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ST085301 It' PLAINTIFF'S EXHIBIT DOW-1631 MANUAL OF ir'.'r INDUSTRIAL HYGIENE AND MEDICAL SERVICE IN WAR INDUSTRIES Issued under the Auspices of the Committee on Industrial Medicine of the Division of Med ical Sciences of the National Research Council PREPARED BY THE DIVISION OF INDUSTRIAL HYGIENE, NATIONAL INSTITUTE OF HEALTH, UNITED STATES PUBLIC HEALTH SERVICE WILLIAM M. GAFAFER, D.Sc Editor W. B. SAUNDERS COMPANY PHILADELPHIA AND LONDON 1943 S TO 8 53012 0 /-?. L ^'/S / Copyright, 1943, by W. B. Saunders Company Copyright under the International Copyright Union All Bifhta Reserved This book is protected by copyright. No part of it may be duplicated or reproduced in any manner without written permission from the publisher MADE IS U. S. A. PRESS or w. B. SAUNDEBS COMPANY PHILADELPHIA ST08530I FOREWORD Ttos urgent demand for doctors and engineers in the military forces has served to deplete industry's pool of experienced indus trial physicians, industrial engineers, and industrial hygienists. This book is therefore intended not only as a source of informa tion for industrial physicians who must meet the changed conditions in industries converted to war purposes, but as a guide for those who patriotically volunteer to take the places of industrial physicians who have gone into the service. I believe the book is sufficiently complete to accomplish these ends. There are' about 17 million workers in the war industries, and their number is steadily increasing. Consequently, they com prise a substantial section of the population, whose health is of immeasurable importance to the war effort. For the protection of their health and for the reduction of sickness absenteeism, which interferes so greatly with production, these workers depend upon an equally substantial proportion of the available civilian phy sicians of the United States. It is hoped that this book will obtain a wide reading among all who have to deal in any way whatever with the health prob lems of war workers, and that it will arouse an awareness among them of the opportunities for usefulness in the produc tion of war material. In behalf of the Subcommittee on Industrial Health and Medicine, I wish to thank the Health and Medical Committee for making this important book possible; and also, Dr. James G. Townsend, Chief of Division of Industrial Hygiene, National Institute of Health, United States Public Health Service; the members of his staff; and the other contributors, for their excellent work. C. D. Selby, M.D., Chairman Committee on Industrial Medicine National Research Council ST0853011* PREFACE The unprecedented growth of industry and the rapid .develop ment of industrial facilities to meet the needs of the Nation at war demand a corresponding increase in industrial health practice. This means the organization of programs and the adoption of policies which, in a large measure, should be uniform in struc ture. Although the literature is abundant in its coverage for the many variables in medical and engineering industrial hygiene, there was not before available a book small enough to give com pact knowledge and yet large enough to cover the entire subject. With this realization, the Committee on Industrial Medicine, Division of Medical Sciences, National Research Council, whose Chairman is Dr. Clarence D. Selby, recommended through the Health and Medical Committee that the Administrator of the Federal Security Agency instruct the Division of Industrial Hygiene, National Institute of Health, United States Public Health Service, through its Surgeon General, to prepare such a text. This we have done, with the knowledge that some may think too much emphasis has been given to certain subjects and not enough to others, and that still other items, important in the viewpoint of some authorities, have not been included. Due con sideration has been given this, and much editing has been neces sary to emphasize the salient points based on the Division's many years of experience in the industrial hygiene field, and yet keep the book within convenient size for reference. Further detailed information may be obtained by writing to either this Division or, if one exists, to the industrial hygiene office of the State Government. Finally, we should like to express our appreciation to those who reviewed a number of the chapters. ' April, 1943 L G. Townsend, Medical Director Chief, Division of Industrial Hygiene National Institute of Health United States Public Health Service Bethesda, Maryland vi >p'ar ce. of uc- :he ne, mCt. ne, jse ;he :he ial lie 1a nk not :he )n- ea- n's /et to ;ne )se ST0853015 LIST OF CONTRIBUTORS OTIS L. ANDERSON, M.D., F.A.C.P. Surgeon, V. S. Public Health Service; Aeeietant Chief, Division of Venereal Dieeaeee J. J. BLOOMFIELD, B.S.Eng. Sanitary Engineer, U. S. Public Health Service; Chief, Statee` Rela tione Section, Division of Industrial Hygiene, National Institute of Health ALLEN D. BRANDT, D.Sc. Passed Assistant Sanitary Engineer, U. S. Public Health Service; formerly Chief, Engineering Unit, Division of Industrial Hygiene, Na tional Institute of Health HUGH P. BRINTON, Ph.D. Statistician, U. S. Public Health Service; Division of Industrial Hy giene, National Institute of Health W. C. DREESSEN, M.D. Surgeon, U. S. Public Health Service; Chief, Medical Unit, Division of Industrial Hygiene, National Institute of Health ROBERT H. FLINN, M.D. Passed Assistant Surgeon, U. S. Public Health Service; Division of Industrial Hygiene, National Institute of Health WILLIAM M. GAFAFER, D.Sc. Senior Statistician, U. S. Public Health Service; Chief, Statistical Unit, Division of Industrial Hygiene, National Institute of Health LYDIA G. GIBERSON, M.D. Medical Division, Metropolitan Life Insurance Company, New York, New York LYMAN D. HEACOCK, D.D.S., M.P.H. Dental Surgeon (R), U. S. Public Health Service; Division of Indus trial Hygiene, National Institute of Health 0. F. HEDLEY, M.D., F.A.C.P. Surgeon, U. S. Public Health Service; Division of Industrial Hygiene, National Institute of Health RICHARD T. PAGE, S.M. * Assistant Sanitary Engineer, U. S. Public Health Service; Division of Industrial Hygiene, National Institute of Health ELIZABETH G. PRITCHARD, A.B. Health Education Specialist, U. S. Public Health Service; Division of Sanitary Reports and Statistics Vll ST085301 6 Viii LIST OP CONTRIBUTORS LOUIS SCHWARTZ, M.D. Medical Director, U, S. Public Health Service; Chief, Dermatoses Sec tion, Divieion of Industrial Hygiene, National Institute of Health HARRY E. SEIFERT, C.E., M.S.P.H. Pasted Assistant Sanitary Engineer (R), U, S. Public Health Service; Chief, Engineering Unit, Division of Industrial Hygiene, National In stitute of Health R. F. SIEVERS, M.D., Ph.D. Assistant Surgeon, U. S. Public Health Service; Division of Industrial Hygiene, National Institute of Health OLIVE M. WHITLOCK, B.S., R.N. Associate Public Health Nursing Consultant, U. S. Public Health Serv ice; Division of Industrial Hygiene, National Institute of Health ST0853017 .^Vv - CONTENTS PART I ORGANIZATION AND OPERATION OP FACILITIES CHAPTER 1 page Wab's Influence on Industrial Hygiene............................................. J. J. Bloomfield, B.S.Eng. 1 CHAPTER 2 Plant Medical Facilities.......................................................................... 0. F. Hedley, M.D., F.A.C.P. 12 CHAPTER 8 Organization of Plant Medical Department....................................... 0. F. Hedley, M.D., F.A.C.P. 25 CHAPTER 4 Medical Services .. ...................................................................................... 48 0. F. Hedley, M.D., F.A.C.P. CHAPTER 6 Nursing Services ......................................................................................... Olive M. Whitlock, B.S., R.N. 66 CHAPTER 6 Dental Services ........................................................................................... Lyman D. Heacock, D.D.S., M.P.H 88 CHAPTER 7 Organization of Plant Emergency Medical Service and Integra tion with That of Community................................... ..................... R. F. Sievers, M.D., Ph.D. 98 CHAPTER 8 Available Services in Industrial Hygiene........................................... 106 J. J. Bloomfield, B.S.Eng. PART II PREVENTION AND CONTROL OF DISEASE IN INDUSTRY Section I CHAPTER 9 The Problem of Occupational Disease.................................................. W. C. DREES8EN, M.D. ix 131 ST 0853018 X CONTENTS CHAPTER 10 pace Occupational Dermatoses............................ ,................................. :... 161 Louis Schwartz, M.D. CHAPTER 11 Engineering Control or An Contamination of the Working En vironment ............................................................................................. Allen D. Brandt, D.Sc. 198 CHAPTER 12 Medical Control or Respiratory Diseases............................................ 267 W. C. Deeessen, M.D. CHAPTER 13 Venereal Disease Control ....................................................................... 278 Ons L. Anderson, M.D., F.A.C.P. CHAPTER 14, Industrial Psychiatry.............................................................................. 291 Lydia G. Gibekson, M.D. CHAPTER 16 Health Education......................................................................................... 297 Elizabeth G. Pritchard, A.B.' CHAPTER 16 Industrial Fatigue: Causes and Control........................................... 308 Robert H. Flinn, M.D. CHAPTER 17 Nutrition in Industry.............................................................................. 326 R. F. Sisters, M.D., Ph.D. Section II CHAPTER 18 Community Sanitation.............................................................................. 336 Richard T. Page, S.M. CHAPTER 19 Plant Sanitation........................................................................................... 346 Allen D. Brandt, D.Sc. * CHAPTER 20 Illumination, Noise, and Radiant Energy........................................... 363 Allen D. Brandt, D.Sc., and Harry E. Seifert. C.E., M.S.P.H. CHAPTER 21 Heating, Ventilattng, and An Conditioning...................................... 373 Allen D. Brandt, D.Sc. ST085301 9 CONTENTS Xi part m 1 THE MANPOWER PROBLEM CHAPTER 22 _ page Maximum Use op Manpower ................................................................... 383 3 Robert H. Flxnn, M.D. ft';**' CHAPTER 23 Women in Industry .................................................................................. 395 7 Huoh P. Brinton, Ph.D. CHAPTER 24 Absenteeism.................................................................................................. 420 3 William M. Gafapeb, D.Sc. Index ...................................!........................................................................ 467 l 7 8 5 6 R 3 3 ST0853020 PART II PREVENTION AND CONTROL OP DISEASE IN INDUSTRY Section I CHAPTER 9 THE PROBLEM OF OCCUPATIONAL DISEASE W. C. Dreessen, M.D. INTRODUCTION Claims paid for occupational disease under workmen's compen sation amount to from 1 to 3 per cent of the amount paid for industrial accidents. This cost comparison, however, does not give the complete picture of their relative importance. In speaking of occupational diseases one ordinarily thinkB of such diseases as occupational dermatitis, lead poisoning, and silicosis. In this country these three groups of diseases constitute the most im portant occupational diseases, with respect to both number of cases receiving compensation and total cost of compensation per case. Based on a year's experience of one State,1 the compensation costs of individual cases are generally lowest for dermatosis cases (averaging about $50 per case) and highest for silicosis cases (averaging about $5,000 per case); lead poisoning occupies a middle position with an average cost per case of about $150. These differences in costs are related to the degree of permanency and duration of the disability. These three* diseases bid well to continue to lead the list in the changeover from peace to war time production. The liability of the employer without proof of fault is the essential principle upon which workmen's compensation is based. Within the limitations of wording or mode of administration 131 ST085302 I 132 PHEVENTION AND CONTROL OF DISEASE IN INDUSTRY of the compensation laws, the provisions common to these acta are the giving of prompt medical care, and payment of monetary benefits, at the cost of the employer without regard to the ques tion of negligence, to an injured or occupationally ill employee or to his dependents in case of death in line of duty. Under the workmen's compensation laws,2 the three common law defenses, namely contributory negligence, the fellow-servant doctrine, and the assumption of risk, are no longer available to the employer. Consequently, the burden of economic loss and waste due to personal injury has been shifted from the employee to industry and thus has been made an item in the cost of pro duction ultimately to be borne by the consumer. Occupational diseases were not specifically covered in the original State workmen's compensation laws. Even as recently as 1920, compensation for such diseases was provided in only seven jurisdictions3 in the United States--California, Connecti cut, Hawaii, Massachusetts, North Dakota, Wisconsin, and the Federal government. Occupational diseases introduced more com plex factors in the administration of law than were encountered with industrial accidents. Occupational Disease Coverage in Various Jurisdictions There is a lack of nationwide coverage for occupational disease.