten doses daily was used. In addition, magnesium sulfate, % ounce (15 gm.), each morning was given. With this regimen, increase in urinary lead was at first seen, and this was followed by a decrease as the patient was presumably deleaded. Table 12--Low Calcium-High Phosphorus Diet (Ratio 1 : 3) Food Weight (Gm.) Applesauce............................................... 100 Grapes....................................................... 103 Banana...................................................... 100 Pineapple juice....................................... 540 Shredded wheat (1)............................... 27 Whole-wheat bread................................ 120 Macaroni.................................................. 30 Egg-yolks (4).......................................... 80 Butter........................................................ 30 Cream, 40 per cent.............................. 70 Lettuce...................................................... 30 Total: Protein, 101.78 gm.; calcium, 0.601 Food Weight (Gm.) Lamb chops............................................. 160 Liver.......................................................... 90 Bacon........................................................ 15 Baked potato.......................................... 100 Tomatoes.................................................. 100 Green peas............................................... 100 Mushrooms.............................................. 60 Celery........................................................ 30 Almonds.................................................... 15 Oranges..................................................... 200 i.; phosphorus, 1.889 gm.; Calories, 2,969.88. With Other Substances.--Other methods suggested for deleading have included the low calcium diet cited above; ammonium chloride, 15 grains (1 gm.) every hour for ten doses daily; and magnesium sulfate, l/> ounce (15 gm.), every morning. Belknap20 used fifteen drops of potassium iodide twice daily or seven drops twice daily of sodium iodide in saturated solution. Sodium bicarbonate, from 5 to 8 drachms (20 to 30 gm.), daily, divided into five or six portions has also been used, as has parathyroid extract. Advisability of Deleading.--As indicated above, there is disagree ment concerning the possibility of deposition of lead in bones by changes in diet or by medication. In addition, the advisability, as well as the possibility and the methods of deleading, is distinctly open to question. Most authorities feel that it should not be attempted before from three to four weeks have elapsed after the acute episode. Most feel that the deleading should be carried out only in the hos pital and with adequate laboratory checks, although Belknap, cited above, deleads patients in mild cases while they are ambulatory but under close supervision. He requires a blood level of 80 per cent hemo globin, 4,000,000 or more red blood cells, stippled cells not more than from 1000 to 5000 per million red blood cells for two to three weeks, and a twenty-four-hour urine lead 0.15 mg. or lower before under taking the deleading. He also deleads no oftener than once in four weeks, and preferably not oftener than once in six or eight weeks. Benefits versus Drawbacks of Deleading.--Those who oppose de leading feel that the danger of producing lead encephalopathy is too 250 OCCUPATIONAL DISEASES great, and that the patient cannot be successfully "deleaded" at any rate. Those who favor it urge that the stored lead represents a con stant potential hazard, since acute episodes, such as infections with acidosis or other periods of metabolic stress, may cause deleading at an undesirable time. Aub27 feels that thorough deleading approx imately halves the period of disability for lead palsies. Ascorbic Acid Therapy.--Holmes, Campbell, and Amberg28 found 100 mg. of ascorbic acid daily of much benefit in lead-intoxication cases, and also observed that the ingestion of alcohol had an un favorable influence and in several instances nullified the benefits of treatment. Others have had no success with this form of therapy. Treatment in Lead Palsy.--In this condition, stretching of fibers of paretic muscles should be prevented. In those cases presenting a wrist-drop, a cocked-up splint, to include the fingers and worn night and day, is used until function returns. Hot-water baths (110 F.), electric stimulation by interrupted galvanic current, and gentle mas sage, preferably by whirlpool, once every day or two are used. Strenu ous massage and violent exercise are avoided. Reeducation exercises are of value. Treatment in Lead Encephalopathy.--Encephalopathy is rare and has not been seen in our clinic in the past five years. When it does occur, lumbar puncture and sedation may be required. Magnesium sulfate, 2 cc. of a 25 per cent solution given intramuscularly from every four to six hours, and barbiturates are used. For convulsions barbiturates, e.g., sodium amytal, from 3% to 7% grains (0.23 to 0.5 gm.), are given intravenously, and avertin is used rectally. Suboccipital or subtemporal decompression in lead encephalopathy has been used successfully.29 Therapy without Deleading.--Many feel that removal from the hazard with symptomatic treatment for pain, weakness, lead palsy, and encephalopathy is all that is needed, with no particular attempt to store or remove the lead. We have usually found this procedure successful in our own clinic. Prophylaxis.--The best method to avoid lead poisoning is, of course, to take measures to prevent it. To this end, Gant30 suggests the following rules and mechanical features:1 2 3 I 1. Hoods with adequate exhaust ventilation to be at any point where dusts or fumes arise 2. All mixing and shaking to be done in enclosed machines 3. All powdered compounds to be transferred by means of ade quate vacuum lines P LEAD 251 4. Work tables to be provided with grated tops, ventilated from below, and equipped with small narrow troughs filled with water, and attached to each side to prevent dust falling to the floor 5. All inlets to exhaust ventilating ducts to be below the level of the nose, as far as possible, to prevent fine dust particles from being inhaled 6. A chemical analysis of samples of air from various parts of the plant to be made at different intervals during working hours. (Any spot showing more than 1.5 mg. of lead per 10 cu. m. is a potential health hazard) 7. Employees in hazardous spots, as found under "6," to wear respirators. Where movements are confined to a small area, forced-draft respirators (fresh air from the outside) to be used. If exposure is to fumes, masks to be provided with canisters charged with activated carbon. (Respirators are only from 70 to 90 per cent efficient and must be inspected and changed frequently) 8. No dust allowed to accumulate on the floor 9. Floors to be wet at frequent intervals, and powdered compounds used, if possible 10. All cleaning to be done with large vacuum lines. No sweeping 11. To prevent the collection of dust on rafters, sills, etc., ventilat ing ducts to be installed, equipped with dust-filters near the ceiling or in mid-air 12. To avoid the contamination of outside air and surrounding terri tory, and as an economy measure, electrostatic precipitators to be installed in the stacks and flues 13. The personal hygiene of the employees to be closely guarded. Locker-rooms with showers, a lunchroom isolated from the plant, and a change of overalls twice a day to be provided. Hands and face to be washed before eating. No eating, chew ing, or smoking during working hours Factory Management.--All of the above find their fulfilment in intelligent plant or factory supervision. The experience of this clinic confirms the observation of others that most cases of lead intoxica tion arise in small, non-supervised establishments. Frequently those in charge do not realize they are handling a lead compound or lead alloy. As an additional preventive measure substitution of non-toxic materials for the lead compounds may, in certain processes, be prac tical. For example, aluminum or ferric oxide paint may in many in stances be substituted for the paint containing a litharge base. 252 OCCUPATIONAL DISEASES REFERENCES 1. Magnuson, H. J., and llaulston. B. 0.: "Lead Poisoning in Roofers," J.A.M.A., 1U (April 20), 1940. 2. Kelioe, R. A.: Address before Central Society for Clinical Research, November, 1939. 3. Aub, J. C.: "To the Editor," J.A.M.A., Ilk (June 1), 1940. 4. Aub, J. C,, Fairhall, L. T,, Minot, A. S,, and Reznikoff, P.: "Lead Poisoning," Medical Monographs, Williams and Wilkins Co., Baltimore, 1926. 5. Aub, J. C., Robb, G. P., and Rossmeisl, E.: "Significance of Bone Trabeculae in the Treatment of Lead Poisoning," Am. J. Pub. Health, 22: 285, 1932. 6. Gray, I., and Greenfield, I.: "High Calcium Therapy," Indust. Med., 8: 507 (Dec.), 1939. 7. Aub, J. C., Reznikoff, P., and Smith, D. E.: "Lead Studies; Effect of Lead on Red Blood Cells, Changes in Hemolysis," J. Exper. Med., i0: 151-172 (Aug.), 1934. 8. Ferguson, A. E., and Ferguson, T.: "Examination of the Blood Films in Relation to the Prevention of Plumbism among Shipbreakers," J. Hyg., 3k: 293 (Oct.), 1984. 9. Shiels, D. O.: "The Ratio of Large to Small Lymphocytes in Persons Exposed to a Lead Hazard," Med. J. Australia, 1: 847-849 (June 20), 1936. 10. Smith, Fred L., H, Rathmell, T. K., Marcil, G. E.: "Early Diagnosis of Acute and Latent Plumbism, Am. J. Clin. Path., 8: 471-508 (Sept.), 1938. 11. Blackman, S. S.: "Intranuclear Inclusion Bodies in Kidney and Liver, Caused by Lead Poisoning," Johns Hopkins Hospital Bulletin, 58: 384 (June), 1936. 12. McCord, C. P., Minster, D. K., and Rehm, M.: "Basophilic Aggregation Test in Lead Poisoning," J.A.M.A., 82: 1759-63 (May 31), 1924. 13. McCord, C. P., Holden, F. R., and Johnston, J.: "Basophilic Aggregation Test for Lead Poisoning and Lead Absorption," Indust. Med., k: 180-185 (April), 1935. 14. Hyler, M. D., and Bradley, W. R.: "Basophilic Aggregation Test as Early Diag nostic Factor in Absorption and Incipient" Poisoning," Indust. Med., 7: 184193 (April), 1938. 15. Barnes, E. C.: "Possibilities of Control of Lead Exposure by Examining Less than 24-Hour Urine Samples, J. Indust. Hyg. and Toxicol., 21: 9, 464-468 (Nov.), 1939. 16. Tompsett, S. L., and Anderson, A. B.: "Lead Content of Blood and Excreta," Lancet, 1: 553-616 (March 11), 1939. 17. McNally, Wm. D.: Toxicology, Industrial Medicine Publishing Co., Chicago, 1937, p. 170. 18. Calvery, H. 0., Laug, E. P., and Morris, H. J.: "Chronic Effects on Dogs of Feeding Diets Containing Lead Acetate, Lead Arsenate and Arsenic Trioxide in Varying Concentrations," J. Pharmacol, and Exper. Therap., 6k: 364-387 (Dec.), 1938. 19. Lederer, L. G., and Bing, F. C.: "Effect of Calcium and Phosphorus on Retention of Lead by Growing Organism," J.A.M.A., Ilk: 2457-61 (June 22), 1940. 20. Taeger, H.: "Calcium Therapy of Lead Poisoning," Klin. Wchnschrijt., 16: 1613 (Nov. 13), 1937. 21. Shelling; H. D., and Hopper, K. B.: "Calcium and Phosphorus Studies," Johns Hopkins Hospital Bulletin, 58: 196, 1936. 22. Kelioe, R. A., and Thamann, F.: "The Excretion of Lead," J.A.M.A., 92: 1418, 1929. 23. Shelling, D. II.: "Effect of Dietary Calcium and Phosphorus on Toxicity of Lead in Rat; Rationale of Phosphate Therapy,"' Proc. Soc. Exper. Biol, and Med., 30: 248-254 (Nov.), 1932. 24. Gray, I., and Greenfield, I.: "Newer Concepts in the Treatment of Lead Poison ing," New York State J. Med., 3$: 1313 (Oct. 15), 1938. LEAD 253 2.3. Gray, I.: "Recent Progress in the Treatment of Plumbism," 10k: 200 (Jan. 19), 1935. 20. Belknap, E. L.: "Control Lead Poisoning in the Worker," J.A.M.A., 10k: 205- 210 (Jan. 19), 1935. 27. Aub, J. C.: "The Biochemical Behavior of Lead in the Body," J.A.M.A., 101: 87-90 (Jan. 12), 1935. 28. Holmes, H. N., Campbell, K., and Ambcrg, E. J.: "The Administration of Vitamin C in the Treatment of Lead Poisoning," J. Lab. and Clin. Med., 2k: 1119-27 (August), 1939. 29. Haverfield, T. W., Bucy, P. C., and Elonen, A. S.: "The Surgical Treatment of Lead Encephalopathy," J.A.M.A., Ilk: 2432-37 (June 22), 1940. 30. Gant, V. A.: "Lead Poisoning." Indust. Med., 7: 693 (Nov.), 1938. CHAPTER XX MERCURY The case of mercurial poisoning as one sees it in accidental, sui cidal, or therapeutic instances is not similar to industrial mercurialism. Industrial exposure to mercury was known to the Greeks as early as 400 b.c., but like lead it is still not well known to the average physician. Freeman reported its occurrence in fur-cutters and hatters in America in 1859. Occupational Hazards.--There are about 100 occupations in which this metal offers a hazard. All of these need not be listed. The fol lowing list is but a few of the hazards and shows the form of mercury used: Mercury ...................................... Mercury nitrate (HgN03, Hg(N03)2) ......... Mercury fulminate (Hg(CNO)2) ....................... Mercury sulfide (cinnabar, HgS) ..................... Mercury cyanide (Hg(CN)2) Mercuric chloride (I-IgCl2) .. Hatting industry (Hg(N03)2) Fire-gilding.................................. Mercury amalgam..................... Mercury pumps ....................... Chemical works......................... Solder for dry batteries Dentists ...................................... Mercury boilers Welders Manufacture of scientific instru ments Felt-hat industry; decorating por celain Constituent of all percussion caps Mining and use as a pigment Making cyanogen Manufacture of antiseptic dress ings Treatment of felt Applying gold mercury amalgam to base metal and driving off mercury by heat For extracting gold and silver from ore To exhaust air from incandescent lamps As HgClo, etc. Mercury amalgams Pathology and Action.--Comparable to lead, the chief mode of en trance of mercury into the body in industry is by the respiratory tract. Ingestion, absorption through the skin, and injection into the 254 MERCURY 255 subcutaneous tissue are primarily used in therapeutic endeavor. The inhalation of mercury produces a reaction peculiar to body tempera ture, according to Biondi. If the inhaled vapors are lower than the body temperature, they circulate in the body as such or in combina tion, eventually to irritate the nervous system. If the mercury vapor in the air is of a higher temperature than the body or mucosa, the mercury is condensed on the mucosa to be absorbed as a mercury compound, giving rise to stomatitis, nephritis, or colitis. When this occurs, it causes inflammation at the point of elimination, as nephritis in the kidneys, stomatitis in the salivary glands, and colitis in the large intestines. Mercury may be stored in the kidneys, liver, spleen, or the bones. It is eliminated in the urine, feces, saliva, sweat, or from the large intestines, bile, or milk. Its effect upon the nervous system may repre sent a diffuse encephalitis or symptoms of the particular center which it happens to predominantly affect. The ethyl group of organic mer curial compounds has an affinity for the cerebral lipoids resulting in a disturbance not unlike that of tetraethyl lead. Mercury vapors in the body affect the lipoid tissue. The pathology of chronic mercurialism is not well understood. Mercury circulates in the bloodstream as an oxychloro-albuminate. Young people and fe males are more susceptible to its constant effects, while infection or alcoholism predisposes to chronic mercurial poisoning. DIAGNOSIS Signs and Symptoms. Tremor.--The most startling symptom, and one which leads to much confusion in the diagnosis, is the tremor which occurs in the voluntary movements. It is an intentional tremor, similar to that observed in paralysis agitans (not so regular), multiple sclerosis, or Basedow's disease. The hands, limbs, head, lips, tongue, or jaw may be affected, and this may be bilateral or unilateral. Text books for years have illustrated the characteristic handwriting of these victims, where the first few words are normal but succeeding words become more and more illegible. An illustration is found in the Mad Hatter in Alice in Wonderland. In New England they were called the ``Danbury shakes." Psychic Disturbances.--Various forms may occur, e.g., unrest, irritablencss, depression, fear, lack of concentration, and loss of selfconfidence. In addition, generalized weakness, pains in the chest, vomiting, metallic taste in the mouth, and cramps in the leg muscles are sometimes present. Tests. Acute Poisoning.--Acute poisoning is rare in industry. Marked gastric disturbance, characterized by alternating diarrhea and 256 OCCUPATIONAL DISEASES constipation, varying degrees of distention with distress, stomatitis, and inflammation of the kidneys may occur. Chronic Poisoning.--Symptoms of chronic poisoning are referable chiefly to the nervous system. When it is suspected or alleged, the urine or feces should be examined for the presence of mercury. If found, its presence does not mean that the patient is poisoned. Like lead, its finding must be combined with the history and symptoms. Blood examination is not of much value. There is frequently a rela-' tive lymphocytosis. The blood chlorides may be decreased. A safe atmosphere for working conditions is that of 2.5 mg. per 10 cubic meters of air, or less. MEDICOLEGAL ASPECTS Temporary Disability.--Most patients respond to treatment and removal from exposure. Patients in mildly severe cases may have a persistence of symptoms from two to three months; in severe cases, they may be disabled for a period of eight to twelve months. Permanent Disability.--Before the present state of hygiene, perma nent tremors were not uncommon. Today, one rarely sees them. If they are present in older persons and those exposed for many years, Kessler1 suggests a 25 per cent total award. Illustrative Cases.--Mercury mining in California was a prominent industry during the first World War, but there followed a period of inactivity. Today these mines are booming because of the removal of Spain as a source of mercury, due to the second World War. How ever, the process is now so carefully guarded that mercurial poisoning rarely occurs. In the city of Los Angeles there are 120 concerns engaged in the manufacturing of hats and furs; yet in the past five years not a single patient with mercurial poisoning has presented himself to our clinic. This is an indication of the high state of preventive medicine in an industry with known hazards. The following case has been selected for illustration because of the description of the tremors that existed and the eventual outcome. The man was a patient of Dr. F. S. Ryan, of San Jose, California, and the case was reported by Dr. Alice Hamilton.2 Case I.--The patient is a Spaniard, employed first as a miner and then as a furnace man, and he was evidently unusually susceptible, for he had several attacks of poisoning while mining cinnabar, where the danger is very slight. An attack would begin with a queer sweetish taste in the mouth, followed by colicky pains and diarrhea. There was never an inflam mation of the mouth or salivation, nor had there been a loss of teeth. MERCURY 257 The most serious symptom was tremor. From the mines the patient went to work in a reduction plant and was put on a Scott furnace where the fumes were very bad. During this time, his tremor was practically constant and very troublesome, especially if he was ex cited. sometimes making it impossible for him to feed himself. He drank a good deal of native California wine but no whisky. In spite of the doctor's warning, he continued to work on the furnaces; then one afternoon at about three o'clock in his home in the mining camp, he suddenly began to have violent clonic spasms of the right leg, which, as he described it, "began to work up and down like a piledriver." The thigh would be drawn up on the abdomen, the leg flexed against the thigh, and then violently extended again, and all the efforts of his fellow-workmen failed to hold it still. According to Dr. Ryan, who saw him about three hours later, the right leg was jerking back and forth rhythmically about sixty times per minute without any variation and with great violence. Morphine had no effect on the spasm, although it induced drowsi ness. There was no change in his condition under treatment by purg ing, by applying hot packs, or by putting ice to the head, nor could he be made to sleep even with morphine. The next morning a supin ator spasm of the right arm developed, synchronous with that of the leg. Chloroform was then tried, but the spasms did not stop until the stage of surgical anesthesia was reached, and then began again before consciousness was regained. There was no cerebral symptom except the insomnia. Thirty-six hours after the onset, sleep was obtained under chloral, and the spasms diminished in violence. Under the continual adminis tration of chloral, purgatives, and sweating, the spasms gradually died down, but did not cease entirely until the seventh day. The exhaus tion was extreme, especially as the patient could only take liquid food and only a very little at a time, for he could not keep still long enough to swallow much. He was discharged from the hospital, emaciated and weak, and for a year after that he could not work. He was a prey to headaches, in somnia, bad dreams, depression, and irritability. Nevertheless, he went back to the furnaces the following year and worked for six or eight months until his increasing tremor finally compelled him to give it up. I saw him at the works where he was employed as a teamster and he told me that he had never recovered his former health. He is always nervous, irritable, and easily upset, a statement which was heartily endorsed by the bystanders. Just recently he had had an operation for gastric ulcers, and under the excitement of preparing for it, his tremor returned for several days. This case-report is an instance of marked tremor, unusual suscepti bility, chronic ill health, and the return of tremors under excitement. 258 OCCUPATIONAL DISEASES It should be pointed out that disability occurred some time prior to 1925. The standards of hygiene as carried out in plant or mines today would not have permitted this patient to remain in the hazard after symptoms became so pronounced, nor would they have permitted him to return to this hazard. One wonders what the status of this case was under the Workmen's Compensation Act in California, where occupational disease was a part of that law at that time. There appears to be no question but that the patient was disabled because of his work and that he was eligible for temporary disability for at least one year. Why this employer or insurance carrier permitted him to return to work is most peculiar in the light of present-day working standards. Case II.--In the Archiv jiir Gewerbepathologie und Gewerbehygiene, Berlin, December, 1938, an observation not mentioned in American literature was found. Fellinger and Schweitzer report the clinical histories of three patients in whom severe vascular impair ments developed in connection with mercurial poisoning. To be sure it is justifiable to inquire whether the vascular lesions are actually the result of a mercurial intoxication or whether their concurrence with mercurial poisoning is merely accidental. Although positive proof is lacking, many factors militate for a causal role of the mercurial poisoning. In all three cases the vascular lesions developed at a time at which, although the early signs of mer curial poisoning had disappeared, the chronic manifestations and sequelae (dental lesions, tremor, and psychic changes) were com pletely developed. This appearance at a time when late lesions and sequelae develop seems to indicate that the vascular changes belong to the other manifestations of mercurial poisoning, the more so as the chronological connection is similar to that which is observed in lead poisoning, in which vascular impairments are comparatively fre quent. Moreover it appears improbable that in comparatively young and hitherto entirely healthy persons, vascular lesions should develop with great rapidity, when it is considered that Raynaud's and Buer ger's diseases generally develop at first sight insidiously, causing only minor symptoms. These and other considerations make it probable that these vascu lar lesions and their sequelae have a causal connection with mercurial poisoning. It was impossible to make anatomic studies on the vessels of the three patients with mercurial poisoning, but the clinical mani festations of the vascular lesions resemble those of the various forms of obliterating endarteritis; however, in their unusually rapid, almost fulminant, course they differ from idiopathic vascular diseases.3 Case III.--Williams and Schram4 report an incident of mercurial poisoning in 1937 when thirty-eight men suffered effects from exposure to this metal following cutting out the tops of stills by means of oxy- MERCURY 259 acetylene torches. The lids of these stills were closed by mercury seals, and over a period of years small quantities of mercury would be spilled on the lids. Those particles which were not removed would be painted over from time to time by a spray process. The symptoms were gingivitis, salivation, headache, abdominal cramps, and in the more severely affected, diarrhea with bloody stools. One patient showed alternate albuminuria and glycosuria. The temporary dis ability was short in all cases, the longest being six days. Case IV.--A fifty-seven-ycar-old general workman for a metal concern, of Los Angeles, presented a claim before the Industrial Acci dent Commission (January, 1941) for permanent disability due to: (1) loss of all teeth and (2) loss of all nails as a result of exposure to mercury. His total length of employment had been two years and nine months, although he had been absent from this process for one year before his final year of service. In 1938, at intervals, the patient was annoyed by "indigestion." His family doctor noted many decayed teeth and advised their removal, believing this would relieve the indi gestion. All teeth were extracted in August of 1938. About five months before being seen by the writer, the patient noted that he was losing his nails, a condition which led to his stopping work. The company for which this claimant worked is engaged in a process of obtaining mercury and antimony by the reduction of livingstonite concentrate, obtained from Mexico. This workman would take sacks of concentrate to a scale to be weighed; then to the elevator where the material was carried to a platform where it was dumped into a hopper (Fig. 44). He then carried the cinders which fell to the bottom of the furnace to a pile where they cooled and were re-sacked. These cinders when hot gave off a strong sulfur fume. The cinders also contained antimony that had been separated from the mercury. For ten minutes every hour the patient worked at the hoe table where mud containing mercury was spread out and under which was a fire. Also, every hour he drained mercury from the condensers into a flask. An industrial engineer, after investigating the plant, reported that the process was carried on in a large building, which had a roof but no side walls. He found only one point where there could be any possibility of inhalation of mercury fumes, although the concentration was well within the permissible limits. This was after the mercury antimony had passed through the rotary kiln. Antimony and mercury are vaporized in this kiln and drawn by suction into a condenser for the first recovery of the metals. Antimony oxide resulting from kiln action is eliminated from the rotary kiln by gravity into a hopper, from which it is conveyed by bucket elevator to an elevated hopper. The oxide is then released from the hopper by means of a sliding door into small muck cars. Farther along in the process in the scrubbing and retort recovery of the mercury and antimony, sulfur dioxide is 260 OCCUPATIONAL DISEASES generated, but this gas is carried off by suction control up to the exhaust chimney which is 102 feet high. The whole process is one de signed to prevent an escape of mercury fumes, for such escape would mean a financial loss. Fig. 44.--Reduction plant for treating livingstonite concentrate for the produc tion of mercury and antimony metal. {Mining and Metallurgical Bulletin, PhenhoelMenardi Engineering Co., Ltd.) Physical Examination.--The patient is an adult male whose given age is fifty-seven. He appeared somewhat underweight. The scalp and hair were normal in appearance. The pupils reacted to light and ac commodation, but were irregular and unequal. Teeth all false. Gums MERCURY 261 clean; no discoloration or pigmentation. Throat: normal. Lungs: clear throughout; no adventitious sounds noted. Heart: sounds some what distant; no murmurs heard, llate of 78, regular. Blood pressure, 138/90. Abdomen: normal in contour; no organs or masses palpated. There was a scar in the right quadrant due to a former appendectomy. Neurological examination revealed no abnormal findings. Right knee jerk normal. Left knee jerk exaggerated. Romberg negative. Gait normal. Examination of the hands revealed a loss of the fingernails of all fingers. This loss was not complete in every instance, there re maining at the tip of most of the fingers a small portion of normal nail. There existed no tenderness of the finger tips or to pressure on the nail bed. Examination of the feet revealed the large and second toes to have lost their nails in a manner similar to that noted of the hands. x-Ray Examination.--Chest: No alteration of either pulmonary field is demonstrated. The markings are not unusually prominent for a patient of the stated age. No evidence of pleural thickening seen. The left ventricle is beginning to be prominent in keeping with the patient's age, but no other changes are recognized. The findings are essentially negative. Laboratory Examination: Blood Hemoglobin.................88 per cent Erythrocytes per cu. mm................... 5,200,000 Leukocytes per cu. mm................ 7,800 Polynuclear neutrophiles ........... 58 Lymphocytes ............. 36 Large mononuclears . 3 Eosinophiles ............... 2 Basophiles................... 1 Blood Wassermann: Negative Urine Voided specimen Yellow color Clear appearance Specific gravity, 1.014 Acid reaction Sugar, 0 Albumin, faint trace Acetone, 0 Microscopic, 0-1pus cells A consultant ruled out arsenic poisoning and fungous infection by laboratory examination of the nails. In his opinion even though the blood Wassermann was negative, the probable etiology was lues. A spinal Wassermann was not permitted. Since arsenic was eliminated from an etiological consideration, there remained antimony, sulfur dioxide, and mercury. Little is known about the effects from chronic exposure to an timony, and it is believed that it is relatively non-toxic. In the foreign literature mention is made of a pustular, necrotic dermatitis com 26*2 OCCUPATIONAL DISEASES mencing as a folliculitis and resulting in atrophic scars. Colic, diarrhea, and loss of weight have also been mentioned by foreign writers. The claimant presented none of these conditions unless the vague type of indigestion he complained of could be considered a result of exposure. Sulfur dioxide produces irritation to the upper respiratory system when inhaled in large doses, but the effect is usually transitory. Mercury primarily affects the central nervous system, and tremors of the hands, legs, head, jaw, lips, and tongue may be noted. Psychic disturbances such as mental depressions, fear, and lack of concen tration are sometimes present. In 1935 Neal and Jones3 made a study of the effect of mercury upon workers in the fur-cutting industry. They found no evidence that mercury fumes or dust affected the lungs, nor was there a single case of pulmonary tuberculosis among their group. A fine intention tremor was noted in forty-three workmen, while tremor of the eyelids, tongue, jaw, head, and legs was also pres ent in less frequency. These two investigators noted a frequency of two types of discoloration of the oral and nasal membranes, one a white line and the other a rich, copper-colored line. With both the membrane was dry, glistening, and when the condition was present it usually extended over the entire oral mucous membrane as far as the upper portion of the pharynx and vestibular portion of the nasal mucous membrane. In their study of the blood picture, no significant changes were noted. The percentage of lymphocytes in the blood was slightly higher than normal, but the percentage of monocytes was within normal limits, so they attached no importance to the slight increase in lymphocytes. Nor could they determine that the amount of mercury in the urine had any significant value, since in persons with pronounced mercurial poisoning, the mercury in the urine was consistently found not to be high. In discussing the paper of Neal and Jones, McCord6 pointed out that in the cartridge industry the mercury fulminate is in a wet state, and therefore the type of exposure is somewhat different from what it is where fumes are in existence. He stated that in those who handle the wet mercury fulminate, ulcer ated fingertips, erosion of the nails, and sore fingers appear. In a report to the Industrial Accident Commission concerning our case under discussion, the author, took the position that he could not state with any certainty whether mercury was or was not the cause of the disturbance to the nails. Onychomadesis is usually considered to be the result of some metabolic disturbance, such as diabetes, or of syphilis of the central nervous system. In this instance, diabetes was ruled out, but syphilis was not completely, and had to be con sidered as a likely cause. Too little is known about the industries using mercury to be dog- MERCURY 263 matic. Our claimant's exposure docs not appear to be exactly com parable to the workers in mercury fulminate referred to by McCord, for in the latter instance it is inferred that these men handled the wet substance, whereas our claimant did not touch the mercury mud. However, the case herein reported is worth while in that it calls at tention to the possibility of nail erosion from this or similar types of mercury exposure. It does not represent a permanent total dis ability, from the standpoint of loss of either teeth or nails. TREATMENT Acute Poisoning.--This is usually the result of intentional or er roneous ingestion of the bichloride of mercury and so will not fre quently be seen in industry. However, as indicated by the cases reported by Williams and Schram, acute exposure may result in symptoms primarily involving the gastro-intestinal tract. Gastro-intestinal Involvement.--In such instances gastric lavage is indicated at once. A number of chemicals have been used with the wash water to precipitate the mercury and to delay its absorption. The most promising agent so far seems to be sodium formaldehyde sulfoxylate. The chief difficulty is that its effect is not great if as long as fifteen or thirty minutes elapse before it is given. A freshly pre pared solution of 10 per cent of the sulfoxylate with 5 per cent of sodium bicarbonate is used for the gastric lavage, and about 200 cc. of the mixture is left in the stomach. An intravenous injection of from 10 to 20 gm. of sulfoxylate in a 10 per cent solution should also be given over a period of from 20 to 30 minutes. Its use except in the acute case seen quite early is open to ques tion, since there is some experimental evidence demonstrating that while sodium formaldehyde sulfoxylate is of value in the prevention of the manifestations of poisoning, it may actually aggravate preexist ing intoxication. Monte and Hull7 felt that its repeated use was in advisable and strongly doubted its efficacy in any instance. It is probable that acute mercury poisoning will be seen earlier in indus trial than in private practice, and hence the therapy outlined may be of considerable value. Lavage with three tablespoonfuls of charcoal and 20 gm. of mag nesium sulfate to a pint of water is advised by McNally. One gram of charcoal binds 180 mg. of bichloride of mercury. Following this lavage two eggs in water and a glass of milk are administered. This is followed by another lavage with water, and finally four tablespoon fuls of charcoal are given by mouth (not to be removed). The milk which is used should have the cream removed, since fats dissolve mercury salts more quickly and aid in the absorption. |,,5 \:X; 264 OCCUPATIONAL DISEASES Pain and Prevention of Shock.--In these conditions, morphine sul fate, % grain (0.016 gm.), every four to six hours is used. For further treatment in shock, caffeine sodium benzoate, 7% grains (0.5 gm.), or epinephrine, 1 ce. of 1:1000 solution, may be given hypodermically, and an intravenous infusion of 10 per cent dextrose in saline (1000 cc.) is indicated. Subsequent Treatment.--Various therapies have been outlined for the subsequent treatment of the patient. Good results have been claimed for the intravenous use of sodium thiosulfate, 15 grains (1 gm.), in 10 cc. aqueous solution, from one to six times daily, for from three to five days. Hashinger and Simons reported a patient treated chiefly by exsanguination-transfusion, with complete recovery. Koranyi!) reported complete recovery of a patient with beginning olig uria, hematuria, and albuminuria by the use of daily venesection (300 cc.), daily oral administration of 5000 cc. Ringer's solution, and the intravenous administration of 20 cc. of a 10 per cent solution of sodium chloride. Others have advised multiple transfusions of from 300 to 350 cc. Cecostomy has been used with good results. It is very important that the lowered blood chloride level should be treated by intravenous administration of physiological saline, and that acidosis be treated as described under "Methyl Alcohol." Sodium citrate or acetate in amounts sufficient to keep the urine alkaline is given by mouth. A regimen consisting of 250 cc. of the following mixture, 250 cc. of milk at hourly intervals has been used: potassium bitartrate, 1 drachm (4 gm.); sugar, 1 drachm (4 gm.); lactose, % ounce (15 gm.); lemon juice, 1 ounce (30 cc.); boiled water, 16 ounces (500 cc). In combination with gastric lavage (with six quarts of sodium bicar bonate solution) and colon irrigation twice daily, daily sweating in a hot pack, and continuous rectal irrigation with a solution of potassium acetate (a drachm to the pint), it has given some good results. For muscular twitchings of uremia, calcium gluconate. 10 cc. of a 10 per cent solution intravenously, is of value. Chronic Poisoning.--No treatment of demonstrated value in chronic poisoning is reported. Removal from the hazard is, of course, absolutely essential. The use of sodium thiosulfate might be of value, 15 grains (1 gm.), in 10 cc. of sterile water intravenously every other day for a short time. Nervous Disorders.--Most of the treatment in the chronic case is directed toward alleviation of the nervous affections. Since many of these patients have symptoms similar to those seen with chronic encephalitic parkinsonism, it has been suggested that a trial of drugs used in that disease be made. The older drugs of this group arc scopol MERCUHY 265 amine hydrobromide (hyoscine), from to Vioo grain (0.0003 to 0.0006 gm.), two or three times per day, or tincture of stramonium, from 60 to 90 minims three times daily. A drug used more recently has been amphetamine sulfate (benzedrine sulfate), from 20 to 30 mg. twice daily, at 8 a.m. and at noon, in conjunction with a drug of the atropine group, or genoscopolamine, in dosage of 0.5 mg. gran ules, one three times a day, increasing the dosage after several days to two or three granules three times a day. The latter is said to have far less toxic effects than atropine, hyoscine, and stramonium.10 Stomatitis.--For this, the following mouth washes may be used: tincture of myrrh, 1 part to from 25 to 50 parts of water; potassium permanganate, 1:8000; or Ounces cc. Thymol (saturated solution) ............................. 2 64.0 Hydrogen dioxide .................................................. 2 64.0 Glycerine ................................................................. 2 64.0 Potassium chlorate (saturated solution) q.s. ad. 8 250.0 Good oral hygiene is imperative. A diet high in vitamins with the vitamin B complex particularly added should be of value. Diarrhea or constipation, if present, should be controlled. REFERENCES 1. Kessler, H. H.: Accidental Injuries, Lea and Febiger, Philadelphia, 1931, p. 718. 2. Hamilton, A.: Industrial Poisons in the United States, Macmillan Co., New York, 1925, p. 240. 3. Fellinger, K., and Schweitzer, F.: "Vascular Diseases after Poisoning with Mer cury," JAM.A., 112 (March 18), 1939. 4. Williams, J. E., and Schram, C. F. N.: "Acute Mercurial Poisoning," Indust. Med.., 6 (Sept.), 1937. 5. Neal, P. A., and Jones, R. R.: "Chronic Mercurialism in Hatter's Fur Cutting Industry," J.A.M.A., 110: 1938. 6. McCord, C. P.: Discussion of above paper. 7. Monte, L. A., and Hull, E.: "Mercury Bichloride Poisoning Treated with Sodium Formaldehyde Sulfoxylate," J.A.M.A., Ilk'- 1433 (April 13), 1940. 8. Hashinger. E. H., and Simon, J. F.: "A Case of Mercuric Chloride Poisoning Treated by Exsanguination-Transfusion," J. Lab. and Clin. Med., 20: 231 (Dec.). 1934. 9. Koranyi, A.: "Successful Treatment of Corrosive Mercuric Chloride Poisoning, with Repeated Venipunctures and Administration of Ringer's Solution," Klin. Wcknschr., 14: 753 (May 25), 1935. 10. Scharf, J. H.: "Genoscopolamine: Its Use in Parkinsonism," J. Nerv. and Ment. Dis., S9: 682 (May), 1939. CHAPTER XXI MANGANESE AND CHROMIUM MANGANESE Manganese poisoning is not a common industrial disease. Little has been written about it. Yet manganese is finding increasing use, and it is to be expected that the cases of manganese poisoning will be increased. The industrial demands for manganese ore have been met mostly by importing it, but it is produced in Montana, Georgia, Arkansas, Virginia, and to a lesser extent in Arizona, New Mexico, Nevada, and California. Occupational Hazards.--Manganese, because it imparts strength and hardness to steel products, is employed in the steel industry in the manufacturing of alloys, such as silicomanganese, silicospiegel, ferromanganese and spiegeleisen, and in combination with copper, zinc, aluminum, and other metals. It is also used extensively in the manu facture of dry-cell batteries and to a lesser extent in calico printing, making of dye, fireworks, pottery, linoleum, and photographic re agents, and in germicides, deodorizers, and fertilizers. Pathology and Action. Effect on Nervous System.--Information regarding its effect has come largely from animal experimentation. From these observations, combined with occasional autopsies on vic tims of this poisoning, it would appear that the central nervous sys tem is primarily involved. Degenerative changes in the pons, caudate nucleus, striate nucleus, large ganglion cells, cortex, and basal ganglia have been variously reported. Interstitial nephritis, biliary cirrhosis, and proliferation of connective tissue in the lungs have also been noted. Effect on Blood.--According to a United States Public Health Service1 report, extensive laboratory examinations of workers indi cated that a low white-cell count with a decreased percentage of neutrophiles, a slightly lowered blood calcium content, and a slight reduction in the middle zone of Lange's test, were often associated with manganese poisoning. A lowered hemoglobin content was ob served in several of the manganese workers. Analysis of the blood for manganese content was of no assistance in this study. Urinary manganese appears to reflect a present or past exposure to manganese compounds rather than evidence of intoxication. Im pairment of kidney or liver function was not observed. 266 PpPVIIPIIPiPf! MANGANESE AND CHROMIUM 267 Effect on Lungs.--Chemical examination of the lungs of a person dying from manganese poisoning was reported to show from 3.07 to 4.87 mg. of manganese per 100 gm. of dry tissues in the right and left lungs, respectively, and very much smaller amounts in the other organs, indicating that he still had a reservoir of manganese in the lungs seven years after his last exposure to this dust. A few months before death he had been found to be excreting small amounts of manganese in the urine. Mild and Severe Effects in Industry.--According to Voss,2 the use of manganese is greater in Europe than in America. He points out that in comparison to the wide technical use of manganese and its compounds, the number of cases of manganese intoxication is small. He believes this is due to the fact that only a small number of per sons have a predisposition for this poisoning; that not all manganese compounds are capable of exerting a toxic action; and that the danger of occupational poisoning occurs only where manganese com pounds are inhaled or swallowed in adequate quantities for a com paratively long time. Voss observed a case of a man who had had a mild exposure for ten months and a severe exposure for seventeen months. Other men working under the same conditions developed no signs or symptoms. This patient showed a masklike face, amyostatic symptoms, disturbances in speech, and gait, micrographia, laughing, weeping, and stuttering. Stored manganese was indicated by the pres ence of this substance in the feces eight months after the cessation of exposure. Nervous lesions in severe poisoning usually remain constant or increase in severity (as noted in the case reported by McNally), but the patient observed by Voss improved. Bryan3 reported a case of manganese poisoning in a forty-sevenyear-old man who sought medical treatment because of disturbance of gait. The initial symptom in three of six patients examined by Gayle4 was a disturbance of gait. Canavan, Cobb, and Drinker5 were fortunate to observe the autopsy findings in a sixty-nine-year-old man who died of cardiorenal disease fourteen years after the onset of symptoms resulting from this occupational hazard. This man had been exposed to manganese for four years. His symptoms had been disturbance of gait, stiffness of the legs, frequent falls, fatigability, and sleepiness. The chief autopsy findings were degeneration of the nerve cells, satellitosis, and gliosis in the basal ganglia. There was also widespread atrophy in various portions of the brain. The bulletin of the United States Public Health Service showed pictures of patients walking but dragging their feet, their difficulty in attempting to walk up an inclined surface, and their falling down when they tried to walk backward (Fig. 45). OCCUPATIONAL DISEASES patients dragged their feet. AND FELL DOWN TRYING TO WALK BACKWARD Fig. 45.--Patients with chronic manganese poisoning. Photographs taken with a motionpicture camera. (U. S. Public Health Service, Bulletin 2/t7.) MANGANESE AND CHROMIUM 269 Diagnosis Signs and Symptoms.--Languor, sleepiness, stolid, masklike facial expression, low monotonous voice, muscular twitching, cramps in the leg muscles, increase in tendon reflexes, ankle and patellar clonus, retropulsion and propulsion, slapping gait, and uncontrollable laugh ter are some of the signs and symptoms in manganese poisoning. The patient is usually aware of muscle stiffness and twitching first, and he then notices difficulty in walking. Differential Diagnosis.--Paralysis agitans, multiple sclerosis, and progressive lenticular degeneration must be differentiated from chronic manganese poisoning. The occupational history is, therefore, impor tant in initiating suspicion that one is dealing with manganese poisoning. Tests.--There is no single laboratory finding which offers conclu sive evidence of manganese poisoning. Manganese may be found in the excreta, but this only indicates the fact that manganese has been absorbed. In suspected cases a low white-cell count with a reduced percentage of neutrophilic leukocytes is a significant confirmatory aid. In the work conducted by the group under the supervision of the United States Public Health Service they failed to find any significant changes in the bones upon x-raying a series of men poisoned by man ganese; nor did they find any value in the study of blood analyzed for manganese. They did note that the blood calcium was lower on the average in the poisoned patients than in the non-affected. A slight rise in the middle zone of the colloidal gold curve was thought to be noteworthy. These workers also noted a reduction in the middle tubes of Lange's test similar to that observed in paralysis agitans. It was held that the Lange test may prove helpful in differentiating manganese poisoning from active multiple sclerosis. Test of Atmosphere.--In cases where a questionable history of ex posure exists, it may be of advantage to test the atmosphere at the place of occupation. It is thought that 50 mg. of manganese per 10 cubic meters of air is a safe atmosphere for workmen. Test of Blood or Urine.--If it is felt necessary to establish the presence of manganese in the body, the urine or blood may be exam ined in the following manner: Blood or urine is evaporated to dry ness in a silica dish in the presence of sodium carbonate and ashed in an electric muffle. Add sulfuric acid until effervescence ceases, then a few drops of nitric (1:3 dilution). Filter, and to the filtrate add five drops of 2.5 per cent silver nitrate, and 0.3 gm. of crystallized potassium persulfate. Place beaker or test-tube containing the un known in warm water. In a few minutes a purple color of permanga nate appears. Run a blank on all chemicals and dishes used. Make 270 OCCUPATIONAL DISEASES up to 50 cc., compare with a standard permanganate solution con taining from .002 to .025 mg. of manganese. (See Sutton's Volumetric Analysis, 11th ed., 1924, p. 209, for details.) Medicolegal Aspects Temporary Disability.--With a short exposure and the removal of the workman early from the hazard, complete recovery may be expected. The length of this temporary disability is extremely variable. It is rarely short. Permanent Disability.--If a severe exposure has occurred and marked neurological symptoms are present, it may be expected that the disability is permanent and may be progressive. However, life may not be necessarily shortened, for patients often live for years, eventu ally to die of some unrelated cause. Illustrative Cases: Case I.--White male, aged fifty. Occupational History.--This man quit working in the manganese plant in 1918, after having worked there for two years running a pulverizing machine. He stated that he was grinding both chrome and manganese ore at that time, working inside the whole time. He stated that the dust conditions were particularly bad, and he did not wear a respirator. He was transferred out of this plant in 1918 because of difficulty in walking. Following this, he worked with the mixing pans in the brickyard for six years and after that running the pump and tending boilers in the brickyard for three years. He was assigned to this light work on account of partial disability. Prior to this indus trial work, he had farmed for thirteen years and had been a muletender in a woolen mill for three years. He had not worked at all since 1928. Personal History..--His wife was living and well. They had two children living. His wife had one miscarriage after influenza in 1927. He admitted being a light user of liquor and a rather heavy user of tobacco, mostly in the form of cigars. Past Medical History.--The patient stated that he had had fre quent severe attacks of tonsillitis. He had typhoid fever at the age of thirteen and was in the hospital for five weeks. He had neuralgia of the face years before when his teeth were bad. He was operated on for hemorrhoids in 1930. He had a chronic, severe cough while work ing in the manganese mill, lasting about one and one-half years. Present Medical History.--Patient dated the onset of his present condition back to 1918, about the time he was transferred out of the manganese plant. It began with a slight weakness, which grew worse and still persists. Marked disturbances in gait, with stumbling, began MANGANESE AND CHROMIUM 271 to trouble him, with inability to lift the right foot. He was troubled with weakness and cramps in the legs, falling down on going back wards, inability to turn around, and difficulty in going up and down hills, especially the latter. He noticed moderate drowsiness, which has persisted. Metallic taste and loss of appetite were noted. He had gen eralized tremor of the muscles, muscular weakness, especially of the right leg, and muscular cramps, worse at night, throughout both legs. He was troubled with numbness and tingling of the forearms, hands, feet, and legs, which was intermittent, and a stuttering, halting speech. He had some difficulty in swallowing food. Since 1925 he had noticed short attacks of impulsive weeping. There had been no change in his sexual functions. His wife had had three pregnancies during this illness. Since the onset of these symp toms he had noticed a slight shortness of breath on exertion. He stated that he had noticed black spots and stars in front of his eyes at various times during the last twelve years. He had occasional slight attacks of palpitation of the heart. He had occasional twitching of the fingers and legs, mostly when sitting down. Several of these symptoms had been improving in the past few years. The trembling of the extremities, and muscle tremor in general, was improving, being intermittent in character and troubling him only occasionally at the time. However, the weakness in the right leg seemed to be getting worse. He believed his ability to talk was improved considerably. Physical Examination.--White male, aged fifty, not acutely ill. Height, 71 inches; weight, 142 pounds; temperature, 97.4 F.; almost white hair; eyes and ears, essentially normal; moderate obstruction to breathing was present in nose; rather marked pyorrhea alveolaris, a slight amount of dental caries, all upper teeth were out; a coarse, moderate tremor of the tongue was noted; neck, normal. () Chest.--Girth at inspiration, 94 cm.; at expiration, 86 cm. The physical examination of the chest was essentially negative. The stereographic x-ray films of the chest were essentially negative. () Circulatory System.--The heart examination was essentially negative except for some diminution of all heart sounds. Before exer cise the heart rate was 80; immediately after exercise, 96; and three minutes after exercise, 80. The blood pressure before exercise was 124/84; immediately after exercise, 126/86. No peripheral arterioscle rosis was noted. The electrocardiogram showed a heart rate of 76; con duction time, 0.12 seconds; left axis deviation and low voltage, 0.45 millivolts. (c) Abdomen.--Except for a left inguinal hernia, supported by a truss, the examination of the abdomen was negative. (d) Extremities.--Examination of the extremities revealed atro phy of the left thigh and calf, the circumference of the left calf being 2y2 cm. less than the right. \ i 272 OCCUPATIONAL DISEASES Neurologic Examination.--Besides the atrophy noted in the left thigh and calf, there was a general diminution in power of all groups of leg muscles. The facial muscles were not affected, except for those of the forehead. Only tongue tremor was observed. The ankle jerks were slightly decreased. Both Achilles tendons were abnormally sensitive to compression. The Romberg test was slightly suggestive but not posi tive. The gait was spastic and slapping in character. He had a right foot drop and had to swing the leg to walk. Retropulsion and propul sion were noted, with the subject falling down on walking backward. On the inclined plane he had marked difficulty walking up, owing to the right foot drop, and he fell down in walking down backwards. Walking sideways was quite slow and tedious. There was no intention tremor in lifting the water glass. There was a slight stuttering ob served with fast economical speech, indistinct at times. Masked facies was not observed. A specimen of handwriting revealed no intention tremor or micrographia. The examination of the skin was negative. The psyche was unaltered. Laboratory Findings, (a) Urine.--Specific gravity, 1.013; amber; acid; no albumin or sugar; 0.006 mg. Mn per 1; no casts; occasional red blood cell; 1 or 2 pus cells per high-power field. (b) Blood.--Erythrocyte count, 4,900,000; 14.5 gm. hemoglobin per 100 cc. (86 per cent); color index, 0.88; reticulocytes, 0.30 per cent; white blood count, 10,200; platelet count, 255,000. (c) Schilling Differential Count.--Showed 53 per cent segmented neutrophiles, 39 per cent lymphocytes, 6 per cent monocytes, 1 per cent eosinophiles, 1 per cent basophiles. (d) Coagulation Time.--1 minute 50 seconds: bleeding time, 3 minutes. (e) Kahn test, negative. (/) Blood Chemistry (mg. per 100 cc.).--Blood glucose, 93; total non-protein nitrogen, 40; serum chloride, 366; serum calcium, 9.5 and serum phosphorus, 3.9. (g) Cerebrospinal Fluid.--Clear and colorless; very faint trace of globulin; cell count, 2; mastic negative; colloidal gold curve, 0001000000; Kahn test, negative. (h) Galactose Tolerance Test.--Only very slight trace of galactose eliminated. Diagnosis.--Chronic manganese poisoning, well advanced. It is interesting to note that although this man left his manganese exposure in 1918 (some 19 years previously), he still had rather marked disability, especially in the use and control of his legs. While many of the symptoms had improved considerably, this case demon strates that there are certain permanent organic changes.1 MANGANESE AND CHROMIUM 273 Case II.--McNally" reports a patient seen by him in 1925. The patient gave a history of having worked in the ore department of a battery company, transporting, loading, and handling in various ways 58 per cent manganese in powdered form. After fourteen months of this type of work, he first noticed that after dumping a wheelbarrow of dust he stepped back and had difficulty in stopping himself from falling. In a week's time the condition became progressively worse. Within the next six months the patient noticed that if he walked too far he developed a rapid gait which ended in a fall unless someone was present to assist him. This tendency progressed until he had great difficulty in walking alone and would not trust himself to do so. The condition was aggravated by fatigue and excitement. He subse quently developed a coarse tremor of the right leg, marked disturb ance in walking; he had propulsion, retropulsion, and lateropulsion. and tremor on effort, such as dressing himself. The tone of his voice became more monotonous, and a mask-like expression of his face per sisted. McNally noted in the laboratory examination a slight increase in the lymphocytes and also in the monocytes. The liver-function test was negative. Treatment Prophylaxis.--The prevalence of this disease can be limited by engineering control. Isolating the process under hoods or exhaust ven tilation, control of the dust by wet processes, the use of mechanical conveyors, and examination of the atmosphere at intervals are all preventive measures. Jones3 observed no cases of intoxication among men working in an atmosphere of less than 30 mg. of manganese per cubic meter of air. He states that this should not be considered a threshold limit and suggests an atmosphere of 50 mg. per 10 cubic meters as a safer one. Quarterly medical examinations should be rou tine in any mill or place where manganese compounds are handled in order to detect early signs or symptoms. Mild neurological signs or symptoms, such as drowsiness, languor, muscular cramps, and twitch ing, perhaps coupled with an otherwise unaccountable low white-cell count, indicate removal of the workman from the hazard. Daily showers following work should be encouraged by installation of shower baths and education of the employee in this regard. Nothing of real value in the treatment of these patients has been described. For those mildly affected, much improvement, perhaps total, will occur on their removal from the exposure. For those severely affected, little improvement may be expected. Vitamin Bx and Calcium.--Well-rounded, adequate diets should be given these patients, and general tonics may be used. There is some question concerning the use of thiamine hydrochloride (vitamin Bt) since experimentally large doses of vitamin Bj encourage retention 18 274 OCCUPATIONAL DISEASES of manganese, and hence Bx might be contraindicated here. Since low blood calcium levels have been demonstrated by some, oral cal cium preparations and milk may well be included in the diet. The patient should be encouraged to drink adequate amounts of fluids and should be given cathartics, if necessary, in order to secure ade quate elimination. Sodium Thiosulfate and Liver Extract.--McNally6 thought a pa tient of his showed some improvement while 15 grains (1 gm.) of sodium thiosulfate in 10 cc. aqueous solution was given intravenously every other day. He cites the feeding by Charles7 of liver to these patients with what appeared to be improvement in some. When im provement under liver was noted, it was rapid and occurred in the first few days or so of the therapy. The use of liver extract intra muscularly, then, in dosages of from 15 to 30 units a day for four consecutive days, and the repetition of this dose two or three times a week over an indefinite period of time, depending upon the individual patient, is suggested. REFERENCES 1. "Chronic Manganese Poisoning in an Ore-Crushing Mill," Public Health Bulletin No. 217, 1940. (Case 71.) United States Public Health Service, Division of Industrial Hygiene. 2. Voss, H.: "Occurrence of Occupational Manganese Intoxication in the Steel In dustry," Arch. j. Gewerbepath. u. Gewerbehyg., 9: 407-507 (July), 1939. 3. Bryan. A. W.: "Chronic Manganese Poisoning," Arch. Neurol, and- Psychiat., 37: 1448, 1937. 4. Gayle, R. F.: "Manganese Poisoning and Its Effect on the Central Nervous Sys tem, Report of Six Cases," JAM.A., 85: 2008-2011, 1925. 5. Canavan, M. M., Cobb, S., and Drinker, C. K.: "Chronic Manganese Poisoning. Report of a Case with Autopsy," Arch. Neurol, and Psychiat., 32: 501-512, 1934. 6. McNally, Wm. D.: "Manganese Poisoning Case," Indust. Med., 1: 349-350 (July), 1935. 7. Charles, J. R.: "Manganese Toxemia; with Special Reference to the Effects of Liver Feeding," Brain, 50: 30, 1927. CHROMIUM Chromium is found in several minerals, chiefly as chromic iron or chromite. Industrially the bichromates of potassium and sodium and chromic acid concern us. Chromium as a metal is inert, but chromic acid and its compounds, because of their caustic action, affect the skin and mucous membranes. Occupational Hazards.--In the manufacturing of coal-tar dyes, wallpaper, electric batteries, and explosives; in textile printing; in cer tain paints, such as lead chromate; in lithography; and most com monly of all in photography and electroplating. Signs and Symptoms.--There have been a few cases reported in literature where some form of the chromium has been ingested with MANGANESE AND CHROMIUM serious or fatal results. These do not deserve consideration in this dis cussion. Ulcers.--Industrially, the acid produces lesions around the base of the nails of the hands, on the knuckles, dorsum of the hands, and the forearms. Occasionally they affect the eyelids and often the nasal mucosa. The ulcers usually develop slowly, and the workman is often unaware of their presence until they become big enough to note upon inspection. Sometimes they may be painful, especially if they occur over the knuckles, where flexion is hindered. These ulcers may become fairly deep (Fig. 46). The ulcers are usually small, varying in size from the head of a match to the end of a lead pencil, but often quite Fig. 46.--Healing chrome holes. The permanent scarring is well seen. (White: ; The Dermatergoses or The Occupational Affections of the Skin, Paul B. Hoeber, New deep. The edges are thick, rounded, often glossy and rarely inflamed. They may persist indefinitely unless treated. On healing there is ft' usuallv a Dermanent residual scar. Invariably they cause no appre- ey occur in the cartilaginous portion of the nose. tions.--Instances of allergic reaction to the chromates ed in which the affected persons developed in addition asthma, fever, nephritis, and the like. Aspects. Temporary Disability.--This is short. Treatips the progress of the lesions, and removal from exployment of preventive measures permits the affected person to continue his work. 276 OCCUPATIONAL DISEASES Permanent disability is not to be considered. Claims for disability almost always are based upon impairment of function of the nose owing to ulcerations of the nasal mucosa or perforation of the septum. Many nasal perforations due to chrome have been seen by the writer, but in no instance did it impair function or constitute a disabling con dition. The British observers failed to note any carcinomatous lesions resulting from chrome ulcers. Teleky1 reports an incidence of lung cancer among chromate workers. When and if such a causative agent for cancer is claimed, the basis for decision must rest upon the pre cepts outlined under "The Medicolegal Relationship of Trauma to Disease." Treatment. Scrubbing Tissue.--If the lesion or lesions ("chrome holes" or ulcers) are small and superficial, the damaged tissue may be scrubbed thoroughly with 5 per cent sodium hyposulfite, water, or saline solutions. The purpose of this treatment is to dislodge all tissue containing chromium compounds so that additional damage by bur rowing will not occur. After this scrubbing, the wound may be treated like any abrasion of similar severity. Wet Dressings.--If the ulcers arc already too deep for such scrub bing, wet dressings of sodium hyposulfite for a period of from three to five days should be applied to aid in the reduction of the chromium compound. Since the chromium in the flesh is not dislodged by sodium hyposulfite, wet dressings of from 5 to 10 per cent solution of sodium citrate, sodium lactate, or potassium and sodium tartrate should be applied to accomplish this. These wet dressings are continued for from three to five days. At times necrotic tissue in the ulcer will re quire curettage. Suppuration rarely occurs in chrome ulcers, but cleansing with a mild antiseptic agent following use of the reducing agents may be used. Treatment appropriate for any ulcer is used fol lowing the above-outlined therapy. It is frequently desirable to remove the worker from his customary duties, at least during the early stages of treatment. Prophylaxis.--Prophylactic measures consist of removal of fumes and dust from the atmosphere, cleanliness within the plant, and con fining the process within enclosures wherever possible. Respirators or gas-masks should be worn. Shower baths and change of clothing should follow the day's work, and the installation of showerbaths and locker-rooms will encourage this procedure. The skin should be pro tected by suitable clothing, rubber gloves, protective ointments, or oils. The nasal mucosa should be sprayed with an oil prior to going to ivork. REFERENCE 1. Teleky, T.: "Occupational Cancer," J. Indust. Ilyg. and Toxicol., 10: 2, 1937. CHAPTER XXII CADMIUM From the amount of space devoted to cadmium poisoning in text books on toxicology and industrial hygiene, one would be led to be lieve that such an intoxication is extremely rare. There is good reason to believe, however, that cadmium poisoning occurs with relative fre quency but remains unrecognized as such. Furthermore, it can be safely assumed that the incidence of cadmium poisoning will increase, especially during these years of intensive production for national de fense. As is the situation with all industrial hazards, the large wellsupervised establishments will prevent the occurrence of this illness by precautionary methods, but the small plant is apt unwittingly to expose workmen to the fumes of this metal. It is obligatory, then, that all who deal with industrial health be better informed regarding cadmium. A recent personal experience with an acute fatal case of cadmium intoxication enables me to present an accurate description of the various phases of this illness. Cadmium was first used as a coating for piano strings and other musical instruments because it formed a protective covering against rust. It was subsequently found to take on a high polish. Cadmium is also included in specialized solders. Since it has a relatively high melting point and is capable of withstanding excessive wear, it is be ing used extensively in the automobile industry. Undoubtedly with the demand for machinery of all types, the need for cadmium will be increased. Pennsylvania produces a large part of this country's sup ply of this metal in the form of cadmium sulfide. The more important compounds of cadmium are the oxides, sulfate, sulfide, chloride, iodide, and bromide. The failure to be concerned about, or to recognize, cadmium as an industrial poisoning is largely attributable to the fact that it is used with other metals and to a peculiarity of the symptoms it produces on undue exposure. Unquestionably, ill effects from the fumes of this metal have invariably been ascribed to lead or to metal-fume fever, as our two cases will show. Also, because the serious symptoms are sometimes delayed, cadmium poisoning may be confused with dis eases of non-occupational origin. Because of this delayed reaction, a workman may fail to withdraw immediately from his exposure. 277 278 OCCUPATIONAL DISEASES Occupational Hazards.--These are encountered largely in the smelting of ores; in the making of alloys, vapor lamps, and storage batteries; in electroplating, glass coloring, spraying of pigments, plat ing of automobile parts and musical instruments, and especially in welding. Pathology.--Because of animal experimentation, the reports have indicated a more extensive pathology than is probably found in the human. Prodan1 fed cadmium to cats to find subsequent involvement of nearly all of the viscera. But industrial cadmium poisoning results from inhalation, not ingestion. Legge2 reported an autopsy of a work man exposed to the fumes of cadmium resulting from the melting of cadmium ingots. According to Legge, the autopsy of this man re vealed inflammation of the lungs, gastro-intestinal tract, kidneys, and spleen. In 1935 from two plants located in Ontario, fifteen cases of cadmium poisoning occurred and were reported by Bulmer, Rothvvell, and Frankish.3 Two of these men died and were autopsied, at which time the findings indicated predominant involvement of the lungs. Ac cording to these men, the postmortem examination gave the following anatomical diagnosis: Cadmium poisoning, edema and congestion of the lungs (chem ical) , hemorrhages into the lung (chemical), partial collapse of lungs, proliferative interstitial pneumonitis (chemical), catarrhal bron chitis (chemical), cloudy swelling of the liver and kidneys, conges tion of the spleen, and fatty infiltration of the pancreas. Microscopic examination of the lungs showed congestion, hem orrhage, edema, alveolar collapse, desquamation of the lining cells of the alveoli, and marked proliferation of the lining cells of the alveolar spaces. This report of these Canadian investigators indicates that the lungs bear the brunt of the assault from cadmium-fume inhalation. Testi mony to this is found in the autopsy of our patient, to be subsequently presented in detail. DIAGNOSIS Signs and Symptoms.--The first symptom is that of a distressing cough, to be followed within a short time to several hours by head ache, dizziness, and eventually by a feeling of constriction within the chest. Accompanying the early symptoms are often dryness of the throat and sometimes nausea or vomiting. At the time the chest pain sets in, shortness of breath is also noted. The patient may feel alter nately hot and cold, but it is an interesting observation that an eleva tion of temperature does not usually occur early but invariably at the terminal stage of the fatal cases. CADMIUM 279 Pidmonary Involvement.--If the exposure is severe, the symptoms become intensified. Of these, the excruciating chest pain and the ex cessively increased respiratory rate are most striking. While the above symptoms point to profound pulmonary involvement, signs within the lungs are meager, if any. The breath sounds may be of the exaggerated bronchovesicular type, but rales are often few or absent until the terminal stage. Also, while the a;-ray may reveal widespread patchy bronchopneumonia, indications of large areas of consolidation are not heard. MEDICOLEGAL ASPECTS No toxic limit has as yet been established. From the author's ex perience, inhalation of even minimal doses is hazardous. Nor is it known how long after cadmium poisoning has occurred that the pres ence of this metal can be found in the body tissues. The cases so far reported have resulted from short, severe exposures. Unless death occurs, the illness is rarely longer than one or two weeks at the most. To date there exists no reason to believe that a permanent disability results. Illustrative Cases.--Before reciting the more interesting details of a fatal case of the writer's experience, a mild illness resulting from inhalation of cadmium fumes will be reported. Case I.--In June 1940, a twenty-four-year-old welder came to the clinic stating that on the day previously he had welded some "gal vanized rods." His respirator was defective, but knowing that the job would be of short duration, he did not secure another respirator. Shortly after finishing this work he noticed an irritating cough, head ache, and slight dizziness. That night he had chills, noted a dryness of the throat, the cough became more constant, and by morning he was aware of a heavy, oppressive feeling in his chest. His examination revealed nothing unusual except increase in the pulse and respiratory rate. The temperature was normal; pulse, 90; respirations, 26; blood pressure, 116/78. The urinalysis and blood count were not significant, and the a;-rays of the lungs were negative for evidence of any pathological process. Since the patient's illness resembled in some respects a metal-fume fever, inquiry was made at the plant where he worked regarding the substance being welded. I was informed that these rods were cad mium-coated. The patient returned to his work six days after exposure free of all symptoms. Similar to the above case is a report4 of an instance of intoxication due to the overheating of cadmium. The exposure, although brief, was followed shortly by a sensation of dryness of the throat, weakness, . ,, ; i i 280 OCCUPATIONAL DISEASES difficulty in breathing, together with pain across the anterior chest. The slightest effort precipitated paroxysms of coughing. The patient was confined to bed for five days and returned to work thirteen days after exposure. Case II.--The following case of the author's experience represents a contribution to the study of cadmium poisoning in that he was not only able to observe this case clinically, but secured complete labora tory studies, postmortem findings, and microscopic slides of the vari ous tissues of the body. History.--A twenty-sevcn-year-old Mexican laborer employed by a metal company, of Los Angeles, was referred to me on April 14, 1941, with, a diagnosis of metal-fume fever. Before proceeding with the de tails of this case, a defense of the physician who made the diagnosis of metal-fume fever is justifiable and illustrates the confusion regard ing cadmium poisoning which was mentioned in an earlier paragraph. This doctor has for years treated workmen from this plant for the ordinary traumata incident to industry, and has also treated numerous patients from this same plant for metal-fume fever and lead poisoning. He was never informed that cadmium was present in a new process used by this company. Furthermore, although a competent industrial physician, he told me in discussing this case that his "reading ma terial" had never mentioned the toxic effects of this metal. This digression well illustrates the fact that employers fail to realize that they expose their workmen to a hazard when cadmium is heated and that the physician has likewise not yet been impressed with the ex treme toxicity of cadmium fumes. To return to our patient: While he managed to walk into the ex amining room, he was so exhausted that he was unable to speak for several minutes. He was obviously extremely ill, and after speaking a few words would stop to regain his breath. No ambulatory cardiac, or even one suffering from a cardiac insufficiency of severe degree and confined to bed, presented more extreme dyspnea. While this patient talked he clutched his upper chest. After considerable waiting, the following meager history was obtained. Three days previously, April II, 1941, he had crawled into a rotary furnace, thirty inches in diameter, to cut V-shaped openings from two longitudinal fins. (Details of his activities will be discussed in the comment on this case.) He wore no mask, and although the fumes caused him to cough, he finished the work, without stopping, in about forty minutes. Upon emerging from the furnace he was coughing con siderably, but continued with other duties for the rest of that day. During the latter part of the afternoon his coughing became distress ing, and he felt dizzy. That night severe headache set in, coughing became constant, and during the night he became aware of a grip ping chest pain. Sleep was impossible. He related that he would try CADMIUM 281 sleeping in bed, then in a chair, then back in bed again. This stirring around increased his cough as well as his shortness of breath. The morning following his exposure, his illness was reported to his em ployer, who sent him to the physician referred to previously. The afternoon of the day following his exposure, the patient's wife had him look into a mirror that he might see how blue his lips were. In spite of the administration of codeine, his chest pain increased in severity. The patient described this chest pain by closing his hands as if he were tightly squeezing something. Physical Examination.--Inspection revealed this Mexican work man to be cyanotic and extremely dyspneic, with a facies that indi cated he was suffering severe pain. His temperature was 98.4 F. upon admission; the throat was not inflamed; and in spite of a respiratory rate of 40 per minute the lung examination showed evidence of no moisture or consolidation. The heart had a regular rate of 122 beats per minute, while the blood pressure was 140 systolic; 90 diastolic. The rest of the examination was not remarkable. Twelve hours after admission, eighty-four hours after exposure, his temperature rose to 100 F.; respirations remained at the rate of 40; the pulse was 130 beats per minute; the lungs remained clear. Pantopon, % grain, did not relieve his chest pain. Unbearable head ache accompanied his chest pain, as did dryness of the throat and cough upon the least exertion. Laboratory Examination.--The initial laboratory findings were as follows: Urine Specimen.......................................................................... Voided Color ................................................................................ Yellow Appearance..................................................................... Cloudy Specific gravity ............................................................. 1.021 Reaction .......................................................................... Acid Albumin............................................................................ One plus Amorphous deposits..................................................... None Pus cells............................................................................ 1-2 Mucous threads............................................................. Numerous Blood Hemoglobin ................................................................... Erythrocytes ................................................................. Leukocytes per cu. mm.................................................. Polynuclear neutrophiles ........................................ Lymphocytes ............................................................. Large mononuclears ................................................ Eosinophiles ............................................................... Basophiles................................................................... Stippled R.B.C................................................................ 89 per cent 5,200,800 14,800 84 per cent 12 per cent 2 per cent 1 per cent 1 per cent None 282 OCCUPATIONAL DISEASES x-Ray of Lungs.--There were mottled increases in density through out both lung fields. The pleural margins were clear. The cardiac shadow appeared to be normal in size. On April 16, two days after admission to the hospital and five days after his exposure, the temperature rose to 104 F., the pulse rate to 140, and the respirations to 50. The leukocyte count was 21,100, with 87 per cent polynuclear ncutrophiles; the urine remained unchanged. A bedside x-ray film revealed multiple patches of increased density throughout the entire lung fields. Worthy of comment is the fact that although this patient had been placed in an oxygen tent at the time of admission, it did not affect his respiratory rate. When under the tent he was definitely more comfortable and the chest pain less severe, but the breathing contin ued to be rapid and shallow, with movement confined to the area of the diaphragm. While the breath sounds were of the exaggerated bronchovesicular type, no moisture could be detected within the lungs. For the next two days there was little change in the patient's gen eral condition except for a drop in the temperature and pulse rate, but the respirations continued to be excessively rapid. There was also no change in the lung findings, although the x-ray film showed wide spread patchy bronchopneumonia. Thinking that a secondary invasion of the pneumococci might be present, we instituted sulfathiazole treat ment, without any effect. During all this time the patient remained perfectly lucid. However, if it became necessary to remove the oxygen tent momentarily for any reason, he would fight for air, toss to and fro, and appear frantic. On the evening of the 19th of April, nine days after exposure, the pulse rate increased to 160, the respirations to 70, but the tempera ture did not rise until just before death. One hour before death he was mentally clear. During the last three days there was no chest pain, but cyanosis became more pronounced. On the morning of his death, April 19, the bedside x-ray revealed the entire lung field to be over shadowed by widespread patchy pneumonia, but there was no evi dence of pleural fluid or solidary consolidation. On this last day scat tered rales were heard within the lungs, but there was nowhere any tubular breathing. The blood count and urinalysis taken on the day of death were as follows: Urine Specimen ........ Color................. Appearance .. Specific gravity Reaction.......... Albumin.......... Pus cells........ Voided Yellow Slightly cloudy 1.020 Acid Trace 0-1 5; l CADMIUM 283 Blood Hemoglobin ............................. Erythrocytes per cu. mm......................................... Leukocytes per cu. mm............................................. Polynuclear neutrophiles .................................. Lymphocytes ....................................................... Large mononuclears............................................ Eosinophiles ......................................................... Basophiles ............................................................. Stabs........................................................................ 90 per cent 4,500,000 30,500 88 per cent 7 per cent 2 per cent 2 per cent 1 per cent 15 During the height of his illness a blood chemistry, blood Wassermann, and blood culture were made. The blood chemistry was normal; the blood Wassermann, negative; and the blood culture showed no growth. Sputum was never obtained for examination, since this patient's cough was non-productive. A dark-brown urine has been reported as present in cases of cadmium poisoning. It was not so at any time in our case. Autopsy Report.--The body is that of a well-developed and wellnourished male of approximately the age stated on the record, twen ty-seven. There are no gross deformities. There are no evidences on the external surface of the body of any injury. The muscles are all well developed. The pleural cavity contains a thin, red fluid. The parietal pleura is smooth and glistening. The lungs do not collapse when the chest is opened. The right lung weighs approximately 900 gm. It feels solid. Frothy fluid escapes from the air passages when pressure is applied, but there are regions, particularly in the lower lobe, in which a seropurulent fluid can be expressed from the smaller divisions of the bronchi. All of the small air passages appear to be distended. The cut surfaces are quite wet. The visceral pleura, par ticularly of the lower lobe, is red and somewhat thickened. The left lung is similar, except that in the lower lobe there are regions up to 6 mm. in diameter, which are quite solid, from which seropurulent fluid can be expressed. Edema of this side is the same as that on the right. The heart is not enlarged. All the valves are normal. No scars are found in the myocardium, but the muscle is somewhat flabby. Both right and left coronary arteries have common origin in the root of the aorta above the aortic cusps. Both arteries are patent throughout their extent. The liver appears to be normal. The capsule is smooth and glistening, and the normal markings are present on the cut sur faces. The gallbladder contains black bile. There is no obstruction to the major bile ducts. The spleen is somewhat enlarged and soft, and the cut surfaces are a grayish red. There are no abnormalities of the pancreas.. Both kidneys are normal in size. The capsules strip off easily. The cut surfaces are somewhat swollen and cloudy, but the normal markings are present. Except for slight grayish discoloration of the medulla in the lower pole, the right adrenal gland appears normal. 284 OCCUPATIONAL DISEASES In the left adrenal gland, the medulla in the lower pole appears to be replaced by gray-white tissue. This is of cartilaginous firmness. This tissue replaces less than one sixth of the medulla and except for this, the gland appears to be normal. The urinary bladder contains clear, yellow urine. There are no abnormalities in the bladder. The mucosa of the stomach is intact. Some swelling and redness are present in the mucosa of the first portion of the duodenum. Except for this, there are no gross changes in the small bowel. The colon is normal. The gross appearance of the brain is normal. From the gross examination, the cause of death in this case is bronchopneumonia, associated with marked edema of the lungs. Microscopic Examination.--Sections of the following tissues were stained with hematoxylin and eosin: () Lung.--In the sections taken from the lower lobes of the lung most of the alveoli are collapsed. There has been desquamation of the lining epithelium, and mingled with these cells there are numerous plasma cells and a few polymorphonuclear leukocytes. The inter stitial tissue is thickened. The cells are swollen and in many places are separated by relatively large clear spaces. In other regions the tissue is quite compact. In the former regions there has been some infiltration with plasma cells and an occasional polymorphonuclear leukocyte. The alveoli which are open contain plasma cells, a few leukocytes, and large pale-staining round cells with centrally placed nuclei and pale-staining acellular debris. The lining epithelium of these alveoli is swollen and stains poorly. () Heart.--There are no noteworthy alterations in the sections of the myocardium. (c) Liver.--There are no alterations of the hepatic cells, and the lobular arrangement of the cells is intact. The capsule is normal. (d) Kidney.--Except for some swelling of the tubular epithelium there are no noteworthy sections of the kidney. The glomeruli are intact, and the tubules are patent. There is no scarring. (e) Adrenal Gland.--The sections have been taken through the lower poles of the adrenal glands. There are numerous, fairly thick strands of fibrous tissue replacing portions of the medulla. The me dullary cells, however, appear normal, and there are no alterations of the cortex. (/) Duodenum.--Sections cut through the first portion of the duo denum: The mucosa is intact and appears normal in approximately half the section. It is absent down to the submucosa, and there is some round-cell infiltration along the remaining surface. The sub mucosal glands are normal, and there are no alterations in the mus cular layers. The blood vessels are distended. (g) Brain.--No noteworthy alterations noted. CADMIUM H'i The manner in which this patient received his cadmium intoxica tion is not only interesting but instructive. The plant where this workman labored had been engaged for a number of years in reclaim ing metal, chiefly lead, antimony, and tin, from discarded scrap metal. During 1940 they noted that another metal was present in the recovered substance, which upon analysis proved to be cadmium. They, therefore, devised a rotary furnace into which the scrap was thrown to be "sweated." This rotary furnace was thirty feet long and thirty inches in diameter. Within the furnace on opposite sides and extending the length of this tubular furnace were two fins which pro jected about four inches from the walls, the purpose of which was to tumble the scrap as the furnace revolved. It was decided that the recovery process could be made more efficient if V-shaped openings were cut at intervals in these two fins. Into this narrow, confined space went this Mexican workman without a mask, to cut with an acetylene torch the fins coated with cadmium residue. The victim did not know he was going to volatilize cadmium, and had he known he would not have appreciated its dangers. The superintendent admitted he was not aware of the toxicity of cadmium, but contended that all the workmen are instructed to wear masks whenever using an acety lene torch to cut metal. Had someone been present to enforce that ruling, this death would not have occurred. When this patient first presented himself with a diagnosis of metal-fume fever, it was felt that the diagnosis was erroneous be cause of two factors, (1) the complaint of severe chest pain, and (2), the presence of extreme dyspnea. There is no acute industrial metal poison, .to the writer's knowledge, which results in such distressing conditions. Just -why they are present in severe cadmium poisoning is not quite clear, but the author believes it can be explained upon the basis of anoxemia. The immediate reaction to the fumes is appar ently an acute inflammation of the respiratory tract so intense and so extensive that in order to lessen pain, massive splinting of the lungs occurs similar to that occurring in pleurisy, but more marked. As the diffuse, patchy bronchopneumonia spreads and edema obliterates the alveolar spaces, the available area for aeration decreases until the blood receives no further oxygen. Successive x-ray films of the lungs of this patient revealed this gradual diminution of available normal lung space. Likewise, the autopsy showed the distention of the first portion of the bronchial vessels which accounts for the bronchovesicular breathing heard throughout the upper chest. The plugging of the alveolar spaces, particularly in the lower two thirds of the lungs explains why rales were not prominent. Both the autopsy findings and 286 OCCUPATIONAL DISEASES the microscopic study indicate a chemical, rather than an infectious, nature of the inflammation. The death in this instance was considered occupational in origin, and the widow was awarded the full death benefits. The only other cause of death to be considered in this case was possibly that due to nitrogen dioxide (N02), which would still make the case a com pensable one. However, cadmium was believed to be the etiological sr factor in this death because of the following facts: 1. It has been shown by investigators that one of the outstanding complaints in severe cadmium poisoning is that of chest pain with severe chest constriction. Our patient complained of this from the beginning, and it remained an outstanding constant symptom. 