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The Principles and Practice of INDUSTRIAL MEDICINE Edited, by FRED J. WAMPLER, M.D. Profteear, Preventive and Induetrial Medicine xmdkx&l coiuaa or mmu CONTRIBUTORS Otis L. Anderson Robert A. Kehoe R. N. Anderson M. H. Kronenberg Anna M. Baetjer B. E. Kuechle J. J. Bloomfield Matthew Lucldesh J. A. Calhoun Willard Machie J. M. Carlisle R. W. McKee George H. Cross Sarah I. Morris Donald E. Cumming Kenneth Morse Charles F. Engel Frank K. Moes John H. Foulger C. M. Peterson Augustus Gibson D. F. Robertson T. Lyle Haslett F. S. Rossiter Albert Hemming William A. Sawyer F. F. Heyroth Louis Schwartz Joanna Johnson Lorin A. Thompson R. T. Johnstone Fred J. Wampler George Zur Williams O' O o' o* Y A William Wood Book <7 &> BALTIMORE THE WILLIAMS & WILKINS COMPAQ 1943 o vO 4?' ST08537I7 ST08537I 8 FOREWORD Advancement in the knowledge of industrial medicine presupposes a far wider dissemination of instruction than that which has obtained to this time. The instructional effort in this field must increase tremendously, both in its purely didactic and in its clinical aspects before the student in medicine may be considered as having received adequate general training. Not only for the student, but for those already engaged in the art of healing is such instruction eminently useful. Concern for the welfare of the industrial worker is no longer a matter in the realm of mere sentiment. It has become a vital, concrete necessity even when completely divorced from its humanitarian implications. The day has actually come when the absence of well-conducted medical depart ments in industry is suggestive of medievalism when measured by the criterion of social progress and of financial obtuseness when measured by the more tangible criterion of profits and losses. Scientific discovery, in its ever accelerating pace, has brought before us new concepts of the relationship of the environment to physical well-being. It is inevitable that industry take cognizance of these facts and be guided by them in providing protection for its workers. The great strides in scientific knowledge have widened the scope of industrial medicine; but our contribution to the worker's health will not be commensurate to the possibilities unless we are, as physicians, aware of the broadened horizon. We have noted, with the utmost gratification, that of recent years many of our medical schools have included training in industrial medicine in their curricula. We have noted, moreover, that the new offering is being re garded less and less as usurping a place in the roster of courses and more and more as an integral part of medical training. This augurs well for industrial medicine and will assure for it an increasing receptivity both from the worker and from management. Warm commendation is justly forthcoming to the editor of this book and to the individual contributors. They have made a signal contribution to the student of medicine whether he be still in school or in the active practice of his profession. Their contribution is, indeed, a particularly timely and loyal service to the nation at a moment wheri a dire need for this service exists. Pittsburgh, Pennsylvania T. Lyle Hazlett, M.D. v I PREFACE The purpose of this book is twofold. In the first place, many practicing physicians are being asked to take on the medical care of industrial workers when they never have had experience in industrial medicine before. This book should give them a general idea of the principles of industrial medicine. Secondly, medical schools should be placing more emphasis on the teaching of industrial medicine to medical students so that the oncoming physicians will know how to step in and do a real job of health protection for the who works. Industrial medicine differs from regular practice principally in the view point. Here the physician is working with well people trying to keep them well. This, then, is a new discipline. Industrial medicine thus becomes the practice of adult health. New techniques have been and are being developed which help the industrial physician better to do the job of keep ing the worker well. Some of these techniques are brought out in this book. Starting with these, the alert physician will develop other methods of his own. I want to record here my appreciation of the willingness with which the contributors undertook their jobs in a time of unusual stress and when there were many demands upon their time. This was done in spite of the fact that some of the men had military and governmental responsibilities thrown upon them that took much of their time after they had promised to contri bute to this book. I wish to express my appreciation to J. Clarence Funk, Sc.D., who read much of this material and made valuable suggestions as to clarity of state ment, and to Prof. Harvey B. Haag, my colleague, for reviewing the chap ters in the toxicological field. I should also here record my appreciation for the work that Mrs. Wampler put on this book. She has done most of the secretarial work in my office in connection with this publication. The thirty-three contributors to the book are now joined together in a little family of workers in a common cause. It has been a pleasure to work with scientific men and women like these. We are sorry to have to record that Professor Don Cumming, one of the youngest, ablest and most genial of the group, lost his life in an airplane accident a short time after he had sent in his manuscript. Richmond, Fo. Feed J. Wampler, M.D. LIST OF CONTRIBUTORS Awdebson, Otis L., BJ3c., M.D., F.A.C.P. . ; Surgeon, United States Public Health Service, Assistant Chief, Divi sion of Venereal Diseases, National Institute of Health, Bethesda, Maryland. Anderson, Richard N., B.A., M.A. Director of the Division of Rehabilitation, Special and Adult Educa tion of the Virginia State Department of Education, Richmond, Virginia. Baitjeb, Anna M., Sc.D. Associate in Physiological Hygiene, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland. Bloomjteld, J. J. Sanitary Engineer, United States Public Health Service, and Chief, States' Relations Section, Division of Industrial Hygiene, National Institute of Health, Bethesda, Maryland. Calhoun, J. A., M.D. Medical Director, American Viscose Corporation, Wilmington, Dela ware. Cahlible, J. M., M.D. Medical Director, Merck and Company, Rahway, New Jersey; Professor of Industrial Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania; Executive Director, Bureau of Industrial Health and Hygiene, New Jersey State Department of Health. Cnoss, George H., M.D. Associate Professor of Ophthalmology, University of Pennsylvania, Graduate School of Medicine, Chester, Pennsylvania. Cummino, Donald E., B.S.* Associate Professor, Department of Medicine, and Director, Division of Industrial Hygiene, University of Colorado School of Medicine, Denver, Colorado. Engel, Chahles F., M.D. Assistant Medical Director, Westinghouse, Electric and Manufactur ing Company, East Pittsburgh, Pennsylvania. Foulgeb, John H., M.D., Ph.D., F.A.C.P. Medical Director, Haskell Laboratory of Industrial Toxicology, Wil mington, Delaware; Associate Professor of Industrial Medicine, Medical College of Virginia, Richmond, Virginia. * Deceased December, 1942. IX ST085372I } X LIST OF CONTRIBUTORS Gibbon, Augustus, M.D. Physician, Merck and Company, Rahway, New Jersey. Haelett, T. Lyle, M.D. Medical Director, Westinghouse Electric and Manufacturing Com pany, Professor, Industrial Hygiene, University of Pittsburgh,Pitts burgh, Pennsylvania. Hxuming, Albert, M.B., Ch.B. Physician, Merck and Company, Rahway, New Jersey. Hxtboth, Francis F., M.D. Assistant Professor of Research Physiology, Kettering Laboratory of Applied Physiology, College of Medicine, University of Cincinnati, Cincinnati, Ohio. Johnson, Joanna, R. N. Supervisor, Industrial Nursing Division, Employers Mutual Liability Insurance Company, Milwaukee, Wisconsin. Johnstone, Rutherford T., 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, Pitts burgh, Pennsylvania. Kkhoe, Robert A., M.D. Research Professor of Physiology, Director, Kettering Laboratory of Applied Physiology, College of Medicine, University of Cincinnati, Cincinnati, Ohio. Kronenberg, Milton H., M.D. Chief, Division of Industrial Hygiene, and Industrial Medical Super visor, Department of Public Health, State of Illinois; Assistant Professor of Bacteriology and Public Health, University of Illinois Chicago, Illinois. Kuechle, B. E., A.B. Vice-President and Claims Manager, Employers Mutual Liability Insurance Company, Wausau, Wisconsin. Luciuesh, Matthew, D.Sc., D.E. Director, Lighting Research Laboratory, General Electric Company, Nela Park, Cleveland, Ohio. Machle, Willard, M.D. Associate Professor of Research Physiology, Associate Director, Ket tering Laboratory of Applied Physiology, College of Medicine, University of Cincinnati, Cincinnati, Ohio. McKee, R. W., Ph.D. Instructor in Industrial Hygiene, School of Public Health, Harvard University, Boston, Massachusetts. LIST or CONTRIBUTORS XI Morbis, Sarah I., M.D., F.A.C.P. Professor of Preventive Medicine, Womans Medical College of Penn sylvania, Philadelphia, Pennsylvania. Morbe, Kenneth, MJ3. Industrial Engineer, Division of Industrial Hygiene, Illinois State Department of Public Health, Chicago, Illinois. Moss, Frank K, E.E. Physicist, Lighting Research Laboratory, General Electric Company, Nela Park, Cleveland, Ohio. Peterson, C. M., M.D. Secretary, Council on Industrial Health, American Medical Associa tion, Chicago, Illinois. Robertson, D. F., M.D. Associate Medical Director, Merck and Company, Rahway, New Jersey. Rossfter, Frank S., M.D. Medical Director, Camegie-Hlinois Steel Company, Pittsburgh, Pennsylvania. Sawter, William A., M.D. Medical Director, Eastman Kodak Company, Rochester, New York. Schwartz, Louis, M.D. Medical Director, United States Public Health Service, and Chief, Dermatoses Investigations Section, Division of Industrial Hygiene, National Institute of Health, Bethesda, Maryland. Thompson, Lorin A., Ph.D. Director, Population Study, Virginia State Planning Board, Rich mond, Virginia. Wampler, Fred J., M.A., M.D., M.P.H. Professor, Preventive and Industrial Medicine, and Administrator, Out-Patient Clinic, Medical College of Virginia; Health Consultant, Southern Biscuit Company, Richmond, Virginia. Williams, George Zur, M.D. Associate Professor of Pathology, Medical College of Virginia, Rich mond, Virginia; Member of Armed Forces, Lt. Com. UJ3.N.M.C.R. CONTENTS I. Note* on Hiatory.......................................................................................... 1 Fred J. Wampler, M.D. II. Method* Employed in the Appraisal and Control of Industrial Health Hasards................................................................................................... J. J. Bloomfield 7 III. Industrial Accidents: Their Cause and Prevention............................... 23 Donald E. Camming, BJS. IV. Medioal Services in Industry and the Industrial Physician................. 35 Fred J. Wampler, MD. V. The Lay-Out of the Medioal Department............................................... 43 Fred J. Wampler, MD. VI. Governmental Agencies in Industrial Hygiene....................................... 48 J. J. Bloomfield VII. Industrial Health Program of the American Medical Association-- 65 C. M. Petereon, M.D. VIII. The Effects of Temperature and Humidity on Industrial Workers-- 69 Anna M. Baeljer, Se.D. IX. The Effects of Abnormal Atmospheric Pressures................................... Si Anna M. Baeljer, Sc.D. X. Light, Lighting and Seeing........................................................................ 101 Matthew Luckeieh, M.D., and Frank K. Moee, E.E. XI. Fatigue........................................................................................................... 133 Larin A. Thompeon, Ph.D. XII. The Physical Examination......................................................................... 144 Fred J. Wampler, M.D. XIII. Medical Control of Industrial Exposure to Toxic Chemicals............... 150 John H. Foulger, M.D. XIV. Survey of Substances which Cause Occupational Poisoning................ 180 Willard Mochle, MD., and Franeie F. Heyroth, M.D. XV. Industrial Lead Exposure and Lead Poisoning....................................... 202 Robert A. Kehoe, M.D. XVI.Carbon Disulfide............................................. .............................................. 241 Ralph W. McKee, Ph.D., and J. A. Calhoun, M.D. XVII. The Toxicity of Certain Organic Solvents in Industry......................... 256 J. M. Carliele, M.D. XVIII. Carbon Monoxide Poisoning...................................................................... 269 Frank 8. Roeeiter, M.D. XIX. Some of the Poisonous Gases...................................................................... 278 Frank S. Roeeiter, M.D. xiii in .s s fln ,i.s . - xiv CONTENTS XX. Electricity................................................................................................ 288 Charlee F. Engel, M.D. XXI. Occupational Diseases of the Skin......................................................... 29A Louie Schwartz, M.D. XXII. Pneumoconiosis (Duet Diseases of the Lung)...................................... 345 Qeorge Zur Williams, M.D. XXlll. Occupation and Tuberculosis................................................................. 375 Sarah /. iforris, M.D. XXIV. Venereal Disease Control in Industry................................................... 394 Otis L. Andereon, MJ>. XXV. What Industry Can Do to Improve Nutrition..................................... 409 William A. Sawyer, MD. XXVI. Eyes in Industry: Care and Prevention of Injury............................... 421 Qeorge H. Croet, MD. XXVII. Traumatic Shock and Burns................................................................. 435 J. M. Carliele, M.D., Augueiue Qibeon, M.D., Albert Hemming, MD., Ch.B., and D. F. Roberteon, MD. XXVIII. The Industrial Back................................................................................ 458 Rutherford T. Johmtone, M.D. XXIX. The Nurse in Industry............................................................................ 483 Joanna Johnson, R.N. XXX. Compensation.......................................................................................... 498 B. E. Kueehle, AD. XXXI. Vocational and IndustrialRehabilitation............................................. 507 Richard N. Andereon, M.A. XXXII. Industrial Medical Service for the Smaller Plant................................ 518 Fred J. Wampler, MD. XXXIII. Women in Industry................................................................................. 523 Milton H. Kronenberg, M.D., and Kenneth Moree, M.3. !1 mi3725 Chapter I NOTES ON HISTORY Fred J. Wampler, M.D. Industrial medicine is largely a development of the last hundred and forty-three years--the machine age--but occupational diseases were known from before the Christian era. The more important stepping stones in the development of our knowledge of occupational diseases will be out lined in this chapter. In the early days labor was performed largely by slaves. The nearest approach to our modem industrial practice was when an individual's slave* would become proficient in some type of work. This Blave owner would then contract for this particular type of service. Ax grinding is known to have been done in this way and mining and other types of work could easily have followed this line of development. Hippocrates (about 460-370 B.C.) described a disease that might well have been hookworm; those suffering from it ate stones and earth, had great intestinal disturbances and were jaundiced. Insanitation of mines up until modem times made them ideal places for the spread of hookworm disease. Other diseases described by Hippocrates are those involving metallur gists, fullers, tailors, horsemen, farm hands and fishermen. He describes the metal worker as being pale and livid, with difficult respiration, a dis tended, hard abdomen, large spleen and a swollen right hypochondrium. Pliny the Elder (23-79) described a protective mask for miners, which consisted of a bladder tied over the mouth to prevent inhalation of poi sonous dusts and vapors. Pliny recommended to wine dealers the use of cabbage and bitter almonds as a protection against alcoholic intoxication. He described poisoning with zinc and sulphur. Galen (131-201), the founder of experimental physiology, has many ref erences to occupational diseases. He visited a copper mine on the island of Cyprus and was nearly overcome with fumes. He writes that the work men who carried out a vitriolic liquid ran with all speed from the mine to avoid death in the midst of their labors. Galen also said students and scholars are exposed to a hazard from the fumes of the tallow candles they were forced to use. Other occupational diseases mentioned by Galen con cerned runners, farmers, wrestlers, wet nurses, gypsum workers and those who used their voices excessively. 1 ST0853726 2 PRINCIPLES AND PRACTICE OP INDUSTRIAL MEDICINE As times advanced others made important contributions in the field of occupational diseases, such as Agricola, Ulrich Ellenbog and Paracelsus. Georg. Agricola (1494-1555), in his treatise on mining and metallurgy, refers to dangers and diseases to which miners and refiners are exposed. Ulrich Ellenbog of Swabia, Germany, described in 1473 the symptoms of mercury and lead poisoning (headache, visual disturbances, paralysis and unconsciousness) and gave advice concerning their avoidance. This was the first work written expressly on the subject of industrial metal poison ing. Paracelsus (1493-1541), a Swiss, wrote a treatise dealing exclusively with occupational diseases. This was not published until 1567, twentyseven years after the author's death. He wrote on metals and minerals known at that time and gave the symptoms caused by each and the thera peutic procedures to be used in case of poisoning. It is supposed that Paracelsus himself was a victim of his enthusiasm in the investigation of the noxious influences found in mines and that he died as a result of heavy metal poisoning. We now come down to Ramazzini (1633-1714), known as the Third Hippocrates and the Father of Industrial Medicine, who wrote an excellent work on the diseases of tradesmen, the "De morbis artificum diatriba." His work was published in Padua in 1700 and was written so well that it was more than one hundred years before it was improved upon. He made an exhaustive review of the literature and his book contained most of the information in this chapter that precedes this paragraph. He described about a hundred different occupations and the special hazards involved in each. His descriptions were based on his own clinical observations. The book was written for practicing physicians that they might be ac quainted with the various trades and to advise the proper treatment and prevention of occupational diseases. Even a brief history of industrial medicine would not be complete with out mention of the influence that the craft guilds had upon the lives of skilled workmen in the fourteenth century and afterwards. The guilds were formed primarily for the protection and the regulation of certain trades; these were generally organized ultimately into monopolies. The guild controlled the admission of apprentices, controlled the hours of labor and regulated wages and the selling price of finished products. The stan dards of the trades were upheld by frequent inspections. It can be seen from this that they completely controlled the personnel and the quality of the finished products of the trades. The physical and social welfare of the individual member of these guilds was considered quite im portant. and this was a step in the advancement of better working condi tions in the production of goods. Some guilds of this general type still NOTES ON HISTOKY 3 exist in China and India although they have long since died out in countries where machinery has taken the place of hand labor. The famous Bidar ware produced in Hyderabad, a native state in India, is a good example ot'such a guild at the present time. Here the guild owns the secret process for making this product. Diamond cutting and some of the Swiss watch making are still done by secret techniques handed down from father to son by the old craft guild system. The introduction of machinery in the production of goods changed the whole industrial picture. In England the factory system developed rap idly in the latter part of the eighteenth century. While workers were generally well paid, the physical welfare of the employee was neglected. Long hours were the rule and machinery was unguarded. Lighting and ventilation were bad. Under such conditions the accident rate was high and industrial diseases prevalent. The mortality rate of workers was higher than that of farmers or other non-factory workers. Child labor was the general rule and oftentimes the child had to work twelve hours in twenty-four. The Health and Morals Act to regulate the labor of bound children in cotton factories was passed by Parliament in 1802. The great prison reformer, John Howard (1762-90) was one of the leaders in laying the foundations of modem hygiene. He visited most of the known prisons of England and Europe and wrote accounts of his findings. He thus gave publicity to the inhuman and often corrupt administrations which he found. He might be said to have established the value of inspec tion and reporting, which are strong arms of modem hygiene. Edwin Chadwick (1800-90), a barrister who became interested in life insurance, studied the effect of environment on the length of life. Chad wick in 1832 was appointed to investigate the workings of the Poor Laws. When a factory commission was set up by the Factory Act of 1833, Chad wick was the secretary and executive officer of the commission which was composed of three appointed members. Professional inspectors were ap pointed by this commission and they were a very potent force in the proper conduct of factories. (See Newsholme.) Labor legislation in the United States has lagged considerably behind that of England (1897) and of the more progressive (Germany 1882) coun tries on the continent. The year 1911 marked the beginning of effective legislation in the United States. In that year California and New York made compulsory the reporting of occupational diseases and New Jersey made certain occupational diseases compensable. Now (1943) all the States, except one, have laws requiring compensation for industrial acci dents. About half of them have laws requiring compensation for at least some of the industrial diseases. ST0853728 4 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE High lights in the history of the development of industrial hygiene in America are given in the following outline: 1837--Committee appointed by Pennsylvania to investigate child labor. 1875--First federal statute relating to labor was passed. 1877--Massachusetts gave inspectors the right to enter into factories. 1884--Federal Bureau of Labor was created. 1895--The first nurses were employed by an industrial organization. 1906--National Committee on Child Labor and the American Association of Labor Legislation were organized. 1910--The first clinic for occupational diseases was established, first American Congress on Industrial Diseases was held, and the United States Bureau of Mines was created. 1911--As noted in paragraphs above, the first American laws for compulsory reporting of occupational diseases were passed by California and New York, and certain occupational diseases were made compensable by New Jersey. 1912--The use of white phosphorus matches was abolished by the establishment of a prohibitive tax, the Children's Bureau in the Department of Labor was created, and the congress authorized the appointment of a Com mission on Industrial Relations. 1913--The National Safety Council was organized. The Public Health Service and the Bureau of Mines did the first study of the health of workers in dusty trades. 1914--In the Public Health Service the office of Industrial Hygiene and Sanita tion was organized as was the Section on Industrial Hygiene of the American Public Health Association. 1916--The first symposium on Industrial Hygiene and Medicine was held at the meeting of the American Medical Association. 1916--The American Association of Industrial Physicians and Surgeons was organized. 1919--The Journal of Industrial Hygiene was established and Wisconsin passed the first clear cut law making occupational diseases compensable. 1920--National Safety Code for protection of heads and eyes of industrial workers was published. 1921--The Safety Code for Foundries was approved and the reporting of mor bidity among industrial workers was begun by the U.S.P.H.S. 1922--Committee on Benzol was established by National Safety Council. 1926--Committee on Industrial Medicine and Traumatic Surgery was appointed by the American College of Surgeons and this same year the College formulated and adopted the Minimum Standard for Medical Service in Industry. 