* Although all of the 48 States, excepting Mississippi, have legislation providing for compensation of industrial in juries, only 25 States have laws providing compensation for occu pational disease. The Federal government also provides com pensation for such diseases under compensation laws for its civil employees, longshoremen and harbor workers, and for such dis eases arising from private employment in the District of Colum bia. Compensation is provided for all occupational diseases or for certain specified ones in the jurisdiction shown in the accom panying list. This list also contains the name and address of the agency administering workmen's compensation in the respective State or jurisdiction. Copies of compensation legislation and the rules and regulations of the administrative agency pertaining to the jurisdiction in whicli he is practicing should be readily avail able to the industrial physician. * The discussion in this chapter has been limited to occupational dis eases. The reader should not overlook compensation aspects of industrial accidents. ST0853022 THE PROBLEM OF OCCUPATIONAL DISEASE 133 List or JuxuoicnoNg in Which Occupational Disease Is Compensated and the Name and Address op the Adminutratiye Agency Arkansas ............................... Workmen's Compensation Commission Rector Building* Little Rock California............ ................ Division of Industrial Accidents ^and Safety State Building, San Francisco Connecticut............................Board of Compensation Commissioners 54 Church Street, Hartford Delaware............................... Industrial Accident Board Ninth and Market Streets, Wilmington District of Columbia............D. C. Workmen's Compensation Act Seventh and E Streets, N. W., Washington Hawaii ................................... Department of Labor and Industrial Relations Bureau of Workmen's Compensation Honolulu Idaho...................................... Industrial Accident Board Boise Illinois ................................... Industrial Commission 205 West Wacker Drive, Chicago Indiana.................................. Industrial Board 404 State Capitol, Indianapolis Kentucky ............................... Workmen's Compensation Board Frankfort Maryland...............................State Industrial Accident Commission Equitable Building, Baltimore Massachusetts.......................Department of Industrial Accidents Statehouse, Boston Michigan ............................... Department of Labor and Industry 630 State Office Building, Lansing Minnesota ............................. Industrial Commission 137 State Office Building, St. Paul Missouri.................................Workmen's Compensation Commission State Office Building, Jefferson City Nebraska ............................... Workmen's Compensation Court State Capitol, Lincoln New Jersey ......................... Bureau of Workmen's Compensation Wallach Building, Trenton New York.............................Department of Labor Division of Workmen's Compensation 80 Centre Street, New York North Carolina ................... Industrial Commission Raleigh North Dakota....................... Workmen's Compensation Bureau Bismarck Ohio .......................................Industrial Commission State Office Building, Columbus Pennsylvania ....................... Bureau of Workmen's Compensation Harrisburg Puerto Rico........................... Industrial Commission San Juan Rhode Island......................... Department of Labor Division of Workmen's Compensation Providence a ST0853023 134 PKEVENTION AND CONTROL OP DISEASE IN INDUSTRY List or Jurisdictions in Which Occupational Disease Is Compensated and the Name and Address op the Administrative Agency (Cont.) Utah .......................................Industrial Commission State Capitol, Salt Lake City Washington...........................Department of Labor and Industries Olympia West Virginia.......................Workmen's Compensation Department Charleston Wisconsin ............................. Industrial Commission 1 West Wilson Street, Madison United States ..................... U. S. Employees' Compensation Commission 285 Madison Avenue, New York, New York Definition of Industrial Disease Briefly stated, an occupational disease is an affliction due to a specific industrial health hazard. Legal connotations, however, tend to either limit or extend the number of diseases embraced by this definition. There are two schools of thought on the sub ject of occupational disease legislation and administration. Thus, one school holds that a disease to be occupational must "arise out of and in the course of employment." In other words, it is something characteristic of the employment and not a hazard to which the public is generally exposed. Such diseases are fairly well exemplified by those listed in certain schedule laws (e.g., poisoning by lead, arsenic, and mercury, and silicosis). The other school holds that any disease contracted by a worker, which arises out of employment or out of an incident of employ ment and yet not necessarily characteristic of employment, is an occupational disease. This viewpoint provides for the inclusion of such diseases as pulmonary tuberculosis and malaria. Thus, nurses and internes have received compensation for pulmonary tuberculosis contracted in the course of their work in tuberculosis sanatoria, and a railroad laborer is compensated for malaria contracted in railway section work. The definition of occupational disease has always been found to be very difficult.4 Much has been written on the subject. One of the commonly quoted definitions is that of the Rhode Island law which states that, "The term `occupational disease' means a disease which is due to causes and conditions which are char acteristic of and peculiar to a particular trade, occupation, process, or employment." In many instances it is seen that the "compensable diseases" are the "occupational diseases." Brahdy's comments5 on this point, however, are pertinent: "When physicians differentiate ST 0 853024 THE PROBLEM OP OCCUPATIONAL DISEASE 135 between the terms, 'occupational' and `compensable,' they recog nize a boundary separating their medical field from the legal administrative field. Physicians--and only physicians--can decide whether a disease is occupational. Lawyers and administrators, but never physicians, must decide if an occupational injury is compensable according to the law of that State." Comparison of Schedule and General Coverage Laws.--In some of the State compensation laws, no clear-cut distinction is made between "occupational disease" and "industrial injury." This is probably related to the fact that before administering agencies had experience in compensating occupational disease, an attempt was made to provide coverage for such diseases by amending definitions of the term "injury" to include occupational diseases in some form, either by listing a few of them or by the use of broad language.0 Two general terms are thus ordinarily applied to laws providing compensation for occupational disease. These acts are referred to as (1) schedule or limited coverage laws, and (2) general coverage or blanket laws. Under the schedule laws, the specific compensable diseases are listed and briefly described. This type of coverage holds in Arkansas, Delaware, Idaho, Kentucky, Maryland, Michigan, Min nesota, Nebraska, New Jersey, North Carolina, Pennsylvania, Rhode Island, Utah, West Virginia, and Puerto Rico. In other jurisdictions the law provides compensation for any disability arising from an occupational disease without at tempting to name it and is the law in California, Connecticut, District of Columbia, Illinois, Indiana, Massachusetts, Missouri, New York, North Dakota, Ohio, Washington, Wisconsin, and Hawaii. The language of some general coverage acts adds qualifica tions to the effect that ordinary diseases of life to which the gen eral public is exposed outside of the employment shall not be compensable, except where the said diseases follow as an incident of an occupational disease. These general coverage acts having a statutory definition of the term "occupational disease" are re ferred to as definitive general coverage laws. Provisions of Compensation Laws The industrial physician should know which occupational diseases are compensable in his State. He should also familiarize himself with the administration of the law so that his reports and opinions will convey the proper meaning. Besides the type ST 0853025 136 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY of coverage referred to above, the laws include such provisions7 as scale of compensation, insurance features, limitations as to type of employment, number of employees, medical benefits, extraterritorial provisions, reporting of occupational diseases, medical boards, accrued liability, and waiver or second-injury provisions. Contrary to industrial accidents which can usually be related to time and place, certain occupational diseases take years to develop and hence as a point of reference the day when disability or incapacity begins is usually recorded as the date of injury. Workmen's compensation laws are designed primarily to fur nish the occupationally ill worker with medical care and monetary benefits during the period of his disability or money payments to his beneficiaries in case of death. Except in some States having a State insurance fund and those States where employees may contribute, the cost of compensation is borne almost entirely by the employer. Compensation for loss of wages usually runs from 50 to 70 per cent of the employee's average wage with minimum and maximum amounts usually specified. Most States provide a certain specified period of time immediately following disability, during which compensation shall not be paid. This period varies from one to 14 days, but is 7 days in most States. Claims must be filed within certain time limitations. Failure to provide full compensation for wage loss is meant to be an incentive for the temporarily disabled worker to return to work as soon as pos sible and to preclude malingering. Medical costs are not borne by the worker in most of the States, but maximal limits as re gards period of time and cost, or both, of this service are usually specified. According to Newquist,8 "the acts of 23 States and of the Federal government do not limit the period for medical bene fits other than by qualifying terms such as `reasonable,' `reason able time,' during `temporary disability,' etc. The stated time limits for medical service range from 2 weeks to 1 year and the limited amounts for medical benefits range from $100 to $1,600. Because of the uncertainties and great potential burdens asso ciated with the present occupational disease situation, a few States have seen fit to limit the medical responsibilities of em ployers for treating workers with such diseases, particularly silicosis or asbestosis." Financing the payment of compensation benefits is usually accomplished through insuring the employer's liability by insur ance with a private company, by State fund, or by self-insurance. STO 853026 THE PROBLEM OF OCCUPATIONAL DISEASE 137 The employer is allowed to insure in a private company in most States, but a few States have exclusive State funds. Whether or not an employer may elect or be compelled to carry insurance varies according to jurisdiction. Depending on the degree of incentive offered employers to accept the benefits and burdens of the compensation law, these laws may be classed as compulsory or elective. According to Daw son,3 "a compulsory law is binding upon every employer and em ployee within its scope; there is no choice. Under an elective act, employers and employees have the option of either accepting or rejecting the act But in case the employer rejects, the customary common-law defenses in personal injury litigation are usually removed, while if the employee rejects, the workmen's compen sation principle of liability of the employer for work injuries without regard to fault is not applicable to an action for damages." Agricultural and domestic workers are excluded from benefits of compensation laws in most States. Among the exceptions are Arizona, California, Connecticut, Illinois, Kentucky, Minnesota, New Jersey, New York, Ohio, South Dakota, Vermont, and some of the territories of the United States. Casual employees are also usually excluded. Employers are also exempt if they employ fewer than a specified number of workers. Special conditions are provided in certain jurisdictions for covering hazardous and pub lic employments as well as disability incurred outside of the State. The limiting provisions relating to silicosis deal with (1) period of employment and exposure within the State, (2) filing of claims, (3) time within which death must occur in com pensable fatal cases, and (4) deductions from death benefits. Some States have included penalty provisions for false state ments as a responsibility of the employee. If as an applicant for employment the employee falsely represents that he has not suf fered from an occupational disease which subsequently causes disability or death, his compensation is forfeited. The term accrued liability has been used to describe potential compensation claims for occupational .disease which existed prior to the enactment of occupational disease legislation. It is par ticularly characteristic of silicosis, a disease which requires years for the pathologic process to maturate and cause disability. It is an accrual of injuries sustained during previous years of employment. In some acts the last employer of the victim of disease (e.g., silicosis) is held fully liable for compensation. At ST 0853027 138 