2. The autopsy findings were in keeping with those reported by others. 3. Cadmium was the metal being recovered in the process to which this patient had been exposed. TREATMENT Drugs for Respiratory Relief.--The less seriously affected usually experience sensations similar to an upper respiratory infection, and measures commonly used for the latter often afford relief. These in clude the use of acetylsalicylic acid, 10 grains (0.65 gm.), every four to six hours; capsules of acetylsalicylic acid, 5 grains (0.32 gm.), phenacetin, 2% grains (0.160 gm.), and caffeine citrate, % grain (0.032 gm.), at three-hour intervals; or capsules of codeine sulfate, % grain (0.016 gm.), and papaverine hydrochloride, % grain (0.016 gm.), at from four- to six-hour periods. A combination of ephedrine sulfate, y8 grain (0.008 gm.), and amytal, % grain (0.024 gm.), at from three- to four-hour intervals, may afford relief in some. Any of num erous cough syrups containing codeine phosphate or sulfate, panto pon, or dilaudid hydrochloride in combination with expectorants, such as ammonium chloride, may be of value, e.g.: Codeine sulfate ......................................7% grains Ammonium chloride.............................. 4 drachms Syrup of citric acid................................ 1 ounce Water to make........................................ 4 ounces Sig.: Teaspoonful every three to four hours. 0.45 gm. 16.00 cc. 30.00 cc. 120.00 cc. Irrigations and Gargles.--Irrigation of the throat with warm salt and soda solution (a teaspoonful each of sodium chloride and sodium bicarbonate in one pint of water), or warm glucose solution ("corn syrup" one part and water two parts) every two hours, may be under- <* CADMIUM 287 taken. If irrigations are not possible, then gargling either with the salt and soda solution, with 1:5000 potassium permanganate, or with five aspirin tablets crushed in a glass of water may be substituted. Neither the use of silver preparations nor the frequent vigorous swabbing of the throat with other preparations is recommended. Inhalations.--In some instances inhalations of the following might prove soothing: Menthol ) Camphor J Oil of eucalyptus Oil of dwarf pine needles aa 15.0 gm. aa 30.0 cc. Sig.: One teaspoonful in one pint of water, steamed, and inhaled. Sedation in the form of barbiturates and intranasal drops may be needed, of from 0.25 to 0.5 per cent neosynephrin, or 0.33 per cent ephedrine in aqueous solution. Oxygen Therapy.--Whenever a patient appears to be moderately or severely overcome by these fumes, placing him immediately within an oxygen tent is strongly recommended. This should be instituted without waiting for any signs of pneumonia for, as indicated by our fatal case, these may be absent. Furthermore, irrespective of the presence or absence of a pneumonia, oxygen therapy affords a relief for the air hunger which exists. If a specific organism is suspected to be present as a secondary invader, appropriate chemotherapy should be introduced. Prophylaxis.--Those responsible for the health of workmen should recognize the danger of cadmium and adopt adequate means of re moving fumes by exhaust systems. Workmen should wear a respirator at all times when in proximity to cadmium fumes. REFERENCES 1. Prodan, L.: "Experimental Cadmium Poisoning," J. Indust. Ilyg., lb: 174, 1932. 2. Legge, T. M.: "Cadmium Poisoning," Ann. Report Chief Inspector of Factories for 1923, London, 72, 1924. 3. Bulmer, P. M. R., Rothwell, H. E., and Frankish, E. R-: "Industrial Cadmium Poisoning, a Report of Fifteen Cases, Including Two Deaths," Canad. Pub. Health J., 29 (January), 1938. 4. Bayhurst, E. R.: "Cadmium Poisoning," Ohio Indust. Hygiene Bull., 1 (May), 1939. CHAPTER XXIII SELENIUM AND VANADIUM SELENIUM Relegated to an obscure place in the textbooks of chemistry and absent from books on toxicology, this metal is practically unknown so far as its industrial uses or hazards are concerned. Chemically, it forms the same compounds as sulfur does. For instance, with hydro gen and the more reactive metals, selenides such as ^Se or FeSe are formed. Many organic selenium compounds have, been formed in which Se replaces S. Certain areas of the country contain a soil high in selenium. In 1936 Smith1 and his co-workers studied the possibility of toxic effects upon the rural population in Wyoming, South Dakota, and Nebraska-from the ingestion of selenium-bearing foodstuffs. The most persistent investigator of this substance has been Dudley,2 who has pointed out that this metal is at present an unrecognized hazard in the processing of selenium-bearing materials. His warning can be better appreciated when it is realized that the domestic consumption of selenium increased from 57,000 pounds in 1921 to 412.000 pounds in 1935. Occupational Hazards: Glass decolorizing Production of ruby glass Production of red and yellow glazes Production of paint and ink pig ments Production and coloring of plastics Manufacture of photoelectric ap paratus Alloying of maehineable stainless steels Alloying of free machining copper base alloys Fireproofing of electric cable Pathology.--The pathology of selenium has not, as yet, been ade quately studied, although considerable animal experimentation has been done. There is, apparently, a divergence between its action upon animals and that upon humans. In animals, subacute poisoning has produced bronchial pneumonia, fatty degeneration of the liver, de generation of the kidney cells, and other minor alterations, which clear up without residual pathology. Gastro-intestinal disturbances noted in the human have been absent in animal experimentation. 288 SELENIUM AND VANADIUM 289 Signs and Symptoms.--Respiratory irritation, cough, edema of the lungs, vomiting, diarrhea, abdominal pain or cramps, loss of reflexes, cerebral irritation as manifested by convulsions, and death. Acute Reactions.--Concerning the severe reactions resulting in convulsions or death, one finds these mentioned, but the author was unable to find any reference to actual death from selenium poisoning other than that of Gadamer in 1909. The garlic odor to the breath has been frequently referred to. Chronic Reactions.--Possibly the best picture of the chronic effects from constant exposure is reported by Smith, Frankc, and Westfall.1 A series of 111 families was studied for clinical evidence of selenium intoxication, and a series of 127 specimens of urine of as many sub jects, representing 90 families, was analyzed for this element. The results of the urinary analysis showed that only 8 per cent of the cases were free, or nearly free, of selenium, while 92 per cent contained amounts varying from 2 to 133 micrograms of selenium per 100 cubic centimeters. This affords definite proof of the absorption of selenium by some of the rural population in the foregoing states. In the 111 families visited, the following disorders, exclusive of the more vague symptoms of anorexia, indigestion, general pallor and malnutrition, were observed: 1. Bad teeth, varying from marked discoloration through all stages of decay, were seen in one or more members of 48 families. 2. Yellowish discoloration of the skin, in many cases a very definite icterus, and in some cases seemingly associated with more or less definite liver disease, was seen in about 46 subjects. 3. Skin eruptions of varying degrees of severity, but not conform ing to any one particular type, were seen in 20 subjects. 4. Chronic arthritis with more or less permanent changes in the joints was present in 15 subjects, varying from the milder types of rheumatoid arthritis to a more severely deforming type of arthritis deformans. 5. Diseased nails of the fingers, and in some cases also of the toes, were observed in 8 subjects. They were usually asymmetrical, atrophic, brittle, and irregular, and often presented trans verse and at times, longitudinal ridging. 6. Subcutaneous edema of probably cardiorenal origin was diag nosed in 5 cases, and peripheral neuritis of doubtful etiology in 2 subjects. Fifteen subjects gave a history of more or less protracted gastro-intestinal disturbances. While this study of Smith, Franke, and Westfall cannot be con sidered an observation of industrial exposure, yet it does offer the 19 290 OCCUPATIONAL DISEASES largest group of cases yet noted in the literature, and many of the symptoms are analogous to those resulting from industrial exposure. Certain observers have noted a close similarity between selenium and tellurium poisoning. Alice Hamilton3 in 1917 investigated selenium poisoning in copper foundries. She reports the chief symptoms were bronchial irritation and digestive disturbances. K. Halter* reports the case of a man working as a mixer in a plant where colored glass was produced. After working with elementary selenium and especially with sodium selenite, used for bleaching green ish glass, he developed headaches, then irritation of the mucosa. After about two days, reddening and swelling of the uncovered skin fol lowed. These symptoms appeared often and increased in severity. Clinical examination disclosed edematous erythema of the face and neck, and several hard, infiltrated, ill-defined foci on the back of hands and fingers. No change appeared on skin protected by clothing. Nasal and laryngeal mucosa was reddened and somewhat thickened. Slight conjunctivitis was present. There was an enlarged liver and increase of porphyrine in the urine. Selenium was detectable in the urine. Basal metabolism increased. No nervous or gastro-intestinal symptoms (in contrast to arsenic poisoning). Inflammation of nasal mucosa and conjunctiva is the direct result of the irritating action of selenium, as is the injury to liver function. Tests.--Selenium can be detected in the urine. The relationship has not yet been determined between the amount of selenium present in the urine and the symptoms. That is, there has not been sufficient experience with this metal to form standards of acceptance such as there has been with lead, for instance. Air also can be sampled for the presence of selenium contamination. Medicolegal Aspects__ As yet there is no recognized toxic limit of exposure, nor has there been a sufficient number of cases studied to form any basis for the estimation of temporary disability. It is held that massive doses cause death. Possibly by the end of this decade, experience will have established a better bas-relief of this metal, as well as of tellurium, thallium, and vanadium. With few exceptions these three closely resemble selenium in regard to toxic effects. Treatment. Prophylaxis.--The air breathed by the workers should be free of this substance, or its presence reduced to a minimum. Frequent sampling is necessary to accomplish this. If this substance is subjected to high temperatures, exhaust ventilation should be in operation. The skin should be protected to prevent involvement as noted by Halter. Workmen with known respiratory conditions, im paired liver function, or arthritic tendencies should be excluded from this hazard. SELENIUM AND VANADIUM 291 In chemists synthesizing organoselenium compounds, absorption through the skin is prevented by frequent changes of new gloves, protective cream, and scrupulous care in handling products. Protec tive devices, such as rubber and synthetic rubber gloves, give only temporary protection, since some compounds, e.g., methylbenzoselenazole, readily penetrate them. Diuretics and Cathartics.--No specific treatment for this poison ing is outlined, but if intoxication has occurred, removal from expo sure with possible hospitalization is necessary. The use of diuretics to secure adequate elimination may be indicated, e.g., ammonium chlor ide, 15 grains (1 gm.), from four to six times daily; or theophylline, 3 grains (0.195 gm.), three times daily. In this regard saline cath artics are useful, such as magnesium sulfate, from % to 1 ounce (16 to 32 gm.); the effervescent preparation of magnesium citrate, 12 ounces; sodium phosphate, 1 drachm (4 gm.); or the effervescent preparation of sodium phosphate, 2% drachms (10 gm.), Relief of Symptoms.--Upper respiratory symptoms may be treated as described under "Cadmium." Intravenous 50 per cent glucose (50 to 100 cc.) may aid in treatment of edema of the lungs, as may from y, to 2 cc. of salyrgan intravenously at from three- to four-day inter vals. If kidney degeneration is present, the use of salyrgan is probably contraindicated, although some believe that salyrgan may be used even in the presence of definite kidney pathology. Inhalations of oxy gen by intranasal tube or by a tent may be needed, and intravenous infusions of 10 per cent dextrose in physiological saline (1000 to 3000 cc. daily) may be necessary if vomiting or diarrhea is present. Diet.--The use of a high carbohydrate diet with an increased water intake has been suggested, as has the use of concentrates of the vita min B complex. Experimental work5' 6i 7 on animals indicated the protective action of a diet high in protein and low in carbohydrate against selenium. There was also some evidence that the ratio of selenium to the protein in the diet seems to determine the toxicity of selenium in food and that the quality of protein, as well as the quantity, was of importance. For example, casein and lactalbumin tend to counteract the toxicity of selenium while edestin and gelatin are not effective.5' 7 The trial of similar diets in selenium poisoning in human beings has not been reported, but the use of diets high in proteins, such as casein, lactalbumin, etc., might well be worth while in treatment of these patients. In addition, when liver damage is present, the use of a high carbohydrate, high protein diet should be followed. Also experimentally,8 sodium arsenite, five parts arsenic per mil lion of drinking water, completely prevented symptoms of selenium 292 OCCUPATIONAL DISEASES poisoning1. Clinical use of this in treatment of selenium poisoning is not reported. REFERENCES 1. Smith, M. I., Frauke, K. W., and Westfall, B. 15.: "Selenium Problem in Relation to Public Health; Preliminary Survey to Determine Possibility of Selenium Intoxication in Rural Population Living on Seleniferous Soil," Pub. Health Rep., 5V. 1496-1505 (Oct. 30), 1926. 2. Dudley, H. C.: "Selenium as Potential Hazard," Pub. Health. Rep., 53: 281--292 (Feb. 25), 1938; Indust. Med., 7: 233-236 (May), 1938. 3. Hamilton, A.: Industrial Poisons in the United States, The Macmillan Co., New York, 1925. 4. Abstracts: J. Indust. Hyg. and Toxicol., 31: 8 (Oct.), 1935. 5. Editorial: JAMA., 115: 2001 (Dec. 7), 1940. 6. Smith, M. K.: "The Influence of Diet on the Chronic Toxicity of Selenium," Pub. Health Rep., 51: 1441 (Aug. 4), 1939. 7. Gortner, R. A., Jr.: "Chronic Selenium Poisoning as Influenced by Dietary Pro tein," J. Nutrition, 19: 105 (Feb. 10), 1940. 8. Maxon, A. L., and DuBois, K. P.: J. Nutrition, 18: 447 (Nov.), 1939, cited in editorial, J.A.M.A., 111: 1083 (March 23), 1940. VANADIUM There is not much in American literature regarding the effects from exposure to vanadium dust. Dutton1 reported a case in 1911. He, with others, has indicated an irritating cough, gastro-intestinal symptoms, and anemia to be present following exposure. In contrast to these reports, the investigation of Symanski suggests that the affec tion is confined to the eye, the upper respiratory tract, and the lungs. Vanadium Pentoxide as Toxic Product.--After calling attention to the fact that the use of vanadium has greatly increased in recent years, Symanski2 reviews the literature on the disorders supposedly caused by it. Reviewing the complicated procedure by which vanadium is produced, he shows that of the various transformation products, it is only the vanadium pentoxide, particularly in the readily absorbable form of dust, which is harmful to the health of the workers. He sub jected the workers who came in contact with this substance to a care ful examination. He describes observations on nineteen men. Signs and Symptoms.--Symanski found a number of character istic disorders. He observed conjunctivitis with inflammatory injection of the conjunctivae, suppurating discharge, and corresponding com plaints such as burning of the eyes, rhinitis with reddishness of the nasal mucosa, and coryza with watery discharge; and also a feeling of soreness in the pharynx, continuous coughing with more or less pro fuse expectoration, occasionally sanguineous pharyngeal secretion, a feeling of dryness in the pharynx, sensations of constriction of the chest, occasionally piercing pains, the typical aspects of a more or less severe subacute or chronic bronchitis, considerable sonorous and sibi SELENIUM AND VANADIUM 293 lant rales in the absence of signs, indicating inflammatory infiltration of the pulmonary parenchyma; he observed no tuberculous complica tions, but there were roentgenological signs indicating a chronic bron chitis. In view of the fact that all examined persons had been active in the production of vanadium for only a few years, Symanski thinks that it is necessary to consider the possibility of the development of chronic changes. Contrary to reports in the literature, he never ob served reabsorptive gastro-intestinal disturbances, renal symptoms, increased nervous sensitivity, disturbances of the central nervous sys tem, or impairment of vision. Moreover, he found no characteristic changes in the composition of the white or red blood picture, espe cially signs of anemia. Treatment. Symptomatic.--Since but few cases have been re ported, and there is no general agreement about the symptoms, treat ment should be directed to the individual case of proved exposure. If Symanski is correct, symptomatic treatment would be directed at the conjunctivitis, the nasopharyngitis, and the bronchitis. Some of the detailed therapy directed at the upper respiratory symptoms as described under "Cadmium" may be followed. Prophylaxis.--All processes in which vanadic acid is liberated in the detailed therapy directed at the upper respiratory symptoms as possible. In mixing rooms, respirators or masks should be worn, and suction apparatus should be installed. Rotation of workers should be practiced, so that they would have days or weeks in which they could recuperate from effects of contact with vanadium. REFERENCES 1. Dutton, W. F.: "Vanadiumism," J.A.M.A., 56: 1648, 1911. 2. Symanski, J.: "Gewerbliche Vanadinschadigungen ihre Entsteliung und Symptoma tology, Arch. f. Gewerbepath. u. Gewerbehyg., 19: 295-313. 1939. (As re viewed in J.A.M.A., May, 1939.) CHAPTER XXIV ARSENIC The solid compounds of arsenic usually cause no serious disturb ance to the body or its functions. Skin lesions in persons handling these solid compounds are fairly common. On the other hand, ex posure to the gaseous form of arsenic (arsine or arseniuretted hydro gen) is dangerous. Arsine has a strong hemolytic action, but the destruction to the red cells is not immediate, there being an interim of from several hours to a day or two. Arsine is never intentionally used or produced in industry. There is always the chance, however, that it may escape in certain processes. Wherever nascent hydrogen is used in a reduction process, as in the making of aniline dyes or coal-tar products, there is a possibility that arsine may be formed. Another source of danger is in the cleaning out of tank cars which have contained sulfuric acid. Occupational Hazards.--Among the following workers, arsenic af fects the skin chiefly: Arsenic-roasters Artificial-flower makers Artificial-leather makers Bookbinders Brass-founders Briquet-makers Bronzers Calico-printers Carpet-makers Carroters (felt hats) Chargers (zinc-smelting) Colored-paper workers Color-makers Compounders (rubber) Copper-founders Copper-smelters Curriers (tannery) Cut-glass workers Decorators (pottery) Dye-makers Electroplaters Enamelers Enamel-makers Farmers and Gardeners Feather workers Felt-hat workers Ferrosilicon workers Picklers Pathology.--Pathology consists chiefly of a local irritation causing lesions to the skin, mucous membranes, and appendages. Acute poison ing, as in suicide, murder, or accident by ingestion, will cause irrita tion of the stomach as well as degenerative changes of the heart, liver, and kidneys. Chronic absorption may lead to changes in the nerve and muscle fibers. 294 ARSENIC 295 Diagnosis. Signs and Symptoms.--Headache, eruptions, and ulcera tions of the skin, perforation of the nasal septum, loss of nails and hair, inflammation of the mucous membranes, nausea, vomiting, diar rhea, and abdominal pains, peripheral neuritis, muscular weakness, and paralysis. Workers with paris-green have complained of an irri tation of the larynx and bronchial tubes. Many of these exhibit a cough or husky voice, which quickly disappears upon withdrawal from exposure. Differential Diagnosis.--Arsenic poisoning must be differentiated from botulism, mercurialism, and from certain poisons such as carbolic acid. In the latter, the burns on the lips or mouth and the carbolic odor are characteristic. Mercurialism is differentiated by the saliva tion and pains in the mouth. Botulism is confined mostly to a gastro enteritis of a day or two's duration. Tests.--Arsenic may be found in the urine, feces, hair, and nails. In chronic arsenic poisoning, it remains for a long time in the hair and nails. It has been found in the hair of an employee two years after cessation of his employment. This substance may be recovered from the bones and other organs after death. Medicolegal Aspects. Temporary Disability.--This varies, but is usually short. Skin lesions may be resistant to treatment, resulting in a temporary disability of several months. Gastro-intestinal symp toms clear up shortly after exposure has ceased. Permanent Disability.--When this occurs, it is usually from a peripheral-nerve involvement. If it is present after a two-year period, the functional loss should be estimated, as in any other partial perma nent disability. Illustrative Cases: Case I.--A fifty-seven-year-old white male, single, had been un employed since November, 1935. In June, 1936, he presented himself with a disabling condition which he attributed to chronic arsenic poisoning from his last employment, that of dye-making. Examination.--Weight 210 pounds. Florid complexion, red bulbous nose. Huge barrel-shaped chest with rales at both bases. Markedly dyspneic. Heart sounds distant and barely audible. No murmurs elicited. Blood pressure, 200/120. Abdomen obese with possible fluid present. The liver was palpable and down to the level of the umbilicus. Pitting edema of both legs. Urine: Albumin, two plus, with occasional casts. Blood count not significant. Blood Wassermann negative. Nails and hair negative for arsenic. It was freely admitted by the patient that he had drunk heavily all his life. During the past ten years he had consumed nearly a pint 296 OCCUPATIONAL DISEASES of whisky a day, with frequent week-end bouts. During the past year he had become a pronounced drunkard. His occupational history re vealed that prior to coming to California in 1925, he had been a sec tion hand on a railroad in Illinois. From 1925 to 1932 he was a longshoreman. He was unemployed during the greater part of the time from 1932 until May of 1935. At this time he obtained employ ment in a dye-manufacturing concern. He worked there for nearly seven months, when he was discharged. While there a young employee alleged that his father had died of arsenic poisoning from working in dyes. Therefore, when this patient became ill, he claimed arsenic as the cause. He appeared honest in his belief. However, his "job" was that of a trucker, conveying finished material to the shipping platform. The details of the case have been given to show how often an obviously non-compensable case must be carefully investigated. Diagnosis.--Cardiovascular renal disease, with hypertension. Cir rhosis of the liver (alcoholic?). The case was not compensable. Case II.--A young Chinese laborer employed in spraying vege tables became weak, lost some weight, and had abdominal pains. He consulted a physician in a nearby town, who diagnosed the case as arsenic poisoning. He was removed from his work, but the symptoms continued. Four weeks later a stool examination revealed numerous eggs of the tapeworm, which was then recovered by administering male fern. No comment is needed. Treatment. General Measures.--As with mercury, phenol, and others, the cases of acute poisoning from arsenic will be rare in indus try. When they do occur, the symptoms of vomiting, painful diarrhea, nervousness, thirst, cyanosis, and circulatory collapse must be treated. Early abundant gastric lavage with warm water is indicated. This is followed by the administration of warm milk. Previously lavage of the stomach with colloidal ferric hydroxide suspension, prepared by adding magnesium oxide to tincture of ferric chloride or a solu tion of ferric sulfate, was advised. This is now considered by most to be obsolete, but as McNally points out, it can do no harm and may delay absorption while the stomach is repeatedly washed out. Relief of Pain and Diarrhea.--Morphine sulfate, ]/j grain (0.016 gm.), every four to six hours, may be needed for relief of the pain and may aid in controlling the diarrhea. Other drugs which may be used for relief of the diarrhea and abdominal pain include bismuth subcarbonate or subnitrate, 15 grains (1 gm.), every four to six hours; tincture of opium, from 10 to 15 drops, every four to six hours; or camphorated tincture of opium (paregoric), two drachms ARSENIC 297 i (8 cc.), every three to four hours. Approximately two hours prior to starting these latter drugs, it is advisable to give a saline cathartic in full dose. For the diarrhea the drugs mentioned above, e.g., tincture of -S ' opium, bismuth subcarbonate or subnitrate, or paregoric, may be used. Porter2 has reported prompt improvement of the diarrhea and neuritis by the use of 2.6 mg. of thiamine hydrochloride daily, but if this vitamin is used, larger dosages, from 50 to 60 mg. per day parenterally, arc indicated. The use of nicotinic acid, from 100 to 200 mg. daily, would possibly be of value in treatment of the diarrhea. Cyanosis, Circulatory Collapse, and Shock.--For cyanosis, oxygen inhalations are given, and circulatory collapse and shock are treated as described in other sections, e.g., "Mercury" and "Fluorine." The intravenous infusion of from 5 to 10 per cent dextrose in 1000 cc. physiological saline is indicated not only for treatment of the shock syndrome, but also for the dehydration and chloride loss which may follow prolonged vomiting and diarrhea. The amount of this intra venous therapy needed will be determined by the patient's course. Sodium Thiosulfate.--The use of sodium thiosulfate intravenously in both the acute and chronic cases is advised. There has been con siderable controversy concerning the use of this drug, but clinically it appears to be of value. Ayres and Anderson1 demonstrated an in crease in the excretion of arsenic in the urine following the injection of sodium thiosulfate in 80 per cent of forty-nine cases. The amount to be used may vary from 15 grains (1 gm.) in 10 cc. of sterile distilled water every four to six hours during the first twenty-four hours of the acute stage to a similar injection two or three times a week over a period of weeks in the chronic case. Skin Reactions.--The ulcerations, pigmentation, and varied forms of a scaling dermatitis which may be present in the chronically ex posed usually disappear after removal from exposure. The following prescriptions may be of value for the dermatitis: I. Salicylic acid .. Sulfur (ppt.) .. Lanolin .......... Ung. aqua rosae n. Salicylic acid .. Menthol............ Lard................... ............. 1.5 gm. ............. 1.5 gm. ............. 6.0 gm. ... .q.s. 30.0 gm. ............. 6.0 gm. ............. 1.2 cc. q.s. ad. 60.0 gm. Fluids should be forced, and some of the drinking-water should be normal saline. Milk and a high caloric, high vitamin diet are of gen eral, value. 298 OCCUPATIONAL DISEASES Peripheral Neuritis.--Vilter, Aring, and Spies'* report striking im provement in a case of arsenic peripheral neuritis, in which 20 mg. of synthetic vitamin Bn in sterile physiological solution of sodium chloride was given twice daily. Improvement was more marked when 50 mg. of alpha-tocopherol was given intramuscularly in conjunction with the vitamin B(i; 50 mg. of thiamine hydrochloride intravenously for three weeks had previously failed to influence the condition. Physiotherapy may also improve the neuritis. Anemia, if present, should be treated by ferrous sulfate, 5 grains (0.32 gm.), two tablets three times daily. Arsine Poisoning.--No specific treatment is available for arsine poisoning. Repeated transfusions are of value, and the administration of iron compounds orally is indicated. Oxygen inhalations will be needed in many cases. The remainder of the treatment should consist of an adequate fluid intake, supplemented by frequent intravenous infusions of from 5 to 10 per cent glucose in physiological saline. The administration, in the early morning, of saturated solutions of mag nesium sulfate, from % to 2 ounces (15 to 60 cc.), flavored with a small amount of compound tincture of cardamom, may help in en couraging flow of the thick bile plugging the biliary passages; this, however, is doubtful. A similar attempt might be made by introduc tion of from 40 to 50 cc. of 33 per cent magnesium sulfate through a duodenal tube (Lyon non-surgical drainage)-. The stimulants fre quently mentioned in other chapters, e.g., "Mercury," are to be used when symptoms of circulatory or respiratory failure appear. REFERENCES 1. Ayres, S., and Anderson, N. P.: "Sodium Thiosulphate and the Elimination of Arsenic," J.A.M.A., 110: 886-887 (March 19), 1938. 2. Porter, W. A.: "Acute Arsenic Poisoning," Virginia M. Monthly, 66: 148 (March), 1939. 3. Vilter, R. W., Aring, C. D,, and Spies, T. D.: "A Case of Arsenic Peripheral Neuri tis Treated with Synthetic Bo and Alpha-Tocopherol." J.A.M.A., 115: 208 (July 20), 1940. ' ' fr r ! r!; CHAPTER XXV ZINC, ANTIMONY, COPPER, AND TIN ZINC The acute intoxication in which zinc plays a part has been de scribed under "Metal-Fume Fever." Chronic Poisoning.--Chronic zinc poisoning is doubted by most &?# investigators. In the older textbooks and literature, instances of 't chronic zinc poisoning were recorded. It is now felt that other metals present in the process in which zinc is used provide the intoxication. In 1926, McCord and his co-workers1 studied the employees in two galvanizing plants. In one plant, where the working conditions were poor and the men had been engaged in this work for a long period of time, they exhibited gastric disturbances varying from gastro enteritis to gastric and duodenal ulcers. In the second plant, where the hygienic conditions were fairly good and the men had a short term of exposure (less than six years), no gastro-intestinal disease was found. They concluded that a long period of time expressed in years (five to twenty), plus poor working conditions and a poor type of worker, favored the production of chronic zinc poisoning. In this same year, Drinker2 and her colleagues found no acute or chronic illness attributable to zinc in twenty-four workmen exposed from two to thirty-five years. Writers in the recent literature are of this same opinion, although duBray3 reported a case in 1938, believed by him to be due to chronic zinc intoxication. Zinc is found in various human tissues and the excreta. Some zinc is found in practically all food. In industry, zinc is involved in the process of mining, smelting, manufacturing of brass and other alloys, galvanizing, and in many other less important procedures. Anyone alleging illness due to zinc warrants thorough study for causes not industrial in origin, as well as careful inquiry into the process to which he is exposed in order to determine the presence of other metals. Medicolegal Aspects.--An allowable concentration is 14 mg. per cubic meter. Temporary disability is short, a few days at the most. There is no permanent disability. Treatment. Prophylaxis.--The preventive measures are the same as those to be adopted with a lead hazard, or any dust hazard apt to 299 1 300 OCCUPATIONAL DISEASES contain lead. Adequate ventilation, avoidance of the deposits of dust, frequent cleaning of all parts of machinery, floors, and walls of dust collections are factors in reducing exposure. Men should be selected who are free from focal infection. Some authors advise periodic changes of work and comparatively short working hours. The inclu sion of adequate fat and milk in the diet is thought to prevent to some degree the occurrence of symptoms in those working with zinc. If a case of chronic zinc -poisoning has been established, the patient should be removed from his hazard at once. Anemia, if present, is treated by ferrous sulfate, 5 grains (0.32 gm.), two tablets three times a day. In acute intoxication, a few days' absence from the work and treatment as described under "Metal-Fume Fever" will suffice. Zinc Chloride Burns.--Treatment of zinc chloride burns consists of removal of the necrotic slough and of filling the wound with sodium bicarbonate. Compresses of a warm solution of sodium bicarbonate are then used. After the lesion has cleaned up to some extent, it is dressed with borated petrolatum, painted with merthiolate, or cov ered with metaphen in collodion. Gloves should be worn by workers handling flux containing zinc chloride. When zinc chloride powder is handled, ordinary washing with soap and water will not remove it as a rule, while a 5 per cent solution of hydrochloric acid will:3 REFERENCES 1. McCord, C. P., and Friedlander, A.: "Occupational Syndrome among Workers in Zinc," Am. J. Pvb. Health, 16: 274-280 (March), 1926. 2. 'Batchelor, R. P., and others: "Clinical and Laboratory Investigation of Effect of Metallic Zinc Oxide and of Zinc Sulphide upon Health of Workmen," J. Indust. Hyg., 8: 322-363 (August), 1926. 3. duBray, E. S.: "Chronic Zinc Intoxication; Instance of Chronic Zinc Poisoning from Zinc Chloride Used in Pillow Manufacturing Industry," J.A.MA., 108: 383-385 (Jan. 30), 1937. ANTIMONY, COPPER, AND TIN These three metals are considered jointly because they represent a group about which little is known. This is especially true of copper and tin, whereas (more is being learned regarding the toxicity of antimony and its compounds. Tin.--Tin is rarely ever used in a form that could cause any symp toms. A transient irritation of the nose and eyes has been noted from the use of tin tetrachloride in silk mills. Copper.--Copper oxide is frequently present with other metals in processes which cause metal fume fever. Following Mallory's con tention that bronze diabetes, characterized by cirrhosis of the liver, diabetes mellitus, and pigmentation of the skin resulted from chronic ZINC, ANTIMONY, COPPER, AND TIN 301 copper poisoning, the British investigators made a careful survey regarding the incidence of such a syndrome among copper workers. They found no evidence that such a disease occurred among copper workers. Antimony.--While antimony has received slight consideration by the toxicologist, it is likely to be subjected to more detailed study, since it is now being more widely used in certain national-defense projects. Occupational Hazards.--The usual exposure to antimony occurs where the ore is being mined, smelted, or refined; and also in processes where it is combined as an alloy with other metals, especially lead, tin, and copper. These allo5's find use in storage-battery grids, pew ters, metal bearings, and type metal. In the defense program it is used especially in the manufacturing of munitions. Pathology.--Most of the references regarding the eifects of antim ony occur in the foreign literature, and a great deal of it is of an experimental nature. A very recent summary of the literature can be found in an excellent paper by Bradley and Fredrick.1 These two workers quote the report of Schrumpf and Zabel, whose observation of workers in a type foundry revealed very few cases of lead poison ing, but a number of men with "remarkable facial expression, com plaints of nervousness, irritability, sleeplessness, fatigue, dizziness, muscular and neuralgic pains, loss of appetite, nausea, gastrointes tinal disturbance, and constipation." Examination of the blood re vealed a diminished leukocyte count and a notable eosinophilia. The blood pressure was lowered. Antimony was recovered in the stools. Experimentally the work of Bradley and Fredrick indicates that the most important pathological effect was the consistent injury to the heart muscle. They could draw no conclusions from their hemato logical studies. The author has never observed a case of intoxication by antimony, although his experience with the metals has been fairly comprehensive. It is possible that antimony has been an unrecognized factor of illness in certain cases thought to be lead poisoning. Obviously, but few industrial processes use antimony except in combination with other metals. A true estimation of its harmful effects upon the human body will have to await the compilation of more clinical data. The experi mental investigation strongly suggests strict hygienic measures in those industries using this metal. REFERENCE 1. Bradley, Wm. T., and Fredrick, Wm. G.: "The Toxicity of Antimony--Animal Studies," hxlust. Med.., 10 (April), 1941. *Kr PART IV THE DUSTS Recognition of the irritating effects from inhaled dust is not re cent. "Fatal dust" was mentioned in the writings of Pliny; and Celsus in the first century described "dust phthisis." Studies of silicosis were conducted in England, Germany, Italy, South Africa, and Australia many years ago, yet it was not until 1915 that the first real investi gation (by Lanza and Higgins) was conducted in this country. Since then much time has been devoted to the dust diseases, especially sili cosis, by the hygienist and pathologist, and volumes have been writ ten concerning them. Confusion about Effects.--In the early years of the depression, the physician and the layman were awakened to a disease called "silicosis." Unscrupulous lawyers grabbed the chance to obtain fees from idle workmen willing to allege a disability to obtain remuneration. Judges and juries were shown a;-ray films with "spots" on them. Untaught physicians testified that such films could represent silicosis. Large awards were made to fraudulent persons. It has been estimated that the cost of these to industry was in excess of $100,000,000. The silic osis racket has abated, but it is not extinct, nor will it be so long as confusion remains in the minds of the court, industrial commission, or the practicing physician, as to the interpretation of the word "harmful." What dusts are harmful? what factors constitute a harm ful exposure? and when is the worker to be considered harmed or disabled? These questions have been answered repeatedly in the litera ture, but possibly they have been obscured by scientific detail. It is hoped that those seeking a ready basis for diagnosis and especially a basis for the determination of compensability will find the following discussion adequate. Distinction between Dusts.--The distinction between gases, fumes, 7l, and dusts in an industrial atmosphere is a very fine one. It has been indicated in the chapter on metals that the body is affected by the inhalation of finely divided dust particles of lead, zinc, mercury, cad mium, manganese, etc. These metallic dusts produce a toxic reaction which is usually acute and temporary; whereas the dusts to be dis '3 cussed in the succeeding chapters have a specific action upon the lung l V tissue, are insidious rather than acute, and their damage is perma Mii nent. This statement excludes those dusts which may affect the upper respiratory tract but which produce no pathological change in the 303 V 304 OCCUPATIONAL DISEASES lung- tissue. Frequently a patient conies to the clinic with a diagnosis of silicosis because he has been in an atmosphere of dust, just any dust, without any effort having been expended to determine if silica or the silicates existed in the exposed atmosphere. Organic and Inorganic Dusts.--The first act to be considered by the physician is the type of dust in the occupation. For this purpose the dusts may be divided into two groups: (1) the organic, and (2) the inorganic. Organic dusts do not cause pulmonary lesions, and, most important of all, very few inorganic dusts can be definitely considered to be offending agents. Definition of "Pneumoconiosis."--Pneumoconiosis means a chronic pulmonary fibrosis due to the inhalation of irritating dusts which pro duce a proliferative reaction. The term is comprehensive and too often misleading. Investigators in dust diseases use the term correctly, but the average physician is prone to assume that it implies a disabling condition. Since silicosis is a condition of pneumoconiosis, the impli cations of this disease are apt to be applied to any dusty exposure. In addition to silicosis, the term "pneumoconiosis" includes asbestosis, anthracosis, aluminosis, siderosis, chalicosis, byssinosis, tabacosis, and other forms not fully understood. Silica versus Silicates.--Confusion also exists regarding the use of the word "silica." I have heard physicians, attorneys, and referees discussing the possible presence of silicosis in a claimant who had been exposed to the silicates without appreciating that there is a world of difference between silica and the silicates. Because that difference is so important, the author feels it expedient to present an elementary review of the chemistry of silica and the silicates. Chemistry.--The chemical individuals that go to make up the igneous rocks, resulting from originally molten material by a process of crystallization, are called "primary minerals." When these primary minerals have been altered by heat, pressure, or water, secondary minerals result. Silica is silicon dioxide, Si02. The most important crystalline form of silica is quartz. Next to feldspar, it is the most abundant of all minerals. Minute aquatic organisms such as diatoms, infusoria, and certain varieties of sponges develop siliceous skeletons which, following death, accumulate on the bottom of the ocean. This substance is known as infusorial or diatomaceous earth. Silica, Si02, is composed of silicate tetrahedra, Si04-------- , a struc tural unit,, which was first revealed by a;-ray. In studying the internal structure of crystals, among other things it was noted that separate Si04-------- tetrahedra alternate in the space lattice with positively charged metallic ions in certain silicates, while others are linked to gether in pairs, with an oxygen ion in common. "Since each oxygen ion is shared between two different silicate tetrahedra, there are only THE DUSTS 305 half as many oxygen ions in the complete solid structure as the for mula SiC>4--------- would seem to suggest; in other words, the formula of the solid structure, extended indefinitely in three dimensions of space, is a triple infinite multiple of SiO-j."1 However, the chemistry of the silicates is not so simple as the foregoing would indicate, owing to the arrangement of the oxygen ions in the structure, for some groups possess oxygen ions which are not linked with other groups, while two ions may be shared with other groups. A chain, for instance, of infinite multiples of Si03 may be formed. The fibrous structure of asbestos is due to the linking of silicate groups in continuous chains. Silicates in Industry.--The silicates of industrial importance are too numerous to consider at this time, but a few deserve mention. The talc used in cosmetics is hydrated magnesium silicate. Closely re lated to talc is soapstone. Hydrated potassium-aluminum silicate is known as mica and is chiefly of use in electrical condensers. Waterglass has many uses and is formed artificially by fusing sodium or potassium carbonate with sand. When added to water in its molten state a viscous colloidal dispersion takes place, and it is in this form that it is most widely used. Various heavy metals may be added to silica to form colored silicates, such as cobalt, copper, chromium, manganese, or the like. Carborundum (silicon carbide) results from adding carbon (coke) to silica at high temperature. Silica Locked in Silicates.--The point in the foregoing discussion is this: The silicates are abundant in industry, whereas pure silica is less so. In the silicates, the silica is bound by the chemical structure so that it is not released to act as a harmful agent to the lungs. There fore, in dealing with all persons presenting a claim involving silicosis, one should first differentiate between a hazard in which silica as such is present and one in which the silica is locked within the chemical structure of the silicates and is, therefore, inert. This fact must be kept in mind when one reads a chemical analysis of a substance which shows the presence of a high content of silicates, but does not reveal the actual content of the silica as such in the mineral. In fact, a chemical analysis of a material is not satisfactory for the determina tion of the exact percentage of silica present. Estimating Silica Content.--When a question arises about the amount of silica present in a substance alleged to be an offending agent, it might be better to resort to the x-ray diffraction method as discussed in Case XIII under "Silicosis." As a final exhortation prior to the consideration of silicosis, the author warns all interested parties that the silicates should be differentiated from silica in a claim of this type. REFERENCE l. Deming, G. H.: General Chemistry, Wylie and Sons, Inc., New York, 1935, p. 482. 20 CHAPTER XXVI SILICOSIS Definition.--The Committee on Pneumoconiosis of the American Public Health Association defined silicosis as a . disease due to breathing air containing silica (SiOo), characterized anatomically by generalized fibrotic changes and the development of miliary nodules in both lungs, and clinically by shortness of breath, decreased chest expansion, lessened capacity for work, absence of fever, increased susceptibility to tuberculosis (some or all of which symptoms may be present) and characteristic x-ray findings."1 Factors in Development of Silicosis.--Four important factors are necessary: Size of Dust Particle.--If dust is to exert a harmful effect upon the lung tissue, it must be small enough to enter the smallest divisions of the lung. Only particles of less than 10 jj. are capable of getting into the lungs. Seventy per cent of the dust in industry measures between 0.5 and 3 /*. Larger particles settle out of an atmosphere more quickly than the smaller ones. A particle of 5 y, will fall, according to measurement, twenty times as fast in one hour as a particle of from 1 to 3 jx. Therefore, an atmosphere which appears to the workman as being too dusty because he can see the dust is apt to be less dan gerous than one which appears free of the particles. Number of Dust Particles 'per Cubic Foot of Air in Breathing Zone. --An allowable concentration is 10,000,000 particles of a size between 0.5 and 5 p. per cubic foot of air. Mineral Composition of Dust Breathed.--The content of the dust should determine the standard fixed for allowable concentration. If a standard of 15,000,000 particles is the limit for a dust containing 35 per cent free silica, then a mineral dust containing 70 per cent free silica shouky be limited to a standard of 7,500,000 particles per cubic foot of air. Concerning the composition of the dust breathed, there exists controversial opinion over the action of silica combined with other substances. Some hold that the action of silica is aggravated by the presence of an alkali, while others maintain it is retarded. McCord 2 and his co-workers concluded that . . the often en countered assertion that co-existence of silica and alkali dust in in dustry constitutes extra hazardous working conditions, is unproved but not necessarily unfounded." 306 SILICOSIS 307 Denny, Robson, and Irwin3 contend that if metallic aluminum (hydrated alumina) is dispersed in an atmosphere containing silica, silicosis will be prevented. Length of Exposure.--No set time can be given as an estimate for development of silicosis. The older literature indicated that ten years or longer was the average. In the more severe exposure, silicosis may develop in from three to five years. Cases resulting from an exposure of less than one year have been reported. Such instances are extremely rare and certainly must involve unusual factors. Occupational Hazards: Mining of hard siliceous rock (copper, gold, silver, zinc, iron, and hard coal) Quarrying of granite, sandstone, quartz, slate rock, and crystal Pottery-making. Ceramic industries Glass-manufacturing Working with talc and abrasive material (sand, sandstone, sandpaper, scouring material, and soaps) Brick-manufacturing where silica is used Stone-finishing Construction work (tubes, tunnels, aqueducts, etc.) Industries where spraying occurs DIAGNOSIS Signs and Symptoms.--Climate, season, soil, heredity, race, age, and sex seem to have no effect upon the development of silicosis. But individual susceptibility varies a great deal, some patients showing marked pathological changes after a comparatively short exposure. Nodulation and Fibrosis in Absence of Symptoms.--The initial effect of a collection of silicotic nodules within the lung is attended by no symptoms. Many persons may develop what appears to be in tense nodulation and fibrosis without evidencing any signs or symp toms during their life. Rales will not be heard, the chest will usually be barrel-shaped, and inspection will generally show some bilateral limitation of excursion. Otherwise these persons appear normal. Even respiratory diseases of another nature, such as pneumonia or bron chitis, may be overcome without aggravating silicosis. Progressive Symptoms.--If the patient does show symptoms, the first is that of shortness of breath upon minor effort. This increases in severity, and palpitation of the heart may be noted. At about this time, a dry, infrequent cough may ensue, which as time goes on be comes moist and frequent. The sputum is usually scant, stringy, and sometimes discolored. Fever is conspicuously absent. Unaware of his 308 OCCUPATIONAL DISEASES true condition, the patient may request lighter work. Further pro gression may include pleurisy pains, epigastric pains, loss of appetite, and marked fatigue. As dyspnea increases, cyanosis appears. Progres sive heart failure may continue until death, but these cases are rare. It is usually at this late stage that tuberculosis enters the picture. This condition, silicotuberculosis, will be described later. Symptoms in Acute Silicosis.--This is an extremely rare form and results when enormous amounts of fine silica dust become imbedded in the lungs. Within from a few months to a year symptoms may ap pear. These may even precede conclusive x-ray findings. Acute and frequently fatal pneumonia often complicates or terminates this type of silicosis. Tests.--The important evidence of pneumoconiosis is obtained by x-ray. The advent of tuberculosis may be proved by the finding of the tubercle bacilli in the sputum. In the absence of the tubercle bacilli, early suspicion may be strengthened by an increased blood sedimentation rate. Pathology. Elimination Mechanisms.--That only a small portion of the dust inhaled ever reaches the lung is a fact not realized by the layman and frequently forgotten by the physician. Most of it is expelled before it reaches the lung by the upward current created by the ciliated epithelium. Further elimination occurs by phagocytosis, the particles being carried back to the ciliated epithelium or to the point where the cough mechanism becomes effective. Inert dusts which pass these barriers usually disintegrate and become short-lived. Sub stances, such as coal dust, which actually enter the lung tissue may cause pigmentation but no pulmonary destruction. Fibrosis at Hilus of Lung.--The pathology of silicosis is one in volving the lymphatic drainage of the lung. The normal lymphatic drainage is toward the hilum. A small area beneath the visceral pleura is drained into the subpleural cistern and from there along the lobar septa to the hilum. Dust which reaches the wall of an alveolus is picked up by the phagocytic cells, and by ameboid movement they pass into the lymph spaces. From here they slowly move on to the minute lymph islands which guard the entrance to the small lymphatic vessels, pass through these and are finally picked up by the lymph glands at the hilus of the lung. It is believed that at this point the dust cells, acted upon by the alkaline body fluids, form a colloidal silica hydroxide which is a strong protoplasmic poison, and its action causes death to the dust cell and necrosis to the immediate surround ing tissue. Scar (fibrous) tissue is formed, which acts as a blockage to the lymphatic channels, and the removal of further inhaled dust be comes impossible.  ffc .... ...... ................... ...... --: f' -- i ; silicosis 309 S]>read o/ Fibrosis.--Additional fibrous tissue forms along the lymphatic vessels which accompany the blood vessels of the lung, in vades the septa between the lobes and spreads into the lung tissue itself. The minute masses of lymphatic tissue become fibrotic nodules (Fig. 47), and these, as time goes on, increase in number to block off large portions of the lung. This blocking of the lymph flow toward the hilus increases the spread of dust cells toward the pleura. These minute nodules of fibrotic material are thus scattered throughout the field and are surrounded by apparently normal lung tissue. *N0Sm Fig. 47.--Simple discrete Modulation of uncomplicated silicosis. (Gardner.) Alveolar Consolidation.--As the process proceeds they tend to coalesce to form massive areas of fibrosis (Figs. 48, 49, 50). This in crease of fibrosis tends to destroy the alveoli and thus provokes en largement of the surrounding alveoli. Such enlargement constitutes emphysema. With the thickening of the alveoli, the elasticity of the lung is interfered with, and aeration decreases. If compensatory em physema is adequate and infection is not present, the condition is that of simple silicosis. But if compensation is not adequate, the first symp tom of silicosis appears, namely dyspnea. However, since only one fourth of one lung is necessary for life, fibrosis must be enormous be fore death can occur from deficient aeration alone. Production of Dyspnea.--That encroachment upon the normal 310 OCCUPATIONAL DISEASES Fig. 48.--Massive areas of confluent nodules. Note the thickened pleura. (U. S. Public Health Service, Bulletin SH-i.) Fig. 49.--Confluent mass of silicotic nodules adjacent to small bronchus and blood vessels. Note the presence of extensive emphysema in patent lung tissue. (U. S. Public Health Service, Bulletin %kk-) Fig. 50.--Section through lung, showing massive areas of confluent, fibrous nodules. Close inspection will reveal the extensive emphysema. (U. S. Public Health Service, Bulletin lung fields by nodulation is the cause of dyspnea is questioned by Cole and Cole*: SILICOSIS 311 It is universally conceded that small, hard, dense nodules in the lung are pathognomonic of silicosis, yet these small, hard, dense, nodules are either absent or relatively infrequent in some cases of ad vanced silicosis in which dyspnea is an outstanding symptom. These silicotic nodules as observed roentgenographically often progress to an extreme stage before they cause dyspnea, yet dyspnea may occur and terminate fatally without a preponderance of the typical well defined nodules. Spherical whorls or nodules are considered pathogno monic of silicosis, yet we believe they constitute a protective mecha nism--a constructive rather than a destructive process--and are not responsible for the outstanding symptom of silicosis, dyspnea. Advanced silicosis is frequently found only by accident, when the patient is being examined roentgenologically for some other lesion or injury, such as a fractured rib. Such accidental discoveries are fre quent, but, on the other hand, roentgenograms may show no evidence of typical nodulation even in a case of advanced silicosis. They are convinced, after making an intensive study of the patho logical changes of acute silicosis, that "dyspnea is caused by morbid changes in the blood and endothelial reticular structures, which in turn result in changes in blood cells, observed in localized regions of the lung." They conclude that large microscopic sections of silicotic lungs show three general manifestations of morbid change: (1) avascular areas, (2) overvascular areas, and (3) a region of invasion. The region of invasion, where collagen constricts the capillaries, is the most important region for intensive study. In the avascular portion, capillary occlusion by external pressure causes a traffic jam of red blood cells, with a damming back of the blood into the arterioles and a lack of drainage of the veins. The blood in the larger vessels in the avascular areas disintegrates. Overvascular areas, where there is immense dilatation of the capillaries and engorgement of the veins and arteries with viable red blood cells, seem to compensate for avas cular regions in different portions of the section. Dyspnea has been explained by two pathological factors: (1) nodulation. and (2) alveolar consolidation. To these Cole and Cole add a third; namely, capillary obstruction and dilatation. From a study of microscopic sections they have made certain deductions which constitute their conception of the life history of silicosis at least as it occurs in some groups of cases. They believe i. that the dyspnea of silicosis is due to capillary occlusion in large ' localized regions of the lung, with compensating capillary dilatation l*-. iy> in other regions. 312 OCCUPATIONAL DISEASES Variety of Morbid Changes.--Most diseases exhibit morbid changes which can be recognized in relatively small sections; for ex ample, certain types of neoplasm can be determined by small groups of characteristic cells; but in silicosis there is a vast variety of morbid changes in various portions of the lung. Different varieties of dust result in different types of morbid change in varying regions of the lung. Tabus 13--A Tabulation of the Roentgenological Changes Found in Silicosis Together with the Underlying Histological Conditions1* Healthy Lungs and Adnexa Roentgenological Appearances Histological Appearances 1. Healthy lungs, as defined by the N.T.A. 1. Essentially the normal tissues of the Committee Report (National Tuber vascular tree, the mediastinum, the culosis Association) bronchi, and trachea 2. Irregular exaggeration of the linear 2. Cellular connective tissue proliferation markings, with possibly some bead about lymphatic trunks in the walls ing, confined to the trunks of vessels and bronchi. Beading may be due to various causes, such as blood vessels seen end on, arterio sclerosis, minute areas of fibrosis in lymphoid tissues along the trunks 3. Increased root shadow 3. Cellular reaction in the tracheobron chial lymph nodes with extensions along afferent lymphatic trunks These changes come within normal variations when not accompanied by recognized organic disease. Simple Silicosis Roentgenological Appearances Histological Appearances i. Modulation. Discrete shadows not ex ceeding 6 mm. in diameter tending to uniformity in size, density, and bi lateral distribution, with well-defined borders surrounded by apparently normal lung shadow. The outer and lower lung fields characteristically show fewer nodules 5. Conglomerate shadows that appear to re sult from a combination or consolidation of nodulation usually with associated em physema manifested by: (a) Localized increased transparency of the lung with loss of fine detail (h) Intensification of the trunk shadows by contrast (c) Depression of the domes with possible tendency toward in dividualization of the costal components of the diaphragm (d) Lateral view. Increase in the pre-aortic and retrocardiac spaces with exaggerated for ward bowing of the sternum and backward curving of the spine. Widening of the spaces between the ribs may or may not be present (Fig. 51) i. Circumscribed nodules of hyaline fibro sis located in the parenchyma of the lung. Occasionally some of these nodules may show microscopic foci of central necrosis 5. The result of coalescence of discrete nodules; an area in which the nodules are closely packed and most of the intervening lung is replaced by more or less hyaline fibrous tissue. The lung architecture is partially obscured. No demonstrable evidence of infection. Emphysema is a compensatory dila tation of the air spaces with or with out thickening of the septa I SILICOSIS 313 Table IS--A Tabulation of the Roentgenological Changes Found in Silicosis Together with the Underlying Histological Conditions--Continued Silicosis with Infection The characteristic appearances described under "Simple Silicosis" are modified by infection as follows: Roentgenological Appearances 6. Localized discrete densities and- or string like shadows accompanying those of simple silicosis described above 7. Mottling. Shadows varying in size, with ill-defined borders and lacking uni formity in density and distribution accompanying simple silicosis 8. Soft nodnlation. The nodular shadows described under "Simple Silicosis" (4) have now assumed fuzzy borders and- or irregularities in distribution. This change may or may not accom pany No. 7 9. Massive shadows of homogeneous den sity not of pleural origin symmetric ally or asymmetrically distributed Histological Appearances (i. Strands of fibrous tissue, often along trunks and septa, with or without areas of calcification; indicative of "healed" infection 7. (a) Areas of bronchopneumonia with or without caseation (acute infec tion) (ib) Lobar areas of proliferative reac tion with or without caseation (subacute or chronic infection) 8. Perinodular cellular reaction either exu date or proliferalive in character 9. Extensive areas of fibrosis probably due to organized pneumonia of tubercu lous or non-tuberculous origin super imposed upon a coexistent silicotic process. Outlines of normal struc tures may be partially destroyed Finally, it must always be remembered that nodulation and forma tion of new fibrous tissue continues in a victim after the exposure to a dust has ceased. The damage produced in the lung is permanent. Roentgen-Ray Diagnosis.--The most important evidence of pneu moconiosis is presented by x-ray films. These should be in stereo, and in questionable cases a lateral view may be of some value. Table 13 was prepared by experts following the Saranac Symposium in 1934. Differential Diagnosis.--In interpreting the films of suspected early silicosis, one must rule out passive congestion from cardiac decom pensation, advanced bilateral bronchiectasis, asthma, malignant dis ease, and mycotic infections. The x-ray diagnosis of silicotuberculosis from that of uncompli cated tuberculosis is frequently difficult. Pancoast and Pendergrass" classify these cases into seven groups:1 2 1. Cases showing x-ray evidence of tuberculosis only, in spite of history of dust exposure 2. Cases showing obvious pulmonary tuberculosis with mild silic osis or pneumoconiosis. (Pancoast believes that these two groups should not be included in the x-ray diagnosis of silico tuberculosis.) 314 OCCUPATIONAL DISEASES 3. Tuberculosis associated with silicosis (interstitial) of short duration but high exposure, as sand-pulverizers 4. Obvious advanced tuberculosis with no evidence of silicosis because obscured by the extent of the tuberculous infection (study of environment essential here) 5. Obvious tuberculosis with evidence of advanced silicosis 6. Advanced silicosis in which there is doubt as to coexistence of tuberculosis 7. Obvious tuberculosis occurring late in persons with progressive and marked silicosis which has appeared many years after exposure to dust has ceased SCHEME REPRESENTING THE SEQUENCE OF LUNG-FIELD MARKINGS IN A TYPICAL CASE OF UNCOMPLICATED SILICOSIS LINEAR NORMAL LUNG MARKINGS & Ist DEGREE EXAGGERATION OF LINEAR PULMONIC MARK INGS. 2N0 DEGREE EXAGGERATION Or LINEAR PULMONIC MARK INGS, WITH OR WITHOUT BEADING. This is the range of markings usually seen on X-ray examination of persons who have never worked in a dusty trade. IST DEGREE DIFFUSE GROUND GLASS OR GRAINY APPEAR '/'/'/A ANCE, NOT OBLITERATING LINEAR MARKINGS. GRANULAR // / / / / * 2* DEGREE DIFFUSE GROUND GLASS OR GRAINY APPEAR ANCE, OBLITERATING LINEAR * MARKINGS. Y- Vv" V These are the earliest markings in the sequence of dust-induced changes which can be elearly differentiated from the changes that usually accompany advancing age, bronchitis, cardiac stasis, etc. NODULAR Ist degree oisseminateo NODULES UP TO SIZE OF MILIARY TUBERCLES. 2*0 DEGREE DISSEMINATED NOOULES EXCEEDING IMM IN SIZE, EMPHYSEMA PRES ENT, USUALLY. * * '** **! .* , , * Cases with granular or nodular markings may be diagnosed as stage I or stage II silicosis depending on signs and symptoms present. COALESCENT NODULES AND CONGLOMERATE SHADOWS CeMPHYSEMA ALWAYS PrtESEMT) r V May be diagnosed stageE or stage H depend ing on signs and symptoms present and degree of disability. Pig. 51.--This scheme gives an excellent graphic impression of the advancing stages of uncomplicated silicosis as interpreted from the a;-ray markings. (U. S. Public Health Service, Bulletin SU, 1939.) Silicotuberculosis.--It has been previously stated that silicosis may exist in a pronounced form without causing death or interfering with health. Tuberculosis likewise may be present in a person for years, causing no impairment of health, or may be easily controlled. But tuberculosis in the presence of silicosis defies treatment or con trol. To understand this, it must be realized that these two diseases do not represent a constant entity but rather a combination of all degrees of the two diseases. Tuberculosis may be present in either a quiescent or active stage before the lung is exposed to silica, or the tubercle bacillus may be implanted in a lung already silicotic. SILICOSIS 315 Evidence of Tuberculosis.--If silicosis is superimposed upon an old inactive tuberculosis, certain characteristics of the preexisting tuber culosis may be in evidence. Gloyne0 lists these as: (1) dense pleural adhesions, especially in the upper part of the pleural sac, tethering the apex of the lung to the apical pleura; (2) fibrotic contraction and scarring of the visceral pleura without adhesions, again especially well marked at the apices; (3) calcified nodules. Gardner, Gloyne, and others have pointed out that the calcified nodules of old healed tuberculosis have certain distinguished characteristics. They are usu ally beneath the pleura, attached to the wall of the small bronchus or in a mediastinal gland. Silicosis "with Infection."--As to whether the frequency of silicotuberculosis is greater in those harboring the tubercle bacilli prior to exposure or in those who become infected with tuberculosis after silicosis has transpired is of interest to the experimentalist or path ologist but not to the practicing physician. What should interest him is that it is estimated that 75 per cent of all silicotic persons die of tuberculosis. There are many instances when it cannot be proved that tuberculosis is the coexisting infection. Under such circumstances, the diagnosis of silicosis with infection is preferred, but the chances are great that the unproved infection is tuberculosis. Silicosis with infection produces certain recognized a;-ray findings. The nodules lose their distinct outline to become fuzzy and "soft" in appearance. They lack uniformity in density and outline. They coalesce, and conglomerate masses appear. While this is in progress, rales may be heard, fever may be present, and tubercle bacilli may be found. Marked weight loss, flattening of the chest, increased productive cough, pleural adhesions with chest pain, and cavitation may become prominent. Complications and Sequelae of Silicosis. Emphysema.--This is an almost constant condition accompanying silicosis. Its production ex plains the barrel chest. Occasionally large emphysematous areas are mistaken for tuberculous cavitation. Cardiac Involvement.--Many of these silicotic persons die appar ently from cardiac failure, yet postmortem examinations rarely reveal valvular lesions or particular involvement of the myocardium. It seems evident to the writer that months or years of cardiac effort against resistance could result in myocardial weakness and a cardiac death. Certainly in the presence of arteriosclerosis, silicosis becomes an added burden on heart function. Electrocardiograms taken of silicotics reveal no significant findings except evidence of displace ment to the right, due to overstraining of the right heart. Bronchitis and Bronchopneumonia.--Secondary infection from S16 OCCUPATIONAL DISKASKS septic invasion is common. Its frequency, compared to that in persons not exposed to silicosis, is not revealed by statistics. Carcinoma.--No evidence exists that malignant disease of the lungs commonly results from silicosis. From a compensation angle it should not be assumed that a worker in a silicosis hazard has in curred cancer because of his exposure. Gardner7 reviews a case re ported by Bradshaw and Chodoff in which roentgenograms of an ex-coalminer with cough, expectoration, loss of weight, and dyspnea showed a localized mass the size of a half dollar in the right hilum. There was no evidence of generalized silicotic nodulation. The sputum was negative for tubercle bacilli; bronchoscopic examination showed an obstructive lesion compressing the right upper lobe bronchus with a tendency to mucosal bleeding. Films taken at the end of expiration showed an obstructive emphysema of the right upper lobe. Tubercu losis was apparently excluded by the absence of hemoptysis, elevation of pulse and temperature, and a persistently normal sputum. Although two bronchial biopsies revealed no evidence of tumor but merely "in flammatory exudate, blood clot, and anthracotic tissue," the probable diagnosis of bronchiogenic carcinoma superimposed upon anthracosilicosis was entertained. Exploratory thoracotomy was advised but refused. One year and five months later, the patient's films showed marked symmetrical elevation of both hila with increased "fibrosis" radiating upward and laterally from both hila. The trachea was displaced to the right, and there was emphysema in the left lower lung field. On bronchoscopic examination the orifice of the upper lobe bronchus was now clearly visualized, but there was an obstruction of the main tube at the level of the middle lobe bronchus. Another biopsy pro duced no cellular elements. Temperature and pulse had remained nor mal, but the patient had lost 21 pounds, and his dyspnea had in creased. A thoracotomy was performed, and the surgeon palpated a stony hard mass in the upper lung covered by dense adhesions between the apex of the lung and the anterolateral chest wall. Only a few small nodes were felt about the hilum of the lung and along the trachea. He then performed a total pneumonectomy, but pneumothorax de veloped on the opposite side and the patient died. Pathological exami nation revealed an anthracosilicosis of conglomerate type involving the upper three fourths of the upper lobe. "The remainder of the lung contains a moderate amount of pigmentation and of fibrotic foci." On autopsy a localized lesion, inferred to be similar in character, was found in the apex of the upper lobe. The authors cite the difficulties in diagnosis, point out that gen- SILICOSIS 317 cralized nodulation was not observed in the roentgenogram and hence silicosis could only be inferred, and plead for more exploratory thoracotomies. The reviewer admits the difficulties but points out that "fibrotic foci" were reported in the lower part of the right lung after removal from the body. They may have been too small to cast definite shadows on a film. In his mind the localization of the massive fibrosis in both upper lobes suggests reaction to dust localized in the scars of healed tuberculosis. In such cases much of the inhaled dust seems to come to rest in the vicinity of the scars, and subsequent retraction of the lung tends to pull nodules upward toward the conglomerate focus. Compensatory emphysema produces the impression that there are few nodules in the lower lung. Conglomerate fibrosis is much more prone to develop in the modified anthracosilicosis than in uncompli cated silicosis. The stony hard consistence of such lesions is one of their major characteristics. The tracheobronchial lymph nodes in car cinoma are generally enlarged and more matted together than in pure a n thracosilicosis. Extrapulmonary Tuberculosis.--A survey made by Cohen at the White Haven, Pennsylvania, Sanitorium, and reviewed by Schnurer,s corroborates the established fact that pulmonary tuberculosis is more common in anthracite-coal miners than in non-miners. Of 541 miners and 730 male non-miners of the same age who came to autopsy, it was the cause of death in more than twice as many miners as non miners. Cohen reports on the occurrence of extrapulmonary tuber culosis in a series of autopsies. Only 20 per cent of 50 anthracosilicotics with pulmonary tuberculosis had intestinal tuberculosis, while in 84 patients with non-anthracosilicotic pulmonary tuberculosis, it was present in 51 per cent. The degree of anthracosilicosis, rather than the age, determines the frequency with which intestinal tuberculosis occurs. It was seen in miners under thirty years of age in 67 per cent because the existing anthracosilicosis was early or only mod erately advanced. In those above thirty years, when the coniosis was advanced, it occurred in only 14 per cent of cases as compared to 41 per cent in the non-mining group of the same age. The author ex plains the comparative rarity of intestinal tuberculosis in advanced anthracosilicotuberculosis on the basis of (1) chronicity of the pul monary process, and (2) the extensive pulmonary fibrosis, particu larly the vascular sclerosis which tends to prevent the spread of tubercle bacilli. There are no definite symptoms referable to the gastro-intestinal tract in those having intestinal tuberculosis associ ated with anthracosilicosis. During the same period of time, laryngeal examinations were 318 OCCUPATIONAL DISEASES made on 365 subjects. Of 100 tuberculous miners, only 27 per cent had laryngeal tuberculosis as compared to 31 per cent of 276 tuber culous non-miners, despite the fact that the tuberculosis in the miners was much more severe. Thus, 57 per cent of the miners died of tuber culosis, while only 12 per cent of the non-miners died of the disease. In those who died, laryngeal involvement was seen in 33 per cent of the miners, and in 59 per cent of the non-mining group. Again, age per se was not important in the incidence of laryngeal tuberculosis. In the same series of autopsies, 32 per cent of the miners had extrapulmonary lesions other than those mentioned, as compared to 46 per cent in non-mining adults. Basis for Diagnosis. Reliable History of Adequate Exposure.-- The patient's statement that he has been working in a silica-laden atmosphere cannot be accepted without investigation. To accept or deny a case for compensation without investigation often instigates unnecessary litigation. An adequate exposure constitutes working within this dusty atmosphere over a period of several years. The claimant may be employed by a firm engaged in handling silica, but he may be a janitor or shipping clerk or employed in an endeavor outside the actual hazard. Furthermore, the time one works in such an atmosphere is exceedingly important. From ten to twenty years is the average length of time in an average concentration. In excessive concentrations, this average time may be as low as two years. Less than two years is to be viewed with skepticism until evidence of unusual factors is obtained. Occupational History.--A claimant may be engaged in an occu pation foreign to silicosis at the time he becomes disabled. His last exposure to silica may have been ten or fifteen years previously. To allocate the responsibility under compensation properly, his occupa tional history since he left school is necessary. x-Ray Findings.--Chest films, preferably in stereo, should be in terpreted by one thoroughly acquainted with the roentgenological manifestations this disease presents. Sputum Examination. x-Ray Diffraction Analysis.-- (See discussion of this method under Case XIII.) Of occasional value only. MEDICOLEGAL ASPECTS The fact that a workman has evidence of silicosis does not necessarily entitle him to compensation. A scar, evident in the pul monary tissue is comparable to a scar on the surface of the body-- if neither interferes with the function of the body or part, it is there fore not compensable. However, if the fibrous tissue of a scar pre- SILICOSIS 319 vents contraction of a finger, for instance, loss of function is to be com pensated. Similarly, when the scar tissue in the lung interferes with its function to the point that one becomes disabled, then compensation is due. Concisely, silicosis is to be compensated for only when dis ability is present. Evaluation of Disability.--But upon what basis is disability to be evaluated or its extent determined? Two men may present comparable results from physical examination, as well as almost identical tc-ray pictures, yet one claims no disability and the other does. Not only physical examination but also history, roentgen-ray studies, exercisetolerance tests, and estimations of cardiac and respiratory efficiency have been suggested as measuring rods. Mayer9 states that pulmonary function may be disturbed in one of three ways: (a) in ventilation, (b) in gas exchange, and (c) in pulmonary circulation. Testing Ventilation.--Ventilation is tested by calculating the vital capacity and multiplying this by the highest rate per minute of respirations which the patient can accomplish. Pulmonary fibrosis associated with emphysema interferes with the capacity of the lung to inflate and deflate. There results an increase in minute volume of ventilation, while at the same time maximal breathing capacity is reduced. Testing Gas Exchange.--The gas-exchange test, with the use of a spirometer, estimates the oxygen intake and the carbon dioxide out put. According to Mayer, it is expressed in the following three ways: () Oxygen Debt.--This is the amount of excess oxygen the nor mal person needs at the end of exertion. It usually takes from one to two minutes to recover the oxygen necessary to relieve dyspnea. Decompensation of the gas-exchange mechanism is evident when the recovery period is longer than three minutes. () Oxygen Deficit.--This is revealed by the excess intake of oxy gen utilized when the patient shifts from air to oxygen inhalation. This is a sign of latent oxygen want, which may be present at rest. It is found, despite full oxygen saturation of the blood, in pulmonary diseases bordering on decompensation. (c) Oxygen Unsaturation.--Oxygen unsaturation of the hemo globin of the arterial blood, as determined by gas anaylsis, is found in disturbed gaseous exchange. Normally the oxygen saturation of arterial blood is about 95 per cent; saturation below 93 per cent indi cates anoxemia, a sign of deficient oxygen supply. Testing Pulmonary Circulation.--Pulmonary circulation is tested by the use of either dehydrochloric acid, sodium cyanide, or calcium, determining the circulation time from arm to arm, arm to tongue, or arm to lung. Intravenous infusion of 1000 cc. of fluid, followed by a 320 OCCUPATIONAL DISEASES study of its effect on the venous pressure and vital capacity, reveals loss in reserve of the pulmonary vascular bed by the proportionate rise in the venous pressure and decrease of vital capacity. Congestive heart failure was observed to be a common occurrence in cases of far-advanced anthracosilicosis by Giering and Charr10 among the hard-coal miners of eastern Pennsylvania. They attempted to determine whether dyspnea in these cases was of cardiac or pul monary origin by studying the vital capacity, the venous pressure, and the velocity of pulmonary circulation. Of twenty-five miners studied, two showed by roentgenograms evidence of heart enlarge ment, while secondary polycythemia and reduction of vital capacity were frequent. No appreciable variation between the normal venous pressure and pulmonary and complete circulation time was noted. Electrocardiograms in the majority of instances showed myocardial damage. There is no question but that the procedures employed by Mayer, Giering and Charr, and others constitute an advance step in the at tempt to better evaluate the disability of the silicotic, but the method is too elaborate and complicated for the average physician. A routine use of these methods by a special examining board might, after a period of time, produce some acceptable standards of measurement. Until then, the question remains largely a matter of clinical judgment. With or without the use of these tests, the examiner must rule out as a partial or complete cause of dyspnea, such conditions as unrelated respiratory disease, unrelated cardiac disease, or mechanical blockage to normal respiration, such as occluded nasal passages, nasal polyps, sinusitis, and the like. Illustrative Cases: Case I.--A thirty-six-year-old Mexican female presented herself to the community surgeon who did the first-aid surgery for a soap manu facturer. Her complaint was that about six months previously she first noticed shortness of breath, which progressed until at the time she was markedly dyspneic on the least effort. Following examination, she was told that she had a bad heart. Digitalis was prescribed and bed rest ordered. Eight months later her employer referred her to this clinic. History taken here revealed that she had worked for fourteen years in abrasive-soap factories. Her :u-ray films showed a bilateral involvement of the lungs with a wide spread discrete nodulation of varying density and size, with fuzziness of the borders and areas of coalescence. In addition to shortness of breath, she complained of chest pains. There was no loss of weight or fever. Subsequently chest pain was increased and there was a notice able weight loss. No tubercle bacilli were found. SILICOSIS 321 This girl went for over eight months without an accurate diagnosis and. therefore, without compensation to which she was entitled. Her first physician failed to take an accurate occupational history or .r-rays. The case was compensable, and she was placed on total dis ability. Case II.--A man fifty-nine years of age, who had been in the em ploy of a monument company for twenty-six years, was discharged when a physical examination, required of all employees of the com pany by its new insurance carrier, showed that he had silicosis. The worker contended at that time, however, to the examining physician that he was all right and could continue to do his work. Subsequently he instituted proceedings under the Wisconsin Workmen's Compen sation Act before the Industrial Commission. An examiner for the commission found that the man was suffering from silicosis in an ad vanced stage, caused by the exposure in his employment and that since as a result he was incapable of more than slight physical exertion and could be employed only in occupations which involved so-called "light" work, he was 50 per cent disabled. The Industrial Commission confirmed those findings and awarded compensation accordingly. From a judgment of the circuit court for the county, affirming the award, the employer and his insurance carrier appealed to the Supreme Court of Wisconsin. In general, the Wisconsin Workmen's Compensation Act provides for compensation for such disability, whether resulting from acci dental injury or from occupational disease, arising out of and in the course of employment, which results in a wage loss. The appellants seem to have contended that the man had suffered no wage loss. Wage, answered the Supreme Court of Wisconsin, is dependent on two fac tors, time and rate of compensation. In Zurich General Accident and Liability Insurance Company vs. the Industrial Commission, 203 Wis. 135, 233 N. W. 772, this court held that a worker who was transferred from a place of exposure to outside work at a diminished wage suffered a wage loss; that is, his rate of compensation per unit of time was diminished. The real source of difficulty, the Supreme Court continued, in silicosis cases is that many men suffering' from the ailment in some of the various stages are able to, and do continue to, work and receive full compensation therefor long after they have sustained what has been referred to as a medical disability, but what might be more properly referred to as a pathological disability, and therefore as a matter of fact sustain no wage loss. It is because the legislature has so far seen fit to withhold compensation for physical impairment which does not immediately result in the physical incapacity of the claim ant to work that the difficulty in these cases springs. There is a feel- 21 322 OCCUPATIONAL DISEASES ing that a person who has sustained loss of physical vigor and had his system invaded by foreign substances, which may and often do result in impairing his ability to work and not infrequently in death, should have compensation. If, however, the legislature had intended the term "disability" to embrace so-called "medical" or "pathological" disability as distinguished from actual physical incapacity to work, it would un doubtedly have said so. "This court," continued the Supreme Court, "has previously held that the injury or wage loss to be compensable must be sustained at a time when the relation of employer and employee existed. An amend ment to the Workmen's Compensation Act adopted thereafter {Laws, 1933, c. 314. Sec. 27) provides that the time of injury or the occur rence of disability shall be deemed to be the last day of work for the last employer whose employment caused the disability. This obviously refers the time of injury or disability back to a point in time when the employer and employee relationship existed. Even if a plant shuts down, and an employee is discharged and is not thereafter employed, if he is thereafter disabled, the time when his disability occurs is referred to as the last day of employment which caused his disability. In the case at bar when it is considered that admittedly Marsz is suffering from silicosis; that as a result of it he is incapable of more than light physical exertion; that by reason of his physical incapacity he can be employed only in occupations which involve so-called light work, this court cannot say that there is no evidence to sustain the finding of the Industrial Commission that Marsz has sustained a wage loss, which, measured by the rate of compensation he had theretofore received, amounts to 50 per cent."11 The award in favor of the worker accordingly was affirmed. This case is recited here to show the legal phase of silicosis and wage loss. Case III.--The workman's employment subjected him to the dust of burnt clay and other vitrified products disseminated by machines used in the manufacture of china, and to silica dust raised by sweep ing. In 1927, after several years of employment, he developed a cough. He became chronically tired and weak. The employer discontinued business in November, 1933, but at that time the workman did not consider his condition serious enough to require medical attention. The following February a physician diagnosed the workman's condi tion as due to a slight temporary inflammation of the lungs. In March, when the patient was treated for injuries from an automobile accident, the physician discovered a tuberculous condition. In May, following roentgen examinations, his condition was diagnosed as pulmonary tuberculosis activated by silicosis. Attributing the silicosis to his former employment, he instituted proceedings for compensation under SILICOSIS 323 the California Workmen's Compensation Act. The Industrial Accident Commission dismissed his claim on the grounds that it had not been filed within six months after the date of injury, as required by the Workmen's Compensation Act. The worker then appealed to the Dis trict Court of Appeal, Second District, Division 2, California. "In cases of the character under consideration," said the District Court of Appeal, "the date of injury, in computing the limitation period set forth in the Workmen's Compensation Act, is not the date of any particular exposure to the hazards of the employment, but the time when the accumulated effects culminate in a disability traceable to the latent disease as the primary cause, and by the exercise of rea sonable care and diligence it is discoverable and apparent that a com pensable injury was sustained in performance of the duties of the employment." 12 In the case cited, the court disapproved the holding of the Com mission that the statute of limitations began to run as of the date the employee first was disabled and indicated that the running of the prescribed period began when the presence of silicosis was, or should have been, diagnosed as the primary and efficient cause of the injury. "It appears quite obvious," said the court in the present case, "that the claimant, from the inception of his cough until he received the roentgen report in May 1934, had no reason to believe he was suffer ing from a compensable injury, silicosis, arising out of his employ ment. Even his visit to a physician in February 1934, disclosed nothing further than the given diagnosis of a slight inflammation of the lungs from which a speedy recovery was assured. "An employee," continued the District Court of Appeal, "is not to be deprived of compensation because he incorrectly diagnoses his condition." The commission in this case found that the claimant should have discovered the character of his condition prior to the date of his final termination of work. "Such a finding," concluded the District Court of Appeal, "is without support in the evidence. It is wholly unreasonable to argue that the worker should, through the exercise of reasonable care and diligence, have known in November, 1933, that which his medical adviser did not discover in February, 1934. " The court accordingly ordered that the award of the commis sion dismissing the claimant's claim be set aside and that the com mission proceed with the determination of the claim.13 The above case from the J.A.M.A.14, illustrates the legal viewpoint in one state regarding the period in which a claim for compensation due to silicosis may be filed. This court intimated that if the claim ant had known or had been informed that he had silicosis and had failed to file for compensation within the six-month period, then the statute of limitations would have held. 324 OCCUPATIONAL DISEASES Case IV.