1929--Safe limits of dust concentration in granite cutting plants were established. 1932--The publication of the magazine of Industrial Medicine was begun. 1934--Adoption of Safety Code for Sanitation of Factories; Federal Conference on Labor Legislation; U. S. joined International Labor Office. 1937--A.M.A. established Council on Industrial Health. 1939--First Congress on Industrial Health was held by AM.A.'s Council on Industrial Health. NOTES ON HISTORY 5 1940_President Roosevelt created Office of Defense, Health and Welfare Service, which appointed Committee on Health and Medicine with Sub-Com mittee on Industrial Health and Medicine. Dept, of Labor appointed National Committee for the Conservation of Manpower in Defense Industries. 1942--American Association of Industrial Nurses was organized. All of the above have had their place in the development of the modem industrial medical and health hygiene programs. Some of the actions and developments, however, were much more important than others. In this important group would be the Federal and State legislation requiring em ployers to pay for accidents and occupational diseases, which did more through bureaus and divisions of government set up by this legislation than other factors toward improving working conditions and reducing industrial sicknesses. Much, however, was accomplished by a number of voluntary organizations and scientific and professional associations. Foremost in this group promoting industrial health have been the National Safety Council, the American Association of Industrial Physicians and Surgeons and the American Industrial Hygiene Association. These last two groups carried the banner for industrial health when many doubters and opposers stood on the side lines. The high standards of industrial medicine and hygiene were made possible by the character and professional strength of the men making up these two organizations. More recently several professional organizations have had a leading hand in carrying forward this program. One of these is The American College of Surgeons which organized its Committee on Industrial Medicine and Traumatic Surgery in 1926. This committee has done excellent work in setting minimum standards for medical services in industry, in surveying the medical departments of industrial plants and accrediting those that measure up to their standards. Another is the Council on Industrial Health formed by the American Medical Association in 1937. This Coun cil has had a strong influence on the continued development in industrial medicine through its Annual Congress on Industrial Health, through its exhibits, and through influencing the state and local medical societies to appoint committees and helping them develop programs on industrial medicine and health. Post-graduate and under-graduate industrial medi cal education are also being stressed by this Council. In the hands of these associations and their councils and committees, industrial medicine should make rapid strides forward in the immediate future. More about organized medicine's part in this program is given in Chap ter VII. Of the governmental bureaus, the Division of Industrial Hy giene, National Institute of Health, Bethesda, Maryland, has at the pres ent time the most widely diversified program and has a large group of ST0853730 Chapter II METHODS EMPLOYED IN THE APPRAISAL AND CONTROL OF ^ INDUSTRIAL HEALTH HAZARDS1 J.J. Bloomfield It is generally conceded that in order to obtain practical results in indus trial hygiene, we need the combined efforts of the physician, the engineer, the chemist, and the nurse. Basically, we can divide our mode of attack on industrial hygiene problems into two parts: first, we must attack those problems concerned with the hygiene of the individual, and second, those dealing with the environment in which the individual works and lives. The first function comes within the scope of the medical sciences and has been treated adequately in the other chapters of this book. The second function deals with engineering practices and forms the basis for the pres ent discussion. Under medical sciences would come the allied professions--nursing and the various medical specialties, such as pathology and physiology. En gineering services would include, in addition to engineering, the work of other public health personnel, such as chemists, bacteriologists, and biometricians. In other words, the functions coming within the province of the medical department are concerned with the individual, while the functions with which the engineer concerns himself deal with the environment. Insofar as the working environment is concerned, it is within the prov ince of the medical department to determine the existence of such diseases as may be due to the working environment, while on the basis of the phy sician's findings the engineer is in a position to learn what unhealthful conditions should be investigated and where control measures need to be ini tiated. It is essential therefore that the various professions clearly under stand the functions of each, and approach the solution of the industrial hygiene problem as co-workers in a joint effort, cooperating with each other to the fullest extent. Ill health and premature death have been associated with the nature of man's livelihood from time immemorial. Studies in recent years have clearly indicated that the health of workers engaged in industry can be affected by the conditions, materials, and processes of work. For these 1 Much of the material in this chapter has appeared in the Industrial Medicine Number of the July 1942 issue of the Medical Clinics of North America. Credit is due to W. B. Saunders Company for permission to reprint this material. 7 ST0853732 8 PRINCIPLES AND PRACTICE OP INDUSTRIAL MEDICINE reasons, important functions in industrial hygiene are the study of the workroom environment and its effect on health, and the subsequent de velopment of methods for the control of environmental hazards. It is realized, of course, that in ordinary times the worker spends only approximately one-third of his day at his place of employment. His health can therefore also be influenced by his home and recreational en vironment. These latter conditions,may also bear an important relation ship to the so-called nonoccupational diseases, which are a major cause of time lost from work. For this reason, attention must also be given to factors outside the workroom which might have a bearing on a worker's health and efficiency. The present chapter will be limited to a discussion of the working environment only. If we examine the literature on industrial hygiene, we are confronted with the fact that methods employed in the study of the effect of industrial health hazards differ but little from those used in investigations of other phases of public health. This is not strange, since in the studies of indus trial diseases it is essential, as in communicable disease investigations, to determine the etiology, pathology, symptomatology, and the application of measures to prevent or control the disease. One may therefore employ the term "industrial epidemiology" when referring to the methods used for the investigation of diseases occurring in industry or among industrial workers, and the subsequent determination of methods of prevention or control of such diseases. It is the purpose of the present discussion to treat some of the methods which are employed in those phases of industrial epidemiology dealing with the workroom environment. THE STUDY OF THE WORKROOM ENVIRONMENT The Reconnaissance Survey One of the functions of an engineer in the field of industrial hygiene is the study of the workroom environment in an effort to determine any re lationship between that environment and its effect on the health of the worker. In all such investigations there are certain preliminary steps of fundamental importance which must be undertaken in order to serve as a guide in the more detailed studies which may be indicated. These prelim inary steps are the basis for the reconnaissance survey and consist of the sanitary appraisal and the occupational analysis of the workroom and its inhabitants (1). The sanitary survey of the workroom consists in noting items of a gen eral sanitary and hygienic nature, such as provisions for ventilation, illu mination, fire protection, accident protection, exposure to specific poisons, such as dusts, fumes, vapors, and gases, fatigue, and so on. In other ST 0853133 APPRAISAL OF INDUSTRIAL HEALTH HAZARDS 9 TOrds, sanitary survey yields information concerning the presence of various health hazards and serves as a guide in determining which hazards require further detailed study in the nature of actual quantitative determinations. One should look upon this type of survey as a listing of the facilities afforded the worker while in the industrial environment and may be likened to the inventory of materials in stock which a business establish ment usually undergoes periodically. The occupational analysis, which is also a part of this inventory or recon naissance survey, permits one to learn of the activities involved, the partic ular hazards associated with each occupation, and the number of persons in each occupation. In order to assist the engineer in the conduct of such reconnaissance sur veys, certain forms are recommended. The forms illustrated have been developed as the result of experience during the past two decades in nu merous investigations of industrial establishments throughout the United States. It has been found that in nearly all instances the filling out of these forms has proved a valuable guide and starting point in the subse quent studies of the workroom environment. The first form lists data of a general nature. It covers items of a sani tary character in order to provide information on housekeeping; provision of certain personal services, such as cloak room, locker rooms, showers, and toilets; and information on various control measures which may be in use, such as ventilation and safety devices. Space is also provided for the list ing of exposures to certain hazards arising from fumes, gases, dusts, and specific poisons. The second form deals primarily with the individual occupation, providing space for the designation of the occupation, the number of persons involved, the nature of the work itself, and the raw materials and by-products associated with each occupation. Space is also provided for noting control measures associated with each exposure and individual occupation. In practice, the reconnaissance survey consists of carefully filling out the two inspection forms and jottingdown any additional notes on items which may not be provided for in the forms. Under certain conditions, such as may exist in a coal mine or a cement mill, some of the items listed on these forms may obviously be omitted. After filling out survey forms for each workroom in an entire plant, a detailed analysis of the data contained in the forms is then in order. It is such an analysis that enables one to furnish a complete picture of the hygienic conditions in each of the workrooms studied and in the plant as a whole. Perhaps one typical illustration from actual experience will demonstrate the value of a reconnaissance survey of an industrial establishment. The Division of Industrial Hygiene of the National Institute of Health ST 0853734 APPRAISAL OF INDUSTRIAL HEALTH HAZARDS 11 4*; Illumination Natural............................................ General impression........................................... Condition of windows................................................................................................ , r Artificial.......................................... General impression........................................... > Type 4 No............................................... Condition............................................... *' Shadow or glare......................................................................................................... fi. 8Arm Hazards {Form 1--Continued] ft. FuMxa and Gasas .r . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . c V Dustt Procissis i IZIIZIII * .................... __ 8i SraciTic Poisons 9. Exposures to Abnormal Temperatures, Dampness, Radiation, Noibx, Etc. ( has been receiving reports from industrial sick-benefit organizations Bince 1922 (2). A study of these reports from the steel industry Bhowed con sistently higher incidence rates for pneumonia in all forms than employees of other industries. For the period 1922 to 1928, inclusive, the pneumonia case rate in the steel industry was nearly 70 per cent above the rate in the reporting public utilities, and nearly 50 per cent higher than all other re porting industries as a group. A five-year inquiry into the causes of high pneumonia rates among iron and steel workers in a representative mill dis closed the fact that the largest number of cases occurred in certain depart ments, such as in the blast furnace and open-hearth steel mills. When one realizes, however, that these departments contain anywhere from 60 to 100 different occupations, the task of a preventive program is almost a hopeless one, unless definite information is obtained concerning such important items as (a) the number of persons in each occupation, (6) the activities associated with each occupation, (c) the health hazards associated with each occupation, and (d) the incidence of pneumonia for each oocupa- ST0853736 APPRAISAL OF INDUSTRIAL HEALTH HAZARDS 13 <<Ctian. Such information may be readily obtained from a reconnaissance ^ survey. Pr.TS. For example, in the reconnaissance survey made in this plant, it was found that the most important exposures associated with the various oc/f cupations were heat with wide changes in temperature, gases (sulfur TabLi 1.--Frequency of Pneumonia according to Occupation and in Relation to the N.. Nature of Industrial Exposure Involved in the Blast-Furnace Department, lMl-tS Sertion* sod occupation* Nature and extent of industrial exposure1 Heat with wide chances in tem Stren uous work pcratue Outdoor work Gases in all and kinds of moke weather Nosberof Annual number of case* CAMS of pnenoaia Approx imate Dost of pneu monia per 1,000 men Actual Ex pected' of rsan of life observed All sections........................ 14.0 36 10 2,578 Stacks and stoves (casting section)....................... 27.2 17 2 Keeper.......... ............... * 0 * 8.3 1 0 first and second helpers......................... 0 e 41.5 12 1 Blowers........................... e 0 0 00 0 00 Hot-blast men................ * 00 00 16.7 2 1 Stove cleaners............... a e 00 00 ** 46.5 2 0 624 120 289 52 120 43 General labor section and ear-dumper laborers.. 0 0 00 0 0 30.7 15 2 489 All other sections'............ 0 0 0 0 2.7 4 6 1,465 1 Symbols for extent of exposure are as follows: 0, no exposure; *, slight or occa sional exposure; **, heavy exposure. 1 Number expected from the rate per 1,000 men in "All other departments." 18 per cent of the men heavily exposed, 23 per cent slightly or occasionally ex posed to heat with wide temperature changes. To strenuous work no one was heavily exposed, and only 6 per cent had occasionally to work strenuously. To outdoor work in all kinds of weather about 8 per cent of the men were heavily exposed, 80 per cent slightly or occasionally exposed. To gases and smoke about 5 per cent were heavily and 26 per cent slightly or occasionally exposed. About 1 per cent of the men were heavily exposed to dust, and about 55 per cent slightly or occasionally exposed. dioxide, hydrogen sulfide, and carbon monoxide), siliceous dusts, strenuous work, and outdoor labor in all kinds of weather. The survey enabled one to note these exposures for those occupations in which they occurred. Table 1 presents the frequency of pneumonia according to occupation in the blast furnace department, in relation to the nature of the exposure, ST0853738 14 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE during the period of 1924-1928. It is obvious that the highest pneumonia rates occurred among those occupations exposed to one or more of the potential hazards cited. The actual number of cases for those occupations not associated with these five exposures (all other sections) were found to be even less than the expected cases of pneumonia for such workers. The reconnaissance survey indicated that, in the blast furnace department, at tention should be centered on the occupations in the casting and general labor sections, in an effort to determine the degree of exposure to gases, dusts, extreme temperature changes, and so on. Such studies are carried out by the engineer and chemist, whose task it is to determine the extent of the occupational exposure to the materials and conditions enumerated. Thus, the engineer is concentrating on the important factors and omitting the unimportant. In this particular study, it was necessary to evaluate the working environment for but a few occupations of the more than 60 in the blast furnace department. It was these few occupations that ac counted for the high pneumonia incidence for the enthe department and once the occupational exposure factor had been evaluated, the engineer was in a position to initiate control measures for the minimization or the elim ination of the hazards demonstrated to be deleterious to health. The Detailed Survey In determining a worker's exposure to materials or conditions incident to his employment, it is necessary to have precise data on such exposures. In some cases the difference between a hazardous and a non-hazardous condition may depend entirely on whether the worker is exposed con tinuously to concentrations of materials bordering on the threshold limit. For example, in the case of exposure to certain lead compounds, for which the threshold limit has been set as 1.5 milligrams per 10 cubic meters of air, it is very important to know whether the worker is inhaling lead dust approximately above or below this limit. Quite often a difference of a milligram or so may spell the difference between a safe or an unsafe con dition. Detailed appraisals of exposure may be said to serve a three-fold pur pose. First, they enable one to determine the extent of a hazard. This is accomplished by obtaining occupational exposures, by precise methods, to the toxic materials pr conditions under consideration. Today, the engineer and chemist have at their disposal delicate instruments and methods of analysis unprecedented in the history of industrial hygiene and our knowledge concerning such matters is increasing from day to day. The guesswork as to actual exposures has been fairly well taken out of industrial hygiene. A second purpose served by the detailed study is the fact that if clinical ST085373S APPRAISAL OF INDUSTRIAL HEALTH HAZARDS 15 investigations are made concurrently with environmental studies, the find ings on occupational exposure may indicate the permissible amounts of the toxic materials which may be tolerated with safety. : And, finally, the third purpose served by this type of study deals with the control of the hazard. In other words, one is in a position to determine the efficiency of any device which may have been introduced for the minimi zation or elimination of the hazard. Some examples illustrating each of the three purposes served by the detailed study follow. Extent of Hazard.--In a study of lead poisoning among storage battery workers, it was important to determine the relationship between the amount of lead dust inhaled by the men and the incidence and severity of plumbism. Such a study is valuable in that it may indicate the maximum amount of lead which may be inhaled with impunity. Table 2 shows the fundamental correlation between the lead dust in the air and the rate of plumbism in the major departments of the plant inwhich a study was made (3). It is evident that a close correlation exists between Table 2.--Lead Exposure and Maximum Monthly Rate of Initial Compensation Cases for Plumbism Department M10Ucluifbriacsmueotefrlseaodf pseirr Muruteleu(mpemr 1o0n0t)hly Mixing................................................................. Pasting................................................................ Burning .. . . Casting................................................................ 120 50 5.7 1.2 44 12 4.4 .18 the lead exposure of workers in different departments and the risk of de veloping a case of lead poisoning. Correlation with Clinical Data.--Figure 1 illustrates the relationship between lead dust exposure, years of exposure, and the percentage of work ers diagnosed as having early plumbism (4). It is evident that 1.5 milli grams of lead dust per 10 cubic meters of air, except for very prolonged ex posure, is the limit of safety under the conditions encountered in these studies. This important finding is of great value to the engineer, since it gives him a basis upon which to develop protective devices in the way of exhaust ventilation, respiratory protection, good housekeeping, and so on. Efficacy of Control.--The detailed survey as employed in studying the efficiency of various methods employed for the control of a hazard will be treated in more detail in the next section, which deals with the control of industrial health hazards. It is desired, however, in closing this portion of the discussion, to point out that the engineering problems in industrial hygiene are constantly increasing in number, especially now when many ST0853740 16 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE new chemicals and processes are being introduced into our industries. Our knowledge of these substances, as to their action on the body, is constantly being augmented by the work of toxicologists and by field studies of the type described herein. It is the engineer's task, once this knowledge is available, to devise ways and means for controlling these injurious materials and conditions, a discussion of which follows. Fro. 1. Percentage of workers with early plumbism. The percentages of storage battery workers in each of 10 exposure groups diagnosed as cases of early plumbiam are represented by the height of blocks. Thus, of the workers exposed more than 15 years to atmospheric lead concentrations in excess of 3 mg. Pb per 10 m* of air, 61 per cent were found to have early plumbiBm. Data taken from table. THE CONTROL OF INDUSTRIAL HEALTH HAZARDS The control of industrial health hazards is also a function of the medical and engineering departments. The physician and his co-workers recognize the existence of diseases due to the workroom environment and exercise medical supervision and initiate studies designed to eradicate the dangerous conditions. The engineer and his co-workers determine the extent of the hazard, and, armed with a knowledge of the toxicity of the material in volved, are in a position to consider methods and equipment for the control of the hazard. No set rules may be established for the mechanical protection to be in stituted in an attempt to control an industrial health hazard. Specific conditions encountered in a plant will determine the type of protection to be employed. In genenj, however, there are five methods which may be attempted in the minimization of an industrial exposure. These are: (a) Substitution of a non-toxic material for the toxic one, (6) isolation of the harmful process, (c) wet methods in the case of some dusty operations, (d) local exhaust ventilation, and (e) respiratory protection. In many instances it may be necessary to employ a combination of the above meth ods in the control of a single exposure. Substitution.--The protection of workers against certain dusts known APPRAISAL OF INDUSTRIAL HEALTH HAZARDS 17 to be toxic may at times be accomplished by the substitution of a non-toxic material for the toxic one. One example of such a procedure is the use of a metallic or other type of artificial abrasive for sand in the sandblasting process in those operations in which it is not necessary to use sand, a sub stance high in quartz content. The data shown in table 3 indicate clearly the lowering in dust concentration when a steel abrasive is employed in stead of sand in a sandblasting room (5). Tabix 3.--Showing Reduction in Concentration and Quartz Content of Duet in Sandblast Rooms with the Substitution of Steel for Sand Abrasive Type of abmaive Average doit concen tration in millioni of particle* percu. ft. Percentage of quarts Sand.................................................................... Steel................................................................... 909 165 43-98 3 Another example of substitution is one recently employed in the hatting industry. For more than 100 years mercury had been employed in the carroting solution which was applied to rabbit fur utilized for the produc tion of felt hats. Certain operations in the preparation of the hatters' fur and in the subsequent manufacture of the hat itself entailed exposure to mercury vapor and dust with accompanying mercurialism among the workers. Recently the hatting industry itself developed a non-mercurial canroting solution which was adopted by the industry, so that mercurialism in the future will be completely eradicated in this industry (6). Isolation.