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY the National Silicosis Conference (1938), the Committee on the Economic, Legal, and Insurance Phases of the Silicosis Problem* felt that such accrued liability should be at least in part recog nized as a public liability. This conclusion is related to lack of nationwide occupational disease coverage. Because of interstate movement of people, States having or planning silicosis coverage fear that they will become the dumping ground for the accrued liability of other jurisdictions. With the passage of compensation laws making employers responsible, preemployment examinations were adopted by em ployers to screen out physically defective workers. As Dawson* points out, this adverse effect upon the employment of handi capped workers was an unforeseen consequence of these laws. Employers considered the increased risk of loss a good cause for refusing employment. To remedy this injustice and to minimize the difficulty which partially disabled workers have in securing employment, some of the States created special "second-injury" funds and amended the compensation act to provide that in case of a second major disability the employer should be held liable only for the second injury considered separately. The disabled employee, however, is compensated for disability resulting from the combined injuries. Statutory provisions for second-injury funds are included in the laws of Arkansas, District of Columbia, Hawaii, Idaho, Illinois, Massachusetts, Minnesota, New Jersey, New York, North Carolina, North Dakota, Ohio, South Carolina, Utah, West Virginia, and Wisconsin, and also in the Federal Longshoremen's Act. In the absence of second-injury funds, waivers and limited, disability have been used to meet the issue: These procedures find application particularly in dealing with accrued liability of sili cosis. Speaking of waivers, Kessler10 states: "These waiver clauses take cognizance of the fact that the workmen's compensation law may be an obstacle to employment. They aim to permit the workman to exchange a right for a benefit he may prize more highly. Though it would be possible to safeguard the employer from the suit of a workman who had waived compensation, to allow the workman so to waive this right is open to various objections and abuses. It might become possible, for instance, for employers to require all persons with any physical disability to sign waivers as a condition of getting employment. ... In prac tice, waivers are restricted or prohibited in most jurisdictions." Where restricted, they are issued in accordance with regulations ST0853028 THE PKOBLEM OF OCCUPATIONAL DISEASE 139 of the agency administering the compensation law. Under limited disability plans the disabled worker may be compensated only for later injury, or the decreased earning power of the handi capped worker is used as a basis of apportioning compensation. In general, it seems that with reference to handicapped workers an exception should be made to the theory of workmen's com pensation which makes industry bear the full burden of respon sibility for industrial disabilities and have the government assume part of the burden. CLINICAL DESCRIPTION OF DISEASES OF PRESENT IMPORTANCE Classification of Diseases or Conditions Dublin and Vane11 classify occupational hazards as follows: (1) abnormalities of air pressure, (2) abnormalities of tempera ture and humidity, (3) dampness, (4) defective illumination, (5) dust, (6) infections, (7) radiant energy, (8) repeated motion, pressure, shock, etc., and (9) poisons. Major Groups of Occupational Diseases.--A review of various compensation laws subscribing to schedule coverage shows that the specified occupational diseases fall into six or so major groups when classified according to causative agent. Thus, under toxic metals or metalloids may be listed poisoning caused by arsenic, zinc (brass), cadmium, lead, manganese, phosphorus, radium, and mercury; under dusts are listed pneumoconiosis and/or silicosis with or without tuberculosis and asbestosis with or without tuberculosis; under gases, vapors, and fumes, poisoning caused by hydrogen fluoride, nitrous fumes, sulfur dioxide, carbon disulfide, hydrogen sulfide, hydrogen cyanide, carbon monoxide, nickel carbonyl, halogenated hydrocarbons, methyl alcohol, ben zene, and nitro and amino derivatives of gasoline, benzene, and phenol; under occupational skin hazards, chrome ulceration or dermatitis, infection or inflammation of the skin or eyes due to oils, cutting compounds, lubricants, dusts, liquids,, fumes, gases, and vapors, epitheliomatous cancer or ulceration of the skin or surface of the eye due to pitch, tar, and bitumen, and dermatitis venenata; under infectious agents may be listed such diseases as anthrax and glanders; and under physical agents may be listed compressed air illness, radioactive substances, cataract, and impaired hearing caused by noise. War Industries and Occupational Disease.--With few excep tions, the serious and prevalent occupational diseases of prewar days may be anticipated as being the sources of difficulty in war- ST 0853029 140 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY -r time industrial production. Cunningham^2 of Canada has given us some idea of what we may expect from the changeover to war production. He states that the number of cases of occupational disease have increased in the Dominion, but up to the present they have come from increased exposure to common substances rather than from new processes, i * Predominance of Industrial Poisoning.--Exclusive of derma toses, industrial poisonings make up the majority of the occu pational diseases. The progressive industrial physician moreover recognizes the need of studying the toxic properties of new sub stances or chemicals prior to the establishment of a new indus trial process. He is aware of the fact that absorption of metals and their compounds does not as a rule induce the same reaction or degree of action in the body as the metal or its compounds when used for therapeutic purposes. In other words, industrial intoxications are characteristically chronic in contradistinction to acute poisonings of usual medico-legal importance. When acute, disability ordinarily occurs on the day of exposure and the disease entity is then usually considered an accident. The portals of entry for industrial poisons are (1) by inhalation, (2) by mouth, (2) through the skin, and (4) through the subcutane ous tissues. Broadly speaking, the, respiratory route is character istic of most industrial poisons. Medical Questions Arising.--Because an occupational disease is related to the personal activity of the worker and is of the nature of the inevitable consequences of a given type of work, medical questions are bound to arise in the settlement of occupa tional disease claims.13 Besides the nature, extent, and duration of disability, questions of etiology and differential diagnosis need to be established. To solve these questions the industrial physi cian should have a clear conception of the time factor in the evolution of these diseases. Related to this time factor is a latent period without disability somewhat analogous to the incu bation period of infectious diseases. In silicosis, for instance, it may require the passage of from 2 to 25 years of industrial dust exposure before the disease manifests itself clinically in a given worker. Needless to say,* it is important to have a record of the nature of exposure in different types of work in the form of an occupational history. This may be a time-consuming inquiry, particularly in the case of a miner who has worked in many different mines over a period of 30 years or so, or in the instance of a worker potentially a victim of metal poisoning from whom ST 08 53030 THE PROBLEM OK OCCUPATIONAL DISEASE 141 the physician endeavors to learn the circumstances, such as the lack of ventilation, chemicals involved, and nature of the work process, which have precipitated the toxic episode. Other steps In diagnosis make the same demands on the physicians's acumen as other disease entities. In the following pages certain selected occupational diseases, which are manifested by systemic reaction, will be briefly dis cussed. A chapter on occupational dermatoses appears subse quently. An endeavor has been made to present an epitomized account of the most significant occupational diseases. 1 :-* Lead Poisoning Industrial Uses of Lead.--About 150 industrial occupations entail a possible lead exposure. The principal hazards14 occur in: Storage battery manufacture Printing industry Punt industry Application of paints Enameling of such articles as bath tuba Welding and- riveting, in enclosed spaces, steel painted with red lead Rubber manufacture Lead ore mining t Pottery glazing Tetraethyl lead manufacture, or Reclamation of lead from junk cleaning tanks in which ethyl gaso line has been stored Lead arsenate manufacture Among the most commonly used lead compounds are lead car bonate, lead chromate, red lead, lead sulfate, litharge, lead ace tate, lead arsenate, and tetraethyl lead. Symptoms.--Lead absorption into the tissues is cumulative in the sense that a part of the relatively small daily doses, indi vidually insignificant, which is absorbed each day, is not elim inated promptly. When physiologic tolerance is exceeded, symp toms and disability occur. Lead enters the body in industrial work principally through the respiratory tract. Organic lead com pounds, for example, tetraethyl lead, may enter through the unbroken skin. The maximal permissible concentration for lead is 1-5 mg. per 10 cubic meters of air, and this quantity may ,be considered as a daily dose which should not be exceeded if disa bility is to be prevented. Industrial lead poisoning ordinarily' occurs following pro longed exposure to lead or its compounds. Classified on the basis of systems, the three more or less distinct clinical types of lead ST085303I 142 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY poisoning* seen currently among American industrial workers are alimentary, neuromotor, and encephalic. Some cases show a combination of two or more of these principal clinical man ifestations. The alimentary type is the most frequent in occurrence. It is characterized by abdominal discomfort or pain which culminates in frank colic in the most severely affected cases. Obstinate con stipation is occasionally preceded by a brief period of diarrhea. Among the other complaints in this type of case are loss of appetite, nausea and vomiting, metallic taste, lassitude, insomnia, general weakness or asthenia, arthralgia, myalgia, irritability, dizziness, and headache. Accompanying these symptoms may be the following signs: ashen pallor, lead line on gums, pyorrhea, malnutrition, abdominal tenderness, basophilic stippling, reduced hemoglobin and red blood cell count (but may be within normal limits), slight albuminuria, and elevation of lead content of blood and urine. When a typical episode of colic is in progress, the patient is obviously in agonizing pain, bathed in cold sweat, has gray-green pallor, and is likely to be doubled up with hands pressing upon his abdomen. During a spasm the abdomen has a board-like rigidity. Between spasms, the abdominal pain is usu ally relieved by firm pressure. The pain of lead colic is usually promptly relieved by intravenous administration of calcium chloride or calcium gluconate. The gingival lead line, if present, will show up as finely punc tate bluish-black deposits in the gum tissue. It should not be confused with the congestion of chronic gingivitis, discolored calculus on the tooth surface, or the normal pigment deposits observed in the gums of Negroes and other dark-skinned races.' The effects of congestion can be overcome by pressure with a transparent applicator such as a glass slide. In the neuromuscular type, the chief complaint arises from weakness, perhaps the paralysis (wrist drop) of the extensor muscle groups of forearm and hand. The paralysis may be uni lateral or bilateral. When unilateral, it is likely to affect the arm most used. If a lower extremity is involved, foot drop may be present. Gastro-enteric symptoms, though not absent, are less disturbing. Arthralgia, myalgia, aching, and stiffness of muscle groups are likely to be more severe than in the alimentary type. * The presentation of the discussion of the clinical manifestations of lead poisoning follows a section (to be published) of a report prepared by the Committee on Lead Poisoning, American Public Health Association. ST 0853032 THE PROBLEM OP OCCUPATIONAL DISEASE 143 Headache, vertigo, insomnia, and disturbed sleep are likely to be prominent symptoms. True palsy is uncommon today; it is . usually the result of prolonged and severe lead exposure, and clinical history may give evidence of repeated episodes of intoxi cation of milder type. Lead encephalopathy is the most severe but fortunately the rarest manifestation of lead poisoning. In the industrial worker it follows rapid, heavy lead absorption. Certain organic lead com pounds, such as tetraethyl lead, are absorbed rapidly (through the skin as well as other portals of entry) into the body and I ;<i- especially into the central nervous system. With these compounds, encephalopathy is the rule. Comparable concentrations of lead are absorbed into the brain from inorganic lead compounds only when the workplace is heavily contaminated with lead vapor, fume, or dust. Lead encephalopathy begins abruptly and is characterized by signs of cerebral and meningeal involvement. The patient may be in a heavy stupor at the onset and go into coma, with or with out convulsion, and die. Excitation, confusion, and mania occur less frequently. Headache, dizziness, insomnia, and somnolence are symptoms in cases recovering and of shorter duration. The cerebrospinal fluid may be increased in pressure and show slight increase in cellular elements and globulin. Laboratory Findings.