--A foundry company had to reinsure its employees. The prospective insurer demanded as a condition precedent to the execu tion of a policy that all employees be examined by a physician se lected by it. Before the examination was made, all employees were discharged. Only those were reemployed who were believed to be physically fit for the duties to be imposed upon them. Five employees who were not reemployed, because they were not physically fit, were awarded compensation by the Industrial Commission, under the Wis consin Workmen's Compensation Act. Thereupon their employer and its insurance carrier brought actions against the commission and the several claimants to set aside the awards. From a judgment modifying and affirming the award in each case, the Industrial Commission, the several claimants, the employer, and the employer's insurance carrier all appealed to the Supreme Court of Wisconsin. The Supreme Court based its decision on the case of one claim ant, as the same questions were involved in all cases. This man, before he was discharged, had worked steadily. He was not aware that he was suffering from any disease. The physical examination, however, showed that he had had silicosis for probably five years or more and was in the second stage of that disease and that tuberculosis had already devel oped. Although at the time of the examination he was able to perform his work, his chance of recovery would be diminished if he remained in the dusty employment in which he had been engaged. Reexami nation three months later showed that his ability to do work requir ing physical exertion was greatly diminished, if he could be said to be able to do it at all. Nevertheless, his employer and its insurance car rier contended that he had suffered no compensable injury in the course of his employment with his employer. "Disability within the meaning of the statute," said the Supreme Court, "occurs when an employee is disabled from rendering further service; that is, when he no longer has physical ability to perform his work in the usual and customary way. Unless he is so disabled he sus tains no compensable injury even though in the course of his employ ment he is subjected to conditions that contribute to disability as an end result. The right of an employee to compensation depends on whether or not, in the course of his employment and because of it, an occupational disease renders him incapable of performing his cus tomary work. ... It has been argued that if an employee is entitled to compensation, as he is when he voluntarily ceases work because of physical incapacity to continue, then an employee who is discharged by his employer because of potential physical disability is equally en titled to compensation. For the latter contingency, however, the pres ent law, which was framed to cover injuries resulting from accident, rather than incapacity resulting from occupational disease, affords no relief. An employee who has been exposed to industrial hazards, who has suffered no 'physical disability that prevents his performing his SILICOSIS 325 work in his usual and customary way, and who is discharged because an examination discloses that such disability may arise in the future, is not entitled to compensation for medical disability." It has been argued that it is against public policy to permit an em ployer to discharge an employee who has been exposed to industrial hazards, in order to anticipate his employee's future disability. "That, however," said the Supreme Court, "is a problem for the legislature and not for the courts. The courts can do nothing more than interpret and administer the statute. The remedy lies solely with the legisla ture." Finding no evidence to show that the claimants suffered dis ability within the meaning of the law during the period of their em ployment with the foundry Company, nor until after the relation of employer and employee had been terminated, the judgments of the courts below in the several cases were reversed and remanded with in structions to enter judgments setting aside the awards of the Indus trial Commission.13 Case V.--The plaintiff, a workman, in the course of his employ ment as a grinder in the defendant company's grinding department, operated emery wheels for a period of five years. Later he sued the company at common law, alleging that, because of the company's failure to fulfil its statutory duty of supplying adequate exhaust fans and sufficient ventilation, he had contracted ". . . the occupational disease of silicosis as a result of inhaling ... a quantity of steel, ascoloy, and carborundum dust." From a verdict in favor of the plaintiff and a judgment denying the defendant's motion for judgment notwith standing the verdict, the defendant appealed to the Supreme Court of Pennsylvania. The Workmen's Compensation Act of Pennsylvania provides that it shall apply to industrial accidents within the commonwealth. It defines the terms "injury" and "personal injury" as meaning "only violence to the physical structure of the body, and such disease or infection as naturally results therefrom." The defendant company con tended: (1) that the plaintiff had sustained an occupational disease, for which no compensation was provided in the Workmen's Compen sation Act; and (2) that he was barred from bringing an action at common law, because silicosis causes "violence to the physical struc ture of the body," thus making the plaintiff's condition an "injury" within the meaning of that act for which the act provided no com pensation. "The Workmen's Compensation Act," said the Supreme Court, "must be interpreted as if to the phrase `violence to the physical struc ture of the body' there was added the phrase `when said violence was due to an accident'; the Act does not apply to all cases in which work men receive injuries which do `violence to the physical structure of the body.' " Every disease affecting human beings is pathologically an 326 OCCUPATIONAL DISEASES alteration of the normal, healthy condition of the human body and as such involves some degree of "violence." The word "violence," how ever, in common usage connotes a vehement application of force and is not ordinarily used to characterize the progress of a disease. "Con ceding," continued the court, "that diseases such as tuberculosis and silicosis may involve `violence' in some degree to the `physical struc ture of the body,' a workman who has contracted the disease in the course of his employment docs not come under the Workmen's Com pensation Act unless that disease had its origin in an injury by acci dent, and occupational diseases do not so arise. In the opinion of the court the plaintiff could not have maintained an action under the Workmen's Compensation Act because he had not sustained a com pensable accidental injury." The Supreme Court was unable to agree with the defendant's contention that in Pennsylvania no action lies at common law for an occupational disease. Even though the Workmen's Compensation Act provides no compensation for such a disease, it cannot be said that the employee must assume the risk and cannot resort to his commonlaw remedy to secure damages provided the disease, whether occupa tional or otherwise, arose from the employer's negligence. The court concluded that the workman had a common-law right of action against his employer for injuries caused by a disease contracted in the course of his employment and owing to the negligent conduct of his employer in violation of a statutory duty. Accordingly, the Supreme Court affirmed the judgment in favor of the plaintiff.10 This is an example of the disputes which frequently occur in those states which have no special occupational-disease schedule regarding the term "injury." (Pennsylvania has since enacted an occupationaldisease schedule.) In the above case no mention is made as to whether or not the patient actually had silicosis. Case VI.--A forty-one-year-old male had been an electric welder for sixteen years. In June, 1937, he fell, striking his chest wall. rc-Ilays revealed no fractured ribs but did show unusual markings in the lung field. His physician informed him that he had silicosis, which the pa tient promptly reported to his employer. When seen by us he had no complaints; his past medical history was negative, and his physical findings the same. a;-Rays of the chest showed nodular shadows which resembled modified silicosis. The patient was informed that he did not have silicosis and that there existed no compensable condition. Examination of his employ ment condition revealed that he had never worked in a confined area and that he inhaled no appreciable amount of dust, but rather the SILICOSIS 327 fumes only from the welding process. This patient had inhaled par ticles of iron oxide which were responsible for the markings noted by the ,-r-ray. Iron deposits (free from silica) cause no functional im pairment of the lungs, no symptoms, or susceptibility to complicating infections. Case VII.--On July 3, 1940.1 examined a sixty-one-year-old miner at the Mojave, California, Hospital, who was in the employ of a min ing company. He had been a timberman for twenty-eight years, eight een of which were spent in a gold mine, and ten in copper mining. His past medical history was not significant. He first noted some short ness of breath in January, 1940, which was not disabling. About June 1, this dyspnea increased to the point where he was forced to quit work. Three weeks later he entered the Mojave Hospital with marked dyspnea, ascites, and edema of the ankles. When seen by the writer he was in the terminal stages of what appeared to be myocardial insufficiency. Propped up in bed, he was markedly cyanotic and dyspneic. Respirations were rapid, shallow, and with little movement of the chest cage, which was of the huge barrel type. Percussion of the chest was dull, and auscultation re vealed many large mucous rales and what appeared to be terminal rhonchi. These excluded any other findings which might have been present except a friction rub in the left posterior base. The heart rate was 120, tones almost imperceptible; and the blood pressure was 110/90. (It was recorded at 160/100 on admission.) The abdomen was distended with fluid, the genitalia edematous, as were the ankles. He died ten hours after this examination. No ar-rays or laboratory inves tigation had been done. The details of the autopsy will be omitted. The anatomical diag nosis was: acute, purulent tracheitis and bronchitis; bilateral pneu monitis; moderately advanced silicosis; enlargement of the right ven tricle of the heart; chronic passive congestion of the liver, spleen, and kidneys; and moderate generalized arteriosclerosis. It was not possible to determine the extent of the silicosis roentgenologically since no films were taken. It appeared to this examiner that the course of events was a rapidly progressive myocardial fail ure, followed by a complicating pulmonary infection which could not be handled by the patient, owing to his heart condition and also to the existing deficient pulmonary aeration. To what degree the sili cosis entered as a cause of death it would be impossible to state, but it was considered a factor in preventing recovery and, therefore, the death was held to be compensable. Case VIII.--Two weeks after the death of the workman referred to in Case VII, a forty-three-year-old miner, employed by the same 328 OCCUPATIONAL DISEASES mining company, reported to the clinic alleging silicosis. He was well acquainted with the details of the preceding case. He claimed that six months prior to the date of examination he had noted shortness of breath, cough, and lassitude. During these six months he thought he had lost twelve pounds. For the past two months the dyspnea had increased to the point where even slight exertion caused shortness of breath. His past medical history was essentially negative, and there was no family history of tuberculosis. Occupational History.--The patient's mining experience consisted of about nineteen years of copper-mining in Arizona, four years in gold-mining, and about four years in gold-prospecting. Fig. 52.--A, Advanced silicosis of a gold-miner referred to in Case VIII. While a co-existing infection appeared likely, tuberculosis was not proved to be present. B, A schematic drawing of third-stage silicosis or silicosis with conglomerate shadows and coalescent nodules. The medial aspect of each lung is especially heavy because of the hilus shadows and the extension of the bronchus in addition to the conglomeration. The first consequence of dust inhalation as seen by s-ray examination occurs in the hilus and adjacent portion. The markings proceed mostly downward and outward and have been purposely exaggerated by this drawing to emphasize this. Physical Examination.--The heart and lung findings were not sig nificant, and the entire examination was essentially negative. Labora tory investigation failed to disclose any evidence of tuberculosis. Elec trocardiogram normal. Stereo rr-ray films showed moderately advanced silicosis (Fig. 52). This case is included owing to the interest provoked by the occu pational exposure. The x-ray films disclosed silicosis to an extent not to be expected in one whose exposure was apparently for only about four years. Furthermore, this four-year exposure was in a mine where a wet process is maintained, and recent dust counts did not indicate a SILICOSIS 329 harmful concentration; and also, the patient wore a respirator. In this regard, it is interesting to note what Dr. Porter Miller, of Los An geles, wrote regarding this patient and his exposure. Dr. Miller17 saw this patient two days after the completion of my examination, and commented as follows: The exposure in this case is interesting. The applicant began min ing in 1914 and has been at it ever since. There were periods when he would be off work and during the interim he would be prospecting. I feel that in the past, too little attention has been directed towards prospecting as a contributing factor in the development of silicosis. It is the general belief that if a man is above ground, or at least not deep within the ground, that the exposure is more or less minimum. In that I would take issue. In the first place, this is all dry mining and we know that Mojave and 29 Palms is a very dusty area, due to the winds which constantly keep the dust in circulation. If a man is con yf stantly digging in the earth's crust which normally contains sixty per 'I cent silica, is it not reasonable to assume that this is quite a factor? I would refer the reader to the United States Public Health reports 50, 1369-1385 (1935), by Brown, Gottlieb, and LaBroun, and their report upon dusty conditions in the dust bowl, which as you know, would be more or less parallel to the man who might be prospecting. It was their findings that during the dust storms silica was present in the air in from 67 to 93 per cent, and they also stated that this would provoke pathologic changes if the exposure was continued long enough, and particle size was fine enough. It would seem that the exposure while prospecting, assuming conditions to be dry, would be equally as great as in a mine where working conditions are regulated, and men have access to respirators, and wet methods and ventilation processes are used to a maximum degree. I cannot refute, or concur in, what Dr. Miller observes. This is the first claim ever presented to me wherein prospecting might be con sidered a factor of exposure; nor have I ever read any comments else where on this point. While it may be true and worthy of consideration, it appears to be a dangerous assumption without knowing the details of the prospecting, the type of dust encountered, the concentration, and a serial study of other prospectors' lungs. An award was made in this case by the Industrial Accident Com mission of California. Case IX.--A twenty-four-year-old male entered a claim for dis ability after being told by his family physician that he had "dust tuberculosis." Upon being referred to our clinic he brought with him a letter from his physician which stated that he had "arrived at this 330 OCCUPATIONAL DISEASES diagnosis after consideration of the patient's symptoms, occupation, and films of the lungs." Briefly, the history was as follows. For the past six months the patient had noticed a loss of weight, increasing fatigue, shortness of breath, cough, and occasionally some blood in the sputum. When closely questioned, he recalled that just prior to this decline he had suffered an attack which he thought was "flu" but for which he did not consult a doctor. His past medical history revealed measles at the age of fourteen, complicated by rheu matic fever. The patient had been engaged as a sprayer for a concrete emulsion company for the five preceding years. This work consisted of first applying an adhesive paint to the facing of buildings which was then quickly sprayed with a 25-mesh silica dust. Then following a repaint ing of adhesive substance, black mica of 80 mesh was rapidly sprayed upon the surface. The workmen wore respirators. Physical Examination.--Temperature 99.4 F.; tonsils cryptic and red, anterior pillars injected. Lungs were normal except for evidence of congestion at both bases. Heart was slightly enlarged, with the apical impulse noted upon inspection. Auricular fibrillation was pres ent, with a diastolic murmur at the apex. The blood pressure was low. Laboratory Findings.--Blood count showed a mild anemia with a leukocytosis of 14,300 v'hite cells. Sedimentation rate increased. Urine showed slight albumin with occasional red blood cells. Repeated spu a tum examinations revealed no tubercle bacilli. Electrocardiogram not done. Stereoscopic films of the lungs show'ed no evidence of tubercu losis or silicosis. The a;-ray film taken by the patient's family physician was a single anteroposterior view, which was greatly overdeveloped and valueless for interpretation. Subsequent stereo views denied the evidence of either tuberculosis or silicosis. The history of rheumatic fever when younger, and a recent exacerbating illness followed by typical findings, resulted in a diagnosis of rheumatic heart disease (mitral stenosis with auricular fibrillation). Foregoing any censorship of the family physician for assuming a "dust tuberculosis" to be present because of the symptoms and occupation, this case is cited in order that it may be emphasized that good roentgenological technique should be em ployed in the filming of suspected silicotic patients, and that these films be interpreted by a roentgenologist or someone experienced in I silicosis. This case was not compensable. ( Case X.--A sixty-four-year-old male reported to his physician be f cause of shortness of breath. Although retired at this time, he had been engaged at intervals in hard-rock mining for a period of approxi I mately twenty-four years. He was cognizant of the effects of silicosis c i % i i l \ SILICOSIS 331 and stated honestly to the examining physician that he. believed his difficulty was due to this disease. His family doctor had informed him that there was only one way to determine the presence of silicosis, that being by x-ray. Accordingly, the patient was referred to a roent genologist who reported that the films showed first-stage silicosis. ' Upon the reception of this report, the patient was informed by his / physician that the dyspnea was due to silicosis. The man, therefore, ; entered his claim for compensation. Fig. 53.--Advanced first-stage or early second-stage silicosis. As mentioned in Case X, patient had arteriosclerosis with hypertension and mitral heart disease. His mild dyspnea on effort was thought to be cardiac in origin. Past Medical History.--The past medical history was entirely negative other than for rheumatic fever at the age of twenty. The patient had maintained his weight for over fifteen years. Physical Examination.--The physical examination of this patient revealed a long, thin chest, not barreled or emphysematous in type. There was no restriction of the respiratory excursion. Auscultation of the lungs revealed no rales or other adventitious sounds. The heart showed a marked mitral stenosis. Blood pressure, 180/100. Generalized i. 332 OCCUPATIONAL DISEASES arteriosclerosis. Albumin and casts in the urine. Mild second-degree anemia. Negative blood Wassermann. The x-ray films confirmed the previous report of first-stage silicosis (Fig. 53). The first physician consulted by this patient never examined him. He correctly stated that the x-ray was the best means of determining the presence or absence of silicosis. When he received the report that first-stage silicosis was present, he informed the patient that this was the cause of his dyspnea. He instituted no search for a cause of the dyspnea and falsely assumed that dyspnea can result from early sili cosis. The diagnosis was mitral heart disease, with generalized arterio sclerosis and first-stage silicosis. The patient was denied compensation on the basis that his disability was due to his heart disease and that first-stage silicosis causes no disability. Case XI.--Collins reviews a case reported by Lovelock18 of a man who had mined steamcoal for twenty-two years in South Wales. He was admitted to the Brompton Hospital for chest diseases, with a diagnosis of tuberculosilicosis. No tubercle bacilli were found, and x-rays raised doubt as to the diagnosis. He was transferred to St. Mary's General Hospital. He lost ground and finally died, but before death, an enlarged liver had indicated the presence of carcinoma. Ex amination revealed anthracosilicosis of both upper lobes and apices, together with carcinoma of the right lower lobe bronchus. A guineapig injected died of generalized tuberculosis. A silica content of the lungs was between eight and nine times normal, amounting to 2.83 per cent in fresh lung and 12.43 per cent in dry lung. This case during life presented great difficulties in diagnosis, and after death raised legal difficulties regarding the claims of the dependents for compen sation because of the industrial origin of the cause of death. Case XII.--A twenty-nine-year-old male had been employed in a pottery works for six months, when in September, 1939, he developed a fever, cough, and pain in his chest. After the patient had been in bed for five days, his physician had the patient's chest x-rayed, and informed him that he had silicosis. The insurance carrier sent the pa tient to this clinic. When seen six weeks after his acute episode, he complained only of occasional pain in the chest. The history revealed that as an inspector he walked through rooms where there was an atmosphere containing 40 per cent silica. He wore no respirator. It was estimated that the total hours spent each day in this atmosphere were three and that the total number of hours during his entire em ployment were ninety. His physical examination, except for enlarged tonsils, was negative. The x-ray films were entirely negative for any type of lung pathology. By actual count there were five small, indis tinct nodules scattered throughout the entire lung field. It was prob- SILICOSIS 333 able that these findings led the physician to assume that silicosis was present. This case has no value except to show the cost of faulty interpre tation. The patient was sure he had silicosis because his "physician said so." He would not accept our diagnosis and took his case to the Industrial Accident Commission, where it was denied. The procedure Fig. 54. Fig. 55. Fig. 54.--This film reveals irregular linear and nodular infiltration involving the greater portion of the upper half of the left lung; also involvement of the right apex. There is a thin-walled cavity, 3 by % cm. in the greatest diameter, at the left apex. There is obliteration of the right coslophrenic angle. The x-ray picture indicates moderately advanced pulmonary tuberculosis. Clinical investigation confirmed the diagnosis. This twenty-seven-year-old Mexican claimed compensation because he had been diagnosed as having pneumoconiosis as a result of operating at intervals, over a five-year period, a carpet-making machine in an atmosphere laden with heavy dust. Fig. 55.--Very early silicosis with questionable apical tuberculosis. This twentynine-year-old male had helped his father prospect for gold at intervals during his youth. He had actually mined gold for a combined period of about one year. He sought compensation in California after being turned down by the Canadian govern ment when he sought to become an aviator in their air force. He had no symptoms of tuberculosis or silicosis. Physical examination and laboratory investigation failed to reveal evidence of tuberculosis. The film is used here to demonstrate the earliest stage of silica deposition in the lung tissue. cost time and money. An accurate diagnosis in the beginning would have prevented this wasteful expenditure. Similar cases are rather frequent. Tuberculosis, cardiac decompen sation, asthma, emphysema, pleurisy, and various forms of pneu monitis are attributed to silicosis in instances where no silicosis ex ists and where the occupation does not involve free silica. The cost to industry where large awards were made is well known, but it is im possible to estimate the aggregate cost of these frequent, unfounded 334 OCCUPATIONAL DISEASES claims which are daily presented to the Industrial Accident Commis sion because of faulty medical opinion when the patient is first seen. Only when the basis for diagnosis, as previously outlined, is adhered to by the practicing physician will this cost be minimized (Figs. 54, 55, 56, 57). Case XIII.--The details of the clinical aspects of this case will not be given since they are not of essential interest. Suffice it to state that an adult male, who had been employed for a number of years, entered a claim for a permanent disability due to a "dust disease of the lungs." The physical examination did not indicate any disability of pulmonary origin. The ic-rays revealed an old, healed, left apical tuberculosis, but no evidence of pneumoconiosis. Fig. 56. Fig. 57. Fig. 56.--Advanced silicosis in a retired fifty-nine-year-old male, who had spent twenty-eight years as a gold-miner. He presented himself at this clinic for treatment of arthritis. His only symptom referable to silicosis was that of mild dyspnea follow ing effort. Fig. 57.--Advanced silicosis in a fifty-seven-year-old male, who had spent thirty years in gold- and copper-mining. Patient complained of mild dyspnea with gradual loss of weight. Tuberculosis not proved to be present. Died of cancer of the bowel. It was recognized that the process in which the claimant was engaged involved the grinding of materials which did contain silicates, but it was also believed that there existed no exposure to free silica. The operation consisted of grinding the barytes obtained from Battle Mountain, Nevada, and bentonite procured from a district east of Daggett, California. To the writer's knowledge, these substances had never before been on trial as a cause of silicosis. In the years of its existence the de fendant company had not been confronted with a similar claim. SILICOSIS 335 Chemistry of Minerals.--A chemical analysis of each follows: Table 14--Typical Analysis of Baiiite Ground A I' LOS ANGELES Percentage by Weigh BaSO., ........................................................................................ BaC03 ...................................................................................... Fe208+Al.,08 .......................................................................... SiOo ............................................................................................ CaO ............................................................................................. Moisture .................................................................................... 91.50 0.50 0.75 6.50 Trace 0.10 99.35 Table 15--Typical Analysis of Hector Mine-Run Bentonite Percentage by Weight Silica (Si02) ............................................................................ Alumina (AloOg) ................................................................... Iron oxide (Fe203) ............................................................... Titanium dioxide (Ti02) ....................................................... Calcium oxide (CaO) ............................................................. Magnesium oxide (MgO) .................................................. Sodium oxide (Na20) ........................................................... Potassium oxide (K2d) ......................................................... Moisture at 105 C.................................................................. Combined water and volatile .............................................. Carbon dioxide (C02) ........................................................... Sulfuric anhydride (S03) .................................................... 31.50 7.21 0.11 0.12 21.42 9.05 6.36 0.65 2.93 4.07 16.42 Trace 99.84 Barytosis is chiefly mentioned in the foreign literature. Fifty cases of pneumoconiosis among workers in the barite mills in Italy were re ported in which the pneumoconiosis presumably did not tend to cause tuberculosis, but rather acute forms of lung affection. The American literature is practically devoid of any mention of barytosis, although Lanza reproduces an tr-ray film showing diffuse, discrete nodulation in a person who worked in barium rock. In view of this to seek all aid available. Dust counts had already established the fact negligible aid from the literature and because the defendant desired to have some concrete evidence against future claims, it was decided that the atmosphere in which the claimant worked was one in which the concentration of the dust was well within permissible limits. x-Ray Diffraction Analysis.--It was decided to submit samples of the bentonite and barytes to Ernst A. Hauser, of the Massachu setts Institute of Technology, for rc-ray diffraction analysis. These samples were: (1) composite Hector mill-run bentonite; (2) com- 336 OCCUPATIONAL DISEASES positc El Portal mill-run barytes; (3) typical Battle Mountain, Oak land, grind barytes; and (for the purpose of comparison) (4) a quantity of Ottawa sand, which is quite pure quartz. To these, also for comparison. Dr. Hauser added a standard pure quartz from his own stock. At the end of his investigation, he reported no evidence of uncombined silica in the samples submitted except that the El Portal barytes "might be faintly contaminated with uncombined silica, but Ottawa -5av*> Fig. 58.--A, x-Ray diffraction of sample quartz used for a standard. Arrows at left of film indicate the heavy silica line. B, A ground silica, about 2 /t in diameter, also used as a standard. C, Ottawa sand, a silica of average 30 n diameter. D, Cali fornia magnesium type bentonite. E, Nevada Battle Mountain barytes (Oakland grind), --325 mesh. F, California barytes, --325 mesh. according to the pattern, the amount of free silica was not over one per cent." This report of Dr. Hauser's offered substantial evidence of the negligible amount of silica present in this grinding process (Fig. 58). A scientific description of this method of detecting the crystalline state of solids is not within the scope of this book, nor is the author capable of detailing such a process. If interested, the reader will find an adequate description of this method in Applied. X-Ray}9 However, SILICOSIS 337 certain elementary facts deserve mentioning. Prior to the use of .r-rays, a knowledge of the crystalline state of matter was limited to the ob servations gained from the appearance of crystals through the use of the microscope and optical goniometers. The external appearance re vealed crystals to be either single entities, with pairs of parallel sur faces, disposed in definite geometric fashion at angles which could be measured, or aggregates of these single crystals. But the internal structure of these substances remained a mystery, although external arrangement suggested a similar, regular internal arrangement. x-Ray analysis now shows that such a regularity does exist in practically every solid substance. A knowledge of the planes is a prerequisite for the understanding of the structural arrangement of these solids-- faces, angles, reflection planes, the unit cell, space groups, space lat tices, and many other phases, including the crystal systems, triclinic, monoclinic, orthorhombic, tetragonal, hexagonal, and cubic. On first thought, the x-ray analysis of the structure of solids may appear as having extremely limited value, as most of us in medicine have con sidered the x-ray only as an adjunct to the study of pathological proc esses. Yet industry is using the x-ray to determine the strength of steel, the corrosion of alloys, the wearing properties of metals, the covering power of pigments, defects in material such as gas cavities, blowholes, cracks, shrinkage, porosity, and the like. x-Ray Diffraction Principle,--The principle of the diffraction method is as follows-": When a beam of monochromatic x-rays is directed toward a finely divided crystalline substance, some of these x-rays are diffracted. If these diffracted x-rays come into contact with a photographic film, a definite pattern is produced and a reference point is formed by the undiffracted and unabsorbed x-rays that pass through the material. The diffraction pattern produced is governed by the nature and arrangement of the atoms in the crystalline material; that is, by the crystalline structure. All evidence so far obtained indicates that no two crystalline sub stances give the same pattern, which in a sense, is the "fingerprint" of the substance. The x-ray diffraction pattern, therefore, serves as a method of identifying crystalline substances. According to the technique developed by Clark and Reynolds21: A pure crystalline powder, known not to be present in the dust being examined, is added to the unknown in a definite ratio and the diffraction pattern registered. The ratio of the density of a line sought to that of a nearby line of the added standard is determined protometrically. The ratio thus obtained is proportional to the line in tensity of the substance sought, which in turn is proportional to the amount of the substance in the mixture. By reference to a curve that 338 OCCUPATIONAL DISEASES is prepared empirically from mixtures of known composition, the per centage of the constituent sought is obtainable at once. Fig. 59 shows the pattern for a typical dust sample compared with a standard pat tern for ordinary quartz. This method, of course, is applicable to the determination of any selected mineral constituent. It is to be appreciated by the reader that the problem in our case was to determine whether or not the claimant was subjected to a silicate-free silica mixture, and if free silica was present, to what ex tent. Some time after our investigation of this case, Louis H. Berkelhamer, of the Saranac Laboratory, reported additional applications of the .r-ray diffraction method. He compares the values of the spec troscopic, chemical, petrographic, and a--rav diffraction methods of analysis in determining the presence of quartz in a given material. According to Berkclhamer22: Spectroscopy is of little value in this instance. Although it can be employed on very small samples, it demonstrates only the presence of the element silicon. By the unaided chemical analysis silicon dioxide is determined without the qualification as to the original state of the silica. Differential solution methods allow for an empirical estimate of quartz, but variations in particle size of the fine quartz fraction have so much influence upon its rate of solution that the results are not always reliable. A petrographic examination permits direct identi fication of quartz and when combined with a chemical procedure, offers a satisfactory means of determining quartz. Petrographic methods, however, are difficult to apply to particles less than 5 p in diameter, and it is particles 3 p and under that are of the greatest pathological significance. In this extremely small particle size range petrographic analysis must give way to x-ray diffraction. Berkelhamer's report is of significant value in that it reveals the application of the various methods of analysis just mentioned to an individual case. A twenty-scven-year-old colored male, who had mined pyrophyllite in North Carolina for twelve years, died and the diag nosis was silicosis resulting from the inhalation of pyrophyllite dust. Petrographic study of hand samples was unsatisfactory since pyro phyllite resembles sericite and talc. (By .r-ray diffraction, the identifi- SILICOSIS 339 cation was relatively simple.) Chemical analysis of the dried lung was made, and the pulverized lung tissue was subjected to the rr-ray diffraction test. But most interesting of all was the analysis of a 67/ tissue section by .r-rav diffraction, thus identifying the minerals pres ent ".. . in the very section of tissue that the pathologist had studied." This case is cited to call attention to a recently discovered type of investigation. It is not likely that the .r-ray diffraction method will - / be used in the ordinary claim for silicosis, but on occasion the phys ician, investigator, or medicolegal consultant may wish to utilize it 1i when other methods of investigation are inconclusive. Treatment--This follows "The Inert Dusts." REFERENCES 1. Committee on Pneumoconiosis of the American Public Health Association: Official Transcript of the Second Silicosis Symposium, Saranac Lake, N. Y., 1935, p. 14(1. 2. McCord. C. P.: "Action1 of Silica as Modified by the Presence of Alkalies." Indust. Med., 5: 17 (Jan.), 1930. 3. Denny, J. J., Robson, IV. D,, and Irwin, D.: "Prevention of Silicosis by Metallic Aluminum," Indust. Med., S: 134 (April). 1939. 4. Cole, L. G., and Cole, ffm. G.: "The Dyspnea of Silicosis: What Causes It?" J.A.M.A., 113: 1216-21 (Sept. 23). 1939. 5. Pancoast, H. K., and Pendergrass, 15. P.: "The Roentgen Classification of Pneu moconiosis, Based upon Roentgen Appearances, with and without Coexisting Tuberculous Process, and Differential Diagnosis," J. Indust. Ilyg. and Toxicol., 16: 327, 1934. 6. Lanza, A. J.: Silicosis and Asbestosis, Oxford University Press, New York, 1938. 7. Gardner, L. U.: "Anthraco-silicosis Simulating Pulmonary Carcinoma." J. Indus!. Ilyg. and Toxicol., SI: 193 (Oct.), 1939. (Abstract.) 8. Schnurer, L. J.: "Incidence of Pulmonary and Extra-pulmonary Tuberculosis in Anthracite Coal Miners," J. Indust. Ilyg. and Toxicol., SI: 194, 1939. (Ab stract.) 9. Mayer, E.: "Clinical Evaluation of Disability in Pulmonary Disease of Industry." J.A.M.A., 116 (Jan. 11), 1941. 10. Giering, J. E., and Charr, R.: "The Heart in Anthraco-silicosis," J.A.M.A., 113 (Aug. 12), 1939. 11. Shaefer and Company vs. Industrial Commission, Wis. 265 N. \\. 390. 12. Marsh vs. Industrial Accident Commission. 217 Calif. 338. 18 P. (2d), 933. 13. Price vs. Industrial Accident Commission. Calif. 49 P. (2d), 294. & 14. "Abstract Silicosis; Period of Claim within Which Claim for Compensation Must Be Filed," J.A.M.A., 106: 1122 (March 28). 1936. 15. North End Foundry Co. vs. Industrial Commission, Wis. 258 X. W. 439. 16. Billo vs. Allegheny Steel Co., Pa. 195 A. 110. 17. Miller, F. P.: "Examination and Report." Letter to Pacific Employers Insurance ...i' Company, Los Angeles, July 19, 1911. 18. Lovelock, J. E.: "Anthraco-silicosis and Bronchial Carcinoma with Quiescent Tuberculosis," J. Indust. Ilyg. and Toxicol., 31: 191 (Oct.). 1939. (Abstract.) 19. Clark, G. L.: Applied X-Ray, McGraw-Hill Book Co., New York, 1940. 20. Ballard, J. W., Oshry, H. j., and Schcnck. H. II.: Report of Investigation No. 3520, U. S. Bureau of Mines. 21. University of Toronto Studies. Geol. Scr., JS: 13, 1935; Indust, and Engin. Cliem., Anal.' Ed.. S: 36, 1936. 22. Berkelhamer. L. H.: "X-Ray Diffraction an Important Tool in Pneumoconiosis Research," J. Indust. Ilyg. and Toxicol., 23: Plate 63 (May), 1941. CHAPTER XXVII ANTHRACOSILICOSIS Most cases of silicosis result from exposure to an atmosphere which contains not pure silica, but rather an admixture with other dusts. Anthracosilicosis is an example of this, and in this country it constitutes a disease confined chiefly to the miners in the hard-coal district of eastern Pennsylvania. Findings in Governmental Survey.--In May, 1933, at the request of the governor of that state, the United States Public Health Service began a survey of the nature and prevalence of chronic incapacitating miner's asthma. During this study the occupational and medical his tories, physical examinations and roentgenological examinations were recorded on 2711 men. At the completion of their work, the following summary and findings were offered.1 Definition.--The term "anthracosilicosis" is a descriptive title for the form of pneumoconiosis commonly called "miner's asthma." It is a chronic disease due to breathing air containing dust generated in the various processes involved in the mining and preparation of an thracite coal. It is characterized anatomically by generalized fibrotic changes throughout both lungs with the presence of excessive amounts of carbonaceous and siliceous material, usually by compensating em physema, and often by cardiac changes in the later stages of the disease. Symptoms.--The chief subjective symptoms found in the early stages were shortness of breath, cough, and pain in the chest: later, weakness and hemoptysis were frequently mentioned. The most com mon objective symptoms were dyspnea, prolonged expiration, de creased chest expansion, clubbing of the fingers, change in breath sounds, altered fremitus, and impaired resonance. In the more ad vanced stages (or in cases complicated by infection), persistent rales, cardiac impairment, loss of weight, and cyanosis were often seen, and usually there was more pulmonary infection, and moderate or marked decreased capacity for work. Lung changes, general in distribution, often with more or less fixation of the diaphragm, were shown by fluoroscopic and x-ray-film examination. Basis of Diagnosis.--Diagnosis was based on three important classes of findings: (a) histories, occupational and past medical; (6) clinical examination, symptoms, and physical findings; and (c) x-ray sro 1 * ANTHRACOSILICOSIS 341 examination, fluoroscopic and film. For a definite diagnosis of anthracosilicosis, information from all three sources is required. In deter mining the role played by specific infection, laboratory examination should supplement the knowledge gained from the three sources men tioned. In certain borderline cases, repeated examinations may be nec essary. A postmortem diagnosis should be based on the results of pathological and chemical examination of the lungs. A complete diag nosis of anthracosilicosis includes a statement of any associated com plications, and of the extent and cause of permanent decreased ca pacity for work, if such is shown. Of the various contributory factors observed in the development, course, and final effect of the disease, pulmonary infection and cardiac impairment appeared to be the most important, especially in the advanced stages of the disease. Groups Studied.--These conclusions in regard to the nature and development of the disease were based on the examination of 711 men (about 96 per cent of the number on the payroll of three repre sentative anthracite-coal-mining companies studied); on the findings for 135 disabled ex-miners who were hospitalized for observation; and on a smaller group examined in a state tuberculosis sanitarium. The coal-mining employees were grouped occupationally, largely in accordance with the proportion of free silica found in the dust to which they were exposed. No cases of anthracosilicosis were found in a control group com posed of hard-coal-mining employees whose dust exposure averaged less than 5,000,000 particles per cubic foot of air. Prevalence and Exposure.--The prevalence of anthracosilicosis among the entire group of employees was found to be about 23 per cent. Among all except rock workers, less than 2 per cent of the men developed anthracosilicosis when the duration of employment was less than fifteen years, regardless of the amount of dust in the air. Among men exposed from fifteen to twenty-four years to dust containing less than 5 per cent free silica, 14 per cent of those who had worked where the average dust count was from 100,000,000 to 199,000,000 particles per cubic foot, 29 per cent of those exposed to from 200,000,000 to 299,000,000 particles, and 58 per cent of the men who had worked for this period in more than 300,000,000 particles per cubic foot, developed anthracosilicosis. Among men employed for more than twenty-five years in dust containing less than 5 per cent free silica, the proportion of persons found with anthracosilicosis under different concentrations of dust was as follows: from 5,000,000 to 99,000,000 particles, 7 per cent; 342 OCCUPATIONAL DISEASES from 100,000,000 to 199,000,000 particles, 54 per cent; from 200,000,000 to 299,000,000 particles, 71 per cent; 300,000,000 or more particles per cubic foot, 89 per cent. With the exception of miners, their helpers, and rock workers, about 25 per cent of all the men employed underground developed anthracosilicosis after a working period of more than twenty-five years. This group was exposed to dust having a quartz content of about 13 per cent. The prevalence of anthracosilicosis among persons who had been exposed for more than two or three years to dust, of which about 35 per cent was free silica, varied from 10 per cent, among those who had worked in concentrations of less than 200,000,000 particles per cubic foot for less than fifteen years, to 92 per cent, among those who had been employed for more than twenty-five years in dust concen trations exceeding 200,000,000 particles per cubic foot, more than two or three years of which time was spent in rock work. Age per se appeared to play a minor role in the development of anthracosilicosis. Safe Limits of Exposure.--Analysis of the data for the purpose of determining safe limits of dust exposure indicated that employment in an atmosphere containing less than 50,000,000 dust particles per cubic foot would produce a negligible number of cases of anthraco silicosis when the quartz content of the dust was less than 5 per cent. In the gangways where the silica content of the dust was about 13 per cent, a safe limit appeared to be from 10,000,000 to 15,000,000 particles per cubic foot. The limit of toleration for rock workers was set tentatively at from 5,000,000 to 10,000,000 particles per cubic foot of air. Respiratory Disease.--Pulmonary infection increased with length of service more rapidly among the men in the haulageways than in the control group, and much more rapidly among the regular miners. The highest rates of pulmonary infection, however, were found among the rock workers of more than fifteen years' service. The prevalence of pulmonary tuberculosis among the hard-coal mining employees at ages below thirty-five was slightly less than that found through studies of tuberculosis among male adults in the gen eral population of the country. In the age-group thirty-five to fortyfour, however, the prevalence of tuberculosis was about twice; at ages forty-five to fifty-four, about five times; and for the ages above fifty-five, it was about ten times the rate found in the general popu lation. The highest prevalence of clinical pulmonary tuberculosis occurred among the rock workers (men who had been employed in rock-loading ANTHRACOSILICOSIS 343 or rock-extraction for more than two or three years). After twenty years' service, of which more than two or three were in rock work, 37 per cent presented evidence of pulmonary tuberculosis. lit a group of 135 completely disabled former anthracite workers, which did not include any known cases of tuberculosis, 10 per cent proved positive for pulmonary tuberculosis. Pulmonary infection (tuberculous and non-tuberculous) was found among 58 per cent of the employed men having early anthracosilicosis, and in 92 per cent of the workers in the more advanced stages. Clinical pulmonary tuberculosis was diagnosed in 15 per cent of those with early anthracosilicosis, and in 43 per cent of those in the more advanced stages. In all groups combined, with the exception of the control group, about 20 per cent of the non-tuberculous workers were diagnosed as having some respiratory disease other than tuberculosis. In the con trol group only 6 per cent had non-tuberculous respiratory disease. In the control group less than 2 per cent were found with moderate or marked physical impairment causing decreased capacity for work as compared with about 10 per cent among the regular miners, and with approximately 13 per cent among the rock workers. With the exception of the rock workers, no group showed moderate or marked physical impairment in excess of that found among the controls when the period of employment was less than twenty years. However, an excess in the prevalence of slight impairment was found among the regular miners and among others exposed to dust containing less than 5 per cent free silica when they had worked from ten to twenty years in atmospheres containing more than 100,000,000 particles per cubic foot. The correlations between exposure to dust and the evidence of constitutional changes left little doubt as to the etiological significance of the dust in the air breathed. Like correlations were found between the silica exposure and the extent of pulmonary changes. Mortality from respiratory diseases was found to be much greater among anthracite workers than in the general adult male population of the country. The data indicated that underground work in the absence of dust did not predispose to fatal attacks of respiratory disease. Signs and Symptoms.--As in silicosis the first symptom is dyspnea. Initially this dypnea does not require the patients to be in bed. but usually at the time they become short of breath on mild effort, their appearance takes on certain changes, there is a beginning loss of weight, the skin becomes pale or dusky, muscle weakness is noted, and the patients appear asthenic. A cough is common and productive 344 OCCUPATIONAL DISEASES of a blackish sputum. Because of the pleural adhesions and the fibrous changes causing fixation of the diaphragm or distortion of the medias tinum. pain is a frequent companion to the cough. Pain appears to be more common and seems to occur earlier than in silicosis with infection. Percussion note is impaired, breath sounds may be decreased or show signs of consolidation depending upon underlying patho logical conditions. Pathology. Gross Appearance.--The lungs are dark gray, firm, and feel heavy. Black linear markings may be noted on the surfaces of the lungs. Adhesions between the parietal and visceral pleura are fre- Fig. 60. Fig. 61. Fig. 60.--Simple pigmentation of uncomplicated anthracosis. The lungs appear almost normal. (Gardner.) Fig. 61.--Details of an anthracosilicotic nodule. (Gardner.) quent. When sectioned these black lines are seen to run through the lungs, and there are also noted the disseminated, black nodules. In severe states, the pleural thickening and adhesions, as well as the fibrosis of the lung proper, tend to distort the shape of the lung. Coalescence of the nodules takes place in this stage, and emphysema tous blebs become larger. Consolidation of these areas occurs usually subapically replacing normal tissue (Figs. 60-65). Microscopic Appearance.--According to Drecsen and Jones,- black particles are present in the macrophages, but they are rarely seen free in the alveolar epithelial cells. Collections of "dust cells'' are AA'THHACOSILICOSIS 345 seen, however, in the perivascular and peribronchial lymphatics and adjacent interstitial tissue. Fibrous hyperplasia is observed quite 7, jj-.- Fig. 63. Fig. 64. Fig. 63.--Conglomerate anthracosilicosis. (Gardner.) Fig. 64.--Conglomerate anthracosilicosis. (Gardner.) early along the lymph channels and increases in certain areas to the formation of nodules. In the center of the smaller nodules, evidence of 846 OCCUPATIONAL DISEASES devascularization may be seen. The centers of larger nodules are for the most part well-formed, white, fibrous connective tissue and com monly reveal evidence of hyaline degeneration but are often free of appreciable amounts of carbon. In the periphery of the nodules, dust laden macrophages are present. Free extracellular dust is noted in large quantities in the adjacent underlying dense connective tissue. As confluence of the nodules occurs, the peripheral coal-dust de posits are enclosed in the larger nodule formed. Areas of central, amorphous, finely granular necrosis are often seen. Fibrous hyperplasia and dense depositions of coal dust arc seen in the peritracheal and Fig. 65.--Anthracosilicosis proved by autopsy. (McCloskey.) pulmonary lymph glands, often to such an extent that histology of the organ is completely obscured. x-Ray Findings.--The first typical appearance is that of an exag geration of the normal linear markings of the lungs. Following this there is some increase in the general fibrosis. With continued exposure the film takes on a "groundglass" appearance, the linear markings tend to disappear, and the generalized fibrosis is increased. At about this time very fine nodules may be scattered throughout the film. Further progress results in increase in number and size of the nodules. These nodules become larger than those seen in miliary tuberculosis, ANTHRACOSILICOSIS 347 and at this time also emphysematous blebs will be noted. Finally, conglomerate masses are much in evidence, the emphysema has in creased, and the generalized fibrosis is marked. Medicolegal Aspects.--The determination of (Usability and the basis for such a determination correspond to those principles outlined under "Silicosis." Treatment.--This follows "The Inert Dusts." REFERENCES 1. U. S. Public Health Service Bulletin 221, Dec., 1938. 2. Dreesen, \V. C., and Jones, It. It.: "Anthracosilicosis," J.A.H.A., 107: 1179 (Oct. 10), 1936. CHAPTER XXVIII ASBESTOSIS The health hazard of asbestos dust has been recognized only re cently. In England, over a number of years, up to 1934, there were only forty-one deaths from asbestosis. There were twenty-six deaths from asbestosis, with silicosis. As late as February, 1927, the first claim for compensation due to a disability from this disease was filed in Massachusetts. In 1936 Lanza1 reported that the files of the Metropolitan Life Insurance Company revealed only nineteen cases. He estimated that there were about 10,000 persons exposed to asbestos in this country. It can be seen that this is small in comparison to 500,000 workers exposed to harmful mineral dusts in mining and industry in the United States. Occupational Hazards.--Asbestos is a hydrated magnesium silicate. The more prominent hazards are offered in mining (especially chryso lite in Canada), handling and crushing crude asbestos, making as bestos mattresses, manufacturing of insulation, the carding and weav ing of fine asbestos, and in certain phases of the automobile industry. Signs and Symptoms.--British investigators feel that the signs and symptoms are more severe in asbestosis than in silicosis, but American investigators believe they are milder. As in silicosis, the first sign is that of dyspnea, the cough is usually dry, and auscultation reveals few, if any, physical signs. Loss of weight is usually notice able, the color is pale, and cyanosis is a fairly early sign. After some time, fine, crackling rales may be heard, and the chest appears emaci ated and lacks the robust character noticed in silicosis. Early asbestosis must be differentiated from acute emphysema. If tuberculosis is pres ent, the symptoms may take on the character of this disease, but this complication is far less frequent than in silicosis. Pathology. Pulmonary Changes.--According to Stewart, as quoted by Auerbach,2 the pulmonary fibrosis of asbestosis is diffuse in char acter, peribronchial and basal in location, in contrast to silicosis in which the fibrosis is nodular in character and present in the upper part of the lungs. As the process continues, the fibrosis extends into almost all portions of the lung tissue. Bronchiolectasis and bronchiectasis arc present within the substance of the fibroid areas, and bronchopneu monia and acute tracheobronchitis often cause the death of these 318 ASBESTOSIS 349 patients. The pleurae, especially in the basal regions, are thickened and adherent. In some cases the pleural sac is completely obliterated; in others a fibrous or serous exudate may be present within it (Figs. 66-70). Action of Asbestos and Silica.--The difference between chrysotile asbestos and quartz silica in their mode of action has caused con- Pig. 66.--Photomicrographs of asbestosis bodies found in sputum. Enlarged 530 times except for E, which is enlarged 310 times. A scale ruled in units of SO n has been drawn beside each asbestosis body. (U. S. Public Health Service, Bulletin 2hi.) sidcrable speculation as well as experimentation. Gardner3 particu larly, at the Saranac Laboratory, has carried on intensive study of these two materials. He feels that while the action of free silica is chemical in nature, the action of asbestos is mechanical. He states; 350 OCCUPATIONAL DISEASES Fig. 67.--Right lung, showing markedly thickened pleura with fusion of inter lobar pleura. Dense fibrous tags over entire surface. (U. S. Public Health Service, Bulletin ikt.) Fig. 6S.--Asbestosis bodies accompanied by giant cells. (U. S. Army Medical Museum, Specimen 52255.) ASBESTOSIS 351 Fig. 70.--X-Ray film of a patient with asbestosis. (Pendergrass.) 352 OCCUPATIONAL DISEASES For the last year or two we have been coming to the conclusion that inhaled asbestos fibres are irritating not because they arc sili cates but because they are stiff fibres which mechanically irritate the lungs. Unlike the free silicas, these minerals will not stimulate fibroblasts in any part of the body; only those in the lungs are affected. It was inferred that these organs were affected because the move ments of respiration are so much more rapid and continuous than those of other viscera. Then it was discovered that if asbestos was ground very finely so that few of the fibres were longer than 2 ^ in length the irritating property of the asbestos was practically de stroyed. Inhalation experiments with such fine chrysotile asbestos have now been continued for three years. No fibrosis has developed in spite of the fact that an average atmospheric concentration of 125 million particles per cubic foot of air has been maintained. In contrast I would point out that in a previously reported experiment one-third this concentration of long fibre asbestos dust produced well marked fibrosis after about two years. If the effect of asbestos were chemical, one would expect that a decrease in size would accelerate tissue response. With free silica large particles have little effect, but as their size decreases cellular reaction becomes more vigorous and even constitutional symptoms may ensue. With fibrous asbestos the' reverse is true. The histology of early asbestosis does not suggest a chemical in jury. Even under the most extreme conditions that can be created by artificial injection there is no preliminary phase of tissue necrosis with infiltration of leucocytes as,occurs with high concentrations of very fine quartz. The connective tissue cells merely multiply very slowly in areas where the asbestos fibres arc caught in the bronchioles. As collagen forms and contracts, the air spaces are obliterated by scar tissue. In experimental animals, at least, this change is not a pro gressive one after cessation of exposure to the dust as is the case in the response to quartz. Perhaps the reason is the deposition of the peculiar iron-containing coating on the surface of the inhaled fibres giving rise to the characteristic "asbestosis bodies." -a;..;- Finally it is most suggestive that among dozens of different silicate minerals only the five known as asbestos, which are unique because they are fibrous in structure, should be commonly recognized as pul monary irritants. The variation in chemical composition within this group is greater than that between them and many other silicates. In fact chrysotile asbestos has the..same chemical formula as a non- fibrous silicate, serpentine, which' is physiologically iiiOftFF)bviously irritation would seem to be associated with the physical,'rather than the chemical composition of these minerals. One point of practical significance may be indicated by these ob servations; namely, that very finely ground asbestos is not dangerous. ASBESTOSIS 353 This conclusion has support in clinical observation, for it has long been known that at the Thetford mills there was no clinical asbestosis even though in former years the atmosphere was very dusty and the dust was extremely fine. The fact that fabrication of fibres of the same mineral in American plants could produce disease was one of the puz zling' features of this disease. But these experiments offer a plausible explanation. The fine dust in the mills is composed of serpentine and extremely short chrysotile fibres; that in the spinning and weaving mills contains many more long fibres. , Microscopic Appearance.--In the early phases of the disease there is a thickening of the alveolar septa as a result of fibroblastic prolifera tion. The alveolar spaces contain numerous alveolar phagocytes. With progression of the disease, fibrosis becomes more marked, the alveolar structure gradually disappears, and in its place there is now dense fibrous tissue. The few remaining alveoli which lie in the area of fibrous tissue are lined by a low cuboidal epithelium and have a glandular appearance. Scattered throughout the lung in both the diseased and healthy parts are spindle-shaped structures (first described by McDonald) known as asbestosis bodies. These bodies are slender in their center and bulbous at each extremity. Many are arranged like strings of graduated beads with the largest at the end of the chain. x-Ray Findings.--Certain distinct peculiarities exist here as con trasted to silicosis. In asbestosis, the lesions may be bilateral or largely unilateral. According to the experience of Pendergrass,4 the roent genological findings in asbestosis are largely limited to the lower half or two thirds of the lung fields, while in silicosis the upper portions of the lungs are also involved. In moderately advanced asbestosis, arrays will reveal lessened ventilation of the lung fields, the parietal pleura is thickened, and there is a "groundglass" appearance to the picture. THe vascular shadows lose their identity. Nodulation is absent. Pen dergrass feels that a roentgenological diagnosis of early asbestosis is unreliable and that the condition must be moderately or markedly advanced to make a differential diagnosis from the roentgenograms. Medicolegal Aspects.--It is felt that the time necessary to develop asbestosis is on the average from seven to nine years in a fairly high concentration. With a less severe concentration, from fifteen to twenty years. The allowable concentration is 10,000,000 particles per cubic foot of air, of a size between 0.5 and 5 y. Once established, the disease is progressive, even after the cessation (^exposure. The basis for diagnosis is similar to that stated under 23 354 OCCUPATIONAL DISEASES Treatment.--This follows "The Inert Dusts.'' REFERENCES 1. Lanza, A. J.: "Asbestosis," 10G: 3G8 (Feb.), 1930. 2. Auerbach. 0.: "Pathology of Asbestosis," Indust. Med., 6: 318 (Jan.), 1937. 3. Gardner, L. U.: "Recent Developments in Relation to Silicosis," Indust. 'Med., 9: 45 (Feb.), 1940. 4. Pendergrass, E. P.: Silicosis and Asbestos-is, Oxford University Press, New York, 1938. CHAPTER XXIX THE INERT DUSTS How deleterious are the various industrial dusts? Ill health as a result of working in a dusty atmosphere is claimed by a sufficient number of workers to make this a problem of frequent incidence in any industrial medical practice. Usually such claims arise from trades where the dust particles are large and plainly visible. It is not diffi cult to understand that men laboring in such circumstances easily imagine all types of harm to the lungs from breathing such dust. Nor has the pathological picture of the inert dusts been sufficiently clari fied in the various textbooks to permit the average physician an adequate understanding of their status. Effects of Inert Dusts.--To date there is no evidence that the inert dusts are relatively harmful. This does not mean that breathing heavy concentrations of any dust may not have an irritating effect upon the upper respiratory-passages. Nor is it to be implied that continuous exposure to a moderately severe or severe concentration of dust may not produce a mild fibrosis. But this reaction is very slow, noticeable by a-ray only after a number of years of continuous exposure and rarely productive of any symptoms. After many years of exposure, dyspnea may be present to mild degrees, but this is not often disabling. Furthermore, to attribute this dyspnea to an existing fibrosis, one would have to rule out unrelated cardiac pathology. Relation to Tuberculosis.--It has long been recognized that the tuberculosis death rate among certain industrial groups exceeds that of the general population. To evaluate this increase, many factors must be considered, such as overcrowding of workers in the shops and plants, thus favoring the spread of tuberculosis; poor ventilation at work as well as in overcrowded homes; faulty diet; ignorance of gen eral hygiene and the like. Tuberculosis is not to be considered a se quela of exposure to inert dusts per se. This point cannot be too strongly emphasized. Supportive evidence of the above statements may be found in sev eral investigations. Clark1 studied men subjected to the effects of inhalation of abrasive substances for a period of twenty-five years. He found that in factories which provide for proper dust removal, the continuous inhalation of abrasive dust (chiefly aluminum oxide) over a period of years did not produce symptoms or a;-ray findings of 355 356 OCCUPATIONAL DISEASES crippling lung fibrosis, that tuberculosis in these workers was not greater than in the community, and that the risk was slight. Some of the common inert dusts will be mentioned briefly with enlargement upon several others: Talc.--Talc powder creates the impression that it is so dense that it must of necessity cause disturbance within those who breathe it. While talc is a mineral often occurring with asbestos or near it in nature, there is no evidence that it causes any undue fibrosis. This observation is based upon the facts that exposure to talc powder is not a new hazard and that there has been sufficient evidence gathered to confirm the above statement. Calcium and Magnesium Carbonates.--From these compounds come limestone rock, marble, chalk, calcined magnesium used for insula tions, furnace linings, and the like.. Men have been exposed to these dusts for years, but there is no evidence that they are harmful to the lungs. Carbon Dust.--This dust is a common constituent of the air in any industrial district where anthracite or bituminous coal is used. Ex posure causes black pigmentation of the lungs, noted in city-dwellers even though they have no specific or intense exposure. Miners reveal a fibrosis greater than that of the non-exposed, but it is a non-dis abling fibrosis, unless the carbonaceous substance is combined with siliceous material. Iron Dust.--Exposure to excessive amounts of iron dust is con fined chiefly to the mining of iron ore. Inhalation of this substance may cause a mottling or staining of the lungs, simulating silicosis to a degree. This condition has been called "siderosis." This is a non-dis abling condition. Tobacco Dust.--Tobacco dust has been referred to in the litera ture of the past as a cause of pulmonary disease. In reviewing'this literature it is interesting to note that practically all, if not all, of these reports were made without the benefit of x-ray. Some of them were purely assumption, such as the observation that tuberculosis was greater in tobacco workers of Baden than in the general population, and it was, therefore, concluded by Stephani that the tobacco dust was responsible. The probability of faulty hygiene, poor working con ditions, long hours of labor, etc., was overlooked. Thus there crept into the literature a condemnation of a dust not proved to be an actual offender. Long,2 after studying a group of tobacco workers over a period of ten years, did not once see the occurrence of this disease. He studied 2254 persons, of whom 1246 had been exposed to tobacco dust wjhile working. By comparison of the findings of these two groups it THE INERT DUSTS 357 was concluded that pneumoconiosis (tabacosis) docs not develop in tobacco workers. The value in his observation lies in the sc-ray and fluoroscopic revelations as compared to the absence of these in other reports. REFERENCES 1. Clark, W. I.: "Dual Hazard in the Abrasive Industries," J. Indust. Ilyg-, 7: 3 to, 1925; 11: 92. 1939; Id: 343, 1931. 2. Long, C. F.: "Tobacco Dust and the Human Lung," Indust. Med., S: 365 (Sept.), 1939. CEMENT DUST Probably the most informative and extensive survey and one which should, for the present time, present a picture of the actual status of inert dusts is the one conducted by the Saranac Laboratory at the request of the Portland Cement Company. This study was begun in 1935, but was not completely reported until September, 1939.1 Table 16 and the following comments are based upon that survey. Chemistry.--The essential ingredients of Portland cement are CaO, Si02, A1203, and Fe203. The chief raw materials which supply these constituents are limestone to furnish the CaO, and shale to supply the other ingredients. An analysis of Portland cement reveals that it contains 19.86 per cent of Si02, yet almost none of this silica exists in a free state. Complete studies were made in eleven plants involv ing 2278 employees. Of these 299 worked in a dust-free atmosphere. Clinical Findings.--Complete physical examinations of 2278 em ployees in eleven different plants situated in widely scattered parts of the country have demonstrated nothing even suggestive of a pneu moconiosis, nor has any other condition common to a majority of cement workers been disclosed. Stereoroentgenograms of the same group have revealed certain variations of the usual pulmonary shad ows. The same abnormalities also occur in the films of other indus trial groups and are in no sense specific for these. Pulmonary Roentgenograms. Classification.--The roentgenographic interpretations have been classified in two categories: linear exaggera tions and nodulation. (a) Pi Shadows.--In the first, the normal shadows, cast largely by the pulmonary blood vessels, are unusually prominent. The slight est degree of exaggeration designated as Pj is so ill-defined that had not all the films been read by one observer there would be little point in discussing them. They will be considered here, not because they have any clinical significance, but because of a tendency among certain roentgenologists to attribute all possible variations from the usual s 358 OCCUPATIONAL DISEASES pulmonary pattern to a dusty occupation. It should be clearly under stood that changes of this intensity are not indicative of a disease process and that they may be produced by a variety of causes whose number increases with advancing age. (b) P2 Shadows.--A more marked accentuation of the linear shadows in the pulmonary roentgenogram, designated for purposes of classification by the symbol P2, is sufficiently unusual that all observ ers recognize it, although there are borderline cases, difficult to dif ferentiate from exaggeration of lesser intensity. The pathological reac tion responsible for the heavier vascular shadows may again be due to different causes, but in groups of men employed in dusty atmos pheres, the inhaled material is much more likely to have produced the change. As a general rule, second-degree linear exaggeration (P2) is not associated with clinical symptoms. Exceptions have been re ported by some observers in patients exposed for prolonged periods to certain types of dust, particularly those containing some free silica, but there is always a question of the causal relationship between this type of pulmonary reaction and the clinical findings. In the experience of the Saranac Laboratory, however, symptoms in men whose arrays show this reaction should be attributed to associated conditions like heart disease or obvious bronchial infection. (c) P3 Shadows.--A still more marked exaggeration of the usual branching shadow pattern has been provisionally designated as P3. The condition is rare, and its cause is not definitely known. The shadows of the peripheral branches of the vascular tree are so heavy that they lose definition and tend to fuse. It is suspected that complicating infection may play a part in producing such appear ances. Roentgenographic Findings.--For purposes of analysis the em ployees were separated into two groups--the first comprising 1979 exposed to more or less dust in occupation (designated "exposed"), and the second, 299 office workers, laboratory employees, machinists, watchmen, and others not often in contact with cement-plant dusts (designated "control"). The roentgenographic findings in the larger group exposed to dusts of various kinds in all parts of the plant are shown in Table 16. Perhaps the most striking feature of this table is the fact that 82.06 per cent of the films showed no abnormality of any kind (Figs. 71, 72). The changes that were noted in this group include 17.45 per cent classified as linear exaggeration of one degree or another, and 0.40 per cent read as silicotic nodulation. The eight cases in the latter category were apparently due to exposures before entering this in dustry. They are of little interest in this study. THE INERT DUSTS 359 16Table --Summary of Roentgenograpiiic Findings by Length of Service-- Exposed Group j Number Per Cent Number | Per Cent Number | Per Cent 1N u m b e r 1 j Per Cent jPer Cent Per Cent ! | Number 1 Per Cent ft0 Hi* P3 Sit Years Num ber 1 -O 3 X 5-9............... 10-14............... 15-19............... 20-24............... 25-29............... 30-34............... 35-39............... 40-44......... .. 45-49............... 50-54............... 55-59........ 503 379 469 271 141 106 56 26 10 9 6 3 454 00 26 316 83 38 386 82.31 217 80.07 97 68.79 74 69.81 39 69.64 19 73.08 7 70.00 9 100.00 4 66 67 0 66.67 42 8 32 6 1.19 0 20 43 14 25 6 1 58 1 0 26 1 0.26 1 0 26 73 15.57 6 1.28 1 0.21 1 0.21 2 0.43 44 16.23 9 3.32 1 0 37 34 24.11 10 7.09 24 22.64 8 7.55 15 26.79 2 3.57 5 19.23 1 3.85 1 3.85 2 20.00 1 10.00 0 33 33 1 33.33 Total------ 1979 1624 82 06 295 14.91 50 2 53 2 0 10 3 0.15 4 0 20 l 0 05 * Pi, ft, P3 indicate the degree of linear exaggerations, t Si, S2, S3 indicate the degree of Modulation exaggerations. Subdividing the cases of linear exaggeration according to the in tensity of the reaction, it was noted that 14.91 per cent were read as Px and 2.53 per cent as P2. There were also two cases (0.10 per cent) of the rare P3 type of change. These figures present a well-marked contrast to those for the group of hard-rock miners, whose films were interpreted by the same observer. In them the total incidence of linear exaggeration was nearly three times as great: Px readings occurred in 32.33 per cent of the films. Many of these miners had been exposed to considerable amounts of free silica, whose capacity to produce pul monary reaction needs no comment. Since the amount of well-marked linear exaggeration in the cement ft workers was so very small, there was a reasonable doubt as to whether any of it was produced by the dust that they had inhaled in this industry. Many of them had also worked in other places where they were exposed to dusts of different kinds. To throw more light on this question a group of 274 plant employees was selected whose histories stated, or whose age in relation to length of service indicated, that they had never worked outside the cement industry, even on farms. None but persons likely to have been exposed to cement dust or its components were included. Of this group, 70 per cent had been employed for periods varying from ten to fifty-five years. The films of 19 (6.93 per cent) were read as Px, and 5 (1.82 per cent) as P2. In other words, among those ex posed only to cement-plant dusts the percentage of first-degree linear exaggeration was about half that for the group as a whole; and the percentage of second-degree reactions was three-fourths as great as 360 OCCUPATIONAL DISEASES in the entire group. This comparison emphasizes the non-specific nature of the linear type of change and indicates that, in the group as a whole, causes other than inhaled cement-plant dusts contributed to its production. The data have been analyzed further to demonstrate the incidence of different types of roentgenographic change in relation to length of employment, to age, to geographic distribution of plants, and to concentration and composition of dust. Fig. 71.--Film of a thirty-five-year-old male who worked in cement dust for twenty years. (A. J. It. Curtis, of Portland Cement Co., and Drs. Gardner and Samp son, of Trudeau Sanatorium.) In this report several of the few cases of nodulation were found in southern California. During a visit of Mr. Curtis, of the Portland Cement Company, to Los Angeles, he described these cases and showed the -ray films. It is rather surprising that, in the long period these southern California plants have operated, more cases of nodula tion have not been acquired from outside. Cement rock is often so located in southern California that it has to be taken out by methods familiar to the mining industry rather than the typical quarrying THE INERT DUSTS 361 processes used in the East. Consequently such help is drawn to a con siderable extent from the hard-rock-mining industries of the state, in which there is in many instances a pronounced silica exposure. Yet no case exhibited other than moderate nodulation disclosed by the roentgenogram. (a) Length of Exposure.--The table reveals a steady increase in the percentage of Px readings in each successive five-year period of dusty trade. This and Fig. 71 serve to illustrate the relatively minor extent of fibrosis resulting from exposure to the inert dusts. (A. J. It. Curtis, of Portland Cement Co., and Drs. Gardner and Sampson, of Trudeau Sanatorium.) employment, starting at 8.35 per cent and reaching a value of 26.79 per cent for men working from thirty to thirty-four years. Then the figures become irregular, but probably not altogether because of the small number of men in the groups. There were 54 employed for from thirty-five to fifty-nine years, inclusive, of whom 9 (16.66 per cent) showed first-degree linear exaggeration (Pi). The less frequent second-degree linear exaggeration (P2) also in creases with duration of employment, but it reaches its greatest fre- 362 OCCUPATIONAL DISEASES quency five years earlier than the Pi reaction and then occurs occa sionally. It is manifested in only 4.5 per cent of the entire group of 110 working for more than thirty years. This lack of correlation between length of exposure and the degree of reaction again suggests an influence of factors other than dust. (6) Dust Exposure and Respiratory Infection.--This group quite thoroughly investigated the relationship between dust exposure and tuberculosis, bronchitis, and pneumonia, and their study indicated that the incidence of tuberculosis and other pulmonary infections is as low as or lower than that in the general population. There is noth ing to suggest that prolonged inhalation of cement dust has altered natural susceptibility to tuberculosis. If this is true of cement dust, it is probably true of other types of inert materials. They likewise found no significant effect of this inert dust on old tuberculosis. It was also noted that the incidence of bronchitis and pneumonia in those work ing in a cement dust varied, as did the figures for the general com munity where the various plants were located. The reports of a low incidence of bronchitis in the dry sections of Texas or Kansas, as contrasted with the high incidence in one of the dampest parts of the state of New York, suggested a marked climatic influence. Ab senteeism due to upper respiratory infections such as coryza was somewhat greater than that in the general community. It is the belief of the author that the above findings regarding a well-known dusty trade should aid in the prevention of too hasty and ill-founded conclusions regarding the action of inert dusts. Details have been given because much of this information is not found in the general literature available to the physician. Cotton and mill dusts are likewise subsequently presented for this same reason. Illustrative Cases: Case I.--A man was employed as a still-cleaner by a petroleum corporation. The work of a cleaner was to rake down coke, burning or smouldering, in stills that escaped the mechanical rake, and sweep it out. The breaking up of these coke deposits gave off dust and a trace of gases. The man worked steadily in that capacity for about ten years, at the expiration of which time he became ill and died. His physician diagnosed his condition as pneumoconiosis. The widow of the workman, as the administratrix of his estate, brought a commonlaw action against the petroleum corporation for the workman's death, alleging that the corporation failed to provide him with a reasonably safe place in which to work and reasonably safe appliances with which to work, and that it failed to warn or to instruct him with respect to the dangers incident to the work. The trial court, at the close of the plaintiff's evidence, directed a verdict for the defendant, and the THE INERT DUSTS 363 plaintiff appealed to the United States Circuit Court of Appeals, Tenth Circuit. Among other reasons for directing a verdict, the trial court was of the opinion that there was no substantial proof that death resulted from the workman's work. The proof was most unsatisfactory, said the Circuit Court of Appeals. Conceding that death resulted from pneumoconiosis, the attending physician's opinion that it resulted from the work was formed, he testified, because he could find no other reason for it. However, said the court, pneumoconiosis concededly re sults from deposits of foreign material, and the man did work in a dust-laden atmosphere. That the physicians who testified never knew of another "still worker" becoming so affected, and that the medical books contain reference to no other case, merely goes to the weight of the evidence. In the opinion of the appellate court, the evidence was sufficient to justify a submission of the question to the jury. If the man died of pneumoconiosis, and if his occupation had anything to do with it, it was because of the dust in which he worked. He knew the dust was present when he took the job, and he kept it year after year. He knew it was harmful to the lungs, for he was furnished with a respirator and told to wear it. While assuming the ordinary, known risks attendant on inhaling dust-laden air, he did not assume the risk of any concealed dangers lurking in the dust. The plaintiff contended that the presence of carbon monoxide and hydrogen sulfide in the stills contributed to the pneumoconiosis. Any finding by a jury, said the court, that hydrogen sulfide or carbon monoxide had anything to do with the pneumoconiosis would rest on speculation. There was nothing in the record to warrant a finding that, after the forced venti lation, there remained in the stills a sufficient amount of the gases to do injury. There was, furthermore, no evidence of acute or chronic poisoning of still workers due to either gas. The petroleum corporation, continued the court, was engaged in the refining of oil, a business attended with some danger as are nearly all constructive undertakings. Its equipment was standard and not defective. It followed the approved practices. It did all that was then known to minimize the risk to its employees. It operated year after year with no occupational disease resulting from the work. It had no reason to suspect any such. "Tested by the principles of fault which underlie recovery for injuries at common law," concluded the court, "we do not believe that the plaintiff has established her case." The judgment of the trial court was consequently affirmed.2 In this case three contentions are made but not verified; (1) there was failure to provide a reasonably safe place to work; (2) death re sulted from pneumoconiosis; and (3) carbon monoxide and hydrogen sulfide gas contributed to the death. 364 OCCUPATIONAL DISEASES The first contention requires the decision of an industrial hygien ist; the second and third, an opinion from a physician based upon knowledge and proof--not assumption. This case illustrates the need for a better understanding of the effects of dust upon the lung, since the dusty trades comprise the largest group exposing the workman to any one material. Case II.--Two longshoremen from the Los Angeles Harbor pre sented themselves to this clinic within an hour of each other with the allegation that recent handling of borax had produced severe chest pain, cough, shortness of breath, and weakness. The histories obtained from each were practically identical and were as follows: On May 15, 1940, together with other men, they were engaged in loading bags of borax to be shipped to England. Patient A stated that on the evening of May 16 he developed shortness of breath, a feeling of oppression in his chest and a cough. He was so "all in" that he was unable to report to the company physician until May 18. Patient B gave an identical history but did not report to the same physician until May 19. Physical examination of A revealed obvious dyspnea upon inspec tion. The chest was barrel-shaped and inspiratory excursion bilaterally limited. Auscultation revealed widely scattered musical rales at the beginning of expiration. The rest of the examination was entirely nega tive. The patient denied ever having had asthma, to his knowledge. The examination of B was entirely negative. The lungs were clear throughout, temperature normal, and no evidence of inflammatory reaction of the nose and throat. These two claims puzzled the writer. For years this clinic has han dled the workmen of the borax company involved. All of these cases have been injuries--the traumata arising out of employment. No claims had ever been presented, at least during the writer's tenure with this clinic, alleging a disturbance of the lungs from occupation. Did this particular shipment of borax, owing to war exigencies, con tain an added ingredient that might have caused an allergic response? I immediately contacted Mr. G. A. Connell, Technical Director for the Pacific Coast Borax Company. His reply was as follows: Dear Dr. Johnstone: I am in receipt of your letter of May 22nd, regarding the complaints of men loading Borax on a shipment made May 15th. I have examined our records and find that on May 15th we shipped to England a parcel of bags containing what we term Calcined Rasorite, at Wharf 90. I have examined our analysis of this parcel and find it to be almost ex actly similar to all other shipments of this nature. We manufacture at our Mines at Boron, California, several hundred tons of this material THE INERT DUSTS 365 a week and to date know of no complaints from our men working with this material or handling the same after it has been bagged. As a mat ter of fact, investigations made by the Insurance Commission and the Mining Bureau of the State have given us a clean bill of health in regard to our products, although the dust condition obviously should be worse than that in loading ships with this material after it has been bagged. We have also had occasion to investigate the effects of borax from an allergic standpoint and tests conducted under a very competent physician indicate that while some people may be allergic to borax, the evidence indicated that this allergy amounted to only about one out of one thousand people. This information indicated the unlikelihood of borax as the cause of the alleged complaints, but it was felt that investigation should not stop at that point. It must be appreciated that one of these patients presented a condition of bronchial asthma. The possibility of a claim for frequent temporary disability or an eventful permanent disability due to the initial onset following the exposure to this dust presented itself. An investigation in the patient's community brought out the following facts. Patient A had been under treatment with a family physician for asthma prior to this contact with borax. A longshore man strike was impending, and it was thought that a layoff was due. So, if these two could be on compensation during that time, they would benefit financially. A drugstore clerk testified that A had met B at the fountain and told him he had another attack of asthma and was going to "fool the doctor" by blaming it on this dust. B thought that was a good idea and asked A just how he felt. The conclusions finally reached by this examiner were that A was suffering from an attack of asthma, which he had experienced before, and that his at tack was coincidental with, but not incidental to, the handling of borax. The negative examination of B and subsequently determined facts led us to believe that he was faking. This illustration offers certain lessons that should be emphasized. In the first place, before a claim is denied where doubt exists, it should be investigated thoroughly. Any doubt in compensation cases is to be given in favor of the workman. If a doubt exists, thorough search to substantiate or deny the claim should be instituted. Snap judgment is unfair to all parties. Time and effort must be expended to obtain facts. When the general practitioner is faced with doubt regarding the cause of his patient's illness, he resorts to his experience and to his textbooks. But the industrial physician is required to go beyond that, to seek into conditions of employment, to examine the plant by personal inspection or by submitting material for analysis. The willingness to do this qualifies the industrial physician as just and fair in his deci 366 OCCUPATIONAL DISEASES sions. Both patients in the above illustration were denied compen sation. REFERENCES 1. Gardner, L. I'.. Durkan, T. M., Brumfiel, D. M., and Sampson, H. L.: "Survey of Twenty-Two Hundred Cement Workers," Indust. Hyg. and Toxicol., 21: 7 (Sept.), 1939. 2. Grammer vs. Mid-Continent Petroleum Corporation, Texas 71 F (2d) 38. COTTON DUST Occupational Hazard.--The cotton industry is an important field of employment in this country. But if this work provides any risk to the workers' health it is not indicated in the American medical litera ture. One case which presented itself aroused the author's interest, and he believes that his study of this case might be of interest to others who may, on occasion, be confronted with the problem of de termining the effect of cotton dust upon the lungs of those exposed. The bulk of comment is to be found in the English literature. In America it is classified as an inert substance, and little thought has been given to its effect, if any, upon the lung. In a report from the English Encyclopedia of Hygiene, Pathology, and Social Welfare (1930), cotton workers' pneumoconiosis (byssinosis) is classified as one of the chief affections of the lungs among the workmen. Possibly their method of sorting, carding, and handling this substance differs from ours, and so in our system there may exist little or no hazard. Nevertheless, there are bound to be occasions when this question will present itself to the practitioner in our cotton-growing states. Signs and Symptoms. Respiratory Effects.