--The mechanical enclosure or isolation of certain operations also serves to protect the worker. In the case of dust exposure, we have an excellent illustration of this type of protection by the use of the modern Bandblast barrel used in the cleaning of small objects. Table 4 illustrates the practical elimination of dust exposure in certain sandblasting opera tions in which well enclosed and isolated operations are contrasted with those not offering this sort of protection. Tabix 4.--Dust Concentrations for Sandblast Installations Regarded by Manufacturers as "Ideal" in Comparison with Other Equipment Average dust count in millioni of particle* per cubic foot Ideal....................... Other....................... Barrels 1.7 29.0 * Tablet 0.2 22.0 Cabinet* 1.9 38.0 Wet Method$.--lii the case of dust, it is possible to protect workers by the substitution of wet for dry processes. This method is illustrated by the results shown in table 5. 18 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE Table 5.--Contrasting Wet and Dry Methods of Rock Drilling and Loading Processes Number of samples Average doit oouat in millions of particles per cubic foot Dry Wat Drilling............................................... 23 568 33 Loading.............................................. 10 636 32 31i.eS801S More recent studies of rock drilling operations have shown that wet methods employed in conjunction with general exhaust ventilation may often result in even lower dust concentrations than those shown in this table (7). Local Exhaust Ventilation.--Perhaps the most universally used method of control of certain workroom conditions which are harmful to health is local exhaust ventilation. This method aims to remove dusts, fumes, vapors, and gases at their source. So much depends upon the correct design and construction of hoods and exhaust systems that they should be laid out and maintained with great care. The past few years have wit nessed the gradual accumulation of a tremendous amount of basic en gineering data on this type of control. Data pertaining to quantity of air necessary at hoods to control hazards or nuisances are rapidly accumu lating. For example, it has been shown that spray painting booths require velocities of 100 to 200 feet per minute at the openings to reduce effectively the presence of vapors to safe limits. For laterally exhausted chromium plating tanks, specific air velocities and air volumes have been developed and are now embodied in a national standard recently promulgated by the American Standards Association (8). In connection with granite-cutting, special hoods have been designed for the control of the hazard in this in dustry (9). In certain instances, down-draft ventilation has been found to be most effective. Such practice materially reduces the air velocities re quired for control and utilizes a natural tendency for heavy dust to set tle (10). The scope of the present article does not permit adequate treatment of this particular method qf control, although when properly considered it is an effective one. Table 6 presents some data concerning required air volumes and other pertinent information regarding local exhaust ventila tion. Respiratory Protection.--It is generally agreed that in the control of exposures to air-bome toxic materials, primaiy consideration should be given to procedures for preventing excessive contamination of the air in A-PPRAISAL OF INDUSTRIAL HEALTH HAZARDS 10 the breathing zone. However, there will always be situations where these procedures will be inapplicable, impracticable, or at times not effective. For these situations, personal respiratory protection will be required, either as a primary means of protection or as an adjunct to other preventive procedures. In recent years, great strides have been made in the improve ment of respiratory protective devices and at present the United States Bureau of Mines is approving such devices after rigid testing (11). Such an approval system has stimulated further research on the part of the manufacturers handling these devices, which has resulted in a better prod- Tabue 6.--Minimum Air Velocities Required to Capture Certain Industrial Duet* and Vapor* Industry Process Required air velocity At point At lace of origin of hood Criterion \[ Hand pneumatic tool 200 FPU GraniU outtin*....... Surfacing machine 1500 FPU l au tool. Elevator boot and heed, garner Spraying booth Band pulverising...... 400 FPU [ Horisontal drilling with 50* Quarrying and min- J Kelley trap inf........................| Vertical drilling with 200* 1 Kelley trap Chromium piftiny 50** '" 1 Steam and add tanks 75-100 Brushing Cutting machines 200* 250* Blowers Saottie midis*........ Waldinf Xetal spraying***.. .| Lead Zinc 2000* 200 300 135 1500 500 50-200 1500 lUduoad oonoaatntion to of. Uni Reduced concentration to safe level Reduoed eonoentration to safe level Vijtul tort Reduoed concentration to safe level Reduoed eonoentration to safe level Reduoed oonoentration to safe level Reduoed oonoentration 0 safe level Rsduwl oosoutntion to mI. Uni Reduced oonoentration to safe level Usual praetioe Uaual prmetioa Uatul pnotiw VUual tot Effective removal of all fumee Cobio foot por minute. Cobio loot por minute per foot of slot (0002000 practice). At opening of booth. uct. The reader is referred to an excellent treatise on respiratory pro tective devices which was prepared by the Subcommittee on Personal Respiratory Protective Devices of the Committee on the Prevention of Silicosis through Engineering Control of the National Silicosis Confer ence (12). It is also not possible to include in the present discussion the important subject of protective clothing, such as goggles, aprons, boots, rubber gloves, and especially the newer type of protective clothing made from plastics, nor is it practicable to go into a discussion of the subject of pro 20 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE ST0853744 tective ointments. The reader is referred to the excellent chapter in this book (Chapter XXI) on this subject by Dr. Louis Schwartz. SUMMARY Today we are witnessing vigorous action on the part of many official organizations in the development of codes and other regulations dealing with the removal of noxious air-borne materials and other environmental hazards in industry. Nonofficial agencies, such as the American Stand ards Association, and various medical and engineering organizations are collaborating with State and Federal agencies and industry toward the de velopment of such codes on a scientific basis. One of the great needs today to aid in the development of such codes is factual data based on studies of existing installations. Table 7.--Exposure of Hatton' Fur Workers to Mercury Vapor and Treated Fur Duet under Controlled and Uncontrolled Conditions Occupation Total mercury espoeore in rnUUnatta per 10 cubic meters Anna air floir, C.FM. Un controlled Controlled Method of control Drummers....................... Clippers........................... Brushers........................... Cutters............................. Sortere*............................ Blowers............................ Pilers................................ Stonge workers and shippers........................ 2.5 1.5 3.1 4.0 3.8 4.6 5.4 7.2 0.6 0.7 1.2 1.8 1.7 0.7 Trace 300 383 383 2,000 Tnce Segregation Segregation Local exhaust ventilation Local exhaust ventilation Local exhaust ventilation Local exhaust ventilation Good natural ventilation Good natural ventilation * Depend on exhausted cutters. It is well-known that in many industries health hazards are being ef fectively controlled. The engineer and the clinician should systematically evaluate the efficiency of the various methods employed so that the data would be available and useful in the preparation of good practice codes. Perhaps it would be proper at this point to give an example of the use fulness of a study of exiting installations. In a survey of the mercury hazard in the hatters' fur cutting industry, the engineers were in a position to evaluate various control measures in vogue in various representative plants in the industry (13). Table 7 indicates the exposure to mercury dust and vapor of some of the workers in this industry under controlled and uncontrolled working conditions. It is apparent that where some measure of control is practiced by such methods as segregation or local exhaust ventilation, a material reduction in the exposure to mercury is APPRAISAL OP INDUSTRIAL HEALTH HAZARDS 21 effected. Although no one plant was found to have all of the control measures in effect, as shown in the table, methods were found in representa tive plants of the industry showing that the mercury exposure for different occupations could be controlled by existing practices. The engineer, in conducting a study of this type in representative plants, is in a position to present to the industry as a whole information showing how certain hazards can be and are being effectively controlled. With further reference to basic standards for the control of hazards in industry, two approaches may be employed. Standards can be based on clinical data, that is, on definite knowledge which shows that exposure to more than a certain amount of a toxic material will involve injury to health. Such knowledge then can be used in engineering design in order to reduce the exposure within the so-called threshold limit. Although our knowledge concerning the toxicity of materials is rapidly becoming more and more abundant, there are still many substances for which we have no basic information at this time concerning their toxicological properties. In such cases it is suggested that standards could be employed which are based on results which can be obtained by good engineering practices. Quite often these engineering practices are found to yield conditions far better than those which might be based on our present knowledge of the toxicity of a material. One must bear in mind that our present ideas concerning the toxic limits of certain substances are subject to change as our methods of diagnosis and analysis improve. Chapter XIII describes in detail recently developed techniques for the early discovery of indica tions of toxic exposure. In closing, it is desired to emphasize that studies of the industrial en vironment necessitate numerous laboratory examinations of a clinical, physical, and chemical nature. These call for highly trained chemists and biochemists. Today, with the added use of chemicals in many of our proc esses, there is a greater need for data concerning the toxic effects of these substances. The proper procedure is a study of these new materials or processes on a small scale prior to their widespread use in industry. This practice, which is now being employed in some of our more progressive industries, calls for a close collaboration between the production and de velopment departments in the plant, and the industrial health maintenance service. Once the problem in industry has been evaluated and everything possible has been done to control unhealthful conditions, it will still be essential for the medical, nursing, engineering, and chemical personnel to maintain close vigilance, in order that safe conditions may be maintained and im proved upon. Constant study of the workroom environment is essential to ascertain whether certain measures are really effective. Such practice ST08531U6 I 22 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE in cooperation with the work of the physician and the nurse appears to afford the best means of controlling industrial health hazards, and their attendant loss of valuable time from work. REFERENCES (1) Bloomfield, J. J.: Preliminary Burveya of the industrial environment. Pub. Health Rep., 48 : 44 (Nov. 3, 1933). (2) Brundaoe, D. K., Russell, A. E., Jones, R. R., Bloomfield, J. J., and Thomp son, L. R.: Frequency of pneumonia among iron and steel workers. Pub. Health Bull. No. 202 (1932). (3) Russell, A. E., Jones, R. R., Bloomfield, J. J., Britten, R. R., and Thomp son, L. R.: Lead poisoning in a storage battery plant. Pub. Health Bull. No. 206 (1933). (4) Drbessen, W. C., Edwards, T. I., Reinhart, W. H., Paoe, R. T., Webster, S. H., Armstrong, D. W., and Saters, R. R.: The control of the lead haiard in the storage battery industry. Pub. Health Bull. No. 202 (1941). (6) Bloomfield, J. J., and Greenbubo, L.: Sand and metallic abrasive blasting as an industrial health hatard. J. I. H. T., XV: 4, 184-204 (July 1938). (0) U. S. Public Health Service, Division of Industrial Hygiene: Use of mercury to be discontinued in hatting industry. Industrial Hygiene, 1: 6, 2-3 (May 1941). Mimeographed. (7) Hatch, T.: Dust control in rock-excavation. Reprinted from The Industrial Bulletin, 16: 9. New York State Department of Labor (September 1930). (8) Bloomfield, J.J.,etal.: American standard for safety in electroplating opera tions--Z9.1. American Standards Association (August 13, 1941). (9) Hatch, T., and Harris, W. B.: Requirements for dust control in stone cutting. Reprinted from The Industrial Bulletin, 18: 12, 379-381. New York State Department of Labor (December 1939). (10) Bloomfield, J. J., and DallaValle, J. M.: The determination and control of industrial dust. Pub. Health Bull. No. 217 (April 1936). (11) U. S. Bureau of Mines, Department of the Interior: Procedure for testing filtertype dust, fume, and mist respirators for permissibility. Schedule 21 (August 20, 1934). (12) National Silicosis Conference: Report on engineering control. Final report of the committee on the prevention of silicosis through engineering control. Bull. No. 21, Part 2. Division of Labor Standards, U. S. Department of Labor (1938). (13) Neal, P. A., Jones, R. R., Bloomfield, J. J., DallaValle, J. M., and Edwards, T. I.: A study of chronic mercurialism in the hatters' fur-cutting industry. Pub. Health Bull. No. 234 (1937). Chapter VII THE INDUSTRIAL HEALTH PROGRAM OF THE AMERICAN MEDICAL ASSOCIATION C. M. Peterson, M.D. Many large corporations in this country and elsewhere have learned by experience through extended periods of time that medical supervision over workers, processes and environment is good business. Many physicians have been associated with such activity in manufacturing operations of every description. They have amply demonstrated that an industrial medical service can be administered to the very great advantage of worker and employer alike, and at the same time in conformity with existing ethical and scientific standards. Concisely expressed, the objectives of a properly organized industrial medical service have proved to be: 1. The prevention of disease or injury in industry by the establishment of proper control over working conditions. 2. The restoration to health and earning capacity as promptly as possible after industrial injury or disease. 3. The conservation of the health of workmen through physical supervision and education. It has been apparent for some time that smaller industrial organizations have been denied the advantages of industrial hygiene, preventive in dustrial medicine and health conservation mainly through lack of properly trained professional personnel and the absence of a plan of industrial medi cal service which could receive wide acceptance by small employers. In recognition of these two material facts, the industrial health program of the American Medical Association is intended to: 1. Acquaint physicians with the special character of industrial medicine, surgery and hygiene and the necessity for the enforcement of standards defining scope and professional competence. 2. Convince employer and employee alike that medical service in industry merits support if soundly organized, economically, scientifically and ethically and that to produce lasting benefits it must be Satisfactory both to those who provide and to those who receive the service. In accordance with this view, improved standards of medical accomplish ment in industry must stem directly from better industrial medical educa tion and efforts at self-improvement and self-discipline administered by the physician's own organizations. To accomplish this purpose the Coun- 65 66 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE cil on Industrial Health of the American Medical Association was established. It was not long until the Council realised that no plan of industrial health training would be successful without full cooperation from 1. Medical and professional schools. 2. State and county medical societies. 3. Medical specialty groups. The Council has on several occasions communicated with the adminis trative officers of medical and public health schools with a view towards stimulating better organization of industrial health teaching, both before and after graduation. A program for improved organization of teaching has been prepared in conjunction with the Committee on Education of the American Association of Industrial Physicians and Surgeons. Improve ment has been gradual, but in a number of medical centers very substantial contributions are being made in the field of industrial health teaching and it seems safe to predict that much greater effort will occur in other institu tions located in highly concentrated and important industrial areas. At the invitation of the Council, 45 states and the District of Columbia have organized committees on industrial health. Each of these agencies acts independently in accordance with local situations and requirements. However, in the interests of concerted and uniform action, the following broad-scale program has been recommended: 1. To train industry and labor to the value of industrial health oonaervation. 2. To develop a clear understanding of the proper (cope and functions of in dustrial medicine and to clarify relationships between private and industrial practice. 3. To keep the medical profession informed about all accepted methods for reducing the frequency and severity of industrially induced disability. 4. To evaluate medical relations under workmen's compensation. 5. To scrutinize all legislation affecting the health of industrial workers. 6. To improve relationships between medicine and insurance. 7. To establish working relationships with all agencies in the state interested in industrial health. 8. To arrange for the adoption of similar activities through cooperating com mittees in the medical societies of the industrial counties. In recognition of the major medical interests involved, it has been felt that each state committee on industrial health should contain representa tion from: 1. Private practice. 2. Industrial medical practice. 3. Medical representation if such exists from each of the following: ST0853748 f I ' ; ] I I PROGRAM OF AMERICAN MEDICAL ASSOCIATION 07 a. State bureau of industrial hygiene. b. State workmen's compensation agency. c. Medical faculties in the state. d. Casualty insurance company. A bulletin has been developed by the Council on Industrial Health to promote inter-change of ideas between committees of the state societies and as a means of estimating progress. In much the same way, representa tives of the state committees attend the Annual Congress on Industrial Health in Chicago each January to report developments and advances. Successful organization of cooperating agencies in state medical societies has suggested that similar objectives and methods be introduced into the county medical societies as a means of mobilizing community resources for general or special industrial health activity. Such committees can establish dependable information about local or regional health exposures in industry and use this knowledge as a basis for early recognition and control and to promote in other ways the physical welfare of workers. There should be many opportunities to provide better professional training in medical society meetings and symposia. The community at large can be instructed in the objectives of industrial health and made aware of the favorable effect of industrial health procedure. Certainly, a county medi cal society committee enables the special technics of industrial practice to be integrated into the general pattern of community medical service and it has already been demonstrated that helpful working relationships can be promptly established with such allied professional groups as the in dustrial hygienists, the safety engineers and the industrial nurses. Following the example set originally by the Section on Dermatology and Syphilology, most of the Sections in the Scientific Assembly of the American Medical Association representing all major specialty groups affected by industry have formed committees to initiate programs which will be of benefit in industrial relationships encountered by specialists and to act in an advisory capacity to the Council on Industrial Health. Al ready these committees have contributed in a very substantial way to our knowledge of occupational medicine and will, it is confidently believed, steadily improve methods of attack on specific problems related to improved case management, disability evaluation and rehabilitation. In addition to improved training and better' national, state and local organization for proper consideration of industrial health relations, the Council has inaugurated and maintained other services calculated to ad vance standards and improve results. Work is going forward in the stand ardization and classification of nomenclature in industrial health, in the determination of better clinical and preventive methods, in medical ad- ministration under workmen's compensation, in improved vital statistics relating to occupational morbidity and mortality, in clearing house service and in the general field of socio-economic development. All these activities indicate that the problems of industrial health, whether in hygiene, medicine, surgery or whatnot are beginning to receive genuine consideration throughout the profession. There is good reason to believe that as industrial health continues to develop, the responsibilities of the medical profession will be well recognized and ably represented. ST0853750 ST085375 I L i Chapter XXII PNEUMOCONIOSIS (DUST DISEASES OF THE LUNG) George Zur Williams, M.D. ! I. THE PROBLEM Early History I It is not tbe purpose of this chapter to discuss the early history of pneumoconiosis at length nor to consider in detail the many disputed hypotheses and results of experimental investigations concerning the ' theories of production and prevention of pneumoconiosis. It will be the purpose of these paragraphs to set forth briefly and as concisely as possible the various practical and proven concepts concerning the etiology, patho genesis, pathology, clinical course, and control of the various dust diseases, ` : particularly that due to silica (silicosis). ! j Dust disease of the lungs is a long recognized entity, but long before ` T: { distinction from other diseases of the lungs Hippocrates mentioned symp.. j toms of breathlessness in certain metal workers who "degenerated rapidly." J Although the disease was differentiated and known to affect miners before , 1899 on the Transvaal, the first commission was not appointed until 1902 to study the effects of dust on miners' lungs. In 1919 the first technical commission was appointed in Australia to use x-ray in the diagnosis of dust diseases of the lungs. Silicosis was first reported in a western state of this country in 1894 and a thorough x-ray study was made and reported by Lanza and Childs in 1917. Many reviews of the literature on the effects of dust in the lungs are complete and should be consulted by the reader who is particularly interested in the details of early work. Dust in the Lungs All normal lungs contain a certain amount of dust, accumulation begin ning soon after birth. Many different dusts are accumulated by the lungs and stored in varying amounts in the small pulmonary lymph centers and hilar lymph nodes. In localities with large amounts of smoke in the atmosphere, children begin to Bhow blackening of the lungs early in life due to accumulation of coal dust. Silica is found in all lungs of adults in small amounts regardless of the occupation of the person. In persons under 48 years of age 50 milligrams per cent to 200 milligrams per cent of dry weight of the lungs is found to consist of silica. The hilar lymph nodes contain from 1,000 to 3,000 milligrams per cent in individuals of from 48 to over 52 years of age. This amount of silica does not produce pathological changes 346 I 346 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE in normal persons. The silica can be found onlv by histo-incineration or by chemical analysis. Definition The pneumonoconioses are conveniently divided into various types de pending upon the character