--Laboratory findings supplement the. j clinical findings and are of considerable assistance in differential diagnosis. They should not be expected to yield the diagnosis. Evidence of the effect of lead on the hematopoietic system is ascertained by a study of the blood picture. Basophilic granula tion or stippling of erythrocytes should be ascertained in quan titative terms and related to an established normal standard. According to Mayers,18 abnormal cell morphology and abnormal cells (including nucleated erythrocytes) are more characteristic than stippled cells and polychromatophilia of lead anemia, even in such cases in which the hemoglobin is as high as 80 per cent and there is a red blood cell count of 4 million. The blood of normal North Americans has an average lead content of 0.03 mg. (range 0.01 to 0.06) per 100 gm. of whole blood.15 Normal urinary lead values average 0.03 mg. per liter with values ranging from 0.01 to 0.08 mg. per liter or ranging from 0.005 to 0.12 mg. per liter, depending on the size of the sample submitted for analysis. The finding of abnormal quanti ties of lead in blood and excreta means only abnormal lead ab- if ST0853033 144 PREVENTION AND CONTROL OP DISEASE IN INDUSTRY sorption and hence points to the existence and severity of lead exposure. Lead intoxication1" occurs rarely if the mean urinary lead concentration of representative groups of workers is kept below 0.10 mg. per liter, and if individual results are generally below 0.15 mg. per liter and very rarely in excess of 0.20 mg. per liter. The upper limit of safety for the concentration of lead in the blood lies somewhere between 0.05 and 0.07 mg. per 100 gm. The blood levels in frank cases of lead intoxication are usually considerably higher (0.09 to 0.30 mg. per 100 gm. of whole blood). Samples for chemical analysis to determine lead content of blood or excreta should be obtained near the height of an acute episode. Extreme care is necessary to avoid contamination from the time of taking the sample until it is completely analyzed.17 Differential Diagnosis.--The alimentary type must be dif ferentiated from such conditions which may require surgical intervention, as acute appendicitis, acute cholecystitis and chole lithiasis, perforated peptic ulcer, intestinal obstruction, and acute pancreatitis. Neglect of a surgical condition is far more serious for the patient than giving undue weight to apparently significant lead exposure. In such cases "it is better to err on the side of surgical exploration." Jaundice in lead poisoning is rare today. Leucocytosis, and abnormal differential count, would favor in flammatory lesions. Hematuria is very rare in lead colic cases. Intestinal obstruction is difficult to differentiate, but if stippling is-absent lead colic may be eliminated. The medical history will afford material differential points and it is particularly helpful in cases of peptic ulcer or coronary thrombosis. With respect to lead neuropathy or encephalopathy, neurologic changes induced by viruses, infections, arsenic, malnutrition, and alcoholism must be ruled out. Treatment.--Treatment may be briefly summarized as fol lows: (1) discontinue the worker's exposure to lead, (2) treat the acute episode with large doses of calcium and calcium-rich diet, (3) later induce catharsis, (4) during convalescence active deleading procedures1* may be instituted, although some investi gators assert that the body will gradually, rid itself of excess lead if lead exposure has ceased, and (5) treat cerebral symp toms and sequelae palliatively. Generally speaking, on recovery from acute lead poisoning, the worker may return to his former occupation provided the lead exposure responsible for his disability has been brought ST0853034 THE PROBLEM OF OCCUPATIONAL DISEASE 145 under control or eliminated. Otherwise, it will be necessary to place him in a job entailing no exposure. Periodic occupational examinations or check-ups to detect early evidence of dangerous lead absorption should be performed on all workers exposed to a lead hazard, but their frequency must be related to the problem at hand. Workers who are exposed to less than 1.5 mg. of lead per 10 cubic meters of air need not be examined regularly more than once or twice a year, but in ex tremely hazardous exposures and in young employees it may be necessary to raise this frequency to every fortnight. Metal Fume Fever Metal fume fever is an acute transient illness often referred to as brass founders' ague, metal shakes, oxide chills, brass chills, galvo, and zinc oxide fever. Although at one time the disease was thought to be caused exclusively by zinc,10*20 it is now known to be produced by other metals, for example, cad mium, lead, manganese, mercury, and magnesium. It follows the inhalation of rather heavy concentrations of finely dispersed metal fumes, usually in the form of oxides. Then, under certain circumstances, toxic proteins or albuminates of the metals are said to be formed which produce a severe transient febrile re action resembling protein shock in nature and symptomatology. Symptoms.--A few hours after exposure,21*22*21 the nose, throat, and substernal region feel dry and sore, burn, and give rise to a dry cough. A feeling of constriction in the chest, head ache, and lassitude may be complained of and sometimes nausea and vomiting occur. Symptoms at this stage are similar to the prodromes of an acute respiratory infection. Within one to several hours, the symptoms become aggravated, the headache becomes worse, vision may become blurred as chilly sensations begin to appear, and the victim usually takes to his bed. Shivering or trembling rapidly increases into a more or less severe rigor which may last from % to 2 or 3 hours. Fever and leucocytosis23 not uncommonly accompany and follow the chill. Myalgia and arthralgia are also usually present q.t this stage. The symptoms associated with the chill end almost by crisis and are followed by profuse perspiration. Considerable prostration usually follows an attack but by the next morning recovery is usually complete. An entire attack seldom lasts longer than from a few to 20 hours, and for this reason compensation is rarely claimed. New workers and employees upon their return to work fol- ST0853035 146 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY lowing a holiday or lay-off are particularly susceptible to an attack. Workers become "immunized", but this artificial im munity lasts only about 6 days.88 The illness is also more likely to develop in winter and is aggravated by chilling the body. If symp toms persist for more than a day, it is necessary to look to lead, manganese, cadmium, and arsenic as specific causes. Malaria, influenza, tuberculosis, leukemia, Hodgkin's disease, acute bron chitis, onset of tonsillitis, and septic processes also must be con sidered in differential diagnosis. Control.--Sayers24 is of the opinion that metal fume fever may be eliminated through the adoption of an adequate medical and engineering program. A study of the industrial exposure responsible for the illness should be requested by the industrial physician. In conducting preplacement or transfer examinations, it should be remembered that the clinical course of chronic res piratory conditions, such as bronchiectasis, asthma, and arrested tuberculosis, and chronic heart disease may be unfavorably in fluenced by the fever and chills. Cadmium Poisoning The great increase in the use of cadmium, not only for coat ing marine hardware but also for many fittings that were for merly zinc coated, has created a new problem in industrial hy giene. Most cases of industrial cadmium poisoning have resulted from accidents or short exposure to excessive concentrations of cadmium dust or fume. Little is known of chronic effects upon humans. Acute industrial poisoning is characteristically produced by inhalation of the fumes, particularly where cadmium has been heated to give off the oxide in yellowish-brown fumes. Symptoms.--The clinical picture26 is characterized by irrita tion of the respiratory mucous membrane which may eventually lead to pulmonary edema, pneumonitis, or bronchopneumonia. The first symptoms are those of metal fume fever, usually dryness of the throat, cough, chills, headache, vomiting, and a sense of constriction of the chest. Later symptoms are predominantly referable to the respiratory system and are characterized by cough, pain in the chest, severe dyspnea, and prostration. A few cases have gastro-intestinal complaints. Differential Diagnosis.--Poisoning with nitrous fumes and methyl bromide may be ruled out by history. Metal fume fever caused by zinc oxide fumes usually clears up within 24 hours. Therefore, the continuance and aggravation of symptoms such ST 0853036 THE PROBLEM OP OCCUPATIONAL DISEASE 147 aa occur with irritant gases which produce acute pulmonary con gestion make it imperative to consider cadmium. These serious delayed symptoms27 should not be confused with nonoccupational diseases. Treatment.--Treatment is palliative. Oxygen should be used in moderately and severely affected cases without waiting for signs of pneumonia. Rest is acutely essential as is the withdrawal of the worker from the source of contact. Manganese Poisoning Manganese is used principally in the manufacture of alloys, for example, ferromanganese, and to a lesser extent in the man ufacture of dry cell batteries, paints, matches, and fireworks, and in leather tanning. In the crude black ore most of the manganese is present in the form of the dioxide. Symptoms.--Industrial manganese poisoning is a chronic disease characterized by neurologic symptoms and is usually the consequence of inhaling manganese dust or fumes. The important symptoms are muscular stiffness, twitching and incoordination, giving rise to difficulty in walking, and propulsion gait. Speech defects, a mask-like facial expression, drowsiness, weakness, and emotional instability may also be present. In differential diag nosis, disseminated sclerosis, paralysis agitans, and progressive lenticular degeneration must be ruled out. Control.--Flinn, Neal, and Fulton28 advise quarterly medical examination of workers exposed to manganese dust and the im mediate transfer to a manganese-free environment of any work ers showing signs of early poisoning, until the hazard has been controlled. Mercury Poisoning (Hatters' Shakes) The principal ore from which mercury is derived is cinnabar, or mercuric sulfide. Some cinnabar mines also yield native quick silver. In 1940 there were 159 mercury-producing mines29 in the United States and Alaska, with the greatest production coming from the States of California, Oregon, and Nevada. Besides the mining of mercury, some other potential sources of mercury hazard arise from its use in thermometers, barometers, extraction of gold from its ores, dental alloys, mercury arc lamps and recti fiers, anti-fouling marine paints, agricultural disinfectants, radio equipment, analytical laboratories, explosives, and certain chem ical industries. Dublin and Vane11 list about 100 occupations in ST0853037 148 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY which mercury may be a hazard. Mercury is being replaced in the fur-hatting industry by less toxic chemicals.80 Industrial mercury poisoning occurs almost exclusively from the inhalation of mercury vapor or dust of the metal and its salts, yet poisoning through the ingestion, cutaneous, and sub cutaneous routes may infrequently occur.81 Elemental mercury gives off vapor at ordinary room temperatures. Mercury is "a general protoplasmic poison." After it gains entrance to the circulation, it is rapidly taken up by the tissues. The form in which mercury circulates in the body is not definitely known32 though some feel it is as an albuminate such as mercury chloroalbuminate, or oxy-chloro-albuminate. Symptoms.--The cardinal symptoms of industrial mercurialism are stomatitis, psychic disturbance, and tremors. These symp toms are not present simultaneously in all cases nor in the same degree.33 Industrial mercury poisoning is typically chronic though cases of severe, rapidly developing mercurialism characterized by colicky pain, diarrhea, painful stomatitis, and excessive saliva tion may occur occasionally "in such jobs as mining metallic mercury, when the silver runs free, as the miners say, and the mine is hot."34 There is rarely much kidney involvement in the industrial form of the disease. A blue line on the gums resembling that due to lead absorption is seen in a few cases. Tremor and other signs of neurologic origin are more characteristic of an insidious, slow form of poisoning. The tremor is observed mainly in the muscles of the face, hands, and arms; it is intention in type, becoming most apparent while the patient is doing an un usual task. As the tremor grows worse, shaking or convulsive movements are added to the tremor, giving rise to the typical picture of hatters' shakes. Mercurial erethism or psychic irrita bility is intimately related to the tremor and may include or lead to loss of memory, insomnia, and depression. Hyperactive knee jerks and scanning speech are frequently present in ad vanced cases.35 Mercury fulminate rarely produces symptoms of systemic mercurial poisoning; the cases are usually characterized by a dermatosis associated with conjunctivitis and inflammation of mucous membranes of the nose and throat.30 Radium Poisoning Because luminous dials are needed on instruments in night operations of the armed forces, there has been a great increase ST0853038 THE PROBLEM OP OCCUPATIONAL DISEASE 149 in the use of luminous paints. These paints are usually a mixture of phosphorescent zinc sulfate and radium, mesothorium, or other similar radioactive substances.