--According to the Eng lish investigators, the effects produced by breathing an atmosphere heavily impregnated with cotton dust are characteristic and indicate a severe irritation of the air passages. Dyspnea is a prominent symp tom, but it is dyspnea of an undoubtedly asthmatic type. It is different from the dyspnea of silicosis, which involves the abdominal efforts and not the marked thoracic efforts of those affected by cotton dust. The cough is dry with little expectoration. Whatever sputum is produced is of an extremely tenacious character. The attacks tend to disappear over the week-end or during a vacation, but reappear with the resump tion of work. Chronic asthma eventually results in loss of weight, in creased dyspnea, emphysema, and the development of the barrel-type chest. Erom reading the English literature it can be assumed that it takes from twenty to twenty-five years for the development of severe symptoms. It is also noted that the coarser grades of cotton contain more dust than the finer varieties and, therefore, constitute a greater hazard. In addition to the asthma and'bronchitis, catarrh of the upper respiratory passages is common. THE INERT DUSTS 367 Allergic Phenomena.--These have been reported by the English investigators as well as by Teleky in Vienna, and Schmidt in Ger many. Weavers do not appear to be affected by this allergic reaction as much as those who prepare the material. In the latter group irrita tion of the upper respiratory passages, a sensation of oppression of the chest, and attacks of coughing with scanty sputum are the com mon complaints. Fibrosis.--Autopsies on cotton-strippers and grinders fail to reveal pulmonary fibrosis. It is thought by most investigators that any fibrosis developed by such cotton workers is the result of a combina tion of bronchitis and asthma and not of the cotton dust itself. In Eng land the Home Office Departmental Committee defined byssinosis as a chronic bronchitis complicated by emphysema in its later stages and by asthma in some cases. It is felt by these investigators that the combination of asthma and chronic bronchitis is due to the action of the protein fraction of the cotton dust inhaled. Non-Pvlmonary Conditions.--Certain non-pulmonary conditions may exist in the industry. Workers in the processing rooms may de velop conjunctivitis or blepharitis (from the burned products of the gassing of double yarn), headaches, lassitude, and loss of appetite (from the high temperatures), in addition to the possible effects of carbon monoxide. Molds and Fungi as Factors.--A comment by Collis1 particularly interested the author in view of the x-ray findings in the case he is about to report. After investigating the cotton mills of England, Col lis concluded that the occasional severe epidemics of coughing among these workers were due to mildew and molds and that these molds were Penicillium glaucum or Aspergillus glaucus. Others have indi cated a relationship between the chest conditions and fungus. The British statistics show a high incidence of upper respiratory diseases in persons engaged in the preliminary operations such as balers, card ers, or sorters. Our patient was a sorter for twenty-eight years. Roentgenographic Studies.--It was disappointing in searching the American and British literature to find no report of T-ray studies of cotton workers. Dr. R. R. Sayers, Senior- Surgeon of the United States Public Health Service, Division of Industrial Hygiene, was appealed to, and he graciously aided in supplying references to the foreign literature but could suggest no source of help in this country. Our films were submitted to certain authorities in America on pneumo coniosis and various interpretations were received. Illustrative Case.--It was because of the history of exposure, symptoms, and the peculiar T-rav findings that this case was of interest. 368 OCCUPATIONAL DISEASES Case I.--In May, 1939, a forty-year-old Negro male presented him self to the writer with a complaint of attacks of nocturnal dyspnea. History.--Since the age of twelve this patient had worked as a cotton-sampler. He had not worked in the cotton mills or been con nected with any other processing phase of the cotton industry; his activities had been confined to the handling of cotton for inspection. The only time he was not exposed to this was during a brief sojourn in the army during the first World War. Until 1918 his work was done in the South, and since that time he had been engaged as a cottonsampler in Los Angeles. About one year previous to this examination he noticed a sensation which he described as a dull weight or oppression between his shoul der blades. He claimed that this was not a pain and never had felt like a pain, but was simply a heavy sensation in the upper posterior chest. Six months after noticing this heavy feeling he began having noc turnal attacks of shortness of breath. He described these attacks as follows: I do not'have any trouble during the day or while I am at work. I am all right until after I have been asleep for a while. I usually fall asleep without difficulty, but about an hour later or sometimes less, I am awakened by a wheezing sensation in my chest. I then start cough ing and get very short of breath. I feel as if my air is being cut off, and I have to get up. When I get up I usually spit up a heavy, thick, sticky substance, and then I start to feel better. I never notice any of this whistling or wheezing in my chest during the day and I rarely cough during the day. I do not have any shortness of breath except if I walk about three blocks of if I climb a flight of stairs in a hurry. Symptoms Referable to the Various Systems.--Essentially nega tive. Past Medical History.--Entirely negative with the exception of gonorrhea contracted while in the army, at which time he also devel oped a sore at the end of his penis to which he gave the familiar term of "hair cut." Physical Examination.--Patient is an adult Negro male; height, 5 feet 8 inches; weight, 191 pounds. He is forty years of age. His in telligence is above the normal, for his race. The pupils reacted to light and accommodation; the eyegrounds were normal. Throat normal, tonsils atrophied. Teeth appear to be in a good state of hygiene. Neck short, bull-neck type. Chest barrel-shaped and measured 41 inches. Following full in spiration it measured 42 inches. There was a moderate limitation of the normal excursion rate bilaterally. There was no noticeable lag on one side over that of the other. Percussion note was slightly duller than normal. Auscultation of the lungs revealed the breath sounds THE INERT DUSTS 369 over the entire chest to be quite distant, almost imperceptible. In spite of the history of wheezing and whistling sounds, we were unable to detect any rales during three separate examinations of this pa tient's chest. Heart rate of 84, sounds distant, no murmurs heard. Blood pressure: right arm, 128/90; left arm, 130/90. Abdomen obese; no organs or masses palpated. Genitalia and rec tal examination negative. Neurological Examination.--Pupils reacted as noted. Knee jerks, 2 plus. Achilles reflexes, positive bilaterally. Romberg sign, negative. Finger-to-nose test, negative. Babinski test, negative. Laboratory Examination.--Urinalysis, negative. Blood count, nor mal. Blood Wassermann, 4 plus. Kahn, 4 plus. Repeated sputum speci men, moderate number of white blood cells; ordinary bacterial flora; acid-fast bacilli not found. No fungi found. Guinea-pig, negative for tuberculosis. This case presented the following similarities to the English cases: 1. Length of exposure. Twenty to twenty-five years is the time in terval they have observed before the pronouncement of se vere symptoms. Our patient had an exposure of twenty-eight years. 2. The symptoms. Cough with scanty but tenacious sputum. (The laboratory technician had to cut specimens in this instance with scissors for material for slides.) Oppression in the chest; this was one of the first things noted by our patient. Dyspnea at night with the presence of rales. Symptoms are more marked in those who handle the raw cotton. (Our patient was a cotton-sorter.) 3. The development of emphysema and barrel-type chest. 4. The possible infestation of fungus. This question had to be con sidered in our case. Roentgenographic Interpretation.--The chief problem was to evaluate the chest plates. These were so strikingly unusual and out side the experience of several clinicians and roentgenologists who viewed them that they were mailed along with the history to several nationally known authorities for their comment. In the base of both lung fields, especially on the left, there were concentric whirlpools as if made by interlacing white threads. These films in stereo were in terpreted by our roentgenologist as follows: a;-Ray examination; stereo of the chest (Fig. 73). There is a definite area of increased radiability along the upper and lateral wall of the left lung field, consistent with a partial pneumothorax or coali tion of several large emphysematous blebs. On the right side there is also noted near the apex and along the upper lateral wall an area of 21 370 OCCUPATIONAL DISEASES increased radiability suggestive of a similar condition. The low, flat diaphragm, together with a rather enlarged chest, bears out the pic ture of general emphysema. There is increased fibrosis around both lung fields near the base of the heart on the left side, but the cause of this is rather obscure. It is very definitely not suggestive of pulmo nary tuberculosis nor does it have the markings of pneumoconiosis. Fig. 73.--A , These films are of the Negro cotton worker referred to under "Cotton Dust." For their interpretation, the reader is referred to the comments in the text. B, Film of the same patient, taken almost one year later, showing no perceptible change. This fibrosis is most likely due to a chronic bronchitis with a coex istent pneumonitis. It is conceivable that these rounded areas of increased density might represent small areas of atelectasis developed on a basis of emphysema plus a partial pneumothorax. Dr. Leroy Gardner, at Saranac, commented: I am most grateful to you for letting us see the films of your negro cotton sampler. Both Dr. Sampson and I have studied them with greatest interest. I have been looking for a long time for such a case, as I have never had opportunity to study any material after long exposure to dust of this kind. We quite agree with you that the anatomic changes are probably not due directly to exposure to cotton dust; that there is a complicat ing infection, but whether this is directly attributable to the dust ex posure or not cannot be established. Dr. Sampson saw the films before he read your letter and because they were marked California he naturally thought of coccidioidal granuloma as a possible etiologic agent of infection. This I would as sume you have excluded. THE INERT DUSTS 371 I certainly feci that the sputum should be examined for all kinds of fungus and unusual bacteria. I quite agree with you that lues can probably be excluded as a cause of pulmonary change. I am sorry that I cannot help you. If you should arrive at any definite conclusions about the case I would be interested to learn about them. Dr. II. L. Sampson, at Saranac, stated: Definite pathological process involving both lungs, more particu larly at the base, and more particularly the left base, with some em physema in the top of each lung. The character of the shadows sug gests this to be non-tuberculous, but it does not have the nodulation characteristic of silicosis. About the best that can be said for the process is that it does not appear to be tuberculous. The possibility of coccidioidal granuloma would have to be considered. After viewing these films, Dr. A. J. Lanza wrote: Both Dr. McConnell, my colleague, and I have viewed these films and see nothing in them to suggest an occupational condition, nor have we at any time seen anything in the films of cotton mill workers that would indicate any specific pulmonary reaction as a result of ex posure to cotton dust. It did seem to us that the appearance in the left base was some what suggestive of gumma. Speaking from my own experience, in a healthy, colored male, with a 4 plus Wassermann, presenting symp toms not readily accounted for, I would be very much inclined to try anti-syphilitic treatment. It would be interesting and well worth while to see what changes there might be in the appearance on the a;-ray films following a few doses of specific therapy. I will be interested to know what the outcome of this case is and would appreciate your informing me. Dr. C. 0. Sappington had this to say: Taking all the information into consideration and making a differ ential diagnosis, it is my opinion that all of the following things must be taken into consideration: Pulmonary tuberculosis; asbestosis; some form of mixed infection; and some form of fungus infestation. I do not believe that there is any reliance to be placed on a diag nosis of byssinosis, because I believe that the symptoms, the clinical course, and the a>ray findings are all out of proportion to any effect that could be produced by cotton dust alone. While it is not entirely possible to rule out tuberculosis, it is unusual that the predominating lesions in pulmonary tuberculosis should be basal in type as they are here. The question of asbestosis is raised merely because of the char 372 OCCUPATIONAL DISEASES acter of the lung changes, and also because of the suggestion of em physema in the upper lobes; however, there is also emphysema at both bases, which is against asbestosis; furthermore, at the left base there are large "snowball-like" changes which certainly do not sug gest asbestosis. There is, of course, no suggestion of silicosis in this film. It is my belief that the greatest possibilities in this case lie between a so-called mixed infection and some sort of fungus infestation. Summary.--From the various opinions expressed regarding the x-ray films, it is evident that the markings indicate (1) a pronounced emphysema and increased fibrosis; (2) the presence of snowball-like or whirlpool configurations of unusual and undetermined character; (3) the possibility of fungous infection; (4) the possibility of gumma. The maintenance of weight, the absence of afternoon temperature, the negative sputa, the negative guinea-pig inoculation, and the char acter of the films argue against the possibility of tuberculosis. Syph ilis of the lung can definitely be ruled out. This patient was first seen in May, 1939. At that time the positive Wassermann was noted, and the patient immediately underwent antiluetic treatment. Examination nearly one year later shows the treatment has changed the complexion of the Wassermann reaction, but the chest films remain unchanged and, if anything, seem further accentuated. According to Sante,2 the lungs are structures relatively, if not entirely, immune from syphilis. Our present knowledge of the action of inert dusts dispels any likeli hood that the markings of the lung as- revealed by x-ray are the result of cotton dust. It is conceivable that the repeated attacks of allergic asthma, in conjunction with continuous inhalation of dust over many years, may finally set up pulmonary changes consistent with a chronic bronchitis and produce a loss of elasticity of the pulmonary tissue. In view of the English observations of certain molds in the ma terial used, the writer questions the possibility of some unrecognized fungous infection in the case at hand. One case of this type is no basis upon which to form an opinion, yet medical history is replete with instances where an isolated finding or suspicion has instigated research into undeveloped fields. The case is not presented as an illus tration of pneumoconiosis, but rather one of unrecognized pathology, suggesting the presence of an unrecognized concomitant factor in cot ton-dust inhalation. REFERENCES 1. Collis, E. L.: English Encyclopedia of Hygiene, Pathology, and. Social Welfare, 1930. 2. Sante, L. R.: "The Chest," Annals of Roentgenology, Paul B. Hoeber, New York, 1930, Vol. XI, p. 386. THE INERT DUSTS 373 MILL DUST Occupational Hazards.--The inert dusts should not be passed over without a word regarding a rather neglected problem in certain mills and grain elevators. While these dusts have no direct effect upon the tissues of the respiratory tract, they do carry certain allergens. In various mills, factories, and plants, the concentration of inert dusts may be very great and yet not affect the majority of workmen em ployed there. A few of these, however, may develop a respiratory or cutaneous allergy, the cause of which may be unrecognized by them selves or their physicians. Particularly is this apt to be true in those who work in or around flour or grain mills. Attention to this problem has been called by the report of Wittich.1 Discharge of Dust into Air.--Wittich points out that in the mill ing of grains the problem becomes one which concerns not only the workmen in these mills but the community, for the dust discharged into the air from "cyclones" atop these mills causes high contamina tion of the air over an area of many blocks. In fact, the dust hazard for the workmen is often controlled while the general community re mains unprotected. This investigator has pointed out that slides ex posed for twenty-four hours inside offices within six blocks of these mills showed numerous grain smuts, rusts, and molds. It appears that the worst offenders are the grass and grain smuts. Smuts.--These are minute, threadlike, parasitic plants of my celium, which enter the growing portion of the seedling and grow up with the host, remaining invisible until the heads of grain appear when they partially or wholly destroy the heads, appearing at that stage as masses of dark substance. These masses contain spores which further propagate by getting on or into the seeds, where they reenact their life after the seed is planted. Due to these smut spores, contact dermatitis, atopic forms of skin allergy, perennial rhinitis, and asthma may occur. These conditions may be fairly abundant wherever condi tions favor the infestation of smut. They are most pronounced in the Middle West, the Pacific Noi'thwest, the South, and the Southwest. Grain or Malt Fever.--There exists another illness among grain workers which, when described by them, sounds fantastic. This con dition, referred to as "grain fever" or "malt fever" came to the writ er's attention just after the printing of this book had begun, so that there was not sufficient time for thorough laboratory investigation of this type of case. A weighman at the grain elevator of a malt company in Los An geles, was hospitalized suffering from a penetrating wound of the chest. In relating his past medical history he described recurrent at tacks of an odd malaise which he attributed to exposure to malt dust. _Vf 374 OCCUPATIONAL DISEASES The other men at this mill were subsequently reached, and the pa tient's story was substantiated. Symptoms.--A description of this illness follows: Several hours after leaving work, or while asleep, the workman becomes aware of a headache, weakness, fever, chills, and cold sweats, as well as nausea, cough, and often vomiting. By morning these symptoms have all sub sided, the victim feels normal, and reports for work. Such nocturnal attacks may continue for several weeks. This strange illness occurs most frequently among men never before exposed to grain dust, or among experienced men at the beginning of a new season or upon re turning to work after a short absence. In this respect it is not unlike metal-fume fever, an illness to which only those constantly exposed appear to develop an immunity. No satisfactory explanation can be offered for this reaction to malt dust, except that it is probably due to a foreign protein. Report of Investigation.--To check our observations, a search of the literature revealed only one reference to "grain fever." In a sur vey of the hazards to which the grain-handlers at Buffalo are exposed, the Division of Industrial Hygiene of New York State reported the occurrence of the aforementioned syndrome. The Buffalo workers empty boats bringing grain from Canada and the western states. The description of "grain fever" occurring in these workers is exactly like that found in our group. While the condition is not disabling and there appear to be no chronic ill effects, it is worthy of recording in the literature. Roentgenographic Findings.--This report of the New York inves tigation not only confirmed our observations but in addition revealed the a;-ray findings of 395 grain-handlers. It is as follows: Men x-Rayed re-Ray diagnosis: Number Percentage Negative ........................................................... 323 81.7 Old healed tuberculosis.................................. 49 12.4 Clinically significant tuberculosis............... 7 1.8 Fibrosis ............................................................. 9 2.3 Non-specific lung infection........................... 7 1.8 Total ........................................................... 395 100.0 The a:-ray finding of greatest interest in this group of grain handlers was that designated as "non-specific lung infection." Such cases showed irregular patchy areas of increased density in the bases or mid-lung fields associated with an increase in linear markings. The appearance sometimes resembled a clearing pneumonitis, sometimes a bronchiectasis.2 THE IXERT DUSTS 375 The report concluded that the significant hazard to men in this occupational group is that of an increased liability to respiratory dis ease, particularly an irritation to the upper respiratory tract. This occupational cause coexists with, and is probably enhanced by, the hazard found in the inclement weather so prevalent along Lake Erie. Medicolegal Aspects.--Florists, gardeners, field workers, and others in similar occupations present themselves with cutaneous manifesta tions of fungus infection or reactions to certain allergens in plants, weeds, etc. But it is not common to have a workman allege his asthma or hay. fever is due to the dust in the mill or plant where he works. Undoubtedly more of these cases occur than arc reported, probably because the workman is not cognizant of the possible etiology. These cases call for intensive search for the actual cause in order to estab lish the compensability of the claim. REFERENCES 1. Wittich, F. W., and Staekman, E. C.: "Case of Respiratory Allergy Due to Inhala tion of Grain Smuts," J. Allergy, 8: 189-193 (Jan.), 1937. 2. Industrial Hygiene Bulletin, Division of Industrial Hygiene. New York State De partment of Labor, Yol. 20, No. 1 (Jan.), 1941. TREATMENT OF DTJST DISEASES There is no specific treatment for silicosis, asbestosis, or anthracosilicosis other than removal from exposure. Treatment used, then, will be symptomatic or preventive. Symptomatic Treatment.--Under symptomatic care, general ton ics, vitamin preparations, an adequate diet, cough mixtures, and mild narcotics, such as codeine phosphate or sulfate, may be listed. If the patient has marked dyspnea or other disabling factors, a regimen of limited activity should be outlined. However, not all patients show ing marked involvement must necessarily join the great class of un employed. Many of them are better off occupied. Cardiac insufficiency, usually of the right-heart-failure type, and emphysema may require special attention, but their treatment will often be very unsatisfac tory in view of the irreversible structural changes which have already taken place in the lungs. Particular care should be taken to guard against respiratory infections, such as colds, acute bronchitis, bron chopneumonia, and lobar pneumonia. Bronchodilator Vapors.--The use of a continuous-spray technique for the administration of vaporized bronchodilator solutions has been described as giving relief of dyspnea, asthma, and cough in patients with chronic fibrosis and emphysema who are confined to bed or who are on a limited ambulatory regimen. This might be found useful in some of the more advanced of these cases. The solutions used are 376 OCCUPATIONAL DISEASES epinephrine, 1:100 solution, or when undesirable side-reactions occur with the former, ncosynephrin, 1:100. This method as described by Richards, Barach, and Cromwell1 is as follows: An oxygen pressure tank, with the usual reducing valve to regulate flow, is used. The out flow tube is attached to the vaporizer, and oxygen is run in at a flow sufficient to produce adequate vaporization. A small motor blower unit can be used instead of a pressure tank, but these units usually convey a slight undesirable odor to the vapor. With a flow of from 4 to 7 liters per minute, 1 cc. of the solution is vaporized in from three to ten minutes. The patient holds the vaporizer nozzle in his oropharynx and breathes quietly. As a vaporizer, Vapco and Vaponefrin models are satisfactory. A convenient schedule suggested by these authors is the inhalation of the vapor of from 0.5 to 1.5 cc. of the solution for from five to ten minutes: (1) on waking in the morning, and before getting out of bed; (2) in the middle of the day, e.g., after lunch; and (3) just be fore retiring at night. With this method significant increases in vital capacity were noted in most cases of chronic fibrosis and emphysema. Measures in Tuberculosis.--If tuberculosis in active form is pres ent, sanatorium treatment is indicated, with the various therapeutic approaches usually directed toward that disease being used. Special care to guard against spread of tuberculosis, if it occurs, is needed. Spontaneous pneumothorax with collapse of a lung from rupture of emphysematous blebs has been described, although its incidence is not great because pleural adhesions usually prevent the occurrence of such collapse even though a bleb may rupture. If such an incident occurs, removal of the compressing air, administration of oxygen, and treat ment of circulatory failure may be required. Prophylaxis.--Preventive measures are of extreme importance, es pecially as they apply to silicosis and asbestosis. Aluminum Dust in Prevention of Silicosis.--Denny, Robson, and Irwin,2 of the University of Toronto, have recently made a discovery which may shortly be of much practical importance in the prevention of silicosis. Their experimental results showed that a very small pro portion of metallic aluminum dust would protect experimental ani mals from silicosis. In these animals the inhalation of aluminum dust in large quantities over long periods of time showed no effect on the general health of the animals and no evidence of toxicity or damage to tissues. The concentration of the aluminum necessary to prevent silicosis was hundreds of times below the explosive concentration of aluminum powder. At the McIntyre mine, by using small quantities of aluminum powders, varying from 3 to 20 gm. dispersed in a dust cloud, reductions in solubility of 90 per cent or better were obtained from THE INERT DUSTS 377 dust samples taken from 150 to 300 feet from the face, following a drift round blast having a volume of 8000 cubic feet. Other Measures in Silicosis Prevention.--Lanza3 listed the follow ing as factors in the prevention of silicosis: (a) Abandonment of Process Producing Dust.--An example of this is the cleaning of metal castings with adherent sand by a wet method instead of by sand- or shot-blasting. (b) Substitutes for Dangerous Materials.--Examples include the use of artificial abrasive wheels for sandstone in metal-grinding; metal Fig. 74.--Exhaust ventilation applied to an unenclosed primary carding machine for asbestos. (U. S. Public Health Service, Bxdletin 2Jtl.) grit or aluminous abrasive for sand or flint in sand-blasting; alumina for placing china biscuitware and for polishing and grinding in the pottery industry. (c) Suppression of Dust Immediately on Its Production.--An ex ample of this is the improved outlook in mining and quarrying in sandstone, granite, and other siliceous rocks and deposits by the use of water alone or combined with foam-producers with suitably modi fied drills. 378 OCCUPATIONAL DISEASES (d) Removal of Dust Near Point of Origin.--This is to prevent its reaching the breathing level. Localized exhaust ventilation by mechan ical means has been widely used (Figs. 74, 75). (e) Exclusion of Persons.--No one should be allowed in the room where a dusty process is being carried on unless he is actually and necessarily employed in it. (/) Protection by Individual Respirators or Breathing Apparatus. --These should have a high filtering efficiency against fine dust, fit accurately, have low resistance, and be reasonably comfortable and cheap. These are not substitutes for dust suppression or removal. (g) Adequate Medical Supervision.--Preemployment examinations should be of an exacting type, with special attention given to the fam ily history for tuberculosis, history of a tendency to respiratory in fections, the past medical history, previous exposure to silica, the pres ent physical condition, and x-ray examination of the lungs. Successful THE INERT DUSTS 379 applicants should be picked men in the best of health from every standpoint. Periodic reexaminations should be made, the frequency depending upon the severity of exposure, type of work done, etc. The first onset of pulmonary symptoms in those engaged in dusty occupa tions should be the signal to abandon the work, since, although the damage already done cannot be remedied, it may be checked to some extent by avoiding further exposure to the dust. (h) Ventilation.--There should be rigid adherence to proper ven tilation, and inspection of the hazard should be periodic to insure the minimal concentration of dust. For those working in the inert dusts, similar but less exacting requirements need to be enforced. Asbestosis.--The control of asbestosis follows very closely the steps outlined above. In asbestosis the dust-control methods are very prac ticable and have been vigorously carried out by asbestos-manufactur ing companies with successful results. Mill Dust.--If alleged symptoms in a workman were, after thor ough investigation, found to be due to grain smuts, rusts, or molds, the obvious treatment would seem to be his removal from expo sure. Some striking results in patients with respiratory allergy due to rusts and smuts following hyposensitization with rust and smut ex tracts have been described.4 The symptoms in these patients subsided after two or three injections. REFERENCES 1. Richards, D. \Y., Jr.: "Use of Vaporized Bronchodilator Solutions in Asthma and Emphysema," Am. J. M. Sc., 199: 225-232 (Feb.), 1940. . 2. Denny, J. J., Robson, W. D., and Irwin. D. A.: "The Prevention of Silicosis by Metallic Aluminum," Canad. M. A. J., 10: 213 (March), 1939. 3. Lanza, A. J.: Silicosis and Asbestosis, Oxford University Press, New York, 1938. 4. Waldbott, G. L., and Ascher, M. S.: "Rust and Smut, Major Causes of Respiratory Allergy," Ann. Int. Med.., Ik: 215 (Aug.), 1940. !_ 'p. j.!- PART Y CHAPTER XXX THE INDUSTRIAL BACK* While backache has not been considered primarily an occupational disease, its prevalence among workmen and the frequency of claims for compensation for this disability render a discussion of this condi tion obligatory. Increase in Number of Claims.--During 1939 every tenth patient presenting himself at this clinic alleged a back sprain. Each year there has been an increase in this percentage over the previous year. What is the reason for this increase? Certainly man's work is not more ardu ous. The jack, crane, hoist, derrick, steam shovel, truck, and other de vices spare him much that was formerly done by purely human effort. Possibly these aids have changed the environmental conditions to the extent of altering the potentialities that man has for work. Be that as it may, there is no question but that the attitude the workman and the physician have toward the benefits of compensation has added to the number of claims. The patient, being- unable to evaluate the rela tionship of his pain to his work, naturally thinks it is the result of effort. The average physician doesn't attempt to make any differen tiation. Because of the existing situation, this relationship was sub jected to a prolonged study, the results of which, it is hoped, will influence an adoption of a saner attitude toward the so-called "indus trial back." Relation of Pain to Work.--In complete disregard of the multiple causes of backache, the tendency in industrial medicine is to "massgroup" all these cases under the diagnosis of back sprain. This error seems to be predicated upon the "locale" of the onset of pain. If it ensues while a man is cutting his own lawn, the term "lumbago" is invariably applied and the condition attributed to causes within the man. But pain arising while stooping, bending, or lifting at the plant is called "back sprain" and considered the result of motion while work ing for someone else. The situation assumes added import when it is appreciated that this disability is becoming one of the most frequent causes of claims for compensation. * This chapter represents a slight enlargement of the author's paper published in the American Journal of Surgery, 4<S (July), 1940. 381 382 OCCUPATIONAL DISEASES DIAGNOSIS Sprain in Presence of Normal Motion.--In the series offered for consideration, an inadequate or negligible history of injury occurred in over 70 per cent of the cases. Obviously, then, the history should determine the basis for investigation before accepting or denying a case as being occupational in origin. The patient brought in disabled because of a fall from a ladder or platform requires such an examina tion as will determine the extent of his injury. But the man who be comes disabled while engaged in a simple motion requires an investi gation upon more divergent lines. It is imperative that criteria of normal and abnormal motion, or movement, be established in the ex aminer's mind. If the origin of pain is to be evaluated and its respon sibility allocated, the above statement must become indelibly fixed in the minds of all industrial physicians. Despite the contention that in the evolution of man instability of the lower back occurred when he assumed the orthograde position, there does exist a normal physiolog ical range of motion. Sprain is defined as an overstrain, the result of excessive motion. Accepting the last two statements as a premise, how can a motion to which one is accustomed, one executed daily in the same manner, one within the normal range and lacking excessive, strenuous, or unusual characteristics, constitute a sprain? Yet, beyond any question of doubt, from mild to severe, disabling pain does occur following a normal motion or a trivial act. Why? It should be appar ent that it would not have occurred had there not been an added fac tor, an unrealized factor, present. It must be this added factor, this added "straw" that breaks the patient's back. The failure to search for it in industrial medicine has resulted in the preponderant diagnosis of "back sprain." Multiple causes and various theories represent this "straw," which will be reviewed briefly. Sacro-iliac Slip.--The sacro-iliac slip or subluxation will receive no mention here other than to state that despite its wide refutation by reputable investigators it still finds wide acceptance as a common cause of backache. Invariably this diagnosis is made without benefit of a;-ray study. There was not a single instance of such a condition in our large series of cases. Indiscriminate use of this term should cease. Sources of Back Pain.--At one time congenital or developmental defects were emphasized as a cause of backache. Then a lack of em phasis followed, and the importance of Bertolotti's syndrome (sa cralization, sciatica, and scoliosis), along with other abnormalities, was minimized. Recently certain of these defects have been receiving more consideration as the cause of back pain. Muscles and Ligaments.--Why is it that certain persons with these defects evidence no back pain, while others have a chronic discomfort THE INDUSTRIAL BACK 383 or disability? It is believed that the reason is based upon the condition of the muscles and ligaments. As long as they maintain their tone, the defect remains an innocent anomaly. If, however, the tone and strength of the muscles and ligaments supporting the lumbosacral area are deficient, then the structural defect becomes a participating factor. Persons with structural defects and mechanical weakness have a lessened capacity to engage in occupations requiring the use of the lower back. In fact, in the presence of this combined weakness, disa bility may occur without direct trauma or excessive strain. Injuries and Toxemias.--Goodwyn1 expressed the belief that cer tain anomalies are a definite source of pain when aggravated by injury or toxemias. He further stated that in the presence of such anomalies, disability can result without injury. Facet Irregidarities.--Putti- particularly has renewed the profes sion's interest in the abnormal placement of the articular facets. Their variation in the lower portion of the back is important when it is realized that the intervertebral canals between the fourth and fifth lumbars and the fifth lumbar and sacrum are the smallest, whereas the fourth and fifth nerve roots emerging from them are the largest. Facet irregularities can only be detected by employing the oblique view of the z-ray. How frequently this irregularity may be passed up by rou tine rc-ray study is obvious. Willis once thought the separate neural arch an important defect, but later expressed agreement with Badgley in doubting its significance. Spondylolisthesis and the horizontal sa crum are unquestionably definite factors in low back pain. Lumbosacral Contracture.--One of the commonest findings in the . routine examination of the back by a;-ray is a narrowing of the lumbo sacral junction. Hodges3 found it in 57 per cent of his cases with backache, Williams4 in even a greater percentage. Its importance has been slighted until recently, and Williams in particular has awakened interest in this possible source of pain. He describes this lesion as a chronic, traumatic, or postural destruction of the lumbosacral inter vertebral disc. Certain muscles weaken through disuse while others become stronger, resulting in several alterations of weight-bearing and a constantly increasing force brought' to bear upon the posterior mar gins of the intervertebral discs of the lumbar and lumbosacral areas. This disc becomes wedge-shaped, and there is constriction of the fora mina with subluxation of the facets. Its high incidence in patients with back pain indicates consideration in the eventual diagnosis. Rupture or Herniation of Intervertebral Disc.--Another phase of intervertebral disc pathology receiving increasing attention is its rup ture or herniation. To appreciate the pathology of disc protrusion or herniation, it is necessary to recall that the body of the vertebra is iW m. 384 OCCUPATIONAL DISEASES composed of cancellous tissue, the major portion of which is uncov ered and not protected by compact bone. iDisc Anatomy.--The disc between the vertebrae is made up of three parts: (a.) The Central Portion (Nucleus Pulposies).--It is firm, elastic, of fluid consistence and is retained in its central position by consid erable tension. It functions as a cushion which serves to absorb and distribute evenly pressure applied along the axis of the column. Be cause of its fluid consistence, it swells or bulges out if extreme pressure is applied, or if the pressure of the surrounding tissue is removed (de generative processes). (6) The Peripheral Portion (Annulus Fibrosus).--This structure lacks the elasticity of the nucleus pulposus for which it forms a cap sule and serves to fix the disc. (c) The Cartilaginous Plates.--These are two thin layers of hyaline cartilage situated between the disc and the body of the vertebra and are found only over the central portion of the disc. They likewise serve to withstand the pressure of the nucleus. Expansion of Disc.--With the above picture in mind, it is not difficult to conceive of the susceptibility of the disc to pressure influ ence, whether it is from a single act of trauma, from repeated trauma, or from degenerative changes. The spine is subjected to constant func tional activity. Just being about our daily business imposes an ele ment of wear and tear. The daily functional imposition placed upon the intervertebral disc is comparable to that placed upon the vascu lar system. Expansion of the disc is seen repeatedly in x-ray films of persons who present no evidence of cord symptoms. That is, the nor mal contour of the intervertebral space is altered, indicating an ex pansion into the body of the vertebra. It was found to be present in 32 per cent of our patients. Whether the incidence is less in the non laboring group as compared to workmen in heavy industries, the writer is unable to say. This nuclear expansion into the body of the vertebra is commonly referred to as "Schmorl's node" (Fig. 76). Just what effect these have in the production of a back disability is as yet not fully known. It is thought by some that reactive changes follow the protrusion of the disc substance into the spongiosa, such as pro liferation of cartilage and bone. It is held that in youth the loss of the disc substance, together with the alteration in shape and size, gives rise to spinal deformities. Retropulsion of Disc.--Probably a more important phase of disc disturbance--certainly one which is receiving widespread considera tion in the present-day literature--is the retropulsion of the disc into the canal space (Figs. 77, 78). It has been definitely established that a THE INDUSTRIAL RACK 385 Fig. 76.--A, Schmorling of the intervertebral disc between the third and fourth vertebrae and to a less extent between the fourth and fifth. No history of serious injury to the back. B, A protrusion of the disc substance into the body of the vertebra (Schmorl's node). ar-Ray films do not reveal the marked degree of indentation indicated by the drawing. Fig. 77. Fig. 78. Fig. 77.--Retropulsion of the disc (herniated intervertebral disc) showing pressure upon the cord--dorsal view. Fig. 78.--Retropulsion of the disc into the spinal cord--lateral view. 2o 386 OCCUPATIONAL DISEASES protrusion of this nature does cause compression of the spinal cord or of one or more of the nerve roots, resulting in a fairly typical syn drome of low back and sciatic pain. In the wake of this discovery there has been a tendency to operate on too many patients suspected of nucleus pulposus without a justifiable diagnostic basis. The symptoms are invariably pain in the lower back extending into the buttock and down the affected leg posteriorly, with a tendency to involve the lateral and anterior surface of the lower leg. The pain is usually con stant but may be intermittent with acute attacks accompanied by sciatic scoliosis. The pain is accentuated usually by coughing, sneez- Fig. 79.--This film is of a patient who had clinical evidence of a ruptured nucleus pulposus. At operation no herniation of the disc was found, but hypertrophy of the ligamentum flavum was present. The shadow is that of Iipiodol in the spinal canal. ing, or sudden increase in the intra-abdominal pressure. The pain may also be increased by hyperextension of the spine, spasm of the lum bar muscles, loss of normal lumbar lordosis, reaction to jugular com pression, and positive Lasegue's and Kernig's signs are helpful diag nostic findings, as are also the diminution or loss of the achilles tendon reflex and frequently atrophy of the lower leg. These findings strongly indicate the presence of a nucleus pul posus, but the diagnosis should be further substantiated by the eleva tion of the total protein content of the spinal fluid (fluid should be withdrawn from the lower part of the lumbar spine), and by finding rc-rav evidence of spinal blockage by using a radiopaque oil (Fig. 79). THE INDUSTRIAL BACK 387 Some investigators object to lipiodol on the belief that if the oil reveals no blockage and is permitted to remain in the canal, since no operation is performed in such a case, it is a source of irritation. These objectors prefer to use air. However, among others, Barr, Hampton, and Mixter3 noted no serious disturbance from lipiodol in twenty patients who were not operated upon. Unquestionably the patient with chronic backache will receive in the future an investigation along the lines just outlined and undoubtedly many a suspected malingerer will have to be reclassified. At the time of operation, a search for a nucleus pulposus has revealed not infrequently the presence of a hypertrophy of the ligamentum flavum, causing cord pressure. Contracture of Iliotibial Band.--To continue with other conditions considered to be the cause of back pain, OberG calls attention to the contracture of the iliotibial band and suggests cutting of this band for the purpose of securing relief. Involvement of Dorsolumbar Junction.--A recent study and report of Judovich and Bates" detracts from the lumbosacral area the im portance that has been ascribed to it and centers attention on the dorsolumbar junction. They have been impressed with the frequency of a syndrome involving the twelfth dorsal and first lumbar nerves, resulting in a neuralgia due to the susceptibility of the dorsolumbar spine to injury and strain. Among some of their contentions are these: That the dorsolumbar area represents a combination of fixed and movable parts which arc more susceptible to injury than the fixed segments found above and below this area; that this area bears almost as much weight as the lumbar spine, yet these segments are smaller and weaker; that because this site is nearly in the middle of the spine it bears more leverage; that the lumbar enlargement of the spinal cord in this region makes vertebral housing relatively smaller. Judovich and Bates' contention, in the main, is similar to Steindler's8 in that there is an involvement in a large percentage of these cases of the posterior division of the spinal nerves. However, they locate the original site higher than Steindler, and disagree with the commonly accepted text book distribution of the twelfth dorsal and first lumbar nerves (pos terior division). They emphasize that tenderness should not be con fused with pain, and that while pain may be confined to any one point, tenderness exists over the entire distribution of the nerve. Their illustrations reveal distribution extending anteriorly and involving the lower anterior wall adjacent to and below Poupart's ligament, ending in the midline. According to their theory, tenderness should exist over this portion of the abdomen as well as over the back. This is not borne out in our study. Circulatory Disorders.--Makaroff8 attributes much back pain to 388 OCCUPATIONAL, DISEASES a vasospastic disorder, believing in many instances it should be treated as a circulatory condition rather than an orthopedic entity. He states that an occlusion of the blood vessels can take place as a result of trauma or focal infection, producing a pain comparable to that in the leg following an ischemia. Ridlon and Berkheiser10 called attention to the calcareous degeneration of the abdominal aorta as a cause of backache (Fig. 80). The author has one such unquestionable case in this series and eight others where this apparent circulatory deficiency was considered contributory. Pig. 80.--Calcification of the abdominal aorta. (Anteroposterior view shows marked calcification of the iliacs.) Patient complained of pain across the lower back and in both legs after climbing stairs or walking a short distance, which was almost im mediately relieved by resting. Fascial Adhesions.--Gratz11 contends that, "Fascial planes func tion as joints, synchronizing motion between muscles, groups of mus cles, nerves and blood vessels. Traumatic and inflammatory lesions may involve these planes resulting in myosynovitis or fascial adhe sions. These are believed to be competent producing causes of muscu lar pain by involvement of the nerves and the limitation of the normal range of motion in the joint by retardation of the gliding mechanism of the muscles." Using air insufflation followed by pneumofasciograms he demonstrated these adhesions. If his viewpoint is ac cepted, manipulation is of value not only in the stretching of muscles but in the freeing of agglutinated surfaces and the breaking of ad hesions. THE INDUSTRIAL BACK 389 Posture, Nutrition, and Exercise.--Faulty posture, poor nutrition, insufficient exercise, and ignorance of how to execute motion arc defi nite sources of back pain. These are daily and frequently exemplified in the workman who presents himself with back pain following a sim ple act. He finds his contrast in the trained pole-vaultcr whose spine and muscles coordinate as he twists, squirms, and turns to ascend to almost unbelievable heights. Consider the contact, impact, and pretzel like positions imposed upon the football player. Yet the painful back in the college athlete is zero compared to that in the industrial worker. Proper food, guided exercise, and knowledge of how to engage in movements involving stress account for the former's seeming immu nity. Industry of the future might well consider the physical director as essential as the guardrail or respirator in the prevention of disa bility among its workers. Miscellaneous Sources.--This passing parade of possibilities must cite allergy and endocrine imbalance. Referred pain from adjacent or gans is common. Finally, but most important, are the secondary effects from systemic or focal infection. Why this source is accorded such negligible recognition by the industrial physician is beyond under standing. Pain occurring in the knee, elbow, or shoulder, with or with out motion, should invariably instigate a search for infection else where in the body. Are the fascial planes and vertebral joints not just as susceptible? Classification of Sources of Back Pain.--Consideration of the varied etiology outlined in the review just completed stimulated a study conducted over a three-year period. That the term "back sprain" could be applied to approximately 80 per cent of these disa bilities appeared unreasonable and unscientific. It was felt that an adequate answer could be obtained only by studying a sufficiently large series of cases and only those cases where the onset of pain allegedly occurred while the patient was working. The series repre sents all ages, races, various social levels, and types of industry. Procedure.--In the clinic where this material was gathered the fol lowing procedure is observed. Excluding the recently traumatized back (severe falls, crushes, and blows) every patient alleging back pain is referred to the Special Examination Department. Following a de tailed, exacting history and a complete physical examination, a;-rays, urinalyses, and blood counts are done routinely. If indicated, and when necessary to establish the diagnosis, further rr-ray examinations of teeth, sinuses, lungs, genito-urinary tract, etc., are made; also blood Wassermann, blood chemistry, blood sedimentation, smears, and cul tures. The data gathered from this three-year study are presented in the following tables: 390 OCCUPATIONAL DISEASES Table 17--Patients in Sukvev X'umbcr of cast's studied from April 1, 1936, to February `28, 1939............................... 8018 Incident to total clinic admissions, 1980................................................................................... 7.0 Incident to total clinic admissions, 1988................................................................................... 10.4 Males................................................................................................................................................... `2799 Females............................................................................................................................................... 219 Average age................................................................................................................................ 80.2 Patients referred to clinic diagnosed its hack sprain................................................ 74 per cent Patients referred to clinic diagnosed its sacro-iliac disease.................................. 5 per cent Attention is called in this table to an increase ot` 2.8 per cent of back claims in 1938 over those of 1936. Of the 219 females represented, over 60 per cent of these had received falls or contusions as a result of their heels catching, or their slipping on a smooth surface. Special attention is called to the group of cases in Table 18. These patients had been diagnosed and treated elsewhere before being re ferred to this clinic. The condition in practically 80 per cent of them had been diagnosed as "back strain." Table 18 represents our opinion of their compensability after study. Taupe 18--Status or Compensability No. of Cases 1936 (April 1 to Dee. 31)........... 1937................................................... 1938................................................... 1939 (Jan. 1 to Feb. 28).............. Totals........................................ 722 1092 1014 190 2018 Accepted 433 564 315 56 1368 Rejected Percentage of Rejections 289 528 699 134 1650 40 49 59 71 57 The reason for this sharp rise in the percentage of rejections found in Table 18 is that in the summer of 1937 a policy of unlimited labora tory investigation was adopted. This resulted in finding pathological conditions which, when considered with a negligible history of injury, formed a basis of rejection. While the entire average rejection over a period of three years was only 57 per cent, the rejections for the years 1938 and 1939 averaged 70 per cent. Table 19--Basis op Rejection Of the accepted cases, a contusion occurred in............................................. 423 or 31 per cent Of the accepted cases, a leukocytosis occurred in.................................................... 3 per cent Of the rejected cases, a leukocytosis occurred in...................................................... 37 per cent Of the rejected cases, abnormal urine, smears, serology, blood chemistry, etc., occurred in........................................................................................................................ 13 per cent Of the rejected cases, a history of previous back disability occurred in........... 42 per cent Of the rejected cases, fever occurred in....................................................................... 11 per cent THE INDUSTRIAL BACK 391 The pathological conditions which were present in the rejected cases are broken down and outlined in Table 20. Table 20--Morbid Anatomy in Rejected Cases Throat infection.................................................................................................................................. 301 Defective oral hygiene, significant degree.................................................................................. 000 Coryza................................................................................................................................................... 127 Pleurisy................................................................................................................................................. 31 Pneumonia; pain in dorsal area first symptom........................................................................ 2 Cholecystitis........................................................................................................................................ 5 Gallstones............................................................................................................................................. 3 Aneurism............................................................................................................................................... 1 Aortitis, with positive serology............................ 0 Coronary heart disease, suspected................................................................................................ 12 Appendicitis, with chief complaint of hack pain...................................................................... 3 Kidney stones...................................................................................................................................... 10 Nephritis, with urinary evidence.................................................................................................. 03 Pyelitis.................................................................................................................................................. 3 Cystitis.................................................................................................................................................. 1 Hydronephrosis................................................................................................................................... 7 Pyonephrosis........................................................................................................................................ 1 Acute gonorrhea, with back pain the reason for examination............................................. 42 History of gonorrhea......................................................................................................................... 312 Enlarged uterus, tumor.................................................................................................................... 2 Abortion; called industrial doctor because of backache......................................................... 1 Abnormal prostate............................................................................................................................. 208 Pylonidal cysts, alleging their presence as resultingfrom contusion or strain................. 20 Pernicious anemia; presented himself because of "sciatica" of legs from heavy lifting 1 Tabes..................................................................................................................................................... 3 Lead poisoning; back pain first symptom.................................................................................. 1 Bronchiogenic carcinoma; presented himself because of dorsal pain................................. 1 Cancer of prostate............................................................................................................................. 3 Obesity, marked, with recurrent back pain, with congenital defective spine................. 9 Adiposogenital dystrophy, age 13, back pain after one day of lifting grocery baskets. 1 Tables 19 and 20 comprise Exhibit A in the indictment of the uni versal usage of the term "back sprain" as a diagnosis of the accepted cases. Of the accepted cases, one third of them revealed a history of actual contusion, leaving only two thirds or 945 out of 3018 cases to be accounted for by unusual stress or strain or extraordinary circum stances. One cannot pass lightly over the fact that of the rejected 51 per cent had abnormal laboratory findings. Nor can one observe the extents of morbid anatomy listed in Table 20 without realizing that the workman is subjected to the same ills all man is heir to and, therefore, the origin of his pain should not be stereotyped. Table 21--Roextgenographic Findings Patients .c-rayed in this series........................................... Lumbosacral pictures........................................................... Cervical pictures................................................................... Dorsal pictures....................................................................... Osteo-arthritis........................................................................ Cancer of vertebral bodies................................................. Tuberculosis of vertebral bodies...................................... Myeloma with involvement of spine.............................. Ktimmell's disease................................................................ Nuclear expansions (Schmorl's cartilaginous nodules) 2414 1929 305 180 24.6 per cent 6 0 1 5 32 per cent 392 OCCUPATIONAL DISEASES The incidence of 24.6 per cent of ostco-arthritis recorded here is conservative. It represents only veil-defined changes. Its place in the etiology of back pain is questionable. Hodges and Peck found it in 23 per cent of their cases of back pain but also present in 28 per cent of their control scries with no back pain. They concluded it had no significance. This conclusion may be applicable to the average group, but the presence of advanced arthritis of the spine- in the elderly laborer cannot be ignored. To our clinic come men from the Goodwill Industries, men older than their years, men who have faced life with Fig. 81.--Marked osteo-arthritis of a sixty-four-year-old Goodwill Industry worker who complained of back pain after lifting bundles of paper (repeated claims of back sprain). the wind of fortune not always at their backs. Invariably they pre sent no sufficient history of injury, but on re-ray examination marked arthritis is observed (Fig. 81). One notes the absence of tuberculosis in this large series of films. So-called "Kummell's disease" was pres ent in two patients who recalled a previous history of injury, and in three who had no history of injury. Invasion of the vertebral bodies by nuclear expansions in this series has already been referred to. Coupled with narrowing of the intervertebral spaces, it is finding in creasing emphasis in recent orthopedic literature. THE INDUSTRIAL BACK 393 Table 22--Variations Found in Lumbosacral Area 1920 Cases Sacralization: bilateral, 5.2 per cent; unilateral, 9.4 per cent........................... 14.0 per cent Failure of fusion (2 found in dorsal area)............................................................... 18.4 per cent Horizontal sacrum.......................................................................................................... 3.4 per cent Narrowed lumbosacral disc......................................................................................... 52 per cent Spondylolisthesis............................................................................................................. 2.8 per cent Posterior displacement of oth lumbar...................................................................... 21 cases Articular facet variations (incompletely studied)................................................. 1.6 per cent Nucleus pulposus herniation into canal: 3 patients injected; 3 revealed blockage A narrowed lumbosacral disc found in 52 per cent of the patients is evidently smaller than that found by Williams and others. Our figure represents patients who showed not only a wedging of this disc but a diminution of the foramina. Efforts to determine cord pressure or blockage by posterior displacement of the nucleus pulposus have been but recently begun in the clinic, so that we have no knowledge of how often it might have been present in this series. Posterior dis placement of the fifth lumbar is found in twenty-one patients in our series. We believe that these are not optical illusions, as Willis12 warns they are apt to be. Tenderness: Table 23--Back Findings Percentage Lumbosacral: bilateral, 10 per cent; unilateral, 18 per cent.................................... 28 Sacro-iliac: bilateral, 6 per cent; unilateral, 13 per cent.................................... 19 Sciatic notch: unilateral......................................................................................................... 28 No tenderness.................................................................................. Limitation of motion, mild......................................................................................................... 03 Limitation of motion, marked................................................................................................... 20 No limitation of motion..................................................................................................... Limitation of straight leg raising: Unilateral.................................................................................................................................... 41 Bilateral....................................................................................................................................... 21 Pain, without motion; constant but aggravated by motion............................................ 56 Pain, on motion only.................................................................................................................... 24 Pain, unclassified, indefinite as to motion or rest............................................................... 20 17 Examination of Patient. Normal Motion versus Abnormal.--It is not to be construed from the foregoing discussion that a case of actual strain should be ruled as non-compensable simply because infection or morbid anatomy is found to coexist. But it is to be reiterated that the physician must carefully evaluate the history of the incident and determine if the factors constitute an abnormal, excessive, overt, or unusual stress; or whether the movement or motion was a normal act and one to which the patient was accustomed. Details of Investigation.--Following the history, and especially if the act which allegedly induced the pain appears to be normal, the patient should be carefully searched for other causes. The vogue of ushering the patient into the physiotherapy room as soon as he has finished his preliminary statement of, "Doctor, I wrenched my back," is to be condemned. The examiner should have the patient describe 25 394 OCCUPATIONAL DISEASES and illustrate, if possible, the exact mechanism of the alleged act. lie should inquire into the weight, size, and type of object being handled, how soon pain ensued after this act, the type of pain and its location, and whether it remained in the same area or moved about. It is con stantly present or only on motion? How frequently does the patient have backache and has he ever had a severe fall or blow to the back? These and many other details must be ascertained. Physical Examination.--This should be done with all clothing removed. It is a good rule to disregard the back until the end of the physical examination, starting and going through the routine that would be carried out in any complete physical examination. Special search for focal infection in teeth, throat, or prostate must be made as well as a search for possible disease in the various organs. This advice may appear redundant, but there exists ample evidence that it is not. Laboratory Investigation.--This should be made as indicated. Most insurance carriers or self-insured employers appreciate the value of, and willingly permit, routine x-vny examination of every case of alleged back strain. Most of them will give consent to special labor atory procedure if they are contacted and informed of the reason for such an examination. (This clinic does the bulk of the work for one large insurance carrier which has agreed to a flat-rate fee for a;-ray ex amination, urine analysis, and blood count of every patient with back pain. While it might seem that such a procedure is costly and useless in many instances, in the end it has proved profitable in the accurate and just dispensation of the claim.) Error of Attributing Back Pain to Occupational Activity Alone. --The investigation of over 3000 cases by the author reemphasizes what has long been recognized--that backache has a multiple and varied etiology. But the amazing revelation to be garnered from this study is that in spite of the recognized causes, and irrespective of the possible pathological conditions which may exist to explain backache, a diagnosis of assumption occurs. The study indicates that the in dustrial physician used this blanket diagnosis in 80 per cent of the cases which were subsequently studied by us and which were reclassi fied because of discovered accountable etiology, so that actually only 30 per cent were considered as having an occupational origin. From this study, it should be appreciated that the disabling back is not an industrial entity. The practice of according it the same occupational earmarks concerning its origin as are attributed to silicosis or lead poisoning, for instance, is a fallacy. The so-called "industrial back" is not primarily an orthopedic problem. It is one for differential diag nosis. From this study it is obvious that disease and infection comprise a considerable portion of the etiology. THE INDUSTRIAL BACK 395 MEDICOLEGAL ASPECTS Figures from this clinic indicate that the average length of tem porary disability in cases of actual strain or sprain was `24.3 days. Prolongation beyond that time should arouse suspicion of other co existing causes. Permanent disability rarely exists from strain in the absence of direct trauma. Illustrative Cases.--It is not necessary to cite instances of actual back strain. Such cases invariably present a history of sufficiently unusual stress, strain, or overexertion. Nevertheless, these patients should receive just as thorough an examination as those without an adequate history of strain. But the coexistence of an unrelated infec tion or disease should not prevent the case from being accepted as compensable. To reiterate a thought which runs as a theme through out this book: the physician should remember that he is not making an examination to disprove the patient's claim or the employer's con tention. In the acute back disability, the patient is not fooling about his pain. The duty of the doctor is to determine the cause of the pain, let the chips fall where they may. On the other hand, the practice of accepting and treating a 'pain in the back as a back sprain when the cause of the pain is an infec tion or disease process is to be condemned. The numerous instances of back pain due to focal infection have been emphasized by our statistical study, and individual cases need not be related. The fol lowing few cases have been selected, not because they represent the infrequent error in assuming that a back sprain exists, but because such mistakes are common. The few illustrations selected serve to warn against: (1) the acceptance of the patient's statement about the cause of his pain; (2) the widespread acceptance of the opinion of the quasi-quack or the increasing lay opinion that a sacro-iliac slip has occurred; and (3) treatment without complete physical and labor atory investigation. Case I.--A sixty-four-year-old janitor received a sudden, severe pain in the back as he stooped to roll a rubber mat. Without benefit of z-ray he was accorded six weeks of physiotherapy with no improve ment resulting and with a steady downhill course on his part. Subse quent history revealed a marked loss of weight over a period of months, generalized weakness and increasing constipation, approach ing obstipation. Examination revealed evidences of loss of weight, anemia, a sharp, angular kyphosis at the twelfth dorsal, first lumbar, which the patient maintained was not present prior to "his accident," and the rc-rays revealed a cancer of the twelfth dorsal vertebra secon dary to the prostate which had not previously been examined (Fig. 82). r i. Fig. 84.--A and B, Films show the presence of a destructive process in the eleventh thoracic vertebra with a complete collapse of the vertebral body so that only a part of the dorsal half remains. Despite the collapse, the intervertebral discs on each side show a space which is relatively well preserved. The anteroposterior film shows the presence of a paravertebral abscess, as well as numerous small chips of bone. Infiltration in the head and neck of the left eleventh rib is indicated by the spotty demineralization in this area. The ventral and cranial corner of the twelfth thoracic vertebra is apparently similarly infiltrated. Malignancy had to be differen tiated from tuberculosis, but in view of the presence of a prostatic malignancy, meta static carcinoma of the spine appeared more probable. C, Schematic drawing to show the collapse of the body of the eleventh thoracic vertebra, the relatively clear disc spaces, and the fragments of bone overshadowing the lower border of the tenth and almost the entire body of the twelfth thoracic ver tebrae. This patient (referred to in the text) was treated for back sprain. 39 G ( THE INDUSTRIAL BACK 397 Case II.--A patient--having a large palpable mass in the right abdominal quadrant; temperature of 101.2 F.; urine loaded with pus; and stones in the right kidney, as noted on -.r-ray examination--was treated for a sprained back because two days after slipping while carrying a radio he developed pain. A diagnosis of a pyonephrosis with stones was confirmed bv an operation (Fig. S3). Case III.--A man who cleaned out boilers for years developed a pain in the upper back and was given physiotherapy for occupational Fig. 83.--This film is of a forty-two-year-old janitor who noted back pain some hours after slipping while holding a small radio in his hands. Because of this history he had been treated for two weeks for "back sprain." Examination revealed a large palpable mass in the right quadrant of the abdomen, a temperature of 102 F., the urine loaded with pus cells, red blood cells, and albumin, and stones as shown by :r-ray film. or positional strain. Subsequent examination after six weeks of treat ment and the payment of compensation revealed a bronchiogenic carcinoma (Fig. 84). Case IV.--A thirty-two-year-old man developed pain at the medial border of the right scapula. He had been treated for: (a) back sprain, (6) subluxation of a vertebra, (c) intercostal neuritis, and (d) pleurisy, by regular practitioners, chiropractors, and osteopaths. Six months after the onset of symptoms he was seen by the author, at which time the following complaints were elicited; deep-seated pain 398 OCCUPATIONAL DISEASES at about the middle of the medial border of the right scapula: exten sion of this pain (about four months after onset of the original pain) to the right shoulder and down the right arm; increasing weakness of grip in the right hand, to the point where he was attempting to educate his left hand to perform the duties ordinarily done by the right, such as using pliers, screwdriver, and the like: inability to sleep because of excruciating pain and failure of ordinary analgesics, such as anacin, to stop the pain; a sensation of swelling around the right eye; and mild, but constant, loss of weight. Cough, afternoon lag, and shortness of breath were denied. Physical Examination.--This revealed no spasm of the muscles of the dorsal area, no limitation of motion, no increase of pain on Fig. 84.--A, Anteroposterior view of the lungs of a forty-six-year-old boiler-cleaner, showing bronchiogenie carcinoma. Patient was treated with diathermy and massage for six weeks for "back sprain" of the dorsal area. B, Right oblique view of same lung as A. Autopsy confirmed x-ray diagnosis. motion, and no tenderness to pressure over the original site of pain. Inspection of the face showed ptosis of the right eye, contraction of the right pupil and anhidrosis, constituting a typical Horner's syn drome. There was moderate atrophy of the muscles of the right shoul der girdle, with marked atrophy of the muscles of the right hand. The grip of the right hand was greatly diminished as compared to the left. Palpation of the arm showed marked loss of tone of the muscles of the forearm. The right palm was very dry (anhidrosis), while the left was moist. There was a tremor to the right hand. The lung find ings were negative clinically except for a mild increase of the whis pered voice sounds. Laboratory and Roentgenographic Examination.--The routine laboratory investigations, such as urine analysis, complete blood count, THE INDUSTRIAL BACK 399 and blood Wassermann, were all negative. The .r-ray film of the, lungs revealed a clouding of the right apex, which was first considered to be a tuberculous process. At this point the neurological surgeon of our staff saw this patient in consultation. He suspected the syndrome to be a pulmonary sulcus tumor, as originally described by Pancoast, and ordered -ray study of the cervical spine and ribs. x-Rays showed: "In the anterior-posterior view thickening of the apex of the right lung, with a dense shadow extending over the apex and with evidence of a small amount of infiltration below it (Fig. 85). "x-Ray of the cervical spine reveals no alteration of the verte bral bodies. It does show a destructive lesion of the vertebral end of the third right rib." Fig. 85.--A and B, Involvement of the right apex and invasion of the right third rib at the vertebral end. Together with the clinical findings, the case represented a tumor of,the pulmonary sulcus. n This case occurred just prior to the publication of this book and, therefore, no biopsy reports can be made. Clinically it conforms in m every respect to the "superior pulmonary sulcus tumor" of Pancoast. # ft In 1924 Pancoast13 reported three cases of what appeared to him it to be a new entity among intrathoracic tumors. He noted that "the tumors in question seemed to occur at the thoracic inlet, were char acterized clinically by pain around the shoulder and down the arm, Horner's syndrome, atrophy of the muscles of the hand and roent- genographic evidences of a small, homogeneous shadow at the extreme apex of the lung, with always more or less local rib destruction and tr? often vertebral infiltration." 400 OCCUPATIONAL DISEASES Pancoast believed that the tumor had its origin from an embryonic remnant of the fifth branchial pouch and represented an epithelioid carcinoma of extrapulmonary origin. In 1932 he reported four addi tional cases. Since then the clinical entity has been fairly well estab lished, but concerning the pathological origin of the tumor there has existed much controversy.11-21 Until further study is made, our case cannot be reported patho logically as a Pancoast tumor, but clinically it conforms to the classi cal picture. EXPLANATION OF SPINAL ANOMALIES From the x-ray files of our clinic, a number of films have been selected which depict the various congenital anomalies described be low. In some instances these defects have been amplified by drawings. It is hoped that these will present an adequate roentgenological and graphic study of spinal anomalies. The drawings used to illustrate the various movements involving the lower back have been done after the manner of those used by Brahdy.22 It has been pointed out that in view of the extension of the Work men's Compensation Act to include the occupational diseases, the general practitioner is confronted with an obligation not heretofore experienced. The so-called "industrial back" is an example, as has been emphasized in the present chapter. It is not unfair to state that in general the office treatment of back pain has consisted of strapping the back, without investigating the cause. When, however, a back dis ability has a medicolegal aspect and investigation reveals certain anomalies which could account for the disability, the general prac titioner is expected to interpret their meaning despite his lack of spe cial training or experience. An appreciation of such irregularities as asymmetry of facets, sacralization, and spondylolisthesis has been lim ited largely to the orthopedist. Now, owing to the expansion of indus trial medicine, the general practitioner also must understand their significance. To the writer's knowledge, no textbook in general medi cine or surgery attempts to define these congenital defects. Therefore, this chapter is augmented by an explanation of these conditions. Asymmetry of Facets (Facet Irregularities, Anomalies of the Articular Processes).--Reverting to Gray's Anatomy, a typical verte bra is described as consisting of two essential parts, an anterior seg ment, or the body, and the posterior part, which is the vertebral or neural arch. These enclose a foramen, the vertebral foramen. The vertebral arch consists of a pair of pedicles and a pair of laminae, and supports seven processes; namely, the four articular, two transverse, and one spinous. The cervical, thoracic, and lumbar vertebrae differ 1 THE INDUSTRIAL BACK SUPERIOR ARTICULAR PROCESS 401 Fig. 86.--A thoracic vertebra. Note the direction of the superior and inferior articular V facets. K TRANSVERSE INFERIOR ARTICULAR PROCESS m Fig. 87.--A lumbar vertebra as seen from above, showing the superior and posterior aspects. Note the plane of the superior and inferior articular facets. in their arrangement of these parts. While the cervical vertebrae present an occasional anomaly, such as the cervical rib or failure of S!G 402 OCCUPATIONAL DISEASES fusion of the spinous process, the majority of anomalies arc to be found in the thoracic and lumbar vertebrae, especially the lumbar. Normally in the thoracic (dorsal) vertebrae the superior articular processes are thin plates of bone projecting upward from the junction of the pedicles and laminae; their articular facets are practically flat, and are directed backward and a little lateralward and upward. The inferior articular processes are fused to a considerable extent with the laminae, and project but slightly beyond their lower borders; the facets are directed forward, a little medialward and downward (Fig. 86). The superior and inferior articular processes of the lumbar verte- Fig. 88.--A, Failure ot fusion--a thin fissure line--of the left inferior articular process of the third lumbar vertebra. This defect on the x-ray film is invariably faint and hard to detect. B, The arrow indicates the failure of fusion of the inferior process with a fissure line which is purposely exaggerated. On x-ray film this line is never so distinct, but on the contrary rather faint and therefore often overlooked. brae are well defined, projecting respectively upward and downward from the junction of the pedicles and laminae. The facets of the superior processes are concave and face backward and medialward; those on the inferior are convex and are directed forward and lateralward (Fig. 87). When the facets do not face in a normal manner as just described, they are said to be asymmetrical, or the condition is referred to in the literature as anomalies of the articular processes. The surfaces of the articular facets are covered with cartilage, and the articular capsules of these joints are lined with synovial mem brane. Hence they are susceptible to changes resulting from infection. THIS INDUSTRIAL BACK 403 i't ;'A- iX Fig. 89.--A, Spina bifida occulta. The defect includes the last lumbar and the first and second sacral segments. B, Spina bifida occulta as shown in A. Vi 8 n k*>- 8 '-x s* u ;.'s i'i I\ < Fig. 90.--A, Failure of fusion of the spinous process of the firth lumbar vertebra, as well as the first sacral segment. The congenital defect of the fifth lumbar had been interpreted as a fracture, the patient being placed in a body cast. B, To show the failure of fusion, the drawing of the film purposely overemphasizes the defect. -7^.- . 104 OCCUPATIONAL DISEASES degenenilive processes and trauma, especially if the primary irrita tion has been induced by alteration of their normal plane of direction. A further anomalous condition of the articular processes is the fis sure line which is occasionally seen (Fig. 88). This line is so fine that it often escapes detection and when seen is sometimes mistaken for a fracture line. Fig. 91.--A, Failure of fusion of the first thoracic vertebra, which was interpreted as a fracture line. A body cast was applied, following which the patient developed a neurosis characterized by marked tremor of the head and right arm. B, Congenital defect of first thoracic vertebra as shown in A. Spina Bifida Occulta.--This term refers to a failure of fusion of the spinous processes of the fifth lumbar and the first sacral segment. Occasionally more than the first sacral segment has failed to fuse. Inspection of the back reveals no evidence of this defect, although in rare instances there may be a small lipoma, tuft of hair, or a dimple in the lumbosacral region to indicate its presence. It is usually noted only by x-ray and rarely is of significance, although it may constitute an instability of the lower back (Fig. 89). THE INDUSTRIAL BACK 405 Failure of Fusion.--This congenital defect occurs in various parts of the posterior portion of the vertebra (the neural arch). It may be seen in one or more of the articular processes and more commonly in the spinous process. It is most commonly seen in the lumbar area, although occasionally elsewhere (Figs. !)0, 91). In itself and without other accompanying congenital defects it is not a cause of back pain, but it is sometimes mistaken for a fracture line. Spondylolisthesis.--This term is applied to that deformity of the lumbosacral region which consists of a gradual slipping forward of the fifth lumbar vertebra on the sacrum (Figs. 92-94). It was first Fig. 92.--A, Spondylolisthesis of the fifth lumbar vertebra. B, The broken line indicates the extent of slipping forward of the fifth lumbar upon the sacrum. Note the narrowed foramen and the complete failure of fusion of the neural arch. noted by obstetricians and considered a disorder among women, but subsequent study reveals it to be more prevalent in men. It is the result of a variation in the ossification of the fifth lumbar vertebra where, instead of one primary center for each half of the vertebral arch, there exist two primary centers in each half, the two parts being united by cartilage extending between the superior and in ferior articular processes, the union being effected by hyaline cartilage only. Normally the apposition of the inferior articular processes of the fifth lumbar vertebra with the articular processes of the sacrum pre vents any forward displacement of the fifth vertebra. But if this 406 OCCUPATIONAL DISEASES continuity does not exist, displacement is apt to occur owing to the strain of the superimposed body weight, which in time overcomes the resistance of the muscular and ligamentous structures. ilFrom a medico legal aspect it is important to appreciate that this; slipping takes place gradually and over a period of years. Claims that a sudden strain or lift produced the condition are to be discounted. There is no set age when this condition progresses to the point that dirability ensues, but it is almost always after the muscles and ligaments lose the tone of youth. Fig. 93. Fig. 94. Fig. 93.--Spondylolisthesis of the fifth lumbar vertebra. Note! the horizontal sacrum. Fig. 94.--Spondylolisthesis of the fourth lumbar vertebra. Note Mure of fusion of the neural arch as well as narrowed intervertebral space between ttbi: fifth lumbar and sacrum. No history of injury. Pain first experienced while pulliiijgi out a cabinet file drawer. Spondylolysis.--This is a term used frequently to indicate a con genital failure of fusion in the neural arch, predisposing to a spon dylolisthesis but before any slipping has occurred (Fig. 9iJ. Sacralization.--This term refers to an elongation of time transverse process of the fifth lumbar vertebra to the point where ill articulates with or is in close connection with the sacrum or sometimes the ilium. It is most often unilateral, but frequently bilateral. It is often referred to in the literature as a "butterfly wing" (Figs. 96, 97, 981}. Its pres- 412 OCCUPATIONAL DISEASES test anil its variations concern the lumbar muscles and the posterior sacral attachments, while the extcnsion-abduction-rotation signs point Fig. 106.--Normal forward flexion from the erect position, accompanied by movement of both spine and pelvis. Fig. 107.--Forward flexion in which the pelvis has rotated to some extent but not accompanied by flexion of the spine. Fig. 108.--Forward flexion of the spine but not accompanied by any pelvic rotation. Fig. 109.--The straight-leg-raising test is illustrated by this drawing. It shows the decrease in the distance from the origin of the hamstring muscle to its point of insertion when the knee is flexed as compared to the distance when the knee is ex tended. to involvement of the hip. The following is a description of the more commonly mentioned signs (Figs. 106-113). THE INDUSTRIAL BACK 413 Lasegues Sign.--This test was designed to distinguish between sciatica and hip-joint disease. The patient lies on his back on the 'M Fig. 110.--This drawing is designed to show the pull on the sciatic nerve when flexion of the hip is engaged in with the knee extended. Dorsiflexion of the foot produces a similar effect. Tension on the nerve is relieved when the knee is flexed. Fig. 111. Fig. 112. Fig. 111.--The specimen is in the supine position showing the gluteus maximus muscle. Just anterior to the muscle lies the ischiogluteal bursa. Fig. 112.--Flexion of the thigh with stretching of the gluteus maximus muscle. examining table and raises the leg with the lower leg straight (ex tended) . The normal person should be able to flex the hip through a range of 90 degrees. In sciatica, pain is produced if the knee is ex- 'T 414 OCCUPATIONAL DISEASES tended when the leg is raised, but no pain occurs in the same motion if the knee is flexed. In hip-joint disease flexion of the hip is painful whether the knee is flexed or extended. Bechterew's Sign.--In sciatica, straight-leg-raising on the opposite side may cause pain on the affected side to a less degree, since the stretched nerve on the unaffected side pulls upon the nerve roots of the opposite side by its attachment in the cord. Pig. 113.--Lesions of the hip joint may produce spasm of the pious magnus ! muscle. This drawing shows the left heel placed on the patella of the opposite leg. Pushing downward on the left knee produces outward rotation and abduction of the thigh which stretches the psoas magnus. If this muscle is in spasm due to hip-joint 1 disease, the movement is painful and limited. S Demianoff's Sign.--The following test is to differentiate lumbago j from sciatica. The straight-leg test is first done. If it is positive, it is | repeated with the examiner's one hand holding the pelvis of the 1 patient firmly to the table. In sciatica the pain is still present, but in lumbago it disappears. Gaenslen's Sign.--One hip is flexed, and at the same time the other hip is extended. Then the procedure is reversed. The test supposedly i THE INDUSTRIAL BACK 415 differentiates lumbosacral from sacro-iliac lesions and between rightand left-sided involvement. The patient lies on his back on the exam ining table. The knee and hip of one leg are flexed as far as possible and held in that position by the patient's hands clasped over the knee. The other leg at the edge of the table is allowed to hang and is further pressed down by the examiner, producing hyperextension of the hip. Pain is said to occur on the affected side. Ober's Sign.--The patient lies on the unaffected side while the examiner places one hand on the pelvis to steady it and grasps the patient's ankle with the other, moving the leg until the knee is flexed at right angles. The thigh is abducted and extended in the coronal plane of the body. Ober contends that if contracture of the iliotibial band is present, the leg will remain abducted. Ely's Sign.--With the patient prone, hyperflexion of the knee may cause, elevation of the pelvis on the same side. Linder's Sign.--If enforced passive flexion of the head occurs with the patient sitting or recumbent and the legs outstretched, pain may arise in the lumbar region or down the leg on the affected side. It is thought that a positive reaction indicates root sciatica. Neri's Sign.--When the patient in a standing position forwardflexes the torso, there is noted flexion of the knee on the affected side. Soto-HaU's Sign.--With the patient lying flat on his back, flexion of the spine beginning at the neck and proceeding downward, pain may be noted at the site of the lesion. TREATMENT Educational Campaign in Prophylaxis.