of dust accumulated in the lungs. In almost all instances a varying amount of coal dust is present and, therefore, the prefix "anthraco" may usually be applied. The following definitions are taken from the National Silicosis Conference Report on Medical Control, United States Department of Labor, Bulletin 21, Part 1: "The committee on pneumonoconiosis of the industrial hygiene section of the American Public Health Association recently defined silicosis as: A disease due to breathing air containing silica (SiOa), characterized anatomically by gen eralized fibrotic changes and the development of miliary nodulation in both lungB, 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 by char acteristic x-ray findings.'' As will be pointed out later, considerable importance may be attached to the difference between the clinical disease, silicosis, and the discovery of moderate nodulation of the lungs caused by inhalation of silica and found incidentally upon roentgenological examination. This difference is of some importance in the disposition of individual cases with relation to control and industrial compensation. Classification There are pulmonary diseases due to inhalation of organic dusts which do not produce nodulation and which are infectious in nature and, there fore, are not properly included under this term. Silicosis is the one true uncomplicated nodular fibrosis which has been proven clinically and experi mentally to be caused by the inhalation of dust containing high concentra tions of free silica. No other dusts than those containing silica will produce true nodular fibrosis. A more diffuse fibrosis and mixtures of nodular and diffuse fibrosis are caused by other dusts, such as asbestos, coal dust, and iron ore dust. Usually, with the possible exception of asbestos, these dusts have a rather high concentration of silica and, therefore, there is yet a question concerning the true etiology of anthracosis and siderosis. Silicosis is the most important of this group of pneumoconioses, particularly from the point of view of industrial medicine and will be discussed in more detail. Occupational Incidence Although the incidence of disabling silicosis is not as high or grave as many reports and the news publicity in recent years would indicate, silica ST0853752 ! PNEUMOCONIOSIS 347 dust occurs in hazardous concentrations in the air of many industrial mines and plants. Silica dust hazard occupations are listed in Occupational Disease Leaflet # 9, 1936, Division of Labor Standards, United States Department of Labor, as follows: Abrasive-powder makers Abrasive-soap makers Blasters (Band) Brickmakers Coal miners Core makers Foundry workers Glaasmakers Glass mixers Granite quarters Hard-rock miners Metal grinders Pottery makers Pneumatic rock drillers Polishers Sanders Stone finishers Slate quarters Slate finishers Sand pulverisers Tunnelers Vitreous enamelers Control Problem Of great importance to society, and particularly to industry, is the prob lem of the control of silicosis. In some states silicosis is now a compensable disease and due to this fact, insurance companies and compensation com missions have stimulated a widespread interest in the prevention of this disease and some control by legislation in certain states provides for pre vention and compensation of this disease. Further details concerning this general problem are discussed in Chapter II. n. the pathogenesis Causative Agent It has been proven beyond doubt, both clinically and experimentally, that silica (SiOs-silicon dioxide) is the primary etiological agent in the pro duction of a nodular fibrosis of the lungs. There is no definite evidence that non-siliceous dusts produce this characteristic fibrosis and when no history of exposure to silica dust can be obtained from a patient suspected of suffering from silicosis, careful investigation of his historical background should be made to determine exposure to any other dust which may have contained dangerous concentrations of silica without the patient's knowl edge. The combined forms are termed silicates and these are of no impor tance in the pathogenesis of disease with the ong exception of magnesium silicate (asbestos). Silica is the most abundant constituent of the earth. It occurs com monly in both free and combined forms. The free silica occurs in the form SiOj and is commonly known as quartz, being the chief constituent of granite, schist, and other rocks, such as sandstone and quartzite. Many ores are deposited in veins which are composed almost entirely of quartz. Another form in which silica occurs commonly is the amorphous hydrated I ST0853754 348 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE type of colloidal origin, abundant in diatomaceous earths. Other forms of free silica occurring in nature, but much more rare, are tridymite, cristobalite, and siliceous glass. Action of Silica Silica is very commonly believed to be insoluble because of its resistance to chemical reagents with the exception of hydrofluoric acid. However, it has been proven by well controlled chemical experiments that silica is rel atively soluble in many agents, including water, and particularly slightly alkaline solutions of salt, when exposed to the solvent in very finely divided particles measuring only a few microns in diameter. Therefore, size of the silica dust particles is important in determining their action upon tissues of the lungs. A second factor determining the action of silica on tissue is the dose (the concentration of the dust in the inhaled air). A third factor is the effect of other dusts mixed with the silica. It has been shown by both chemical and animal experiments that silica particles of very small size, i.e. measuring micron or less in diameter, are relatively innocuous if aspirated into the lungs because they are so rapidly dissolved that most, if not all, of the silica is excreted through the kidneys in dissolved form. Recent experiments show that unusually high concen trations of silica of this small size may produce extremely toxic effects, but no nodular fibrosis is produced. Particles of silica from 10 microns in size to larger are also more or less innocuous when introduced into the lungs in high concentrations. This probably is due to the fact that these particles are too large for phagocytosis by the alveolar cells and also that their rate of solution is so slow there is no stimulation of the phagocytic activities of these cells. As a result they are swept back out into the trachea and the pharynx by the ciliary activity of bronchial and tracheal mucosal cells. Silica particles of the sizes between } micron and 10 microns, and partic ularly those of the size from 3 to 5 microns, are the sizes found to be most injurious in producing experimental nodular fibrosis of the lungs. These sizes permit some solution with resulting "toxic" paralysis of mucosal cilia. Large numbers of experiments have been completed to determine the dust concentration required to produce this nodular fibrosis. It is generally found that dust concentrations between 5,000,000 and 10,000,000 particles per cubic foot are capable of producing nodular fibrosis in only a very small number of exposed animals or individuals, but that dust concentrations above 10,000,000 particles per cubic foot are definitely hazardous and pro duce a nodular fibrosis in the majority of exposed individuals. Dust con centrations below 3,000,000 particles per cubic foot are very rarely haz ardous. The third factor is that of a mixture of various other dusts. Early ex- PNEUMOCONIOSIS 349 perimcnts led to tin; conclusion that carbon dusts in the form of coal dust in hard coal miners protected the miners from silicosis because it was found that apparently hard coal minors developed less silieosis and of less severity and in fewer numbers than did other hard rock miners. However, this contention has not been proven and in other studies of hard coal miners such results are not always found. It has been found that, alkaline dust when mixed with silica dust apparently renders it innocuous. Experimental evi dence has been obtained explaining this effect as due to the fact that the silica dust particle carries a negative static charge. The alkaline dust particle carries a positive static charge. When negative dusts are com bined with statically positive dusts, agglutination of neutralization occurs and the dusts precipitate into large clumps and fall out of the air. The concentration of silica in the dust is greatly lowered by precipitation due to this electrical agglutination and the particles of agglutinated dust become so large that solubility is decreased in the bronchial secretions and the cilia sweep them outwardly before phagocytic action can occur. Experimental proof is lacking to show that iron dust, aluminum dust, and other metallic dusts have any effect whatsoever on increasing or decreasing the injurious action of silica on lung tissues. Related Anatomy There are certain aspects of the anatomy of the human and animal lungs which become important factors in predisposing to, or protecting the lungs from, the action of silica. Animals possess two types of pulmonary lymph drainage systems. These air termed the "open" and the "closed" types of lymphatic drainage. The human lung, the guinea-pig lung (fig. la), and the pig lung have the "open" type. The rabbit, dog, rat (fig. lb), and mouse lung art' of the "closed" type. Microscopic examination of these lungs reveals large numbers of small lymphocytic nodules scattered throughout the lungs extending into the peripheral portions in the dosed type. Special studies have demonstrated that lymph drainage occurs bv collection in small lymphatics which traverse the lung along the vessel courses and drain through the numerous chains of lymphocytic nodules into the hilar lymph nodes at the root of the lung. On the other hand, in the open type of lymphatic system, there are no such lymphocytic filter centers in the course of lymph drainage from the periphery of the lung to the hilus. In this type foreign particles, fragments, and organisms picked up by the lymphatic system in the periphery of the lung arc transported directly to the first filtering nodes which occur at the hilum. In animals and man possessing the open type of lymphatic drainage, there occurs a significant change to the closed type as the result of many acute and chronic respiratory infections. In the guinea-pig it will be found .'?o0 I'ui.vrii'i.Ks \nd i'll\rrrri; of ivDi sruiAr. ui'.mrrxF. Fig. 1a Fiq. 1b Fig. 1a. (X 50) Normal Kuinea pin lunn--''open" type lymphatic system. Note absence of lymphoid nodules in parenchyma Fig. In. (X 50) Normal rat limn--"dosed" type lymphatic system. Note dark lymphoid nodules adjacent to peripheral bronchioles PNEUMOCONIOSIS 351 that following pneumonia or bronchitis, this change occurs by the enlarge ment of microsocpic collections of a few lymphocytes into nodules of many lymphocytes which accumulate during the infection and persist for long periods thereafter (fig. lc). These nodules may become very large and are frequently found peripherally as far as the pleura. They occur usually at the bifurcation of the blood vessels and are so constructed that the lymph filters through the nodule. It is important for the reader to keep in mind these two types of lymphatic system and to remember the basic fact that chronic infection and inflammation will change the open lymphatic system of the human lung to the closed type when considering predisposing factors to silicosis. Predisposing Factors Many experimental findings have partially explained numerous puzzling problems disclosed by study of large numbers of silicosis cases. Some of the problems consist of exceptions to the general rule; for instance, individ uals who were exposed for long periods of years to high concentrations of silica dust without developing silicosis, and on the other hand, patients who were exposed to lower concentrations of dust for short periods and yet have developed a rapidly progressing typical silicosis with nodular fibrosis and complicating infections. The clinical experiments and observations on large numbers of mine workers, sand blasters, etc., as well as thorough and well-controlled animal experiments have shown that there are several important predisposing factors which cause considerable variation in the type of silicosis produced and in the length and dose of exposure required to produce a disabling fibrosis. Acute and chronic pulmonary and upper respiratory infections are known to produce many changes in the lungs which may be found at post mortem examination. Chronic sinusitis with a persistent poBt-nasal drip, frequent colds with complicating bronchitis, pneumonia and its residual changes, bronchiectasis, and tuberculosis are among the chief contributory conditions. These inflammatory conditions are known to act in two ways. In the acute types of pulmonary infection, there is produced a focal lymphocytic accumulation in the peripheral lung fields thereby closing portions of, or all of the lymphatic system which was previously an open type. All inflammatory scars which produce extensive fibrosis along lymphatic channels will cause obstruction and thereby further modify the lymph drainage. Secondly, certain acute and more especially the chronic respiratory infections, such as low grade tuberculosis, bronchiectasis, and repeated attacks of bronchitis, will cause a loss of the ciliated epithelium of the bronchi and replacement by non-ciliated squa mous cells. This loss of cilia permits the accumulation and stagnation of y 53758 352 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE secretions in the bronchi and bronchioli which in turn promotes accumula tion of inhaled dusts. Certain gaseous irritants in mine gases and explosive gases have been found experimentally to paralyze cilia of the tracheal and bronchial mucous membranes. Certain experiments apparently demon strate that dissolved silica from very small particles of dust will have a Blowing or paralyzing effect on ciliary activity. Thus, the normal pro tective mechanism of the ciliary sweep of secretions to the pharynx is^ destroyed. Stagnation of dust and secretion allows the phagocytes longer_< periods to engorge themselves with silica particles and to traverse theo alveolar walls into the lymph spaces. CO Aside from the general anatomical changes and the ciliary paralysis and destruction, there is apparently a particular increased susceptibility of tuberculous patients to silicosis. This phase will be discussed more fully below. Progressive Development Silicosis is not a complicated disease from the point of view of patho genesis. Although predisposing factors in various degrees of severity pro duce a large number of variations, the actual pathogenic cycle of inhalation of dusts with the subsequent production of fibrosis appears to be a rather clear-cut process. Inhaled silica of a size from 1 to 10 microns in diameter is phagocytosed by the alveolar cells. These accumulate in large groups in the alveoli and gradually pass through the alveolar walls into the lymph spaces. They are collected by the draining lymph and carried into the lymphatics and thence to the hilar lymph nodes. Thus, the primary accumulation of silica occurs in the hilar nodes in cases of open lymphatic system. During this transportation, the phagocytes which are engorged with large numbers of small particles (J to 3 microns in diameter) seem to become "mummified'' and inactive or are killed by the toxic action of the dissolving silica. These cells lose their mobility and, therefore, accumulate in groups obstructing the lymphatics. The cells disintegrate and the liberated particles of silica are again phagocytosed by fresh cells (histio cytes) which are apparently attracted to this focus. These continue migra tion until they in turn are also destroyed by the toxic action of the dissolving silica. This process is repeated many times until eventually the dust may reach the hilar lymph nodes. It is obvious that in the instance of lungs in which previous inflammation has "closed" the lymphatic system, these masses of dust-laden phagocytes (dust cells) will accumulate and remain in the peripheral foci (fig. 2a). These groups stimulate the production of early fibrotic nodules (fig. 2b). In each of these foci the gradual dissolution of silica from the disintegrating cells seems to produce a toxic or stimulating factor which causes further ST0 8 53759 I! ST0853760 354 PRINTIPt-KS AND I'RACTrfF, OF T \TU STItl A r, MBDIOIXK fibroblastic reaction and collagen deposition. Some may interpret this as a protective action on the part of the tissues to wall-off the accumulation of dust cells. As the fibrosis progresses the "mummified" dust cells dis integrate and the silica lies free in the centers of these fibrotic nodules. The nodules grow by peripheral concentric accumulation of layer upon layer of dust cells eventually producing a whorl-like collagenous structure (fig. 2c). Much of this collagen appears to be deposited without the usual number and activity of fibroblasts found microscopically in other types of fibrosis. This acellular type of fibrosis seems to be peculiar to silicosis. As these fibrotic nodules progress in size they grow closer together and finally coalesce into large masses of collagen with numerous centers of ac cumulated and trapped dust (fig. 2d). The dissolution of the dust does not stop with the walling-off by fibrous tissue, but continues as small but con stant amounts of tiasue fluid diffuse into and out of these nodules. There fore, in the young and small silicotic nodule there is less fibrosis and a large amount of entrapped silica dust, while in the old nodule (particularly in the individual who has been removed from dust exposure for a period of years), there may lie very marked fibrosis, but much less silica dust. This is the picture of the development and progress of so-called simple silicosis. A further complicating histological finding, especially in hard rock and coal miners, is coal dust in the form of carbon particles which arc found mixed with the silica dust in all the nodules. Add to this the com plicating picture of scarring and chronic inflammation due to infection of the lungs and the pathology of complicated silicosis is complete. Nodular fibrosis is not the only type which occurs in silicosis. Even in the simple form there is always a second type which may be termed linear fibrosis: a thickening of the walls of the lymphatics often causing complete obstruction of the lymphatic channel. This is probably caused by constant deposition of collagen in the region of scattered dust cells along the walls of the lymphatics. Many studies have shown that although progressing more slowly than the fibrosis of the nodules in the lymph nodes and lymphoid centers, this fibrosis is definite and eventually obliterates the lymphatics. This results in stagnation of peripheral lymph in the lung and thereby in creased accumulation of the dust cells and subsequent fibrosis peripheral to the obstructed lymphatic channels. Therefore, in lungs without pre vious or concomitant chronic or acute inflammatory changes, continuous exposure to hazardous concentrations to silica dust will eventually result in a fibrosis of the entire lung from hilum to pleura. It is obvious that with complicating infection, this extensive fibrosis will be much more rapid. Acute Silicosis The pathogenesis of so-called "acute silicosis" is different from that de scribed above according to reports of several investigators. Cole and Cole PNEUMOCONIOSIS 355 have published their studies of lungs from patients suffering with acute silicosis (especially sandblasters in whom the duration of the disease was in terms of months rather than years). By special stains (Masson trichrome) for collagen, fibrous tissue, and blood vessels, they have found that in the instances of exposure of workers to enormous concentrations of very finely divided particles (which are rapidly soluble in slightly alkaline tissue fluid), there occurs a thickening of the pulmonary capillary walls. They have produced evidence that this is true collagen deposition. They report focal capillary obstruction which causes marked respiratory embarrassment with out accompanying severe fibrosis. In later stageB there is actual collagen deposition and fibrosis of the capillary walls and the lymphatics resulting in characteristic linear peribronchial fibrosis revealed by roentgenological examination. Although this hypothesis of capillary obstruction due to the toxic action of rapidly dissolving silica in the acute cases has not been confirmed by other workers, it is at present the only plausible explanation. The reader is referred to the monograph of Cole and Cole on pneumonoconiosis for further details concerning this aspect of silicosis. III. THE DISEASE Roentgenological examination of various portions of the body reveals . abnormal tissue conditions and, therefore, constitutes a method for the study of pathological processes. Consequently, the x-ray appearance or roentgenopathology, histopathology, and gross anatomical changes will be described together. For purpose of convenience the silicotic changes in the lungs will be described in several stages: the early non-clinical stage found only by roentgenological examination or accidentally on post-mortem ex amination when death is caused by intercurrent disease or accident, ad vanced simple silicosis, and complicated silicosis, particularly silico-tuberculosis. The clinical manifestations of silicosis and its complications are best divided into several phases for clarity of discussion. In all cases of dust exposure, silicosis should be suspected and in alHndividuals with pulmonary symptoms, a careful history should be obtained to determine exposure to silica dust. History Complete occupational history always should be obtained and this must include detailed information concerning all occupations and industries in which the patient has been employed throughout his working life. It is often advisable to record this history in chronological order and if any data indicates probable or definite exposure, this particular portion of the history must be obtained in detail including description of any symptoms during this period of exposure, the exact length of exposure, the industry, 356 PRINCIPLES AND PRACTICE OF IXDUSTRL\L MEDICINE ST0853762 and details concerning the patient's exact duties, hours of work per day, precautions taken, if any, etc. All facts of ill health or upper respiratory infection immediately before or during the time of exposure to the dusty occupation should be carefully noted. Past medical history, particularly in relation to upper and lower respiratory infections, is an important aid to diagnosis and the date of onset and duration and severity of any such illnesses are to be recorded. History of pneumonia, "flu," and bronchitis must not be overlooked because these diagnoses not infrequently inad vertently cover tuberculosis of which fact the patient and his attending physician remain ignorant. Acute or Rapidly Developing Silicosis Diagnosis.--The patient always complains of sudden onset and rapid development of shortness of breath, cough, and sometimes chest pain. There will be a history of progressive weakness, loss of weight, digestive disturbances, and occasionally, the patient will complain of palpitation and pain over the heart. Examination reveals objective symptoms of pulmonary and cardiac embarrassment and these findings may cause con fusion of this disease with such conditions as pulmonary edema, lobar pneumonia, bronchial asthma, cardiac decompensation with pulmonary congestion, or advanced tuberculosis. The cough is usually dry, but may be productive. Hemoptysis is rare, but if there is a superimposed pneu monitis, this may occur. Chest expansion is definitely decreased and the expiratory movement is prolonged over the inspiratory movement. Per cussion elicits moderate hyperresonance over emphysematous areas when such have developed. Increased dullness over much or all of the lung field is the more common finding. Breath sounds may be increased over these areas of congestion and partial alveolar collapse while beginning focal pulmonary exudation and transudation may produce sibilant or musical rales. There are no findings of consequence in the examination of the peripheral blood. Urinary examination reveals nothing except by special chemical tests which will demonstrate the presence of excessive dissolved silica in the urine according to King. Especially in cases exposed to high concentrations of silica, relatively large amounts are reported to be eliminated in the urine. This test is not practical in routine diagnosis of industrial cases and fs of only experimental use at the present writing. Sputum examination for silica is considered of some diagnostic value. Examination of fresh sputum under the microscope by dark field reveals large characteristic refractile silica particles in the alveolar phagocytes. By the experienced worker, this dust can sometimes be seen with bright field illumination. Smears, which have been incinerated, will reveal large concentrations of silica dust in the phagocytes of the sputum. Chemical PNEUMOCONIOSIS 357 teats for silica can be used with larger quantities of sputum, if obtainable, but the tests are rather complicated and will not be found practical in routine industrial investigations. Prognosis.