*7 Another source of industrial disease is in the mining and refining of radioactive ores. The harmful effects of radium are caused by ingestion, in halation, injection of radioactive substances, or whole body exposure to gamma radiation. It is necessary to understand the genetic connection of all members of the radium family because J:. these elements taken all together produce the -effects ascribed to radium. The damage produced by various types of radiation is de (termined by their nature and properties,38 thus, (1) alpha rays have enormous energy but low power of penetration and to pro duce injury they must come in intimate contact with the tissues t they injure, (2) beta rays penetrate several feet of air, and (3) the gamma rays can penetrate several centimeters of lead. All radium39 disintegrates at a slow but definite rate into radon, a radioactive gas. In the body of a victim of radium poisoning, some of the radon is exhaled and that which is not exhaled disintegrates in situ into a series of solid radioactive substances, eventually becoming lead. Like lead, radium has been shown to be stored largely in the bones. Radium induces bone injury as well as damage to the hematopoietic system. It is elimI inated mainly in the feces. Although only about 10 per cent of i the amount of radium taken into the body becomes fixed in the I tissues, this fraction exposes the tissues to the destructive action I of the radiations from the various members of the radium family. Among dial painters tissue damage is almost entirely due to alpha radiation, as studies of bone deposits show that about 92 per cent of the radiation is alpha and only 8 per cent beta and gamma. The common industrial form of radium poisoning,40 such as occurred in radium dial painting, should not be confused with the deleterious effects of external application. The industrial form is an insidious chronic disease. The patient for many years I after exposure remains in good health. According to Martland40 ! patients having 120 to 180 micrograms of radium in their bodies /' will usually develop extensive radiation osteitis within 1 to 5 years. A complicating bacterial, dental infection will not uncom monly lead to extensive necrosis of the jaw bones. Macrocytic, hyperchromic anemia may develop at first, followed by aplastic anemia. Patients retaining 2 to 20 micrograms of radium often escape jaw necrosis, but tend to develop crippling bone lesions 6 I ST 0853039 150 prevention and control op disease in INDUSTRY such as coxa vara, osteoporosis of the flat bones of the skull, deformities of the spine, spinal fractures, and osteogenic sar comata. l\ Even such small amounts as 1 to 2 micrograms may produce ' definite bone change.** When the amount of radium a worker has deposited in his body exceeds 0.1 microgram, as revealed by the expired air test, immediate change of his occupation and treatment by decalcification therapy or other mode of therapy which may have been developed is recommended.*7 Curtiss** states that if a sample of exhaled air is found to contain more than 10-12 curie of radon per liter, it indicates that at least 0.1 1 microgram of fixed radium exists in the body. Treatment is largely symptomatic. The decalcifying therapy of a low calcium diet and ammonium chloride, as used by Aub and his coworkers, has been shown to increase the excretion of radium, but it does not greatly reduce the total deposition of radium in the body. This method of therapy is possibly of value early in the disease when the radium is contained in the trabeculae rather than in the cortex of the bone. As regards medical control, thorough medical and dental ex aminations should be performed before employment. The com plete blood count made at the time of preemployment examination serves as a reference index for subsequent blood counts. Periodic occupational examinations including hematologic studies should be made at intervals of about one month and particular attention given to the trend of successive blood counts. Many authorities prefer to have the expired air radon test, which is made at intervals of six months or one year, because a dangerous radium accumulation may be detected in this way before it has had time to induce changes in the blood picture. Leucopenia, relative lymphocytosis, or beginning anemia calls for careful investiga tion and possibly change of occupation for the worker concerned. Silicosis (Occupational Pulmonary Fibrosis, Pneumoconiosis) Definition.--Pneumoconiosis is a broad generic term applied to all dust affections of the lungs. In a more restricted sense, it means pulmonary fibrosis induced by inhaled mineral dust. The committee on Pneumoconiosis of the American Public Health As sociation42 defines silicosis as "a disease due to breathing air con taining silica (Si02), characterized anatomically by generalized fibrotic changes and the development of miliary nodulation in both lungs, and clinically by shortness of breath, decreased chest I ST 08530U0 THE PROBLEM OF OCCUPATIONAL DISEASE 151 expansion, lessened capacity for work, absence of fever, increased susceptibility to tuberculosis (some or all of which symptoms may be present), and by characteristic X-ray findings." Classification.--On the basis of the structural changes induced in the lung and the type of dust, the pneumoconioses or pul> monary fibroses may be classified as follows (compare referjT ence 43): 1. Simple benign pneumoconiosis, which is virtually a deposi tion of dust in the pulmonary tissues usually accom panied by pigmentation, and includes, for example, anthracosis induced by coal dust and siderosis induced by iron. It does not incapacitate and roentgenologically shows as a maximum change only an exaggeration of linear pulmonic markings and is of clinical interest only by way of differential diagnosis. Such cases should never be diagnosed as silicosis. 2. Silicosis, which is a pathologic pulmonary reaction due to free silica; for example, sandblasters' silicosis. This type of pneumoconiosis results in a classical nodular fibrosis of both lungs, demonstrable both in the X-ray and at post mortem. Massive fibrosis, varying degrees of pig mentation, atelectasis, emphysema, fibrous pleurisy, bronchitis, cavitation, and pneumothorax are among the concomitant pathologic changes.44 3. Mixed forms, that is, silicosis resulting from the inhala tion of mixtures of varying amounts of free silica and more inert pneumoconiogenic dust constituents, for ex ample, anthracosilicosis and siderosilicosis. Most cases of silicosis undoubtedly come under this classification. 4. Asbestosis, a characteristic diffuse, interstitial fibrosis of the lungs induced by fibrous minerals which, according to animal experimentation, is due to the mechanical ac tion of the asbestos, producing a ground-glass appear ance on the X-ray. It may cause disability and a few fatal cases have been recorded. Etiology.--Silicosis is incurable and large numbers of work men are potentially exposed to conditions favoring the develop ment of the disease. The majority of cases of this chronic pulmonary disease occur among workers engaged in mining,45 quarrying, ceramics industry, tunnel construction, sandblasting, and foundry work. Inhalation of siliceous dust almost invariably results in sili- f ST085304 I 152 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY coeis if a certain set of conditions has prevailed during the work ing experience of the worker. Among these silicosis-producing conditions are: 1. The dust must be of respirable size (usually 0.6 to 3 microns). 2. The dust must be present in the atmosphere at the breath ing level of the worker in concentrations exceeding 6 million particles per cubic foot. 3. The dust must be inhaled for a number of years. 4. The dust must contain silica in a free state, such as quartz. Generally speaking, the inhalation of high concentrations of respirable high quartz dust produces disabling disease in a shorter period of time than the inhalation of low concentrations of dust or dust of low quartz content. Legislation.--The following States, which include the 11 States subscribing to blanket coverage, either list silicosis in schedule occupational disease laws, or make certain provisions for the disease:48 Arkansas, California, Connecticut, Delaware, Idaho, Illinois, Indiana, Kentucky, Maryland, Massachusetts, Michigan, Missouri, Montana, New York, North Carolina, North Dakota, Ohio, Pennsylvania, Utah, Washington, West Virginia, and Wisconsin. Incidence.--It has been estimated on the basis of the 1930 census that between 500,000 and 1,000,000 workers are exposed to silica dust.45 Clinical investigations, including X-ray studies, imvarious dusty trades have shown that from 8 to 25 per cent of the employed workers have potentially disabling pneumoconiosis; thus a high proportion of workers in these dusty trades would appear to have escaped the disease. This resistance of some workers, however, is more apparent than real47 if consideration is given to the relatively long latent period required before the disease can be demonstrated clinically or even by X-ray study. A great majority of the cases develop after at least 7 years of exposure, although a few cases have developed in as short a period of time as 114 years. At the other extreme, with exposures to low concentrations of free silica, more than 30 years may have to elapse before the disease develops to a stage when it can be diagnosed.45 Symptoms and Signs.--The worker showing X-ray evidence of an early to a moderate amount of simple silicotic involvement has few symptoms. Moreover, symptoms and physical signs are of little help in determining whether the patient has a silicosis, a modified silicosis (for example, anthracosilicosis), or asbestosis. ST0853042 THE PROBLEM OF OCCUPATIONAL DISEASE 153 Symptoms and signs do, however, assist in the determination of disability. Among the symptoms and signs of importance are shortness of breath, particularly upon exercise; cough, usually dry; chest pain, varying from a feeling of tightness in the chest to the sharp, excruciating pain typical of pleurisy; hemoptysis; general complaints such as digestive disturbances, insomnia, and dizziness; decrease in chest expansion; prolonged expiration, especially in association with emphysema; altered breath sounds; rales; and the presence of areas of increased density in the lungs. Infection may complicate the picture at any time and is usually manifested by pleural pain, fever, night sweats, weight loss, aggravation of dyspnea, anorexia, weakness, and a cough produc ing large amounts of blood-tinged sputum. Diagnosis.--In establishing a diagnosis of one of the pneumo conioses, all of the following three factors should be considered.* 1. An occupational history which reveals definite prolonged exposure to siliceous dust or asbestos dust. 2. Symptoms and physical signs which furnish valuable in formation in (a) gauging the extent to which pneumo coniosis has progressed, (6) showing the degree of dis ability, and (c) excluding other diseases. 3. X-ray findings, which, if classified on the basis of the sys tem recommended by the U. S. Public Health Service, show bilateral ground-glass, nodular, or a more ad vanced type of lung-field marking. So long as the chest roentgenograms show predominantly linear pulmonic markings, silicosis or modified silicosis need not be given serious consideration. It is when the shadows in the lung field assume a ground-glass, granular or nodular appearance that they become specific and assume more diagnostic charac teristics. Using Irvine and Steuart's analogy,48 the usual linear pulmonic markings are likened to the branches of a tree and the granular, stippled, or nodular lung-field markings simulate the leaves. Complete foliation then means silicosis. Viewed stereoscopically, the films at this stage will show fine nodulation. Some writers describe a related change in .the lung-field appearance as reticulation.49 Although not definitely determined, this type of lung-field marking may result from the inhalation of mixed dusts. Later stages will show massive areas of fibrosis, and if infection is present the X-ray shadows tend to be asymmetrical. Asbestosis is exceptional from the standpoint that the pul- * In the field of forensic medicine it has been frequently demonstrated that autopsy studies will yield essential information. ST 0853043 154 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY monary fibrosis is caused by dust containing little if any free silica. The asbestotic patient will usually show clinical symptoms and signs which are out of proportion to the apparently small amount of pulmonary involvement shown by the chest roent genogram. Large massive shadows are very rarely seen in the chest roentgenogram except in the presence of a complicating infection. On the contrary, the diffuse interstitial fibrosis is manifested by a ground-glass appearance, frequently with fine pinpoint stippling of the middle and lower lung fields. It pro gresses to terminal diffuse fibrosis usually without nodular pre dominance in about twenty years/'0 A shaggy appearing cardiac silhouette due to involvement of superimposed lung structures and pleuropericarditis is not infrequent. Asbestosis bodies may be demonstrated in the sputum or the lung tissue. Medical Control Measures.