--Industry as yet has not fully awakened to the tremendous cost of the disabling back, nor are any general preventive measures being adopted. True, while these measures are not so simple as merely installing ventilation or exhaust systems, the incidence of the disabling back can undoubtedly be re duced. Education of the industrial public upon the dangers residing in certain types of moving parts, punches, blades, and the like, by a safety-first campaign greatly reduced the severe traumata occurring in industry. Such a campaign should be similarly directed toward back disabilities. Moving-pictures of correct and incorrect methods of lift ing, pushing, or pulling could be shown; and posters placed so as to catch the workman's eye would warn against faulty tendencies. Peri odic lectures by one trained in physical education would be extremely valuable. Such a person could service a number of plants during a month's time, each company sharing the cost of his salary. Setting-up exercises twice daily would relieve the monotony of work and strengthen the muscles. If they are of value to nondescript soldiers 416 OCCUPATIONAL DISEASES entering the army, they would also be of aid in industry. And, finally, careful selection of the right type of men for the various jobs should be attempted. How frequent, and at the same time how ridiculous, it is to see a frail, undersized laborer struggling with a heavy object, while close by stands a flagman or gateman of normal stature and physically fit! Specific Treatment.--This depends upon the determination of the etiological factors. Actual sprain, strain, or contusion is best treated by conservative measures. In our clinic approximately eleven hundred such patients are treated each year by conservative procedures with very satisfactory results, particularly in regard to shortening the period of disability. Physiotherapy.--A routine of physiotherapy treatment daily or on alternate days, depending upon the severity of the case, is usually instituted. This physical adjunct to treatment is useless unless car ried out adequately. This physiotherapy does not consist of carelessly placing the patient under an infra-red lamp for from fifteen to thirty minutes. Instead, he is first given from fifteen to twenty minutes of infra-red therapy, and this is followed by fifteen or twenty minutes of diathermy. Finally, a gentle but adequate massage by a trained physiotherapist is given to the involved parts. For the first three to seven days we try to avoid strapping the patient's back, so that at home he may apply heat more effectively to the low back area. He is encouraged to take hot sitz baths for from thirty to forty minutes twice daily and to apply controlled electric pads, small heating lamps, hot-water bottles, or hot applications to the involved area, in addition to the baths. Most of these patients will be more comfortable and will improve more rapidly if boards are placed lengthwise on top of the springs underneath the mattress. During this period, acetylsalicylic acid, from 10 to 15 grains (0.65 to 1 gm.) four time daily, perhaps in combination with codeine phosphate, from % to 1 grain (0.0325 to 0.065 gm.), may be needed, and one of the barbiturates may be necessary to obtain adequate sleep. At the end of this time if the patient still has back pain and a feeling of weakness, the low back is strapped adequately with three-inch adhesive tape (Fig. 114). It may be necessary or desirable in some to apply the strapping when the patient is first seen, but if this is done it should be removed for physio therapy treatments and then replaced. Exercise.--We feel that it is particularly important to encourage these patients to be as active as their discomfort will permit. In our experience, hospitalization with absolute bed rest and the sometimes advised traction, definitely prolong the period of disability. The pa tient appears to develop a tenseness and tightness of the low back THE INDUSTRIAL BACK 417 from such procedures and for these requires an additional period of treatment. In this encouragement of the patient to remain active, exercises play an important role. These should be outlined carefully, and it is particularly important to attempt by some exercises to cor rect faulty posture. These may be started at the end of seven or ten days, although by this time many of our patients will have returned to active work or are ready to do so. This matter of activity is similar to some extent to the treatment of the sprained ankle, as outlined by Alexander,23 in which definite shortening of the usual period of dis ability is obtained by the use of novocaine injection, strapping, and early use of the ankle. .1 lv Kt : Fig. 114.--A, The back is first painted with compound tincture of benzoin to protect the skin. Three or four strips of 3-inch adhesive tape are then applied so that they extend over the flanks onto the abdomen. On top, these two adhesive straps are crossed so that they anchor each anterior superior iliac crest. Posterior view. B, An terior view. C, Short strips of tape such as illustrated here are inadequate and of no value. These back sprains and contusions do not need casts, braces, or belts, and their use may actually do harm in many instances and pro long disability. Manipulation.--Manipulation has its place, although its sphere of application is relatively small. Occasionally dramatic results are obtained from its use, but also occasionally great aggravation of the pain is brought about by it. Not infrequently we have referred to us patients who have been manipulated and whose pain has been made much worse by the procedure. In the hands of physicians trained in this art, it may be of some value. It cannot be too strongly urged, how ever, that before resorting to manipulation, a thorough history, physical examination, and investigation as outlined earlier in this chapter be 'done, since much harm may follow manipulative treatment 27 IP! 418 OCCUPATIONAL DISEASES of such conditions as a herniated nucleus pulposus, a cord tumor, an acute arthritis, or disease residing in adjacent organs. Details of these manipulative procedures are outlined in standard orthopedic texts. Eucipin in Oil.--Much relief of pain in these patients and much . shortening of the period of disability has been reported from the use ^ of injections of eucipin in oil. Invig2'1 outlined the following technique: l ' With the patient lying on the abdomen, the sacro-iliac region is surgically sterilized. A 5 cc. syringe with a 1% inch 21-gauge needle is used for the injection. To locate the point of injection, the course of the lumbar spine and the crest of the ilium posteriorly are palpated. A line is drawn parallel and 1 in. to 1% in. lateral (according to thick ness of spine) to the spinous processes of the vertebrae. A second ( line is drawn along the upper border of the ilium and continued posteriorly until the two lines intersect in the lumbo-sacral region of the back. This is the point of injection. The needle is inserted ver tically to its hilt with a quick pressure, the plunger of the syringe is withdrawn slightly, and if no blood is aspirated, the injection of t 2 cc. of eucipin solution in oil is begun. The greater amount of the oil is deposited in the deeper parts. The injection is continued as the needle is withdrawn and should be completed when less than onethird the length of the needle is above the surface of the skin. This 1 procedure obviates the injection of the oil solution into the super:: ficial tissues. The parts should be massaged vigorously after the in* jection. The needle does not endanger vital structures on full insertion. |. He used: * Eucipin base................................................................................ 0.1 | ' Ethylaminobenzoate................................................................. 3.0 \ Benzyl alcohol ............................................................................ 5.0 Oil sweet almond...........................................................q.s. ad. 100.0 He later found that eucipin solution in 2 per cent iodized oil pos sessed even greater therapeutic possibilities than the plain oil. He pointed out that such injections should not be considered a panacea for all cases of low back pain. In our experience this procedure has not greatly added to the treatment outlined. Perineural injections of 0.1 per cent /3-eucaine in normal saline were also employed around the sciatic nerve in some instances by Invig. The treatment of those cases of back pain felt to arise from causes other than trauma, e.g., foci of infection, will not be discussed here, since they, generally speaking, will not fall into the classification of compensation cases. Correction of Congenital Defects.--Cases in which congenital de fects are demonstrated, and on which an acute low back pain sprain ! ! THE INDUSTRIAL BACK 419 is superimposed, frequently respond well to conservative therapy as outlined, and this should first be tried. In these the use of braces or back supports may become necessary later and be of much value. Operative Treatment.--As a last resort various operative pro cedures have been described. These in most instances should not be performed until an adequate period of conservative therapy has been followed, and, if possible, financial settlements made, although this latter is frequently not allowed by industrial accident commissions. Ober'-5 described the use of fasciotomy in cases in which there was demonstrated a contracted iliotibial band as the cause of sciatica and back pain. Gratz11 has used air insufflation for treatment of back pain thought to be due to fascial adhesions. Haggart,-<! after a definite trial of conservative treatment, treated cases of unstable lumbosacral joints by spine fusion. He stated that fully 95 per cent of patients with chronic low back pain were best treated by a conservative regimen, and only 2.5 per cent of 2000 patients with low back pain semi by him in a three-year period were subjected to arthrodesing operations. Operation for herniation of a nucleus pulposus, or hypertrophy of the ligamentum flavum, may at times be necessary, although here again if such morbid anatomy is demonstrated, the role trauma played in its production needs to be very carefully weighed before responsi bility is assigned to a specific, and frequently minor, incident. Here again conservatism and an adequate period of observation should be followed at first. In compensation work, too, the end-result is frequently not so gratifying as that described following operations in private practice, since the desire for a large financial settlement frequently causes con tinuation of the previous complaints or the simulation of new ones, even though the cause of the backache has been removed. A regimen for the correction of structural defects should be di rected by an orthopedist; and diagnosis and surgical correction of herniated nucleus pulposus or hypertrophied ligamentum flavum should be made by a neurosurgeon. REFERENCES 1. Goodwyn, T. P.: "Effect of Trauma oil Mechanically Weak Back," Am. J. Surg., 43: 577-581 (Dec.), 1938. 2. Putti, V.: "New Concepts in Pathology of Sciatic Pain," Lancet, 3: 53-60 (July 9), 1927. 3. Hodges, F. J., and Peck. W. S.: "Clinical and Roentgenological Study of Low Back Pain with Sciatic Radiation; Roentgenological Aspects," J. Roentgenol., 37: 461-466 (April), 1937. 4. Williams. P. C.: "Lesions of Lumbosacral Spine; Acute Traumatic Destruction of 420 OCCUPATIONAL DISEASES Lumbosacral Intervertebral Disc," J. Bone and Joint Surg., 19: 343, 363 (April), 1937. 5. Barr, J. S., Hampton. A. 0., and Mixler, IV. J.: "Pain Low in Back and `Sciatica' Due to Lesions of Intervertebral Discs," J.A.M.A., 109: 1265-1270 (Oct. 16), 1937. 6. Ober, F. R.: "Role of Iliotibial Band and Fascia Lata as Factor in Causation of Low Back Disabilities and Sciatica," J. Bone and Joint, Surg., 18: 105-110 (Jan.), 1936. 7. Judoviclx, B. D., and Bates, IV.: "Low Back Pain; Study of Over 1,000 Cases," Indust. Med., 8: 160-165 (April), 1939. 8. Steindler, A.: "Differential Diagnosis of Pain Low in Back; Allocation of Source of Pain by Procain Hydrochloride Method," J.A.M.A., 110: 106-113 (Jan. 8), 1938. 9. Makaroff, W. N.: "Etiology of Lumbago and Sciatica," Indust. Med., 8: 1-4 (Jan.), 1939. 10. Ridlon, J., and Berkheiser, E. J.: "Calcareous Degeneration of the Dorsal and Lumbar Aortae as a Cause of Backache," J.A.M.A., 80: 1831-33 (June 23), 1923. 11. Gratz, C. M.: "Fascial Adhesions in Pain Low in Back and Arthritis," J.A.M.A., 111: 1813-18 (Nov. 12), 1938. 12. Willis, T. A.: "Backward Displacement of the Fifth Lumbar Vertebra; Optical Illusion," J. Bone and Joint Stirg., 17: 347 (April), 1935. 13. Pancoast, H. K.: "Importance of Careful Roentgen Ray Investigations of Apical Chest Tumors," JA.M.A., 83: 1407 (Nov. 1), 1924. 14. Pancoast, H. K.: "Superior Pulmonary Sulcus Tumor, Tumor Characterized by Pain, Horner's Syndrome, Destruction of Bone and Atrophy of Hand Muscles," JAM.A., 99: 1391 (Oct. 22), 1932. 15. Browder, J., and DeVeer. J. A.: "The Varied Pathologic Basis for the Symp tomatology Produced by Tumors in the Region of the Pulmonary Apex and Upper Mediastinum," Am. J. Cancer, 2k: 507 (July), 1935. 16. Jacox, H. W.: "Superior Pulmonary Sulcus Tumor," J.A.M.A., 103: 84 (July 14), 1934. 17. Steinder, P. E., and Byron, F. F.: "Primary Lung Carcinoma," Am. J. Cancer, 22: 776 (Dec.), 1934. 18. Morris, J. H., and Harken, D. E.: "The Superior Pulmonary Sulcus Tumor of Pancoast in Relation to Hare's Syndrome," Ann. Surg., 112: 1 (July), 1940. 19. Clark, B. E.: "Superior Pulmonary Sulcus Tumor (Pancoast)," abstr.. Am. J. Path., 10: 693 (Sept.), 1934. 20. Fried, B. M.: "Sternoclavicular Branchioma," Am. J. Cancer, 25: 738 (Dec.), 1935. 21. Graef, I., and Steinberg, I.: "Superior Pulmonary Sulcus Tumor," Am. J. Roent genol., 36: 293 (Sept.), 1936. 22. Brahdy, L.: "Mechanics of Physical Signs in Lower Trunk Injuries," Surg., Gynec. and Obst., 60: 802-817 (April), 1935. 23. Alexander, II. II., Jr.: "Treatment of a Sprained Ankle," Am. J. Surg., 50: 581584 (Dec.), 1940. 24. Irwig, F.: "Treatment of Low Back Pain," Indust. Med., 8: 105-112 (March), 1939. 25. Ober, F. R.: "Back Strain and Sciatica," J.A.M.A., 10k: 1580-83 (May 4), 1935. 26. Haggart, G. E.: "Early Operation (Spine Fusion) in Unstable Lumbo-sacral Joints," JAMA., 115 (Dec. 21). 1940. CHAPTER XXXI HERNIA Hernia, like the "industrial back," cannot be considered an in dustrial disease in the true sense of the word, yet its presence in the workman is invariably attributed to occupational activity. The diag nostic features of a hernia are familiar to every practitioner and need not be discussed. Likewise, the cause of a hernia is well understood, and medical opinion in this respect has not changed with the passing years, but the legal attitude has. Originally, before a hernia was con sidered to be compensable, certain prerequisites had to be fulfilled in the establishment of the claim. These are now being ignored by the referees of our industrial accident commissions not only in California, where I am familiar with the opinions rendered, but in most other states. In this situation the physician has become a sort of nonentity. It is imperative that either the legal attitude be clarified or the status of a hernia be reclassified. Compensability of Hernia.--Some states exclude hernia from the list of compensable conditions unless it is the result of direct trauma. Certain other states consider hernia as compensable if it occurred after unusual exertion or sudden strain, and in some commonwealths, as in California, the act does not specifically mention hernias. Their compensability is tested the same as any other incident occurring in industry for which benefits are claimed. The policy followed originally by the California commission was that if an inguinal hernia followed an industrial overexertion or strain it was considered compensable. They held: It is unimportant whether, from a medical or scientific standpoint, hernia be classified as a disease or a malformation; or be otherwise designated; or that the employee be predisposed thereto. "When a hernia results from a strain during the course of and arising out of the employment, and is given impetus to appear at that time and place, the injured man is entitled to compensation.1 In view of the subsequent discussion, the reader is asked to note the phrase given impetus to appear at that time and place quoted in the previous sentence. Prerequisites to Compensation.--With but slight variation the majority of states list the following prerequisites as necessary in con sidering a hernia compensable: 421 422 OCCUPATIONAL DISEASES 1. That the hernia is of recent origin 2. That its appearance was accompanied by pain, discoloration, and evidence of a tearing of the tissues 3. That it was immediately preceded by some strain arising out of and in the course of employment 4. That a protrusion or mass appeared in the area immediately fol lowing the alleged strain In some states decision is not final until the allegation is affirmed or denied by the operative findings. Allegations of Workman.--In analyzing a large number of claims. I find the workman alleges his hernia to be due to one of the three following causes: (1) direct trauma, severe or trivial; (2) excessive strain or overexertion; (3) minimal exertion, or to follow a normal act engaged in while at work. Let us consider the merits of these con tentions: Direct Trauma.--It is the consensus that direct trauma cannot be held responsible for a hernia unless there is demonstrable evidence of a laceration of the overlying structures. This was recently contended by Moorehead2 after an analysis of 1376 herniotomies. His opinion is concurred in by Early3 after an operative experience of over 5000 herniotomies during twenty-five years of industrial surgery. A direct traumatic hernia implies an open-wound hernia. Obviously such must be rare. Excessive Strain or Overexertion.--If hernia results from an overt act or undue strain, it must be because of the indirect action of the increased intra-abdominal pressure. To dilate suddenly the intact rings and the canal, the force of the intra-abdominal pressure would have to be great. And if this action could produce a hernia where none previously existed, why is an inguinal hernia not a common compli cation of severe abdominal blows or crushing injuries? Why is it that in falls from great heights which result in visceral injury, or in crush ing injuries in which fractures of the femur or pelvis occur, acute inguinal hernias are not also found? Dr. Wilmot F. Pierce, of our surgical staff, has treated a large number of patients having injury to the abdominal viscera following direct blows to the abdomen. In these cases he has observed laceration or rupture of the kidney, spleen, liver, and intestines, but no instance of acute hernia. Furthermore, if the inguinal rings and fascial coverings are to be forcibly dilated, pain should be intense and immediate. It has been pointed out that in countries where military service is compulsory, the presence of a hernia may be sufficient to cause rejection. Thus, it is reported, many seek the avoidance of military service by submitting to the produc- HERNIA 423 tion of a hernia by a professional dilator, who frequently must attempt manual dilatation three or more times, during which procedure the patients faint from pain. It is also common knowledge that before the peritoneum can be handled at operation an anesthesia must be administered. To believe that a hernia is suddenly produced, one must expect some or all of the following symptoms to be present: pain, nausea, local tenderness, swelling, and discoloration. To believe that a sac could be forced through narrow openings and through a canal so innervated and so well supplied by blood vessels without producing the aforementioned signs and symptoms is to ignore the anatomy and pathology of an inguinal hernia. Trivial Exertion or a Normal Movement.--In view of the previous discussion, it is obvious that an acute hernia does not result from slight exertion or a normal movement, and no further consideration of such an alleged cause is necessary. Medicolegal Status of Lump.--Since we believe, as all thoughtful physicians do, that certain signs, symptoms, and causative factors must be present in order to consider a hernia compensable, why is it that cases lacking these requisites are accepted by the commission? The answer can be given in these few words--the presence of a lump. The present philosophy of those who rule on these claims appears to be this: The man swears he never had a protrusion before, he has one now, so the alleged incident must have caused it. Such reasoning can be appreciated when it is realized that referees are not physicians, although they do have a rough idea of the modus operandi of a hernia. In fact, one wonders if this little knowledge is not a bad thing. In other types of claims less frequently heard by them, they evidence a willingness to learn and consider all the facts. But in the case of a hernia there is a tendency to consider only the fact that the claimant has or does not have an inguinal protrusion. Recently, before a local referee, a physician was asked by an attorney to describe the steps in the production of a hernia. The referee stopped the testimony, say ing that such was not necessary since the court understood these things. Obviously, the only value the physician had in that court was to state whether or not the claimant had a hernia. Mechanism of Hernia.--What can be said regarding the lump which appears and was not present prior to some alleged act? The answer is that a hernia is a slowly progressive (chronic) enlargement of a preformed sac. Over a period of time the sac, filled with intestine, or omentum, or both, keeps exerting gradual pressure upon the rings until they dilate sufficiently to permit passage of this sac to the point where it can be observed; or, that the sac bulges through at a time 424 OCCUPATIONAL DISEASES when the muscles are relaxed. The final stage may be symptomless or accompanied by some distress. The distress, burning sensation, or mild pain may be the result of the sac's twisting, or of gaseous dis tention, or of the pulling on the adjacent tissue as it further distends. The medicolegal status of the final appearance of this "lump" might be understood by the citation of one or two analogies. A ship ping clerk has a large boil on his arm which is about to rupture. One evening as he removes the dressing he notices that it has broken through the skin and drained. He recalls that during the day he brushed against a box and thinks he noticed his arm hurt a little at that time. Should any further medical care and loss of time be as sumed by his employer? Obviously the brushing against the box didn't cause the boil, and it would appear ridiculous to consider the incident the aggravating cause of its erupting through the gradually thinning skin. Eventually it would have erupted because of the very nature of the infection. Just as ridiculous is it to consider a hernia compensable in one who while undressing notices a lump and then recalls that during that day or several days before, he had lifted some thing and therefore might have strained himself. For another example, I should like to enlarge upon the analogy used by Moorehead. He likens the inguinal canal to the birth canal, the internal ring representing the internal os and the external ring the external os. Before the fetus can be expelled, the internal and ex ternal os must slowly dilate. Unfortunately for women, the cervical canal doesn't just suddenly and painlessly dilate and presto, there is the infant. The eventual appearance of the infant cannot be attributed to the final contraction of the uterus. A birth could not be consum mated unless all the preliminary stretching of the tissues took place. So with the hernia. The protrusion is the final result of previous gradual alteration of the rings, fascia, and muscles. Its appearance may be "silent", or accompanied by mild distress. But no unusual act or endeavor is necessary for its appearance. It may show up with stooping, bending, or lifting at the shop but may just as likely appear while at stool at home. As with the industrial back, the "locale" of its being first noticed seems to have some determination in its being considered due to occupation. Accident Commissions versus Medical Opinion.--It can be safely stated that the preceding opinion is acceptable to the medical pro fession. Yet in no comparable instance is medical opinion so ignored by the Industrial Accident Commission. Opinions written by physi cians on this type of case are apparently held in disdain, all of which creates for the doctor an undesirable and unwanted situation. If the industrial accident commissions of the various states desire to award HERNIA 425 compensation and treatment to all workmen with a hernia, irrespec tive of the history or physical findings, then let the existing act or its meaning be revised and let all parties concerned be informed of the intention. If they would do this, the physician would only be asked to state whether or not the protrusion was a hernia, but he would not have to indulge in a discussion of why he did or did not believe it was compensable. It might not be amiss to state that while the present attitude of the Industrial Accident Commission is, on the surface, benevolent to the working-man, it will result in subsequent harm to the very class it is intended to aid. If the majority of hernias are to be considered compensable, and since a potential inguinal hernia exists in a large proportion of males, the employer can protect himself only by recourse to a preemployment examination. An applicant, particularly in the heavier industries, who has a potential hernia would be rejected. Obviously, this discrimination would work a hardship upon many otherwise employable persons and would create a situation for which as yet there is no remedy. Many of these men, informed of a potential condition, are willing to sign a statement assuming full responsibility regarding it, but the law does not permit this. MEDICOLEGAL ASPECTS Grants in Various States.--This involves primarily the responsi bility for medical and hospital cost and the loss of wages. However, the law varies in the various states. Many grant only the medical and hospital costs, while the employee assumes the full wage loss. Some states grant not only medical and hospital costs, but compen sation for the length of time the patient is prevented from working owing to his hernia. In such states it is necessary for the physician to state whether or not the existing hernia is disabling. For instance, the workman may present himself for examination and likewise pre sent his claim to the insurance company. Several days or a week are consumed by the carrier before the claim is acted upon. Then, if the claim is denied, weeks more may elapse before the case reaches the commission for a decision. This body desires to know if the patient has been disabled during that interval so that it can adjust the wage compensation in case the decision is against the carrier. Temporary Disability.--The temporary-disability period follow ing operation varies, usually extending, however, from four to six weeks. Permanent Disability.--This does not exist in hernia unless the hernia is considered inoperable. Permanent disability resulting from 426 OCCUPATIONAL DISEASES the complications of hernia or from an operation for hernia has been claimed, as will be illustrated later. Operation Refused by Workman.--Hernias are considered remedi able by operation. If an operation is tendered by the employer, carrier, or by the award, and the patient refuses to have this operation, then within a reasonable length of time the carrier may be released from responsibility upon proper petition. Illustrative Cases: Case I.--Claimant, along with a helper, carried a case of books from one room to an adjoining room on the same floor. Two nights later while taking a bath he noticed a swelling in the right groin. He was ignorant of its nature or cause. At the time of medical examina tion he stated he had never been nauseated, nor had he been aware of any pain. Following the medical report of an incomplete inguinal hernia of congenital origin, the carrier denied his claim. He went be fore the Industrial Accident Commission and told the same story he told the physician except he stated that he later recalled that at the time he was carrying the books he noticed a tingling sensation in the groin where the mass later appeared. None of the accepted criteria for the development or aggravation of a hernia was present in this case. No pain, no nausea or vomiting, and no tenderness were present, and the mass appeared two days after the alleged incident. Many causes could have been present during the non-working hours in the interval between the carrying of these books and the presence of the mass. The physician denied the occupational origin, but the referee awarded the patient compensation, medical care, and costs. Case II.--A workman was engaged in reconstruction of a bridge following a flood. This bridge crossed a stream, which during most of the year was dry or nearly so. After the water had receded, he was working in deposited silt and sand. While holding a piece of timber he started to sink, became frightened, and attempted to free his right leg. He pulled and struggled until he got a new footing. At this time he developed a pain in his right groin. He reached shore, felt sick, and stretched out on the ground. The sharp pain diminished within from a half to three quarters of an hour, but the discomfort persisted. That evening he reported to a physician, who found a hernia. Examination revealed the rings to be thickened and well relaxed. A similar condition existed on the opposite side but with no pro trusion of the gut. Regardless of the fact that this patient probably had had a potential condition for years, he had a history of aggra vation. Therefore, the case was held compensable. HERNIA 427 Case III.--A tliirtv-two-year-old Mexican became acutely ill and was treated for three weeks by a Los Angeles County physician. The diagnosis was acute bronchitis. About the time he was ready to return to work he noticed a lump in his left groin, was examined by his physician, and was told he had a hernia. He entered claim for treat ment and compensation. He admitted to the county physician and to a physician at our clinic that it appeared without his knowledge of any strain or overexertion. He had never had any discomfort at the area of the hernia. Subsequently, before the commission he stated that he had lifted a bundle of laundry and noticed a burning sensa tion at the time in the involved groin. He was awarded an operation and compensation, regardless of the testimony of the only two physi cians who examined him. This case is inserted only to illustrate the point previously made about the futility of medical opinion. Case IV.--The claimant's husband had suffered from hernia since childhood. While the hernia had troubled him frequently, he had worked as a miner for at least thirty years. On March 12, 1937, in the course of his employment in a mine, he assisted in moving a piece of slate weighing about 700 pounds. About thirty minutes later he complained of being sick and went home. His condition continued to grow worse, and a physician was called, who caused the employee to be taken to a hospital where he was operated on for a strangulated hernia. A secondary operation was performed some days later; pneu monia developed, and the employee died on March 18. His widow, the claimant in the present case, filed a claim for compensation, which was denied by the compensation commissioner. This denial- was af firmed by the compensation appeal board, and the claimant appealed to the Supreme Court of Appeals of West Virginia. The Workmen's Compensation Act of West Virginia provides that an employee may be compensated for hernia: (1) if there was an in jury resulting in hernia; (2) if the hernia appeared suddenly; (3) if it was accompanied by pain; (4) if the hernia immediately followed an injury; and. (5) if the hernia did not exist prior to the injury for which compensation is claimed. The act, in the opinion of the court, intended to bar compensation for hernia in cases in which the dis ability existed prior to an injury for which compensation is sought. It refers to "all claims for compensation for hernia," and to obtain compensation therefor certain things must definitely be proved to the satisfaction of the commissioner, the first being "that there was an injury resulting in hernia." It cannot be said, the court concluded, that a hernia resulted from an injury in a case, such as the one at bar, in which the hernia had existed from childhood. For the reasons stated, the denial of compensation was affirmed.1 428 OCCUPATIONAL DISEASES Obviously this claim was denied because the law in West Virginia rules against any case in which the hernia was known to exist prior to alleged disability, regardless of the possibility of aggravation by some act incurred while employed. In most states, provided there was sufficient evidence of unusual stress, this claim would have been ac cepted upon the basis of aggravation. Case V.--The claimant developed a right inguinal hernia as a re sult of lifting a heavy keg of nails in the course of his employment, and submitted to an operation. For a number of years prior to the operation he had a chronic inflammation of the spine and "hyper trophic spondylitis, that being a growth of bone and cartilage from the spine, causing pain." The long confinement in bed incident to the herniotomy aggravated these conditions and also caused spastic colitis. As a result of these sequelae, he was unable to do any manual work. The industrial accident board awarded him compensation in accord ance with a special provision of the Texas Workmen's Compensation Act pertaining to hernia, which authorizes, in the event of a suc cessful operation, compensation for a limited period in addition to expenses for necessary medical and surgical care. The claimant then sued his employer's insurer to set aside the board's award and to re cover instead compensation for total permanent disability under the general provisions of the act. From a judgment in favor of the claim ant, the insurer appealed to the United States Circuit Court of Ap peals. The Texas Workmen's Compensation Act, said the Circuit Court of Appeals, authorizes compensation for certain specific injuries, in cluding hernia, and also for injuries in general resulting in partial or total incapacity for work. An employee who suffers a specific injury is not confined to the compensation allowed for that specific injury if that injury, or the proper or necessary treatment, causes other in juries which render him unable to work. The court was of the opinion that the aggravation of his preexisting ailments and his consequent total incapacity for work were traceable to his injury received in the course of his employment, and to the treatment called for by that injury. The court held, therefore, that the claimant was entitled not only to compensation for the hernia directly caused by the accident but also for the total and permanent disability resulting from the aggravation of his preexisting ailments, which prior to the operation had had no disabling effects. The judgment of the trial court was therefore affirmed.3 The contention that the operation and the period of convalescence aggravated a preexisting spondylitis and caused a spastic colitis ap pears to be so extremely remote as to question the equity of this decision. HERNIA 429 Case VI.--The employee in this case was injured on September 11, when his left leg broke through the wood cover of a manhole. He quit work immediately and had difficulty in getting to his house. He com plained of nausea and of pain in the lower left side of his abdomen. That evening a pronounced swelling and tenderness were present in the left inguinal region. Two days later his condition was diagnosed as traumatic hernia. Rest until the swelling and tenderness disappeared was advised. A herniotomy was performed on October 29. Twelve hours later the employee's abdomen became distended, and within a day or two his condition was described as toxic. He died on November 3, the immediate cause of death being "paralytic ileus; i.e., paralysis of the small intestine." The employee's widow was awarded compen sation under the Workmen's Compensation Act of Wisconsin, and the employer and insurer appealed to the Supreme Court of Wiscon sin after the circuit court had affirmed that award. The appellants contended that, since the operating physician found conditions at the time of the operation which clearly indicated that the hernia was not of recent origin, the commission was not justified in finding that the employee sustained a hernia as a result of the accident. But, said the Supreme Court, it was immaterial whether the hernia had existed prior to the accident. If it did exist, it was certainly greatly aggravated by the accident and resulted in a compensable injury. While there was no suggestion of carelessness or lack of skill on the part of the operating physician, it was clear, in the opinion of the court, that the commission was warranted in finding that an acci dent occurred; that it resulted in an injury which reasonably neces sitated an operation; and that as a result of the operation infection entered the abdomen which ultimately caused death. Whether the infection entered in spite of the exercise of the highest skill, or as a result of lack of skill or carelessness, was immaterial. If an employer must compensate an employee for injuries caused by the malpractice of a physician who treats the employee for an industrial injury, and such is the law, an employer must likewise compensate an employee, or his dependents in case of his death, for injuries resulting from an operation skillfully performed. The award of compensation was affirmed.0 Case VII.--The worker, while engaged in the course of his employ ment in lifting railroad ties, sustained a strain which resulted in the strangulation of the contents of an existing hernial sac. A gangrenous condition ensued, and an operation performed three days later failed to avert death. An award of compensation in favor of the widow by the Workmen's Compensation Bureau of New Jersey was affirmed by the Court of Common Pleas but was reversed by the Supreme Court. The widow then appealed to the Court of Errors and Appeals of New Jersey. 430 OCCUPATIONAL DISEASES The Workmen's Compensation Act specifies, in detail, the circum stances under which a hernia must occur in order to constitute it a compensable injury. The Supreme Court held that the death was not compensable because the hernia did not occur under the circumstances set forth in the act. But, said the Court of Errors and Appeals, the rea soning of the Supreme Court did not take into consideration the essen tial difference between the occurrence of a hernia and the traumatic aggravation of that bodily deformity. Manifestly, the workman in this case could not have met the requirements of the act, for the hernia did not follow but long preceded the accident made the basis of the claim for compensation. His widow did not seek compensation for the hernia but for the death directly traceable to the accidental aggrava tion of the preexisting diseased condition of the body. Concededly, the workman's death was caused by the strangulation and the super vening gangrenous condition of the intestinal content of the hernial sac. If extraordinary strain resulting from the lifting of the ties was the causative agent of the strangulation, the fatality was the conse quence of an accidental injury within the meaning of the New Jersey Workmen's Compensation Act. The Workmen's Compensation Bureau found there was a definite and direct relation between the accidental strain suffered by the workman and his death three days thereafter. An accident which sets in motion the undeveloped and dangerous physical conditions with mortal consequences, is properly classifiable as the proximate cause of the fatality. The court, therefore, reversed the judgment of the Supreme Court and ordered an award for the widow.7 The ultimate decision favored the claimant upon the grounds that an aggravation of a preexisting condition occurred. The author ques tions whether the simple act of lifting a railroad tie constitutes an injury or undue strain when unattended by unusual factors of strain or stress. Case VIII.--The claimant in this case contended that in the course of his employment he fell and immediately experienced a sharp pain in his left groin. He reported the accident to his foreman and was referred to the first-aid station. What was found there is not shown by the record, but the claimant applied for compensation, alleging that an inguinal hernia had resulted. From an order of the Workmen's Compensation Commission reversing an award that the deputy labor commissioner had entered in favor of the claimant, the claimant ap pealed to the Supreme Court of Michigan. At a hearing before the deputy commissioner, a physician who had examined the claimant a few days after the alleged accident and again about two months later testified that he had found on both occasions a left indirect inguinal hernia. On behalf of the employer, however, a HERNIA 431 physician who had examined the claimant in the interval between these two examinations testified that he had found an enlarged in guinal ring on each side, the ring on the left side being somewhat more enlarged than that on the right, but that he found no hernia. The condition that he found might be referred to, he said, as a potential hernia, but in his opinion nothing is a hernia unless there is a pro trusion of a viscus or organ from its natural cavity. There was no protrusion of a viscus in the present case, although there was palpated "a sharp mass by inserting your fingers in the rings and getting up on to the abdominal cavity." "Some men," said this witness, "call any such sharp mass a hernia, but others refuse to call it a hernia until after it has descended." In this case, in the opinion of this witness, the viscus had not descended through the rings. Quoting an earlier decision of its own,8 the court said: "All the experts seem to agree that the visible evidence of the hernia is the protrusion through the inguinal ring of the peritoneum and its contents; the hernia is the peritoneum going through, accom panied by the intestines or some other substance." In the present case, said the Supreme Court, there was no pro trusion through the internal inguinal ring, and the evidence sustained the finding of the Commission on Labor and Industry holding that the claimant had a potential hernia or a predisposition to hernia. The order of the commission denying compensation was affirmed.11 TREATMENT Herniotomy.--Treatment in cases of hernia in most instances con sists of herniotomy by whatever method the surgeon handling the case feels to be best adapted to the individual case and to give the best results in his experience. In our own clinic a modified Bassini tech nique is used, with very satisfactory results. Most of the herniotomies here are done under spinal anesthesia. Contraindications.--As in all surgical cases, a careful preoperative check of the patient is made to exclude those cases in which contra indications to operation, e.g., respiratory and genito-urinary tract in fections, might be present. If acute infections are present, the herni otomy is delayed until these have cleared. In general, uncomplicated hypertensive vascular or cardiovascular disease is not felt to be a definite hindrance to successful management of these cases, and a large number of elderly persons have been operated on without post operative complications occurring. The usual routine calls for from twelve to fourteen days' hospital ization, with an additional four-week convalescent period. At the end of this six-week period the patient is returned to his ordinary work, whether it is heavy or light. 432 OCCUPATIONAL DISEASES Trusses.--The use of trusses will not offer a solution for cases of hernia ruled as being either due to or aggravated by industrial occupa tion any more than it will in other non-industrial cases. In inguinal hernias, the use of a well-fitted truss may enable a patient to continue with his work without particular discomfort while his case is being settled or while he arranges his economic situation satisfactorily prior to the six-week period of inactivity. Such a truss does not cure the hernia, but it may during the period prior to operation lessen the pos sibility of strangulation. If the truss is ill-fitting, however, it may ac tually encourage strangulation or incarceration. For femoral hernias trusses are rarely satisfactory, and the danger of strangulation fre quently seems to be increased by their use. No truss should be worn for treatment of any irreducible hernia. Injection Method.--The question of the feasibility of injection of hernias10 frequently arises. In our clinic this method is not used ex cept in rare instances. If the point is simply that the patient refuses operation and instead wants the injection method of treatment, we refer him elsewhere to obtain it, since we do not feel justified in its use under these circumstances. Industrial workers will frequently be attracted by the chance to continue with their work while receiving the injection treatment, since even though compensation may be awarded for the period of disability necessary for the operation, quite a substantial loss is incurred by the worker. If he happens to be in a state where only the medical and hospitalization cost is covered, this is doubly true. Then, too, some people inherently fear surgery and will do anything to avoid being subjected to an operation. The present status of the injection method of treatment for hernia was reviewed by the Council on Pharmacy and Chemistry of the American Medical Association recently. Their report11 was based on replies to a questionnaire addressed to a selected list of hospitals throughout the country and was a sequel to a previous report on a similar questionnaire in 1936. The literature since publication of the last report had also been well reviewed. About 65 per cent of the hos pitals consulted did not employ the injection method for hernia. The review of the recent literature, however, indicated that the weight of evidence was preponderantly in favor of the acceptance of the injec tion method of treatment of hernia in carefully selected cases. Most observers agree that the injection treatment should not supplant sur gery and, except in certain cases, does not offer as favorable a perma nent result as the latter. The criteria for safe and successful use of the injection method given by various observers were cited in this report and were as follows: 1. Selection of Cases.--Thin young adults with good muscula- HERNIA 433 ture. (Obese or aged persons with atonic or atrophic supporting tis sues are not suitable.) 2. Type of Hernia.--Recent, small, reducible, indirect inguinal hernia with external inguinal ring not over 3 cm. in diameter. (Scrotal, direct inguinal, femoral, umbilical, ventral, and incisional hernias are unsuitable. Sliding hernia associated with undescended testis and incarcerated hernias are contraindications.) 3. Truss-Fitting.--Skilled, adequate truss-maintained reduction before, between, and after injections. (Incompletely or inadequately maintained reduction may occur with improper fitting or uncoopera tive patients.) 4. Injection Technique.--Knowledge of inguinal anatomy and skill during injection are fundamental. (Surgical asepsis is, of course, imperative.) 5. Choice of Solution.--Sterile, non-toxic, fibrous-tissue-stimulat ing, non-irritating solution is ideal. The fatty acid (soap) solutions approach nearest to these criteria. (Powerful sclerosing solutions are to be avoided and are believed responsible for many complications.) 6. Follow-Up.--Repeated examination for periods of from six months to three years is necessary to determine length of treatment and period of truss-wearing required for cure. (Inadequate treatment and truss support blamed for failures.) Not for General Use.--The council then voted to adopt the report that the injection method of treating hernia may not be recognized for general use and should be employed only by those with special experience and with full cognizance of the dangers involved in the use of such solutions. It then stated that it concurred in the opinion that the method involves less danger of serious complications than surgery when employed only in selected cases of hernia by those skilled in the injection of suitable standardized solutions of known composition and action. None of the solutions are council-accepted. Those reported as be ing used include a mixture of oil of thuja, phenol, and alcohol; sodium linsoleate; sodium psylliate; tannic acid; and proprietary preparations, such as pina-mestre solution, galtanol, and proliferol. Complications.--Complications reported in the literature include mild infections, the development of fibrous masses of cutaneous tissue, failure of the method to correct the hernia, painful scarring, occasional cases of swelling of the testis, a few instances of subsequent impo tence, gangrene, death following perforation of the bowel from acci dental intraperitoneal introduction of the needle, intestinal obstruc tion due to adhesions from inadvertent intraperitoneal injection, or strangulation from failure to maintain reduction, perirectal abscess. 28 434 OCCUPATIONAL DISEASES fecal fistula, and thrombosis of deep epigastric, iliac, or femoral ves sels. Most observers indicate that all serious complications can be avoided by skilful technique. Evaluation of Results.--That a prolonged period of follow-up, rather than a six-month-to-year period, is needed for actual evaluation of the "injection cures" is evidenced by the report of Dobson.12 In this he reported the results on 101 hernias in 70 males and 4 females operated on between September, 1935, and June, 1938, including 68 indirect inguinal, 21 direct inguinal, 10 postoperative inguinal, one postoperative femoral, and one umbilical hernias. Eighty of these were followed up for periods of from six months to two and a half years. Six months after beginning of the injection treatment, the results had been most promising, and it seemed that all types and sizes of hernia were being cured. But then there began disappearance of scar tissue and recurrence of the hernias. There was a recurrence percentage of 37.73 per cent in indirect inguinal hernias; 68.42 per cent in direct in guinal hernias; and 100 per cent in all postoperative hernias. Harris and White13 reported on the follow-up of 573 cases, only 41 per cent (236) of which could be utilized for this check. In these 236, there were 57 per cent cures, 28 per cent possible cures, and 15 per cent complete failures after a six-month-to-three-year period. Many more long-term follow-up studies are needed to evaluate this method. REFERENCES 1. Campbell, D. A.: Workmen's Compensation, Parker, Stone, and Baird Co., Los Angeles, 193o, Vol. 1. p. 306. 2. Moorehead, J. J.: "The Relation of Trauma to Inguinal Hernia," Am. J. Surg., 27: (Feb.), 1940. 3. Early, C. E.: Chief of Staff. Golden State Hospital, Los Angeles, personal com munication. 4. Jordan vs. State Compensation Commissioner, IV. Va. 197 S. E. 20. ;5. General Accident and Liability Insurance Company vs. Daffern, Texas 81 F. (2d) 179. 6. Stiger vs. Industrial Commission, TVis. 265 N. TV. 678. 7. Furferi vs. Pennsylvania Railroad, N. J. 189 A. 126. 8. Robbins vs. Original Gas Engine Company, 191 Mich. 122, 157 N. TV. 437, 438. 9. Cessante vs. Ford Motor Company, Mich. 278 N. TV. 671. 10. Riddle, P.: Injection Treatment, TV. B. Saunders Co., Philadelphia, 1940. 11. "Present Status of Injection Treatment of Hernia. Report of the Council on Pharmacy and Chemistry." J.A.M.A., 115: 553 (August 17). 1940. 12. Dobson, L.: "The Late Results of the Injection Treatment of Hernia," Surgery, 7: 836 (June), 1940. 13. Harris, F. I., and While. A. S.: "The Evaluation of the Injection Treatment of Hernia," J.A.M.A., 111: 2009-13 (Nov. 26). 1938. PART VI CHAPTER XXXII THE DERMATOSES Any clinic devoted to industrial medicine is certain to have a fairly large admission of patients with skin lesions. Since there is no full time dermatologist on our staff, it falls to the author either to make the diagnosis, or as is frequently the case to refer the patient to an outside dermatologist. It is with a full appreciation of the difficulties commonly encountered that the author sought to make the following discussion a concise but accurate description of only the more frequent occupational dermatoses, since obviously this subject in its entirety is too vast for discussion in other than a separate textbook. The ma terial has been provided largely through the efforts of the collab orator.* Incidence and Statistics.--Schwartz1 estimates that the proportion of dermatoses to all other occupational diseases is 69 per cent; the average loss of time for compensated cases is ten weeks; the average compensation paid is $100; the average cost for medical care is about $90; and the annual loss for the occupational dermatoses in the United States is approximately $4,000,000. The U. S. Public Health Service made studies of 100,000 workers in various occupations and found that 1 per cent were affected by skin lesions resulting from contact. This figure excluded burns, splashes by alkalis or acids, and pyogenic invasion of occupational skin wounds. These figures should give a proper conception of the importance of this phase of industrial medi cine. Occupational Hazards.--It is impossible to list the occupational hazards, for it may be truthfully said that the majority of all trades present such a hazard to certain persons. It is known that any sub stance encountered in any trade or occupation may produce a derma titis in one who is susceptible. The handling of oils, chemicals, dyes, paints, solvents, metals, fabrics, rubber, and heavy dusts, cement in particular, leads the list. Epitheliomas and carcinomas resulting from occupational origin will be mentioned elsewhere in this book. * Written in collaboration with Nelson Paul Anderson, M.D. 435 436 OCCUPATIONAL DISEASES Definition: An industrial dermatitis is any inflammatory disease of the skin for which industrial exposure can be shown to be a major causal, con tributory, or eliciting factor. Industrial dermatitis is a subcategory of occupational dermatitis, for occupational dermatitis includes not only industrial dermatitis but also all other dermatitides attributable to any occupational pursuit.2 General Considerations of Etiology.--That allergy plays a role in the production of many types of occupational dermatoses seems to be an established fact. In spite of the tremendous amount of investigation on this subject, little is known regarding the true mechanism of the production of an allergic state. For practical purposes the physician handling occupational dermatoses should realize that allergy and hypersensitivity do exist. He should, however, fully realize that there are many other factors which may play an important part in the causation of dermatitis in industry, and that these factors may or may not deal directly or indirectly with allergy. Many of the skin conditions met with are due to primary cu taneous irritants. These substances, which are generally strong acids, alkalis, or corrosive salts, are sufficiently irritating to produce a der matitis in a large percentage of persons with normal skin. The presence of focal infections in the teeth, tonsils, and sinuses undoubtedly contributes to the production of a dermatitis in certain cases. Superficial fungous infections of the feet and groin give rise to many perplexing problems in industrial dermatitis. The type of skin, perspiration, diet, and personal cleanliness are all factors which must be taken into consideration. Finally, as pointed out by Sulzberger,2 there are many eruptions which are due to an interaction of many elements and to a complex effect attributable to the cooperation of many factors. He terms this action "synergic" or "synergistic." DIAGNOSIS Certain lesions resulting from occupational exposure constantly present the-same clinical manifestations. "Chrome holes" on the hand, or of the nasal septum, have constant characteristics which should .y. entail no diagnostic difficulty when appearing in a man working with these fumes or with the chromates. The same may be said of the i furunculosis occurring in oil or cement workers, due to mechanical blockage of the pores of the skin, or the acne from the action of tar. : ji: For these and many others, the industrial cause is usually apparent. The industrial physician, practicing in an area given to the manu- THE DERMATOSES 437 facturing or processing of certain substances, rapidly learns the char acteristics to be expected in lesions apt to result from such exposure. On the other hand, there are a vast number of what appear to be nondescript eczematous lesions of occupational origin which are most baffling. With these it is not such a simple matter to find the causative agent. Furthermore, these lesions do not take on a characteristic ap pearance such as the chrome ulcer, but instead present an eczematous appearance similar to many other dermatoses. A dermatitis from a plant, a dye, a solution, a cosmetic, or a fungus may be clinically in distinguishable by the physician. It is this type of case which must frequently be referred to the dermatologist. History.--A careful and detailed history should be taken before proceeding with the examination of the patient. This history must include an inquiry into all past illnesses of the patient and his family, with particular reference to any previous skin trouble, asthma, hay fever, urticaria, or other allergic disorders, and of any drugs recently taken. Detailed chronological statements should be obtained, concern ing both the particular type of work done by the patient and the onset of the present eruption. Inquiry can-be made about the working conditions, including light, heat, ventilation, and factory hygiene. One should try to obtain a complete and vivid picture of the patient's daily routine while at work. While doing this, a list can be made of substances, chemicals, or other materials which the patient contacts while at work. The history is completed with information regarding the patient's outside activities, conditions of home life, and hobbies. Removal of Clothing.--There is one admonition which cannot be too strongly stressed. Any patient presenting a skin lesion should be examined with all clothing removed. A Colles fracture may be exam ined and diagnosed with only the forearm bared, but a skin lesion of the wrist requires removal of the entire clothing for adequate diag nosis. Criteria for Diagnosis.--In order to establish proof of the indus trial nature of a given dermatitis, Sulzberger and Finnerud2 listed cer tain criteria which should be of aid. These are quoted as follows, except that under their "Criteria of the Second Order" I have con siderably altered their seventh point. Criteria of the First Order 1. Inception.--The dermatitis appears at any time during a period of industrial exposure or even after a lapse of a reasonable incubation period, following the cessation of the industrial exposure (usually a maximum of from two to three weeks). 2. Amelioration.--The dermatitis regularly disappears or is re- 438 OCCUPATIONAL DISEASES peatedly improved within a reasonable period (days, weeks, or even months) after cessation of the causal industrial exposure. (While this is usually the case, retention of causal agents, complications, or ensu ing polyvalent sensitization may prolong the course even for several years after the last industrial exposure.) 3. Recurrences and Exacerbations.--The dermatitis shows a tend ency repeatedly to recur or to exacerbate when the worker returns to the identical industrial exposure after a certain period of absence (provided that there has been no change in working conditions or in the patient's manner of working, or in his susceptibility). Criteria of the Second Order (Adjuvant Criteria) 1. The dermatitis appears first in, and is usually confined to, the areas of maximum exposure (in a small percentage of cases it spreads to, or may begin in, apparently unexposed areas or even becomes gen eralized) . 2. The character and localization of the dermatitis correspond to the character and localization of dermatitis known in other cases to have been caused by exposure to the same or similar industrial haz ards. (While many different substances and procedures can produce similar or identical eruptions, there are certain classes of substances and of procedures which regularly produce fairly characteristic lesions.) 3. The application of the presumptive causal agents to an un affected site close to the site of the dermatitis produces a reaction, pro vided this application is made either during the active phase or after the proper interval following the cessation of the dermatitis. 4. The cutaneous test produces reactions of the same fundamental nature as the dermatosis under investigation. 5. Other workers similarly occupied are or have been similarly affected. 6. The dermatitis appears soon (days or weeks) after the patient begins work involving new potential hazards. 7. The dermatitis is proved to be of possible occupational nature; that is, it is shown to be of the type which may result from the indus trial exposure sustained. Skin Disorders Unrelated to Occupation.--The physician should recognize that such skin disorders as psoriasis, scabies, pityriasis rosea, seborrheic dermatitis, impetigo, erythema multiforme, and lichen planus are practically never related to occupation. Nevertheless, pa tients with these diseases frequently present themselves, believing the skin disorder to be caused by their work. It occasionally happens that a preexisting skin condition, particularly seborrheic dermatitis, may THE DERMATOSES 439 be a predisposing factor in the production of an industrial derma titis. Patch-Test Technique.--The patch test is performed as follows: The substance to be tested is placed upon a small square of gauze, several layers in thickness. This gauze square is most convenient when about three-fourths the size of a postage stamp. In general, powders or dry substances must be moistened slightly with water. This small patch is then placed upon the skin in such a manner that the sub stance to be tested comes in direct contact with the skin. Any area of the skin may be selected as the test site. The areas preferred are the Fig. 115.--Positive reaction to patch test from 1 per cent formaldehyde. back, inner aspects of the upper arms, and the anterior surfaces of the thighs. In industrial practice, particularly if one has any suspicions of the integrity of the patient, the back is the best location for testing. The patch is then covered by a square of impervious material, such as wax paper or cellophane. This covering should be about four times the size of the test patch. These are covered by wide strips of adhe sive and left undisturbed for forty-eight hours. The patient should be instructed to remove the patch, at once if burning, stinging, or marked discomfort occurs. In cases of known sensitivity to adhesive tape the patches may be held in place by flexible collodion, nail polish, or rubber cement. 440 OCCUPATIONAL DISEASES Delayed Reaction.--After removing the patches, the test areas may be encircled with 2 per cent mercurochrome or 2 per cent gentian violet, in order to facilitate the correct reading of delayed reactions. The reading of the test is performed twelve to twenty minutes after removal of the patches and should be checked by subsequent read ings at forty-eight- and ninety-six-hour intervals. Characteristics of Positive, Reaction.--A positive reaction is char acterized by a sharply defined square of redness, corresponding in size and shape to the central test area (Fig. 115). Papules and vesicles are also usually present, corresponding to the appearance of the original eruption. Only rarely is a positive reaction manifested by redness and inflammatory edema. Such a positive reaction can best be determined by feeling or stroking the test area with the finger. Evaluation of Negative Reactions.--Having performed patch tests, one would think it a simple problem to evaluate the results of such tests. In the ordinary case this is true. There are, however, numerous pitfalls in the interpretation of such tests. Negative reaction to patch tests with suspected irritants can present several sources of error: 1. The dermatitis in question may not be the result of any sub stances contacted at work. 2. Local skin sensitivity may be present. This phenomenon is rare, but it occasionally happens that patch tests on sound skin give nega tive results. In such cases the test may be repeated, using a site adja cent to that of the original eruption. It may be necessary to wait until the original condition has disappeared and then repeat the test on the healed area.3 3. The actual causative substance producing the eruption may not have been tested; or, if tested, it may have been used in too weak a concentration, or incorporated in an unsuitable vehicle. 4. Theoretically possible, but actually quite rare, is the occur rence of a refractory period of skin reactivity. During such a time the skin may fail to react to a definitely causative substance. If the patch test is performed during such a refractory period, one can easily see how erroneous conclusions can be drawn. 5. The actual conditions of industrial exposure are never dupli cated by patch tests. It is well known that the noxious effects of many substances are magnified by numerous external factors. These include perspiration, heat, cold, sunlight, repeated cleansing with soap and water, repeated exposures and prolonged immersion in liquids leading to maceration of tissues. None of these contributory factors can be adequately reproduced by the patch test. 6. Occasionally, patch tests done with all suspected irritants are negative in spite of fairly definite clinical evidence that some indus trial contact is causative. In such cases there seems to be definite evi- THE DERMATOSES 441 dence to show that two or more substances act in combination or synergistically to produce the occupational dermatitis.4 This is par ticularly true in the so-called "baker's dermatitis." In other instances, in addition to exposure to some irritant, an additional physical agent, such as sunlight or heat, is necessary to produce a positive reaction. Evaluation of Positive Reactions.--Positive reactions to patch tests with suscepted irritants can present several sources of error: 1. Either substance tested may be a primary irritant which would produce irritation of any normal skin; or, if not a primary irritant, it may have been used in too strong a concentration in performing the test. Under no condition should the concentration employed in testing exceed that which occurs in exposure at work. The use of solutions in too strong concentration may give rise to localized gangrene and widespread irritation, and may even be responsible for the generaliza tion of the heretofore localized process.5 In fact, there are medicolegal possibilities in using the patch test. Certain chemicals must be in corporated into vehicles before testing. The proper vehicle and the concentration to employ have been made the subject of considerable study.0 2. A positive patch test with a substance contacted at work does not necessarily prove that the eruption was caused by this substance. Such a positive test may indicate only a latent sensitivity, and the real cause may be some substance not tested but contacted by the patient outside of his work. 3. The interpretation of the positive patch test is always open to the criticism that such a test can never actually duplicate the condi tions of industrial exposure. 4. Marked difficulties of interpretation arise in cases where several different substances produce positive reactions to patch tests. This occurrence of polyvalent sensitivity, however, may furnish a clue to a non-industrial irritant and at the same time aid the physician in avoiding contact dermatitis as a result of his own therapy. Of course, a patient found positive to mercury among other things would not be treated by mercurial ointments or antiseptics. 5. For a substance to be incriminated as the cause of an eruption there must be a definite history of contact with the suspected ma terial.7 6. Although stated elsewhere, it may be said that with one or two exceptions (cement), the elimination of contact with the suspected irritant should produce either a cure or marked amelioration of the skin condition. In the following paragraphs consideration is given to a few repre sentative and fairly common types of occupational dermatitis. 442 OCCUPATIONAL DISEASES Epidermophytosis.--The relationship of superficial fungous infec tions or eczematoid ringworm of the extremities to industrial derma titis is one that gives rise to more discussion and dissension than occurs perhaps in any other skin disorder. As Blaisdell8 states, "Broadly speaking, it would apparently be easy enough to discrimi nate between the case entitled to compensation and the one that is not, but considering the cases individually it is oftentimes difficult to give a judgment that is fair to both the worker and the insurance company." There are definite instances where epidermophytosis might be di rectly related to the occupation, e.g., an attendant in Turkish baths. There are also cases where a true contact dermatitis of industrial nature may be followed by secondary infection with ringworm organ isms. Again, a contact dermatitis may be superimposed on a super ficial fungous infection. This not infrequently happens in cases of ce ment dermatitis. In every case of suspected industrial dermatitis of the hands, the experienced clinician will examine the feet for evidence of any super ficial fungous infection. Such examination should include microscopic study of scales for mycelia. There is considerable clinical evidence to indicate that some of the eruptions on the hands in such cases are allergic manifestations of the fungous infection on the feet,9,10 e.g., epidermophytosis, and hence not of an industrial nature. However, in the presence of a positive patch test to some suspected and con tacted irritant, such an infection of the feet may be looked upon as producing a non-specific irritability of the hands. In other words, such a fungous infection of the feet lowers the threshold of sensitivity of the hands and hence acts as a predisposing etiological agent. The trichophyton intradcrmal test is believed to be of value if properly used. Lewis11 is of the opinion that while a positive intradermal trichophyton reaction is of little or no significance, a negative trichophyton reaction at least excludes the possibility of a given skin disorder's being an epidermophytid. Infectious Eczematoid Dermatitis.--Traumatic wounds of all types are extremely liable to the development of infectious eczematoid der matitis (Fig. 116), often erroneously considered to be a ringworm12 infection because of its tendency to annular configuration. The usual picture is one of a person who sustains an injury to an extremity in the form of a scratch, abrasion, laceration, or crushing injury. In the latter event an amputation of one or several digits follows. During the period of healing an acute eczematous dermatitis develops about the wound margins. This is characterized by an annular or circinate red ness with the presence of small pin-head-sized papulovesicles, produc- THE DERMATOSES 443 ing a weeping surface. The condition may spread only in the neighbor hood of the wound, but often patches are found far removed from the original site. Severe itching occurs, and the scratching which this Fig. 117.--Diffuse infectious eczematoid dermatitis arising from multiple draining osteo myelitic foci. causes may give rise to new lesions. It may also give rise to sec ondary infection in the form of lymphangitis, cellulitis, and regional adenitis. A similar eruption may develop about draining sinuses subsequent to osteomyelitis and compound fractures (Fig. 117). Occasionally such an eruption is a true ringworm infection. In other instances the der- 444 OCCUPATIONAL DISEASES matitis may be due to sensitivity to mercurial or other antiseptics which have been applied. Turpentine Dermatitis.--Turpentine is a frequent cause of con tact dermatitis in industry. According to Schwartz, it produces about l per cent of all cases of occupational dermatitis. Turpentine derma titis may occur in those engaged in its manufacture; however, it is most frequently seen in painters (Fig. 118). Since it usually develops in people who have followed the painting trade for many years, it may present a serious problem both to the patient and to the insur ance carrier. To the painter, turpentine dermatitis represents a seri ous obstacle to the pursuance of his trade. To the insurance car- Fig. 118.--Contact dermatitis of the eyelids due to varnish-remover. Such in volvement of the eyelids may occur through fumes, but is usually from actual contact through the medium of the hands. rier it represents a compensable occupational dermatitis, in which the initial temporary disability is often a matter of several weeks and recurrence is practically universal. There is no doubt that different kinds of turpentine vary a great deal in their irritating and sensitizing properties. Destructively dis tilled wood turpentine appears to be the least irritating. Baker's Dermatitis.--Dermatitis in bakers is not uncommon and may result from contact with flour, sugar, cake dough,13 bread dough,13 cinnamon,14 vanilla, various spices, and so-called "flour im provers," chiefly ammonium persulfate. However, only about two thirds of the patients present positive reaction to ordinary patch tests. In such cases one must perform additional patch tests, using different THE DERMATOSES 445 combinations of the ingredients encountered at work. Even then there remains a considerable percentage of cases of unexplained origin. The eruption involves the hands (Fig. 119) and at times the fore arms and occasionally the face. It is usually of a dry, scaly, eczcma- Fig. 119.--Dry, scaly, hyperkeratotic dermatitis occurring in a baker who was proved sensitive to both cinnamon and nickel. Fig. 120.--Occupational dermatitis of the hand due to cinnamon, in a pastry worker. tous15 nature. In general, the eruption tends to be diffuse, and sec ondary ridging of the finger nails occurs in long-standing cases. In volvement of the nails alone may occur.10 There arc not other special clinical characteristics (Fig. 120). 446 OCCUPATIONAL DISEASES Cosmetician's and Barber's Dermatitis.--Occupational dermatitis is common in those engaged in beauty-shop work. Barbers are prone to develop a trade dermatitis from quinine, which occurs in many scalp tonics, the perfumes used in many hair lotions and from pro longed and repeated immersion of the hands in soap and water. Cosmeticians handle many chemicals which may produce a con tact dermatitis. These include p-phenylenediamine (Fig. 121), which is the active ingredient of most all hair dyes, nail polish, nail-polish removers, finger-wave solutions, perfumed creams, rinses of all types, Fig. 121.--Occupational dermatitis in a hairdresser. Contact dermatitis of hand due to p-phenylenediamine; positive patch tests to same on thigh. shampoos containing various oils, and above all formaldehyde, which is used frequently for the dry sterilization of combs and brushes. Regardless of other factors, it is important to find out the exact cause of the eruption in any given case. Once this has been determined, it is often possible for the beauty operator to continue in the same line of work, provided there is no exposure to or contact with the offending substance. The patch test with formaldehyde should be done with a 1 per cent solution. Cement Dermatitis.--Dermatitis from cement is exceedingly com mon in masons, bricklayers, plasterers, and tile-setters (Fig. 122). It THE DERMATOSES 447 differs from the ordinary contact dermatitis in that the eruption not only involves the exposed areas of the hands and forearms, but also occurs about the ankles and other covered parts of the body. Its per sistence for weeks and even months after exposure has ceased and the tendency to secondary pyogenic infection are noteworthy. It is one of the most disabling of all the industrial dermatoses,17 and from many standpoints deserves more consideration from the dermatologist,18 cement-manufacturers, and insurance carriers than it has received. It should be noted that these patients may be sensitive to only one type of cement10 and yet be able to handle other cements. Fig. 122.--Contact dermatitis of the hand due to cement. Dermatitis Artefacta.--One of the most difficult dermatological problems confronting the physician is that of self-produced eruptions. Usually occurring in emotionally unstable but nevertheless intelligent persons, such artificially produced lesions have the following charac teristics20:1 1. Conform to no other known type of skin condition 2. Occur in circumscribed areas, the surrounding skin being nor mal 3. Can usually be reached by the hands, and are often unilateral, 448 OCCUPATIONAL DISEASES being on the left side of the body in right-handed persons, and vice versa 4. Other features of hysteria, e.g., absent pharyngeal and conjunc tival reflexes, may be found To the above may be added the observations that practically every patient has suffered some sort of trauma before the appearance of the first feigned lesion; and also that the first manifestation is often in the immediate neighborhood of the preceding injury. Such feigned lesions are most frequently produced by acids, al kalis, caustics, or vesicants. They are usually ulcerative in character Fig. 123.--Dermatitis artefacta. Patient's first lesion was due to sulfuric acid from a storage battery. He subsequently intentionally produced the lesions seen in this picture in order to prolong compensation and avoid alimony payments. but may be erythematous, papulovesicular, or.bullous. Gangrenous21 lesions on apparently intact skin should immediately arouse the sus picions of the physician. Frequently in industrial practice, dermatitis artefacta is produced from self-evident motives, e.g., compensation. At times other consid erations come into play, including revenge or domestic difficulties (Fig. 123). From a therapeutic standpoint, nothing is ordinarily gained by directly accusing the suspected person. Time and money will be saved THE DERMATOSES 449 by hospitalization, the use of occlusive dressings sealed with collodion or adhesive tape. If the latter is used, it should be marked in such a way that tampering with the dressing may be readily detected. Con tinuous strict observation must be carried out day and night, but in such a manner that the malingerer does not realize that he is undersuspicion. Onychia.--Involvement of the fingernails and paronychia] tissues occurs more frequently in industry than generally realized.-2 Defor mity, ridging, and transverse striations of the nails occur especially in soda-fountain workers, cannery workers, fruit-juice-stand employees, and others who have their hands immersed in liquids over long periods of time (Fig. 124). Fig. 124.--Paronychia with multiple involvement of the periungual tissues and secondary nutritional deformities of the nails. A common condition in soda-fountain workers. Syphilis.--With the exception of doctors, nurses, and laboratory workers, syphilis does not ordinarily enter into the question of com pensable dermatoses. Situations do occur in which trauma acts as a contributory factor. The most important of these conditions is inter stitial keratitis, which may first appear in a congenital syphilitic fol lowing an eye injury. The criteria for the acceptance of such a diag nosis are well defined and have been aptly stated by Barkan23:1 1. Trauma must be positively ascertained and more than such as the person is exposed to in the course of his employment 2. Trauma must be of the cornea itself and cause a definite irrita tion 3. An expert must determine that the interstitial keratitis is not present at the time of injury, and that the consequence of the injury is an interstitial keratitis 29 450 OCCUPATIONAL DISEASES Unilateral tertiary squamous syphilides of the palm occasionally appear to be induced by frequent and repeated minor traumatisms. Such a syphilide must appear on the right hand in a right-handed person, and vice versa. Further, the location of the syphilide must correspond to the area traumatized. Finally, annular and circinate nodular and nodulo-ulcerative syph ilitic gummata may appear in any area after trauma, or after the re moval of a foreign body. In general, compensability in all cases com plicated by syphilis lasts only until the disappearance of the external manifestations of the disease. MEDICOLEGAL ASPECTS While the industrial dematoses are probably the most frequent of all industrial claims for compensation, the hearings of these cases before industrial accident commissions are infrequent. The insurer is usually willing to accept the diagnosis from a trained dermatologist. Less than 2 per cent of the cases handled at this clinic have ever been contested. Insurance companies also appear to be more willing to accept the skin lesion, since there is not the fear that permanent dis ability will face them if they accept the case as compensable. Temporary Disability.--This ceases with the disappearance of the lesion, when the lesion does not interfere with ability to work, or when employment can be offered which is considered not apt to aggra vate or produce further lesions. In some instances, loss of a wage difference between former occupation and the offered one has to be compensated. Permanent Disability.--This is rare. Occasionally, limitation of, motion follows contraction scars or keloids from skin lesions. If so, they should receive a rating based upon the percentage of loss of function of the part. Disfigurement of the body as a result of altera tion of the former appearance of the skin is ordinarily considered as not compensable. TREATMENT Prophylaxis.--Preventive measures are highly important. Preem ployment examinations should uncover the history of repeated skin lesions or the tendency to react to even mild irritants. In occupations which involve a special liability to dermatitis the employer would do well to insist on a routine examination of the skin of prospective em ployees.24 Such an examination should take into consideration the im portance of any existing skin condition. Special emphasis should be placed on seborrhea, ichthyosis, hyperhidrosis, the general type of complexion (blonds and red-haired persons are very susceptible to cu taneous irritants), and the presence of epidermophytosis of the feet. THE DERMATOSES 451 Protective Procedures.--Each new workman should be given care ful instruction as to maintaining good hygiene, avoidance of undue exposure, and the wearing of certain protective devices. Wherever Fig. 125.--Contact dermatitis of forearms and arms in a janitor due to "sweeping"' compound. Fig. 126.--Occupational dermatitis due to leather. This liat-band dermatitis caused by safety helmet in an oil-field worker. dust, grease, oil, grime, and the like, are prevalent in the work (Figs. 125, 126), the men should have two sets of lockers--one for the clean street clothes, and the other for the working apparel. At the end of the day's work, he should deposit his working clothes in one locker. v 452 OCCUPATIONAL DISEASES shower well, and then proceed to the second locker for his clean clothes. Men working where the substance is such that it may easily penetrate the clothing, such as many dusts, cement, or oils, should wear thick, closely woven clothes or rubberized material. Properly fitting gloves are often neglected where they would be advantageous. A film of oil or vaseline may be a protection to unprotected parts. Their value is questioned by most dermatologists, however. It is astonishing how many small plants fail to supply the above-mentioned protective devices. Immersion of the hands in irritating chemicals is often done without gloves, when these could be easily employed. It can be laid down as a general rule that in all industries involving ex posure to chemicals, dyes, drugs, coloring materials, or fluids, it is always advisable to rinse the hands or exposed parts with a weak solution of some reducing agent. If the offending agent is alkaline, then a weak neutralizing solution of vinegar, acetic acid, lime water, or weak sulfuric acid may be employed. For general purposes, espe cially where acid is apt to affect the skin, a weak alkaline reducer may be used as, for instance, a weak solution of sulfate of soda. These reducing agents should be supplied and should form a routine part of the workman's hygiene. After the use of a reducing agent, the parts may be washed in distilled water. Proper Use of Cleansing Agents.--It is no exaggeration to state that a very considerable percentage of cases of so-called "industrial dermatitis" is due to the improper use of cleansing agents rather than to the actual contact of some specific industrial irritant. This entire field of industrial dermatitis has been extensively studied by Klauder and his collaborators. The physician encountering negative reactions to patch tests in apparent and obvious cases of occupational derma titis should take cognizance of this broad field. In probably 10 to 15 per cent of cases of proved contact etiology, soap, water, and other cleansing agents act as a definite contributory factor. The use of scouring or grit soaps, soap powders, washing powders, and laundry soaps is often followed by the onset of a dermatitis. Substitute for Abrasive Soaps.--The proper cleansing agent for any particular plant or branch of industry can only be determined after proper study. As an efficient substitute for the popular mechanic abrasive soaps, Klauder recommends the following: Formula 12: Co. Sulfonated neat's foot oil......................................................... 45.0 Light liquid petrolatum........................................................... 45.0 Gelatin, 25 per cent aqueous solution.................................. 10.0 THE DERMATOSES 453 This mixture is added to granulated corn meal in the proportion of P/2 parts by weight of corn meal, and one part by weight of the above oil mixture. To prevent the growth of mold, a 0.5 per cent solution of chlorobutanol is added. Protection against Chrome Compounds.--In industries where chromic acid and chrome compounds are encountered (Fig. 127), that is, in dyeing, tanning, electroplating, and blueprinting,2'" a 10 to 30 per cent solution of sodium bisulfite (NaHSO;i) may be used as a reducing agent. It can be applied before exposure and allowed to dry on the skin and is also used as a wash after exposure. Fig. 127.--Contact dermatitis in a printer. Patient was sensitive to the bichromates used in this industry. Protective creams, liquids, ointments, and pastes may also be em ployed, their formulae and composition depending upon the require ments in each case. Klauder gives a number of such formulae appli cable to protection against prolonged contact with soapy water, or against dust-borne irritants. The industrial physician confronted with such a problem would do well to consult this article.21-' Changing Working Conditions.--Confronted with a severe and un doubted case of industrial dermatitis (Fig. 128), there are two possible courses open. The first is to transfer the affected patient to another job, allowing most of the etiological factors to remain for the next susceptible person. The second and more important procedure, par- 454 OCCUPATIONAL DISEASES ticularly if numerous cases occur from the same source, is to change either the process or the working conditions. This involves an exact knowledge of all the processes involved. Such steps at times are made due to poison oak. Fig. 129.--Contact dermatitis due to rubber gloves. At times the very measures used to protect an employee may be the cause of a dermatitis. only when either governmental authorities or the insurance carrier exerts pressure on the insured. In most instances when a person severely afflicted with an occupa tional dermatitis changes his work, the skin condition clears and re mains well. However, the skin condition may persist (Fig. 129). Even THE DERMATOSES 455 if one continues at the same line of work, a certain percentage will eventually clear, although at least an equal number will continue to have skin trouble.27 Local Measures.--In the actual therapy of industrial dermatitis, certain local measures should be mentioned. If the dermatitis is acute and accompanied by vesicles and bullae, together with weeping and exudation, cold wet compresses are advised. Liquor aluminum acetate (liquor burrowi, N.F.)........ 480 Cc. Sig: Dilute twelve to sixteen times with cold tap water and use as a continuous moist compress. Such compresses should be changed or remoistened every two to three hours. If the process is acute and oozing but accompanied by any evi dence of pus formation, the use of wet dressings of from 0.25 to 0.5 per cent of an aqueous solution of silver nitrate is indicated. Wet dressings of Alibour water (see "Infectious Eczematoid Dermatitis") are also of value. As the weeping and exudation subside, which they generally will within from forty-eight to ninety-six hours after the proper use of continuous wet compresses, soothing ointments may be used, such as the following: if Liquor aluminum acetate.......................................................... 15.0 Lanolin, anhydrous.................................................-................. 25.0 3 Lassar's paste, plain ................................................................... 20.0 Sig: Apply locally two or three times daily. If some evidence of infection still persists, either ammoniated mercury (2 to 3 per cent), or sulfur precipitate (2 to 3 per cent), may be added to the above ointment. When a stage of chronicity has been reached and the skin lesions are dry, scaly, and thickened, the use of some tar-containing prepara tion is indicated. In milder cases this may consist of ichthyol, 2 per cent in Lassar's paste. Later, a 5 per cent oil of cade ointment may be applied. The most useful of all the tars, however, is white crude coal-tar paste (see "Infectious Eczematoid Dermatitis"). Constitutional Therapy.--This is rarely of aid in occupational der matitis. Dainow28 has reported desensitization from the administration of vitamins A and D. In very stubborn cases, removal of foci of infection may be necessary. Infectious Eczematoid Dermatitis.--Notoriously resistant to ther apy, this moist, vesicular, eczematous condition may often be ameli orated or cured by the application of a 2 per cent aqueous solution of gentian violet twice daily. As long as the oozing persists, continuous 456 OCCUPATIONAL DISEASES wet compresses of from 0.25 to 0.5 per cent aqueous solution of silver nitrate may be used. Another highly satisfactory wet compress to use in this disorder is the following: Alibour water: Gm. or Cc. Copper sulfate ..................................................................... 1.6 Zinc sulfate........................................................................... 5.6 Saturated camphor water ....................................q.s. ad. 240.0 Sig.: Use 2 tablespoonfuls of the above in a glass of tap water and use as a continuous wet dressing. Change dressing every two to three hours. In addition, small doses of unfiltered roentgen rays are of value. In persons tolerant to tar, White's crude coal tar paste is often very efficacious, especially after the weeping has subsided: White's crude coal tar paste: Gm. or Cc. Crude coal tar..................................................................... 4.0 Zinc oxide.............................................................................. 