--The prognosis of acute silicosis is usually very grave. The great amount of dust already inhaled before the patient is discovered will produce a progressive fibrosis in spite of removal of the patient from the dusty occupation. Fatal complications are most frequently superimposed respiratory infections, but instances of cardio-vascular decompensation have been reported. Simple Silicosis The fibrosis produced by inhalation of silica dust only is rarely seen except in experimental animals. Occasionally, it is seen in rapidly ad vancing silicosis of young workers such as sandblasters and drillers employed in tunneling through sand under river beds. In the early stages of this disease, the x-ray findings are identical with those described below (Stage 1). In the later stages of simple silicosis, the histopathological picture remains free from inflammatory changes and pigmentation by coal dust. Otherwise the clinical and pathological picture is identical with that of anthracosilicoBis. Anthracosilicosis This is the most common form of silicosis occurring in patients and dis covered incidentally upon routine examination of miners and workers in dusty trades. Early (Stage 1) Roenigenopathology.--The earliest stages of silicosis and anthracosili cosis are always asymptomatic and produce no physical signs. This stage is discovered only by routine x-ray examination. The roentgenogram of the lungs reveals typical discrete miliary nodulation of both fields, par ticularly in the mid portions, with characteristically clear bases (fig. 3a). The miliary nodules are seen as uniformly distributed small densities. In some instances there are also increased linear peribronchial marlringa due to peribronchial lymphatic fibrosis in an early phase. Histopathology.--In the affected areas of lung tissue, many patches of alveoli contain accumulation of alveolar phagocytes which are engorged with minute refractile granules which by special processes may be identi fied as silica dust and larger particles of carbon. There is moderate thickening of the inter-alveolar tissue by accumulation of dust cells and beginning deposition of collagen. A bit later young fibroblasts will be \ 358 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE seen. In older areas uniformly small nodules occur. These are made up of collagenous tissue with a center of hyaline matrix in which there may or may not be multinucleated giant cells loaded with silica dust. Around the collar of collagen there is a zone of degenerating dust cells and round cells. In the regions of early fibrosis there is also found a hyaline thicken ing of the walls of the lymphatics due to deposition of collagen. Fibroxo blasts may or may not be present. In carefully prepared sections and--I particularly in experimental animals, there are frequently seen one or moreO layers of dust cells coating the lymphatic walls. Frequently, flat, plaque- like, thickened, hyaline apical scars immediately beneath the pleura are^j found to contain large amounts of anthracotic dust. These scars are^j densely fibrous and lack typical silicotic or tuberculous nodulation, butcn have been found to contain abnormal quantities of silica and probably^" result from areas of poor aeration and stagnation. They have not been proved tuberculous as long claimed. Intermediate Stage (Stage 2) Symptoms.--With the onset of symptoms the progress of silicosis may be stated to have entered the intermediate stage. The onset is insidious and the patient first notes that upon excessive exertion shortness of breath is more marked than he has experienced before. This shortness of breath gradually becomes more noticeable and later there may be added a slight dry cough. The patient is normal in all other respects having lost no weight, frequently being robust and healthy in appearance. Chest pain is rare, but may occur in this stage, particularly in the more rapidly advanc ing type of silicosis. When present it is described as being a sense of painful compression of the chest. The dyspnea is unusual and character istic in that there is no orthopnea and the patient will complain that he obtains no relief from sitting up in bed. Hemoptysis is rare. Signs.--Definite signs are not always present at the beginning of the second stage. However, as this disease progresses and respiratory embar rassment becomes evident, chest expansion will be decreased; the expira tory phase of respiration becomes prolonged; dyspnea following exercise becomes more marked; there may be a slight increase in tactile fremitus of uniform distribution over the entire chest and to percussion there may be found decreased diaphragmatic excursion and some slight impairment in resonance over all the lung areas except those involved by emphysema. Upon osculatory examination decrease in breath sounds may be general, particularly as the condition progresses. A few subcrepitant rales are heard in occasional cases of silicosis and these clear up following cough, but only upon the development of extensive emphysema are wheezing musical rales commonly heard. Decreased chest expansion is not a reli able sign because there is much variation between chest expansion of PNEUMOCONIOSIS 359 various individuals and only upon repeated examination of the same patient can a progressive decrease in the amount of expansion ho deter mined and considered significant. As pulmonary fibrosis progresses, signs of disability may appear or he elicited by exercise tests. Increasing dyspnea is the outstanding symptom and repeated examinations over a period of several years in the average case will disclose progressive lengthening of the recovery period for the respiratory rate to return to normal after a given amount of exercise. Diagnosis.--Although anthracosilicosis is a very clear-cut disease with a single well-proven etiological agent and a definite progressive course, the' pathologic changes cause symptoms which are not particularly character istic because they are often associated with many other cardiac and respiratory diseases. Roentgenopatiiology.--Although more reliable, the roentgenological find ings are not absolutely characteristic. Considerable experience and thor ough familiarity with all aspects of this disease are required to qualify a physician as competent in the differential diagnosis of silicosis especially when complicated by infection. The roentgenologist must examine the patient carefully, obtain his occupational and past history, and lx: informed concerning all aspects of the case before he can properly interpret the roentgenological findings. Otherwise, the roentgenologist should phrase the report in descriptive terms for interpretation by the physician who is thoroughly familiar with the patient. This correlation of all facts and findings for accurate diagnosis and the legal aspects of the problem, which place important responsibility upon the medical profession, are especially emphasized in the National Silicosis Conference Report on Medical Control (1938). The shadows seen on roentgenological examination are larger conglom erate patches of densities due to coalescence of the smaller nodules w ith increasing fibrosis. Hie large patches are still separated by areas of well aerated lung, but loginning emphysema is found. Although areas of clear normal lung in the bases and extreme apices may persist, the apices are usually found involved in this stage. The domes of the diaphragm may be moderately depressed and there is always considerable intensifica tion of the trunk shadows. Enlarged hilar nodes are extremely dense, but may not be visualized due to the large oyerlying patches of con glomerate nodules (fig. 3b). Pathology.--'Hie lungs are grossly filled except in apices and bases bv minute uniform hard nodules which are dull greenish-black or black and which arc prominent on (lie anterior surface of the lung specimen. More involvement is manifested by scattered larger areas of coalescent nodules and intervening patches of crepitant emphysema. As would be expected the microscopic picture is that of coalescence of $T0853766 granular degeneration. There are fewer giant cells and the periphery of the nodules consist of active fibroblastic proliferation and intermixed PNEUMOCONIOSIS 361 accumulation of dust cells. Trapped between many of the coalescing nodules are areas of atelectatic lung tissue and small gland-like structures of bronchiolar cuboidal epithelial cells. Laboratory findings are of little help in establishing the diagnosis except in those instances where the patient is being exposed to high concentra tions of silica dust in the occupational atmosphere. In such cases exami nation of the Bputum will often reveal large numbers of dust cells and the silicotic dust content may be identified by histo-incineration, dark field examination, or, if available, by careful chemical analysis. Differential diagnosis of stage 2 silicosis is frequently difficult due to the many pulmonary diseases, such as early bronchiectasis, disseminated tuberculosis, and pulmonary lymphatic extension of metastatic carcinoma or primary carcinoma of the lung, which may mimic the pathological and roentgenological findings in this stage. Experienced roentgenologists can differentiate the characteristic findings of silicosis from other pulmonary diseases by x-ray examination and the above described laboratory findings are diagnostic when positive. However, from clinical history and physical examination alone, a diagnosis can never be conclusively established, merely suspected. It must be remembered that many patients who have been exposed to silica dust at some previous time, or are under constant exposure to moderate concentrations of silica dust may contract lung dis eases other than silicosis and these should not be ignored in making a differential diagnosis. Before disability develops, definite diagnosis can be established only by the most cautious and complete studies with exclu sion of all other diseases which produce similar roentgenographic, labora tory, and physical manifestations. Progress with Disability.--As stage 2 of this disease approaches the more advanced type, disability may become apparent and is usually manifested by shortness of breath upon exertion and rarely by so-called asthmatic paroxysms. Weakness is not a common complaint even with marked dyspnea. The chief complaint is usually inability to continue work be cause of shortness of breath upon normal exertion required by the occupa tion. This symptom becomes worse until it advances to the profound dyspnea of stage 3. Advanced Stage (Stage 3) Symptoms.--The term, stage 3, is only a convenient designation for the most advanced type of silicosis in which disability is marked. Disability is due to severe shortness of breath, inability to work, and in some cases, cardio-vascular complications caused by the abnormal load upon the heart. It is questionable whether or not a normal heart, which has not previously been injured by some other disease, will undergo hypertrophy, fibrosis, or I ST0853768 362 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE other pathological change in response to decreased pulmonary vascular bed alone. It is claimed that in the most severe cases and in so-called acute silicosis, rapid reduction of the vascular bed may produce cardiac dilatation even in the previously uninjured heart. Signs.--As would be expected, the signs of advanced fibrosis of the lung include widespread dullness over both lung fields anteriorly and poste riorly; decreased or absent breath sounds due to emphysema and fibrosis; and frequently, patches of coarse rales heard over localized areas of bronchi ectasis and pneumonic infiltration. Diagnosis.--Laboratory diagnostic procedures are practically useless because usually the patient has been long removed from exposure to dust and no silica can be found in the alveolar cells of the slight sputum pro duced. Coughing may become persistent, but is only productive when there is a complicating infection. Dyspnea may advance to the stage of cyanosis. In long standing cases with cardio-vascular involvement, club fingers and cyanotic nails are occasionally seen. Differential diagnosis in this stage is not difficult because of characteristic roentgenological signs of massive conglomerate and complete opacity of the lungs. Roentgenopathology.--The x-ray picture of this late stage reveals a mass of large dense shadows leaving little or no normal aerated lung (fig. 3c). Emphysema is marked and trunk shadows are completely obliterated by the large conglomerate shadows. The apices and bases have become dif fusely involved. The domes of the diaphragm are depressed and fre quently there is exaggerated posterior bowing of the spine. If the emphysema is extreme, there will be increased widening of the inter costal spaces. Pathology.--Grossly the lung is a voluminous "petrified" specimen, stony throughout with only small irregular areas of softer, paler tissue. The cut surface is granite-like, but possesses blacker mottling. Microscopic sections from lungs of the third stage reveal massive areas of fibrosis obscuring the individual nodules. These masses of hyaline tissue appear to be closely packed together and the narrow intervening and peripheral spaces of emphysematous lung are seen in conspicuous contrast. Prognosis.--Occasionally, termination is due to cardio-vascular failure with pulmonary edema and acute dilatation of the heart, but more fre quently complicating pulmonary infection in the form of a nonspecific pneumonia or tuberculous pneumonia is the fatal end result. Prognosis of simple silicosis in the earlier stages may be said to be good for life and disability if the patient is removed from exposure to hazardous concen trations of silica dust. Fibrosis will progress even though the patient is removed from such surroundings, but will gradually reach a maximum and from that point become static and no further involvement of the lung PNEUMOCONI08IS 363 tissue will take place. The prognosis of advanced silicosis is definitely grave because of the extreme susceptibility to complicating nonspecific or specific infection of the lungs leading to a fatal pneumonia. Ques tionably, in cases with normal heart, and certainly in instances where the heart has previously been damaged by some other disease or by arterio sclerosis, advanced silicosis will produce marked overwork of the cardio vascular system and not infrequently may cause fatal cardio-vascular decompensation. rv. COMPLICATED HLICOBIB (SILICOSIS WITH INFECTION, SHJCO-TUBEBCUI1O8I8) Very few proven cases of simple silicosis are on record. Partly due to the common and widespread incidence of respiratory infection of all types, but particularly because of increased susceptibility of tuberculous patients to silicosis and of silicotic patients to tuberculosis, mixed infection and silicosis is the usual picture found at necropsy. Chronic bronchitis, pneu monia, active tuberculosis, and other infections are frequently associated with silicosis and, therefore, complicate the pathologic picture and the clinical differential diagnosis. The industrial physician will rarely see uncomplicated simple silicosis and he will be confronted with vexing prob lems concerning the source of the disability and its proper compensation. Bronchopneumonia in Silicosis Whenever silicosis is complicated by bronchopneumonia, the patho logical picture is that of the advanced silicotic fibrosis superimposed by infiltration of monocytes and polymorphonuclear leukocytes into the emphysematous or partially collapsed alveoli. The inflammation may. be caused by any one of the many microorganisms which affect the lung. Silica-tuberculosis From the earliest recognition of silicosis students of this disease have noted that Bilicotic patients are apparently much more susceptible to pulmonary tuberculosis than other individuals. A great amount of labo ratory and clinical research has been done to explain this apparent in creased susceptibility. It is impossible in this brief consideration to include an exhaustive discussion and review of the thebries and findings resulting from this work. However, it can be stated definitely that the incidence of tuberculosis among sufferers from silicotic fibrosis of the lungs is defi nitely much higher than that in the general population. Pathogenesis.--Many laboratory studies, including animal experiments and test tube cultures by workers at the Saranffc Laboratory and the University of Toronto and others, apparently indicate that the presence ST0853770 I 364 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE of silica in culture media or in the animal lung or other animal tissue definitely favors the growth of tubercle bacilli. This may explain the apparent increased susceptibility of silicotic patients to complicating tuber culous infection. Another factor which must not be overlooked is the decrease of aeration in the lungs due to marked silicotic fibrosis. The numerous stagnant pockets formed by scarred areas containing imprisoned bits of bronchi which later dilate and accumulate secretion and the de creased circulation through the fibrotic areas and their vicinity undoubt edly are significant physiological and physical factors favoring infection and inflammation. Therefore, any type of infection may become seated in these areas, but because of the general susceptibility of the man to tuberculosis, this infection more frequently obtains a foot-hold in the less resistant lung. It is conceivable that if enough cases of non-silicotic types of long standing chronic advanced fibrosis of the lung could be collected and thoroughly studied, a high incidence of complicating tuber culous infection might be found due to the same physical and physio logical circumstances outlined above. Too few cases of severe x-ray fibrosis of the lung have yet been accumulated to justify conclusions from study of this type of fibrosis. Reports thus far published to support the claim that silicotic fibrosis of the lung breaks down old calcified or fibrous tuberculous scars and reac tivates an old tuberculous infection are not conclusive or convincing. It is much more probable that because of the well known wide distribution of tubercle bacilli, a reinfection tuberculosis occurs in the silicotic indi vidual. It is certain that in mines and many other industries there is sufficient opportunity for the silicotic employees to be exposed to other individuals who are open cases of tuberculosis. This fact and the low incidence of tuberculous complication in workers (including silicotics) reported from certain isolated or selected industries and mines may be accounted for by the varying incidence of tuberculosis in these communities. Symptoms and Signs.--The manifestations of silico-tuberculosis are those of a fibrosis as described above under simple silicosis plus those of tuberculous infection. The roentgenological findings are definitely sug gestive and sometimes almost conclusive to the experienced roentgenolo gist. The signs are those of bronchial and pulmonary infection at first in localized areas and later in large areas denoting pneumonic involvement. Tuberculous pneumonia is not uncommon as a terminal process in the advanced silico-tuberculous patient. In fact, frequently the typical find ings and symptoms of tuberculosis may overshadow those of silicoBis to the extent that the latter is not diagnosed until the necropsy. Diagnosis.--Undoubtedly, many cases of so-called silico-tuberculosis which have been reported in the literature are not true tuberculous infec tions since no definite proof by culture or guinea-pig inoculation has been PNEUMOCONIOSIS 365 produced to show the presence of tubercle bacilli. Roentgenological find ings are frequently inconclusive, but there are certain manifestations of complicating infection which can be properly interpreted and evaluated by the experienced roentgenologist, particularly if he has available the complete history, laboratory findings, and data concerning exposure to silica dust. It is the author's opinion that the diagnosis of silico-tuberculoeis should never be made in any case until tubercle bacilli are demon strated in the sputum or a positive guinea-pig test completed. Otherwise, even though definite findings of infection are seen on roentgenograms and are apparently confirmed by physical findings (rales, increased breath sounds, areas of pneumonic dullness, and productive cough) the diagnosis of "silicons with infection" is preferable. Differential diagnosis is estab lished only by the finding of tubercle bacilli in the sputum. All the labo ratory studies, such as tuberculin test, sedimentation time, complement fixation test, leukopenia with predominating monocytes, guinea-pig inocu lation with the production of tuberculosis in the animal, will, of course, aid in establishing a diagnosis. Progrtts.--Clinical pictures of progressive silico-tuberculosis are as protean as those of tuberculosis. The numerous variable controlling fac tors include the degree of silicotic fibrosis, the dose and virility of the tubercle bacilli causing the reinfection, the so-called natural resistance or biological resistance of the particular patient to this disease, the physical and atmospheric surroundings, continuation or cessation of exposure to the reinfecting source of tuberculosis, the degree of allergic response of the particular patient to the tuberculous infection, the continuance or cessation of exposure to silica dust, the general working conditions, and the physical condition of the patient. These factors combine in various forms and degrees of inter-relation to produce innumerable manifestations of tuber culosis complicating silicosis. Roentgenopathology.--In silico-tuberculosis the roentgenologic findings are much more confusing and complicated than in either anthracosilicosis or uncomplicated tuberculosis. There is mottling characterized by shadows which are ill-defined with "fuzzy" borders and vary in size and distribution. These shadows usually denote infla.mms.tnry infiltration. In more advanced cases the "soft" nodulation acquires flocculent irregular and indistinct borders larger but of irregular size, varying density, and distribution. Massive shadows of homogeneous density not of inflamma tory origin with asymmetry of distribution denote the presence of silicotic fibrosis. Diffuse, dense opacity of entire lobes usually indicates tuber culous pneumonia superimposed upon the silicotic nodular fibrosis. Out lines of normal structures, such as the vascular bed and bronchial tree, will be partially or completely obliterated. Pathology.