--All applicants for employment in dusty trades should be examined by X-ray. Periodic medical ex aminations at intervals of one year to possibly three years, in cluding X-ray study of the chest, should be made of all workers in dusty trades in order to detect evidence of active pulmonary tuberculosis and early silicotic changes. The length of the inter val between examinations depends mainly on the degree of haz ard and the prevalence of endemic tuberculosis. Clinical study of patients suspected of having pulmonary tuberculosis should be made to determine the dynamic status of such complication. No worker should be rejected on preemploynfent examination or removed from work, which he is accus tomed to perform, merely because of a diagnosis of simple silicosis, but rather the atmospheric dust in which he works should be brought within safe limits. The worker whose first roentgeno gram shows healed primary tuberculosis should not be denied employment in a dusty trade on this account alone. If the worker has minimal, arrested, or healed reinfection tuberculosis, he should be allowed to continue his work.but should be observed with the same precautions as a man with simple silicosis. Close medical supervision is recommended for all silicotic workers in order to control or prevent serious complications of the common respiratory infections. Benzene (Benzol) Poisoning Benzene (benzol) is an excellent solvent for gums, resins, fats, and oils, and as such has found many industrial applica tions. It is used in the manufacture of rubber, rubber goods, ST 08530UU THE PROBLEM OF OCCUPATIONAL DISEASE 155 linoleum, quick drying paints, lacquers, stains, paint removers, and plastics. Benzene should not be confused with the less toxic petroleum product, benzine, which is a mixture mainly of ali phatic hydrocarbons. The most characteristic pathologic changes51 in cases of ben zene poisoning are seen in the bone marrow which may show gradations of change from hyperplasia to hypoplasia and occa sionally complete aplasia of the myeloic cells. Other parts of the hematopoietic system may also be involved. Depending on the degree of exposure, secondary degenerative changes are observed in the liver, kidneys, and heart. Symptoms.--Acute benzene poisoning follows the inhalation of benzene vapors in high concentration and provokes narcotic symptoms such as inebriation, fatigue, sleepiness, vertigo, tin nitus, nausea, vomiting, and headache. If exposure is prolonged, muscular twitching, convulsions, paralysis, and loss of conscious ness may result. With very large doses, unconsciousness, con vulsions, and death due to respiratory paralysis may occur rapidly. The more typical industrial benzene poisoning is chronic, and is a complex hematologic syndrome characterized by anemia, pur pura, and granulocytopenia. The associated subjective complaints are fatigue, somnolence, headache, vertigo, general debility, and gastro-intestinal disturbances. The blood picture may be variable. A drop in white cell count (especially involving polynuclears) below 5000 to 5500 is usually considered a sign of incipient poi soning. Anemia and corresponding change in hemoglobin usually occur after toxic effects on white blood cells become manifest. Leucocytosis, eosinophilia, and polycythemia are occasionally observed. The urine may contain albumin, casts, and bile pigments. In the proper placement of personnel, juvenile and pregnant workers and those suffering from chlorosis, tuberculosis, organic heart disease, hemorrhagic diathesis, and anemia should ordi narily be excluded from positions entailing a hazardous exposure. Medical Control,--Occupational examinations of exposed em ployees, including blood studies, should be made at intervals of approximately one month, gauging the frequency to severity of exposure. The ratio of inorganic to total sulfates should be deter mined, a reduction of which will indicate the existence of ex posure to benzene.52 In case, upon repeated examination, the percentage of organic sulfate is 30 per cent or more, the concen-  ST 0853045 156 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY tration of benzene in the air of such operations should be deter mined and reduced by proper engineering methods.51 Carbon Monoxide Poisoning Carbon monoxide poisoning may occur in a great number of industrial operations.5* The gas, CO, is formed by the incomplete combustion of organic materials. Its action on the body is related to its affinity for hemoglobin which is 300 times that of oxygen. When inhaled it forms carbon monoxide-hemoglobin, and thus causes anoxemia in proportion to the amount of carbon monoxidehemoglobin in the circulation. Carbon monoxide poisoning is usually acute. Whether or not chronic carbon monoxide poisoning exists as an entity is controversial and seems largely dependent on the interpretation of the word "chronic." It appears that con tinued exposure to moderately toxic concentrations will result in disturbances of the circulatory and nervous system. Symptoms.--Blood saturation up to 15 per cent HbCO rarely produces symptoms, but when the blood saturation is from 16 to 20 per cent, tightness across the forehead, possibly slight headache, and dilation of cutaneous blood vessels are observed. When the blood saturation is SO to 40 per cent, the common symp toms are severe headache, weakness, dizziness, dimness of vision, nausea and vomiting, and collapse. Coma with intermittent con vulsions, depressed heart action, and possibly death are symp toms occurring with HbCO concentrations of 60 to 70 per cent. With exercise, latent symptoms often become manifest and exist ing symptoms are aggravated. On exposure to high concentra tions, the victim may notice few, if any, symptoms, yet he may without warning become unconscious and die without regaining consciousness. Treatment.--The treatment of carbon monoxide poisoning should always be carried out by a qualified physician, although first aid must be given pending his arrival. In summarizing expe rience with the treatment of carbon monoxide poisoning, the fol lowing procedure, outlined by Sayers,5S'54 is recommended: 1. The victim should fie removed to fresh air as soon as possible. 2. If breathing has stopped, is weak and intermittent, or present in but occasional gasps, artificial respiration by the Schafer method should be given persistently until normal breathing is resumed or until after the heart has stopped. 3. Pure oxygen or a mixture of 5 per cent carbon dioxide and 95 per cent oxygen should be administered using an inhaler, beginning as soon bb possible and continuing for at least 20 minutes in mild ST0853046 THE PROBLEM OF OCCUPATIONAL DISEASE 157 eaaea and as long as 8 hours, if naeMagry, In eevare eases if the patient does not regain consciousness* Th* administration of oxy gen or of the mixture of carbon dioxide and oxygen when given immediately will greatly lessen the number and severity of the symptoms from carbon monoxide poisoning and will decrease the possibility of serious after-effects, 4. Circulation should be aided by rubbing the extremities of the patient and keeping the body warm with blankets, hot-water bottles, hot bricks, or other devices, care being taken that these objects have been wrapped or do not come in contact with the body and cause burns. 5. The patient should be kept at rest, lying down to avoid any strain on the heart. Later he should be treated as a convalescent and should be given plenty of time to rest and recuperate. Exercise was at one time recommended; however, the procedure is haz ardous, as the patient quite often loses consciousness, and in some cases death occurs. CONCLUSION Occupational disease legislation hps been discussed and cer tain occupational diseases have been briefly described. It is apparent that in the practice of industrial medicine, many ques tions of compensation arise. It is for this reason that the indus trial physician should have a thorough knowledge of the occupational disease laws applying to the workers for whom he is responsible. Many of the questions that arise in connection with such compensation are medical in nature and demand med ical solutions. As more and more handicapped workers must be taken into industry, deficiencies in present compensation laws become ap parent Legislation amending certain of the laws is indicated in many instances, and, in others, enlightened administration of the law is needed, particularly as related to waivers and secondinjury provisions. In his daily practice, the industrial physician should secure accurate and complete occupational and other histories, perform thorough physical examinations, and, in the instance of a claim, submit his impartial report promptly to the administrator of compensation. The physician has a major role to play, not only in the treat ment but also in the control and prevention of disease in in dustry. BIBLIOGRAPHY L Sappington, C. 0.: Medicolegal Trends: Occupational Diseases. Indust. Med., 7:331 (June) 1938. 2. Dodd, W. F.: Administration of Workmen's Compensation. Common wealth Fund, New York, 1936. ST0853047 158 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY 8. Dawson, Marshall: Problems of Workmen's Compensation Administra tion (in the United States and Canada). U. S. Bureau of Labor Statistica Bull. No. 672. Government Printing Office, Washington, D. C., 1940. 4. Occupational Diseases. In Occupation and Health. 2 vole. International Labor Office, Geneva, 1980-34. VoL II, p. 372. 5. Brahdy, L.: Occupational and Compensable Disease. Indust. Med., 11: 148 (April) 1942. 6. Dorsett, J. D.: The Administration of Workmen's Compensation Laws. Casualty and Surety Jour., .*58 (November) 1942. 7. Sharkey, C. F.: Principal Features of Workmen's Compensation Laws as of July 1, 1940. Appendix, Bull. No. 672, cited in reference . 8. Newquist; M. N.: Medical Service in Industry and Workmen's Com pensation Laws. American College of Surgeons, Chicago, 1988. P. 53. 9. U. S. Department of Labor, Division of Labor Standards: National Sili cosis Conference. Report on Economic, Legal, and Insurance Phases. Bull. No. 21, Part 3. Government Printing Office, Washington, D. C., 1938. 10. Kessler, H. H.: Accidental Injuries: The Medico-legal Aspects of Work men's Compensation and Public Liability. Lea and Febiger, Phila delphia, 1941. P. 766. 11. Dublin, L. I., and Vane, R. J.: Occupation Hazards and Diagnostic Signs. Division of Labor Standards Bull. No. 41. Government Printing Office, Washington, D. C., 1942 (revised). P. 51. 12. Cunningham, J. G.: The Health of the Worker in Industry in Wartime. Canad. Pub. Health Jour., .*562 (November) 1941. 13. Hussey, Raymond: Workmen's Compensation and Medicine. Med. Clinics North America, 6:1035 (July) 1942. 14. McDonald, J. M.: Metallic Poisons. Indust. Med., 10:447 (October) 1941. 15. American Public Health Association: Lead Poisoning--The Recognition of Hazardous Industrial Lead Exposure. First section of a report pre pared by the Committee on Lead Poisoning, Industrial Hygiene Sec tion. 1942. 16. Mayers, M. R.: Prevention of Lead Poisoning. Indust. Bull. (New York), 1:286 (August) 1942. 17. Dreeasen, W. C., Edwards, T. I., Reinhart, W. H., Page, R. T., Webster, S. H., Armstrong, D. W., and Sayers, R. R.: The Control of the Lead Hazard in the Storage Battery Industry. U. S. Pub. Health Bull. No. 262. Government Printing Office, Washington, D. C., 1941. 18. Aub, J. C., Fairhall, L. T., Minot, A. S., and Reznikoff, P.: Lead Poison ing. Williams and Wilkins Co., Baltimore, 1926. 19. Collier, H. E.: Outlines of Industrial Medical Practice. Williams and Wilkins Co., Baltimore, 1941. P. 258. 20. Drinker, P., and Hatch, T.: Industrial Dust. McGraw-Hill Book Co., New York, 1936. P. 75. 21. Kober, G. M., and HayhuTst, E. R.: Industrial Health. Blakiston's Son and Co., Philadelphia, 1924. P. 331. 22. Drinker, P.: Certain Aspects of the Problem of Zinc Toxicity. Jour. Ind. Hyg., 4:177 (August) 1922. 23. Sturgis, C. C., Drinker, P., and Thomson, R. M.: Metal Fume Fever. I. Clinical Observation on the Effect of the Experimental Inhalation of Zinc Oxide by Two Apparently Normal Persons. Jour. Ind. Hyg,, 9: 88 (March) 1927. ST 0853048 THE PROBLEM OF OCCUPATIONAL DISEASE 159 24. Sayers, R. R.: Metal Fume Fever and IU Prevention. U. S. Pub. Health Rep., 55:1080 (July 1) 1988. Reprint No. 1958. 25. Turner, J. A., and Thompson, L. R.: Health Haaards of Brass Foundries. U. S. Pub. Health BulL No. 157. Government Printing Office, Wash- ington, D. C., 1926. P. 24. 26. National Institute of Health, Division of Industrial Hygiene: Cadmium Poisoning. U. S. Pub. Health Rep., 57:601 (April 24) 1942. Reprint No. 2371. 27. Johnstone, R. T.: Occupational Diseases. W. B. Saunders Co., Philadel phia, 1941. 28. Flinn, R. H., Neal, P. A., and Fulton, W. B.: Industrial Manganese Poisoning. Jour. Ind. Hyg., 25:374 (October) 1941. 29. U. S. Bureau of Mines: Minerals Yearbook. Government Printing Office, Washington, D. C., 1940. 30. Mercurialism in the Felt Hat Industry. Current Comment. Jour. Am. Med. Assn., 118:54 (January 8) 1942. 31. Neal, P. A.: Mercury Poisoning from the Public Health Viewpoint. Am. Jour. Pub. Health, 25:907 (August) 1938. 32. Goodman, Louis, and Gilman, Alfred: The Pharmacological Basis of Therapeutics. Macmillan Co., New York, 1941. P. 732. 33. Hope, E. W., Hanna, W., and Stallybrass, C. O.: Industrial Hygiene and Medicine. Bailli&re, Tindall, and Cox, London, 1923. P. 128. 34. Hamilton, Alice: Industrial Toxicology. Harper Brothers, New York, 1934. P. 73. 