2.0 ' Corn starch ............................................................................ 15.0 Petrolatum .............................................................................. 15.0 REFERENCES 1. Schwartz, L., and Tulipan, L.: Occupational Diseases of the Skin, Lea and Febiger, Philadelphia, 1939. 2. Sulzberger, M. B,, and Finnerud, C. W.: "Industrial Dermatitis; Definitions and Criteria for Diagnosis," J.A.M.A., 111: 1528-32 (Oct. 22), 1938. 3. Kesten, B., and Laszlo, E.: "Dermatitis Due to Sensitization to Contact Sub stances," Arch. Dermat. and Syph., 23: 221, 1931. 4. Bernstein, J. C.: "Dermatitis Due to a Sulfur-Meat Complex," Arch. Dermat. and Syph., IfO: 414, 1939. 5. Bechet, P. E.: "Patch Test; Evaluation of Its Possible Dangers," Vew York State J. Med., 39: 829, 1939. 6. Rostenberg, A., Jr., and Sulzberger, M. B.: "A List of Substances for Patch Test ing and the Concentrations to be Employed," J. Invest. Dermat., 2: 93 (June), 1939. 7. Sulzberger, M. B.. and Wise, F.: "The Contact or Patch Test in Dermatology," Arch. Dermat. and Syph., 23: 519, 1931. 8. Biaisdell, J. H.: "Epidermophytosis as an Industrial Disease," Urol, and Cutan. Rev., 31: 414, 1927. 9. Peck. S. M.: "Epidermophytosis of the Feet and Epidermophytids of the Hands," Arch. Dermat. and Syph., 22: 40, 1939. 10. Osborne, E. D., and Putnam, E. D.: "Industrial Dermatoses," J.A.M.A., 99: 972 (Sept. 17), 1932. 11. Lewis, G. M., McKee, G. M.. and Hopper. M. E.: "The Trichophyton Test-- Its Value as a Diagnostic Aid," Arch. Dermat. and, Syph., 38: 712, 1938. 12. McNealy. R. IV., and Lichenstein. M. E.: "Tinea! Dermatitis in Traumatic Sur gery," Illinois M. J., 55; 298, 1929. THE DERMATOSES 457 13. Parsons. A. C.: "Report on Baker's Dermatitis."' Brit. J. Dermat., 36: 193, 1924. 14. Tulipan. L.: "Dermatitis from Cinnamon,'' Arch. Dermat. and Syph., 25: 921, 1932. 15. Van Vonna. N. C., Struyeken, J., and Bonnevie. P.: "Contribution to Knowledge of Baker's Eczema," Acta Dermat,.-Venereal., 15: 343, 1934. 16. Cummer, C. L.: "Onychia Due to Handling Sugar," Soc. Trans. Arch. Dermat. and Syph., hi: 142, 1930. 17. Meherin, J. M., and Schomaker, T. P.: "The Cement Burn; Its Etiology, Path ology and Treatment," J.A.M.A., 112: 1322 (April 8), 1939. 18. Burckhardt, \\\: "Mason's Eczema," Arch. f. Dermat. u. Syph., 178: 1, 1938. 19. Schmidt, F. R.: "Occupational Skin Diseases," Urol, and Cutan. Rev., 35: 586, 1931. 20. Sequeira, J., cited by Brown, F. IV.: "The Psychological Investigation of a Case of Dermatitis Arlefacta," Guy's Hasp. Rep., SS: 356, 1938. 21. Towle, II. P.: "Gangrena Cutis Hysterica," Med. Rec., 72: 581, 1907. 22. Ilaldin, Davis H.: "Onychia as an Occupational Disease." Brit. M. J., 2: 845, 1931. 23. Barkan, H.: "Industrial Trauma in Relation to the Development of Ocular Tuber culosis, Syphilis and Neoplasm," Arch. Ophth., 51: 103, 1922. 24. Gardiner, F.: "Occupational Dermatitis," Brit. J. Dermat, 3h: 297, 1922. 25. Parkhurst, II. J.: "Dermatosis Industrials in a Blueprint Worker, Due to Chromium Compounds," Arch. Dermat. and Syph., 12: 253, 1925. 26. Klauder, J. V., Gross, E. R., and Brown, H.: "Prevention of Industrial Dermati tis, with reference to Protective Hand Creams, Soap, and the Harmful Role `of Some Cleansing Agents," Arch. Dermat. and Syph., hi: 331, 1940. 27. Koch, F., and Peters, L.: "Follow-Up of Occupational Eczema," Dermat. Wchnschr., 108: 222, 1939; Abstr. Brit. J. Dermat., 51: 489, 1939. 28. Dainow, I.: "Treatment of Occupational Dermatoses by Vitamins A and D," Acta Dermat.-venereal., 20: 191, 1939. PART VII CHAPTER XXXIII OCCUPATIONAL CANCER No space will be given in this chapter to the relationship of single trauma to the production of cancer, although it is by far the more involved and constitutes a more delicate determination than cancer Fig. 130.--Gas tar cancer on the wrist. The man is aged twenty-nine, and has worked during the last seven years as a gas-retort stoker. He says he frequently gets splashes of tar on this arm. At the age of fourteen he became a scavenger in the mule-spinning room of a cotton mill. Four years later he joined the army, in whichhe served four years. He thinks the growth has been present about eighteen months. The rest of his skin is apparently healthy. (White, The Dermatergoses or The Occu pational Affections of the Skin, Paul B. Hoeber, New York.) which arises in workmen in certain industries. This immediate dis cussion concerns itself primarily with cancer occurring in workmen in those industries dealing with substances or elements recognized as having a carcinogenic tendency. 459 460 OCCUPATIONAL DISEASES Substances with Carcinogenic Properties.--These are chiefly tar, dyestuffs, paraffin, aniline, pitch, and actinic rays (Figs. 130, 131). It is rather startling to note that the majority of noxious agents dealt with in this book are derivatives of the hydrocarbons, and then to observe that in the field of occupational cancer the coal-tar and petroleum products are the chief causative agents. In addition to the ones mentioned--and to a less and very questionable degree, sulfur-- arsenic, chromate, and fumes of acids and caustics have been alleged the cause of cancer. Fig. 131.--Gas tar cancer on the scrotum. A man, aged sixty, worked all his life as a gas-works stoker. (White: The Dermatergoses or The Occupational Affections of the Shin, Paul B. Hoeber, New York.) Site of Assault.--Occupational cancer is considered to be the endresult of chronic inflammation produced by exposure to irritating substances. It appears that there is a predilection for the skin, scrotum, and urinary bladder. Epidermoid carcinoma on the lip of fishermen has been observed. Cancer of the lung resulting from chronic exposure to dusts, gases, or fumes has never been established. Relationship of Silicosis and Pulmonary Cancer.--Klotz1 reviewed 50 cases of silicosis and compared the incidence of pulmonary cancer to that noted in 4500 necropsies performed in the Toronto General Hospital. He suggested that the incidence of cancer in those exposed to silicosis was higher than in the general population. To the author OCCUPATIONAL CANCER 461 this appears as an unfair comparison and is not in agreement with authorities on silicosis. Kuroda2 in Japan noted cancer of the lung in several employees of gas works and began an investigation of this problem. He believed there was a relationship but would offer no conclusions until he had completed his study. Coal-Tar and Petroleum Products.--It is not definitely known or understood just what the carcinogenic property is in the coal-tar or petroleum products. It is evident that the incidence of cancer among workers with these substances is greater in England than in America. Certain investigators have held that the carcinogenic property is less in the petroleum than in the coal-tar series. Others maintain no such differentiation can be made. Some feel that this agent is present to a greater extent at a certain fraction of distillation, supposedly from 200 to 450 C. It is contended by a few that the intensity of action and not the specific agent is responsible. It should not be assumed that all petroleum oils have carcinogenic properties. This was brought out by Heller, who, under the auspices of the Rockefeller Foundation confirmed the earlier work of Wood in noting no scrotal cancer among the oil-refinery workers in Penn sylvania but did find it among the same class of workmen in the MidContinental oil fields of Ohio and Indiana. He stated that the latter oils contained carcinogenic compounds not present in the Pennsyl vania oils. It is not uncommon to find in these refinery workers that the carcinomas are preceded by warts. Wax boils are common. No statistics can be found regarding the incidence of cancer among .the California or Gulf Coast oil workers. These oils resemble the MidContinental oils more than they do the Pennsylvania oils, in that they have an asphalt base. Dr. Alfred Soiland, head of the Cancer Clinic in Los Angeles, told me that he knew of no cases of cancer from this source. Mr. Phil Jones, of the Research Department of the Union Oil Company in Los Angeles, stated that if such cases did occur the inci dence was so low as not to be brought to his attention. It is not known that the "cracking process" so commonly in use in this state creates or enhances the carcinogenic properties of oil, although Leitch5 sup posedly rendered an inert California oil active by heating it to 600 C. Tar.--Tar cancer is not infrequent in fishermen. This substance is used on the nets to keep them from rotting. It becomes smeared on the hands, especially in hot weather, and is carried from the hands to the face. Fishermen have a habit of holding the needle in their mouths while the net is being mended. Shambaugh7 studied this type of affliction among the fishermen of Gloucester and reported eight cases of cancer of the lip. He believed that the tar was the cause and not the constant exposure to the sun. 462 OCCUPATIONAL DISEASES Behan8 pointed out the dangers of coal tar, and intimates that the constant inhalation of the dust and dirt of asphalt or tarred roads may subject the autoist to all the hazards of coal-tar cancer. This likelihood appears far-fetched indeed. Dyes.--Gehrmann reports the incidence of cancer in dye workers at the du Pont plant in Wilmington, Delaware. He states that while it has been observed that prolonged exposure to relatively low con centrations of certain aromatic amines (aniline, a- and /^-naphthalenes, and benzidine) are known to cause the development of tumors in cer tain persons, the mechanism of development is not clearly understood. Absorption is by respiration, through the skin, and by the intestinal route, the latter being relatively unimportant. The lesions are pre dominantly papillomas or carcinomas of the urinary bladder. The classical symptoms are hematuria, frequency, urgency, burning, and pain. In his experience these occur only in well-advanced cases. Benign papillomas occur frequently and may be destroyed by figura tion. From his report it is evident that malignant growths occur only after prolonged exposure. The average length of time was twelve years. Aniline Tumors.--Hueper9 and his associates experimented with the production of "aniline tumors" in animals in order to establish some foundation for study of the occupational neoplasms and to ob serve any systemic effects following the prolonged exposure to one of the suspected carcinogenic aromatic amines. For this study they selected /3-naphthylamine. By oral feeding and the subcutaneous in jections of commercial /J-naphthylamine they were able to produce preneoplastic and neoplastic papillomas or carcinomas in thirteen out of sixteen female dogs. Generalized papillomatosis was a frequent phenomenon. In addition, prolonged administration of this substance produced blood destruction, degenerative changes in the tubular epithelium of the kidneys and in the parenchyma of the liver. Chromate Dust.--Teleky10 contends that the inhalation of chro mate dust by workers in this exposure produces a relatively high incidence of pulmonary cancer and possible cancer of the gastro intestinal tract. McNally11 makes no mention of this possibility, and Hamilton12 fails to cite any instance of it. She even mentions that the British medical inspectors were unable to find a single instance of carcinomatous degeneration of chrome ulcers. Cancer of the Eye.--From eye clinics, institutions devoted to the study of cancer, from eminent ophthalmologists, and from the medical services of large industrial plants, Lane13 collected 1000 cases of can cer of the eye. One hundred and fifty-four different occupations were represented. Her classification included exposure to oils and lubricants; sunlight and tar; sunlight and chemicals or irritants; coal, pitch, tar, OCCUPATIONAL CANCER 463 radioactive substances; and metals. Compared to the average general cancer rate per thousand, there was some increase in the number of workers exposed to oils in the automotive field. There was no increase among those who occasionally use oil in their trades, such as printers, plumbers, steamfitters, and the like. Workers exposed to the elements, tar, and chemicals showed a large increase, especially farmers and laborers. In the miscellaneous group, however, more than half had no occupational hazard; more than one third of the entire 1000 were housewives. The average age of the patients with ocular carcinoma was 57.15 years, and 48.5 for those with malignant melanomas (sarcoma). Her study does not convince this writer of the especial significance of occupational cancer of the eye. Certainly one should be very hesi tant in attributing cancer of the eye in a fifty-seven-year-old farmer, for instance, to his occupation. Any such allocation would require a careful ruling out of all other factors. Medicolegal Aspects.--The incidence of cancer of unquestionable occupational origin is low when consideration is given to the vast army of Workers in contact with the alleged carcinogenic substances. Cancer of the skin from these substances develops slowly, usually taking from ten to fifteen years, at least. The growth is considered to be of low malignancy. Metastasis from these growths is rarer. Any patient presenting himself with a cancer allegedly due to occu pation warrants a thorough investigation upon the following lines: 1. The nature of the substance alleged as the causative agent. Is it known to have carcinogenic properties? 2. The location of the lesion. Is it in an area commonly assaulted by such substances; or is it in a tissue or organ rarely if ever involved by these agents? 3. The time element. How long has the patient been exposed? Have others in the same industry been known to have de veloped similar lesions? Upon the evaluation of such an inquiry should the decision rest. Treatment.--The same hygienic measures recommended for all skin lesions apply to this disease. Clean working-clothes should be furnished daily, showers after work, protection of the skin by gloves, oilcloth aprons, head hoods, and ointments over the exposed parts. Operations employing suspected carcinogenic substances should be under a suction hood when possible or within an enclosed booth em ploying suction. In those occupations offering a known or suspected hazard, frequent physical examinations should be done in order to reveal early lesions. 464 OCCUPATIONAL DISEASES REFERENCES 1. Klotz. M. 0.: "Association of Cancer and Silicosis of the Lung," .1 in- J. Cancer, to: I-I.-I8 (Jan.), 1939. 2. Kurodu, S.: "Occuputiomd Pulmonary Cancer of Generator Gas Workers," Indust. Med., <i: 304-300 (May). 1937. 3. Heller, L: "Occupational Cancers," J. Indust. Huy., 12: 109-197 (May), 1930. 4. Wood, H. B.: "Skin Lesions among Tar Workers," J. Cancer Research, Id: 54-.->9 (Marc!)), 1929. 5. Leiteh, A.: "Mule-Spinner's Cancer and Mineral Oils," Brit. M. J., 2: 941-943 (Nov. 22), 1924. 0. Gehrmann, G. II.: "Papilloma and Carcinoma of Bladder in Dye Workers," J.A.M.A., 107: 143(5-39 (Oct. 31), 1930. 7. Shambaugh, P.: "Tar Cancer of Lip in Fishermen," J.A.M.A10b: 2320-29 (June 29), 1935. 8. Behan, B. J.: Relation of Trauma to New Growths, The Williams and Wilkins Co., Baltimore', 1939. 9. Hueper, W. C., Wiley, N. II., and Wolfe, H. D.: "Experimental Production of Bladder Tumor in Dogs by Administration of Beta-Naphthylamine," J. Ind. Ilyy. and Toxicol., 20: 1-90 (Jan.), 1938. 10. Teieky, L.: "Occupational Cancer of the Lung," J. Indust. Ilyy. and Toxicol., 19: 73 (Feb.), 1937. 11. McNally, Win. D.: Toxicology, Industrial Medicine, Chicago, 1937. 12. Hamilton, A.: Industrial. Toxicology, Harper and Brothers, New York, 1934. 13. Lane, L. A.: "Occupation in Relation to Cancer of the Eye and Adnexa," Am. J. Ophtk., 22: 239-350 (March), 1939. 't CHAPTER XXXIV HEAT AND CLIMATIC AFFECTIONS Heat exhaustion, heatstroke, and heat cramps constitute an occu pational hazard to firemen, stokers, mill and boiler-room workers, and to others forced to exert themselves in an atmosphere of high tem perature. Under extreme heat conditions the discomfort becomes un bearable as the humidity rises. The peripheral vessels dilate, and there is an increase in the circulating blood volume. Hick1 and his co workers noted that if there was no rise in the rectal temperature the cardiac output remained the same, but if there was a rise in tem perature there, an increase in oxygen consumption and cardiac output resulted. This state of hyperpyrexia which may be present in either heat exhaustion or heatstroke may terminate in death. In heat ex haustion there is an embarrassment to the heat-regulating center, while in heatstroke there is a paralysis of this center. Circulatory Adjustment.--A person's ability to withstand exces sive heat is a matter of circulatory adjustment. Keeton2 and his associates studied this adjustment with healthy medical students and nurses under controlled conditions. All subjects were observed twelve hours after their last meal and after a satisfactory rest, being there fore under basal conditions. The environments used were hot dry (11.5 F. dry bulb and 70 F. wet bulb), and hot wet (99.5 F. dry bulb and 90 F. wet bulb). Their study involved observations chiefly with regard to the effect of posture. Circulation is well maintained in hot environments by healthy subjects while they are lying down. The adjustment of the circulation to the erect position becomes in creasingly difficult for normal persons as environment becomes hotter and fever appears. Failure of this adjustment to the erect position leads to symptoms of faintness or fainting. These circulatory changes consist of a rise in the diastolic pressure, a lowered pulse pressure, and an increase and then leveling off of the pulse rate. DIAGNOSIS Signs and Symptoms. Heat Exhaustion.--In heat exhaustion, the symptoms simulate traumatic shock. The patient feels exhausted and faint. His face becomes pale, and the pulse quickens and becomes weak. Frequently if these patients are seen some time after they have been withdrawn from the heat environment they will show a normal 30 465 466 OCCUPATIONAL DISEASES mouth temperature. However, if the rectal temperature is taken it will show fever. This lagging of the rectal temperature was noted not only by Keeton and his co-workers but also by McConnell and Houghton,3 Adolph and Fulton,4 and others. Heatstroke.--In heatstroke (heat retention, sunstroke) the head ache is pronounced, and dizziness is marked, as is visual disturbance. The skin becomes dry and hot, the face flushed, and the pulse full and rapid. Unconsciousness usually ensues, and the temperature may rise as high as 109 F- Heat Cramps.--Heat cramps, with violent spasm of the abdomen and limbs, occur in workmen in hot atmospheres who drink too much water and perspire excessively, with a resultant loss of the body chlorides. Fever or elevated body temperature is not common, and the patient does not appear to be gravely ill. This condition is dis appearing in industry, owing to the preventive measure of supplying chlorides to the workmen. Pathology.--The pathological changes found in these cases of heat exhaustion or heatstroke at autopsy show certain alterations from the normal which occur quite regularly. In some instances they appear to be quite widespread, as indicated in the report of thirty-seven autopsies by Nuzum and LeCount.5 They found edema of the brain and leptomeninges, marked general passive hyperemia, especially in the lungs and brain, edema in the lungs and spleen, cloudy swelling of the liver, kidneys, and myocardium, and hemorrhages into the \ mucous membrane and skin. Most of the reports in the literature, however, emphasize the hyperemia and edema of the brain, together ;< with vascular changes of the nervous system. Cold Weather and Cold Atmospheres.--Frostbite, pneumonia, bronchitis, coryza, and allied conditions associated with lowered tem peratures frequently become claims for compensation. Policemen, firemen, cold-storage workers, and the like, as well as those of the general populace who are victims of weather abnormalities, consti tute the group who present compensable or non-compensable disabili ties. There is no need to discuss the signs, symptoms, or pathology of these conditions. Their status of compensability is the chief concern and is discussed under "Medicolegal Aspects." MEDICOLEGAL ASPECTS The medical phase of the various conditions pertaining to heat and cold is well known. The terseness of the description indicates the needlessness of informing the physician of their symptoms. But the misunderstood legal aspect of the claims which arise is worthy of a more lengthy discussion. HEAT AND CLIMATIC AFFECTIONS 467 Arising Out of Employment.--To reiterate the principle explained in Chapter I, to arise "out of the employment" an injury or illness must be one that follows as a natural consequence from the hazard of the work being performed. Injuries resulting from inclemencies of the weather, heat, cold, lightning, tornadoes, etc., are accidental injuries. When these occur and are presented to the physician, he must de termine if the disability is due to and arises out of the character of the employment. A man may suffer heat prostration while employed in a hot country, or in a district subjected to a heat wave. Such an illness is not compensable, since it is obvious that the heat is caused by the sun, over which the employer has no control, and the tem perature is not the result of his employment. The general rule ac cepted by most states is clearly expressed in a decision in Wisconsin: As a general rule, an employer is not responsible for damages caused to a workman by lightning, storms, sunstroke, freezing, earth quakes, floods, etc. These are considered as forces of nature, which human vigilance can neither foresee nor prevent. On the other hand, should one be required to fire a boiler during a period of excessive heat and suffer heat prostration, then the dis ability arises out of the work because the employee is exposed to a special risk that intensifies the general heat and directly contributes to the disability. This same may apply to policemen forced to walk a beat during extreme temperatures, or a fireman who fights a fire and becomes soaked with water during zero or freezing weather. The common-sense test in this, as in most industrial disease conditions, is: What did the employment, as contradistinguished from other causes, directly have to do with the disability? Aggravation of Existing Disease.--An even more difficult problem than that of estimating the relationship between cause and sudden, acute affection, is the aggravation of an existing disease. For instance, exposure to cold may cause subjective symptoms of Buerger's disease to become manifest. Cold or frostbite cannot produce Buerger's dis ease, but it is to be conceded that an-element of aggravation exists. Cold-storage men, or butchers who are frequently in and out of the refrigerator, claim colds, pneumonia, and arthritis as a result of their exposure. The justification of their claim is difficult to assay. Since there is such an element of commonalty to these conditions, the writer takes the viewpoint that the relationship is so questionable that responsibility should be the employee's. Questionnaire on Heat Exhaustion.--Finally, the author wishes to discuss three phases of heat exhaustion which are not mentioned in J S'.. 468 OCCUPATIONAL, DISEASES textbooks: (l) Can heat exhaustion have its onset some hours or days following an exposure to high temperatures? (2) If heat exhaus tion does not terminate in death, are permanent sequelae apt to ensue? (3) What is the average length of temporary disability? The experience of this clinic was too meager to satisfactorily answer the above questions. Most of these cases arise in large plants, or mills, where a plant physician, or medical director, is available, and we do not, therefore, see them. To obtain a complete answer, I sent seventyfive questionnaires to industrial physicians throughout America who have had adequate experience in such cases, as in the mills and plants of Carnegie-Illinois Steel, General Motors, Westinghouse Electric and Manufacturing Company, du Pont, and a number of the larger rail road shops. The questionnaire was as follows: Table 21--Questionnaire on Heat Exhaustion l. Where does the onset of signs or symptoms occur? () Always while in the heat environment?---------------------------------------------------------- ;------() Have you, in your records, instances of men leaving an excessive heat environ ment apparently normal, only to develop evidence of heat exhaustion some hours, or days, later? (r) How many (or approximate percentage)?-------------------------------------------------------------(d) If you believe the onset of heat exhaustion could occur some time after depar ture from exposure, what limit would you establish as the maximum interval? 2. What has been the average length of temporary disability? 8. Have you had any permanent disabilities? (a) If so, what was the incidence or percentage? (6) Of what has the permanent disability consisted? 1. Do your first-aid men or plant physicians routinely record a rectal temperature in all suspected cases? 5. (a) Are a majority of these cases definitely heat exhaustion without complications? (6) Or do the majority present complicating factors, such as cardiac disease, alcoholism, etc.? Sixty-six questionnaires were returned completely answered; two were returned with the statement that they had insufficient experience to formulate a reply, and no replies were received from seven ques tionnaires. An analysis of the replies is as follows: Question 1.--Sixty-four physicians stated that the onset always HEAT AND CLIMATIC AFFECTIONS 469 occurred while the victim was in the heat environment. One set the upper limit of the interval between exposure and onset of symptoms as two or three hours, while the other set it at six hours. Question 2.--The average length of temporary disability indicated from the replies was not longer than twenty-four to thirty-six hours. Question S.--In the experience of these sixty-six qualified phys icians there had not been a single instance of permanent disability. Such positive evidence makes one wonder if the morbid anatomy reported in heat exhaustion is present only in extreme instances, in which the organs have been suddenly overwhelmed, causing immediate death; if they do not produce immediate death, the changes are transient. I feel that the observations of these experienced physicians, many of whom have been leaders of thought in industrial medicine, will greatly aid in clarifying the status of those claims which, not fre quently, but occasionally present themselves. Illustrative Cases: Case I.--The claimant, during the course of his employment as a carpenter, collapsed from sunstroke or heatstroke. The temperature was 106 F. The state industrial commission awarded compensation for temporary total disability, and the employer and his insurance carrier brought suit in the Supreme Court of Oklahoma to review the award. The circumstances under which sunstroke may constitute a com pensable injury, said the court, were set forth in Stanolind Pipe Line Co. vs. Davis, Okla. 47 P. (2d) 163. In that case it was held that an injury caused by sunstroke arises out of employment when the em ployee is placed, by the nature of his work, in a position or under cir cumstances subjecting him to a greater hazard of injury by sunstroke than other people in the same vicinity who are not engaged in such work. In other words, the employment must increase the danger of being injured by sunstroke. In the present case, the conditions under which the claimant worked were, in the opinion of the court, such as to accentuate the heat and subjected him to a risk greater than that to which other persons not similarly- employed were exposed. The injury was, therefore, compensable. The claimant, however, was awarded compensation for temporary disability for a longer period than he had actually proved. The cause was remanded to the commission, therefore, for further hearing as to the actual duration of the claimant's disability.7 Case II.--The claimant, a policeman, sustained frostbite of his hands while on night patrol duty during the winter. Gangrene set in, and "some amputation was necessary." From an award of the work men's compensation bureau granting him compensation, the township 470 OCCUPATIONAL DISEASES of Woodbridge, his employer, appealed to the Supreme Court of New Jersey. The weather was unusually cold, said the Supreme Court, and the claimant's employment obliged him to use his hands and prevented him from seeking shelter. He was exposed to a risk different from that of the public generally, because lie was on duty from 6 p.m. to 4 a.m., with the exception of a lunch hour. The claimant, the court concluded, sustained a compensable accidental injury arising out of and in the course of his employment.8 Case III.--Death from exposure to the elements, including the heat of the summer and the cold of the winter, said the Supreme Court of Iowa, is not compensable if the hazard is the same as that to which the general public is exposed. For compensation to be recover able for death from sunstroke, the deceased must have been subjected to a greater hazard from heat than that to which the public generally in that locality was subjected. This distinction is recognized by all the authorities. Compensation was denied in this case/1 Case IV.--The claimant's husband was employed by the defendant company to deliver ice on a commercial route. On July 11, 12, and 13, the heat was extreme, the temperature reaching a maximum of 106 F. during the day. On the evening of July 11 he was more tired than usual after his day's work. On July 12, after delivering ice until noon, he quit for the rest of the day. He complained of the heat and stag gered on walking. On July 13 he returned to work, but a helper made most of the deliveries for him. Late that afternoon, on his way home from work, he was overcome by the heat and suffered what was de scribed in the medical testimony as a "collapse." He died the follow ing day, and an autopsy confirmed the diagnosis of heatstroke as the cause of death. The claimant thereupon brought proceedings under the Workmen's Compensation Act of Minnesota against the employer for compensation for the death of her husband. From an order of the industrial commission awarding compensation, the employer appealed to the Supreme Court of Minnesota. The employer contended that the claimant's husband had not sustained an accident within the meaning of the Workmen's Com pensation Act because this particular heatstroke was "of slow, gradual onset." The Supreme Court, however, could not agree with that con tention, citing Minnesota cases to show that in that state heatstroke is accidental fer se. Following those decisions, the court held that the heatstroke in the present case was accidental. Furthermore, in the opinion of the court, the accident occurred in the course of the de ceased's employment even though his collapse had not occurred during his working hours. It is enough, said the court, that the causative agency was applied during the employment and was followed directly and immediately by the collapse without the intervention of a cause HEAT AND CLIMATIC AFFECTIONS 471 independent and unrelated to the employment. Accordingly, the Su preme Court affirmed the order of the industrial commission award ing compensation.10 One notes in this case the peculiar line of defense set up; that is, the contention that the condition was not an accident, owing to the slow, gradual onset. And also is noted the wording of the court that "the causative agent was applied during employment." This reason ing is directly opposite to than handed down in the preceding case. It is contrary to the accepted viewpoint. Case V.--The claimant, in the course of his employment as a truck-driver for a transportation company, was exposed to the rain and to chilling winds because of the lack of glass in the windows of the cab. He contracted a severe cold. Congestion of his throat, chest, and lungs, associated with an elevated temperature and the coughing up of blood, developed. Finally he was forced to go to bed, where' he remained for about three weeks. He then attempted to return to work but was so weak and suffered such pains and aches that he went back to bed. Thereafter he was unable to perform manual labor. He claimed that as a result of his illness he tired easily; was unable to work more than a few minutes at a time; that his heart had been affected, caus ing him pain and suffering at intervals; that he had lost weight and was debilitated; and that his lungs had been affected and weakened. The industrial accident board denied him compensation under the Workmen's Compensation Act of Texas, whereupon he brought suit to set aside the board's decision. From a judgment of the trial court denying relief, he appealed to the Court of Civil Appeals of Texas, Fort Worth. The purpose of the Workmen's Compensation Act, said the court, is to compensate an employee for injury sustained during the course of employment. The injury contemplated is defined by the act as "dam age or harm to the physical structure of the body and such diseases or infection as naturally result therefrom." It was not contemplated that the act should cover health insurance. It is a matter of common knowledge that colds, influenza, and pneumonia are the result of germs attacking the body and that many such germs appear to be in the very atmosphere surrounding us at all times. Any and every per son is exposed to them without being conscious of the fact. Medical science teaches that human beings fall victims of these germs because at the time they are not physically able to withstand the assaults of the germs. If, said the court, the employee in this case is permitted to recover compensation, then every employee who is engaged in labor which tires the body and causes what the layman calls a "run down condition" can recover compensation by showing that his work weakened him and lowered his resistance and caused him to succumb 4-72 OCCUPATIONAL DISEASES to the attack of a disease which he would otherwise have been able to resist. Attempts so to enlarge the purpose of the Workmen's Com pensation Act will destroy its usefulness, it was ruled. Accordingly, the Court of Civil Appeals affirmed the judgment of the trial court upholding the order of the industrial accident board denying compensation.11 Case VI.--A butcher employed in a chain store in the suburbs of Los Angeles awoke one night with a nosebleed which defied home treatment. The patient was taken to the hospital where periodic bleed ing occurred over a period of ten days. The workman was unemployed for two additional weeks. He filed for compensation, alleging that the frequent trips in and out of the refrigerator during the warm weather had produced this condition. He was substantiated in his belief by his physician. The past medical history was unimportant, his only illness being typhoid fever twenty years previously. The physical examination was essentially negative. The blood pressure six days after onset was 138/80. According to his physician it was 142/80 at the time of onset. Urine showed a heavy trace of albumin; the blood count was normal at the time of hospitalization. Blood Wassermann negative. The nosebleed occurred nine hours after he left his employment and while at rest in bed. No known cause could be found to account for it. The defense contended that nosebleeds are common and appear in many persons without known provocation. It had never been re corded that nosebleed occurs in refrigerator workers or cold-storage men more frequently than in men of other occupations, and medical literature fails to reveal any association. It was held that the claim ant's viewpoint was untenable. The decision in this case denied the patient's claim. Case VII.--The plaintiff was employed by the defendant to operate a machine removing snow from the highway. His work required him to keep his eyes constantly on the snow. On March 23 he worked at his task for twelve hours, the day being "quite warm for that time of year" and the sun shining brightly. At the end of the day he was burned about the face, as if sunburned, and his eyes were inflamed. The skin of his face was desquamated. His eyes grew worse, and dur ing the week an ulcer developed in the right eye, and on or about May 18 another developed in the left eye. There was a severe infec tion and ulceration on the conjunctivae and the corneas of both eyes, with the appearance of pus. The plaintiff instituted proceedings against his employer, under the Nebraska Workmen's Compensation Act. An award in his favor by the compensation commissioner was sustained by the district court, and the employer appealed to the Supreme Court of Nebraska. HEAT AND CLIMATIC AFFECTIONS 473 The condition of the plaintiff, said the Supreme Court, was pro duced by "snow blindness" or "snow ophthalmia." The condition is rare in the climate in which the plaintiff was working, and therefore the court concluded that it was unexpected and unforeseen. There was no dispute as to the existence of a "burning" in snow blindness, and the injury to the eyes of the plaintiff was therefore violence to the physical structures of the body. The injury, said the Supreme Court, was due to the reflection of ultraviolet rays of sunlight from the bright snow, which had to continue for several hours before it manifested itself or became known to the person exposed. In this instance, the condition manifested itself on the day of exposure and therefore may be said to have occurred suddenly. In the light of these facts, the judgment of the court below sustaining the award of the compensation commissioner was affirmed.12 Case VIII.--For about ten years the workman in this case had been employed by the defendant petroleum company to fire furnaces and boilers. On May 28, in adjusting a valve on a particular boiler, he was forced to look at the flame for five minutes to adjust the flame to a target in the boiler, a task he had performed many times before. Thereafter he became blind and instituted suit under the Workmen's Compensation Act of Louisiana. The trial court gave judgment against the workman, and he appealed to the Court of Appeal of Louisiana, first circuit. The evidence before the trial court showed that the workman had had syphilis for several years before the incident to which he at tributed the loss of his sight and that his vision had been impaired. A physician who had examined the workman about fourteen months after the alleged industrial accident testified that he found him suffer ing from an advanced stage of neurosyphilis and that the optic nerve was atrophied. There was medical evidence to the effect that syphilis is the principal cause of atrophy of the optic nerve, although it is not the sole cause. Medical experts testified that heat and glare, without some severe burns around the eyes, would not cause atrophy of the optic nerve and that exposure to heat and glare in firing a boiler would not affect or aggravate a syphilitic condition so far as it re lates to the optic nerve. If, said the Court of Appeal, the glare and heat from the boiler or furnace served to aggravate or hasten the atrophy of the optic nerve because of the weakened condition of the nerve brought on by syphilis, and if this heat and glare on that par ticular day was unusual and out of the ordinary routine of the day's work, it could be said that the heat and glare from the boilers had a causal connection with the blindness, and the workman would be entitled to compensation. There was, however, no evidence to this effect. On the contrary, the evidence showed that the atrophy of the optic nerve and the resulting blindness were caused by syphilis, not 474 OCCUPATIONAL DISEASES by the exposure of the workman to the heat and glare of the boilers. The workman, therefore, failed to show that his disability was caused or superinduced by an accident or injury in the course of his employ ment. The judgment in favor of the employer was accordingly af firmed.13 TREATMENT Prophylaxis in Reactions to Heat.--As aids in the prevention of heat exhaustion, heatstroke, and heat cramps, better working and im proved living conditions, rest periods, and suitable light clothing are of value. Stokers, firemen, and the like, often find it of value to wear heavy shirts which are kept soaked with water, instead of light cloth ing. Certain employments, where excessive heat is necessary, have introduced air-conditioning systems, but these are not always feasible. Sodium Chloride.--The most valuable preventive measure, how ever, is the use of sodium chloride tablets for periodic daily ingestion; or, still better, the use of 0.1 to 0.5 per cent solution of sodium chloride chilled to a temperature of from 45 to 50 F. for drinking-water. The sodium chloride tablets may cause gastric irritation, while the physiologic saline solution does not. Glucose.--For the prevention of heat exhaustion, the use of glu cose in the form of jelly drops containing approximately equal parts of glucose and granulated sugar has been reported to be very effective. Beverages, such as lemonade sweetened with sugar, may be equally beneficial, and the lemonade will help with the glucose to prevent acidosis. These procedures are also of value in the prevention of heat stroke, and in addition it has been stated that heatstroke is abso lutely preventable if the patient is treated immediately as a case of hyperpyrexia as soon as he presents himself with a dry skin indicative of suppression of perspiration. The Medical Director of E. I. du Pont de Nemours and Company writes14: . . . since we have subjected all of our men who are exposed,to high temperatures to a very careful examination, with special efforts to determine any disease of the circulation and eliminating any who have any circulatory disturbance as shown by careful examination, we have had no difficulty. Furthermore, most of our men who are exposed to high temperatures are now and have been taking at least, 100 Mgm. of vitamin C each day, and this seems to be a very decided factor in preventing any circulatory changes as a result of heat ex haustion. Heat Cramps.--The treatment in heat cramps depends on the replacement of sodium and chloride ions in the blood serum. This is accomplished by the administration of 0.9 per cent sodium chloride HEAT AND CLIMATIC AFFECTIONS 475 by intravenous infusion and orally, or by hypodermoclysis. Intra venous infusions of this physiological saline with from 5 to 10 per cent dextrose may also be used. The patient should be kept quiet for from twenty-four to forty-eight hours and encouraged to drink milk and other salt-containing fluids and foods. Heat Exhaustion.--The treatment in heat exhaustion is similar to that in shock. The patient should be kept warm if the temperature is subnormal, and care should be taken that the temperature does not rise quickly to dangerously high levels. Intravenous infusions of 0.9 per cent sodium chloride with from 5 to 10 per cent dextrose should be given. The use of one of the following may be necessary for treat ment in circulatory collapse: caffeine sodium benzoate, 7% grains (0.5 gm.); epinephrine, 1:1000 solution, from % to 1 cc.; coramine, 1.5 cc.; or metrazol, from 1Y2 to 4% grains (0.1 gm. to 0.3 gm.). Heatstroke or Sunstroke. Lovoering Body Temperature.--In heat stroke or sunstroke, the opposite treatment is given. The patient is re moved to a cool atmosphere at once, and the body is sprinkled or sponged with cool water, with fans placed to evaporate the water. This is continued until the body temperature is lowered to normal, although some authorities advise not lowering it below 101 F. During this time the head is elevated, and the cutaneous circulation is maintained by vigorous friction. The use of ice baths, packs, or enemas is usually not advised, since they may so diminish the circulation of the skin as to drive the blood to deeper portions of the body and thus contribute to further circulatory collapse. Fluids.--These should be given orally, intravenously, or by hypo dermoclysis. For the intravenous infusions 0.9 per cent sodium chloride with from 5 to 10 per cent dextrose is used, while the physiological saline without dextrose is usually used for the subcutaneous adminis tration. Venesection of from 400 to 500 cc. is performed if cyanosis, venous distention, or pulmonary edema is marked. Artificial Respiration and Circulatory Stimulants.--Artificial respi ration may be necessary, as may also the circulatory stimulants men tioned above in the treatment of heat exhaustion. These stimulants are to be avoided as much as possible, however, since they sometimes make the patient worse and are reported frequently to produce nu merous petechial hemorrhages in these cases. Following the acute stage there should be advised prolonged rest in bed, and the patient should avoid high temperatures for the remainder of his life. Prophylaxis in Reactions to Cold.--Prevention of reactions to cold atmospheres is best secured by interrupting work in such atmospheres by short periods of rest in a warm atmosphere. At the first sign of numbing and blanching of the skin, the worker should leave the cold 476 OCCUPATIONAL DISEASES environment, since the longer he is exposed to such cold the more severe will be the degree of frostbite. Footwear and handwear should be carefully fitted and should in no instance be constricting. Those suffering from cardiovascular diseases or from diabetes mellitus should not be employed where they will be subjected to cold atmosphere. Sensitivity to Cold.--For sensitivity to cold the immediate treat ment consists of injecting epinephrine hydrochloride, or of immediate plunging of the arms into water at 107.6 F. for relief of the local lesions. Desensitization of these patients can sometimes be accom plished by the taking of cold baths with gradual decrease of the tem perature of the bath and increase of the length of the period of im mersion. Gradually increasing doses of subcutaneous histamine have also been used. Frostbite.--For frostbite no well-proved method of treatment is known. The lesions should be thawed slowly, since severe pain, burn ing, and tingling are apt to occur if they are otherwise treated. In addition, rapid thawing at times seems to give rise to the development of an inflammation of an exudative type which is accompanied by more damage than that produced by the freezing alone. Some authors, however, hold that the rapidity of thawing makes little difference. Vertical suspension during the thawing and for several days thereafter has been advised, as has the use of heated air. A cold cloth or ice may be used in a rubbing process to cause friction and thus induce re establishment of circulation. If open lesions are present, strict surgical cleanliness is needed, and surgical dressings should be applied to blis tered areas. Minor traumatism or infection should be warned against. For the general treatment of those who have suffered from extreme cold, hot blankets, a heat cradle, and hot drinks internally are indi cated. REFERENCES 1. Hick, F. K., Keeton, R. W., Glickman, N., and Wall, H. C.: "Cardiac Output, Peripheral Blood Flow and Blood .Volume Changes in Normal Individuals Subjected to Varying Environmental Temperatures," Heating, Piping, and Air Conditioning, 2: 50 (Jan.), 1939. 2. Keeton, R. W., Hick, F. K., Glickman, N., and Montgomery, M. M.: "The Per ipheral Type of Circulatory Failure in Experimental Heat Exhaustion; the Role of Posture," Heating, Piping, and Air Conditioning, IS: 122 (Feb.), 1910. 3. McConnell, W. F., and Houghton, F. C.: "Some Physiological Reactions to High Temperatures and Humidities," Heating, Piping, and Air Conditioning, 29: 129, 1923. 4. Adolph, E. T., and Fulton, W. B.: "Effects of Exposure to High Temperature upon Circulation in Man," Am. J. Physiol., 67: 573, 1924. 5. Brahdy, L., and Kahn, S.: "Heat Exhaustion and Heat Stroke," Trauma and Disease, Lea and Febiger, Philadelphia, 1937, p. 345. 6. Hoenig vs. Industrial Commission, 159 Wis. 646, 150 N. W. 990, L. R. A. 1916-A, 339 (1915). HEAT AND CLIMATIC AFFECTIONS 477 7. Smith vs. Zweifel, Okla. 54 P. (2d) 649. 8. Matthews vs. Woodbridge Tp,, N.J. 183 A. 150. 9. Wax vs. Des Moines Asphalt Paving Corporation, Iowa 203 N. W. 333. 10. Ueltschi vs. Certified Ice and Fuel Company, Minn. 27G N. W. 220. 11. Amann vs. Bepublic Underwriters, Texas 100 S. \V. (2d) 778. 12. Hayes vs. McMullen, Neb. 259 N. W. 165. 13. Laughlin vs. Magnolia Petroleum Co., La. 182 So. 178. 14. Personal communication from Dr. G. H. Gehrmann, Medical Director, E. I. du Pont de Nemours and Company. CHAPTER XXXV ELECTRICAL INJURIES Injuries to the body resulting from lightning or. electrical forces are so comparable that no differentiation is to be made here, nor is it of practical importance to consider the factors which are likely to play a part in determining the extent of injury, such as voltage, am perage, and type of current, for it is not probable that a knowledge of these factors will enter into the diagnosis, treatment, or medico legal aspect. A discussion of electrical injuries finds a place in this book since the effects are primarily medical, in contrast to the surgical nature of most traumas. Another interesting fact regarding electrical injuries is that whereas in most occupational diseases the etiology or occupational origin is to be questioned, it is readily apparent in this instance, since the occasion and effect of such an injury are dramatic, instantaneous, and often observed by others at the time of occurrence. It is the questionable sequelae with which the medicolegal phase is most concerned. Occupational Hazards.--These need not be delineated since elec tricity is a necessary adjunct to almost any phase of man's endeavor. However, some workers are under a greater hazard than others; for example, electricians, linemen, power-plant operators, tree surgeons, operators of electrical transportation equipment, and the like. Physical Findings and Symptoms. Burns.--Next to bone, the skin is most resistant to electrical current and, therefore, burns are almost an invariable finding. The lesions vary in appearance. Some may appear punctate or may resemble a bullet wound; others are oblong, round, or linear. "The area is slightly elevated and pale gray, grayish-white, yellowish-gray, or yellow. The heat makes the horny substance of the epidermis plastic." 1 Deep burns may extend into the underlying structures, muscles, and even bone. Flash burns of the eye are not infrequent. Cataracts, with minute tears to the lens capsule, have been reported and have been thought to be due to a concussion effect. Cataracts resulting from high-tension current and appearing two years later have also been reported. The reason is not clear to the writer, and any instance of such a claim should be referred to the ophthalmologist. Unconsciousness.--If seen soon after the electrical contact, the patient may be unconscious. This phase may be from a few seconds 478 ELECTRICAL INJURIES 479 to several hours in duration. Restlessness, excitement, and muscular twitchings or convulsions are sometimes present. Cyanosis has been noted. If the contact has been severe, the patient is invariably in shock. After regaining consciousness the patient may complain of ringing in the ears, light flashes, and other hallucinatory phenomena. Paralysis of one or more of the extremities, with sensory disturbance, may occur. Upon recovery from immediate effects of the injury, symp toms resembling a disorder of the nervous system may have to be evaluated. These strongly resemble a hysteria and will subsequently be discussed. Pathology.--Since animals differ greatly in their resistance to elec trical currents, experimentation has been of little value. Most of the pathological studies are to be found in the foreign literature. Such re ports indicate that a fairly frequent incidence of neuropathological conditions is to be found following electrical injury. Most of the arti cles reviewed in the American literature quoted the observations of Critchley.2 The following abstract of Critchley's description was made by Pollock3: (a) Focal petechial hemorrhages scattered throughout the brain, especially the medulla. They may be found in the spinal cord, chiefly in the anterior horns. When the cranium has been struck by lightning, large vascular tears may be found in the cerebrum. (b) Chromatolysis, especially of the pyramidal cells, of the medul lary nuclei, and of the anterior horns and the Purkinje cells of the cerebellum. The changes are patchy in distribution, so that healthy and diseased cells may lie in close proximity. (c) Curious wide dilatation of the perivascular spaces, bridged across by delicate strands, and surrounded by a zone of condensation, supposed to be due to bubbles of gas, occur ring particularly in cases of electrocuted criminals. (d) Changes in the peripheral nerves, such as fragmentation and tortuosity of the axons, breaking down of the sheath of Schwann, and infiltration of the epineurium with endo thelial cells. (e) After very severe injury, as from a direct stroke of lightning, or in experimental electrocution with high tension currents, the entire brain and parts of the cord may be swollen, soft ened, and even diffluent. The neuronic changes are variable, and Critchley was unable to demonstrate them in three cases, in one of which death occurred after a shock of 66,000 volts, in another seventeen days after a shock of 132,000 volts, and in the third, eight days after a shock of 19,000 volts, death being due to the burns and toxemia. The 480 OCCUPATIONAL DISEASES changes described in the literature are not specific for elec trical injury, as it is difficult to differentiate these changes from those produced by heat, toxemia, and cerebral con cussion. Thus it is apparent that both the clinical findings and the path ology indicate that the nervous system alone is damaged by strong electrical current. When death is immediate, however, it may be due to paralysis of the respiratory muscles or from fibrillation of the heart, or both. Postmortem examinations fail to reveal any lesions in the heart due to electrical injury. The heart is often empty, although the right side may be full of fluid blood. It should be reiterated that al though ventricular fibrillation is the common cause of immediate death, there exists no evidence that permanent damage exists in the heart of one who has recovered from electrical injury. Medicolegal Aspects. Temporary Disability.--Complications of the burn may prolong the temporary disability; otherwise temporary dis ability is short. It is sometimes difficult to get patients who have been injured by electricity or lightning to believe that they have not been seriously injured. I do not mean the patients who evidence hysteria or malingering, but rather a small group who believe that electric shock is a devastating experience and who require time to adjust themselves. Diplomatic handling of these patients by the physician at the time of injury will usually prevent such an attitude, or at least greatly allay their fears. Permanent Disability.--Permanent disability is not common. Damage to the brain or spinal cord may leave a permanent disability of varying degree. It is held that disability may appear months after the injury, owing to necrosis, secondary hemorrhage, or disturbance of the central nervous system due to cell degeneration. Such instances have not been experienced at this cfinic. When a disability is claimed because of a heart defect, hysteria or malingering must be suspected. In the chapter on neurosis and malingering it is mentioned that the element of fright or severe mental shock is considered by some as a causative factor of the so-called "traumatic neurosis."If fright and shock are to be accorded recognition as causing neurosis or hysteria, then it would be expected that the incidence of neurosis or hysteria following electrical injury would be great. However, it does not seem to be a prevalent aftermath. True epilepsy, paralysis agitans, and multiple sclerosis are to be differentiated from the sequelae of electrical shock. Naville has been unable to find in the literature an indisputable example of epilepsy, general paralysis of the insane, or multiple sclerosis following elec trical injury. ELECTRICAL INJURIES 481 Treatment. Prophylaxis.--The prevention of these injuries depends upon educational measures designed to indicate the inherent dan gers in electrical force and upon the use of measures for safety in in dustry and in the general public. Artificial Respiration.--The patient who has suffered a severe elec trical shock should immediately be given artificial respiration by the Schaefer method. This is continued until he breathes naturally or until all evidence that life has ceased is present. The criteria for death in such cases differ to some extent from those in other cases, since no reflex reactions may be present whatsoever. The patient should not be pronounced dead until rigor mortis sets in or until cooling of the body occurs. Artificial respiration may need to be continued for hours. If natural breathing ceases after it has been once restored, artificial respiration should be commenced again. Prevention of Ventricular Fibrillation.--The use of epinephrine in these cases is to be particularly avoided. Ventricular fibrillation ap pears to be a common cause of death from electric shock, and it has been shown that epinephrine may also induce fatal ventricular fibrilla tion in conditions in which the heart is hyperirritable from the effects of poisoning such as benzene and chloroform. Hoff and Nahum3 used acetyl-/?-methylcholine chloride for the prevention of ventricular fibrillation by electric shock and found that epinephrine counteracted the effect of the acetyI-/f-methyicholine chloride, or in larger doses increased the possibility of fatal ventricular fibrillation. This work to some extent explains the reasons for avoiding epinephrine in treat ment of other cases of poisoning, e.g., carbon tetrachloride, and raises the question of whether epinephrine may not be inadvisable in most of the toxic states which have been discussed in this text. The clinical use of acetyl-/3-methylcholine in these cases is suggested by this work of Hoff and Nahum. Rest.--Patients in severe cases of electric shock should be kept in bed for two or three weeks because of emotional as well as physical shock. There may also be latent effects which may to some extent be avoided by such bed rest. Measures in Burns.--Electrical burns may frequently be treated like other burns. Hemorrhage rarely immediately follows such burns, but secondary hemorrhage may occur after shock has been controlled and the arterial blood pressure rises. All of these burns are treated as serious, no matter how trivial they may appear at first examination. Most authorities recommend avoidance of early surgical intervention, but some recommend early debridement and excision of the burned region beyond the hyperemic margin, followed by suturing. The con servative method permits nature to build up new tissue beneath or 31 482 OCCUPATIONAL DISEASES around the destroyed tissue, and is felt by most to lead to the most satisfactory ultimate results. It is felt particularly that tendon sheaths, etc., may be opened to infection by early surgical intervention. Ed wards and Bowie,! gave details of a conservative regimen which had given very satisfactory results in their experience. According to their routine, the surrounding skin was thoroughly cleaned with soap and water, and then dried with ether followed by alcohol. Compresses were used on the surrounding skin for from twenty-four to forty-eight hours. Then sterile dry dressings were applied until the coagulum be gan to separate. The surrounding normal skin was then covered with vaseline or lanolin, and azochloramide in triacetin or olive oil (prefer ably olive oil) was applied to the burned area. Dressings were changed daily, and the coagulum was permitted to curl. The curled, loosened edges were removed as rapidly as possible. When the base of the ulcer presented uniform, healthy granulations, skin-grafting was done. REFERENCES 1. Jaffe, R. H.: "Electropathology," Arch. Path., 5: 837, 1928. 2. Critchley, M.: "Neurological Effect of Lightning and of Electricity," Lancet, 1: 68, 1934. 3. Pollock, L. J.: "Trauma and Diseases of the Nervous System," Trauma and Dis ease, Lea and Febiger, Philadelphia, 1937, p. 334. 4. Davidson, H. A.: "Neurosis and Malingering," Am. J. M. Juris., 2 (Feb.), 1939. 5. Hoff, H. E., and Nahum, L. H.: "Role of Adrenalin in the Production of Ven tricular Rhythms and Their Suppression by Acetyl-/3-Methylcholine Chloride," J, Pkarrn. and Exp. Therap., 52: 235 (Nov.), 1934; and Am. J. Physiol., 110: 675 (Jan.), 1935. 6. Edwards, C. R., and Bowie, H. C.: "High Tension Electric Burns," Am. J. Surg., A7: 299 (Feb.), 1940. CHAPTER XXXVI CAISSON DISEASE Caisson disease, frequently referred to as "the bends," or less fre quently as "compressed-air illness" or "diver's palsy," is caused by a sudden reduction of the atmospheric pressure at a ratio which exceeds 2.0 or 2.5 to 1. Few physicians will be called upon to diagnose this disease or institute treatment for it, since it is peculiar to a type of employment in which the danger is so well known that trained men are constantly on hand to recognize the symptoms and treat the pa tient promptly. Occupational Hazards.--Those affected are: divers, builders of tunnels and bridges, or wherever compressed air facilitates construc tion underneath water. Pathogenesis.--The solution of gases in fluid depends upon their partial pressures (Dalton's law). Variations in pressure in a man's normal environment are negligible; therefore, no symptoms are pro duced, but under high barometric pressure, blood reaching the lungs is exposed to increased partial pressures of nitrogen and oxygen which are taken up in amounts dependent upon the existing pressure. These are carried to the tissues where the oxygen is readily absorbed, but the nitrogen, being inert, is not absorbed and so accumulates and diffuses into the tissues. This process of taking on nitrogen in the lungs and giving it off into the tissues is repeated as long as exposure exists. All tissues do not absorb the nitrogen in like amounts. While fat is saturated more slowly than other tissue, it has a greater capacity and desaturates more slowly. Hence nitrogen storage occurs to a high degree in the white matter of the central nervous system. The gray matter is less affected. Upon the reduction of the barometric pressure, the nitrogen in the blood escapes into the alveolar air, and the nitro gen in the tissues comes out of solution. If this occurs rapidly (without proper decompression) bubbles of nitrogen will form in the tissues, veins, venules, and capillaries. These bubbles, or more accurately air emboli, compress the tissues, obstruct the blood flow and cause hem orrhage. Because of multiple hemorrhages, the pathology is varied. Signs and Symptoms.--Abdominal pain, often girdlelike in type and excruciating in severity, is common, the victim usually bending over--hence the phrase "the bends." Dizziness, nystagmus, and vomit ing are frequently associated symptoms. Pulmonary edema may be 483 484 OCCUPATIONAL DISEASES present with evidence of dyspnea. In the more severely exposed, aphasia, diplopia, changes in the visual fields, monoplegias or para plegias, and such manifestations of cord involvement as urinary in continence, are observed. Requarth and Benson1 state that at low pressure a blockage of the eustachian tube, with attendent inability to equalize the pressure in the middle ear, is apt to occur, especially in those who are troubled with pharyngitis and sinusitis. Medicolegal Aspects.--The etiology of the disability is always ob vious. Temporary disability is usually short, but will depend upon the resolution of hemorrhagic areas. Permanent disability may result. Treatment. Prophylaxis.--Preventive treatment is dependent upon a careful physical examination and proper selection of applicants. Men above thirty should not be employed unless they have had pre vious experience and are known to tolerate the exposure. Men above forty should not be employed. In addition to age, other factors barring employment should be obesity, vascular impairment or scleroticchanges, alcoholism, and upper respiratory disease or a disposition to such, and limitation of the number of working hours. Decompression.--Operations in compressed air are now generally carried out in such a manner that the workman who is returning to the normal atmosphere passes through chambers which are graduated in their pressure so that by the time he reaches normal atmosphere he has been gradually decompressed. Actual decompression is still car ried out upon the lines suggested by Haldane in 1906. The first step is to reduce the absolute pressure by one-half. A time interval is then permitted to elapse during which the body comes into equilibrium. Pressure is again reduced by one-half, then another time interval is allowed, and so on until normal pressure is reached. The duration of the intervals depends upon the extent of maximum pressure and the duration of exposure. Recompression.--In the actual treatment of caisson disease, recom pression is the best therapeutic measure. Specially designed chambers have been constructed in which the various levels of atmospheric pres sure may be controlled and the stages of decompression repeated. Helium, because it diffuses more rapidly, has been proved experimen tally to be of extreme value. As yet it has not had extensive clinical trial. REFERENCE Requarth, Wm. H., and Benson, R. E.: "Compressed Air Illness," Indust. Med., 9 (March), 1040. PART VIII CHAPTER XXXVII THE MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE The original design of this book did not provide for any discussion of the relationship of trauma to disease. But in collecting material for the preceding pages, in hearing and reading the testimony given before the Industrial Accident Commission, and in the perusal of case reports submitted to me for an opinion, it became apparent that in medico legal controversies, medical opinion is frequently not based upon pos tulates which are recognized as acceptable. Nor does the average med ical witness appear to know where these postulates might be found. It was believed therefore that a book of this nature would serve its purpose better by including the precepts concerning the relationship of trauma to disease which have been evolved from the experience of the passing years. Obviously space will not permit the application of these precepts to all of the diseases of the various systems. What fol lows is merely a concise consideration of the general principles which should be applied to any given case in rendering an opinion regard ing the occupational relationship. Desirability of Scientific Approach.--Can trauma cause diabetes, acute yellow atrophy of the liver, tic douloureux, or appendicitis? Will a strain cause a gastric ulcer to rupture, or produce hemorrhoids, or epididymo-orchitis, or kinking of the ureters? What is the relation ship between a single trauma and cancer, syphilis, or tuberculosis? Confronted by claims of this nature, a physician may make dogmatic statements not founded upon past experience or in accord with the prevailing opinion. He may succumb to the wishful thinking of the claimant or defendant. The following cases serve to illustrate this point. Case I.--On December 5, 1932, a workman fell, contusing his back and hip. For this he was paid compensation. On March 21, 1933, he was operated upon for appendicitis. On July 31, 1935, more than two years later, he was operated upon for a strangulated bowel resulting from adhesions. The following day he' died, and his widow then brought suit for death benefits on the grounds that the fall in 1932 485 486 OCCUPATIONAL DISEASES had caused the appendicitis in 1933, which resulted in adhesions, causing strangulation of the bowel and death in 1935. A physician who treated the patient just prior to his death testified that he be lieved that, "The inflammation resulted from the industrial accident and, by a process of contiguity, progressed through the muscles, or gans and tissues of the body from the locus of injury through the psoas and other muscles, organs and tissues in the lumbar region and through the peritoneum and finally reached the appendix, necessitat ing the appendectomy three months later." Upon the decision of the jury a verdict was rendered in favor of the widow. The decision was eventually reversed by the Texas Court of Appeals. Or, consider the merits of the following case, which the author was asked to review prior to a hearing before the industrial accident commission. Case II.--A welder had assisted three other men in lifting a piece of sheet metal. He noted nothing that day, but two days later he de veloped abdominal cramps and diarrhea. In trying to account for this condition he recalled the lifting episode of two days previously. He related this history to his physician, who made a diagnosis of mucous colitis following strain. The patient entered claim for med ical care for a disease resulting from industrial trauma. A third example of "loose thinking" can be found in this instance of recent experience. Case III.--A twenty-two-year-old male presented himself, stating that he was suffering from pains in the joints, especially in the hips, knees, and wrists. Thirteen months previously he had slipped while mopping the floor and fell into a sitting position. This accident was so trivial that he continued working and did not seek medical care. One year later he noted the multiple joint pains, some loss of weight, shortness of breath, and general fatigue. At this time he consulted a physician who told him he had arthritis. The boy then told the physician of the previous accident and wondered if the condition could have been caused by this fall. The physician said it was likely that the fall had caused or aggravated the arthritis. At the time he was ex amined at our clinic he had a history of repeated attacks of tonsil litis, and the examination presented a typical picture of rheumatic fever. These three examples illustrate a credulity manifested by some physicians that is not warranted by the facts or findings. A healthy skepticism, bred of long experience and of considered thought, appears desirable. It has been constantly reiterated within these pages that MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE 487 the meaning of the Workmen's Compensation Act has been extended within recent years. Previously the awards of compensation were to victims of an obviously direct injury in which the elements of time and place as related to injury were not remote. Today laymen present claims wherein the relationship of trauma to disease is very remote or entirely absent. An entire book could be filled with such instances. For this state of affairs, the medical profession can be held largely accountable. Reason for Discredited Testimony.--As a profession we are steeped in the belief that ours is an art, not a science. Yet our advancement is due to scientific discoveries. It is fallacious to think that our entire success has been due to the laying on of hands. Our specific thera peutic measures are based upon proved procedures, as in the treat ment of lues or diphtheria. Much of our present knowledge concern ing the diagnosis and treatment of certain diseases resulted from the establishment of positive corollaries by investigators after prolonged observation of the behavior of diseases, such as tuberculosis, small pox, malaria, typhoid, and the like. But despite the fact that we daily rely upon proved truths, we are inclined to feel that we deal only with the speculative. In contrast, the legal mind relies upon precedent, even though mistakes of past decisions are perpetuated and project themselves into future decisions. In legal practice, what is infallible today may be erroneous tomorrow. Because of this atti tude of sureness on the part of the legal profession and the tendency on the part of the physician to vacillate, the courts are inclined to discredit medical testimony in concrete questions. Law takes advan tage of the old adage--when doctors disagree. It is high time the med ical profession realized that certain fundamental facts concerning the aspects of disease are constant or rarely vary. We need to create a greater spirit of solidarity in the expression of our opinions. Formulating Relationships between Trauma and Disease.--In ac cepting or denying a single act of trauma as the cause or aggravating factor of a disease, some of the cautions cited in the first portion of the book bear repeating. Common sense, balanced judgment, and a mind free from preexisting prejudice are the first essentials of a sound opinion. Next in importance is a knowledge of the disease under con sideration and of the accepted postulates regarding the production of disease by trauma. Also, the physician on the witness stand must guard against being induced by the legal inquisitor to make an ad mission of probability when under studied circumstances the physi cian would hesitate to admit a remote possibility. One of the pitfalls of medicolegal controversy is the confusion and delusion arising out of the meaning of the words "likely" and "perhaps." 488 OCCUPATIONAL DISEASES Classification.--How should the physician proceed in formulating his opinion regarding the relationship of trauma to disease? He rea sons best who fashions his thoughts in an orderly manner. Heraclitus once said of his predecessors that they had much knowledge but little sense. The sensible application of knowledge resides in logical deduc tions--especially is this true in the type of case under discussion. When any given case presents itself, it should first be classified in one of the three following groups: 1. A group representing cases which obviously are the result of trauma, as infection in the site of a burn, laceration, or fracture 2. A group representing cases which never result from trauma, as diphtheria, trichinosis, or hemophilia 3. A group which consists of diseases usually not produced by trauma but which might on occasion result from or be aggra vated by trauma, as toxic goiter; urinary calculi forming after a fracture of one or more vertebrae; or a rupture of a gastric ulcer following a forceful blow to the stomach The first two groups do not concern us at this time. If the case under consideration falls into the third group, then the validity of the claim must be tested by applying further reasoning. This is done by comparing the factors of the case in question with the recognized postulates as they are applied to a given disease. These postulates vary in their application to different diseases. For instance, those which are adhered to in a case of alleged traumatic appendicitis differ from those to be considered in a case of carcinoma. As previously stated, space forbids a discussion of all the possible diseased conditions which might arise from trauma. A few illustrations must suffice. Trauma and Appendicitis.--Let us consider the debatable ques tion of traumatic appendicitis. There are those who hold that a di rect, severe contusion to the right lower abdominal quadrant may initiate appendicitis in an otherwise healthy, normal appendix. Moorehead2 sees no more relationship between external trauma and appen dicitis than between a blow on the neck and tonsillitis. Others deny the possibility of initiating appendicitis by trauma but admit the pos sibility of aggravating a previously diseased appendix. This state of uncertainty regarding traumatic etiology of appendicitis is true of many other conditions. But the experience of the majority should aid in forming an opinion in most cases. Postulates to Be Satisfied.--Rhodes and Birnbaum3 (quoting Shutkin and Wetzler) set forth postulates which to the writer appear most sound. They are: MEDICOLEGAL RELATIONSHIP OF TRAXJMA TO DISEASE 489 1. There must have been absolute freedom from abdominal com plaints associated with pain, nausea, vomiting, and tender ness before the trauma. 2. Direct trauma must be severe and forcible, involving the ab dominal wall in the right half especially. 3. Indirect trauma must be violent, acute, and unexpected. 4. Symptoms must appear immediately after the trauma. 5. Symptoms must be persistent and progressive, assuming the signs and symptoms of acute appendicitis. 6. The pathological findings must indicate a suppurative, destruc tive, or necrotic process. With these postulates before us, let us apply them to two cases. Case I.--A board from a ripsaw flew back with great force strik ing the operator on the right side of his abdomen. He suffered immedi ate pain, which subsided greatly within a half hour. He felt too knocked out however to continue working, so he went home. During the night he was awakened with cramps in his belly, and at noon of the next day he began to vomit. Late on the second day after injury, his condition being worse, he was operated upon. At that time the abdominal wall was rigid, especially on the right, where he also had marked tenderness. The skin in the lower right quadrant showed deep, purplish ecchymosis. He had a temperature of 101.2 F.; pulse of 108; leukocytes, 16,500; with a polymorphonuclear count of 84 per cent. Upon opening the abdomen there was evidence of hemorrhage into the muscles, the appendix was lying over the pelvic brim, and was gangrenous at its distal end, with a small perforation present. There was no evidence of adhesions or previous inflammation. This case satisfies the postulates previously outlined. The blow was direct and forceful, symptoms appeared immediately after injury; they were persistent, progressive, and assumed the recognized signs and symptoms of acute appendicitis. The findings at operation indi cated an acute process with no evidence of previous inflammation. Case II.--While cartons of furniture polish were being stacked, one of them fell from the stack a distance of two feet, striking the workman a glancing blow across the right upper abdomen. He subse quently alleged that it hurt him at the time but that he continued working. Three weeks later while in a movie he became nauseated. The next day he vomited several times and noted mild pain in his right side. The vomiting and pain subsided but four days later recurred more severely, at which time he was operated upon. Following re covery he entered claim for compensation and medical costs. The operative notes of his surgeon stated that the appendix was rectocecal 490 OCCUPATIONAL DISEASES and bound down by adhesions. The pathologist reported the lumen obliterated and healed sears in the submucosa and in the interstices of the musculature. The facts in this case do not satisfy the postulates for traumatic appendicitis. The blow was neither severe nor direct. No symptoms were produced immediately or reasonably soon afterwards. The oper ative and pathological findings gave evidence of previous attacks. A check-up among his fellow employees revealed that the patient had complained on prior occasions of "stomach-ache" or "indigestion." Appendicitis Folloioing Strain.--Many cases could be cited in which the allegation is made that appendicitis followed a strain of varying degrees of severity. None of these will be illustrated, since I have never seen nor read of a case of appendicitis following strain which came near satisfying the requirements of the above postulates. In my experience the relationship of strain to appendicitis has been either coincidental or too remote to be seriously considered. The pos tulates outlined for traumatic appendicitis can be applied in most in stances to other acute abdominal conditions, such as rupture of a pep tic ulcer, or of the intestines, spleen, liver, and so forth. Trauma and Tuberculosis.--Let us consider the relationship of trauma to tuberculosis. Lesions other than pulmonary tuberculosis will be dispensed with by simply stating that tuberculous infection of traumatized tissue, the finger for instance, by way of the bloodstream from a distant focus rarely, if ever, occurs. The truth of such a state ment resides in the knowledge that subjects with active tuberculosis of the lungs frequently injure themselves without developing this type of infection in the traumatized part. Also, we know that trauma to the chest or lungs does not initiate tuberculosis. The study of wounds to lung tissue incurred during the first World War is sufficient proof of that. But how shall we judge the case wherein the claim is made that pulmonary tuberculosis set in after an injury to the chest or lungs? I suggest that when a claim of this type awaits a physician's opin ion, he first consider the general known facts about tuberculosis. It is a widespread, infectious disease, occurring in all walks of life without being induced or aggravated by trauma. Its incidence among the unskilled laboring class is greater than in the non-industrial class. Its incidence is greater in the productive years, between twenty and fifty years, than at any other time. In weighing the facts, other statistics must not be overlooked. Men in industry receive frequent injuries to the chest, yet the claims for tuberculosis arising from injury are less than the incidence of tuberculosis in the general population. In MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE 491 Kessler's series of 1107 cases of chest injuries, less than 2 per cent claimed tuberculosis as a result of injury, which is the normal inci dence of this disease among the American population. If tuberculosis is higher among the laboring class and injury common, we would ex pect the incidence to be far higher if a relationship existed. In addition to these general considerations, the elements of time, severity, location of injury, past medical history, the worker's health at the time of injury and whether tuberculosis already existed, are to be evaluated. Postulates to Be Satisfied.--The following postulates are suggested when considering the acute, immediately active case of tuberculosis: 1. Severe injury, as indicated by: (a) Ecchymosis, fracture of ribs, tear of muscles, etc. (b) History from eye witnesses 2. Immediate (or within a few hours) evidence of: () Hemoptysis () Pneumonia or bronchopneumonia (c) Pneumothorax (d) Pleurisy with effusion (e) Fever 3. Good health just prior to alleged injury 4. Positive findings of tuberculosis: (a) Tubercle bacilli in the sputa (b) Manifestation of a tuberculous process in the a;-ray films In applying the above postulates I believe one should demand a trauma of sufficient degree before admitting it as the aggravating fac tor (Fig. 132) . It is true that cases have been reported where an acute active tuberculosis followed a trivial strain. In such an instance I should want to be most certain that the subject was not about to have a "breakdown" and that the strain was not purely coincidental. And also, a sudden, active tuberculosis should not be attributed to a trauma which allegedly occurred a year or two previously, when in the interim the patient has been in good health and has not com plained of any disturbance following the trauma. It is held by some that severe trauma to the chest may induce pathological changes which permit the slow progression of the disease with the appearance of signs or symptoms six weeks or several months later. Let us apply these postulates to several examples. Case I.--A fireman in the course of his duty one cold winter night became drenched with water. He was in these wet clothes a number of hours. The following day he developed chills, fever, and cough; and examination of the lungs revealed congestion. Pneumonia set in, which failed to resolve, and subsequently he developed a dry cough, after 492 OCCUPATIONAL DISEASES noon temperature, night sweats, loss of weight, and other indications of tuberculosis. Examination revealed tubercle bacilli in the sputa, and the a;-ray films showed right apical involvement. The severity of injury was sufficient. While not a direct trauma to the chest or lungs, it was an injury to the body which lowered his resistance, permitting pneumonia to set in, which further lowered the resistance and gave rise to the activity of tuberculosis. The onset was immediate. The immediate signs and symptoms indicated lung Fig. 132.--Tuberculous pleural effusion. This case was not discussed in the text. A thirty-four-year-old carpenter fell twelve feet, striking his chest against a projecting cornice. No ribs were fractured. Four days later he began to spit up blood, developed a cough, and noted fatigue. Twelve days later his malaise was so marked that he was forced to bed. This film was taken one month after injury, at which time tubercle bacilli were profuse in the sputum and were recovered in the aspirated fluid. History of previous good health was proved. infection. His previous health had been established, for he had three weeks before passed his medical examination. Finally, the tubercle bacilli were recovered from the sputa, and the x-ray films revealed apical involvement in keeping with the picture of tuberculosis. Case II.--Following the accidental release of the brakes of a heavy truck, it crushed the driver between the endgate and a loading plat form. He suffered great pain and within half an hour had a severe hemoptysis. These occurred at intervals for the next several days. MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE 493 During the first two weeks he complained of severe pain resulting from three fractured ribs. The stereo films revealed several small cavities as well as one large cavity in the right apex with bilateral fibrosis. During the first few weeks he was markedly ill, ran a fever, and coughed a great deal, and tubercle bacilli were present in the sputa. The trauma was severe, and evidence of injury was present. The evidence of lung involvement was immediate. At the time of trauma his general state of nutrition was good, his weight in keeping with his age and height. He had worked on the same job for ten years without loss of time due to illness, and his employer stated that the patient had been unusually energetic. Tuberculosis was proved to be present soon after the injury. Although the x-ray examination left no doubt of a previous pulmonary tuberculosis, the patient denied knowing he had ever had it. Regardless of any skepticism one might have in an instance of this type, it must be admitted that all evi dence pointed to his being apparently well, healthy, and able to work prior to the trauma. One must, therefore, conclude that the case was compensable. Case III.--A girl, occupied as a file clerk, alleged that as she pulled out a cabinet drawer she noted a pain in her side. That night she coughed up some blood. A continuous cough with occasional bloodstreaked sputum over the next several days induced her to see her family physician, who found active pulmonary tuberculosis present. Some months later she filed for compensation, alleging the act of pull ing open the drawers of the cabinet "weakened her and brought about the onset of tuberculosis." Investigation showed that she was twentytwo years old, 5 feet 8 inches tall, and weighed 102 pounds. The em ployment record indicated frequent absences from work over a period of two years due to colds, and one month prior to her discovery of the disease she had been sick with a "very heavy chest cold." Her fellow-employees testified that they had noted her coughing a great deal for a number of months and that she had complained to them of a loss in weight and constant fatigue. The family history showed the mother had died four years previously of pulmonary tuberculosis. When the postulates are applied to this case, it fails to meet them. The drawers of the file were on ball bearings, light and easy to manage. The alleged cause, therefore, could not be considered in any way a trauma, from either single or accumulative effort. The history indi cated an insidious progression of the disease over a long period of time. A known contact existed in that the mother had had tubercu losis. Finally, the presence of hemoptysis on the evening of the day 494 OCCUPATIONAL DISEASES she noted a pain in her side was coincidental and not the result of a single effort. Claim {or Latent Tuberculosis.--All claims do not contend that the signs and symptoms of tuberculosis present themselves immedi ately following a trauma. There are numerous cases recorded, or have been personally examined, where the claimant alleged his pulmonary tuberculosis was the result of an injury sustained a year or more previous to the onset of the disease. In contrast to the immediately active tuberculosis, this type of case might be called the claim for latent tuberculosis. For such the following postulates might be con sidered: 1. Sufficiently severe trauma 2. Reasonable length of time between the trauma and onset of the disease 3. Presence of one or more signs or symptoms during the interim-- the bridging evidence 4. Good health prior to the alleged injury 5. Positive findings of tuberculosis Case IV.--A cook, upon entering the kitchen early one morning to begin the day's work, noted the presence of strong fumes and dis covered a leak in the refrigerator. While attempting to locate the leak, he was almost overcome by these fumes. His eyes burned; he coughed violently and suffered a throbbing headache along with a feeling of constriction in the chest. The cough lasted for several days, as did the sense of constriction in the chest. Within one week the victim was entirely normal, being discharged from further medical care. One year and four months later he consulted a physician because of a dry cough and afternoon fatigue. A diagnosis of early pulmonary tubercu losis was made and'confirmed. Sometime later he filed for compensa tion, alleging the tuberculosis to be the result of the previous gassing. Investigation brought out these facts. The gas was sulfur dioxide, a single exposure to which produces no permanent effect upon the lung. Following this exposure he continued working for that employer for six months, during which time he made no complaint of any resid ual disturbance. Following this six-month period, he changed posi tions twice, each time being required to undergo a physical examina tion. Six weeks prior to the discovery of pulmonary tuberculosis he went fishing in the high Sierras, caught a cold, and was absent from work for ten days. Workmen exposed to the fumes of sulfur dioxide are frequently seen in our clinic. The writer has personally seen in the last five years about one hundred such patients. In none of them has there been a temporary disability beyond a few days or a week or two, at the most. MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE 495 In none has there been any permanent morbid anatomy of the lung. In many, the initial exposure has been much greater than that ex perienced in the ease under discussion. So, we can conclude that the trauma or injury was not severe. The interval of time is too long between date of injury and the onset of symptoms. This gassing cer tainly did not introduce tubercle bacilli into the lungs, and if it had aggravated a preexisting condition, the evidence of aggravation should have been apparent sooner than one year and four months. There were present no bridging symptoms--such as cough, fatigue, loss of weight, afternoon temperature, and the like. The condition of health prior to injury was good, but an illness which could have lowered his resistance was known to have been present six weeks previous to the onset of the signs and symptoms of tuberculosis. This case does not satisfy the postulates. Case V.