--The lungs are stony, bizzare masses of infected gray foul I ST0853772 366 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE tissue and granite blackened by carbon dust and silica. Gross cavitation with exudate of secondary infection is common. Normal anatomic struc tures are often not recognizable. There is much disagreement in the literature concerning the origin of many of the pathological lesions found in so-called silico-tuberculosis. The Saranac group are of the opinion that the early caseation of tuberculous nodules cannot be distinguished histo logically from the acute necrosis of silicotic nodules which also may produce an acute monocytic inflammatory reaction in the peripheral zone. Many other students of silicosis disagree with this statement and claim ability to differentiate the characteristic histologic features of silicotic and tuber culous nodules. For the purpose of the student of industrial medicine, it suffices to emphasize that in this disease, regardless of pathological con troversies, the diagnosis can be established only by characteristic roent genological findings and the demonstration of tubercle bacilli in the sputum or (and) a febrile reaction to the Mantoux, patch or percutaneous tuber culin test. In almost all cases of silico-tuberculosis, there will he demon strated either an old silicotic fibrosis with superimposed inflammatory tuberculous giant cell nodules, caseation necrosis with or without cavita tion, or the opposite picture of old fibro-caseous tuberculosis or arrested quiescent tuberculosis with calcification of hilar nodules and peripheral scars and a more recent uniformly distributed miliary non-necrotic silicotic nodular fibrosis. Large areas of caseous pneumonia with the character istic accumulation of masses of monocytes and caseous necrotic debris leaves no doubt about the tuberculous nature of the pneumonitic reaction. Cavitation is frequent, but may be bordered by walls containing silicotic nodules. In specimens examined under the dark field after histo-incineration, there will be found very little or no silicotic dust in the central portion of tuberculous scars whereas the peripheral zones will contain varying amounts of silica depending on length of exposure to silica. The reverse pattern of much silica in the predominating silicotic fibrous tissue in contrast to much less in the superimposed inflammatory tissue is re vealed by histo-incineration. As will be pointed out in the paragraph on control, it is needless to caution that the open case of silico-tuberculosis is as great a hazard to his fellow workers and members of his immediate family and to society as is any case of active tuberculosis. It is also obvious that in cases of active silico-tuberculosis, all treatment should be focused on the control of the tuberculosis since this complication will sooner or later completely incapaci tate the individual so far as industry is concerned. In occasional instances when the diagnosis of tuberculous complication is made in the middle stage of silicosis or early in the tuberculous phase of the disease, properly instituted treatment including rest, diet, fresh air, removal from exposure to source of infection, etc., may arrest the disease and eventually permit PNEUMOCONIOSIS 367 the patient to return to moderate physical activity. However, almost all cases are discovered in a later stage when the tuberculous infection is advanced. Progress of the infection in these cases is always rather rapid and ever increasing involvement of the lungs due to the widespread silicotic scars and poor aeration and circulation may be expected. The extension of the tuberculous infection is usually by aspiration due to the many areas of poorly functioning bronchi with accumulated debris and secretion and also by contiguous tissue due to the poorly vascularized silicotic scars. Aerated lung may be infiltrated by characteristically monocytic cells and large areas of caseation necrosis as seen at necropsy. In some instances this process may progress rapidly into all the uninvolved por tions of the lungs and result in a rapid fatal termination. Prognosis.--The prognosis is obviously very grave. However, progno sis must be guided by consideration of the variable factors outlined above, and in the more mild infections of low virulence with manifestly better resistance, patients may survive for considerable periods of time and occa sionally are able to earn a living at some minor trade for a period of years. Unfortunately, the greater proportion of cases do not follow this course. If diagnosis could be established earlier and effective treatment for the tuberculous infection instituted, prognosis would certainly improve. The question concerning the increased susceptibility of old cases of pulmonary tuberculosis to fibrosis produced by silicotic dust in the lungs will be mentioned only to point out that it is the author's opinion that there is a definite increased susceptibility of tuberculous patients to silicotic fibrosis, but that this is due to the closed lymphatic circulation produced by the tuberculous infection and in no way is related to any specific affinity for silicosis or silicotic scarring to tuberculous areas. It is the author's belief that any other type of widely distributed scarring or necrosis produced by an infection and resulting in closure of the pulmonary lymphatic system would produce a similar degree of so-called increased susceptibility to silicotic fibrosis. Silicosis of Other Organs Silicotic nodulation of the liver and spleen is described in experimental work. Occasional silicotic nodules have been discovered in post-mortem examination of individuals exposed to high concentrations of silica dust. No clinical manifestation or significant injury has been demonstrated to arise from such accumulations of silica in the viscera. V. COMPENSATION OF SILICOSIS In order to adequately cover the involved subject of industrial compensa tion in silicosis, an entire chapter would be required. Only a few pages can be devoted to the problems peculiar to silicosis. 368 T a b le 1.--Workmen'* Compensation Provision* fo r S ilic o n * (Summary of Coverage Provisions fo r Silicosis as of January 1, 1038) PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE ST0853774 370 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE ST0853776 Disability and Compensation Although it is well proven that silicosis definitely produces disability, the problem of compensation for disability has caused much legal and medico-legal confusion and has resulted in many law suits involving large damage claims against industries and mining companies. The term, dis ability, is defined in the National Silicosis Conference Report as "a decrease in capacity to do work required of an individual in the course of his usual occupation." It may vary from partial to complete and may persist as partial or, in the case of progressive fibrosis due to large amounts of previously inhaled silica or continuous exposure to dangerous levels of silica dust in the industry, may progress to serious and permanent total disability. In many states disability due to silicosis is still not compensable, but the various states which have passed compensation laws including this disease are given in table 1. As a result of the large amount of legal action and legislation concern ing silicosis disability in many states, it has become the general precaution of employers in industries involving silica dust hazards, to reject for employment any persons who have already developed silicotic fibrosis or other types of fibrosis of the lungs demonstrable by x-ray examination. This causes much hardship upon employees who have learned their trade well and become experienced over a period of years in occupations involving the silica dust hazard. It is the opinion of many medical experts that whenever pre-employment examination discloses fibrosis of the lungs in a person who has been exposed in a dusty industry for a period of years and that whenever this fibrosis is not disabling and is not complicated by infection, this person should be recommended for employment as a good risk, furthermore, provided that the silica dust hazard has been eliminated and the concentration of dust in the new job is below the hazard level. There are several obvious advantages to such a procedure, the chief advantage being that such a person has already been tested, so to speak, concerning his ability to withstand silicotic fibrosis without suffering com plicating respiratory infection, particularly tuberculosis. Also, such a person has developed a certain skill in that particular occupation which is of value both to himself and his employer. He is a much smaller risk than a younger man who* is inexperienced, untrained, and whose reaction to silica dust exposure is unknown even though examination may fail to disclose any respiratory infection. Tests for Disability.--Much research, both clinical and laboratory, has been reported concerning practical tests for measuring the degree of dis ability produced by silicotic fibrosis of the lungs. Most of these tests are based upon methods of measuring lung function. Many of these tests are PNEUMOCONIOSIS 371 impractical because the necessary equipment and time for their perform ance are not generally available. The practical test which is suggested by the National Silicosis Conference Report on Medical Control is as follows: The individual places one foot upon a chair or firm stand, 18 inches in height, and raises his body to an erect position 25 times in 30 seconds. Those with marked respiratory or cardiac disturbances cannot be subjected to such a test, but in the course of examining persons already employed or applying for work few of such individuals will present themselves. The pulse and respiration are taken with the examinee at rest, immediately following the exercise test, and after a 2-minute rest period. It is evident that such a test is not one whose results are affected by respiratory conditions only, but one which is influenced by various factors, such os weight, heart condition, age, general physical condi tion, and numerous metabolic differences. It does serve as an indication of de creased capacity for work. When we consider all factors, definite information concerning respiratory capacity is available. Regardless of the presence of slight cardiac defects or changes due to age, etc., the individual with appreciable pulmonary fibrosis will not only exhibit shortness of breath following the exer cise, but the increased respiratory rate will persist well beyond the 2-minute rest period, and the altered respiratory rhythm is characteristic. The expiratory phase is markedly prolonged often to such an extent that the rate of respiration is much less than in the case of a person with pulmonary infection or cardiac dis turbances. Due to loss of elasticity of the lung, the individual cannot empty his lungs rapidly enough to allow for a great increase in respiratory rate. In fact, the rhythm approaches that of the asthmatic before exercise. The condition may be differentiated from bronchial asthma by the absence of the rales and other clinical data. In cases of well-established silicosis, prolonged expiration may be elicited by careful observation during the course of physical examina tion, prior to any exercise test. VI. CONTROL OP SILICOSIS Because silicosis is caused only by silica dust, but is complicated by infection and because of the apparent predisposing action of healed or latent tuberculosis and other chronic infections of the lungs, all methods of control must take cognizance of both exposure to silica dust and the health of the workers before employment in a dusty occupation. Thus, the control of silicosis may be divided into two general types: First, the medical control through physical examination before employ ment, periodic health examination during employment, and education of the employees and employers concerning general hygienic measures, and maintenance of good health with reduction of upper respiratory and pul monary disease; and secondly, mechanical control whereby the actual con centration of silica dust in the air to which the workers are exposed is reduced to a level less than the hazardous concentration and maintained by continuous efficient operation of the mechanical devices. These methods of control are discussed in detail in Chapters II, XIII and XV. I ST0853778 372 PRINCIPLES AND PRACTICE OP INDUSTRIAL MEDICINE VII. OTHER PNEUMOCONIOSES There is considerable disagreement in the medical literature concerning the exact etiology of certain types of pulmonary fibrosis due to dust inhalation other than silica dust. Asbestosis, siderosis, and anthracosis are the most important of these fibroses. Asbestosis It has been well proven that a peculiar type of linear pulmonary fibrosis is caused by minute asbestos fibers inhaled by workers in industries utilising asbestos for the manufacture of fire resisting material, insulation, certain fabrics and ropes, paints, roofing, tile, etc., as well as the manufacture of asbestos itself. Asbestos is magnesium silicate and is the only silicate which has experi mentally been proven to produce a pulmonary fibrosis without exposure to silica. The onset and clinical course of asbestosis is similar to that of slowly progressing silicosis and the symptoms in the later stages are identical. Fatal termination is usually by complicating pneumonitis, cardio-vascular decompensation, or tuberculosis. The roentgenopathology is typical and not difficult to differentiate from silicosis. Gloyne and Merewether state that the roentgenological appearances of asbestosis are revealed typically as a general lack of tranelucency with a fine pinhead mottling. This is the characteristic "ground glass" appearance. The film should always be compared with a film of a normal patient and a film of a silicotic patient taken with the same exposure. The diagnosis depends upon a definite history of exposure to asbestos dust including sufficient period of exposure, roentgenological appearance, decreased pulmonary capacity, and the finding of asbestos bodies in the sputum of patients not yet removed from exposure to the dust. These asbestos bodies are well described and usually illustrated in most text books of clinical pathology. The pathology may be summarized in the single statement that it consists of a persistent, progressive, diffuse perialveolar fibrosis of the lungs. The fibers may be seen on histological examination to lie embedded in the fibrous walls of alveoli and bronchioli and each fiber appears to be encrusted by an iron-containing yellow pigment. As would be expected, in the later stages the fibrosis becomes confluent and massive. Siderosis Siderosis is chiefly a red pigmentation of the lung tissue due to inhalation of iron-containing dust frequently found in hematite miners. Experi mentally, fibrosis has not been produced by pure iron or iron oxide dust PNEUMOCONIOSIS 373 and only when mixed with hazardous concentrations of silica dust does fibrosis result. Therefore, unless the patient is also affected with silicosis siderosis by itself is asymptomatic and produces no roentgenological or clinical findings. Antkracosia Black pigmentation of the lungs due to inhalation of smoke and other types of carbon particles is common particularly in residents of large industrial cities. Most marked blackening is produced in coal miners. There is some controversy concerning the question as to whether or not carbon dust of itself can produce a pulmonary fibrosis. There is no con clusive experimental evidence that pure carbon dust will produce fibrosis. It is the author's opinion that all instances of fibrosis in anthracotic lungs are due to an admixture of silica dust in the inhaled air or an inflammatory fibrosis due to respiratory disease. Anthracosis is asymptomatic and produces no clinical findings or disability. REFERENCES American Public Health Association: Report (joint) of the Committee on Pneumo coniosis and the Committee on Standard Practices in Compensation of Occupa tional Diseases, Year Book, 1933, p. 100. Belt, T. H., Ibwin, D., and Kino, E. J.: Silicon and dust deposits in the tissues of persons without occupational exposure to siliceous dusts. Canadian Med. Assoc. J., 34 (2): 125-133, 1936. Buree, H. E.: The detection of mineral particles in the sputum in silicosis. J. Ind. Hyg., 17 : 27, 1935. Cole, L. G., and Cole, W. G.: Dyspnea of silicosis: What causes it? J. A. M. A., 113: 1216, 1939. Cummins, S. L.: The augmentation of action of anthracite and other dusts by dead tubercle bacilli. Brit. J. Exp. Path., 21: 64-70, Feb. 1940. Drinker, P., and Hatch, T.: Industrial Dust. McGraw-Hill, 1936. Ellman, P.: Pulmonary asbestosis: its clinical, radiological and pathological fea tures, and associated risk of tuberculous infection. J. Ind. Hyg., 16: 165, 1933. Gardner, L. U.: Pathology of so-called acute silicosis. Am. J. Pub. Health, 23: 1240, 1933. Gardner, L. U.: The pathology and roentgenographic manifestations of pneumo coniosis. J. A. M. A., 114: 535-545, Feb. 17, 1940. Gardner, L. U.: Recent developments in relation to silicosis. Ind. Med., 9 : 45-49, Feb. 1940. Gardner, L. U.: Studies on experimental pneumonokoniosis. V. The reactivation of healing primary tubercles in the lung by the inhalation of quartz, granite, and carborundum dusts. Am. Rev. of Tuberc., 20 (6), 833, (Dec. 1929). Glotne, S. R., and Merewether, E. R. A.: Asbestosis. O. A H., (Brochure), 1938. Hatch, T., and Thomfbon, E. W.: A rapid method of dust sampling and approximate quantitation for routine plant operation. Ibid., 16: 92, 1934. International Labour Office: Pneumoconiosis, a list of references, studies and reports, series F (Ind. Hyg.), No. 15, 1932. 374 PRINCIPLES AND PRACTICE OF INDUSTRIAL MEDICINE ST 0853780 Irwin, D. A.: The histological demonstration of siliceous material by micro-incinera tion. Can. Med. Assoc. J., 31: 135, 1934. Kino, E. J., and Belt, T. H.: The silica content of tissues, with and without silicotic lesions. J. Path. & Bact., 61: 269-275, 1940. Lanza, A. J., McConnell, W. J., and Fehnel, J. W.: Effects of the inhalation of asbestos dust on the lungs of asbestos workers. U. S. Pub. Health Reports, 60: 1, 1935. McCann, W. S., et al.: Disability in pulmonary fibroses. J. Am. Med. Assoc., 103: 810, 1934. McNallt, W. D.: Acute silicosis. J. Ind. Hyg. & Tox., 23:45-49,1941. National Silicosis Conference Report on Medical Control, United States Depart ment of Labor, Bulletin 21, Part 1 (1938). National Silicosis Conference Report on Engineering Control, United States Depart ment of Labor, Bulletin 21, Part 2 (1938). National Silicosis Conference Report on Economic, Legal, and Insurance Phases, United States Department of Labor, Bulletin 21, Part 3 (1938). Pancoast, H. K., and Pendergrass, E. P.: Roentgenological aspects of simple sili cosis and silico-tuberculosis. Am. Rev. Tuberc., 29: 43, 1934. ' Vorwald, A. J., and Delahant, A. B.: The influence of silica on the natural and acquired resistance to the tubercle bacillus. Am. Rev. of Tuberc., 38: 347-362, 1938. INDEX A Abnormal atmospheric pressure, 91-100 below eea level, 91, 92 caisson's disease, 93-97 prevention, 94-96 symptoms, 93-94 treatment, 96-97 effects of, 91-100 high pressure, mechanical effects of, 92, 93 Abortion, in benzene poison, 239 Absenteeism, 637-349 control of health, safety and`welfare facilities, medical care, 640 married versus single women, 540 home responsibilities, 540 national health survey, 537-638 tables on, 539 non-occupational conditions, 543 dysmenorrhea, 544 fatigue, 546 menopause, 544 menstruation, 544 noise, 647 nervous manifestations, 548 occupational illness dermatitis, 541 lead, 543 organic solvents 643 radium poisoning, 542 synovitis of arm, hand, wrist, 542 women versus men, 537-640 Boston Edison Co., 537-538 Absorption of solvent vapors, 249-250 Acetone, 285, 266 careful selection of workers, 266 Accidents, 23-34, 424, 484, 506 causes of, 26-27 control, 30 compensation lawa, 484, 505 costs, 30, 424, 484, 505 direct, 30, 484 indirect, 30, 484 occupational, 23 Accident proneness, 27-29 Newholds table for determining, 29 Acid, 192, 195, 281-283, 430-431 burns of eye, 430-431 hydrocyanic, 281-283 nitric, 283 phosphoric, 192 sulphuric, 195 Actinic causes of cancer, 326 Acute pneumoconiosis, 366-367 Acute silicosis, 364-866 Acute transient inflammatory reaction, 78 Age, 24, 303 as factor in accidents, 24 as factor in skin diseases, 303 Agricola, 2, 296 Air conditioning, 87 Air hose accident to eye, 429-430 Alameda Medical Society, 521 in medical education, 521 in medical service to small plants, 521 Alcohol methyl, see methanol Allergy, 304-308 factor in skin disease, 304-306 Alkali burns of eye, 430-431 Allen, T. D., 426 on protecting eyes, 425 Alpers, B. J., 248 on pathology in CSi poison, 248 Aluminum, 188, 189 American Association of Industrial Phy sicians and Surgeons, 4, 5, 66, 518 committee on education, 66 committee on nutrition, 409 results of survey, 409-413 American Association of Labor Legisla tion, 4 American Association of Public Health Nursing, 5, 496 American College of Surgeons, 4,5 committee on industrial medical and traumatic surgery, 4 minimum standards for medical service in industry, 4 American Dietetic Association, 414 training of dietitians, 414 American Industrial Hygiene Associa tion, 4, 5 American Medical Association Council on Industrial Health, 4, 5, 65-68, 518, 521 first Congress on Industrial Health, 4 medical education post-graduate, 66 under graduate, 65, 66, 518 first symposium Industrial Hygiene and Medecine, 4 Section on Industrial Hygiene, 4 557 558 INDEX ST0853782 American Public Health Association, 4, Baths, supervised, 322 346 as protection against skin irritants, 322 section on industrial hygiene formed, 4 Beasley, Ada, 487 American Red Cross, 33 1st nursing visit to industrial policy first aid training, 33 holder, 487 American Standards Association, 186, Bechterew's sign, 476 197,244 Bends, 99 allowable concentration of CS in air, in caisson workers, 244 Benzene (benzol), 259 on harmfulness of cadmium fumes, 186 acute poisoning on safe concentration of manganese death from, 259 dust, 197 signs and symptoms, 259 Anderson, Otis L., 394 chronic form, 259 Anderson, Richard N., 507 abortion in, 259 Anemia, 272, 273 signs and symptoms, 259 in carbon monoxide poisoning, 272,273 cutaneous dryness and cracking, 260 Anemia, aplastic, in benzene poison, 259 diagnosis, 259 Anthracosilicosis, 357-363 effect on girls and pregnant women, 259 Anthracosis, 373 Antimony, 190, 193-194 prophylaxis blood count weekly, 260 Aprons, 32, 322 education of employees, 260 Appraisal of visual defects in industry, protective ointments, 260 423 synthetic rubber gloves, 260 Argon,181 ventilation, 260 Army, 379 urinalysis for sulfates, 260 4x5 x-ray film, 379 treatment Arsenic, 190, 192-193, 329 remove from exposure, 260 as cause of cancer, 329 special treatment as necessary, 260 as impurity in metals, 192 Benzine, 261 symptoms of poisoning, 192-193 see gasoline dermatological, 193 Benzol, 259 Asbestosis, 372 see benzene Asphyxiation, from electrical shock, Berkeley plan, 521 292-294 in medical education, 521 theories, 292 in medical service to small plants, 521 treatment, 292-294 Beryllium, 182 Association of American fi^edical Col Bills, Arthur G., 134 leges, Industrial Medical Educa factors influencing mental output, 134 tion, 518 Bismuth, 190,194 Atmospherio pressure, 91 Blindness, 264 Austria, 3, 498 wood alcohol poisoning, 284 labor legislation, 3, 498 Blood in treatment of traumatic shock Auten, H. L., 427 care of eye injuries, 427 Aviation medicine, 172, 179 Journal of, 171 and burns, 435 Blood pressure, 155-176 effect of continued abnormal, 176 in exposure to toxic chemicals, 155-179 B measurement of, 157 scoring, 158-160 Baetjer, Anna M., 69, 91 Barium, 182,183 registration of score, 160-162 things affecting, 169-175 pneumonoconiosis in Italian mill workers, 183 Baron, 188, 189 Barth, E., 221 on accumulation of lead in bones, 221 useful levels, 157-158 Bloomfield, J. J., 7, 48 Blumer, F. M. R., 193 on arsenio in hair of normal and ex posed personsj 193 INDEX 559 Brieger, H., 248 hematological survey in CSt poisoning, 248 Bristol, Leverett D., 494 on public health nurse, 494 British X-ray and Radium Protective Committee, 186 on safe exposure to x-rays, 186 Bromine, 197,199 Brown, A. L., 431 on epidermal or mucous membrane grafts following chemical burns of eye, 431 Bulson, Jr., A. E,, 428 on foreign bodies in eye, 428 Bureau of Labor Statistics, 60, 396 on employment, 396 Bureau of Mines, 4, 33, 60, 60 functions, 66 first-aid course, 33 Bureau of Standards, 426 on colored eye protective glasses, 426 Bums, 441-467 acid, 430 alkali, 430 Berkow's method for estimation of burned surface, 457 electrical, 288 eyeball, 430 infection, 452 thermal burns in major catastrophe, 441-446 anticipation of, 445 Bum shock, 438-447 Bums, treatment of, 465 general amino-acid, 449 barbituatea, 448 blood transfusions, 438, 449 chemotherapy penicillin, 444, 456 sulfa group, 455 morphine, 447-448 oxygen, 448 plasma transfusions, 438, 449 saline, 438 , 448 water, immersion in cold, 448 local boric acid ointment gauze and pres sure dressing, 451 cleansing of surface, 450 envelope method, 454 miscellaneous methods, 454 Pickrell's translucent pliable film, 452 saline bath, 454 sulfa drugs, 461-462, 466 tanning-tannic acid, silver nitrate, Dymixal, 461 Burns, treatment orders, 466 emergency, 466 laboratory, 466 routine, 466 vitamin requirements, 466 C Cadmium, 186,186 symptoms of poisoning, 186 toxicity of fumes, 188 Cafeterias in industrial plants, 413-417 dietitian in, 414 importance of, 413 operation of, 414-416 Caisson's disease, 93-97 prevention, 94-96 helium-oxygen mixture, 96 hours of work, 95 inhalation of pure oxygen, 95-96 nitrogen-oxygen mixture, 96 proper selection of personnel, 96 rate of decompression, 94-95 treatment, 96, 97 oxygen-helium mixtures, 97 oxygen-nitrogen mixtures, 97 recompression, 96 Calcium, 182, 183 Calcium fluoride, 198 California, 4, 57, 486, 526 Industrial Accident Commission, 57 law on work for women, 528 nursing consultant, 486 passed early law on reporting occupa tional diseases, 4 Calhoun, J. A., 241 Calvery, H. O., 193 public health aspects of arsenic sprays, 193 Candle power, 103 Carbon, 98, 99,189, 275, 279,281,287, 294 carbon dioxide, 189 effects of at high pressures, 98, 99 with oxygen, 275, 279, 281, 287, 294 solid carbon dioxide, 189 solid, freezes and destroys tissue, 189 Carbon disulphide, 241-255, 264 absorption, 249 clinical manifestations local, 245 general, 245-246 differential diagnosis, 247 excretion, 249 exposures, 244 560 INDEX ST0853784 Carbon disulphide--continued manufacture, 242 mechanism of toxicity, 261 method of determinations, 243-244 pathological changes, 248 poisoning, 246 prevention, 252 therapy, 253 properties, 241 reactions, 241 use, 242 Carbon monoxide, 174, 189, 269-277, 281 absorption, 269 chronic poisoning, 273 factors to