35. Neal, P. A., Flinn, R. H., Edwards, T. I., Reinhart, W. H., Hough, J. W., DallaValle, J. M., Goldman, F. H., Armstrong, D. W., Gray, A. S., Coleman, A. L., and Postman, B. F.: Mercurialism and Its Control in the Felt Hat Industry. U. S. Pub. Health Bull. No. 263. Government Printing Office, Washington, D. C., 1941. P. 44. 36. Legge, Sir Thomas (edited by S. A. Henry): Industrial Maladies. Ox ford University Press, London, 1934, P. 77. 37. U. S. Department of Commerce, National Bureau of Standards: Safe Handling of Radioactive Luminous Compound. National Bureau of Standards Handbook H27. Government Printing Office, Washington, D. C., 1941. 88. Curtiss, L. F.: Prevention and Control of Hazards in Radium Dial Painting. Jour. Ind. Hyg. 24:131 (June) 1942. 39. Evans, R. D., and Aub, J. C.: Recent Progress in the Study of Radium Poisoning. Occasional Publications of the A.A.A.S., 4:227 (June) 1937. Reprint No. 415, Cancer Commission of Harvard University. 40. Martland, H. S.: Radium Poisoning. In Practitioners Library of Medi cine and Surgery, Supplement. D. Appleton-Century Co., New York, 1938. P. 208. 41. Reznikoff, Paul: Poisoning from Lead and Other Heavy Metals. In Industrial Hygiene, edited by Lanza and Goldberg. Oxford University Press, New York, 1939. P. 443. 42. Pneumoconiosis. American Public Health Association Year Book, 193233. P. 100. Supplement to Am. Jour. Pub. Health, 25 (June) 1933. 43. Gardner, L. U.: The Pneumoconioses. Med. Clinics North America, 6: 1239 (July) 1942. 44. Pneumoconiosis. American Public Health Association Year Book, 1941- ... TT 42' 117- Supplement to Am. Jour. Pub. Health, 52: (March) 1942. 45. U. S. Department of Labor, Division of Labor Standards: Summary Re- S T 0 8 53049 160 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY ports of the Nations] Silicosis Conference. Boll. No. IS. Government Printing Office, Washington, D. C., 1988. 46. U. S. Department of Labor, Division of Labor Standards: Chart--Work men's Compensation--Silicosis. Summary of Statutory Provisions as of January 1,1942. 47. Dreeasen, W. C., Page, R. T., Hough, J. W., Trasko, V. M., Jones, J. L., and Franks, R. W.: Health and Working Environment of Nonferrous Metal Mine Workers. U. S. Pub. Health Bull. No. 277. Government Printing Office, Washington, D. C., 1942. 48. Irvine, L. G., and Steuart, W.: The Radiology and Symptomatology of Silicosis. Silicosis--Records of the International Conference, Johan nesburg, August 13-27,1930. International Labor Office, Geneva, 1930. 49. Hart, P. D'Arcy, and Aslett, E. A.: Chronic Pulmonary Disease in South Wales Coal Miners. 1. Medical Studies. A. Report by the Committee on Industrial Pulmonary Disease. B. Medical Survey. Medical Re search Council, Report No. 243. H. M. Stationery Office, London, 1942. 50. Pendergrass, E. P.: Roentgen-Ray Diagnosis. In Silicosis and Asbestosis, edited by Lanza. Oxford University Press, New York, 1938. 51. National Institute of Health, Division of Industrial Hygiene: Benzene (Benzol), Its Toxicity and Potential Dangers. U. S. Pub. Health Rep. 56:519 (March 14) 1941. Reprint No. 2248. 52. Yant, W. P., Schrenk, H. H., Sayers, R. R., Horvath, A. A., and Rein hart, W. A.: Urine Sulfate Determinations as a Measure of Benzene Exposure. Jour. Ind. Hyg., 18:67 (January) 1936. 58. National Institute of Health, Division of Industrial Hygiene: Carbon Monoxide, Its Toxicity and Potential Dangers. U. S. Pub. Health Rep., 56:421 (March 7) 1942. Reprint No. 2242. 54. Sayers, R. R., and Davenport, S. J.: Review of Carbon Monoxide Poison ing. U. S. Pub. Health Bull. No. 195. Government Printing Office, Washington, D. C., 1986 (revised). ST 0853050 CHAPTER 11 ENGINEERING CONTROL OP AIR CONTAMINATION OF THE WORKING ENVIRONMENT Allen D. Brandt, D.Sc. Wherever materials are being processed, whether changing the physical or chemical state or the physical size, some of the mate rials in form of dusts, fumes, mists, gases, or vapors will escape into the air:of the workroom with the exception of those rare cases where tfifr processing is done in an air-tight system. Even under these conditions, some air contamination will result when the various parts of the system are serviced or repaired. From the point of view of industrial hygiene, these contaminants may be differentiated as follows:1 Dusts: Solid particle* generated by handling, crashing, grinding, rapid impact, detonation and decrepitation of organic or inorganic materials such as rock, ore, metal, coal, wood, grain, etc. Dusts do not tend to floc culate except under electrostatic forces; they do not diffuse in air but settle under the influence of gravity. Fumes: Solid particles generated by condensation from the gaseous state, generally after volatilization from molten metals, etc., and often ac companied by a chemical reaction such as oxidation. Fumes flocculate and sometimes coalesce. Mists: Suspended liquid droplets generated by condensation from the gaseous to the liquid state or by breaking up a liquid into a dispersed state, such as by splashing, foaming, and atomizing. Gases: Normally formless fluids which occupy the space of enclosure and which can be changed to the liquid or solid state only by the combined effect of increased pressure and decreased temperature. Gases diffuse. Vapors; The gaseous form of substances which are normally in the solid or liquid state and which can be changed to these states either by in creasing the pressure or decreasing the temperature alone. Vapors diffuse. Some of the air contaminants such as benzene,2 lead,8 mer cury,4 and silica* are very harmful to exposed workers while others such as acetone, coal dust, calcium carbonate, and mag nesium oxide are relatively nontoxic. However, even for those relatively harmless contaminants, which are classified as nui sances, there is a degree of atmospheric contamination which should not be exceeded lest the health of the exposed workers be affected adversely. To insure the utmost efficiency from all work- 198 S T 0 8 5 305 I f#7. * ^ ENGINEERING CONTROL OF AIR CONTAMINATION 199 ers, it is necessary that the degree of contamination of the in spired air be maintained at a value which is known to present no harmful effects or in the absence of specific knowledge on the toxicity of the contaminant, the atmospheric concentration should be kept as low as is feasible with good engineering prac tice. GENERAL CONSIDERATIONS Control of atmospheric contamination is primarily a respon sibility of the industrial hygiene engineer and may be accom plished by means of one, or more than one, of the following meth ods: (1) control at point of generation or dissemination, (2) dilution with uncontaminated air, (3) isolation of those processes which produce contamination, (4) substitution of less toxic ma terials, (5) reduction of the concentration of contaminant in the inspired air by means of respiratory protective devices, and (6) maintenance, housekeeping, and the education of the worker. Very rarely do we encounter an operation where toxic mate rials are processed--and practically all air contaminants are toxic if the concentration is high enough--that may be controlled efficiently by only one of the above methods; a combination of several methods is usually most effective and practicable. Control at Point of Generation or Dissemination The methods commonly used to control atmospheric contami nants at their point of origin are (1) local exhaust ventilation, (2) wet methods, and (3) good housekeeping. Local Exhaust Ventilation.--Of the various methods of con trol of air contamination, this is the most important single method. Few are the industries where local exhaust ventilation is not employed in one form or another and in some large indus tries the complete local exhaust ventilation system is almost as extensive as the production equipment. In new buildings the ventilation system should form part of the structure and equip ment, if the best results are to be accomplished. If the ventilation system is designed and installed after the building and equipment installation have been completed with little or no thought having been given to a ventilating system, the ventilating engineer is handicapped tremendously and at best cannot do a good job. Consideration must be given to the location of those operations which liberate toxic materials into the atmosphere as regards, among other things, doors and windows, other. similar equip ment, and densely populated areas. $ T 0853052 200 PREVENTION AND CONTROL OP DISEASE IN INDUSTRY A local exhaust ventilation system consists essentially of four parts, as follows: (1) hoods or enclosures, (2) air ducts, (8) collector, and (4) exhauster. 1. Hoods or Enclosures.--Of the four parts, the hoods or en closures are probably the most vital. The purpose of the hood is to enclose the contaminant or to produce air movement at the source of contaminant production of suitable magnitude and act ing in the proper direction to capture the escaping contaminants and convey them into the exhaust system. A thorough knowledge of the laws of air flow into suction openings and of the way in which the various contaminants react is essential to the design of an efficient hood. A hood is efficient when it collects effectively the contaminant with a minimum of air removal, and is of proper design when it is efficient and does not hinder the operation of the tool or machine. While the design of a good hood involves many considerations, the following specific rules should be kept in mind at all times: (1) Enclose the source of contamination as much as possible, (2) locate the hood in line with the natural direction of move ment of the contaminant or contaminated air, (3) locate hoods, which do not enclose source of contamination, as close to the source as possible, and (4) for hoods which must be located at some distance from the source of contamination, use as large hood openings as practicable and flanges, if possible. The velocity of air movement at the source of contamination -necessary to capture the contaminant may vary from as little as 75 to 100 feet per minute (f.p.m.), a velocity sufficient to over come normal air currents at the surface of an evaporating liquid, to as high as 2000 or more f.p.m. at a'high velocity dust produc ing machine such as a "jack hammer." Table 1 will serve as a guide in the selection of the proper minimum control velocity for any operation, and shows that the minimum control velocities for the great majority of operations are in the range of 75 to 300 f.p.m. Even though these velocities will do a satisfactory job if the operation is carried out as intended, and if other adverse influences are prevented, it is very easy to create conditions which will render the local exhaust system ineffective. For in stance, any unusual motion in the area of the source of contam ination will interfere with the control air currents created by the hood and render the control ineffective. Also opening doors or windows near a local exhaust hood on a moderately windy day will impair the effectiveness of the control. To obtain a clearer ( ST0853053 ENGINEERING CONTROL OP AIR CONTAMINATION 201 picture of the importance of this particular item, namely, that the operation be carried out as intended when the hood was `designed and that all adverse influences be avoided, it is only nec essary to reflect upon three facts: (1) most minimum control velocities are 800 f.p.m. or less, (2) the average person walks at the rate of about S50 f.p.m., and (S) the velocity of air move ment through open doors and windows on a moderately windy day is in the order of 1000 f.pjn. Hence little disturbance is required to upset the control velocity pattern at most operations "Sf? Table 1.--Minimum Aik Velocities Recommended fob the Capture of Dusts, Fumes, Mists, Gases and Vapors Released in Certain Manu facturing Processes Conditions of Generation of Contaminant Recommended Minimum Velocity (Feet per Minute) Examples of Processes Released 'without notice able air movement......... Released with low air ve locity ............................... Active generation............... Released with great force.. 75-100 100-200 200-500 500-2000 and higher Evaporation or escape of liquids from open vessels such as degreasing, pick ling, or plating tanks: manual handling of small amounts of dry materials. Spray paint booths, cab inets and rooms: dump ing dry materials into hoppers; welding. Some spray painting op erations m small booths and with high pressures; active barm filling; load ing conveyors. Grinding; abrasive blast ing. with the result that some of the contaminant will escape into the general room air. This conclusion is most important since it is not uncommon to find that open doors and windows near opera tions provided with local exhaust ventilation render such control measures essentially useless. The fault lies' in the design of the plant layout; operations of this nature should not he located near doors and windows. However, with construction completed and the plant in operation, the only solution is in the education of the worker to open doors and windows judiciously. In small rooms or bays where all operations must of necessity be located ST 0853054 202 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY near the doors or windows, the education of the worker in the proper operation of the process and the wise regulation of doors and windows is the only solution. To obtain the velocities cited in Table 1, it is necessary to know what quantity of air mast be exhausted through the hood. Here again the individual circumstances must be taken into con sideration, but very frequently the following equations will suf fice for the four major types of hood. (1) An unrestricted hood at a short distance from the source of con tamination.