--While lumber was being stacked, the pile gave way, causing the patient to be buried underneath it. Upon being removed, the patient complained of chest pain and was brought to the clinic. aj-Ray study at that time was confined to a picture of the lower rib cage, which showed fractures of the ninth and tenth right ribs. He was accorded the customary treatment, but he was the father of eight motherless children and because of financial circumstances refused to stop working. Nine months after the trauma to the chest, the patient was incapacitated from further work because of active pulmonary tuberculosis. He was sent to a sanatorium. He did not suspect or claim any relationship of his disease to the trauma of the chest, but an in quiring friend did. Investigation revealed that a public health nurse visited his chil dren, one of whom was a cripple. She testified that shortly after the accident to the claimant, the children told her their father was not well, that he coughed a great deal, was observed to spit up some blood occasionally, complained of fatigue, and had been losing weight. On one occasion a physician, called in to see the crippled child, exam ined the father and told him he had bronchitis. This case was opposed by the insurance carrier. It was my testi mony that the relationship of the trauma to the disease could not be denied. I based my opinion chiefly upon two of the postulates. First, he had suffered a sufficiently severe trauma. Secondly, there was evi dence of definite bridging symptoms. The children of this claimant were good witnesses, although they did not realize the significance of their testimony. Their observations were made to a nurse without prompting or prejudice. These bridging symptoms began soon after the injury and were progressive. In the writer's experience, this is the 496 OCCUPATIONAL DISEASES only case of latent tuberculosis that satisfies the postulates, and my opinion was that the trauma aggravated an inactive tuberculosis. Case VI.--A lifeguard at the beach slipped on the steps of his observation platform, skinning his right knee and right chest. Two years later he developed pulmonary tuberculosis. A claim of tubercu losis resulting from the injury mentioned was filed. During the interim, as a student at a local college, he was a member of the water-polo team, and of the track team. Periodic health examinations by the school physician revealed no evidence of disease. This case does not meet the stipulations of the postulates. His trauma was not severe, no immediate lung disturbance appeared. Dur ing a period of two years there were no bridging symptoms, and the claimant exhibited extraordinary strength and vigor. Trauma and Cancer.--That cancer can follow a single act of trauma is a highly controversial question and one which must await further scientific investigation before dogmatic statements can be made. At the present time any such relationship remains speculative and doubtful. Regarding this relationship, Leila Knox states4: In studying the possibility of the production of a malignant tumor by a single injury, it is important to keep in mind the established facts concerning the etiology of cancer and to understand clearly all the fac tors which are thought to be involved in the production of a neo plasm. These biological and chemical facts may or may not find their way into the evidence which determines legal liability, in cases where a decision has to be made as to the influence of a single trauma in the causation of a malignant growth. Since verdicts and claims are pre sumably based upon such evidence as is presented before the court, legal decisions are not the final word concerning the possible relation ship between a trauma and a malignant tumor, for the evidence ad duced may not be of such a nature as to afford a true explanation of the occurrence. Possibly such evidence is, at the moment, not avail able. The fact that it is not available may be determined by the lack of medical knowledge concerning the plaintiff's state of health previous to the alleged accident, and by the absence of other important data necessary for reaching a conclusion as to the true nature of the condi tion under consideration. The patient may refuse a biopsy on the tumor on legally justifiable grounds, and thus prevent a microscopic study of the tissues, which is regarded by the medical profession as essential for diagnosis. Thus, in any human case, many scientific facts may be missing, and the court must render its decision upon what is produced before it in evidence. Hence, it is possible that, under cer tain conditions, the decision may of necessity be contrary to the real MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE 497 Facts, which can only be revealed at autopsy after the plaintiff's death. The use of modern methods of investigation, such as the roent gen ray study of tumors of bone, has helped to establish the fact that many neoplasms, which in the past were considered to be due to injury, are definitely not of traumatic origin. The court also is largely dependent upon the competence of the medical evidence, and it is sometimes impossible for any accurate opinion to be rendered, when the evidence is more or less contradictory. A remedy for this phase of medical testimony has long been discussed but no practical solution of the problem has been reached. History.--In considering the relationship of a single trauma to cancer, a complete, exacting, and relevant history is most important. Such a history must evaluate the patient's viewpoint, for in most every instance the patient is swayed in his story by his own wishful thinking or by ideas which have been disseminated to the laity re garding cancer. Such a history must be supplemented by facts ob tained from every available source, which includes friends and rela tives, fellow-workmen in the shop, neighbors, family physician, and previous employment examinations. Postulates to Be Satisfied.--A set of postulates to test a claim of cancer resulting from single trauma has been suggested by various writers and in the main is as follows: 1. Authentic trauma To establish this, not only the patient's statement, but others from eyewitnesses must be secured. Sometimes these cannot be ob tained and, therefore, the validity of the claim will have to depend upon the remaining postulates. 2. Sufficiently severe trauma This may be described by the patient or by eyewitnesses. Also, medical reports of one or more physicians who have seen the patient immediately after the injury are to be sought. The presence or absence of evidence of trauma such as swelling, ecchymosis, laceration, hem orrhage, and the like, aids in the estimation of the adequacy of the trauma. 3. Normal tissue in wounded part before injury While the patient may claim that his health was normal and the part of the body involved was in a healthy condition just prior to injury, such fact cannot be assumed as true or accurate from a medical and scientific standpoint. This is a difficult postulate to adhere to in many instances. However, occasionally biopsy, x-ray examination, or 39 498 OCCUPATIONAL DISEASES other procedures may establish the fact that the tissue involved con tained a growth or neoplastic change which by its character must have been present prior to the date of injury. 4. Tumor or malignancy in the area that was damaged by trauma Occasionally this cannot be held to in a rigid sense, as in lung injuries in which the principle of contrecoup might be applied, the lesion being found in contralateral lung. Brain injuries often follow this principle. However, the site of the tumor must be related to the site of the injury. 5. Reasonable time interval between trauma and appearance of tumor No set rule can be applied for this postulate, for the interval is variable. This is easily understood when one realizes that a tumor may be present for a considerable length of time but yet be unnoticed by the victim. In addition, there is a relationship between the time interval and the type of malignancy; for instance, it is believed that sarcoma may develop much more rapidly than carcinoma. In general, it can be held that the longer the interval, the less likely the tumor should be considered the result of trauma. 6. The presence of bridging symptoms This postulate considers the evidence of a continuity of symptoms between the time of injury and the period of malignancy. For in stance, when normal tissue has been traumatized and the wound fails to heal or continues to discharge for a long period of time, or a swell ing fails to recede, then the relationship between the development of malignancy to the preceding injury must be strongly considered-- a relationship which if proved in any medicolegal case would be most difficult to deny. 7. Diagnosis of neoplasm Often a biopsy may prove the presence of a slow-growing tumor which antedated the injury. Often, however, the biopsy can throw no light on the length of time the growth has been present. x-Ray exami nation of parts of the body distant to the malignancy may reveal a primary lesion and thus establish that the part claimed to be malig nant as the result of injury is actually a metastatic lesion. Limitation of space forbids any consideration of the effects of trauma to the heart, nervous system, or to other systems not men tioned here. The purpose of this short discussion of an extensive sub MEDICOLEGAL RELATIONSHIP OF TRAUMA TO DISEASE 499 ject is to offer a pattern which can be followed or enlarged upon by the reader. It is hoped it suggests to the reader that, in a majority of cases, definite opinions can be expressed by the physician based upon sound thought and reasonable postulates and that we physicians do not need to vacillate in medicolegal testimony. REFERENCES 1. Texas Employer's Insurance vs. Burnett, Texas 105 S. W. (2d) 200. 2. Moorehead, J. J.: "The Relationship of Trauma to Inguinal Hernia," Am. J. Surg., 37 (Feb.), 1940. 3. Rhodes, G. K., and Birnbaum, W. D.: "Traumatic Appendicitis," California and West Med., 53 (Oct.), 1940. 4. Knox, L. C.: "Trauma and Neoplasms," Trauma and Disease, Lea and Febiger, Philadelphia, 1937, p. 441. 5. Kessler, H. J.: Accidental Injuries, Lea and Febiger, Philadelphia, 1931, p. 352. 6. Brahdy, L,, and Kahn, S.: Trauma and Disease, Lea and Febiger, Philadelphia, 1937, p. 442. CHAPTER XXXVIII NEUROSIS ASSOCIATED WITH TRAUMA--MALINGERING Ordinarily the name applied to any disease entity has a uniform meaning to all physicians. When lues, bronchopneumonia, malaria, or measles is spoken of, the clinical and pathological picture of each dis ease registers no gross dissimilarity upon the individual minds of a varied medical audience. But what does "traumatic neurosis" mean? From the profuse material to be found in medical literature devoted to this subject, it is impossible to extract a clear-cut definition that finds universal acceptance. The condition has been referred to as "terror neurosis," "litigation neurosis," and "post-concussional neu rosis." Traumatic neurosis usually follow injuries to the head, but it frequently follows injury to other parts of the body as well. In my experience, back disorders not easily recognizable as of psychic origin form a large group. By comparing the opinions of a few of the out standing thinkers in the field of neuropsychiatry concerning this sub ject, the reader may be aided in forming a concept of practical value. In order that the starting-point for the evaluation of traumatic neurosis may be of common origin, patients with objective signs of brain injury and those with definite evidence of brain damage or de fect, in the nature of convulsions or mental deterioration, should be excluded from consideration. Elements of Syndrome.--Wechsler1 breaks down the remaining post-traumatic syndrome group into the four following divisions: (1) malingering, (2) traumatic hysteria, (3) concussion or traumatic en cephalopathy, and (4) traumatic neurosis. Since malingering is to be subsequently and separately discussed, it will be omitted here. Of the remaining three groups, Wechsler writes: Traumatic Hysteria.--The diagnosis of traumatic hysteria must be based on one set of negative and one set of positive criteria. Patients falling in this group give either no history of unconsciousness or only a history of very brief loss of consciousness, show no clinical signs of brain injury, no evidence of fracture on the a;-ray plate, no history of subarachnoid bleeding in cases in which a spinal tap was done, and, in cases in which grave doubt as to diagnosis justify an encephalogram, no evidence of a cerebral pathologic condition. Merely negative evi dence, however, is not sufficient, and the diagnosis cannot be made by exclusion alone. There must also be positive evidence that the trauma 500 NEUROSIS ASSOCIATED WITH TRAUMA 501 called forth psychogenic symptoms; that there is a hysterical reaction in an individual who has an underlying neurotic personality make-up. The patient makes unconscious use of the trauma to solve person ality difficulties. The accident brings to a head a series of inner and outer conflicts which the patient was unable to face squarely or to solve adequately. The trauma precipitates the neurosis, sets in motion the same mental mechanisms as in any other hysteria and serves as a convenient solution of industrial, social, marital, familial or psychosexual conflicts. It should be emphasized that the individual is not consciously aware of the mental mechanisms; when he is, one is not dealing with hysteria. Nor must the litigation motif be paramount. Not that litigation and compensation do not play some role; but when they play the chief role or become the sole cause for the perpetuation of symptoms one comes dangerously close to malingering. The trauma may therefore be regarded as a definite precipitating and, in this sense only, as a causative factor. It is interesting to note that com pulsion and obsessional neuroses are never, or rarely ever, precipi tated by head trauma. Concussion or Traumatic Encephalopathy.--This occurs in a fairly large percentage of patients suffering trauma to the head. In eleven cases in the series the diagnosis of encephalopathy was made outright and in seventeen a diagnosis of concussion plus hysteria was made; that is, a total of 28 per cent. In every case there was a history of more or less prolonged unconsciousness. The symptoms were entirely subjective in all of them and in but few more were there even minimal clinical signs of organic disease of the nervous system. There is an increasing tendency to speak of concussion of the brain in terms of traumatic encephalopathy; in fact, the two terms are beginning to be used interchangeably. There is no doubt that the old definition of a molecular disturbance docs not hold any longer.The presence of minute hemorrhages, glial changes, cell and fiber de generation, disturbed dynamics of the cerebrospinal fluid within the skull, ventricular distortion, and brain atrophy justifies the designa tion of traumatic encephalopathy. Martland's work on brain changes in prize fighters threw great light on the subject. The investigations of Foerster and Penfield and of Bielschowsky also added to the knowl edge. More recently Rand and Courville have studied the effect of head trauma on the fiber system of the brain. The encephalographic studies of head injuries by Friedman and others have shown the ex tent of ventricular and brain changes in patients whose main com plaints were of a subjective nature. Kennedy has laid down a few ex cellent criteria for the appraisal of the effects of head injuries. Without citing further references to the literature it may be emphasized that concussion is not a simple process and that it consists of fairly definite pathologic changes consequent on trauma to the head, which is ac 502 OCCUPATIONAL DISEASES companied by unconsciousness at the time of the accident. The diag nosis of concussion or encephalopathy is beginning to depend, there fore, more and more on other criteria than on those furnished by the symptomatology. In itself this differs in no wise from that of traumatic hysteria. One must rely chiefly on the history of prolonged uncon sciousness, on the presence of "small signs" of neurologic involvement, on the absence of psychogenic causal factors, on the persistence and severity of symptoms, and on the evidence furnished by the enceph alogram when other facts are not sufficient to establish a positive diagnosis. Traumatic Neurosis.--This is, in my opinion, a comparatively un common condition. I made the diagnosis in but five of the hundred cases of head injury. The correctness of the statement as to its infre quency obviously depends on the acceptance of certain criteria for diagnosis. If traumatic neurosis and traumatic hysteria are used synonymously and interchangeably, the terminology is not only con fusing but rests on sheer caprice, in which case one of the terms should be discarded. If, on the other hand, one is dealing with two distinct neurologic entities, as I believe to be the case, then it becomes incum bent to delimit them and, if possible, to adhere to a more strict defini tion of each term. The clinical syndrome of traumatic neurosis differs little from that of hysteria but is not dependent, as far as one can tell, on the uncon scious use of the accident to solve difficulties that have nothing to do with the trauma. That is, one is not dealing with a patient who had a neurotic personality to begin with. As far as possible the existence of concussion or traumatic encephalopathy must also be excluded. This leaves a small group of previously well adjusted individuals, who, fol lowing a serious threat to life, in which there was comparatively mild or even trifling injury to the head, beget a stubborn set of symptoms which are not amenable to suggestive therapy or other forms of psy chotherapy. Their condition bears resemblance to some of the war neuroses of soldiers who had been through particularly harrowing ex periences, which they subsequently relived in their dreams. To use a psychoanalytic explanation, there is narcissistic regression, but the ego instincts rather than the psychosexual instincts are affected. Trau matic neurosis might possibly be grouped with the true or actual neu roses, in which neurasthenia, anxiety neurosis and hypochondriasis are included, but the intrapsychic conflict with regard to the ego or selfpreservation instincts, which is assumed to exist in traumatic neurosis, would argue against its inclusion. Whatever the explanation, the fact remains that there is a small group of patients, without demonstrable cerebral pathologic changes, in whom hysterical mechanisms cannot be demonstrated, in whom compensation or litigation does not play a predominant role, who are resistive to treatment and who find it diffi NEUROSIS ASSOCIATED WITH TRAUMA 503 cult or impossible to return to their occupation at which they sus tained the accident. It is to this group that the diagnosis of trau matic neurosis may be correctly applied. Traumatic Neurosis as Effort to Resolve Conflict. -- Davidson2 states: A neurosis is a set of symptoms which, to the best of our knowl edge, do not spring from organic or structural change in the body. It is an effort to solve a conflict. Traumatic neurosis is no exception. Here, too, an unconscious conflict tills the soil from which the symptoms bloom. Conflict between what factors? First, at the time of the trauma, is the fright, the shock, the pain--in a word the body-threat ening and life-threatening experience of the accident itself. Second appears the influence of suggestion. The patient hears the physician remark to the nurse: "Look at the way those nerves are damaged. He's lucky the whole arm isn't paralyzed." And the suggestion thus offered burrows into the patient's unconscious mind until it has be come part of it. Third comes resentment at real or fancied lack of sympathy or understanding. An over-anxious plant doctor urges the still neurotic patient to return to work, implying that his symp toms are unreal. The brusque company examiner barks commands of "Stand-up!" "Put out your tongue!" et cetera, until the patient feels that he is being treated like a piece of machinery. The skeptical ad juster drips disbelief as he lists the symptoms with undisguised con tempt. In all, the injured plaintiff faces a battery of unsympathetic, disbelieving officials, whose authority breeds resentment and evokes unconscious memories of punishing school principals, driving foremen and military martinets. Finally, the mind of the patient, already traumatized by pain and shock, influenced by suggestion, humiliated by disbelief, is challenged by one of life's fundamental conflicts: the conflict of adventure vs. security. The security of damages or compen sation forms one horn of the dilemma; the adventure of being an independent wage-earner forms the other. Here, then, is the basic source of the conflict which underlies traumatic neurosis. Independent employment is uncertain, but adventurous. Offering theoretically un limited opportunities for earning money, it carries the seal of com munity approval and self-respect. It stands for uncertainty. Against this is the security which comes with a check for several thousand dollars, or a guaranteed weekly compensation payment. Between the unconscious desire for adventure and community approval and the unconscious desire for security, is a genuine conflict. To say that the patient coolly weighs the advantages of being healthy and employed, against the advantages of being idle but compensated, and then makes a deliberate decision to stay sick, is to be blind to the complex psychologic factors involved. 504 OCCUPATIONAL DISEASES Classification Based on Etiology.--Fetterman,3 who, as Examiner for the Industrial Accident Commission of Ohio, has had a wide ex perience with a large number of cases, makes the following classifica tion. It is not based on symptomatology but upon the principle of dominating causative factor: Type I: "Injury" neuroses due to severe trauma to central nervous system (a) Traumatic encephalopathy with symptoms of a neurosis Type II: "Industry" neuroses induced by relationship of injured per son to work (a) The trauma offers an "escape," a flight into illness from duties which are disagreeable or dangerous Type III: "Indemnity" neuroses motivated by a combat for compen sation (a) The possibility of indemnity mobilizes the neurotic tendencies towards illness Type IV: "Inherent" neuroses due to essential nervous difficulties (a) The injured individual (always nervous) "projects" the blame upon the trauma for his inherent weakness There are many mixed forms. Insurance as Motivation.--Reinhardt4 believes that after the pa tients with severe trauma to the brain are excluded, the remainder, many of them with concussion, are influenced in their emotional symptoms by the factor of insurance. He cites the experience that among the uninsured and in the pre-insurance era, patients who suf fered a concussion of the brain cleared up in a shorter time than those who are insured. As Psychological and Sociological Problem.--Lewy3 takes the stgnd that the problem is primarily a psychological and sociological one and contends that compensation should be denied every patient with post-accident neurosis if no permanent organic damage exists, believing that when the general public became aware of such a law, there would be a rapid decline of claims. He says: A definite change of opinion came when the existence of a volitional factor as a contributing element was discovered by more careful psy chological examination. It became evident that neither the event of the accident nor the subjective experience of being in an accident created the accident neurosis. The accident neurosis was created in part by the subjective conviction of having been in a compensative accident. In addition to the definite volitional factor, different favor ing circumstances may exist for the patient--financial worries, family troubles, a wish to escape from responsibility--but they only provide NEUROSIS ASSOCIATED WITH TRAUMA 505 the motive for the volitional factor. Those responsible for the damage cannot be held responsible for the wishful thinking on the part of the patient, even though we grant that this volitional factor is a stranger to the conscious mind of the patient. The volitional factor becomes a purposeful factor in a post-accident neurosis and the de velopment from the genesis of the dominating idea of being incapaci tated to the hysterical accustoming and fortification of the whole psychological set-up is a simple one. But the results of any severe shock will wear off after a short time if there is no volitional factor seeking to gain something from the experience. Interpretation in Terms of Subconscious and Organic Factors.-- Strauss and Savitsky6 evidence an attitude diametrically opposite to that of Lewy. They say: The clinical features--headache, dizziness, irascibility, abnormal reaction to effort, vasomotor instability, fatigability, intolerance of intoxicants and of changes in weather, are evidences in almost all cases of alteration of the activity of the intracranial tissues. Precisely the same reactions occur in non-litigation patients as in those who can claim compensation. In a later paragraph these two observers qualify their opinion somewhat: While we admit the frequent existence of a volitional trend, its role and significance can be evaluated only in the setting of the sub conscious and organic factors. Its importance must not be overesti mated. When such a volitional element is discerned, there exists an all too frequent tendency to consider the whole reaction as malinger ing and to evaluate the whole case from this angle. Strauss and Savitsky feel hurt by the attitude of a large part of the medical profession. They feel that: The frequent expression of unjustifiable skepticism on the part of examiners engenders resentment, discouragement, and hopelessness, and too often forces people to resort to more primitive modes of re sponse (hysteria). As Evidence of Organic Changes in Brain.--The paper of Strauss and Savitsky from which the above quotation was taken was read at the Fifty-Ninth Annual Meeting of the American Neurological Association, Washington, D.C., May 9,1933. At this same meeting and immediately following this paper was one read by Winkelman and Eckel.7 This second paper dealt with the histopathology of the brain during the early stages; that is, a histological study of the brain in 506 OCCUPATIONAL DISEASES persons who died soon after injury. It made the following admissions prior to the presentations of case histories--that there is an increase of patients in head-injury cases seeking compensation and redress; that the duration of unconsciousness is usually in direct proportion to the severity of the brain injury; that symptoms following a head trauma are usually uniform even in the absence of legal complica tions; that the brain of a patient who dies after a severe head injury reveals a remarkably uniform finding of subarachnoid hemorrhage with maceration of the brain on the under surfaces of the frontal and temporal lobes; and that it was their purpose to attempt to determine all the minute changes in the brain after trauma and to correlate the clinical and histological features. After presenting seven cases, one of their conclusions was: Sufficient evidence has been found in the brains of patients with severe head trauma, especially those in whom unconsciousness had been prolonged, to convince us that most of these persons have organic changes in the brain, the result of trauma. These changes explain the post-traumatic symptom complex usually characterized as "traumatic neurosis." Organic Changes Not Always Present.--Believing that this conclu sion expressed by Winkelman and Eckel regarding the relationship of trauma to neurosis is not justified, I wish to quote the remarks of Bernard Sachs,8 who criticized the paper at the time it was read as follows:I I should like to say in connection with the whole subject, so as to avoid one danger that neurologists seem to be steering for, that the cases that have been presented are instances of rather serious head injury and I do not think there has been any doubt that organic lesions have followed such injuries. However, before one absolutely dismisses the idea of anything like the picture of traumatic neurosis, an important question and one that has great practical value, particularly in medicolegal experience, is what happens in the far greater number of cases of rather slight injuries to the head and to the spine, in which there is a remarkable similarity in the claims made and in the symptoms that are supposed to follow. Whether or not there is distinct organic change in those eases is still open to discussion. At all events, I think it should be allowed that there may be something in the form of a general neurosis or of neurotic symptoms not necessarily based on actual organic changes which frequently follows mild injury to the brain or to the spinal cord. The mistake that should be avoided is the insistence that in all cases of head injury there are the changes that have been NEUROSIS ASSOCIATED WITH TRAUMA 507 shown here. It has been valuable to see the evidence of the changes that occur, particularly in such cases as Dr. Winkclman presented, but one should not jump at the illogical conclusion that there are organic changes in all cases of skull trauma. I am inclined to feel that evidence is lacking that there are organic changes following even the milder forms of skull trauma. Review of Literature.--The following "brevities" are concise ex tractions of opinion found in the literature: Hassin9: That the majority of neuroses once considered functional are actually pathological and microscopic changes in the nervous tis sue can be demonstrated. Winkelman10: In studying a series of cases histologically was "sur prised to find changes in the brain that were indisputable. In many cases of these, hysteria had been considered as a diagnosis." Riggenbaeh11: Cranial trauma may produce not only a neurosis but even a psychosis. Charcot11: Could see no fundamental difference between the neu roses that followed trauma and those of ordinary life. Page11: Suspense of litigation, want of occupation, and anxious reflection influence recovery. Iligler11: Increase in the incidence of traumatic neurosis since the introduction of insurance. Lottig11: Attempted a differentiation between an illness caused by the immediate factors of injury and that arising because an existing neurotic tendency preceded the injury. Fetterman11: Suggested a distinction between those nervous be fore, and those nervous after, an accident (pre- and post-traumatic groups). Volitional Factor versus Organic Basis.--The review of the litera ture just presented reveals that among authorities there is general disagreement concerning two phases of the so-called "traumatic neu rosis syndrome," namely the presence or absence of psychogenic and organic factors, and the estimation of the extent of injury. From the preceding discussion it will be noted that there are those who feel that traumatic neurosis arises entirely from a functional or volitional factor and that this volitional factor, possibly minor in character at the beginning, progresses into a strong purposeful factor with or without manifestations of hysteria. Opposing this viewpoint are those who contend that there is always an organic basis for the neurosis following trauma, even though the extent of the trauma may be minimal. Here again, "the extent of injury" comprises a phase of the syndrome about which there is dispute. 508 OCCUPATIONAL DISEASES Effect of Concussion, on Consciousness.--Some hold that trauma of a degree sufficient to produce significant intracranial changes must result in unconsciousness, that the possibility of concussion without unconsciousness is not to be considered. Others hold that concussion can be present without unconsciousness (a minority viewpoint). They feel that a mental dysfunction without unconsciousness may follow a head blow, and cite instances of prizefighters who, although they continued to fight, were so dazed by a blow that the events of the fight and those following it were not remembered.12 Finally, there are those who maintain that neither a history of unconsciousness nor of severe trauma is necessary for varying degrees of disability to be present following a head injury. Unfortunately, there seems to be no common ground or unified understanding of the definition of concussion. The majority of commentators have discarded a belief in the molecular disintegration or anatomical change theory, but lend support to the theory that concussion occurs following the disturb ance of the cerebral vasomotor mechanism. Regarding this, Munro13 says: The primary and simplest form of craniocerebral injury is true concussion. The term has been widely used to cover all forms of brain injury regardless of the pathology present. It should be restricted solely to those cases in whom a blow on the head has produced some degree of unconsciousness but who on recovery present no residual symptoms or signs whatsoever. Upon it as a foundation are built the complicated and more serious succeeding brain injuries. It is probable that the primary unconsciousness practically always associ ated with craniocerebral injuries is due to this concussion. Wechsler's concept of concussion has been stated in a previous paragraph. Bennett,14 in his classification of concussion includes a mild form "in which no loss of consciousness occurs at all." Strauss8 prefers to think of concussion clinically as "a series of events resulting from a blow to the head severe enough to cause a disruption of intra cranial equilibrium." Malingering. Definition.--Before summarizing and attempting to clarify the situation so far as the viewpoint of the writer is concerned, malingering should be defined. A person becomes a malingerer only when he consciously and purposely, in order to deceive, to evade re sponsibility, or to derive gain, feigns illness and voluntarily tries to reproduce signs and symptoms which he really does not have, or extravagantly exaggerates minor ones which he has.1 Invariably the claims made by a malingerer follow a minor injury and one in which the initial symptoms have been slight. The malingerer is to be dis NEUROSIS ASSOCIATED WITH TRAUMA 509 tinguished from the neurotic, for in the latter the symptoms arc un consciously manifested. The experienced clinician usually has no difficulty in spotting true malingering, although on occasion a cun ning person will perplex one. In the specialized fields, such as ophthal mology or otology, tests will establish the allegation to be true or false. These are too detailed for description here. Difference between Malingerer and Neurotic.--The following is a broad classification of the malingerer as compared to the neurotic: Table 25--Differentiation of tiie Malingerer from the Neurotic Malingerer Neurotic Attitude towards Work and Play* Claims inability to work, but enjoys ball games, movies, cards, or participates in light games, such as billiards Cannot get interested in games. Evidences no desire to be a participant or spectator Attitude toward.!! Treatment Unfaithful and irregular in reporting for treatment or in taking medication. Proffer of an operation is usually refused. Annoyed by reexaminations or exam inations by "specialists" Faithful to all details of treatment and medication. Willing to submit to an operation. Willingly submits to fre quent and repeated examinations by many doctors Attitude as Revealed by Past History and Background Irresponsible, occupational migrant; has not held responsible positions; not a community worker or asset Responsible, absentee record good; long duration of employment for one or more employers; active in community or civic enterprises Attitude as Revealed by Investigation When away from doctors or observers uses Condition of disability constant parts allegedly, disabled (as revealed by movies, detectives, etc.) Attitude towards Rehabilitation R efuses work offered which could be done without involving part of body allegedly disabled. Unwilling to accept state re habilitation schooling to fit him for a new trade Accepts work of a limited nature which he may be able to do. Distinction here not readily discernible, since many neurotics feel they cannot function in any ca pacity Nomenclature.--That there is need of a better descriptive title for the traumatic neurosis syndrome is evident. The one used as a title for this chapter "Neurosis Associated with Trauma" was borrowed from Fetterman,3 who remarked that such a name suggests at once the distinct types or forms of the disorder and does not prejudice the relationship of cause and effect which is implied by the terms "compensation neurosis," "purpose neurosis," "traumatic neurosis," and the like- Procedure in Classification.--With this definition as a startingpoint, the following procedure should be employed to classify any given patient: History.--The history in these cases is of great importance. Ob taining a complete story calls for tact, ability to bring out the whole 510 OCCUPATIONAL DISEASES story, to create an atmosphere which the patient feels is congenial and an attitude which the patient senses is not prejudiced. Repeated history-taking is invariably necessary in order that a picture of the entire background of this patient's life be obtained--conflicts of youth, his past and present social and economic status, congenial or conflict ing factors in his present occupation, evidence of being a responsible or irresponsible type, his previous compensation or litigation expe rience--all these and many more need to be weighed. Only after repeated observations and a complete compilation of facts, together with the physical and laboratory findings, should a final classification be made. >$ Physical Examination.--This includes not only the general and neurological examination, but frequently a special examination by an ophthalmologist, otologist, or other specialist. It is not infrequent that symptoms considered to be of nervous-system origin, and arising out of an injury, may be found to.have their cause in an unrelated systemic disease. For example, a man claimed headache, vertigo, lack of concentration, and loss of weight two months after a trivial head injury. One physician contended the man was a malingerer; another that his symptoms were due to his injury. Neither of them evaluated, or at least mentioned, the findings of a blood pressure of 210 systolic, 120 diastolic, generalized arterial sclerosis, sugar in the urine, and a blood sugar of 280 mg. per 100 cc. Laboratory Investigation.--This should include routine measures, such as urine and blood studies, rr-ray examination, spinal tap, and (when strongly indicated) encephalograms. Psychiatric Examination.--Undoubtedly this should be more fre quently employed. When the physician feels that organic causes do not account for the symptoms claimed and if he feels he is not suc cessful in getting an adequate picture of the patient's mental back ground, the psychiatrist should be called into the case. Basis for Diagnosis.--In considering the neurosis associated with trauma we are not concerned with the patient in whom the history of severe injury is accompanied by compatible signs and symptoms, but rather with the patient alleging a disability following a minor or negligible injury. The importance of an adequate history, a complete physical examination, and exhaustive laboratory study has been emphasized. But after all that is done, many of these cases will still remain a puzzle. It appears to me that in a case of neurosis associated with trauma, ultimate opinion is influenced by three situations: 1. Character and Background of Claimant.--The following char acteristics were mentioned under "History," but bear repeating: (a) Stability, Solidity.--Has worked for the same employer for NEUROSIS ASSOCIATED WITH TRAUMA 511 many years; rarely been absent from work because of illness; never been involved in litigation or compensation claims; is not an agitator in labor activities; obviously is not of a nervous disposition. (b) Instability.--Is constantly changing jobs and is dissatis fied with his present employment; has had previous experience in liti gation or compensation; is an agitator and feels that labor is unjustly dealt with; is a type that obviously has always been nervous; his economic status is such that compensation, although a reduced in come, is adequate for his needs. To illustrate the difference in character between two persons hav ing the same type of injury and in whom the age, build, and constitu tion were comparable, a fracture of the right transverse process of the first lumbar vertebra occurred in both a longshoreman and a welder. The longshoreman took off from work only that time required for an examination. The welder, employed at much lighter work, had a temporary disability of eight weeks. The welder, in this instance, is not cited as being a malingerer, but a study of his character revealed his attitude towards work. It has been previously stated in this book that the average work man is not a malingerer. This is most certainly true, but the incidence of malingering is not so rare as some writers state. Case after case can be extracted from our files wherein the claimant has faked the same injury in several states to gain compensation. A case in point is here recited. After receiving a minor head injury, an oil-field worker alleged that he had headache, got very dizzy when he had to bend over or walk at high levels. Following an award for total permanent disability, he and his wife retired to a little home in the Mariposa Woods, where they had a garden and he could hunt. More than a year later, without the man's knowledge, movies revealed him to be doing all the acts he alleged he couldn't do. He admitted deceit, but stated he liked that kind of life. In this instance compensation had created a situation desirable to the injured one. Space does not permit the recounting of numerous other cases. Truly, the incidence is not high, but certainly not rare. 2. Character of Circumstance in Which Injury Occurred.--In view of subsequent statements, consider the following conditions: (a) A man sustains a head injury in a home which he owns. He has no one to blame but himself, and he has no insurance; (6) a man, driving his own car, fails to traverse a bend in the road because of speeding, strikes a tree, and receives an injury but has no insurance of any type; (c) the same conditions as case "b" except that the man has insurance to cover his accident; and (d) a man falls from a platform, receiving an injury covered by the Workmen's Compensation Act. 512 OCCUPATIONAL DISEASES It is possible that all four men in the above-mentioned circum stances would evidence no subsequent malingering or neurosis. But if cither of these two conditions arose, would it be likely to occur in the first or the second two instances? The answer is obvious. It is impossible to ignore the factor of possible financial reward for an injury suffered. To believe or insist that the element of compensation or award from a civil court does not enter into the allegation of dis ability is to ignore the increased incidence of such claims. The validity of the claim should not be ignored because the clement of possible award exists, but the character of the circumstances in which injury occurred must be evaluated. 3. Character of Experience of Physician Offering Opinion.--Medi cine has always placed major emphasis upon the importance of ex perience. In a case of questionable yaws, an opinion from one such as myself should be held of no value when compared to an opinion from a medical missionary who has seen large numbers of these cases. A neuropsychiatrist may well define the psychogenic components which comprise a neurosis, but in any given case is his experience such that his definition considers the changing complex of living? Does his definition consider the social philosophy newly adopted by a class of people previously denied justifiable rights? The definition of a neurosis offered years ago remains largely unaltered, but the peo ple to whom it is on occasion applied have changed markedly. Intimate association with any group of people teaches one to un derstand their characteristics, tendencies, attributes, and philosophy. This experience constitutes an inestimable factor in the country doc tor's "acumen." He may not have the specialized training of his urban confrere, but he knows his people. This is likewise true of the physician who is associated with industry. If he believes that the claims pre sented today show an increased tendency towards a wilful or voli tional purpose of obtaining more than is justly due, it is not evidence that he is prejudiced. It is evidence that he is acquainted with the attitude of the age. In substantiation of the writer's viewpoint, one fact must not be overlooked. Most of the expressions of opinions reviewed in this chap ter were made prior to the date when the complete legislation of acts designed to aid the victims of this depression became effective or reached the height of their effectiveness. One wonders if there would not now be a revision of opinion from those who disallowed the influ ence of financial award in the neurotic. Would not the trained soci ologist agree that social legislation--such as old-age pension, unem ployment insurance, the eight-hour day, and the five-day week--has influenced the attitude towards work? The movies, the radio, and the NEUROSIS ASSOCIATED AVITH TRAUMA 513 automobile have encouraged newer concepts of living. Who of us that have sons or daughters around the age of fifteen years does not deprecate their attitude toivards Avork? Would anyone say that their attitude towards work is not different from that of their parents or grandparents? Finally, the character of one's experience varies not only as to the degree of contact but also as to the state of society one deals with. How often would malingering or neurosis be noted among the stolid, rugged men inhabiting the outposts of civilization. Would Dr. Grenfell, of Labrador, have noted the frequency of neurosis that a doctor prac ticing in Detroit or Pittsburgh, or a similar industrial center, expe riences? Manifestly, no; because in the first instance the very life of the individual is dependent upon his own efforts. He cannot fall back upon any benevolence created for his misfortune. The argument offered in the summary of this chapter is that the physician who considers the element of compensation as a factor in his estimation of the cause of neurosis or malingering should not be condemned as prejudiced. He is only considering all the factors Avhich comprise the entity and is just as sincere as the naval doctor who con siders lues in an old sea dog. REFERENCES 1. AVechsler, I. S.: "Trauma and the Nervous System," J.A.M.A., 104: (Feb. 16), 1935. 2. Davidson, H. A.: "Neurosis and Malingering," Am. J. M. Juris., 2: (Feb.), 1939. 3. Fetterman, J. L.: "The Neurosis Associated with Trauma," Indust. Med., 4: (Jan.), 1935. 4. Reichardt, quoted by Fetterman, ibid. 5. Lewy, E.: "Contribution to the Problem of Compensation Neurosis," Mellinger Clinic Bulletin, 4: (May), 1940. 6. Strauss, L, and Savitsky, N.: "Head Injury--Neurologic and Psychiatric Aspects," Arch. Neurol, and Psychiat., 31: (May), 1934. 7. Winkelman, N. W., and Eckel, J. L.: "Brain Trauma, Histology during Early Stages," Arch. Neurol, and Psychiat., 31: (May), 1934. 8. Sachs, B.: Remark made in discussion of AVinkelman and Eckel's paper, op. cit. 9. Hassim, G. B.: Remarks made in the discussion of AVechsler's paper, op. cit: 10. Winkelman, N. W.: "Brain Trauma, Histology during Early Stages," Arch. Neurol, and Psychiat., 31: (May), 1934. 11. Fetterman, J. L.: Op. cit. 12. Tunney, Gene: "A Man Must Fight," Collier's, March 26, 1932. 13. Munro, D.: "The Modern Treatment of Craniocerebral Injuries with special ref erence to the Maximum Permissible Mortality and Morbidity," New England J. Med., 213: (Nov. 7), 1935. 14. Bennett, W.: "Some Milder Forms of Concussion of the Brain," in Allbutt, T. S., and Rolleston, II. D.: A System of Medicine, by many writers. The MacMillan Co., London, 1910, Vol. 8, p. 231. 33 CHAPTER XXXIX THE PREEMPLOYMENT EXAMINATION Workers' Objections to Examination.--On first thought it would seem that there could be no possible objection on the part of the workman to the preemployment or routine periodic physical exami nation in industry. Actually, however, there exists a great deal of opposition. Workmen feel that the physician is an agent of the em ployer and as such will convey to him information ordinarily con sidered confidential. They fear that some minor physical defect may be detected and because of it, employment be denied. Labor unions have objected especially to the periodic examination of men under hire, claiming that this system is used by employers to get rid of men who the employer feels are undesirable or agitators. Objections to a physical examination are not without some valid reasons. The preemployment examination may be unjust to a work man in certain instances, especially in those states which arc extremely liberal in the granting of compensation for aggravation of a preexist ing condition. The potential hernia serves to illustrate this point. When it is detected and reported, the applicant is usually turned down for employment, even though the position sought is one not apt to call for excessive manual labor. But the employer knows that if the potential condition becomes an actual hernia, he will be held responsible by the accident commission. The applicant often is will ing to sign a statement relieving the employer of any responsibility, but this is not acceptable to commissions in the majority of states. The unfortunate victim of such a system is obviously the man who presents a minor physical defect and yet is able to work. Concerning the periodic physical examination, the objection raised is that if a physical defect is discovered, the workman will be discharged. Some industries honestly attempt to care for such an employee by changing his position and placing him in a department where effort is reduced. However, this commendable act is often blocked by the labor unions. In centers where the labor unions are strong, they insist in upholding the right of seniority and insist that if the man is placed in a dif ferent department, he goes in as a new man, losing his seniority. The answer to this dilemma is certainly up to the "National Labor Rela tions Board," or a similar governmental agency. 514 THE PREEMPLOYMENT EXAMINATION 515 Capacity to Work of Men of Forty.--Allied closely with the above two phases of the physical examination is the problem of the aging. Gerontology is now a unit of the National Health Institute. It is not a new problem, for Cicero wrote De Senectute in 45 or 44 b.c., but the period of "old age" has been extended in both directions. Thanks to medical science, the present mean life expectancy at birth has been increased to sixty-one years. Yet the prevailing opinion in industry is that the age when a man becomes old has been lowered. Thus a man in his forties today has difficulty obtaining a job because he is looked upon as being old. Men in the late forties and fifties are being replaced by younger men, thus being forced to sit idly by and increase the aging process. To any physician this is a great mistake. Sir Hum phrey Rolleston once stated', "There is more danger to the individual rusting out than wearing out." Except for certain occupations, not man's age but rather his capacity to work should determine his status. It is a pitiful thing to see the anguish on a man's face who wants to work, but who has been replaced by a younger man. In the vast socialization program being conducted by our government, there should be some system evolved which will find employment for these older men--not just a pension. Extent of Examination.--A preemployment examination should be comprehensive, and records should be of permanent value. When a defect is noted, the applicant should be informed, and he should be referred to his family physician. The latter should be permitted to have access to the findings noted by x-ra.y or laboratory examina tion. The plant physician has a great opportunity to advance pre ventive medicine by cooperating with the community physician in this respect. In some plants, a copy of the examination is given to the applicant so that he will understand why he has been rejected and so that he will attempt to remedy his defect. Routine ,-r-ray exami nation of the chest and tests for lues are advisable. Employee's Permission to Report Findings.--The physician who makes preemployment examinations and periodic reexaminations should be warned that this practice presents a legal problem. Roemer1 points out that by reporting to an employer the findings of a physical examination without first securing the permission of the employee, a doctor violates the patient's trust and in many instances the civil law of the state relating to confidential communications. According to Roemer, it is not safe to assume that when a workman submits to an examination at the request of his employer, he gives tacit per mission to the physician to communicate the findings to the employer. While the risk of a suit for slander is certainly not great, it is ad visable for a physician to protect himself by obtaining the written 516 OCCUPATIONAL DISEASES consent of the patient to make the examination and to disclose the findings to the employer or organization requesting the examination. This consent should (a) Grant permission to the physician to disclose the findings to the employer (b) Waive the patient's rights or other person's in the provisions of the law relating to confidential communications (c) Be signed by the patient (d) Dated as of the day of the examination Routine and Classification.--The best advice the author can give is that a comprehensive routine and a satisfactory method of classifi cation be established. Of all those that have been suggested, the method employed by Selby,2 at General Motors, appears best. The following is the substance of his discussion: Provision for Handicapped Workman.--In discussing this code, tuberculosis will be used as an example. Arrested tuberculosis falls in Class C. There are many occupations at which workmen with ar rested tuberculosis may be employed, provided they have medical supervision, and periodic examinations sufficiently often to guarantee them against aggravation by employment. Obviously, they cannot be employed on dusty work, regardless of the type of dust. Active tuberculosis (Class D) renders workmen unemployable. They are possible sources of the disease to others, and they need treatment, probably in a sanatorium. There are many men with defects requiring medical attention who are employable. Management is content to leave the responsi bility of that problem with the plant physician. He always gives the benefit of the doubt to the workman, and this is exactly as it should be. With him, the only question is whether or not employment will be harmful to the handicapped workmen. This should be the consideration with reference to the placement of this Class C group. Of course, on the reexaminations, Class C men should not be dis charged. The reason for the reexamination is to assist them to main tain their health while employed, to give them a longer period of gainful occupation. The details of the placement cannot be specified. Every doctor has to work them out for himself. He cannot do it unless he knows his plant. The doctor with imagination and inquisitiveness, who goes out in the plant and familiarizes himself with every possible occupation that may have influence on health, avails himself of the service of the in dustrial hygienist and works with the engineer for the control of the occupational-disease exposures, examines employees thoroughly be THE PREEMPLOYMENT EXAMINATION 517 fore placement, examines them after employment often enough to guarantee them against diseases that might result out of occupation, and institutes a complete health-maintenance program, in cooperation with the local general practitioners of medicine and health authori ties, is determining the place of physical examination in industry and effectively placing employees. He is the symbol of modern industrial medicine. Examination Record Code.--Findings are recorded by minus (--) or plus (+) signs to show absence or presence of defects, except where figures are called for, as with age, height, weight, pulse and blood pressure, or where special comments are needed, as with *-ray, etc. If description is required, an identifying numeral (1), (2), (3), etc., is placed after the plus sign in this manner (1), and details are recorded under "Remarks," with, the identifying numeral preceding the description. An applicant who has no defects (minus signs through out) is given a placement rating of Class A. Extent and degree of defects are recorded by one (-)-), two (-|--(-), or three (-|--|--1~) plus signs, and the placement rating is Class B, C, or D. Placement Code Class A (--).............. Physically fit for any work Class B (-)-)...............Defect negligible or correctable; otherwise fit for any work Class C (-1--[-).......... Defect limits fitness for work and may or may not need medical attention, but does require medical supervision Class D (-)--|--)-) ... .Defect requires medical attention and disquali fies for employment Classes A and B may be employed. Classes C and D may not be employed while qualifying conditions exist. If already employed, these classes require handling subject to instruction of the physician in conformity with restrictions set forth by him. 518 OCCUPATIONAL DISEASES Name: Table 20--Physical Examination- Record Address: Xalionalily: 1. Date 2. Reason 3- Age _1 \ ---- -- 4. Temperature 5. Height 0. Weight 7. Type 8. Vision--Par -- -- -- -- -- 9. Vision--Near 10. Eyes 11. Ears -- 12. Nose 13. Teeth 14. Throat -- -- 15. Neck 10. Fingers -- 17. Arms 18. Back -- 19. Equilibrium 20. Skin 21. Lungs 22. Heart ---- 23. Pulse 24. Hernia -- 25. Perineum 26. Legs 27. Feet -- -- 28. Abdomen !9. Blood Pressure -- >0. Rating d. Doctor THE PREEMPLOYMENT EXAMINATION Si. Urinalysis 38. Blood Analysis 31. Fluoroscopy 35. .T-Iiay Remarks: 519 Illustrative Classification.--No attempt is made to set up stand ards for exclusion, because medical judgment must be the basis of all decisions. The following classification is merely illustrative: Group I Epidemic, Endemic and Infectious Diseases: Acute infectious diseases, including measles, scarlet fever, erysipelas, ac tive tuberculosis (any organ)..................................................................... Class D Arrested tuberculosis............................................................................................. Class C Venereal diseases, acute........................................................................................ Class D Chronic venereal diseases undertreatment...................................................... Class B or C General Diseases: Group II Cancer--all forms................................................................................................... Class D Cancer--postoperative cure.......................................... Class C Benign tumors, disabling................... Class D Others..................................................................................................................... Class B or C Acute rheumatic fever, acute arthritis............................................................. Class D Chronic arthritis, marked deformity................................................................ Class D Other forms........................................................................................................ Class B or C Diabetes mellitus............................................................................................. Class D Under diet and control..................................................................................... Class C Pernicious anemia................................................................................................... Class D Under diet and control...................................................................................... Class C Secondary anemia, severe..................................................................................... Class D Mild......................................................................................................................... Class B or C Leukemias.................................................................................................................. Class D Hodgkin's disease.................................................................................................... Class D Chronic poisoning, lead, etc................................................................................. Class D Drug addiction......................................................................................................... Class D Diseases of the Nervous System: Group III General diseases such as encephalitis, meningitis, sclerosis, cerebral hem orrhage or thrombosis, epilepsy, chorea, convulsions, psychosis, im becility, neurasthenia (severe), brain tumor......................................... Class D Neurasthenia (mild), neuritis, etc...................................................................... Class B or C 520 OCCUPATIONAL DISEASES Diseases of the Eye: Vision 20/100 or hotter, both eyes, without correction.............................. One eye blind or defective 20/200 or less with or without glasses......... Both eyes 20/200 or less with or without glasses......................................... Trachoma, glaucoma, etc...................................................................................... Class B Class C Class D Class D Diseases of the Ear: Chronic suppurative otitis media, one ear. ............................................... Class C Both ears............................................................................................................... Class D Hearing normal tones of voice............................................................................ Class A Otherwise................................................................................................................... Class B Disease of the mastoid, not resolved................................................................. Class D Diseases of the Circulatory System: Gnoup IV Active pericarditis, endocarditis, myocarditis, angina pectoris................ Class D Other diseases of the heart, if well compensated.......................................... Class C Decompensation or history of severe decompensation................................ Class D Diseases of the Arteries: Aneurysm, severe embolism or thrombosis, varicose veins with ulcer, hemorrhoids, severe....................................................................................... Class D Varicose veins, moderate...................................................................................... Class C Varicocele................................................................................................................... Class B Hemorrhoids, moderate......................................................................................... Class B or C Diseases of the Respiratory System: Ghoup V Sinusitis, acute............................................. . Chronic.................................................................. Bronchitis, acute..................................................... Chronic.................................................................. Asthma, mild............................................................ Severe..................................................................... Silicosis, first stage................................................. Second stage........................................................ Third stage........................................................... Pneumonia, pleurisy, empyema, gangrene. . . Class D Class C Class D Class C or D Class B or C Class D Class B Class C Class D Class D Diseases of the Digestive System: Group VI Acute tonsillitis, quinsy, acute peptic ulcer, acute enteritis, pancreatitis, acute appendicitis, acute yellow atrophy, acute cholecystitis......... Class D Chronic peptic ulcer, chronic cholecystitis, chronic appendicitis............ Class B or C Hernia, unsupported.............................................................................................. Class D Supported.............................................................................................................. Class C Gkoop VII Diseases of the Genito-urinary System: Acute nephritis, acute cystitis, acute pyelitis, acute prostatitis, acute salpingitis.......................................................................................................... Class D Chronic infections as above if under treatment............................................ Class C Pregnancy.................................................................................................................. Class D Pregnancy if self-support necessary, first four months only..................... Class C Diseases of the Skin: Gnoup VIII Acute abscesses, carbuncles, poison ivy, extensive dermatitis, severe eczema, scabies................................................................................................ Class D THE PREEMPEOYMENT EXAMINATION 521 Guocp IX Diseases of the Bone and Organs of Locomotion: Osteomyelitis, acute and chronic....................................................................... Amputations, fingers, limited.............................................................................. Many fingers or other extremities..................................................................... Scoliosis, kyphosis, lordosis, ankylosis, myalgia............................................ Class D Class C Class C or D Class B, C, or D REFERENCES 1. Roemer, M. L.: "Sued for Slander," Med. Economies, 18: 67, 1941. 2. Selby, C. D.: "The Place of Physical Examinations in Industry," read before the Occupational Disease Symposium, Northwestern University Medical School, Sept. 26, 1938. APPENDIX Table of Toxic Thresholds of Common Industrial Substances The following list of suggested maximum permissible concentra tions of potentially harmful industrial dusts, gases, vapors, and fumes is recommended by the Industrial Accident Commission of California. With but few exceptions it agrees with the one compiled by Bowditch, Drinker, et al.1 Substance Dusts: Asbestos.............................. Cement.............................. Organic.............................. Pottery.............................. *Silica (25 to 35% Si02) Silica (over 75% Si02).. Slate.................................... Talc.................................... Limit Million Particles per Cubic Foot ........... 5 (0.5 to 10.0 n) .................... 15 .................... 50 (0.5 to 5.0 n) ............. 4 ............. 10 (0.5 to 5.0 ti) .................... 5 (0.5 to 5.0 n) ................... 15 .................... 15 Gases and Vapors: Acetone....................... Ammonia.................... Amyl acetate............. Aniline...................... .. Arsine.......................... Benzol......................... Butanol....................... Butyl acetate............ Carbon disulfide.... Carbon dioxide......... Carbon monoxide. .. Carbon tetrachloride Chlorine...................... Chloroform................ Dichlorbenzene......... Dichlorethyl ether. . Ether (ethyl)............. Ethyl alcohol............ Ethyl bromide.......... Ethyl chloride........... Ethylene dichlorido. Formaldehyde........... Gasoline...................... Hydrogen cyanide. . Hydrochloric acid... Parts per Million 200 100 400 . 1 100 100 400 15 5,550 100 100 1 100 75 15 400 250 1,700 20,000 100 20 1,000 20 10 * Dust count (million particles per cubic foot of air), multiplied by percentage of free silica (silicon dioxide), should be less than 5. 523 524 OCCUPATIONAL DISEASES Gases and Vapors: Parts per Million Hydrogen fluoride......................................................................................... Hydrogen sulfide........................................................................................... Methanol.......................................................................................................... Methyl bromide............................................................................................. Methyl ehloride............................................................................................. Monochlorbenzene........................................................................................ Naphtha........................................................................................................... Nitrobenzene.................................................................................................. Nitrogen oxides.............................................................................................. Ozone................................................................................................................ Phosgene.......................................................................................................... Phosphine........................................................................................................ Phosphorus trichloride................................................................................ Sulfur dioxide................................................................................................. Tetrachlorethane........................................................................................... Tetrachlorethylene........................................................................................ Toluol............................................................................................................... Triehlorethylene............................................................................................ Turpentine...................................................................................................... Xylol and coal-tar naphtha....................................................................... 3 20 100 50 500 75 5,000 1 10 1 1 2 0.7 10 10 200 100 200 700 100 Metallic Dusts and Fumes: Milligrams per Cubic Meter Cadmium........................................................................................................... 0.1 Chromic acid.................................................................................................... 0.1 Lead..................................................................................................................... 0.15 Manganese........................................................................................................ 50 Mercury.................................................................................................. 0.1 to 0.2 Zinc oxide.......................................................................................................... Chlorodiphenyl................................................................................................. Pentachlornaphthalene.................................................................................. Trichlornaphthalene....................................................................................... 15 1.0 0.5 5.0 REFERENCE 1. Bowditch, M., Drinker, C. K., Drinker, P., Haggard, H. H., and Hamilton, Alice: "Code for Safe Concentrations of Certain Common Toxic Substances Used in Industry," J. Indust. Hyg. and Toxicol., 99 (June), 1940. INDEX Abdomen, traumatic conditions, 490 Abdominal pains from arsenic, 295 from back pain, 387 from caisson disease, 483 from ethylene dichloride, 145 from heat cramps, 406 from lead, 222 treatment, 247 from methyl chloride, 164, 167 from selenium, 289 Abortion from arsenic, 239 from plumbism, 239 Abrasive dust, effects, 355 materials, worker, silicosis hazard, 307, 320 soap dermatoses, 452 Absorption of lead, 222 Acceptance in workmen's compensation, 9 Accident commissions on hernia, 424 operation, 43 from carbon monoxide poisoning, 181 in workmen's compensation, 4 occupational, effects, 4 prevention, 45 Acetone breath from methyl chloride, 165 Acetonitrile, 199 Acetonuria in methyl chloride poisoning, 165 Acetyl-/3-methylcholine in ventricular fibril lation, 481 Achilles tendon reflex in retropulsion of in tervertebral disc, 386 Achylia from benzene, 73 Acid dermatoses, 436 care, 452 fumes, carcinogenic, 460 in dermatitis artefacta, 448 therapy, effect on serum lead, 234 Acidosis from carbon dioxide, 161 from carbon tetrachloride, 102 from deleading, 250 from heat affections, 474 from mercury, 264 from methyl alcohol, 169 from nitrobenzene, 144 from nitrous fumes, 206 from sulfur dioxide, 163 Acne from tar, 436 Act, compensation, first real, 2 Employer's Liability, 1 Workmen's Compensation, purpose, 2 Actinic rays, carcinogenic, 460 Activity, limited, in dust diseases, 375 Actuarial background of permanent disabil ity, 34 Addiction to trichlorethylene, 139 Adenitis in infectious eczematoid derma titis, 443 Adjustment of claim, 27 Administration of workmen's compensation, 3, 7 Adrenal gland, cadmium and, 284 Aeration in carbon dioxide poisoning, 161 Age in anthracosilicosis, 342 in cement dust exposure, 360 in disability ratings, 35, 37 in estimation of benefits, 28 in eye cancer, 463 of employee, misconduct and, 26 Agents in adjustment of claim, 27 Aging, preemployment examination and, 515 Ague, brass-founders, 208 metal, 208 Air analysis in benzene poisoning, 79 concentration of ammonia, 171 of anthracite particles, 341 of asbestos, 353 of carbon monoxide, 178 of carbon tetrachloride, 102 of hydrocyanic acid, 199 of lead, 237 of manganese, 269, 273 of mercury, 256 of methyl alcohol, 168 of nitrous fumes, 205 of silica dust, 306 of sulfur dioxide, 161 of trichlorethylene, 137 of zinc, 299 emboli of nitrogen, 483 insufflation in back pain, 419 lead dust, sampling, 237 Airplane dope employees, benzene hazard, 67 Albuminuria from carbon monoxide, 184 from carbon tetrachloride, 102 from gasoline, 96 from mercury, 259 Alcohol, caisson disease and, 484 carbon disulfide and, 121, 125 carbon monoxide and, 183 carbon tetrachloride and, 102, 113 gases and, 65 in hernia injection, 433 lead and, 250 mercury and, 255 nitrobenzene and, 143 phenol and, 173, 174 Alibour water in dermatoses, 455 in infectious eczematoid dermatitis, 456 Aliphatic solvents, sources, effects, 65 Alkali dermatoses, 436, 452 dust, silica and, 306 in dermatitis artefacta, 448 Allegations of workman in hernia, 422 525 526 INDEX Allergy in back pain, 389 Aniline, carcinogenic, 460 in dermatoses, 436 dyes, making, hazard of arsenic, 294 in epidermophytosis, 442 of benzene, 67 to borax, 364 of methyl alcohol, 167 to chromates, 275 of nitrobenzene, 142 to cotton dust, 367 poisoning, stippled cells in, 225 to gases, 65 tumors, 462 to mill dust, 373 Ankle clonus from manganese, 269 Alloys corrosion, x-rays and, 337 sprained, treatment, 417 manufacture, hazard of antimony, 301 Annulus fibrosus, 384 of cadmium, 278 Anorexia from antimony, 301 of manganese, 266 from benzene, 73 Almond odor from cyanides, 200 from benzine, 89 Alpha-tocopherol in arsenic neuritis, 298 from carbon dust, 367 Aluminosis, 304 from carbon monoxide, 179 Aluminum acetate in dermatoses, 455 from carbon tetrachloride, 102 dust, silicosis and, 307, 376 from lead, 222 manufacture, hazard of fluorine, 146 from nitrous fumes, 205 of manganese, 266 from silicosis, 308 oxide, effects, 355 from trichlorethylene, 137 in cement, 357 Anoxemia from carbon monoxide, heart and, in welding, 211 185 Alveolar consolidation from silicosis, 309 treatment, 197 Amblyopia, causes, 120 from cyanides, 199 from carbon tetrachloride, 102 symptoms, 187 from trichlorethylene, 137 Aphasia in caisson disease, 484 Amido compounds, effect on blood, 142 Anthelmintic use of carbon tetrachloride, Ammonia, 171-172 103 Ammonium carbonate in nitrous-fume poi Anthracite-coal miners, hazard of anthraco- soning, 206 silicosis, 340 chloride in deleading, 249 of tuberculosis, 317, 342 . persulfate dermatitis in bakers, 444 Anthracosilicosis, 340-347 Amphetamine in mercury poisoning, 265 carcinoma and, 316 Amputation, results, rating, 36 conglomerate, 345 Amyl nitrite in cyanide poisoning, 204 definition, 340 Amyostatic symptoms from manganese, 267 disability in, 39 Analgesia in back pain, 416 prevalence, 341 in cadmium poisoning, 286 treatment, 347 in metal-fume fever, 209 Anthracosis, 304 in nitrous-fume poisoning, 207 Antifreeze-makers, methyl alcohol hazard, Anemia from arsenic, 298 167 from benzene, 69, 73 Antimony, 301 treatment, 81 from livingstonite concentrate, 260 from benzine, 89 lead and, 218 from carbon disulfide, 117 Antiseptic-dressing manufacture, mercury from carbon tetrachloride, 113 hazard, 254 from gases, 63 Anuria from methyl chloride, 164 from lead, 220, 232 Anxiety from tetraethyl lead, 91 from methyl alcohol, 168 Aorta, degeneration, in back pain, 388 from methyl chloride, 164, 167 Apathy from carbon monoxide, 179 from nitrobenzene, 142 from petroleum, 88 from petroleum, 88 Aplasia, medullary, benzene and, 68 treatment, 99 Appendicitis, lead and, 217 from telrachlorethane, 134, 136 strain and, 490 from vanadium, 292 traumatic, 488 from zinc, 300 cases, 489 stippled cells in, 225 postulates, 489 Anesthesia from carbon tetrachloride, 102 relationship, 485 from methyl chloride, 164 Application for adjustment of claim, 27 spinal, in herniotomy, 431 Aprons, oilcloth, in cancer prevention, Anesthetics, chlorinated naphthalenes and, 463 128 Arc radiation from welding, 210 Angina pectoris from carbon disulfide, 121 Arguments in workmen's compensation, 5 from carbon monoxide, 186 Arm, loss, period of payment, 19 Angle, lumbosacral, 409 rating, 34 INDEX 527 Aromatic amines, cancer from, 462 Autopsy in benzene poisoning, 77 solvents, sources, effects, 06 in cadmium poisoning, 283 Arsenic, 294-298 in chlorinated naphthalene poisoning, 130 carcinogenic, 460 - in heat affections, 466 Arsine, 294 in hydrogen sulfide poisoning, 156 effect on liver, 64 in trichlorethylene poisoning, 137 poisoning, treatment, 298 Awkwardness in disability estimation, 31 Arteriosclerosis, plumbism and, 238 in workmen's compensation, 5 silicosis and, 315 Azochloramide in electrical burns, 482 Artery diseases, employability and, 520 Art-glass workers, fluorine hazard, 146 Back, congenital defects, correction, 418 Arthritis from selenium, 289 contusion, treatment, 416 in butchers, 467 disorders, traumatic, neurosis in, 500 Arthrodesis in unstable lumbosacral joints, industrial, 381-419 419 pain, cases, 395 Articular facets in back pain, 383 examination of patient, 393 process, failure of fusion, 402 from benzine, 89 spine, anomalies, 400 medicolegal aspects, 395 Asbestos action, silica and, 349 relation to work, 381 handling, asbestosis hazard, 348 sources, 382 silica in, 305 classification, 389 Asbestosis, 304, 348-354 sprain, causes, 382 bodies, 352 diagnosis, 382 control, 379 examination of, 53 disability in, 39 findings, 393 medicolegal aspects, 353 rejected basis, 390 treatment, 354 status of compensability, 390 .-c-ray findings, 353 treatment, 415 Ascorbic acid in benzene poisoning, 83 strain, treatment, 416 in plumbism, 250 supports for congenital defects, 419 Aspergillus glaucus in cotton dust, 367 Backache, 4 Asphalt roads, cancer hazard, 462 Bacteria, effect of metal fumes, 208 Asphyxia from carbon monoxide, 176, 178 Baker's dermatitis, 441, 444 delayed symptoms, 179 Balers, cotton dust hazard, 367 from gasoline, 89 Barber's dermatitis, 446 from hydrogen sulfide, 156 Barbiturates in fluorine treatment, 153 types, 176 Barite ground, analysis, 335 "Assumption of risk," 1 Barium rock hazard, 335 Asthenia from anthracosilicosis, 343 Barytosis, 335 Asthma from borax, 365 Basal metabolism increase from selenium, from chromium, 275 290 from cotton dust, 366 Basophilia, 224 from fluorine, 153 Basophilic aggregation test, 226 from smuts, 393 Bassini herniotomy, 431 from sulfur dioxide, 162 Bathtub enameling, lead hazard, 216 miner's, 340 Battery manufacture, hazard of benzene, 67 silicosis and, 313 of lead, 216 Ataxia from ethylene dichloride, 145 Bechterew's sign, 414 Atmosphere analysis in benzene poisoning, Bed rest in back pain, 416 74 "Bends," 483 cold, effects, 466 Benefits, death, 12, 26 Atrophy of leg in retropulsion of interver in disability, enforcement of payment, 28 tebral disc, 386 partial, permanent, 15 Atropine in methyl alcohol poisoning, 170 period of payment, 19 Attendants, gasoline-station, poisoning in, 89 total, permanent, 13 Attorneys in adjustment of claim, 27 temporary, 17 Autohemagglutination in benzene case, 83 in workmen's compensation, 3 Autoist, hazard of carbon monoxide, 181, limitation by states, 20 195 maximum, 12-18 of coal-tar cancer, 462 by states, 21 Automobile workers, hazard of asbestosis, medical, limitation, 48 348 minimum, 12-18 of cadmium, 277, 278 payment, 7 of oil, 463 workmen's, limited, 3 of petroleum, 88 Bentonite, analysis, 335 528 INDEX Benzene, 67-87 Blood, manganese in, 269 conjugation in liver, 64 oxygen, effect of carbon monoxide, 177 effect on blood-forming organs, 66 of silicosis, 319 in gasoline, 89 picture in poisoning by benzene, 70 in lymphatic leukemia, 63 by methyl cellulose, 74 occupational hazards, 67 by nitrobenzene, 142 poisoning, diagnosis, 73 by tetraehlorethane, 134 illustrative cases, 75-79 pressure, effect of antimony, 301 latent effects, 64, 69 of carbon dioxide, 160 medicolegal aspects, 74 of carbon tetrachloride, 109 pathology, 67 of hyperpyrexia, 465 prophylaxis, 79 of metal fumes, 208 stippled cells in, 225 of methyl chloride, 165 treatment, 79 of tetraethyl lead, 91 Benzol, 64, 67. See also Benzene. saturation of gases, solvents, 65 Benzine, 67, 88 tests in carbon monoxide poisoning, 179, Benzoin in back strapping, 417 182 Benzonitrile, 199 transfusions in poisoning by arsine, 298 Bertolotti's syndrome, 382 by benzene, 81 Bichromates, 274 by carbon monoxide, 198 Bile salts in tetraehlorethane poisoning, 135 by carbon tetrachloride, 113 Biopsy in benzene poisoning, 74 by mercury, 264 in traumatic cancer, 498 by petroleum, 99 Bladder tumors from amido compounds, 143 by tetraehlorethane, 136 Blast-furnace workers, hazard of carbon by trichlorethylene, 140 dioxide, 160 vessels in silicotic lungs, changes, 311 of carbon monoxide, 176 volume, effect of heat, 465 of sulfur dioxide, 161 Blue line of gums, 224 Bleachers, hazard of chlorine, 154 Boards in bed for low back pain, 416 of fluorine, 146 Boards, industrial, 3 of sulfur dioxide, 161 Body functions, effect on stored lead, 219 Bleeding from benzene, 72, 81 Boiler workers, blindness from flame, com Blepharitis from cotton dust, 367 pensability, 473 Blind spot, carbon disulfide and, 120 hazard of carbon dioxide, 160 Blindness from carbon monoxide, 179 of heat, 465 from trichlorethylene, 137 of mercury, 254 Block, intraventricular, from carbon monox Boiling of blood for carbon monoxide, 183 ide, 189 Bone diseases, employability and, 521 Blonds, dermatoses in, 450 effect of arsenic, 295 Blood calcium, effect of carbon tetra of fluorine, 148 chloride, 102 lead in, factors affecting, 247 of fluorine, 147 marrow in benzene poisoning, 68, 77, 80, of manganese, 266 83 carbon disulfide in, 117, 121 oils extraction, carbon disulfide hazard, cells, lead content, 235 115 red. See Erythrocytes. solvent, trichlorethylene hazard, 137 white. See Leukocytes. storage of lead, 218 chlorides, effect of mercury, 256 jr-rays, for lead, 237 collection for lead analysis, 237 Bookbinders, arsenic hazard, 294 count in poisoning by benzene, 74, 79 Borax, dust hazard, 364 by carbon tetrachloride, 109 Botulism, arsenic versus, 295 by lead, 232 Bowel perforation in hernia injection, 433 by mercury, 262 Braces for congenital back defects, 419 effect of benzene, 72 Bradycardia from tetraethyl iead, 91 of /3-naphthylamine, 462 Brain atrophy from manganese, 267 of carbon disulfide, 120 edema from tetraehlorethane, 134 of carbon tetrachloride, 109 from tetraethyl lead, 91 of gases, solvents, fumes, 63 in heat affections, 466 of manganese, 266 effect of carbon disulfide, 119 of nitrous fumes, 205 of carbon monoxide, 177 forming organs, effect of benzene, 66 of traumatic neurosis, 505 of petroleum, 88 hemorrhage from benzene, 75 lead content, 234 from electricity, 479 after removal from exposure, 236 1 from ethylene dichloride, 145 fate, 218 from tetraethyl lead, 91 INDEX 529 Brain irritation from selenium, 28!) Cadmium, effect on liver, 64 subarachnoid hemorrhages, benzene and, fumes from welding, 211 69 poisoning, cases, 279 Brass chills, 208 delayed reaction, 277 founders, ague in, 208 incidence, 277 hazard of arsenic, 294 medicolegal aspects, 279 of nitrous fumes, 20,5 treatment, 286 of zinc, 299 Caffeine in carbon monoxide poisoning, 198 Bread-dough dermatitis in bakers, 444 Caisson disease, 483-484 Breath, garlic odor, from selenium, 289 workers, hazard of carbon dioxide, 160 sounds, change, from anthracosilicosis,340 of hydrogen sulfide, 156 Breathing, asphyxia and, 170 Cake-dough dermatitis in bakers, 444 capacity in silicosis, 319 Calcined magnesium, inert dust, 356 Brewers, hazard of carbon dioxide, 100 rasorite, effects, 364 of fluorine, 146 Calcium carbonate hazard, 356 Brick manufacturing, silicosis hazard, 307 fluoride in welding, 211 Bricklayers, cement dermatitis, 446 in deleading, 246 Bridge builders, caisson disease, 483 in poisoning by benzene, 83 Briquet-makers, arsenic hazard, 294 by carbon tetrachloride. 