consider in diagnosing, 274 elimination, 269 fatigue and, 174 prevention, 275 prognosis, 271 reacts with metals, 189 symptoms, 271 tests for, in blood, 276-277 tests for, in air, 276 toxicity at high altitudes, 174 treatment, 275 Carcinoma, 184, 327 in radium workers, 184, 327 in x-ray operators, 327 Carlisle, J. M., 256, 435 Carman, H. F., 425 on protecting eyes in industry, 425 Case, . M., 99 toxicity of gases at high pressure, 99 Case finding in syphilis, 401 Case finding in tuberculosis, 388 Cellulose xanthate, 241 Central nervous system, 196, 246, 260, 271 progressive depression in toluene poi soning, 260 carbon disulphide poisoning, 246, 247, 248 , 265 carbon monoxide poisoning, 271 manganese poisoning, 196 Cerium, 189 Cesium, 181 Chadwick, Edwin, 3 investigated working of poot laws, 3 secretary of factory commission, 3 Chemical irritants, 307-308, 383 in dermatitis, 307-308 in tuberculosis, 383 Chemical poisoning, 150-179 acute result of accident, 152 result of carelessness, 152 temporary inadequacy of personnel, 152 chronic, 152-154 physical examinations in control of, 150-179 Chilblains, 78 Children's Bureau, 4, 50 Chimney sweep's cancer, 296 China, 326 kang cancer, 326 Chlorine, 197, 199, 278-280 action, 278 prognosis, 279 symptoms, 278 treatment, 2fe-'Z80 2n 'V Chromium, 194-195 Cleanliness, 212-213, 258, 263, 322-323, 562 personal 258, 263, 322-323 plant, 212-213, 322, 552 Cleveland Railway Co., 28 study of accident proneness, 28 Clothing, 80, 88, 320-322, 531-532 change of, 80, 257, 264, 320-321 protective, 283, 320-322 work, 320-321, 531-532 frequent laundering, 320-321 Coagulation therapy of burns, 453 disadvantages of, 453 constriction of blood vessels, 453 difficulty in detection of infection beneath coagulum, 453 liability to produce rigid scar, 453 Cobalt, 197 Colorado, 526 law on work for women, 526 Columbium, 190 Commission on Industrial Relations, Congress authorized appointment, 4 Committee on Education, American As sociation of Industrial Physicians and Surgeons, 66 Committee on Nutrition, 409-413 American Association of Industrial Physicians and Surgeons, 409 results of survey, 409-413 Commonwealth of the Philippines, 391 all occupational diseases compensable, 391 Compensation, 498-506 accident and disease prevention, 505 compensation laws, 505 physical examinations, 505 administration and review, 503 industrial commissions, 504 labor departments, 504 ST0853785 INDEX 561 benefit*, 601 disability, 601 death, 602 permanent partial, 601 permanent total, 601 coverage, 499 groupe not covered, 600 maritime and interstate commerce, 600 injuries, 600 historical Europe, 498 United States, 498 Wisconsin, 498 insurance and security requirements, 604 private, 604 self-, 504 state, 604 medical and rehabilitation, 502 eye injuries, 424, 433 limited in time and cost, 602 selection of physician, 502-603 rehabilitation, 603 objectives, 499 Public Health Administrators, 68-69 silicosis, 367-371 table on, 368-369 voluntary election on part of employer, not covered, 600 Compressed air illness, 93-97 prevention, 94-96 helium-oxygen mixture, 96 hours of work, 96 inhalation of pure oxygen, 95-96 nitrogen-oxygen mixture, 96 proper selection of personnel, 96 rate of decompression, 94-95 treatment, 96, 97 oxygen-helium mixtures, 97 oxygen-nitrogen mixtures, 97 recompression, 96 Congress, 4, 600 authorized appointment of Commis sion on Industrial Relations, 4 jurisdiction over maritime and inter state commerce employment, 500 Connecticut, 486, 496, 528 law on work for women, 526 nursing consultant, 486 program, man power conservation, 496 Contact finding, 389, 401 in syphilis, 401 in tuberculosis, 389 Control of accidents, 30-34 Control of diseases, 211-226, 319-823 Converse, J. M., 430 on war injuries to eye, 430 Copper, 181-182 Cost of hiring and dismissal, 421 Costs of compensable accidents, 30, 424, 484 Congenital defects, 466-467 in industrial back conditions, 465-467 correction of, 487 Craft guilds, 2-3 Cross, George H., 421, 428 Cumming, Donald E., 23 Curriculum Guide for Public Health Nursing, 496 Cyanogen, 281-283 chloride, 281-283 D Dean, H. T., 199 on mottling of teeth, 199 Defense, Health and Welfare, Office of, 6 Committee on Health and Medicine, 5 Subcommittee on Industrial Health and Medicine, 5 Demianoff's sign, 476 De morbis ariificum diatriba, 2, 296 Delaware law on work for women, 526 Denny, J. J., 188 on exposure to aluminum dust, 188 Department of Agriculture, 531 booklet on work clothing, 631 Department of Interior, 4, 33, 50, 56 Bureau of Mines, 4 , 33, 50, 56 Department of Labor, 50,56,395,433,504 see U. S. Department of Labor Dermatitis, 541-542 in industries using organic solvents, 257-258 in women, 541-542 Dermatoses investigation, methods of, 330-341 contact and explain to superintendent, 330 examine medical records, 331 inspect plant, 331 inspect workers, 331 make card record, 332 perform patch test, 332-341 de Vries, W. M., 328 scrotal cancer in briquette workers, 328 Diastolic blood pressure in exposure to toxic chemicals, 155-179 difference between two arms, 158 normal limits, 158 ST0853786 562 INDEX Diet, 302, 262 as factor in dermatitis, 302 high protein, high carbohydrate in tetrachlorethane poison, 262 Dietary supplements, 171, 233-234, 418-- 410 in lead industry, 233-234 vitamins in, 418-410 in exposure to toxic chemicals, 171 Diethylene oxide, 266 Dimethyl ketone, 265-266 Dioxan, 266 Direct costs of accidents, 30, 484 Direct lighting, 104 Disability benefits, 501 death, 502 permanent partial, 501 permanent total, 501 Disease, toxic exposure and, 174 Diseases of sldn. See occupational diseases of skin, 296-341 District of Columbia, 391 all occupational diseases compensable, 391 Division of Industrial Hygiene, 9 61, 62 four major fields in war effort, 61 Division of Labor Standards, 50, 56 Drinker, C. K., 274 CO poisoning in metropolitan New York, 274 Dry ice, 189 Dublin, L. I., 23, 376 death rates from accidents in America vb. Canada and England, 23 Dunn, Mary J., 496 curriculum guide for public health nursing, 496 Dust concentration safe limits in granite cutting, 4 Dust diseases, 345-374 Dysmenorrhea, 544 E Eastman Kodak cafeterias, 414 Economic importance of visual dis ability, 424 Education of ophthalmologists, 422 Education program * nutrition, 419-420 prevention of industrial backache, 478 tuberculosis control, 389 venereal disease control, 402 Effects of abnormal atmospheric pres sures, 91-99 increase below water, 91-92 mechanical effects of high pressure, 92-93 Effects of temperature and humidity on workers, 69-88 high temperatures effects on health, 79-81 acute respiratory diseases, 80-81 tuberculosis, 383 effects on work and accidents, 81-83 endurance table, 86 recommended for industry, 83-88 air conditioning, 87 air movement, 85 toxic exposure and extremes of low temperatures, 173-174 acute transient inflammatory reac tion, 78 chilblains, 78 frost bite, 78, 79 occurrence, 78 treatment, 79 Electricity, 288--295 injuries produced by, 288, 432 Elimination of solvent vapors, 250 Ellenbog, Ulrich, 2 Ely's sign, 476 Emotional factor, 148, 536, 549 consider in physicial examination, 148 in accidents, 536 in fatigue, 549 women vb. men, 536 Employees of Federal government, 500 compensation for, 500 Employer resistance to using disabled, 512 Employers Mutual of Wisconsin, 487-488 program within industry, 488 services outside industry, 488 Employment poll :y and venereal disease control, 404 Engel, Charles F., 288 England, labor legislation, 3, 498 Everts, Glenn 5., 518 medical service to small plants, 518 Exposure to toxic chemicals, early effects of, 154-156 Eye accidents, 421-433 air hose, 429-430 burns acid, 430-431 alkali, 430-431 compensation, 424, 433 concussion, 429 contusion, 429 coets, 424 ST0853787 INDEX 563 factors in, 425 foreign bodies, 429 in cornea, 426 intra-ocular, 427 tolerance to, 428 prevention of, 424 the problem, 421-422, 424 Eyes, care and prevention of injury, 421-433 F Factors in accident production (eye), 425 Factory Act (England), 3 Fair Labor Standards Act, 527 on employment of women, 527 Family physician, 37, 145, 518 Fatigue, 133-143, 154, 155, 174, 254, 382, 425, 547-548 avoid in CS exposure, 254 definition, 133 factor in accident production, 138, 425 length of work week and work day, 135-138 measures against change of pace, 133 favorable environment, 139 food, 133 lighting, 139 rest pauses, 133 production curves, 138 psychological factors, 133, 135 boredom, 141 foremen, like or dislike, 139 loyalty to company, 139 monotony, 141 noise, 135, 547-548 reaction to rules, etc., 139 wage incentive, 140 tuberculosis and, 382 unnecessary toxic exposure and, 174 women, 547-548 Federal Employer's Liability Act, 500 compensation in maritime and inter state commerce, 500 Federal Government, 500 administers compensation acts: Federal Employer's Liability Act, 600 Longshoremen's and Harbor Workers' Compensation Law, 500 Merchant Seamen's Act, 500 employees, of, 500 First aid personnel training, 33 for eye protection, 423 First aid training, 33, 423 American Red Cross, 33 Bureau of Mines, 33 for eye accidents, 423 First nursing visit to industrial insurance policy holder, 487 Fluorine, 197-199 Footcandle, 103 recommendations for more difficult tasks, 124 table of recommendations, 123 Footcandle scale of effectiveness, 120-122 Footlambert, 103 Foreign bodies in eye, 427 locating by electro-magnet, 427 Foulger, John H., 74,150 and Weaver, W. L., 74 vitamins in control of heat cramps and heat prostration, 74 France, 498 Frequency rate (industrial accidents), 24-25 Frostbite, 78, 79 treatment of, 79 Fungi in skin diseases, 312-313, 320 active treatment in organic solvent plants, 258 infections of foot, prevention, 320 G Galen, 1 Gallium, 189 Gasoline, 261-262, 273 anaesthetic effect, 261 dermatitis, 281 prophylaxis, 261 protective clothing, 261 ventilation, 261 treatment, 262 Gehrmann, G. H., 328 on papillomata and carcinoma of bladder, 328 General plus lighting, 104 General practitioner, 37 relation to industrial physician, 37 Georgia, 486 nursing consultant, 486 Germanium' 190 Germany, labor legislation, 3, 498 Gibson, Augustus, 435 Glare, 103,125-129 Gloves, 32, 322 Gloyne, S. R., 372 roentgenological appearances of asbestoeis, 372 Goenslen's sign, 476 stosss'iss 564 INDEX Goggles, 32, 436 in protection against eye accident and injury, 32, 436 Gold, 181,182 Gordy, S. T., 246,247 symptomalogy of chronic CS, poison ing, 246, 247 Governmental agencies in industrial hygiene, 48-64 state and local health departments, 62-60 functions, 63-64 chemical, 54 engineering, 54 medical, 64 nursing, 54 integrated service, 54-66 interdepartmental relationship, 56- 58 Greenburg, L., 424 economic importance of visual dis ability in industry, 424 Greenwood, D. A., 199 on mottled teeth, 199 H Hafnium, 190 Hair, long, 532 hazard to women workers, 532 Haggard, H. W., 249 on absorption of toxic vapors, 249 Hamilton, Alice, 244, 246, 540 on CSj exposure, 244, 246 on susceptibility of young women to poisons affecting nervous system, 540 Haldane, J. B. S., 99, 272 effects of gases under high pressures, 99 on oxygen consumption, 272 Harmon, F. L., 135 Harrower, J. R., 244 procedure for determining CSj in blood, 244 Health and Morals Act, 3 Health facilities in control of absen teeism, 540 Heim, J. W., 174 toxicity of CO at high altitudes, 174 Helium, 181 caisson work, 93, 96 oxygen mixture, 96 Hemming, Albert, 435 Henderson, V., 249 on absorption of toxic vapors, 249 Heyroth, F. F., 180 Hippocrates, 1 Hoffman, Frederick L., 204 occupational distribution of cases of plumbism, 204 Holland tunnels, 274 CO concentration, 274 Home responsibilities of married women, 540 Houghten, F. C., 87 on body temperatures, 87 Hours of work, 136, 535 fatigue and, 536 production and, 136, 636 Housekeeping, 9, 212, 322, 308, 552 necessity for good, 322, 662 plant construction and, 212 Homard, John, 3 inspection and reporting, 3 Humidity, high, effect on industrial worker, 86-87 Hunter, A. W., 244 procedure for determining CS* in blood, 244 Hydrocyanic acid, 281-283 action, 282 after effects, 283 post-mortem findings, 283 prevention, 283 treatment, 283 Hydrogen fluoride, 197-198 acute poisoning, 197-198 symptoms, 197-198 chronic poisoning, 198 roentgenological findings, 198 safe limits, 198 Hydrogen sulphide, 285-287 prevention of poisoning, 286 symptoms sub-acute poisoning, 286 gas eyes, 286 symptoms acute poisoning, 286 paralysis of sense of smell, 286 toxicity, 285 treatment, 287 I Idaho, 57-68, 486 law forming Bureau of Industrial Hy giene, 57-58 nursing consultant, 486 Illinois, 486 Illumination, 103, 110, 111, 112, 122, 426 poor, and accidents, 425 precision and production, 112 recommended levels of, 122 speed of vision and, 111 type size and visibility, 111 visual acuity and, 110 ST 0853789 INDEX 565 Indiana, 486, 626, 628 accidents to women, 629 law on work for women, 626 nursing consultant, 486 Indium, 189 Indirect costs of accidents, 30, 484 Indirect lighting, 104 Industrial accidents, their cause and prevention, 23-34, 136, 421-434 causes of accident proneness, 27 environmental factors, 28 individual factors, 27 length of work day, 136 control, 30-34 costs, 30, 484 emergency care, 33 eye, 421-434 factors influencing, 23 rates by industries, 24, 25 records, 29 safety committee, 32 safety supervisor, 32 Industrial back, 458-482 backache: causes of, 463 congenital defects: articular facets, 467 horizontal sacrum, 467 failure of fusion, 466 sacrolization, 466 spondylolisthesis, 466 spondylolysis, 466 herniated nucleus pulposus, 469 infection, 473 sacroiliac slip, 469 visceral disease, 464 examination for, 473 history, 474 incidence, 458 physical examination, 475 signs Bechterew's, 476 Demianoff's, 476 Ely's, 476 Gaenslen's, 476 Lasegue's, 476 Linder's, 476 Neri's, 477 Ober's, 476 Soto-Hall's, 477 x-ray, 477 other laboratory, 478 treatment educational campaign in prophy laxis, 478 specific treatment, 479 correction of congenital defects, 487 eutipin in oil, 480 exercise, 479 manipulation, 480 medicolegal aspects, 482 operative, 487 physiotherapy, 479 Industrial cleansers, 323 Industrial Commissions, 504, 607 Industrial diseases, 4, 296-341, 367-371, 600-601 compensation, 367-371, 600-601 dermatoses, 296-341 first American Congress, 4 Industrial engineer, 21 function, 7, 8, 36, 64 in state and local bureaus, 54 Industrial Health, 65-68 program of the American Medical Asso ciation, 65-68 purpose of, 65 Industrial health clinics, 519 smaller industries, 519 Industrial health hazards, methods em ployed in appraisal and control, 7-22 appraisal of study of workroom environment, 8 detailed survey, 14-16 reconnaissance survey, 8 accident protection, 8 exposure to specific poisons, 8 fire protection, 8 housekeeping, 9 illumination, 8 individual occupation, 9 ventilation, 8, 9 control of isolation of hazardous process, 17, 212 local exhaust ventilation, 17 respiratory protection, 18 substitution, 16 wet method, 17 Industrial housekeeping, 9, 212, 552 Industrial hygiene: development of, in U. S., 49-51 governmental agencies in, 48-64 organization, 51 problem, 48, 49 control of health hazards, 16-20 survey, forms of, 10, 11, 12 survey, reconnaissance, 8-14 survey, detailed, 14-16 war effort and, 61-63 ST 0853790 566 INDEX Industrial hygiene division*, 0, 52-54, 62, 387, 402 National Institute of Health, 9, 62 state and local health departments, 62-64, 387, 402 portable x-ray, 387 tuberculosis control, 387 venereal disease control, 402 Industrial medicine, 1-6, 49-51, 296, 399, 448, 498-606 cost of, 399 financial saving, 399 history, 1-6, 49-61, 296 Bureau of Mines, 50 Craft Guilds, 2 Department of Labor, 60 Division of Industrial Hygiene, 5, 49-60 federal and state legislation, 5 labor legislation, 3, 448, 498-606 non-official agencies, 50-61 organised medicine, 5, 66-68 magazine Industrial Medicine began publication, 4 Industrial medical education, 5, 66-66, 422, 518, 520-622 better, 65 ophthalmologists, 422 postgraduate, 5, 35, 519 Council on Industrial Health, 5, 66 American Association of Industrial Physicians and Surgeons, 65 undergraduate, 5, 35, 618 Council on Industrial Health, 5, 6566 American Association of Industrial Physicians and Surgeons, 65 Industrial physician, 35, 40, 79, 248 attributes, 37 duties, 37, 217-218, 253 education, 35, 36 function, 7, 21, 150-151, 162 health education, 41 office equipment, 46 place in industrial Bet-up, 40 preparation, 35-36 relation to family physician, 37 relation to foremen, 36 relation to management, 36 relation to workmen, 37, 216 relation to state health department, 37 relation to state industrial commis sion, 37 relation to state rehabilitation com mission, 37 responsibilities, 36, 58 Industrial workers, 69-90, 216,395 effects of temperature and humidity on, 69-90 high temperature, 70-77 heat cramps, 72 heat exhaustion, 74 heat prostration, 74 heat stroke, 75 sun stroke, 75 low environmental temperatures, 77-79 acute transient inflammatory reac tion, 78 chilblains, 78 frost bite, 78-79 number of men, 395 women, 395 relation to plant physician, 216 Infections contributing to tuberculosis, 382 Infection of injuries, precautions against, 33 Injuries by electricity, 288-294 burns, 288 eye, 294, 432 factors in, 290 flashes, 288 glare, 288 morbid anatomy, 289-290 resuscitation, 292-294 shock, 288, 293 symptoms, 291 treatment, 292 International Labor Office, 4 U. S. joined, 4 International Ladies Garment Workers Union, 491 Intra-ocular foreign bodies, 427 non-magnetic steel, 427 Iodine, 197, 199 Iridium, 199 Iron, 189, 199 carbonyl, fatal poisoning, 189 Irwin, D. A., 188 on exposure to aluminum dust, 188 Isolation of hazardous processes, 17, 212 Italy, 498 Ivy, A. C., 545 fatigue in industry, 545 J Japan, 326 kiro cancer, 328 Jewelry, 532 hazard in industry, 632 ST085379I INDEX 567 Jirouch, E. A., 266 on toxicity of butyl ethylene glycol, 266 Journal of Aviation Medicine, 171 Journal of Industrial Hygiene, 4 established, 4 Johnson, Joanna, 483 Johnstone, Rutherford T., 468 E Kansas, 626 law on work for women, 526 Kashmir, 326 kangri cancer, 326 Kehoe, Robert A., 202 Kentucky, 486 nursing consultant, 486 Keratitis, occupational, 432 Keratoconjunctivitis, 431 Koch, Sumner, L., 460 treatment of burns, 460 Kronenberg, Milton H., 623 Kuechle, B. E., 468 Kuhn, H. 8., 423 appraisal of visual defects in industry, 423 L Labor, 4, 387,392, 491, 604,524 American Association of Labor Legis lation, 4 attitude, 39 Bureau of, created, 4 Child Labor National Committee, 4 Department of, 604 First Federal Statute passed, 4 nursing programs, 491 organized, 524 responsibility, 392 unions provide health service, 387 Labor legislation, 3, 4, 498, 600, 527, 529 Austria, 498 England, 3, 498 Federal Conference, 4 Federal legislation, 527 Fair Labor Standards Act, 527 Walsh-Healy Act, 527, 529 France, 498 Germany, 3, 498 Italy, 498 Russia, 498 United States, 498 California, New Jersey, New York, 3,4 Wisconsin, 498-600 Laboratory, 44 in medical lay-out, 44 Laboratory technicians, 40, 46 Laird, Donald A., 136 noise adaptations, 135 Lasegue's sign, 476 Latka, A. J., 23 death rates, accidents, 23 Lead exposure, industrial, 202-240 control, 211-225 engineering, 211-214 construction of building, 212 equipment location, 212 housekeeping facilities, 212 localize toxic processes, 212 medical facilities, 213 Banitary facilities, 213 locker rooms, 213 lunch rooms, 213 toilet rooms, 213 wash rooms, 213 ventilation, 212 medical, 214 medical work and facilities, 215 medical records, 217 periodic examinations, 216 plant physician, 217-218 pre-employment examinations, 216 significance of observations lead analyses, 218 in blood and urine, 220-225 lead line, 219-220 normal blood metabolism, 220 stippling of erythrocytes, 218 detection, 206 history of, 226 measurement of, 208 air analysis, 208 blood analysis, 209 urine analysis, 209 feces analysis, 209 safe, 210 Lead poisoning, industrial, 15-16, 190, 202-240 clinical picture, 226 diagnosis, 226 differential diagnosis, 232 industrial, 225 laboratory findings, 218, 230-232 management after recovery, 236 occurrence in industry, 202 prophylaxis, 233-34 symptoms, 226 tetraethyl lead, 261 treatment, 234 568 INDEX Length of work day and work week accident production, 138 fatigue, 138-138 production, 137-138 Leukopenia, 259 in bensene poisoning, 259 Lewey, F. H., 248, 247 eymptomaiogy of chronic CSi poison ing, 246, 247 Light, lighting and seeing, 101-132 Lighting, 102, 104, 123-124, 425 American practice, 123-124 benefits of, 102 direct, 104 general plus, 104 indirect, 104 poor, factor in accidents, 425 quality of, 123,129 science of, 101 semi-direct, 104 semi-indirect, 104 supplementary, 104 systems of, 103 Lighting, systems of, 103, 104 Lighting terms and units, 103-130 brightness, 103 candle power, 103 diffuse reflection-factor, 103 footcandle, 103 footlambert, 103 glare, 103, 125-129 illumination, 103 reflection factor, 103 specular reflection-factor, 103 Linder's sign, 476 Lithium, 181 Local exhaust ventilation, 17, 212, 284 Locker, 213, 551 double or separate for street and work clothes, 213, 551 Locker rooms, 213, 551 Longshoremen's and Harbor Workers' Compensation law, 500 compensation in maritime employ ment, 500 Lost time due to illness, 80-81 acute respiratory diseases, 80-81 Luckeish, Matthew, 101 Luckeish-Mass Visibility Meter, 115 Luckeish-Taylor Brightness Meter, 107 Lunch rooms (cafeterias), 213, 413-414 M Machie, Willard, 180,198 fluorine storage in bones, 198 Magnesium, 182-183 Malnutrition, 382 contributing to tuberculosis, 382 Manganese, 196-197 Mantoux test, 388-389 student health services, 384 Manufacturers Associations Connecticut, 496 National, 399 Martime and interstate commerce com pensation coverage, 600 Married women, 646-547 home responsibilities, 546 night and shift work, 546-547 Maryland, law on work for women, 526 Masks, 213, 259 not desirable method of control, 214 Massachusetts code--safe limit on hydrogen fluoride, 197 inspector's right to enter factories, 4 law on work for women, 526 Massachusetts General Hospital, 446 Masurium, 196 MatthewBon, S. B., 140 wage incentive, 140 Mayer, L. L., 422 on ocular service for industry, 422 Mayo, Elton, 137 rest pauses and length of day, 137 McConnell, W. J., 50, 520 medical care for small plants, 520 non-official agencies in field of indus trial health, 50 McKee, Ralph W., 241, 244 Medical care in the control of absen teeism, 540 Medical department, 43-47 equipment, 46-47 floor plans, 43-46, 213 layout of, 43-47 Medical occupation and tuberculosis, 383-385 Medical personnel in industry, 35-42 industrial physician, 35-40 insurance physician, 39 nurses, 40 specialists, 39 technicians, 40 Medical records, 46-47,146-147, 215, 217, 332, 403, 490 in compensation court, 47 in tuberculosis control, 389-390 in research, 41 necessity for, 47, 391 nurse and, 490 space for, 46-47 ST0853793 INDEX 569 Medical services for the smaller plant, 488, 818-422 industrial health clinic, 619 maHiral training and, 818-619 medical semes plans Alameda Medical Society, 621 Berkeley, 621-622 New Haven, 620-621 New Haven physicians, 620 Philadelphia, 620 University of California, 621 Yale School of Medicine, 520 nursing, 489 Medical service in industry, 36-40,41,42, 473, 483-497, 518-622 dental service, 42 health education, 41 industrial health clinic, 473, 519 nurse in, 483-497 pairing for, 40 physicians in, 35-40, 619 research, 41 smaller plants, 618-622 women physicians, 42 Medical students tuberculosis in, 384-386 undergraduates in industrial medical education, 518 Medication, improper, 171 toxic exposure and, 171 Melanosis, 315 Msnopause, 544 Mental hygiene in industry, 496 nurses part in, 496 Menstruation, 544 Merchant Seamens Act, 600 Compensation in maritime employ ment, 500 Merewetber, E. K. A., 372 roentgenological appearances of asbestoeis, 372 Mercury, 185, 188-188 safe concentrations of vapor, 188 uses, 187, 188 Mercury poisoning from inhalation of vapor, 188-187 in fur and felting industry, 187 kidney damage in, 187 nephrosis in, 187 symptoms of, 187 Methanol (wood alcohol), 284-285 absorption gastro-intestinal tract, 264 inhalation, 264 skin, 284 action accumulative, 284 eye, 264 irritant to skin, 264 prophylaxis, 264 protective clothing, 264 ventilation, 264 wash from skin, 264 symptoms, 264 treatment, 264-265 Methyl chloride, 265 Metropolitan Life Insurance Company, 28, 376, 380, 387, 487 nursing service, 487 study of accident proneness, 28 Michigan, 486 nursing consultant in industrial hy giene, 486 Minton, J., 421 eye accidents in London, 421 Missouri, 486 nursing consultant in industrial hy giene, 486 Molybdenum, 194,195 Morbit MetaUiout, 296 Morgan, J. J. B., 135 distractions on performance, 135 Morris, H. P., 221 on lead accumulation data, 221 Morris, Sarah I., 375 Morse, Kenneth, 523 Moss, Frank K., 101 Mule spinners cancer, 329 Mumford, Eleanor W., 486 nursing services for eyes in industry, 486 Myers, C. S., 140 monotony pertut fatigue, 140 N Narcotic effect of, 190, 259, 283 benxene, toluene and xylene, 259 nitrogen, 190 trichlorethylene, 263 National Association of Manufacturers, 399 on cast of medical program, 399 National