* Q = V (10xI+A) where Q = quantity of air to be exhausted in cubic feet per minute, V = recommended minimum control velocity in feet per minute (selected from Table 1), x = distance in feet from face of hood to source of contamination, and, A = area of hood opening in square feet. This equation is accurate only for unobstructed flow into an open hood. If the hood lies on a flat surface of large dimensions so that air flow is cut off from one side of the hood, the value of Q may be decreased as much as one-third for unusually favorable conditions; whereas, if there is an obstruction or some other interference between the hood opening and the source of con tamination, the value of Q must be increased accordingly. _ (2) A hood which partially or wholly encloses the source of contamina tion.* Q = VA where Q, V and A are the same as above except that A is the total area of all openings in the enclosing hood. (3) Canopy hoods located above tanks or tables.* Q = 1.4 VPD where Q and V are the same as above, P = the perimeter of the hood in feet, and, D = the distance in feet from the hood face to the table or tank top. (4) Slot type hoods located along the upper edges of tanks. (a) Pickling and electroplating tanks.7. * Q = 50 LW (b) Degreasing tanks. Q = 120 (L+W) where Q is the same as above, L = the length of the tank in feet, and, W = the width of the tank in feet c S* t' :' % ' | jefv , ^ y, % '< ST0853055 ENGINEERING CONTROL OP AIR CONTAMINATION 203 It should be borne in mind at all times that the quantity of air removed by a local exhaust system from a room or building must be permitted to enter the building at some appropriate point or points. This is sometimes overlooked with the result that a negative pressure exists in the building or room and the exhaust ventilation control measures do not operate satisfactorily. 2. Air Ducts.--The air ducts or piping serve to connect the various hoods to the collector and exhauster, and thus convey the contaminated air from the hoods to the Collector or to the outside. The ductwork is usually constructed of light gage sheet steel, either unpainted, black, stainless, or galvanized. For some corrosive gases or abrasive dusts, the ducts should be lined with special protective coatings such as asphaltum, or special alloy sheets should be used. The thickness of the material employed in ductwork of different sizes is usually as follows: Diameter {Inches) Gage 8 and less...................................................................... 24 8.1 to 18 ....................................................................... 22 18.1 to 30 ..................................................................... 20 Over 30.......................................................................... 18 Square or rectangular ductwork should be made of material about two gages heavier than round ducts of corresponding sizes. The duct size for the various branches and main lines is gov erned by the amount of air which must be moved to collect the contaminant effectively as given previously, and the velocity nec essary to convey the contaminant which is being removed. The recommended minimum conveying velocities vary from as little as 2000 f.p.m. for vapors, gases, light fumes, and very light dusts to as high as 5000 f.p.m. or more for large particles of heavy materials, such as lead dust, or the large stone dust produced by some operations. While any piping system can be made to work after a fashion with suitable dampers and a very powerful exhauster; such a system is not economical to install nor to operate. If the system is to be effective and at the same time economical, it is necessary that it be designed completely by a capable engineer. Blast gates or dampers are to be avoided, if possible, because they get out of adjustment very readily and unbalance the entire system. Exces sive velocities in the various ducts are to be avoided also because the power consumption increases out of proportion to the velocity increase. To avoid deposition of the solid materials being con- ST 0853056 204 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY veyed, to avoid unnecessary abrasion, and to keep power con sumption low, it is essential that all connecting fittings such as branch connections to main ducts, duct to collector, duct to fan, and branch pipe to hood be streamlined. This will serve to reduce the turbulence and shock losses common to poorly designed ex haust systems. The contaminated air should be discharged to the outside and not recirculated except in very rare instances. The discharge stacks should be located at a point which will prevent the con taminated air. from reentering any occupied buildings. Where the heat loss is a serious consideration owing to the large amount of air removed from the building in cold climates, some air may be recirculated if., the contaminant is removed effectively from the return air by a suitable collector. The efficiency of the collector should be checked routinely to guard against a breakdown which would permit abnormal amounts of contaminant to be returned to the building. 3. Collector.--Not all local exhaust ventilation systems re quire collectors. They are used in those instances where the col lected material is valuable, abrasive, corrosive, or where the unfiltered air would produce a nuisance or health hazard in the surrounding community. Some of the types of collectors commonly employed are set tling chambers, cyclones, cloth filters, oil and water air-washers, electrostatic precipitators, centrifugal separators, and fan-type collectors.10 The selection of the proper collector depends upon many considerations, of which the following are most important: (1) type of contaminant, that is, whether dust, gas, or mist; (2) efficiency of collection required; (3) cost of operation and main tenance; (4) cost of installation; (5) amount of recirculation, if any; and (6) nature of contaminant, that is, whether corrosive gas, explosive dust or other type of substance. 4. Exhauster.--The fan or exhauster serves to move the air through the hoods, ductwork, and collector. In addition to fans, air-, steam-, or water-operated ejectors are employed on some local exhaust ventilation systems, particularly in the explosives manufacturing industries. For low velocity exhaust systems, pro peller-type fans are satisfactory, while for the more common high resistance systems, centrifugal-type fans are required. The trend at present is toward the low velocity systems wherever feasible. In the selection of the best type and model of exhauster, the ST 0853057 ENGINEERING CONTROL OP AIR CONTAMINATION 205 following items must be considered in addition to any special items presented by the nature of the system: (1) type of contam inant to be handled, that is, whether corrosive, abrasive, or explosive; (2) resistance of the system; (3) volume of air to be handled; (4) whether or not collector is to be used in the system; (5) cost of operation and maintenance; (6) cost of installation; and (7) whether in operation 24 hours a day, one eight-hour shift per day, or intermittently. It is advisable in all cases to locate the exhauster downstream of the collector, particularly if abrasive dust, explosive dust, or corrosive gases are handled. Wet Methods.--The use of water or other suitable liquid at operations producing dust or fumes, or both, will generally allay the particulate matter satisfactorily. However, this method of control is necessarily limited to a small number of different oper ations such as grinding, drilling, and sweeping. Also the method has one inherent weakness in that the particulate matter may not be wetted successfully or that it may be readily redispersed into the atmosphere as the collecting liquid dries. When used properly, however, it is a very practical method of control and produces worthwhile results. Good Housekeeping.--Dust and other particulate matter in the air of industries is settling out continuously at a rate depend ent upon the physical characteristics of the material and the air currents. As a result, the dusts or fumes are depositing constantly on the floor; ledges; stationary machinery; workers' arms, faces, and clothing; and other objects. Vibration, shock, or unusual air currents will tend to dislodge and redisperse some of this mate rial into the air, thereby increasing the workers' exposure need lessly. Also the skin contact of the workers is increased. All of this may be avoided by good housekeeping. The floors, ledges, overhead structures, stationary machines, and other objects should be cleaned frequently and routinely. This should be done by means of suitable vacuum systems. Blowing the dust off of machines and ledges is taboo since it is merely redispersed into the air; in other words, the atmospheric concentration is in creased since more dust is kept in th'e air than if it were per mitted to settle out. Dry sweeping also is not recommended; it should be done wet. As a general rule, more good can be accom plished per dollar invested by good housekeeping than by any other single method. ST 0853058 206 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY General or Dilution Ventilation The object of general or dilution ventilation is to dilute the contaminated air of a workroom with a sufficient quantity of clean air to reduce the atmospheric concentration of the con taminant to a safe value. There is a certain amount of dilution taking place at all times in nearly all places. The air movement or ventilation may be natural as through open doors, windows, roof stacks, and chimneys, or it may be artificial or mechanical, if produced by fans or ejectors. Dilution ventilation as a rule provides adequate control only if the degree of air contamination is not excessive, and particularly if the contaminant is released at a substantial distance from the breathing zone so that the contaminated air can be diluted satis factorily before it is inhaled. For specific operations and particu larly if the operator is stationed nearby, local exhaust ventila tion is more practical and dilution ventilation should not be used. The amount of clean air which must be supplied in a given area for suitable dilution of the contaminated air is determined by the following equation:11 where Q = the rate of ventilation in cubic feet per minute, X = the quantity of toxic substance released in cubic feet per minute, and, m = the maximum allowable concentration of the contaminant per cubic foot of air. This equation assumes that the contaminated air is diluted completely before it enters the respiratory zone of any worker. Where workers are close to the source of contamination, the rate must be increased considerably, and the clean air should be sup plied near the source of contamination. For evaporating liquids the value of X in the above equation may be obtained directly from the volume of the liquid evaporated since one gram molecular weight of the vapor occupies approxi mately 0.8 cubic foot at normal temperature and pressure. Even though dilution ventilation is limited in scope, as indi cated above, much may be accomplished by the judicious use of doors, windows, chimneys, roof stacks, roof ventilators, fans, and ejectors. Where mechanical means are employed to obtain dilution ventilation, the following factors should .be borne in mind: (1) location of air mover with respect to workers and ST0853059 ENGINEERING CONTROL OF AIR CONTAMINATION 207 source of contamination, (2) natural drafts, (3) convection cur rents, (4) temperature of entering: air, and (5) specific gravity of contaminant. Isolation In many instances, those operations or machines which lib erate large amounts of contaminants require the immediate at tention of only a few workers. Because of lack of foresight in the plant layout, however, large groups of workers are frequently located in proximity to these operations. A practical and very satisfactory method of controlling hazards of this nature is to isolate the offending operations or machines, thereby limiting the exposure to a few workers who may be protected by suitable respirators, if necessary. This method is particularly useful in those instances where the process does not lend itself readily to one of the other measures of control. Substitution The substitution of a nontoxic for a highly toxic material is one of the most effective methods of controlling the atmospheric health hazard. This method is, however, very limited in applica tion. Examples of its application are the substitution of steel shot for silica sand in abrasive blasting, and the replacement of the very toxic benzene in the solvent industry with the less toxic toluol or the petroleum naphthas. Sometimes the substitution of a less toxic material results in an inferior product. In such in stances, one of the other methods of control should be empioyed rather than substitution. Respiratory Protective Devices While practically all operations may be controlled by one of the foregoing methods, it is not infrequent that the cost of con trol by one of these methods is not justified, particularly if the exposure is intermittent and limited to a small number of work ers. In such cases, the workers may be protected by wearing ap propriate respirators. The respirators commonly used as routine measures in indus try may be divided into two major classifications: (1) air-puri fying respirators, and (2) supplied-air respirators.12 See Table 2 for respirator classification. In no instance should respirators be employed as a substitute for other more satisfactory methods of control of air contamina-