111 Bromine, 154 by ethylene dichloride, 145 Bronchiectasis from grain, 374 by fluorine, 152 in asbestosis, 348 by manganese, 273 in silicosis, 313 by mercury, 264 Bronchiogenic carcinoma, back pain in, 397, by methyl chloride, 167 398 by tetrachlorethane, 136 Bronchiolectasis in asbestosis, 348 in welding, 211 Bronchitis, effect of cement dust, 362 metabolism, effect of carbon tetrachloride, of sulfur dioxide, 161 102 from cold, 466 of lead, 218 from cotton dust, 366 Calculation of disability indemnity, 25 from hydrogen sulfide, 156 Calico printing, hazard of arsenic, 294 from silicosis, 315 of manganese, 266 from vanadium, 292 California, permanent disability in, 31 Bronchodilator vapors in dust diseases, 375 rating schedule, 37, 38 Bronchopneumonia from asbestosis, 348 Workmen's Compensation Act, digest, 21 from cadmium, 279, 282 Cancer, gas tar, 459 from hydrogen sulfide, 157 in back pain, 391 from petroleum, 98 lung, chromium and, 276 from silicosis, 313, 315 non-occupational, 60 Bronze diabetes, copper and, 300 silicosis and, 316 Bronzers, hazard of arsenic, 294 occupational, 435, 459-464 of benzene, 67 treatment, 463 Buerger's disease, effect of cold, 467 of eye, 462 Buffers, petroleum hazard, 88 of prostate in back pain, 395, 396 Bullae in dermatoses, treatment, 455 traumatic, 496 Bureau of Industrial Accident Prevention, history, 497 45 postulates, 497 Bureaus, industrial, 3 Cannery workers, onychia, 449 Burial expense in industrial death, 26 Capillary occlusion in silicosis, dyspnea Burns from carbon tetrachloride, 107 from, 311 from electricity, 478 Carbohydrates in carbon tetrachloride poi treatment, 481 soning, 112 from fluorine, 147 in selenium poisoning, 291 treatment, 153 Carbolic acid poisoning, arsenic versus, 295 from zinc chloride, 300 Carbon arc booths, nitrous-fume hazard, trauma in, 488 205 Butchers, disease aggravation in, 467 gases from, 212 epistaxis, compensability, 472 types, 212 "Butterfly wing" sacralization, 400 dioxide, 160-161 Butyn in hydrogen sulfide poisoning, 159 from carbon arcs, 213 Byssinosis, 304, 366 in carbon monoxide poisoning, 197 in welding, 211 Cachexia from cyanides, 201 occurrence, 160 Cadmium, 277-287 disulfide, 67, 115-126 compounds, 277 effect on nervous system, 66 34 530 INDEX Carbon disulfide, group study, ] 1.3 Ceinenlersof rubber, methyl alcohol hazard, poisoning, eases, 143-135 167 diagnosis, IIS Ceramic industries, silicosis hazard, 307 medicolegal aspects, 144 Certificate of consent to self-insure, 42 symptomatology, composite, 121 Cervical rib, 401 treatment, 143 Chalicosis, 304 production, Iivdrogen sulfide hazard. Chalk, inert dust, 356 150 Charcoal burner employees, carbon dioxide dust, 356 hazard, 160 monoxide, 175-198 carbon monoxide hazard, 170 carbon dust and, 307 in mercury poisoning, 263 effects, 60 Chauffeurs, petroleum hazard, 88 from carbon arcs, 213 Chemicals, eye cancer from, 462 from welding, 211 handlers, hazard of dermatoses, 435 hemoglobin, 177 of hydrogen sulfide, 157 poisoning, cases, 191 of mercury, 254 chronic, 179 of selenium, 291 diagnosis, 177 Chemotherapy in cadmium pneumonia, 287 in gasoline-station attendants, 89 Chest burning from chlorine, 154 medicolegal aspects, 190 from vanadium, 292 sequelae, 183 oppression in cotton dust exposure, 368 tetrachloride, 100-113 pain from anthracosilicosis, 340 effect on liver, 64 from cadmium, 278 in uremia, 64 from gasoline, 93 occupational hazards, 100 from mercury, 255 poisoning, cases, 104-111 from silicosis with infection, 315 diagnosis, 102 from trichlorethylene, 137 epinephrine, avoidance, 481 signs in asbestosis, 348 exposure outside industry, 103 Chills, brass, 208 medicolegal aspects, 103 from malt dust, 374 treatment, 111 zinc, 208 Carbonol, 167 China manufacture, silicosis hazard, 322 Carborundum, silica in, 305 Carcinoma. See Cancer. Chlorides in heat cramps, 466 Chlorinated diphenyls, 127-133 Carders, cotton dust hazard, 367 naphthalenes, 127-133 Cardiac. See Heart. Chlorine, 154-155 Carding, asbestosis hazard, 348 Chloroform in mercury poisoning, 257 Cardiovascular diseases, effect of cold, 476 makers, methyl chloride hazard, 164 Carpenter, heatstroke, compensability, 469 tetraehlorethane and, 134 Carpet-makers, arsenic hazard, 294 Chlorohydrocarbons, effect on liver, 66 Carroters, arsenic hazard, 294 Cholesterol, serum, effect of carbon disul Cartilaginous plates of intervertebral disc, fide, 120 384 Chromate dust, oancerogenio, 402 Casein in selenium poisoning, 291 Chromatolvsis of nerve cells from electricity, Cataracts from electricity, 478 479 Catarrh, chronic, from sulfur dioxide, 161 Chrome dermatitis, protection against, 453 respiratory, from cotton dust, 366 "holes," 436 Catharsis in poisoning by carbon tetra Chromium, 274-276 chloride, 113 carcinogenic, 460 by manganese, 274 silica and, 305 by selenium, 291 Chrysolite mining, asbestosis hazard, 348 Caustics fumes, carcinogenic, 461 Cilia in dust elimination, 308 in dermatitis artefacta, 448 Cinnabar mining, mercury hazard, 256 Cavitation from silicosis with infection, Cinnamon dermatitis in bakers, 444 315 Circulation time in silicosis, 319 Ceeostomy in mercury poisoning, 264 Circulatory adjustment in hyperpyrexia, Cellulitis in infectious eezematoid derma 465 titis, 443 collapse from arsenic, 297 Cellulose acetate tetraehlorethane hazard, from carbon tetrachloride, 114 134 from petroleum, 98 workers, sulfur dioxide hazard, 161 in heal exhaustion, 475 Cement dermatitis, 446 complications from fluorine, treatment, dust, 357 152 handlers, dermatosis hazard, 435 disorders in back pain, 387 furunculosis, 436 measures in heatstroke, 475 INDEX 531 C'ii'culutory measures in poisoning by Color makers, hazard of methyl chloride, ammonia, 172 164 by cyanide, 203 Colored-paper workers, arsenic hazard, 294 by phenol, 173 Columbia spirits, 167 system diseases, employability and, 520 Coma from carbon dioxide, 160 Cirrhosis, liver, from carbon tetrachloride, from carbon disulfide, 118 100-102 from carbon tetrachloride, 102 from manganese, 200 from fluorine, 147 Claim adjustment, application, 27 from hydrogen sulfide, 156 handling, 49 from methyl alcohol, 168 number, increase, for back sprain, 381 from methyl chloride, 164 rejection, 0 from nitrobenzene, 142 ('lay worker, silicosis hazard, 322 from tetrachlorethane, 134 Cleaning, gasoline in, poisoning and, 90 Commission, industrial, 3 Cleanliness in occupational dermatoses, 430 on excluded employments, 22 Cleansing agents, dermatoses, 452 Common-law right of action in silicosis, 326 Climatic affections, 405-477 workmen's compensation in, 2 arising out of employment, 407 Commonwealth liability in silicosis, 42 Clonus from manganese, 209 Compensability of back sprains, status, 390 Clothes, care, in dermatoses, 437, 451 of cases, 5 in poisoning by ammonia, 172 of hernia, 421 by chlorine, 155 prerequisites, 421 by nitrobenzene, 143 Compensation, 24 by phenol, 173 acts, first real, 2 by sulfur dioxide, 162 by employer in silicosis, 40 in prevention of heat affections, 474 by state in silicosis, 41 Clubbed fingers from anthracosilicosis, 340 department of Industrial Accident Com Coagulation time in benzene poisoning, 73 mission, 44 Coal, carbon dust, 356 enforcement, time limit, 27 eye cancer from, 462 elective, 7 gas, 176 forfeitures, 26 miners, hazard of carbon dioxide, 160 in benzene poisoning, 69 of carbon monoxide, 176 in Employer's Liability Act, 2 of silicosis, 307 insurance carrier, 22 tar, carcinogenic, 460 nature, 24 paste in dermatoses, 455 neurosis, 509 arsenic hazard, 294 penalties, 26 chromium hazard, 274 rejection, 9 Cobalt, silica and, 305 variability in states, 10 Codeine in fluorine poisoning, 152 workmen's, purpose, 1 Coke-oven workers, sulfur dioxide hazard, Complexion from carbon disulfide, 119 161 in preemployment examinations, 450 Cold, effect on Buerger's disease, 467 Complications in hernia injection, 433 reactions, prophylaxis, 475 Compressed-air illness, 483 sensitivity, 476 Compulsion in workmen's compensation, 7 weather, effects, 466 Concentration, lack, from mercury, 255 Colds, effect of sulfur dioxide, 161 Concussion, 500, 501 in butchers, 467 effect on unconsciousness, 508 Cold-storage workers, disease aggravation Condensers, electrical, chlorinated naph in, 467 thalene hazard, 127 hazards, 466 Confusion from carbon monoxide, 179 Colic from antimony, 262 from phenol, 173 from benzene, 73 from trichlorethylene, 137 from lead, 221 Congenital anomalies of spine, 400 Colitis from mercury, 255 Congestion from trichlorethylene, 137 Collapse from carbon monoxide, 178 Conjunctivitis from ammonia, 171 Collar-fusing workers, methyl alcohol haz from cotton dust, 367 ard, 167 from cyanides, 200 Collodion in patch testing, 439 from petroleum, 99 Colloidal gold curve in manganese poison from vanadium, 292 ing, 269 Consciousness, effect of concussion, 508 Colon irrigation in mercury poisoning, 264 Consolidation of lung from anthracosili Colonial spirits, 167 cosis, 344 Color index in benzene poisoning, 72 Constipation from antimony, 301 makers, hazard of arsenic, 294 from fluorine, 153 532 INDEX Constipation from lead, 222 Cough from cadmium, 278 from nitrous fumes, 205 from carbon tetrachloride, 102 Constitutional therapy in dermatoses, 455 from chlorine, 154 Construction work, silicosis hazard, 307 treatment, 155 Contaminant, nature, concentration, 64 from cotton dust, 366 Contracture, lumbosacral, in back pain, 383 from fluorine, 152 Contrecoup in traumatic lung cancer, 498 from malt dust, 374 "Contributory negligence," I from nitrous fumes, 205 Contusion in hack pain, 390, 410 from selenium, 289 Convalescence in tetraethyl lead poisoning, from silicosis, 307 92 with infection, 315 Convulsions from benzene, 78 from vanadium, 292 from carbon monoxide, 179 in dust elimination, 308 from carbon tetrachloride, 102 mixtures in dust diseases, 375 from cyanides, 199 syrups in cadmium poisoning, 286 from electricity, 479 Court testimony, 50 from fluorine, 147 Coverings in welding, 211 treatment, 153 Cracker Stillman, hydrogen sulfide hazard, from hydrogen sulfide, 156 from methyl chloride, 164 157. Cracking of oils, effect on carcinogenesis, 461 treatment, 167 hydrogen sulfide hazard, 157 from nitrobenzene, 142 Cranial nerves, effect of lead, 221 from petroleum, 88 Creams, protective, in dermatoses, 453 from selenium, 289 Crepe soles, manufacture, trichlorethylene Cooks, carbon monoxide hazard, 176 hazard, 137 Cooling in heatstroke, 475 Crying from carbon disulfide, 118 Copper, 300-301 Cryolite, 146 alloy making, hazard of antimony, 301 Crystal quarrying, silicosis hazard, 307 of selenium, 288 Crystalline substances, diffraction pattern, dipping, nitrous-fume hazard, 205 337 mining, silicosis hazard, 307 Curriers, arsenic hazard, 294 silica and, 305 Cut-glass workers, arsenic hazard, 294 sulfate test for carbon monoxide, 183 Cyanides, 199-204 workers, hazard of arsenic, 294 poisoning, carbon monoxide and, 176 of manganese, 266 cases, 201 Coramine in trichlorethylene poisoning, 140 medicolegal aspects, 200 Corn oil extraction, trichlorethylene hazard, tests, 200 136 Cyanogen, 199 Cornea, injury in welding, 212 chloride, 199 opacities from chlorine, 154 compounds, 199 from ethylene dichloride, 145 making, mercury hazard, 254 reflex, effect of carbon disulfide, 121 rash, 200 smoking, from ethylene dichloride, 108 Cyanosis from anthracosilicosis, 340 ulcers from hydrogen sulfide, 159 from arsenic, 297 from sulfur dioxide, 163 from asbestosis, 348 Coronary disease from carbon monoxide, from electricity, 479 186 from gasoline, 93 occlusion, carbon monoxide and, 190 from methyl chloride, 165 Corpuscular hemoglobin, mean, in benzene from nitrobenzene, 142 poisoning, 71 from nitrous fumes, 205 volume, mean, in benzene poisoning, 71 from phosgene, 140 Corrosion from fluorine, 147 from silicosis, 308 Coryza from cement dust, 362 Cylindruria from carbon tetrachloride, 102 from cold, 466 from vanadium, 292 Cosmetic dermatitis, 437 "Danbury shakes" from mercury, 255 Cosmetician's dermatitis, 446 Death, benefits in, 12 Cotton dust, 362, 366 life pensions and, 34 hazard, case, 367 time limit for collection, 27 Cottonseed oil extraction, trichlorethylene burial expense, 26 hazard, 136 criteria, in electrical injuries, 481 Cough from ammonia, 171 from carbon dioxide, 160 from anthracosilicosis, 340, 343 from carbon disulfide, 118 from arsenic, 295 from carbon monoxide, 178 from asbestosis, 348 from carbon tetrachloride, 102 INDEX 533 Death from chlorine, 15-1 Desensitization in dermatoses, 458 from electricity, -480 to cold, 476 from hernia injection, 433 Detoxication by liver, 64 from hydrogen sulfide, ISO Dextrose in benzene poisoning, 83 from hyperpyrexia, 405 in carbon tetrachloride poisoning, 112 from methyl aleohol, 108 in tetracldorethane poisoning, 135 from methyl chloride, 104 Diabetes mellitus, effect of cold, 470 from nitrobenzene, 143 trauma and, 485 from petroleum, 88 Diagnosis, errors, in compensation, 0 from phenol, 173 Diarrhea from antimony, 202 from selenium, 289 from arsenic, 295 permanent disability and, 34 treatment, 290 Debility from hydrogen sulfide, 157 from ethylene diehloride, 145 "Decap" paper, carbon disulfide hazard, 123 from fluorine, 147 Decompression in caisson disease, 484 from hydrogen sulfide, 150 in lead encephalopathy, 250 from mercury, 255 Defecation from cyanides, 200 from selenium, 289 Degeneration, fattv, from tetracldorethane, Diathermy in back pain, 416 134 Diatomaceous earth, silica in, 304 from trichlorethylenc, 137 Dichlorodifluorometliane, 144 from manganese, 200 Dichloropropane, carbon tetrachloride and, from nitrobenzene, 142 105 from tetraethyl lead, 91 Diet in deleading, 240 in vertebra, 404 in dust diseases, 375 Degreasers, hazard of benzene, 07 tuberculosis, 355 of carbon tetrachloride, 100 in occupational dermatoses, 430 of ethylene dichloride, 144 in poisoning by benzene, 83 of petroleum, 88 by carbon disulfide, 125 Dehairing, cyanide hazard, 199 by carbon tetrachloride, 112 Deleading, 219 by chlorinated naphthalene, 132 advisability, 249 by cyanide, 204 by high calcium diet, 246 by ethylene dichloride, 145 by low calcium diet, 248 by manganese, 273 Delirium from hydrogen sulfide, 150 by nitrobenzene, 143 from methyl alcohol, 168 by petroleum, 99 Delousing, carbon tetrachloride hazard, 100 by selenium, 291 Delusions from tetraethyl lead, 91 by tetracldorethane, 135 Demianoff's sign, 414 by trichlorethylene, 140 Dental caries from selenium, 289 Digestive disturbances from hydrogen sul Dentists, mercury hazard, 254 fide, 157 Deodorizers, making,manganese hazard, 266 from sulfur dioxide, 101 Dependents, benefit, death, 26 system diseases, employability and, 520 Depression from carbon dioxide, 100 effect of carbon disulfide, 119 from mercury, 255 of lead, 223 from methyl alcohol, 168 Digitalis in carbon tetrachloride poisoning, from tetraethyl lead, 91 112 Dermatitis or dermatosis, 435-457 Diphenyls, chlorinated, 127-133. See also amelioration in, 437 Chlorinated naphthalenes. artefacts, 447 Diphenylthiocarbazone method for serum diagnosis, 436 lead, 235 criteria, 437 Diplopia in caisson disease, 484 etiology, 436 Dipping process, cyanide hazard, 199 exfoliative, from chlorinated naphthal Disability, calculation, 25 enes, 132 claims in carbon monoxide poisoning, 179 from antimony, 201 estimation, 28, 55 from benzene, 81 evaluation, 7 from chromium, 275 in silicosis, 319 from smut spores, 373 extent, benefits and, 12-18 from trichlorethylenc, 137 from ammonia, 171 treatment, 139 from anthracosilicosis, 347 incidence, statistics, 435 from arsenic, 295 local measures, 455 from back sprain, 395 medicolegal aspects, 450 from benzene, 74 protective procedures, 451 from cadmium, 279 treatment, 450 from caisson disease, 484 534 INDEX Disability from carbon dioxide, 100 from carbon disulfide, 122 from carbon monoxide, 191 from carbon tetrachloride, 104 from chlorine, 151 from chromium, 275 from cyanides, 201 from dermatoses, 450 from electrical injuries, 180 from fluorine, 150 from gases, 05 from heat exhaustion, 409 from hernia, 425 from hydrogen sulfide, 157 from lead, 239 from manganese, 270 from mercury, 256 from metal-fume fever, 209 from methyl alcohol, 108 from methyl chloride, 105 from nitrobenzene, 143 from nitrous fumes, 206 from petroleum hydrocarbons, 92 from selenium, 290 from solvents, 65 from sulfur dioxide, 161 from tetrachlorethane, 131 from trichlorelhylene, 137 from zinc, 299 in occupational diseases, 39 in silicosis, 39 indemnity, 23, 25 in permanent partial disability, 25 injury and, 9 partial, permanent, 25 benefits, 15 rating, 35 permanent, actuarial background, 34 basis, 35 definition, 33 estimation, 29 in California, 31 in general, 33 in occupational diseases, 39 rating form, 32 schedule, 35, 37 temporary and, concurrent indemnity, 37 temporary, estimation, 28 total, permanent, benefits, 13, 17 temporary, weekly indemnity, 25 ultimate, 4 Disc, intervertebral, expansion, 384 retropulsion, 384 lumbosacral, narrowed, 393 Discoloration in hernias, 422. , Disease, communal origin, care, 56 existing, aggravation by climate, 467 general, employability and, 519 medicolegal relationship of trauma, 485499 non-occupational, definition, 5 occupational, 1 compensation, variability in states, 10 definition, 5 Disease, occupational, states compensating, 9 workmen's compensation and, I of workers, employability and, 519-521 possibilities, 50 probabilities, 50 Disfigurement from dermatoses, compensa bility, 450 Disinfectants, hazard of carbon disulfide, 115 of chlorine, 154 of sulfur dioxide, 161 Disseminated encephalitis from carbon mon oxide, 177 Distention from mercury, 256 Dithizone litrimetric extraction of urine for lead, 232 Diuretics in carbon tetrachloride poisoning, 113 in selenium poisoning, 291 Divers, caisson disease, 483 carbon dioxide hazard, 160 palsy, 483 Dizziness. See Vertigo. Doctor. See Physician. Dog, effect of carbon disulfide, 118 Domestics, exclusion from compensation, 22, 48 Dopeyness from nitrous fumes, 205 Doping of airplane wings, carbon tetra chloride hazard, 100 Dorsolumbar junction in back pain, 387 Dough dermatitis in bakers, 444 Dreams from tetraethyl lead, 91 Driving ability, effect of carbon monoxide, 180 Drowsiness from carbon dioxide, 160 from cyanides, 200 from hydrogen sulfide, 156 from methyl alcohol, 168 from methyl chloride, 164 from nitrobenzene, 143 from petroleum, 88 Drugs in carbon monoxide poisoning, 198 Drunkenness from trichlorethylene, 137 Dry cell battery manufacture, manganese hazard, 266 ice, effect on skin, 160 Drycleaners, hazard of benzene, 67 of carbon tetrachloride, 100 of ethylene dichloride, 144 of methyl alcohol, 167 of petroleum, 88 of trichlorethylene, 130 Dullness, mental, from trichlorethylene, 137 Dust or dusts, 303 asbestos, hazard, 348 bowl workers, silicosis hazard, 329 carbon, 356 care of clothes, 451 "cells" in anthracosilicosis, 341 cement, 357 cotton, 366 counts, 39 diseases. See under names of specific con ditions. INDEX 535 Dust, elimination mechanisms, 308 exposure, 307 in anthracosilicosis, safe limits, 342 handlers, hazard of dermatoses, 433 harmfulness, 303 inert, 3.55 effects, 355 fate, 308 iron, 356 lead, in air, sampling, 237 precautions in industry, 251 mill, 373 mineral composition, 306 particle, size, in silicosis, 306 "phthisis," 303 storm, silicosis hazard, 320 tobacco, 356 toxic thresholds, 523 "tuberculosis," 320 types, 304 Dwelling fumigation, cyanide hazard, 199 Dye dermatitis, 437 handlers, hazard of dermatoses, 435 in tetraethyl lead gasoline, 90 workers, hazard of ammonia, 171 of arsenic, 294 of cancer, 462 of chlorine, 154 of cyanide, 199 of fluorine, 146 of manganese, 266 of methyl alcohol, 167 of methyl chloride, 164 of sulfur dioxide, 161 Dyestuffs, carcinogenic, 460 Dynamite, nitrous fumes from, 206 Dyspepsia from benzine, 89 from nitrous fumes, 205 Dyspnea from anthracosilicosis, 340, 343 from asbestosis, 348 from benzine, 89 from cadmium, 278 from caisson disease, 484 from carbon dioxide, 160 from cotton dust, 366 from inert dusts, 355 from nitrobenzene, 143 from phenol, 173 from phosgene, 140 from silicosis, 306, 309 from trichlorethylene, 137 Dysuria from hydrogen sulfide, 156 Ear diseases, employability in, 520 hearing, loss, period of payment, 19 ringing from carbon dioxide, 160 from carbon monoxide, 178 from electricity, 479 sensation in carbon tetrachloride poison ing, 106 Earthquakes, effects, medicolegal aspects, 467 Ecchymosis from benzene, 70, 77 from nitrobenzene, 142 Eczemas, occupational, 437 Eczematoid dermatitis, infectious, 442 Edema from benzene, 76 from selenium, 289 lung, from nitrous fumes, 206 from phosgene, 140 from sulfur dioxide, 161 Educational campaign in back sprain, 415 Eggs in mercury poisoning, 263 Election in compensation, 7 Electric battery manufacture, chromium liazard, 274 cable, fireproofing, selenium hazard, 288 condensers, chlorinated naphthalene haz ard, 127 silicate in, 305 furnaces, carbon monoxide hazard, 176 injuries, 478-482 ophthalmia, 212 pads in hack pain, 416 shock from welding, 210 welding, iron hazard to lungs, 326 Electricians, electrical hazard, 478 Electrocardiogram in carbon monoxide poi soning, 185 in silicosis, 315 Electroplaters, hazard of arsenic, 294 of benzene, 67 of cadmium, 278 of chromium, 274 of cyanide, 199 Electrostatic precipitators for lead, 251 Elimination of carbon disulfide, 116 of carbon monoxide, 197 of mercury, 255 Ely's sign, 415 Emergency treatment, 5 Emery wheel grinder, silicosis problem, 325 Emotional change from carbon monoxide, 179 Emphysema from anthracosilicosis, 340 from asbestosis, 348 from cotton dust, 366, 369 from silicosis, 309, 315 Employability of diseased workers, 519-521 Employees, employer and, relationship, 1 misconduct, in compensation, 26 number, in compensation exemptions, 10 permission to report findings in preem ployment examination, 515 physician and, 55 rotation, in benzene exposure, 81 in carbon tetrachloride industry, 113 in vanadium poisoning, 293 Employer, compensation, in silicosis, 40 employees and, relationship, 1 insured, 23 lack of compensation, 22 liability, 23 act, 1 for compensation, 23 insuring, 7 misconduct, in compensation, 26 notice to, 24 physician and, 56 536 INDEX Employer, responsibility, 8 Ethyl isonitrile, 199 in dust diseases, 89 Ethylene dichloride, 144 security, 22 poisoning, 107 Employment, accidents in, 4 glycolmonomethyl elher, 168 casual, 27 Eucaine injection about sciatic nerve, 418 compensation and, 4 liucipin in oil injection in hack sprain, 418 excluded in compensation, 22 Eustachian tube blockage in caisson disease, types, compensation in, 3 484 Enamelers, hazard of arsenic, 294 Exacerbations in dermatoses, 438 of benzene, 67 Examinations in benzene poisoning, 79 of lead, 216 in carbon disulfide exposure, 125 Encephalitis from carbon monoxide, 177 in industrial medicine, 53 from lead, 221 in neurosis, 510 from mercury, 25(5 in reopening a case, 47 Encephalography in concussion, 501 preemployment, 514-521 Encephalopathy, lead, 249 record code, 517 disability from, 239 Excitement, effect on mercury tremors, 257 traumatic, 500 from carbon tetrachloride, 102 Endarteritis from hydrogen fluoride, 152 from chlorine, 155 from mercury, 258 from electricity, 479 Endocrine imbalance, gases and, 65 from hydrogen sulfide, 156 in back pain, 389 from tetraethyl lead, 91 Endurance in disability estimation, 31 from trichlorethylenc, 137 Enforcement of compensation, time limit, 27 Excretion of phenol, 172 Engines, gasoline, employees, poisoning, 89 Exemptions, number of employees and, 10 Engravers, benzene hazard, 67 Exercise in back pain, 389, 415 Environment, exposure, occupation and, 6 in carbon disulfide poisoning, 126 Eosinophilia from antimony, 301 tolerance tests in silicosis, 319 Ephedrine in cadmium poisoning, 286 Exertion in hernia, 421, 422 Epidemic diseases, employability in, 519 Exhaust system, automobiles, carbon mon Epidermoid carcinoma, lip, 460 oxide and, 181 Epidermophytosis, 442 in carbon tetrachloride industries, 113 in preemployment examinations, 450 Exhaustion from heat, 465 Epididymo-orchitis, trauma and, 485 Expiration, prolonged, from anthracosili- Epigastric burning from carbon tetrachlo cosis, 340 ride, 102 Explosives-makers, hazard of ammonia, 171 from silicosis, 308 of chromium, 274 Epilepsy from electrical injury, 480 of nitrous fumes, 205 from petroleum, 92 of nitrobenzene, 142 Epileptoid seizures from trichlorethylenc, Exposure in anthracosilicosis, safe limits, 137 342 Epinephrine in cold sensitivity, 476 in benzene poisoning, 69, 74 in dust diseases, 370 in dermatoses, 438 in ventricular fihrillation, avoidance, 481 patch test and, 440 Epistaxis from benzene, 73 in dust diseases, 39, 375 Epithelial cells, etfect of metal fumes, 208 in occupational diseases, 9 Epitheliomas, occupational, 435 in silicosis, diagnosis, 318 Epsom salts in deleading, 247 to cement dust, 361 in poisoning by arsine, 298 to gases, 66 by mercury, 263 to petroleum, 88 by methyl alcohol, 170 to solvents, 66 by nitrobenzene, 144 Exsanguination-transfusion in mercury poi by petroleum, 98 soning, 264 Eruptions from arsenic, 295 Extension-abduction-rotation sign in hip in Erythema multiforme, non-oeeupational, volvement, 412 438 Extraction processes, carbon disulfide haz Erythrocytes, basophilic aggregation, 228 ard, 115 counting, in basophilic, aggregation test, Extremities, swelling, from carbon tetra 231 chloride, 108 effect of benzene, 71, 73 Exudation in dermatoses; treatment, 455 of lead, 220 Eye cancer, 462 non-nucleated, in bone marrow, 81 diseases, employability and, 520 stippling, from nitrobenzene, 142 effect of ammonia, 172 Etchers, fluorine hazard, 146 of carbon tetrachloride, 106, 110 Ether, petroleum, 88 of chlorine, 155 INDEX 537 Eye, effect of hydrogen sulfide, 119, 156 Femoral hernia, truss and, 432 treatment, 150 Ferric hydroxide lavage in arsenic poisoning, of electricity, 478 290 of fluorine, 147 Ferromanganese manufacture, manganese of sulfur dioxide, 1 (i 1 hazard, 200 of tin, 300 Ferrosilicon workers, arsenic hazard, 294 of vanadium, 292 Fertilizer manufacture, hazard of ammonia, protection in welding, 211 171 sight, loss, period of payment, 19 of cyanide, 199 ulcers in snow machine operator, 472 of fluorine, 147 Eyeballs, frozen, from sulfur dioxide, 101 of manganese, 206 Eyelids, contact dermatitis to varnish- Fetal life, effect of lead, 238 remover, 444 Fever from cadmium, 278 swelling, from carbon tetrachloride, 108 from malt dust, 374 ulcers, from chromium, 275 grain, 373 in back pain, 390 in heatstroke, 460 "F-I2," 144 lack, in silicosis, 307 Fabric handlers, hazard of dermatoses, 435 metal-fume, 208 Face, baker's dermatitis, 445 Fibrosis, conglomerate, in anthracosilicosis, Facets, asymmetry, spine, 400 317 irregularities in back pain, 383 from asbestosis, 853 Factory management for lead, 251 from inert dusts, 355 work, symptoms from, 188 from silicosis, spread, 309 Fainting from hyperpyrexia, 405 lung, from cotton dust, 367 Farmers, arsenic hazard, 294 Fibrous masses in hernia injection, 433 exclusion from compensation, 22, 48 Fifth nerve paralysis from trichlorethylene, tar hazard, 403 137 Fascial adhesions in back pain, 388 Fights in workmen's compensation, 5 air insufflation, 419 Financial award in neurosis, 512 Fasciotomy for contracted iliotibial band, Financing payment of benefits, 7 419 Fines of employer, compensation and, 23 `Fatal dust," 303 Finger, index, loss, period of payment, 19 Fatigue from antimony, 301 little, loss, period of payment, 19 from benzene, 73 loss, permanent disability, 33 from lead, 222 middle, loss, period of payment, 19 from manganese, 207 ring, loss, period of payment, 19 from silicosis, 308 Fire extinguisher manufacture, carbon tetra from sulfur dioxide, 101 chloride hazard, 100 from tetraethyl lead, 91 from welding, 210 from trauma, 505 gilding, mercury hazard, 254 Fats, absorption of nitrogen, 483 Firemen, hazard of carbon monoxide, 170 extraction, hazard of benzene, 07 of cold, 460 of carbon disulfide, 115 of heat affections, 465 of trichlorethylene, 130 of traumatic tuberculosis, 491 in poisoning by benzene, 83 Fireworks making, manganese hazard, 266 by cyanide, 204 First-aid measures in phenol poisoning, 174 by zinc, 300 Fishermen, epidermoid carcinoma of lip, 460, solvent, hazard of carbon tetrachloride, 401 100 Fissure line of articular process, 404 of ethylene diehloride, 144 Fixtures, enameling, lead hazard, 210 of tetrachlorethane, 134 Flame arc, 212 Fatty acid solutions in hernia injection, 433 Flatulence from cyanides, 200 Fear from mercury, 255 Flavoring extracts, nitrobenzene hazard, 142 Feather workers, arsenic hazard, 294 Floods, effects, medicolegal aspects, 467 Fecal fistula in hernia injection, 434 Floor polishes, nitrobenzene hazard, 142 Feces, arsenic in, 295 Flour dermatitis in bakers, 444 manganese in, 207 dust, 373 Fee, doctor's, 49 Flower, artificial, makers, arsenic hazard, Feet, dragging, from manganese, 268 294 Feigning illness, 508 Fluids in arsenic poisoning, 297 Feldspar, silica in, 304 in heatstroke, 475 Felt-hat makers, hazard of arsenic, 294 in manganese poisoning, 274 of methyl alcohol, 167 Fluorine, 140-153 of mercury, 254 gases from carbon arcs, 213 538 IXDEX Fluorine poisoning, cases, 151 Gait, effect of nitrobenzene, 143 medicolegal aspects, 1.50 Galtanol in hernia injection, 433 treatment, 152 Galvanized roofing nails, lead hazard, 217 Fluoroscopy in anthracosilicosis, 04(1 Galvanizing plants, zinc hazard, 299 Flushing from heatstroke, 40(1 Gangrene from hydrogen fluoride, 152 Focal infection in back pain, 080, 004 in hernia injection, 433 in dermatoses, 430, 455 in patch testing, 441 zinc poisoning and, 000 Garages, carbon monoxide poisoning in, 197 Fog, sulfur dioxide and, 161 mechanics, carbon monoxide hazard, 176 Folliculitis from antimony, 262 Garbage solvent, trichlorethvlenc hazard, Foodstuffs, selenium-hearing, 288 ^ 137 zinc in, 299 Gardeners, arsenic hazard, 294 Foot, dorsiflexion, lest, in sciatica, 410 Gargles in cadmium poisoning, 287 loss, period of payment, 19 Garlic odor from selenium, 289 Footwear in frostbite prevention, 476 Gas or gases, 63 Forearms, baker's dermatitis, 445 carbon monoxide in, 175 Forfeitures in compensation, 26 classification, 65 Formaldehyde dermatitis in cosmeticians, effects, 63 446 exchange in silicosis, 319 patch reaction, 439 from carbon arcs, 212 Formates in urine in methyl chloride poison from welding, 210 ing, 165 manufacturing, carbon monoxide hazard, Formic acid from methyl alcohol, 169 176 Formula 12 for cleansing, 452 masks in chrome poisoning, 276 Foundry workers, hazard of lead, 243 in sulfur dioxide poisoning, 163 of silicosis, 324 poisoning from welding, 211 of sulfur dioxide, 161 tar cancer, 459 Fractures, anatomic result in, 29 toxic thresholds, 523 functional result in, 30 Gasoline, 88 rating of disability, 29 cracked, safety, 88 sinuses, infectious eezematoid dermatitis, hazards, 89 443 poisoning, cases, 93, 96 Freezing, effects, medicolegal aspects, 467 straight-run, safety, 88 '"Freezing" in history taking, 52 Gassing, after-effects, 63 "Freon," 144 in tuberculosis, 494 Friction in frostbite, 476 Gastric analysis in benzene poisoning, 78 in heatstroke, 475 distress from carbon tetrachloride, 102 Frostbite, 5 lavage in poisoning by arsenic, 296 from cold, 466 by cyanide, 203 prevention, 476 by fluorine, 152 treatment, 476 by mercury, 263 Fruit decay, carbon dioxide from, 160 by nitrobenzene, 143 Fruit-juice-stand employees, onychia, 449 by phenol, 174 Fumes, 63 ulcer, plumbism and, 221, 238 carcinogenic, 460 trauma and, 485, 488 classification, 65 zinc and, 299 from welding, 210 upset from mercury, 255 toxic thresholds, 524 Gastro-enteritis from zinc, 299 Fumigation, hazard of cyanide, 199 Gastro-intestinal cancer from chromate of ethylene dichloride, 144 dust, 462 of fluorine, 147 tract, effect of cadmium, 278 Fungus dermatitis, 437 of cyanides, 200 contact dermatitis and, 442 of mercury, 263 in cotton dust, 367 of selenium, 288 infections in occupational dermatoses, 436 of vanadium, 292 Fur-cutters, mercury hazard, 254 of zinc, 299 Furnace-tenders, carbon monoxide hazard, Geuito-urinary system diseases, employabil 170 ity and, 520 Furunculosis in handlers of oil or cement, Gentian violet in infectious eezematoid der 436 matitis, 455 Fusion, failure, in vertebrae, 405 Germ cells, effect of lead, 238 Germicides, making, manganese hazard, 266 Gaenslen's sign, 414 Gerontology, 515 Gait, effect of manganese, 267 Giant ceils, asbestosis bodies and, 350 of methyl chloride, 164 Giddiness. See Vertigo. INDEX 539 Gingivitis from mercury, 209 Hartmann's buffer solution in carbon tetra Glass coloring, cadmium hazard, 278 chloride poisoning, 112 decolorizing, selenium hazard, 288 Hat-band dermatitis, 451 finishers, fluorine hazard, 140 Hatters, mercury hazard, 254 manufacturing, silicosis hazard, 307 Hazard, environmental, 6 Glazes, colored, production, selenium haz of antimony, 301 ard, 288 of arsenic, 294 Glazing, lead hazard, 216 of asbestosis, 348 Gliosis in basal ganglia from manganese, 207 of benzene, 67 Gloves in cancer prevention, 403 of cadmium, 278 in dermatoses, 452 of caisson disease, 483 Glucose in chlorinated naphthalene poison of carbon dioxide, 160 ing, 132 of carbon disulfide, 115 in prevention of heat affections, 474 of carbon monoxide, 176 Gluteus maxiinus muscle, stretching, 413 of carbon tetrachloride, 100 Glycerin in phenol poisoning, 173 of chlorinated naphthalenes, 127 Glycosuria from carbon monoxide, 183 of chlorine, 154 - from cyanides, 200 of chromium, 274 from mercury, 259 of cotton dust, 366 from metal fumes, 208 of cyanides, 199 Glycuronates from benzol, 04 of dermatoses, 435 Goiter, toxic, trauma in, 488 of electricity, 478 Gold extraction, mercury hazard, 254 of fluorine, 146 miner, silicosis hazard, 307, 328 of gases from carbon arcs, 212 Goniometers, optical, in study of crystals, of gasoline, 89 337 of hydrogen sulfide, 156 Governmental survey of anthracosilicosis, of lead, 216 340 of manganese, 266 Grain dust, 373 of mercury, 254 fever, 373 of metal fumes, 215 smuts from mill dust, 373 of methyl alcohol, 167 Granite quarrying, silicosis hazard, 307 of methyl chloride, 164 Granulopenia from benzine, 89 of methylene dichloride, 144 Grass smuts from mill dust, 373 of mill dust, 373 Gray stage in phosgene poisoning, 140 of moving-picture projection booths, 213 of anoxemia from chlorine, 155 of nitrobenzene, 142 Grease, care of clothes, 451 of nitrous fumes, 205 removing, in home, carbon tetrachloride of petroleum hydrocarbons, 88 hazard, 100 of selenium, 288 Greasepaint, plumbism from, 243 of silicosis, 307 Green wood spirits, 167 of sulfur dioxide, 161 Grime, care of clothes, 451 of talc, 356 Grit soaps, dermatoses, 452 of tetrachlorethane, 134 "Groundglass" .r-ray in anthracosilicosis, of tetraethyl lead, 90 346 of tin, 300 Guanidine in carbon tetrachloride poisoning, of trichlorethylene, 136 112 of welding, 210 Gummata, traumatic, 450 of zinc, 299 Gums, bleeding, in benzene poisoning, 73, Head, flexion, in sciatica, 415 75 hoods in cancer prevention, 463 line from lead, 224 traumatic neurosis, 500 from mercury, 262 Headache from arsenic, 295 solvent, tetrachlorethane hazard, 134 from benzene, 73, 78 from benzine, 89 from cadmium, 278 Hair, arsenic in, 295 from carbon dioxide, 160 dye dermatitis, 446 from carbon disulfide, 118 Hallucinations from electricity, 479 from carbon monoxide, 178 Hands, baker's dermatitis, 445 from carbon tetrachloride, 102 chrome holes, 275, 436 from cotton dust, 367 loss, period of payment, 19 from cyanides, 199 Handwear in frostbite prevention, 476 from gasoline, 90 Hard-coal miners, anthracosilicosis hazard, frontal, 90 340 from heatstroke, 466 Hard-rock mining, silicosis hazard, 330 from hydrogen sulfide, 156 540 IN'DEX Headache from malt dust, .`174 Hemorrhages from nitrous fumes, 205 from mercury, 259 from tetraethyl lead, 91 from methyl alcohol, 108 Hemorrhoids, trauma and, 485 from nitrobenzene, 142 Hepatitis, chlorinated naphthalenes ami, from nitrous fumes, 205 128 from petroleum, 88 Hernia, 4, 421-434 from phenol, 173 aggravation, 427 from tetraethyl lead, 91 cases, 426-431 from trauma, 505 medicolegal aspects, 423, 425 Health maintenance program, 517 open-wound, trauma and, 422 Hearing, effect of carbon disulfide, 120 potential, preemployment examination for adjustment of claim, 27 and, 514 loss, period of payment, 19 rating, 34 Heart attacks, seasonal incidence, gas and, status in compensation, 48 188 treatment, 431 effect of anthracosilieosis, 340 Herniation of intervertebral disc in back of antimony, 301 pain, 383 of benzine, 89 Herniotomy, contraindications, 431 of carbon monoxide, 184-190 Hexylresorcino! in carbon tetrachloride poi compensability, 190 soning, 113 of carbon tetrachloride, 102 Hiccoughs from methyl chloride, 164 of electricity, 480 Highway exposure to carbon monoxide, 180 of heat, 465 Hip, extension-abduction-rotation sign, 412 of hydrogen sulfide, 156 hyperextension in back sprain, 415 of petroleum, 88 joint disease, Lasegue's sign, 413 of silicosis, 308, 313, 315, 319, 320 psoas magnus spasm, 414 of sulfur dioxide, 103 Histamine in cold desensitization, 476 of tetraehlorethane, 134 History in back sprain, 382 of tetraethyl lead, 91 in dermatoses, 437 impairment in anthracosilieosis, 341 in industrial disease, 52 stimulants in methyl chloride poisoning, in workmen's accidents, 5 106 of compensation cases, 49 Heat affections, 465-477 Hodgkin's disease, benzene poisoning and, cramps, 465 84 diagnosis, 466 Hood, suction, in cancer prevention, 463 treatment, 474 Horseplay in workmen's compensation, 5 exhaustion, 5, 465 Hospital benefits, limitation, 48 treatment, 475 Hot-water bottles in back pain, 416 in chlorine poisoning, 155 Household domestic service, lack of com in dermatoses, 441 pensation, 22 in frostbite, 476 refrigeration, sulfur dioxide hazard, 161 reactions, prophylaxis, 474 Housewives, carbon monoxide hazard, 176 retention, 466 eye cancer, 463 Heatstroke, 465 naphtha poisoning, 92 diagnosis, 466 petroleum hazard, 88 treatment, 475 Huskiness from arsenic, 295 Helium in caisson disease, 484 Hydrocarbons, carcinogenic, 460 Helmets, positive-pressure, in carbon tetra chlorinated, poisoning, stippled celts in, chloride poisoning, 113 225 Hematopoiesis, effect of benzene, 68, 73 petroleum, 88-99 of lead, 220 Hydrocephalus, internal, from carbon mon Hemoglobin, carbon monoxide in, 177 oxide, 177 in benzene poisoning, 71, 72 Hydrochloric acid, gastric, in benzene poi reduction from lead, 232 soning, 72 from manganese, 266 Hydrocyanic acid, 156, 199 Hemograms in plumbism, 221 Hydrogen, arseniuretted, 294 Hemolysis from arsine, 294 fluoride, 146 Hemolytic jaundice, stippled cells in, 225 peroxide in cyanide poisoning, 203 Hemoptysis from anthracosilieosis, 340 sulfide, 156-159 Hemorrhages from benzene, 75, 78 noxiousness, 110 from carbon monoxide, 179, 186 poisoning, cases, 157 from carbon tetrachloride, 109 medicolegal aspects, 157 from electricity, 479 symptoms, 119 from heat affections, 466, 475 treatment, 158 from nitrogen air emboli, 483 use, arsenic hazard, 294 INDEX 541 Hygiene, gases and, 65 in dust tuberculosis, 355 Hyperacidity in plurabism, 221 Hyperemia, passive, in heat affections, 466 Hyperhidrosis in preemployment examina tion, 450 Hyperplasia, marrow, benzene and, 08 Hyperpyrexia, 465 Hypersensitivity in occupational derma toses, 486 Hypertension, plumbism and, 238 Hyoglossal nerve paralysis from trichloreth- ylene, 137 Hypoplasia, medullary, benzene and, 68 Hyposensitization to rusts, smuts, 379 Hysteria from electricity, 479 in dermatitis artefacta, 448 traumatic, origin, 505 Ice man, heatstroke, compensability, 470 Ichthyol in dermatoses, 455 Ichthyosis in preemployment examination, 450 Icterus from selenium, 289 index in benzene poisoning, 76 in carbon tetrachloride poisoning, 102 Iliotibial band, contracted, fasciotomy for, 419 in back pain, 387 Ober's sign, 415 Illness, chronic, from gases, solvents, 65 occupational, 4 Illuminating gas, 175 Immunity to metal fumes, 208 Impetigo, non-occupational, 438 Impotence from welding, 210 in hernia injection, 433 Incarceration from trusses, 432 Incline, walking, effect of manganese, 268 Indemnity, assignment, 27 concurrent, in temporary and permanent disability, 37 disability, 23, 25 in employee misconduct, 26 in employer misconduct, 26 in permanent disability, 37 neuroses, 504 weekly, in great disability, 26 in temporary total disability, 25 Individual susceptibility to carbon tetra chloride, 102 to gases, solvents, 65 Industrial Accident Commission, 3, 22 estimation of disability, 28 operation, 43 Industrial back, 381-420 dermatitis, definition, 436 exposure, patch test and, 441 gassing with chlorine, 154 neuroses, 504 physician, attitude, 55 practice, physician and, 57 substances, toxic threshold, 523 Inert dusts, 355 Infarction, kidney, from carbon tetrachlo ride, 102 Infections, effect on stored lead, 219 in anthracosilicosis, 341 in hernia injection, 433 in herniotomy, 431 in mercury poisoning, 255 in vertebrae, 402 upper-respiratory, lead and, 217 Infectious diseases, employability in, 519 eczematoid dermatitis, 442 treatment, 455 Inflammation from cadmium, 278 Influenza, metal fumes and, 208 Infra-red therapy for back pain, 416 Infusorial earth, silica in, 304 Ingestion of cadmium, 278 of chromium, 274 of lead, 216 of manganese, 267 of mercury, 254 bichloride, 263 Inhalation in bronchitis from carbon tetra chloride, 113 of cadmium, 278, 287 of manganese, 267 of mercury, 254 of trichlorethylene, 139 Inherent neuroses, 504 Injection of hernia, 432 evaluation of results, 434 Injury, definition, 9 electrical, 478-482 in back pain, 383 in compensation, 23 neuroses, 504 period of payment, 19 "personal," 3 reporting of, 23 self-inflicted, in compensation, 26 treatment, reasonable cost, 24 Injuries, types, 4 Ink-pigment making, selenium hazard, 288 Inoperable hernia, 425 Inorganic dusts, 304 Insecticide manufacture, hazard of carbon disulfide, 115 of fluorine, 146 of trichlorethylene, 137 Insecurity in disability estimation, 31 Insomnia from benzene, 73 from benzine, 89 from mercury, 257 from nitrous fumes, 205 from tetraethyl lead, 91 Instability in neurosis, 511 Instrument making, mercury hazard, 254 Insulation manufacture, asbestosis hazard, 348 Insulin in carbon tetrachloride poisoning, 112 Insurance carrier in Employer's Liability Act, 2 physician and, 56 role, 23 542 INDEX Insurance in traumatic neurosis, 504, 507 Kidneys, effect of petroleum, 88 requirements of workmen's compensation of tetraehlorethane, 134 laws, 8 excretion of lead, 236 Insured employers, 23 inflammation of. See Nephritis. Interstitial keratitis, trauma and, 440 tubules, inclusion bodies, in plumbism, Intervertebral disc, destruction, in back 221 pain, 383 Kilns, carbon monoxide hazard, 176 Intestine, effect of fluorine, 147 Knee in straight-leg-raising lest, 412 of lead, 221 Korsakoff's svndrome, carbon disulfide and, of nitrobenzene, 142 121, 125 obstruction in hernia injection, 433 KiimmelFs disease in back pain, 391, 392 rupture, traumatic, 490 tuberculosis, silicosis and, 317 Intoxicants, intolerance, from trauma, 505 La grippe, metal fumes and, 208 Intoxication from carbon disulfide, 118 regimen, 209 from lead, 222 Labor, agricultural, excluded in compensa from petroleum, 88 tion, 22 in compensation, 5, 20 unions on preemployment examination, Intra-abdominal pressure in hernia forma 514 tion, 422 Laboratory findings in cadmium poisoning, Intradermal test, trichophyton, 442 281 Intranasal drops in cadmium poisoning, 287 in plumbism, 238 Iodides in deleading, 249 investigation in occupational diseases, 53 Iodine extraction, carbon disulfide hazard, studies, abnormal, in back pain, 390 115 in gases, solvents, 65 Irascibility from trauma, 505 workers, syphilis compensability, 449 Iron dust, 356 Laborers, tar hazard, 463 effect on lungs, 327 Labyrinthine disturbance from carbon mon hardening, cyanide hazard, 199 oxide, 188 in arsine poisoning, 298 Laceration, trauma in, 488 in benzene anemia, 83 Lacquerers, hazard of benzene, 67 in welding, 211 of carbon disulfide, 115 mining, silicosis hazard, 307 of carbon tetrachloride, 100 oxide in cement, 357 of ethylene dichloride, 144 Irrigations, throat, in cadmium poisoning, of nitrous fumes, 205 286 Lacrimation from cyanides, 200 Irritability from antimony, 301 from tetraehlorethane, 134 from mercury, 255 Lactalbumin in selenium poisoning, 291 Irritatidn from gases, solvents, 65 Lactate-Ringer's solution in acidosis, 161, from hydrogen sulfide, 156 170 in occupational dermatoses, 436 Lamps in back pain, 416 non-industrial, in patch testing, 441 Lange's test in manganese poisoning, 266 Isonitrile, ethyl, 199 Languor from manganese, 269 methyl, 199 from nitrobenzene, 143 Laryngeal tuberculosis, silicosis and, 317 Lasegue's sign, 413 Janitor, contact dermatitis, 451 in retropulsion of intervertebral disc, Jaundice from carbon tetrachloride, 102 386 from chlorinated naphthalenes, 127 Lassar s paste in dermatoses, 455 from tetraehlorethane, 135 Lassitude from cotton dust, 367 Joint, amputation, rating, 33 from metal-fume fever, 209 immobility, rating, 33 from sulfur dioxide, 161 Lateropulsion from manganese, 273 Laughter from carbon disulfide, 118 Keloids from dermatoses, 450 from manganese, 269 Kerosene in stamp cleaning, 90 Laundry soaps in dermatoses, 452 Kernig's sign in retropulsion of interver workers, carbon monoxide hazard, 176 tebral disc, 386 Law, enactment, prior disability and, 40 Kidneys, effect of cadmium, 278 workmen's compensation, 2 of carbon monoxide, 184 Lead, 216-253 of /3-naphthylamine, 462 alloy, antimony hazard, 301 of tetrachloride, 102, 111 chromate making, chromium hazard, 274 of fluorine, 147 circulating, symptoms and, 220 of gases, solvents, fumes, 64 encephalopathy, treatment, 250 of lead, 223 fate in body, 218 I i INDEX 543 Load intoxication, 222 levels, blood, 235 urine, 233 modes of entrance, 210 palsy, treatment, 250 poisoning, cuses, 240 from welding, 210 medicolegal aspects, 238 signs and symptoms, 223 treatment, 240 without deleading, 250 tetraethyl, hazard, 90 Leather dermatitis, 451 workers, hazard of arsenic, 294 of benzene, 07, 75 of methyl alcohol, 107 of trichlorethylene, 130 Leg cramps from benzine, 89 from manganese, 209 from mercury, 255 loss, period of payment, 19 rating, 34 raising test in back pain, 409 stiffness from manganese, 207 Legal aspect of workmen's compensation, 7 department of Industrial Accident Com mission, 45 viewpoint in silicosis, 321-326 Lemonade in prevention of heat affections, 474 Lens-capsule tears from electricity, 470 Lenticular nucleus, softening, from carbon monoxide, 177 Leptomeninges edema in heat affections, 466 Lethargy in benzene poisoning, 73 Letter as medical report, 51 Leukemia from benzene, 64, 68, 69 from petroleum, 88 gases and, 63 stippled cells in, 225 Leukocytes, effect of benzene, 71 of lead, 220 Leukocytosis from benzine, 89 from lead, 232 from metal fumes, 208 from methyl chloride, 165 from petroleum, 88 in back pain, 390 Leukopenia from antimony, 301 from benzene, 70 from benzine, 89 from manganese, 266 Liability Act, Employer's, 1 Liability, definition, 3 employer's, limited, 3 of employer, 23 placement, 2 Libido loss from carbon disulfide, 119 Lichen planus, non-occupational, 438 Life expectancy in silicosis, 41 pensions, death benefits and, 34 Lifting in hack pain, 415 in hernia, 426 Ligaments, calcification, fluorine and, 148 in back pain, 382 Ligaments in spondylolisthesis, 400 Ligamenlum flavnm hypertrophy, 380 operation in, 419 Light flashes from electricity, 479 Lightning injuries, 478 medicolegal aspect, 467 Limbs, spasm, from heat cramps, 400 Limestone in cement, 357 rock, inert dust, 356 Linder's sign, 415 Linemen, electrical hazard, 478 Linoleum-making, hazard of manganese, 266 of methyl alcohol, 167 Linotype operator, plumbism in, 240 Linseed oil extraction, trichlorethylene haz ard, 136 Lip cancer in fishermen, 460, 461 Lipiodol in nucleus pulposus study, 387 Lipoid tissue, effect of iead, 255 Lipoma in spina bifida occulta, 404 Liquids, protective, in dermatoses, 453 Listlessness from lead, 222 Litharge use, lead hazard, 216 Lithographers, hazard of benzene, 67 of chromium, 274 Litigation neurosis, 500 Liver, effect of benzene, 68, 77, 86 of cadmium, 278 of carbon tetrachloride, 100-102, 105 treatment, 111 of chlorinated naphthalenes, 127 of chlorohydrocarbons, 66 of ethylene dichloride, 145 of fluorine, 147 of gases, solvents, fumes, 64 of lead, 221, 239 of metal fumes, 208 of /3-naphthylamine, 462 of nitrobenzene, 142, 144 of petroleum, 88 of selenium, 289 of solvents, 131 of tetrachlorethane, 134 of trauma, 485 of trichlorethylene, 137 extract in poisoning by benzene, 78, 83 by carbon disulfide, 126 by manganese, 274 functions, 64 rupture, traumatic, 490 Livingstonite concentrate, reduction plant, 260 Locomotion diseases, employability and, 521 Longshoreman's act, insurance require ments, 8 Lubricants, eye cancer from, 462 Lumbago, 381 Demianoff's sign, 414 Lumbar muscles, leg-raising test, 412 puncture in lead encephalopathy, 250 ribs, congenital, 411 vertebrae, 401 fusion of bodies, 411 laminae, failure of fusion, 410 spondylolisthesis, 405 544 INDEX Lumbosacral angle, 40!) area, away findings, 393 Malpractice in hernia, compensabilitv, 429 Malt fever, 373 contracture in back pain, 383 Manganese, 200-274 disc space, narrowing, in back pain, 409 effect on liver, 04 joints, unstable, spinal fusion, 419 in welding, 211 lesion, Gaenslen's sign, 41.5 poisoning, cases, 270 Lump, hernia and, 423 differential diagnosis, 209 Lung cancer from chromate dust, 402 medicolegal aspects, 270 non-oecupational, 00 treatment, 273 occupational, 400 reservoir in lungs, 207 silicosis and, 400 silica and, 305 edema from caisson disease, 483 Manhattan spirits, 107 from chlorine, 155 Mania from methyl alcohol, 108 from heat affections, 400 Manipulation in back sprain, 417 from nitrous fumes, 205 of back, signs in, 409 from pneumonia, 171 Manson methylene blue stain for basophilic from selenium, 289 aggregation, 230 from tetraethyl lead, 91 Marble, inert dust, 350 from trichlorethyleno, 137 Masklike face from manganese, 269 effect of anthracosilicosis, 340, 344, 340 Masks in metal-fume fever, 210 of asbestosis, 348, 350, 351 in poisoning by hydrogen sulfide, 158 of benzene, 77 by vanadium, 293 of cadmium, 211, 278 Masons, cement dermatitis, 440 of carbon dust, 356 Massage in back pain, 416 of carbon monoxide, 170, 183 Mattress-making, asbestosis hazard, 348 of cement, 357 McBride's method of estimating disability, of grains, 374 30 of iron dust, 327 Mechanical action of asbestos fibers, 352 of lead, 218 Mechanism of hernia, 423 of manganese, 200, 207 Medical department in compensation de of petroleum, 88, 98 partment, 44 of silicosis, 300, 309, 312, 314, 319 examinations in manganese mills, 273 of sulfur dioxide, 161 opinion on hernia, 424 of tetrachlorethane, 134 futility, 427 of tetraethyl lead, 91 report, 51 of vanadium, 292 supervision in dusty occupations, 378 of welding, 211 Medicine, art versus science, 487 hilus, fibrosis, 308 industrial, new field, 55 lead entrance, 216 workmen's compensation and, 1 Lymph nodes, fate of dust, 308 Medicolegal aspects of asbestosis, 353 in anthracosilicosis, 346 of back pain, 395 in benzene poisoning, 85 of caisson disease, 484 Lymphangitis in infectious eczematoid der of dermatoses, 450 matitis, 443 of electrical injuries, 480 Lymphatic drainage of lung in silicosis, 308 of heat affections, 400 Lymphocytes, effect of lead, 220 of hernia, 423, 425 Lymphocytosis from mercury, 256 of mill dusts, 375 Lyon non-surgical gallbladder drainage in of occupational cancer, 463 arsine poisoning, 298 of patch testing, 441 of poisoning by benzene, 74 by cadmium, 279 Machine-parts hardening, cyanide hazard, by carbon disulfide, 122 199 by carbon monoxide, 190 Machinery-making, cadmium hazard, 277 by carbon tetrachloride, 103 Macroeytosis in benzene poisoning, 71 by chlorinated naphthalene, 128 Magnesium carbonate hazard, 350 by cyanides, 200 oxide in fluorine burns, 153 by fluorine, 150 in welding, 211 by hydrogen sulfide, 157 sulfate. See Epsom sails. by lead, 238 Malaise from malt dust, 373 by manganese, 270 Malignancy of lung, silicosis and, 313 by mercury, 250 Malingering, 508-513 by petroleum, 92 classification, 509 by selenium, 290 in dermatoses, 449 by tetrachlorethane, 134 Malnutrition, carbon tetrachloride and, 102 by triehlorethylene, 137 INDEX 545 Medicolegal aspects of silicosis, 318 Mica, silicate in, 305 relationship of trauma to disease, 485-499 Micrographia from manganese, 267 Melanomas, malignant, of eye, 463 Microscope in study of crystals, 337 Members, artificial, injury, compensation Mildew in cotton dust, 367 in, 23 Mileage fees, 49 injury, indemnity, 25 Milk for carbon tetrachloride employees, Mental changes from carbon monoxide, 179, 113 191 confusion from methyl chloride, 164 in heat cramps, 475 in poisoning by arsenic, 297 depression from benzine, 89 by manganese, 274 excitement from carbon dioxide, 100 by mercury, 263 Mercurialism, arsenic versus, 295 by zinc, 300 Mercury, 254-265 Mill dust, 362, 373 from livingstonite concentrate, 200 control, 379 in infectious eczematoid dermatitis, 444 medicolegal aspects, 375 poisoning, cases, 256 workers, heat affections, 465 medicolegal aspects, 256 Mineral mining, fluorine hazard, 146 treatment, 263 primary, secondary, 384 Metabolism, effect of gases, solvents, fumes, Miners' asthma, 340 64 Mining, hazard of asbestosis, 348 of lead, 219 of fluorine, 146 Metal or metals, 215 of hydrogen sulfide, 156 ague, 209 of iron dust, 356 bearings manufacture, antimony hazard, of mercury, 254 301 . of nitrous fumes, 205 burning, lead hazard, 216 of silicosis, 307 defects, x-rays and, 337 of zinc, 299 degreasing, carbon tetrachloride hazard, of cement, 360 100 of mercury, 256 dusts, 303 Misconduct, employer, in compensation, 26 toxic threshold, 524 Mitral valve, effect of carbon monoxide, etching, nitrous-fume hazard, 205 186 eye cancer from, 463 Molds in cotton dust, 367 handlers, hazard of dermatoses, 435 in mill dust, 373 wearing properties, x-ray and, 337 Monocytes, abnormality, from carbon di Metal-fume fever, 208 sulfide, 117 cases, 209 lymphocyte ratio in lead poisoning, 220 from cadmium, 283 Monocytosis from lead, 220 from copper, 300 Mononuclear increase from tetrachlorethane, from lead, 222 134 from welding, 210 Monoplegia in caisson disease, 484 from zinc, 299 Monotonous voice from manganese, 269 Metallic taste from mercury, 255 Monument worker, silicosis hazard, 321 Metallurgy, cyanide hazard, 199 Mortality from respiratory diseases of min Metalware-enameling, lead hazard, 216 ers, 343 Metastasis in occupational cancer, 463 Moth fumigant, ethylene dichloride hazard, Methanol, 167 144 Methemoglobin from nitrobenzene, 142 Motion in back pain, 382, 389, 393 in moving-picture operators, 213 Motor fuels, 88 Methyl alcohol, 167-170 Mouth care in benzene poisoning, 83 effect on optic nerve, 66 washes in nitrous-fume poisoning, 207 from methyl chloride, 164, 166 Moving-picture projection booths, hazards, poisoning, cases, 168 213 chloride, 164-167 Mucosae, effect of arsenic, 284 fate in body, 164 of benzene, 73 poisoning, cases, 165 of chromium, 274 treatment, 166 of mercury, 255, 262 hydroxide, 167 of nitrous fumes, 205 isonitrile, 199 of selenium, 290 Methylene blue in poisoning by carbon Mucous colitis, traumatic relationship, 486 monoxide, 198 Multiple sclerosis, electrical injury and, 480 by carbon tetrachloride, 112 plumbism and, 239 by cyanide, 203 Munitions manufacture, antimony hazard, Metrazol in poisoning by trichlorethylene, 301 140 Muscles in back pain, 382 35 546 INDEX Muscles in spondylolisthesis, 400 Nausea from methyl chloride, 164 twitching from manganese, 20!) from petroleum, 88 from petroleum, 88 from tetrachlorethane, 134 weakness. See U'ea/itiexs. from trichlorethylene, 137 Musical-instrument making, cadmium haz Neoplasms in benzene poisoning, 69 ard, 277, 278 stippled cells in, 225 Myalgia from lead, 222 Ncosynephrin in dust diseases, 370 Mycosis of lung, silicosis and, 813 Nephritis from carbon tetrachloride, 104, Myelocytes in benzene poisoning, 72 100 Myeloma in hack pain, 391 from chromium, 275 Myocardial failure from carbon monoxide, from ethylene dichloride, 145 18G from lead, 238 weakness from silicosis, 315 from manganese, 266 Myosynovitis in back pain, 388 from mercury, 255 from phenol, 174 Neri's sign, 415 Nails, arsenic in, 295 Nervous system, diseases, employability in, diseased, from selenium, 289 519 galvanized, lead in, 217 effect of benzine, 73, 89 in baker's dermatitis, 445 of carbon disulfide, 66, 116, 117,119 injury in industry, 449 of carbon monoxide, 177, 184 loss, from mercury, 259 of chlorine, 154 polish dermatitis, 446 of electricity, 479 in patch testing, 439 of heat, 466 Naphtha, 88 of hydrogen sulfide, 156 jag, 88 of lead, 219, 221, 223, 239, 247 poisoning, 92 of manganese, 266, 267 case, 97 of mercury, 255 wood, 167 of methyl chloride, 164 Naphthalenes, cancer from, 462 of petroleum, 88, 92 chlorinated, 127-133 of solvents, 66 poisoning, medicolegal aspects, 128 of trichlorethylene, 137 treatment, 132 nitrogen storage in caisson disease, 483 effect on liver, 64 Nervousness from antimony, 301 Naphthols, absorption, 172 from benzene, 73 Naphthylamine tumor, 462 from cyanides, 200 Narcissistic regression in traumatic neurosis, from petroleum, 92 502 treatment, 98 Narcosis from carbon tetrachloride, 102 from tetrachlorethane, 134 from methyl chloride, 164 from tetraethyl lead, 91 from nitrous fumes, 205 Neural arch failure of fusion, 406 from trichlorethylene, 137, 139 poisoning by carbon disulfide, 117 Narcotics in dust diseases, 375 Neuritis, peripheral, from arsenic, 295, 297 Nasal irritation from sulfur dioxide, 161 from carbon monoxide, 196 from tetrachlorethane, 134 from lead, 238 from tin, 300 from selenium, 289 mucosa, ulcers, from chromium, 275 retrobulbar, from petroleum, 92 polyps, silicosis and, 320 Neurologic examination in manganese poi septum, chrome holes, 436 soning, 272 perforation from arsenic, 295 signs in concussion, 502 from chlorine, 154 Neuromvelitic complex from trichlorethyl Nasopharyngitis from sulfur dioxide, 161 ene, 137 Natural gas, 176 Neuropathy from carbon disulfide, 121 Nausea from antimony, 301 Neuroretinitis, plumbism and, 238 from arsenic, 295 Neurosis associated with trauma, 500-513 from cadmium, 278 classification, 509 from carbon disulfide, 118 plumbism and, 239 from carbon monoxide, 178 traumatic, 480 from carbon tetrachloride, 102 Neurosurgeon in low back pains, 419 from cyanides, 199 Neurotic, 509 from ethylene dichloride, 145 New York compensation act, 1910, 2 from hernia formation, 423 Nickel dermatitis in bakers, 445 from malt dust, 374 Nicotinic acid in arsenic diarrhea, 297 from metal-fume fever, 208 Nitric acid manufacture, hazard of ammo from methyl alcohol, 168 nia, 171 INDEX 547 Nitric acid manufacture, hazard of chlorine, Onychomadesis, causes, 262 154 Operation. See also Surgery. oxide, 204 of industrial accident commission, 43 Xitro compounds, effect on nervous system, Ophthalmia, electric, 212 142 snow, 473 Nitrobenzene, 142-144 Ophthalmological care in carbon disulfide poisoning, case, 140 poisoning, 126 Nitrogen absorption in caisson disease, 483 Opinion, expert, in estimation of disability, dioxide, 204 28 effects, 59 Optic nerve, effect of methyl alcohol, 66, 167 fixation by carbon arcs, 213 of trichlorethylene, 138 peroxide from welding, 211 Ore mining, fluorine hazard, 146 Nitrous fumes, 204-207 smelling, cadmium hazard, 278 from carbon arcs, 213 Organic basis of traumatic neurosis, 507 from welding, 211 dusts, 304 poisoning, case, 200 Organs, effect of arsenic, 294 oxide, 204 of carbon monoxide, 177, 183 Nocturnal attacks from malt dust, 374 of chlorinated naphthalenes, 130 Nodulation in x-rays in cement workers, 357 of heat, 466 Nodules in lung, dyspnea and, 311 of methyl alcohol, 167 in silicosis, 310 of methyl chloride, 164 Nose. See also Nasal. of nitrous fumes, 206 care in benzene poisoning, 83 of phenol, 173 Notice of compensation insurance, 23 of selenium, 288 to employer, 24 of solvents, 66 Novocaine injection in ankle sprain, 417 mercury storage, 255 Nucleus pulposus, 384 Ornament manufacture, plumbism in, 242 herniation, operation in, 419 Orthopedist in low back pains, 419 Nurses, syphilis compensability, 449 Osteo-arthritis in back pain, 391, 392 Nutrition in back pain, 389 Osteomyelitis sinuses, infectious eczematoid Nystagmus in caisson disease, 483 dermatitis, 443 Overcrowding in dust tuberculosis, 355 Oxides of nitrogen from carbon arcs, 213 Ober's sign, 415 Oxy-acetylene torches in welding, poisonous Obesity, caisson disease and, 484 gases from, 211 gases and, 65 Oxygen, blood, effect of carbon monoxide, injection of hernia and, 433 177 Obstipation from cyanides, 200 consumption, effect of heat, 465 from fluorine, 153 exhaustion by welding, 210 Occupation in estimation of benefits, 28 in poisoning by arsenic, 297 standard in disability rating, 37 by arsine, 298 Occupational activity in back pain, 394 by cadmium, 287 Odor, almond, from cyanides, 200 by carbon dioxide, 161 of hydrogen sulfide, 156 by carbon monoxide, 197 Oil, care of clothes, 451 by carbon tetrachloride, 111 extraction, hazard of benzene, 67 by chlorine, 155 of carbon disulfide, 115 by cyanide, 199, 203 of carbon monoxide, 176 by fluorine, 152 of dermatoses, 435 by gasoline, 89 of eye cancer, 462 by nitrous fumes, 206 of hydrogen sulfide, 156 by petroleum, 98 of trichlorethylene, 136 by selenium, 291 heavy, 88 by trichlorethylene, 139 in phenol poisoning, 174 unsaturation in silicosis, 319 of cade in dermatoses, 455 Ozone from carbon arcs, 213 workers, cancer incidence, 461 furunculosis, 436 Ointments in cancer prevention, 463 Pi shadows in cement workers, 357 in dermatoses, 453, 455 P2 shadows in cement workers, 358 in trichlorethylene poisoning, 139 P3 shadows in cement workers, 358 Olefins, 67 Pain from anthracosilicosis, 344 Oliguria from carbon tetrachloride, 102, 108 from antimony, 301 Olive oil, extraction, trichlorethylene haz from arsenic, 296 ard, 136 from chlorine, 155 Onychia, 449 from mercury, 264 548 INDEX Pain from retropulsion of intervertebral Perivascular spaces, dilatation, from elec disc, 386 tricity, 479 in hernias, 422, 424 Permanent disability. See Disability, per Paint-handlers, hazard of benzene, 07 manent. of chromium, 274 Pernicious anemia, stippled cells in, 225 of dermatoses, 435 Peroneal nerve, effect of carbon disulfide, of lead, 245 121 of methyl alcohol, 107 "Personal injury," 3 of selenium, 288 Personality, effect of carbon monoxide, 192 of turpentine dermatitis, 444 of petroleum, 92 Pallor from asbestosis, 348 Perspiration from carbon dioxide, 160 from heat exhaustion, 465 from occupational dermatoses, 436 from lead, 222 Petrographic analysis of quartz, 338 Palm, syphilides, traumatic, 450 Petroleum cancer, 461 Palpitation from benzene, 73 ether, 88 from nitrous fumes, 205 hydrocarbons, 88-99 from silicosis, 307 poisoning, cases, 92-98 Palsies, lead, deleading and, 250 diagnosis, 88 Pancreas, effect of cadmium, 278 medicolegal aspects, 92 Papaverine in carbon tetrachloride poisoning, treatment, 98 113 products, carcinogenic, 460 , Paper works, chlorine hazard, 154 refiners, sulfur dioxide hazard, 161 Papilloma, urinary bladder, from dyes, 462 still worker, dust hazard, 362 Papillomatosis, generalized, from /3-naph- Pewter-making, antimony hazard, 301 thylamine, 462 Phagocytosis in dust elimination, 308 Paraffins, 67, 88 Phalanges, loss, rating, 34 carcinogenic, 460 Pharynx, soreness, from vanadium, 292 Paralysis agitans, carbon disulfide and, 122 Phenol, 172-174 electrical injury and, 480 in hernia injection, 433 from arsenic, 295 poisoning, cases, 173 from carbon dioxide, 160 p-Phenylenediamine dermatitis in cosmeti-' from carbon monoxide, 191 cians, 446 from cyanides, 200 Phosgene from trichlorethylene, 136 from electricity, 479 poisoning, symptoms, 139 Paraplegia in caisson disease, 484 Phosphate fertilizers, fluorine hazard, 147 Paresthesias from benzine, 89 Phosphoric acid in deleading, 248 from trichlorethylene, 137 Phosphorus in lead metabolism, 219, 247 Paris-green workers, arsenic hazard, 295 Photoelectric apparatus, manufacture, sele Parkinsonism, carbon disulfide and, 122 nium hazard, 288 from carbon monoxide, 179, 193 Photo-engraving, nitrous-fume hazard, 205 mercury and, 264 Photographic-film making, nitrous-fume haz Paronychia, 449 ard, 205 Pastes, protective, in dermatoses, 453 reagent-making, manganese hazard, 266 Patch test, delayed reactions, 440 Photography, hazard of chromium, 274 negative reactions, evaluation, 440 of methyl alcohol, 167 positive reaction, 440, 441 Physical director in industry, 389 technique, 439 examination record, 518 Patellar clonus from manganese, 269 Physicians, attitude of industrial, 55 Patient, examination in back pain, 393 change in compensation, 28 physician's attitude toward, 55 experience in neurosis, 512 questioning in carbon disulfide poisoning, 122 fee, 49 function in workmen's compensation, 47 Payment of benefits. See Benefits. r6le in silicosis diagnosis, 333 Payroll size, excluded employments and, 22 in workmen's compensation, 5 Pelvis movements, 412 selection in compensation, 24 Penalties, in compensation, 23, 26 syphilis, compensability, 449 Penicillium glaucum in cotton dust, 367 vacillation in legal courts, 487 Pennsylvania Bureau of Workmen's Com wishful thinking in medicolegal relation pensation on silicosis, 40 ship of trauma to disease, 485 Pentnucleotides in benzene leukopenia, 83 Physiotherapy in arsenic neuritis, 298 Peptic ulcer, rupture, traumatic, 490 in back pain, 416 Percussion caps, mercury hazard, 254 Piano-string making, cadmium hazard, 277 Perfumes, nitrobenzene hazard, 142 Picklers, arsenic hazard, 294 Peripheral nerves, effect of electricity, 479 Pigmentation from arsenic, 297 Perirectal abscess in hernia injection, 433 of lung in anthracosilicosis, 344 INDEX 549 Pigments, covering power, x-rays and, 337 Posture, effect on circulatory adjustment to production, selenium hazard, 288 hyperpyrexia, 465 use, hazard of cadmium, 278 in back pain, 389, 417 of mercury, 254 Potassium permanganate in cyanide poison Pina-mestre solution in hernia injection, ing, 203 433 Potential hernia, 431 Pitch, carcinogenic, 460 Pottery manufacture, hazard of arsenic, 294 eye cancer from, 462 of lead, 216 solvent, trichlorethylene hazard, 136 of manganese, 266 Pityriasis rosea, non-occupational, 438 of silicosis, 307 Placement by plant physician, 516 Powder in patch testing, 439 code, 517 soap, dermatoses, 452 Plant dermatitis, 437 talc, hazard, 356 distribution in cement exposure, 360 Power-plant operators, electrical hazard, Plasma, lead content, 235 478 Plasterers, cement dermatitis, 446 Predisposition for manganese poisoning, 267 Plastics-making, selenium hazard, 288 Preemployment examination, 514-521 Platelets in benzene poisoning, 72 extent, 515 Plating of metals, cadmium hazard, 278 in dermatoses, 450 Play, malingerer versus neurotic, 509 Pregnancy, chlorinated hydrocarbons and, Pleura in anthracosilicosis, 344 128 in asbestosis, 349 Pressers, tailor, carbon monoxide hazard, in silicosis, 308, 333 176 in silicotuberculosis, 315 Printers, hazard of chromate dermatitis, 453 in tuberculosis, 492 of lead, absent, 216 Plumbism. See Lead poisoning. of methyl alcohol, 167 Pneumoconiosis, cotton workers', 366 Probabilities in industrial diseases, 50 definition, 304 Proceedings for compromise, physician in, tuberculosis and, .r-ray of, 313 48 Pneumonia, cement dust and, 362 Proliferol in hernia injection, 433 from carbon monoxide, 179 Propionitrile, 199 from chlorine, 154 Propulsion from manganese, 269 from cold, 466 Prospecting, silicosis hazard, 329 from cyanide, 202 Prostigmine in cramps from methyl chloride, from grain, 374 167 from nitrous fumes, 205, 206 Proteins in poisoning by carbon tetrachlo in butchers, 467 ride, 102, 112 in silicosis, 308, 313, 333 by phenol, 174 Pneumothorax, spontaneous, in tubercu by selenium, 291 losis, 376 by tetrachlorethane, 13.5 Poison oak dermatitis, 454 Prothrombin level in tetrachlorethane poi Poisoning. See under names of etiological soning, 135 agents. Protrusion in hernia, 431 Policeman, cold hazard, 466 Psoas magnus spasm in hip joint lesion, 414 frostbite compensability, 469 Psoriasis, non-occupational, 438 Polycythemia from carbon monoxide, 180 Psychiatry in carbon disulfide poisoning, 126 from cyanides, 200 in neurosis, 510 Polyneuritis of limbs from trichlorethylene, Psychic disturbances from mercury, 255 137 from trauma, 501 Pontocaine in hydrogen sulfide poisoning, Psychology in traumatic neurosis, 504 159 Psychoses from carbon monoxide, 181 Porcelain decoration, mercury hazard, 254 from cranial trauma, 507 Portal of entry of carbon disulfide, 116 from cyanides, 201 of cyanide, 202 Pulling in back pain, 415 of dyes in cancer production, 462 Pulmonary circulation, testing, in silicosis, of lead, 216 319 of mercury, 254 infection in anthracosilicosis, 341 of metals, 215 sulcus tumor, back pain in, 399 of methyl alcohol, 168 Pulmotor in carbon monoxide poisoning, 197 of petroleum, 88 Pulse rate, effect of carbon dioxide, 160 of phenol, 173 of hyperpyrexia, 465 Portland cement, chemistry, 357 of metal fumes, 208 Post-concussional neurosis, 500 Pumps, mercury hazard, 254 Postulates in relation of trauma to disease, Pupils, effect of benzene poisoning, 75 488 of carbon disulfide, 121 550 INDEX Purpose neurosis, 509 Respiration, allergy from mill dust, 373 Purpura haemorrhagica from benzene, 07, artificial, in electrical injuries, 481 69 in heatstroke, 475 Pus in dermatoses, treatment, 455 in poisoning by carbon dioxide, 161 Pushing in back pain, 415 by carbon disulfide, 126 Pyogenic infection in cement dermatit is, 447 by carbon monoxide, 197 Pyonephrosis, back pain in, 397 by hydrogen sulfide, 156, 158 Pyrophyllite mining, silicosis hazard, 333 by trichlorethylene, 140 effect of ammonia, 171 of anthracosilicosis, 342 Quarrying, silicosis hazard, 307 of bromine, 154 Quartz light in chlorinated naphthalene poi of caisson disease, 484 soning, 132 of carbon dioxide, 160 silica in, 304 of cement dust, 362 .l'-ray diffraction, 330 of chlorine, 154 Quinine dermatitis in barbers, 440 of cotton dusts, 366 of cyanides, 199, 200 of dusts, 375 Radioactive substances, eye cancer from, of electricity, 480 403 of fluorine, 147, 152 Railroad employees, excluded in compensa of hydrogen suifide, 156 tion, 22 of selenium, 289 Rash, cyanogen, 200 of silicosis, 319 Ratings, statutory, schedule, 36 of sulfur dioxide, 101, 163 Rayon manufacture, hazard of carbon di of vanadium, 292. 293 sulfide, 115 hazards from welding, 210 of hydrogen sulfide, 150 measures in poisoning by ammonia, 172 Recompression in caisson disease, 484 by cadmium, 286 Records in compensation cases, 49 by cyanides, 203 Rectal irrigation in mercury poisoning, 264 by methyl chloride, 166 Recurrences in dermatoses, 438 by nitrobenzene, 143 Red blood cells. See Erythrocytes. Redheads, dermatoses in, 450 by phenol, 173 | by selenium, 291 Reducing agents in chrome ulcers, 276 by trichlorethylene, 139 in dermatoses, 452 system diseases, employability in, 520 Reeling from carbon disulfide, 118 Respirators in dust diseases, 378 References on compensation, 49 in metal-fume fever, 210 Refinery workers, hazard of cancer, 461 in poisoning by cadmium, 287 of lead, 216 by chrome, 276 Reflexes, effect of carbon disulfide, 121 by lead, 251 of selenium, 289 by vanadium, 298 of tetraethyl lead, 91 in welding, 210, 211 Refrigeration, hazard of ammonia, 171 Rest in electrical injuries, 481 of carbon dioxide, 160 periods in prevention of heat affections, of dichlorodifluoromethane, 144 474 of methyl chloride, 164 Restlessness from benzine, 89 of sulfur dioxide, 161 from electricity, 479 Refuse plants, carbon monoxide hazard, from methyl chloride, 167 176 from nitrous fumes, 205 Regimen, la grippe, 209 from petroleum, 98 Rehabilitation, malingerer versus neurotic, from tetrachlorethane, 134 509 Reticulocytosis in benzene poisoning, 73 physician and, 48 Retrobulbar neuritis from trichlorethylene, power, 35 137 Rejection of claims, 6 Retropulsion from manganese, 269 Release settlements, physician in, 48 of intervertebral disc, 384 Relief for injury, "compensation," 24 Rheumatic fever, trauma and, 486 Renal. See Kidneys. Rhinitis from smuts, 373 Reports in industrial diseases, 51, 57 from vanadium, 292 Requirements, insurance, of workmen's Ribs, lumbar, congenital, 411 compensation laws, 8 Roads, tarred, cancer hazard, 462 Reserve of insurance carrier, 55 Rock workers, anthracosilicosis hazard, Resin solvent, hazard of carbon tetrachlo 342 ride, 100 tuberculosis incidence, 342 of trichlorethylene, 130 Roofers, lead hazard. 217 INDEX 551 Rotation of employees in benzene exposure, Scopolamine in mercury poisoning, 264 81 Scotoma from carbon disulfide, 120 Rotogravers, benzene hazard, 67 from trichlorethylene, 137 Routine in preemployment examination, 516 Scouring-material workers, silicosis hazard, Rubber cement in patch testing, 43!) 307 compounders, hazard of arsenic, 294 soap dermatoses, 452 of benzene, 67 Scrap-melting, lead hazard, 216 of carbon disulfide, 115 Scrotum, gas tar cancer, 460 of carbon tetrachloride, 100 Scrubbing of chrome ulcers, 276 of dermatoses, 435 Scudder's method of estimating disability, of hydrogen sulfide, 150 of methyl alcohol, 167 , 29 Seborrhea in preemployment examinations, of trichlorethylene, 136 450 glove dermatitis, 454 Seborrheic dermatitis, non-occupational, Rubberized clothes in dermatoses, 452 438 Ruby-glass making, selenium hazard, 288 Security, employer's, 22 Rupture of intervertebral disc in back pain, in traumatic neurosis, 503 383 Sedation in back pain, 416 Rusts from mill dust, 373 in poisoning by cadmium, 287 by carbon tetrachloride, 113 by fluorine, 152 Sacrai, attachments, leg-raising test, 412 by lead, 250 Sacralization, 382, 406 by methyl chloride, 167 Saero-iliac lesions, Gaenslen's sign, 415 by nitrous fumes, 207 slip, 382 by petroleum, 98 Sacrum articulation, sclerosis, 407 Sedimentation rate in benzene poisoning, 72 horizontal, in back pain, 383 in tuberculosis, 308 horizontal position, 40!) Seed-oils extraction, carbon disulfide hazard, Safety factor in disability estimation, 31 115 Industrial Accident Commission and, 43 Selenium poisoning, 288-292 Salivation from mercury, 25!) Self-confidence, loss, from mercury, 255 from tetrachlorethane, 134 "Self-insurance" of liability, 7 Salt solution. See Sodium chloride. Sensitivity to cold, 476 Salts, corrosive, in dermatoses, 436 polyvalent, in patch testing, 441 Epsom. See Epsom salts. Sensory disturbance from electricity, 479 Salyrgan in poisoning by nitrous fumes, Serpentine, asbestos and, 352 200 Serum in chlorine pneumonia, 155 by selenium, 291 lead content, 234 Sampler, cotton-dust hazard, 368 Sewer workers, hazard of ammonia, 171 Sand workers, silicosis hazard, 307 of hydrogen sulfide, 156 z-ray diffraction, 336 Sex in back pain, causes, 390 Sandblasting, abandonment, 377 Sexual power, loss, rating, 34 Sandpaper workers, silicosis hazard, 307 Shakes, spelter, 208 Sandstone quarrying, silicosis hazard, 307 Shellackers, hazard of benzene, 67 Satellitosis from manganese, 267 of methyl alcohol, 167 Scabies, non-occupational, 438 Shiftograins in plumbism, 221 Scars from dermatoses, 450 Shinglers, lead hazard, 217 from hernia injection, 433 Ship employees, excluded in compensation, Schedule, disability rating, use, 38 22 on statutory ratings, 36 fumigation, cyanide hazard, 199 permanent-disability, in California, 37 Shock from arsenic, treatment, 297 Schmorling of intervertebral disc, 385 from chlorine, treatment, 155 "Schmorl's node," 384 from electricity, 479 Sciatic scoliosis, intervertebral disc and, 380 from fluorine, treatment, 152 Sciatica, 382 from mercury, 264 Beehterew's sign, 414 from phenol, 173 Demianoff's sign, 414 from trichlorethylene, 140 Lasegue's sign, 413 Shoe dyes, nitrobenzene hazard, 142 Linder's sign, 415 Shot-blasting, abandonment, 377 Scientific approach in medicolegal relation Showers in cancer prevention, 463 ship of trauma to disease, 485 in chlorinated naphthalene hazards, 132 Sclerosis, caisson disease and, 484 in chrome poisoning, 276 multiple, carbon disulfide and, 1-22 in manganese poisoning, 273 of articular facets of spine, 410 Siderosis, 304, 356 Scoliosis, 38 Sight loss, rating, 34 552 INDEX Sign, extension-abduction-rotation, 412 Skin, effect of carbon monoxide, 177 in low back pain, 413--115 of chlorinated naphthalenes, 127 leg extension, 409 of chromium, 211, 274 Silica, chemistry, 304 of cosmetics, 243 in barytes, 336 of cyanide, 200 in bentonite, 336 of dry ice, 160 in cement, 357 of electricity, 478 locked in silicates, 305 of petroleum, 88 x-ray diffraction, 336 of selenium, 289 Silicates, chemistry, 304 of solvents, 66 colored, 305 grafting in electrical burns, 482 in industry, 305 in heatstroke, 466 Silicomanganese manufacture, manganese occupational, 435-457 hazard, 206 occupational cancer, 460 Silicon dioxide in welding, 211 protection in poisoning by chromium, 276 Silicosis, 303, 306-339 by trichlorethylene hazard, 139 acute, 308 reactivity, refractory period, 440 cases, 320 sensitivity, local, in patch testing, 440 complications, sequelae, 315 tests in dermatoses, 438 definition, 306 Skull trauma, brain changes in, 507 development, factors, 306 Slate-rock quarrying, silicosis hazard, 307 diagnosis, 307 Sleepiness from hydrogen sulfide, 156 disability in, 39 from manganese, 267, 269 effects, 60 Sleeplessness from antimony, 301 first-stage, disability, 332 Slip, sacro-iliac, 382 lung cancer and, 460 Smell disturbance from sulfur dioxide, 161 medicolegal aspects, 318 Smelters, hazard of cadmium, 278 prevention, 377 of lead, 216 with aluminum dust, 376 of sulfur dioxide, 161 racket, 303 of zinc, 299 simple, 312 Smoke from welding, 210 treatment, 339 Smuts from mill dust, 373 tuberculosis and, 314 Snow blindness, 473 with infection, 313, 315 machine operator, sunburn, compensabil x-ray changes, 312 ity, 472 Silicospiegel manufacture, manganese haz Soap dermatoses, 452 ard, 266 in barbers, 446 Silicotuberculosis, 308, 314 makers, hazard of methyl alcohol, 167 Silk manufacture, hazard of hydrogen sul of silicosis, 307 fide, 156 Soapstone, silicate in, 305 of tin, 300 Sociology in traumatic neurosis, 504 of trichlorethylene, 136 Soda-fountain workers, onychia, 449 Silver care, cyanide hazard, 199 Sodium arsenite in selenium poisoning, 291 extraction, mercury hazard, 254 bicarbonate in acidosis, 161 mining, silicosis hazard, 307 from methyl alcohol, 169 nitrate in dermatoses, 455 in deleading, 249 in infectious eczematoid dermatitis, 456 in zinc chloride burns, 300 Sinks, enameling, lead hazard, 216 bisulfite in chrome-dermatitis protection, Sinuses, infectious eczematoid dermatitis, 453 443 chloride in acidosis, 161, 169 Sinusitis, silicosis and, 320 in poisoning by carbon monoxide, 198 Sitz baths, hot, in low back, pain, 416 by mercury, 264 Skin absorption of cyanide, 202 in prevention of heat affections, 474 of lead, 216, 254 fluoride, 146 of phenol, 172 formaldehyde sulfoxylate in mercury poi allergy from mill dust, 373 soning, 263 from smuts, 373 hyposulfite in chrome ulcers, 276 care in benzene poisoning, 83 lactate in acidosis from methyl alcohol, in selenium poisoning, 290 169 diseases, employability in, 521 r-molar, in acidosis, 161 disorders unrelated to occupation, 438 linsoleate in hernia injection, 433 dusky, from anthracosilicosis, 343 nitrite in cyanide poisoning, 203 effect of ammonia, 171 oxide in welding, 211 of arsenic, 294, 297 phosphate in deleading, 248 of benzene, 77 psylliate in hernia injection, 433 INDEX 553 Sodium thiosulfate in poisoning by arsenic, Sputum from silicosis, 307, 308 297 Stability in neurosis, 510 by cyanide, 203, 204 Staggering from hydrogen sulfide, 156 by manganese, 274 Staining of stippled cells, 225 by mercury, 264 Standard for disability ratings, 37 xanthine in poisoning by carbon tetra wood spirits, 167 chloride, 113 States, benefits in death, 12 Softening of brain from electricity, 479 in disability, partial, permanent, 15 Solders, hazard of cadmium, 277 total, permanent, 13 of mercury, 254 temporary, 17 Solidity in neurosis, 510 maximum, 21 Solution dermatitis, 437 and minimum, 12-18 in hernia injection, 433 compensation in occupational diseases, 9 of gases, effect on toxicity, 06 in silicosis, 41 Solvents, 63 insurance fund of California, 6 aliphatic, sources, effects, 65 Department of Industrial Relations of aromatic, sources, effects, 66 California, 6 classification, 65 elective compensation in, 9 hazard of benzene, 74 employees, compensation of, 22. of carbon tetrachloride, 100 fund in compensation, 7 of dermatoses, 435 insurance requirements of workmen's of trichlorethylene, 136, 137 compensation laws, 8 Sorters, cotton-dust hazard, 367 system in compensation, 7 Soto-Hall's sign, 415 limiting benefits, 20 Spasm, clonic, from petroleum, 88 making numerical exemptions, 10 Specific action of solvent, 66 period of payment in injuries, 19 Spectroscopic analysis of quartz, 338 waiting time required, 11 Speech disturbance from manganese, 267 Spelter shakes, 208 Statute of limitations in compensation, 47 Steel industry, hazard of cyanide, 199 Spice dermatitis in bakers, 444 of manganese, 266 Spiegeleisen manufacture, manganese haz of selenium, 288 ard, 266 strength, x-ray and, 337 Spina bifida occulta, 403, 404 Stereoroentgenograms of cement workers, Spinal anomalies, explanation, 400 357 cord compression by intervertebral disc, in silicosis, 330 386 Sterility, plumbism and, 239 hemorrhages from electricity, 479 Stiffness from fluorine, treatment, 153 deformities, intervertebral disc and, 384 Stippled-cell count, 225 fluid, carbon monoxide in, 183 Stippling of erythrocytes, 220, 224 in nucleus pulposus, 386 Stokers, gas works, cancer hazard, 459 puncture in methyl chloride poisoning, heat affection, 465 165 Stolid expression from manganese, 269 Spine fusion for unstable lumbosacral joints, Stomach contents, fluorine in, 150 419 in tetraehlorethane poisoning, 134 movements, 412 Spinning of asbestos, hazard, 353 ulcers, plumbism and, 221, 238 trauma and, 485, .488 Spinous process, failure of vision, 403 zinc and, 299 Spirits, Columbia, Colonial, Manhattan, 167 Stomatitis from mercury, 255, 265 Spirometer test in silicosis, 319 Spleen, effect of benzene, 68, 77, 84 Stone-finishing, silicosis hazard, 307 Stools, antimony in, 301 of cadmium, 278 Storage of gases, solvents, 65 of fluorine, 147 of lead, deleading and, 219 of heat, 466 rupture, traumatic, 490 Storage-battery making, hazard of anti mony, 301 Spondylolisthesis, 405 in back pain, 383 of cadmium, 278 melting, hazard of lead, 217 Spondylolysis, 406 Storms, effects, medicolegal aspects, 467 Sponges, silica in, 304 Stove enameling, lead hazard, 216 Sprained ankle, treatment, 417 Strain in hernia, 421, 422 back, treatment, 416 in spondylolisthesis, 406 Spraying industries, silicosis hazard, 307 Stramonium in mercury poisoning, 265 of pigments, cadmium hazard, 278 Strangulation from trusses, 432 Sputum, asbestosis bodies, 349 of hernia, 427, 429 black, from anthracosilicosis, 344 injection, 433 from cotton dust. 366 Strapping of low back, 416 554 INDEX Stumbling from manganese, 270 Stupor from benzine, 89 from carbon disulfide, 118 Tabacosis, 304, 356 Tabes, carbon disulfide and, 121 Tachycardia from benzine, 89 from methyl alcohol, 1G8 from inethyl chloride, 165 Stuttering from manganese, 267 from petroleum, 88 Subarachnoid hemorrhage in brain trauma, Talc, 350 506 making, silicosis hazard, 307 Subconscious in traumatic neurosis, .505 silicate in, 305 Subluxation, sacro-iliac, 882 Talkativeness from carbon disulfide, 118 Submarine workers, carbon dioxide hazard, Tank-ear cleaning, arsenic hazard, 294 160 Tankage solvent, trichlorelhylene hazard, Sucrose in methyl alcohol poisoning, 170 137 Suction apparatus in vanadium poisoning, Tannery workers, hazard of ammonia, 171 293 of hydrogen sulfide, 156 Suffocation from chlorine, 154 Tannic acid in hernia injection, 433 Sugar dermatitis in bakers, 444 test of blood for carbon monoxide, 182 Suggestion in traumatic neurosis, 503 Tanning, cyanide hazard, 199 Sulfanilamide in chlorine pneumonia, 155 Tar cancer, 461 Sulfapyridine in chlorine pneumonia, 155 eye cancer from, 462 Sulfathiazole in chlorinated naphthalene ointment in dermatoses, 455 poisoning, 132 solvent, trichlorethylene hazard, 136 in chlorine pneumonia, 155 workers, acne, 436 Sulfoxylate, sodium formaldehyde, in mer Taste disturbance from sulfur dioxide, 161 cury poisoning, 263 Teeth, loss, rating, 34 Sulfur, carcinogenic, 400 mottling from fluorine, 148 dioxide, 161-163 Tellurium poisoning, selenium and, 290 eases, 162 Temperature in heat cramps, 466 tuberculosis and, 494 in heat exhaustion, 466 dye works, hydrogen sulfide hazard, in heatstroke, lowering, 475 156 Temporal pain from methyl alcohol, 168 extraction, carbon disulfide hazard, 115 Tenderness in hernia formation, 423 Sulfuric acid dermatitis artefacta, 448 Tendon reflex increase from manganese, 269 makers, sulfur dioxide hazard, 161 Terminal infection in benzene poisoning, 83 Sunlight, eye cancer from, 462 Terminology in industrial medicine, 49 in dermatoses, 441 Terror neurosis, 500 Sunstroke, 5, 466 Testimony, discredited, in relation of effects, medicolegal aspects, 467 trauma to disease, 487 treatment, 475 in court, 50 Support in back sprain, 417 Testis swelling in hernia injection, 433 Surgeon's first report, 51 Tests, basophilic aggregation, 226 Surgery in electrical burns, 481 for carbon monoxide, 182 in hernia, workman's refusal to permit, for cyanides, 200 426 for lead, 225 in low back pain, 419 ' for manganese, 269 Susceptibility to silicosis, 307 for mercury, 255 to gases, solvents, 65 for selenium, 290 Sussmann-Weindel stain for basophilic ag in dermatoses, 438 gregation test, 230 Tetrachlorethane, 134-136 Sweats from malt dust, 374 effect on liver, 64 Sweeping-compound dermatitis, 451 Tetraethyl lead, 90, 216, 255 Swelling in hernia formation, 423 Textile workers, hazard of carbon tetra Sympathy, traumatic neurosis and, 503 chloride, 100 Symptoms, bridging, in traumatic cancer, of chlorine, 154 498 of chromium, 274 in traumatic tuberculosis, 495 of trichlorethylene, 136 delayed, from nitrous fumes, 205 Thallium poisoning, 290 from gases, solvents, fumes, 66 Thawing in frostbite, 476 Syncope from hyperpyrexia, 465 Theory of permanent disability rating, 37 Syndrome of traumatic neurosis, 500 Thiamine in arsenic neuritis, 297 Synergy in occupational dermatoses, 430 in benzene poisoning, 78 Syphilides, traumatic, 450 in trichlorethylene treatment, 140 Syphilis, carbon disulfide and, 121 Thoracic vertebra, 401 compensability, 449 Throat, burning, from ammonia, 171 trauma and, 485 from nitrobenzene, 142 Systemic infection in back pain, 389 care in benzene poisoning, 83 INDEX 555 Throat, constriction from cyanides, 199 Traumatic neurosis, effort to resolve con dryness from cadmium, 278 flict, 503 from carbon tetrachloride, 100 volitional and organic factors, 507 from metal-fume fever, 208 Treating process, cyanide hazard, 199 inflammation from chlorine, 154 Treatment, attitude, malingerer versus neu irritation from sulfur dioxide, 161 rotic, 509 Thrombocytopenia in benzene poisoning, 73 inclusions, 28 Thrombosis of vessels in hernia injection, Tree surgeons, electrical hazard, 478 434 Tremors from benzine, 89 Thuja oil in hernia injection, 433 from mercury, 255 Thumb, loss, period of payment, 19 from methyl chloride, 164 Tic douloureux, trauma and, 485 from tetraethyl lead, 91 Tile glazing, lead hazard, 216 Trial by jury in estimation of disability, 28 setters, cement dermatitis, 446 Trichlorethylene, 136-141 Timberman in mining, silicosis hazard, 327 poisoning, cases, 138 Time in asbestosis formation, 353 medicolegal aspects, 137 in onset of heat exhaustion, 469 symptoms, 139 in traumatic cancer, 498 Trichophyton intradermal test, 442 limit to enforce compensation, 27 Trinitrotoluene, effect on liver, 64 waiting, in each state, 11 Truck-drivers, carbon monoxide hazard, 180 Tin, 300 cold, compensability, 471 alloy, antimony hazard, 301 Trusses, 432 Tinnitus from phenol, 173 fitting, in hernia injection, 433 Tissue absorption of nitrogen, 483 Tuberculosilicosis, carcinoma and, 332 analysis for carbon tetrachloride, 102 Tuberculosis, asbestosis and, 348 cell oxidation, cyanides and, 199 cement dust and, 362 Titanium dioxide in welding, 211 classification, 516 Tobacco dust, 356 extrapulmonary, silicosis and, 317 a-Tocopherol in arsenic neuritis, 298 in anthracite miners, 342 Toe, loss, period of payment, 19 in back pain, 391 permanent disability, 33 in dust diseases, 376 Toluene, 67 in tobacco workers, 356 Tongue tremor from manganese, 272 inert dusts and, 355 Tonics in dust diseases, 375 latent, claim for, 494 Tornadoes, effects, medicolegal aspect, 467 silicosis and, 306, 314 Toxemias in back pain, 383 trauma and, 490 Toxic effects. See under names of etiological cases, 491 agents. compensability, 491-496 states, effect on stored lead, 219 postulates to be satisfied, 491 thresholds of common industrial sub x-tay in, 313 stances, 523. See also Air concentra Tunnel-builders, hazard of caisson disease, tion. 483 Tracheobronchitis in asbestosis, 348 of hydrogen sulfide, 156 Traction in back pain, 416 of nitrous fumes, 205 Transportation operators, electrical hazard, Turkish-bath attendant, epidermophytosis 478 in, 442 Trauma, appendicitis and, 488 Turpentine dermatitis, 444 cancer and, 496 Twitching from benzine, 89 disease and, formulating relationships, from carbon monoxide, 179 487 from electricity, 479 in hernias, 421, 422 from phenol, 173 in industry, 9 Type-metal making, antimony hazard, 301 in interstitial keratitis, 449 in occupational cancer, 459 in workmen's compensation, 4 Ulcers from chromium, 275 medicolegal relationship to disease, 485- gastric, plumbism and, 221, 238 499 trauma and, 485, 488 neurosis associated, 500-518 zinc and, 299 to low back, prevention, 415 Uncertainty in traumatic neurosis, 503 to vertebrae, 404 Unconsciousness from benzene, 78 tuberculosis and, 490 from carbon monoxide, 178 Traumatic encephalopathy, 500, 501 from concussion, 501 hysteria, 500, 502 from electricity, 478 neurosis, 480, 502 from gasoline, 90 classification, 504 from heatstroke, 466 556 INDEX Unconsciousness from phenol, 173 Ventilation in poisoning by trichlorethylene, United States, civil employees, insurance re 139 quirements, 8 by zinc, 300 Urea clearance in benzene poisoning, 78 in welding, 210 Uremia from carbon tetrachloride, 64, 102 metal-fume fever and, 210 Ureter kinking, trauma and, 485 of lungs in asbestosis, 353 Urinalysis in methyl chloride poisoning, 104 in silicosis, 319 Urinary bladder, carcinoma, dyes and, 462 of projector lamps, 214 occupational cancer, 460 Ventricle, left, effect of carbon monoxide, calculi, trauma in, 488 186 incontinence in caisson disease, 484 Ventricular fibrillation from electrical in Urination from cyanides, 200 juries, 481 Urine, arsenic in, 295 Ventriculin in benzene anemia, 83 excretion of lead, 219 in benzene poisoning, 78 Vertebrae, 400 failure of fusion, 405 in lead poisoning, 222, 232, 235 lumbar, sacralization, 406 manganese in, 266, 269 Vertigo from antimony, 301 selenium in, 289 from benzene, 73 sulfate and, ratio in benzene poisoning, 72 from benzine, 89 Urobilinuria in benzene poisoning, 73 from cadmium, 278 from caisson disease, 483 from carbon dioxide, 160 Vagus nerve, effect of hydrogen sulfide, 156 from carbon disulfide, 118 Van den Bergh reaction in carbon tetra from carbon monoxide, 178 chloride poisoning, 102 Vanadium, 292-293 from carbon tetrachloride, 102 from cyanides, 199 pentoxide, 992 from ethylene dichloride, 145 Vanilla dermatitis in bakers, 444 from gasoline, 96 Vapor-lamp making, cadmium hazard, 278 from heatstroke, 466 Vapors, bronchodilator, in dust diseases, 375 from hydrogen sulfide, 156 toxic thresholds, 523 from methyl chloride, 164 Varnish-making, hazard of benzene, 67 from nitrobenzene, 143 of carbon disulfide, 115 from nitrous fumes, 205 of contact dermatitis, 444 from petroleum, 88 of lead, 216 from phenol, 173 silk workers, hazard from ammonia, 171 from tetrachlorethane, 134 Vascular disease, caisson disease and, 484 from tetraethyl lead, 91 impairment from mercury, 258 from trichlorethylene, 137 Vaseline, 88 from trauma, 505 in dermatoses, 452 Vesicants in dermatitis artefacta, 448 Vasomotor center, effect of fluorine, 147 Vesicles in dermatoses, treatment, 455 instability from trauma, 505 Vessels, effect of heat, 465 symptoms from carbon disulfide, 121 Viosterol in deleading, 248 Vasospasm in back pain, 388 Viscera, congestion, from tetraethyl lead, 91 Vatmen, carbon dioxide hazard, 160 effect of cadmium, 278 Venereal disease, status in compensation, 48 Viscose rayon, carbon disulfide hazard, 115, Venesection in heatstroke, 475 124 in poisoning by carbon monoxide, 198 Vision, effect of caisson disease, 484 by chlorine, 155 of carbon disulfide, 119, 120 by mercury, 264 of carbon monoxide, 179 by petroleum, 99 of carbon tetrachloride, 102 by phosgene, 140 of heatstroke, 466 by sulfur dioxide, 163 of nitrobenzene, 143 Venous pressure in silicosis, 320 of nitrous fumes, 205 Ventilation in asbestos plant, 377 of petroleum, 88 in benzene exposure, 81 of tetraethyl lead, 91 in dust tuberculosis, 355 of trichlorethylene, 137 in dusty occupations, 378 permanent disability, 33 in plumbism, 250 Vital capacity in silicosis, 319, 320 in poisoning by carbon disulfide, 125 Vitamin B in poisoning by carbon disulfide, by carbon tetrachloride, 103, 113 125 by chlorinated naphthalene, 132 by selenium, 291 by hydrogen sulfide, 158 Bi in manganese poisoning, 273 by manganese, 273 B in arsenic neuritis, 298 by selenium, 290 C in prevention of heat affections, 474 INDEX 557 Vitamin D in deleading, 247 Weakness from metal-fume fever, 209 K in tetrachlorethane poisoning, 135 from tetraethyl lead, 91 Vitamins in dermatoses, 455 in disability estimation, 31 in dust diseases, 375 Weather change, intolerance from trauma, in poisoning by arsenic, 297 505 by carbon tetrachloride, 112 medicolegal aspect, 467 by lead, 248 Weaving, asbestosis hazard, 348, 353 by mercury, 265 cotton-dust hazard, 367 by nitrous fumes, 207 Weeks for payment in injuries, 19 by petroleum, 99 Weeping from manganese, 267 Volitional factor in traumatic neurosis, 507 in dermatoses, treatment, 455 Vomiting from arsenic, 295 Weevils fumigant, ethylene dichloride haz from cadmium, 278 ard, 144 from caisson disease, 483 Weight in spondylolisthesis, 406 from carbon tetrachloride, 102 loss from anthracosilicosis, 340, 343 from cyanides, 199, 200 from antimony, 262 from fluorine, 147 from asbestosis, 348 treatment, 153 from benzene, 73 from malt dust, 374 from benzine, 89 from mercury, 255 from cotton dust, 366 from metal-fume fever, 208 from cyanides, 201 from methyl chloride, 104 from fluorine, 148 from petroleum, 88 from hydrogen sulfide, 157 from selenium, 289 from lead, 222 from tetrachlorethane, 134 from nitrous fumes, 205 from trichlorethylene, 137 from petroleum, 88 Vulcanizers, hazard of benzene, 67 from silicosis with infection, 315 of sulfur dioxide, 161 Welding, 210-212 hazard of aluminum oxide, 211 of benzene, 67 Wage loss, determination, in compensation, of cadmium, 278 321 of mercury, 254 silicosis and, 322 Well workers, hydrogen sulfide hazard, 156 percentage, in death, 12 in disability, 25 Wet clothing in prevention of heat affec tions, 474 partial, permanent, 15 compresses in dermatoses, 455 payments, 12-18 dressings in chrome ulcers, 276 total, permanent, 13 Whipple grid in basophilic aggregation test, temporary, 17 231 Wallpaper manufacture, chromium hazard, White blood cells. See Leukocytes. 274 White's crude coal tar paste in infectious War, gassing with chlorine, 154 eczematoid dermatitis, 456 Warmth in heat exhaustion, 475 Wire insulation, chlorinated naphthalene in poisoning by methyl alcohol, 170 hazard, 127 by petroleum, 98 Wood naphtha, 167 Warts in refinery workers, 461 spirits, green, 167 Washing-powder dermatoses, 452 standard, 167 Wassermann test in preemployment exam Woodworkers, methyl alcohol hazard, 167 ination, 515 Wool extraction, trichlorethylene hazard, Water blisters from carbon tetrachloride, 136 106 Work capacity, decreased, from anthraco- dermatoses, 452 gas, 176 hot, in cold sensitivity, 476 silicosis, 340 from silicosis, 306 changing, age and, 35 in dust suppression, 377 malingerer versus neurotic, 509 Waterglass, silica in, 305 Working clothes in cancer prevention, 463 Weakness from anthracosilicosis, 340, 343 conditions, changing, in dermatoses, 453 from arsenic, 295 hours, caisson disease and, 484 from benzene, 77 Workman, allegations in hernia, 422 from benzine, 89 compensation act, digest, 21 from carbon dioxide, 160 from carbon tetrachloride, 102 miscellaneous provisions, 27 purpose, 2 from lead, 239 administration, 7 from malt dust, 374 physician's function, 47 from mercury, 255 purpose, 1 558 INDEX Workman, diseased, classification, employ- .r-Rny findings in compensation cases, 49 ability, 519 in cotton-dust exposure, 307, 309 handicapped, provision for, 51(1 in gasoline poisoning, 93-95 objections to preemployment examina in grain-handlers, 374 tion, 514 in infectious eczematoid dermatitis, selection in prevention of caisson disease, 450 48-t in lead poisoning, 237 Wounds, infectious eczematoid dermatitis in manganese poisoning, 209 in, 442 in nucleus pulposus, 380 Wrist drop from lead, 221 in pneumoconiosis, 308 gas tar cancer, 459 in preemployment examination, 515 in silicosis, conglomerate shadows, 312, 313, 318 z-Ray analysis of solids, 337 localized discrete densities, 313 bone, effect of fluorine, 148 massive shadows, 313 changes in silicosis, 313 mottling, 313 diffraction analysis of barvtes, bentonite, 335 nodulation, 312 soft nodulation, 313 in silicosis, 318 with infection, 315 for silica, 305 in tabacosis, 356 principle, 337 in traumatic cancer, 497 examination in back pain, 394 Xylene, 07 findings in anthracosilicosis, 340, 340 in asbestosis, 351, 353 in back pain, 383, 391 in barytosis, 335 Zinc, 299-300 in benzene poisoning, 83 chills, 208 in cadmium poisoning, 282 chloride burns, 300 in cement workers, 357, 358 manufacture, manganese hazard, 266 in chlorinated naphthalene poisoning, mining, silicosis hazard, 307 132 smelting chargers, arsenic hazard, 294