Committee on Conservation of Man Power in Defense Industries, 6 National Conference of Governmental Industrial Hygienists, 492 National Health Survey, 537-538 National Industrial Conference Board, 525 training for industrial work, 525 National Institute of Health, 5,9,51,485 ST 0853794 570 INDEX National Organisation for Public Health Nursing, 486, 488, 489 section on industrial nursing, 486, 488 National Safety Code, 4 protection of heads and eyes of indus trial workers, 4 National Safety Counoil, 4, 6, 425, 494, 496, 511, 521 oommittee on bensol established, 4 National Silicosis Conference Report on Medical Control, 346 National Society for the Prevention of Blindness, 486 eye problems, 486 National Tuberculosis Association, 379 Navy, 379 35 mm. x-ray film, 379 Naphtha (see gasoline), 281-282 naphtha jag, 261 Neal, P. A., 188 studies on mercury vapor concentra tions, 188 Nebraska, 528 law on work for women, 526 Necrosis of jaw, 191,327 in phosphorus workers, 191 in radium workers, 327 Neon, 181 Neri's sign, 477 Neuritis of the arm, hand and wrist, 642 Neuro-psychiatrist, 248 New Jersey, 4, 486, 528 certain occupational diseases com pensable, 4 law on work for women, 526 nursing consultant, 486 New Hampshire, 526 law on work for women, 526 New Haven Industrial Medical Service, 520 New Haven plan, 520 medical care for small plants, 520 New York, 526 law on work for women, 526 New York City, 186, 379 mass survey, 379 sanitary code, 186 Nickel, 199 carbonyl, fatal poisoning, 189 Nightingale, Florence, 483, 494 Night work, 546-547 factor in high labor turnover, 547 laws on, 526-527 men and, 547 women and, 528-527, 546-547 Nitric acid, 283 Nitrogen, 97, 190, 283-286 narcotic effects at high pressure, 97 nitrous fumes, 283-286 nitrous oxides, 288-285 prevention of poisoning, 284 symptoms of poisoning, 284 treatment of poisoning, 284-286 Noise, 139, 536, 547-648 in absenteeism, 645 in fatigue production, 139 nervousness in women, 536 Non-occupational illness factors, 543-649 in absenteeism, 543 North Carolina, 57, 486 industrial occupational disease law, 57 nursing consultant, 486 North Dakota, 528 law on work for women, 526 Nuck, 248-247 symptoms from CSi exposure, 246-247 Nucleus pulposus (herniated), 469-473 description of case, 471 diagnosis, 471-473 differential, 472-473 location, 470 pain in, 471-472 Nurse in industry, 40, 483-497 Dunn, Mary J., 496 eye problems and, 486 first nurses employed in industry, 4 functions of in governmental bureaus, 54 home accidents, 494 insurance companies, 487 opportunity for advancement, 496 part in safety program, 485, 494 psychic readjustment, 390 post-graduate preparation, 496 Proctor Marble Co., 487 qualifications, 488 relation to public health nursing, 484 U. S. Public Health Service, 485 relationship to physician, 493 Wanamaker Department Stores, 487 Nursing consultants, 486 Bureaus of Industrial Hygiene, 486 functions of, 486 National Society for Prevention of Blindness, 486 states having, 486 Nursing programs for small industries, 489-493 Employers Mutual, 487 Henry Street, 490 in the Berkeley plan, 521 in the New Haven plan, 520 ST 0853195 un>xx 571 in the Philadelphia, plan, 520 Metropolitan Life Ineuranoe Co., 487 nutritionist and, 480 Pittsburgh Public Health Nursing As sociation, 491 under supervision of physician, 492 Visiting Nursing Association of De troit, 490 Nursing students, 384 tuberculosis in, 384 Nutrition: adequate in CS* exposure, 264 toxic exposure and, 170-171 visiting nurse program, 490 Nutrition, what industry can do to im prove, 409-420 between meal snacks, 134, 418 cafeteria, 418-417 attractiveness, 413 dietitian to supervise, 414 efficient serving, 416 non-profit basis, 414-416 study problems, 416 educational program, 419-420 lunch box, 416 contents, 417 result of survey, 409 sufficient time to eat, 416 vitamin supplements, 171,233,418-419 O Ober's sign, 476 Ocular service for industiy, 422 Occupational Diseases, 4, 68 first clinic, 4 first laws for compulsory reporting, California and New York, 4 first laws for compensation of, New Jersey, 4 first clear cut law compensation, Wis consin, 4 reporting of, 68 Occupational keratitis, 432 Occupation and tuberculosis, 375-393 compensation for, 390-392 contributing factors: age and sex, 380 chemical irritants, 383 dusts, pneumoconiosis and silicosis, 383 fatigue, 382 heat and humidity, 383 heredity and race, 380 infections, 382 malnutrition, 382 trauma, 382 general discussion, 876-379 general picture, 878-876 in medical occupation, 888-386 in medical students, 384-386 nurses, 384 other service groups, 385 responsibility for, 890 tuberculosis in industry, 385-390 control of, 387-390 adequate records, 389 case finding, 388 contact finding, 389 diagnosis, 388 health education, 389 health supervision, 390 know problem in community and plant, 388 rehabilitation, 390 safeguard workers, 388 Occupational diseases of skin, 296-341 cancer, 296 actinic causes, 326 aniline, 328 arsenic, 329 chimney sweeps, 296 mule spinners, 329 petroleum, 328 prevention, 329-330 tar, 327 trauma, 326 causes, 300-313 predisposing, 300 age, 303 allergy, 304-306 diet, 302 lack of cleanliness, 303 other skin diseases, 303 perspiration, 302 race, 301 season, 303 sex, 303 actual, 306 biological agents, 312 bacterial infections, 312 fungi, 312-313 chemical, 307 inorganic irritants, 308 organic irritants, 308 sensitizers, 309-313 diagnosis, 314 appearance of lesion, 315 history, 314 melanosis, 315 site of eruption, 315 ST 0853796 572 INDEX Occupational diseases of skin--continued differential diagnosis, 315 chronic eczema, 317 fungus infectiona, 317 patch teste, 310 historical, 290-200 incidence, 200 prevention cleanliness, 322 clean plant, 322 clean machinery, 322 clean workers, 323 select safe industrial cleanser, 323 pre-employment examinations, 310 protective clothing, 320 cotton, 321 impervious material, 321 leather gloves, 322 synthetic material, 322 protective ointment, 323 classes, 324 properties, 324 ventilation, 320 symptoms, 314 table of, 336-340 treatment, 318-319 Occupational poisoning, survey of sub stances, 180-201 Official Agencies, responsibilities of, 58- 60 Office of Defense, Health and Welfare, 60 Ohio, 486, 526 law on work for women, 526 Oklahoma, law on work for women, 526 Ophthalmologists, 421, 422, 423, 427, 420, 430 duties of, 423 education of, 422 Oregon, 526 law on work for women, 526 Organic solvents in industry, 256-268 effects on skin, 257-258 effects on system, 258-259 general considerations, 256-259, 266- 268 signs and symptoms, 259 toxicity of 256-268 Organic solvents, toxicity, 256-268 action, 256-259 effects on skin: dermatitis, 257 prevention: aprons, 257 cleanliness, 257 gloves, 257 protective clothing, 257 protective ointments, 258 containing chemicals of value against allegens, 258 containing a light screen, 258 containing neutralising chemi cals, 258 to facilitate removal of irri tant, 258 to prevent irritant from touch ing the skin, 258 pre-placement examinations, 258 don't use people with acne, 258 don't use people with allergic ecsema, 258 don't use people with athlete's foot, 258 don't use people with history of dermatitis, 258 systemic effects: clinical signs and symptoms, 250 central nervous system, 259 effects on liver, kidney, heart and blood systems, 250 gastro-intestinal irritation, 259 portal of entry: absorption through skin, 258 inhalation, 258 prophylaxis, 258-259 adequate ventilation, 258 exhaust systems, 258 masks, 259 respirators, 259 selection of employees, 259 Organized labor, 491-492 health programs, 491-492 Osmium, 199 Osteosarcoma, in dial painters, 184 Oxygen, 95-98, 195 in prevention of: caisson's disease, 95-96 compressed air illness, 95-06 toxic effects at high pressure, 97-98 symptoms of, 98 Oxygen in treatment, 96-97,262,275,279, 281, 287, 294 burns, 448 CO poisoning, 275 Cl poisoning, 279 COCU poisoning, 281 caisson's disease, 96-97 compressed air illness, 96-97 electrical shock, 294 H]S poisoning, 287 ST0853797 INDEX 573 gasoline poisoning, 262 Oxygen want, 174, 448 in burns, 448 in toxio exposure, 174 P Pain, 227, 264, 471-472 abdominal: lead poison, 227 wood alcohol poison, 264 ruptured intervertebral disc, 471-472 Palladium, 199 Paralysis in caisson's disease, 94 Parkinsonism, 196, 246, 247 Parran, Thomas, 647. on lengthening shift periods, 547 Patch tests, 316-318, 332-334 Paying for medical service in industry, 40 Penicillin, 444 Pennsylvania, 526, 529 accidents to women in, 529 law on work for women, 526 Pennsylvania Committee on Child La bor, 4 Peracelsus, 2, 296 Peterson, C. M., 65 Petroleum as cause of cancer, 328 Philadelphia Health Council and Tuber culosis Committee, 520 medical care in small industries, 520 Philadelphia plan, 520 medical care in small industries, 520 Physicians, 35-39, 145, 421, 422, 518, 519 industrial, 35-39, 421, 422, 619 attributes, 37 duties, 37-38, 519 full time, 38-39 insurance, 39 part time, 39 preparation, 35-36 responsibilities, 36-37 specialists, 39, 421, 422 general practitioner, 37, 145, 518 Phosgene, 280-281 action, 280 pathological findings, 280-281 prognosis, 281 symptoms, 280 treatment, 281 Phosphine, 192 Phosphoric acid, 192 Phosphorus, 190, 191 red, 191 white, 191 yellow, 191 Physical examinations, 144-149, 150-164, 215-216,258,319-320,405,421,505 control of accidents, 505 control of disease, 505 labor and, 505 medical control of exposure to toxic chemicals, 150-179 Wisconsin program, 57, 505 periodic, 100, 115, 151, 215-217, 422 analysis of results, 164-175 frequency of, 216, 422 in chemical industry, 151 in lead exposure, 216 determined by medical depart ment, 145 for failing vision, 422 use of results, 175 pre-employment, 100, 144, 150, 216, 405, 421 benefits, 144 blanks for, 146, 147 classification, 148, 149 eye in, 421 method, 145 psychological aspects, 148 purpose, 144, 151 rejections, 145, 148, 404, 405 time necessary for, 145 Pickrell, K. L., sulfa drugs in translu cent pliable film, 452 Pitchblende, mining of, 183 Plant construction, 212-213 locker rooms, 213, 551 lunch rooms, 213, 413-414 sanitary equipment, 213, 549-652 toilets, 213, 550 wash rooms, 213, 551 Plasma in traumatic shock and burns, 435 Plumbism. See lead poisoning, 202 Pneumonia, 11-14 , 80 , 272, 273 in steel industry, 11-14 steel, mining and outside occupations, 80 Pneumonoconiosis, 345-374 the disease, 355-363 acute, 356-357 anthracosilicosis, 357-363 advanced stage, 361-363 early stage, 357-358 intermediate stage, 358-361 diagnosis, 356 , 359, 362 pathology, 357-358, 359, 362 prognosis, 357 , 362 signs and symptoms, 358. 361-362 simple, 357 574 INDEX Pneumonoconiosis--continued pathological findings, 280 the problem, 346-347 prognosis, 281 classification, 348 symptoms, 280 control problem, 347 treatment, 281 definition, 346 Polonium, 195 dust in lungs, 345 Post-graduate education, 5, 65, 66, 496, early history, 345 519 incidence, 346-347 medical, 5, 519 in Italian mill workers from inhaled Council on Industrial Health, 5, 66 dust of barium sulfate, 183 American Association of Industrial pathogenesis, 347-355 Physicians and Surgeons, 65 action of silica, 348 nursing: acute silicosis, 354-355 Curriculum guide for public health caasative agent, 347-348 nursing, 496 predisposing factors, 351-352 Simmons College, 496 progressive development, 352-354 Postgraduate medical education, 519 related anatomy, 349-351 Potassium, 181 with silicosis Pott, Percival, 296 bronchopneumonia in, 363 Pregnancy, 545 silico-tuberculosis, 363-367 Pressure, abnormal atmospheric, 91-100 diagnosis, 364 Prevention of eye injuries, 424-425 pathogenesis, 363 Princeton University, Department of pathology, 365-367 Economics and Social Institutions prognosis, 367 Industrial Relations section, 525 progress, 365 training of workers, 525 roentgenopathology, 365 Private insurance companies, 504 signs and symptoms, 364 in compensation insurance, 504 other Proctor Marble Company, 487 anthracosis, 373 early use of nurse, 487 asbestosis, 372 Proden, L., 186 siderosi8, 372 on toxicity cadmium oxide fumes, 186 Poisonous gases, some, 278-287 Profit versus cost of visual correction, CO, 269-277 422 chlorine, 278-280 Protective clothing, 320-322 action, 278 Protective ointments, 323-325 prognosis, 279 Protoactinium, 190 symptoms, 278 Psychiatrist, neuro in CSt poisoning, 248 treatment, 279 Psychology: hydrocyanic acid and cyanide group, consider in examinations, 148 281-283 in fatigue, 133, 135 after effects, 283 Psychologist in pre-placement examina post-mortem findings, 283 tions, 148 prevention, 283 Public Health Administrators, 58, 59 symptoms, 282 treatment, 283 hydrogen sulphide, 285-287 prevention, 286 symptoms of acute poison*, 286 symptoms of subacute poison, 286 treatment, 287 nitrous fumes, nitrogen oxides, 283-285 prevention, 284 Public Health Service, 51-52, 387, 394, 399, 400, 485 Puerto Rico, 391 some occupational diseases compens able, 391 Pulse pressure, 156-160 in exposure to toxic chemicals, 156-160 normal limits, 158 symptoms, 284 treatment, 284-285 Q phosgene, 280-281 Quality of lighting, 129-130 action, 280 Qualifications of nurse in industry, 488 ST 0853799 INDEX 575 R Radium, 182, 183-185, 327, 642 carcinoma, 184, 327 dial painting, 184, 642 ventilation requirements, 185 women, 542 necrosis of jaws, 184, 327 osteosarcoma, 184 radon gas exhaled through lungs, 184 stored in bones, 184 Radon, 181, 184 Ramazzini, 2, 296 Reconnaissance survey, 8 Red phosphorus, 191 Reflection-factor, 103 Rehabilitation, vocational and indus trial, 390, 603, 507-617 compensation and, 503 Federal and State Rehabilitation Serv ice, 507 extent of, 511 U. S. Office of Education, 611 functioning of consultation and guidance, 614 discovery of proper cases, 513 physical restoration, 514 placement, 515 selection of trainees, 513 vocational or trade training, 514-515 origin of service, 510-511 maimed troops, 510 workmen's compensation, 510 purpose, 507 problem: economic, 511 employer resistance, 512 inadequate staff, 512 social, 512 selection of cases for, 508 , 513 factors affecting, 508-510, 513 tuberculosis, 390 Veterans Rehabilitation Service, 510, 511 Resnick, L., on cost of eye injuries, 424, 432 Respiration, artificial Schafer- prone pressure method, 275 Respirators, 32, 213, 214, 259 Respiratory protection, 18 Resuscitation, 275, 294 Drinker apparatus, 294 E. and J. Resuscitator, 275 pulmotor, 275 Schafer prone pressure method of arti ficial respiration, 275 Rhenium, 196 Rhode Island, 57 Rhodium, 199 Robson, W. D., 188 on exposure to aluminum dust, 188 Robertson, D. F., 435 Roentgen rays, 183 Rossiter, Frank S., 269 , 278 Rothwell, H. E., 193 on arsenic in hair of normal and ex posed persons, 193 Routes of absorption of toxic chemicals: ingeBtion, 204, 205 inhalation, 204-206, 258 Bkin, 204-206, 258 Royal Eye Hospital, London, 421 eye accident statistics, 421 Rubidium, 181 Russia, 498 Ruthenium, 199 S Safety code: for foundries approved, 4 sanitation of foundries adopted, 4 Safety committee in control of acci dents, 32 Safety facilities in control of absentee ism, 540 Safety shoes, 532 Safety supervisor in control of accidents, 32 Sanitary equipment, 213 , 549-552 Sawyer, William A., 409 Sayers, R. R., 270 table on time required of various con centrations of carbon monoxide for certain per cent of blood satu ration, 270 Schafer prone pressure method of artifi cial respiration, 275, 292, 293 Schrenk, H. H., 266 on exposure to dioxan, 266 Schwartz, Louis, 20, 257, 258, 296-341 Scott, C. N,, 425 on protection of eyes, 425 Second injury funds, 503 Secretary of labor, 527-528 rules for .working of girls, 627-528 Section on dermatoses investigation, 298 Section on industrial hygiene formed, 4 American Public Health Association, 4 Seeing, 104-131 aids to, 130-131 ease of, 118-123 precision and production, 112-114 Selenium, 195 ST 0853800 576 INDEX Self-insured, 604 Sulfur, 195, 286-287 Self-medication, toxic exposure and, 173 irritation of skin, 195 Semi-direct lighting, 104 Sulfuric acid, 196 Semi-indirect lighting, 104 Service groups and tuberculosis, 336 Severity rate (industrial accidents), 24-26 Sex and accidents, 24 Superficial foreign bodies in cornea, 428 Supplementary lighting, 104 Surgeon General, 400 on shift work, 400 Sweet, William M., 427 and skin diseases, 303 and tuberculosis, 380 Shift work, 546-647 on localizing position of foreign body in eye, 427 Symblepharon, 431 frequency of shift, 547 single people and, 547 women and, 546 factors against, 546-647 Synovitis of the arm, hand and wrist, 542 Systolic blood pressure, 155-179 in exposure to toxic chemicals, 165-179 difference between two arms, 168 Shoes, safety, 532 SiderosU, 372 normal limits, 158 Silica, 189 Silicosis (see pneumonoconiosis), 16-20, 148, 214-218, 368-369, 606 compensation of, 367-371, 506 disability and, 370-371 tests for, 370-371 table on, 368-369 T Tantalum, 190 Tar as cause of cancer, 327 Tasks, visibility of, 117 Taylor, J. H., 135 studies on fatigue, 135 control of, 371 Technicians, 40, 46 mechanical, 16-20, 371 medical, 148, 214-218, 371 * laboratory, 40, 46 x-ray, 40 Silico-tuberculosis, 363-367 Silver, 181, 182 Tennessee Valley Authority, 61 Tellurium, 195,196 Simmons College, 496 course for nurses in industry, 496 Single women, 547 poisoning, 196 symptoms, 196 Territory of Hawaii, 391 night work, 547 shift work, 547 Skin diseases, 296-341 see occupational disease of skin, 296- 341 all occupational diseases compensable, 391 Tetrachlorethane, 262-263 action, 262 irritation, 262 Snell, A. G., 433 narcotic, 262 Snellen Chart, 46, 111, 421 Sodium, 181 solvent, on skin, 262 prophylaxis, 262-263 Soto-Hall's sign, 477 South Carolina, 526 law on work for women, 526 Spine, 459-463 symptoms, 262 treatment, 282-263 Tetraethyl lead, 206, 261 poisoning, 206, 261 anatomy and physiology, 459-463 Thallium, 189 Sprain, 479 Stippling, 218 of red blood cells, 218 Strain, 473, 474, 479, 544 Strontium, 182, 183 Thompson, Lorin A., 133, 141 Thorium, 190 Tin, 190 Titanium, 190 Toilets, 213, 550 Substitution, 16 of less toxic Bubstance, 16 accessible, 550 entrances, 550 Sulfa drugs, 171-172, 455 equipment, 550 in toxic exposure, 171-172 markings, 550 in treatment of burns, 455 one for each 15 women, 550 ST 085380 I INDEX 577 Toluene (see benzene), 259, 260 central nervous system, depression in poisoning, 280 narcotic effect, 259 Tompsett, S. L., 221 on progressive accumulation of lead in bones, 221 Toxicity of gases and vapors, high alti tudes, 174-175 Training of first-aid personnel, 423 Training of physically impaired, 514-515 Trichlorethylene, 263, 264 action: narcotic, 263 skin irritant, 264 solvent, on skin, 263 prophylaxis ventilation: closed Bystem, 264 downward draft, 264 protective ointments, 264 Transfusion, 439, 440 technic of, 439 blood grouping, 439 reaction following, 440 Trauma, as cause of cancer, 326 and tuberculosis, 382 Traumatic shock, 435 clinical features, 436 pathological features, 435 treatment: plasma, 438 saline solution, 438 whole blood, 438 dosage of above, 439 Trumper, M., 246, 247 symptomatology of chronic CSt poi soning, 246, 247 Tuberculosis and occupation, 375-393 see occupation and tuberculosis Tungsten, 194, 195 Twort, C. C. and J. M., 329 carcinogenic tars, 329 U Uniforms for women workers, 531-532 U. S. Army, 379 United States Department of Agricul ture, 531 United States Department of Commerce, 185,425,542 Bureau of Standards, 425 control of radium poisoning, 185, 542 United States Department of Interior, 4 , 33 , 50 , 56 Bureau of Mines, 4, 33, 50, 56 training in first aid, 33 first study of health of workers, 4 United States Department of Labor, 50, 56, 346, 347,395,433 Bureau of Labor Statistics, 50, 395 Children's Bureau, 4, 60 Division of Labor Standards, 50, 56, 347 National Committee on Conservation of Man Power in Defense Indus tries, 5 Women's Bureau, 50, 529, 530, 531 United States Employees Compensation Act, 500 Compensation for Federal Government employees, 500 U. S. employment service, 524, 526 United States Federal- Security Agency, 61,62 War Production Board, 61, 62 U. S. Navy, 327, 379 cancer of lip and skin, 327 miniature x-ray films, 379 United States Office of Education, 511 rehabilitation, 511 U. S. Public Health Service, 4,51-62,298, 387,394,399,400,485,537,547 Division of Industrial Hygiene, 9, 62 First study of health of workers, 4 National Health Survey, 537 Office of Industrial Hygiene and Sani tation, 4 reporting morbidity among indus trial workers, 4 Section on dermatoses investigation, 298 surgeon general, 400, 547 Uranium, 194 Utah, 57 V Vanadium, 190 Venereal disease control in industry, 394-407 administration of program, 401 confidential records, 403 employment policy, 404 follow-up, 406 frequency, 395 informational program, 402 industry's responsibilities, 396 integration with community program, 397 morbidity reporting, 406 ST 0853802 578 INDEX Venereal disease control in industry --continued objectives, 401 preliminary approach, 400 reasons for program, 398 Ventilation, 8, 9,17,197, 212, 268, 320 designed for specific need, 212 in manganese industry, 197 in organic solvent plants, 258, 259, 262 local exhaust, 17, 320 downward draft, 262, 264 skin diseases, 320 Vermont, 486 nursing consultant, 486 Visibility, 108, 114, 115, 117 measurements of, 114 Luckiesh-Moss Visibility Meter, 115 physical factors and, 108 tasks, 117 Visiting nurses, 487-491, 492, 494 Association of Detroit, 490 Henry Street Settlement, 490 home accidents, 494 Metropolitan Life Insurance Com pany, 487 nutritionist and, 490 Pittsburgh Public Health Nursing Association, 491 Visual acuity, 110 Visual defects in industry, appraisal of, 423 Vitamin supplements in industry, 171, 233, 418-419 in exposure to toxic chemicals, 171 in industry, 418-419 in lead exposure, 233 Vitamin therapy, 74, 456 requirements in burns, 456 requirements for wounded, 456 Vitelles, Morris, defines fatigue, 133 Vocational training, 514-515 Valtmer, 246-247 symptoms from CSi exposure, 246-247 Voluntary election in compensation law, 500 von Oettingen, W. F., 266 on toxicity of butyl ethylene glycol, 266 W Walker, S., 427 caring for injuries to eyes, 427 Walsh-Healy Act, 527, 529 on employment of girls, 527 Wampler, Fred J., 1, 35, 43,144, 518 Wanamaker Department Stores, 487 early nursing service to employees, 487 War Production Board, 61, 62 section of industrial health, hygiene and safety, 62 Washington, 526 law on work for women, 526 Wash rooms, 213, 551 Watt, S., 141 on factors influencing output, 141 Weaver, W. L., 74 vitamins in control of heat cramps and heat prostration, 74 Welfare facilities in the control of ab senteeism, 540 Wet method in dust control, 17, 197 in manganese industry, 197 White-Calvert apparatus, 243 White phosphorus, 4, 191 matches abolished, 4 Wiley, F. H., 244 procedure for determining CS in blood, 244 Williams, George Zur, 345 Wisconsin: compensation, 500 first law, 498 industrial commission, 530 law on work for women, 526 legislative committe, 499 night work for women, 526 nursing, 493 physical examination program, 57 Womens Bureau, 50, 529, 530, 531, 546 detailed study of accidents, 529 Women in industry, 623-555 absenteeism and illness, 537 health factors, 536 non-occupational illness, 543 fatigue, 545 menstruation factors, 544 nervous manifestations, 548 noise, 547 pregnancy, 545 occupational illness, 540 dermatitis, 541 other diseases, 542 radium dial painting, 542 prohibited employment, 527 Federal laws, 527 night work, 526 states prohibiting certain work, 527 safety factors, 529-536 emotional stability, 536 falls, 529 fatigue, 535 jewelry, 532 long hair, 532 S T 0853803 INDEX 579 machine guarding, 631 physical limitations, 633 lifting, 633-636 shorter, 633 smaller, 633 strength, 633 safety shoes, 632 state regulations, 636 training, 630 work clothes, 631-633 caps, 631 gloves, 631 shoes, 631-633 uniforms, 631-632 sanitation facilities: dressing and rest rooms, 651 housekeeping, 652 maintenance, 662 toilet facilities, 660 washing facilities, 651 selection and training, 624 welfare facilities, 562 child care, 664 recreation and social activities, 563 seats, 653 Wood alcohol (methanol), 264, 265 Work clothing, 80, 213, 257, 264, 320-321, 631-632, 561 changes of, 80, 213 , 267 , 264, 320-321, 631-632,661 Work day, length of, 136-138 accident production, 136 fatigue, 136-138 production, 137-138 Work week, length of, 136-138 accident production, 136 fatigue, 136-138 production, 137-138 Workmens Compensation Act, 482 objectives, one of, 482 X Xenon, 181 X-ray, 387-380 in diagnosis of: backache, 477 sacroiliac slip, 469 spina bifida occulta, 466 in medical lay-out, 44 periodic examinations, 145 pre-employment examinations, 146, 147 tuberculosis case findings, 379, 384, 388-389 mass surveys, 379 paper films, 379 sub-standard films, 379 portable, 387 precautions against, are necessary, 183 value of technicians, 40 Xylene (see bensene), 259, 260 Y Yale University Medical School and New Haven plan, 520-621 Yant, W. P,, 206, 270, 272 colorimetric test for carbon monoxide in blood, 272 on exposure to dioxan, 266 table on time required of various con centrations of carbon monoxide for certain per cent blood satura tions, 270