Document ga4DD6R9NjVm2En8KE7qaGbXG

3PT) ,Pebruary 23 1944 Mr. Iran Sabourin ALdred Building Montreal, P* Q* Canada Dear Mr. Satwurln* While tha aattar la atlll fresh la ay mind Z aa writing you at length on ay lapresslonof tha situation oa Asbestosis In Quebec la #o far aa It involves relationships betveen the producers, the nodical profession and tha Compensation Commission* One conference with Mr. Sharp, Or* Vidal and Mr* Oleic gave aa a aueh clearer picture than Z had gotten previously* Before doing so Z offer a fee consents on autopsy aaterial. Z aa enclosing ay report on the lung tissues of Phlleaon Tardlf* Of necessity the conclusions are not too satisfying aa they are baaed only upon examination of two blocks of tissue, ap proximately 2x4 eentlaeters in disaster without even aa indication of the parts of tha lung froa which they were taken* However, they like the , . aaterial froa the two previous eases, do deaonatrate that the Yhetford <: operations produce Halted amounts of indisputable Asbestosis* In the presence of advanced tuberculosis this lssfeoaeured and not likely to be identified exeept on aleroseople exaalnatlon of pulmonary tlssuo* X-ray during life will not shoe it* Today Z have also examined in gross the sagltal section through the entire right lung of Majorlqus Perron which we collected yesterday froa the toxleologleal laboratory in Montreal* This is a a more satisfactory apeelaen with which to work* Zt likewise shows a blastion pf widespread chronic tuberculosis upon a background which will probably prove on alcroccoplc exaalnatlon to be minimal Aabeatosla* Sections will be prepared aa soon aa possible for aleroseople exsatnation* xan -gghlfl 4yaftm a Jalf iuaaarv oftha occupationaland eiiniSi history including* How long eaployed, character and date of first ayaptons, date of quitting work, whether Eoch's bacillus was found la sputua and date of death* Z neglected to copy this information from your record* this autopsy material on fatal eases and tha X-rays that are now reaching the Coaaisslca are bouctf to create in their nit*a ! the impression that tuberculosis la an all too coapUaationof Axbe*tosia# If I were in their position with ay experience limited to evidence of this kind Z would find it difficult to resist the conclusion that there la causal relationship between even alight amounts of s Mr. lean Babourln (2) February 23, 1944 asbeatosis and tuberculosis of the lungs. Z bar* told you ** I told Mr. Sharp, yesterday that I did not agree with this Conclusion but I doubt vhathcr ha or Dr. Vidal will be persuaded whan thay aaa a succession of caaas Ilka those which ara now passing before thaw. Thay wust ba aada to realise that thaaa eaaaa ara tha axcaptlona rathar than the rule and that thara is a great majority of cwployeea in tha aabaatoa Industry who are free from tuberculosis* Z would therefore urge that laredlate steps ba taken t _ : surra:- awary employee it) the asbestos industry In Quebec so that tha iiSfeHaAFS" iVatlatlea can ba essaablad. L)r. SxAVeKSfonTs X-ray files airs CaEan on tha wan at Asbestos will prowlds you with notarial for a prelialnary report. Coupled with this thaerae eight ba an analysis of aartal data contr* c. tha total death rata from tuberculosl* Lit TbStlurSlSS^'Xjbd'stoT with thhaat in othcF'lrgastrial conmualtlea"of tha Provided.' Xt would be' still'morV'cbnTineirii If you could show the Separate rates of._ and females unless the nusber of tha latter employed in the -^asbestos slants constitutes an appreciable proportion of tha feeala popu. IstlonV Finally tha age distribution of deaths froe tuberculosis in > those employed in tha USastos plants es contrasted with that in other occupations would help in determining whether the occupational factor taj contributory* *y own obserrations elsewhere and your intimation that the rate for tuberculosis was higher in St. Hyacinth* than in Thetford and- / or Asbestos make me confident that the .companies would acquire Information of greatest serriee to themaelves by such a survey and *n*lysls* Zf asbestosls specifically is predisposing to tuberculosis in the ease sense as silieosls does the effeet should be just as apparent In forth Carolina and Pennsylvania as it seems to be in Quebec or England But the films of eaployed asbestos workers in the States show a very low incidence of associated tuberculosis* Zt is ay firm belief that in Quebec and England, factors outside the occupation are responsible. A Z sensed the situation in Montreal yesterday the V asbestos Industry will have to produce evidence to prove this point end * 'tart on it innedietely or the industrial eoanisslon will become ini'^Jetrreuaths*lngly convinced that our position la biased and not founded upon . Furthermore the industry would undoubtedly profit tar __ v undertaking a general program of community control of tuberculosis* By --^instituting case'TtfiJIngTBiSKlnery hot ehly 'among mploye^s but among tha members of their families, the open eases of tuberculosis would bo discovered and the sourees'of spread of the infection could be removed* Ur. Ivan Sahourin O) February 23, 1944 One of the iron alaIn* companies whom we serve has such a program with a public health nurse, a program for tuberculin testing of sehool children and follow up of tha contacts of every mown ease of opart tuberculosis. Tha program haa paid dlaidanda by practically sllminating v tuberculosis with resultant lowering of compensation costs and tha good ** will of tha employees la unmeasurable. The asbestos industry of Quebec has a serioui problem because Its labor force Is drawn from a population in which the tuberculosis rate Is high but their situation is no worse than that which our other clients attacked successfully In an Iron mining community. Tha aaeond point which la becoming Increasingly appsrent to me Is that the a^bestosls of tha Quebee mines and mills Is quits generally less severe end extensive than tha asbastosls of tha fabricating plants of the States. Comparison of the X-ray findings In the two groups r&veals very few cases with typieal patterns among Thetford or Asbestos mill men. 6oae asbastosls la unquestionably produced for we have microscopic sviesnee of It 1st tbe four autopsy casts now available but it is rot adveneeu enough to replace much Of the functional parts of the lungs end thus cause the X-ray anadows that are generally recognised as . charsctsris tic of the ulseass. (Host of us disagree vlth Or. Pendergrass when ho s.ty* In L&nxa's book that there la no characteristic pattern of <bestosls). If my observations ar correct this relatively slight amount of disease should not enus disability for only the framework of tha lunge Is involved leaving most of the parts that carry on the .functions of ... respiration Intact. - But here again the Canadian industry is on the defense against Its medical profession and their representatives o<; the advisory board to the 1no us trial commission. The doctors have seen only their own local manifestations of asbestos!? elthout opportunity to compare It vlth the really savers manifestations that are produced aleewhere. They find the abnormal shadows in tha X-ray films of exposed workman, which they re convinced must ecuse symptoms and disability. They find asbastosls bodies in tha lungs of autopsiad cases associated with Minimal tissue reactions or overwhelming manifestations of concurrent pulmonary in fections and now they are sure of their ground. Xn order to oefend Itself tha Industry la Quebec must have more facts which will require time to collect* analyse and publicise. ; These findings will have to be contrasted with tbcea la the fabricating (plants either in Asbestos or elsewhere. Xn tha elty or Asbestos the v spinning and weaving mill has baaa In operation for only four years which is tha minimum tine to produce much disease in those exposed, but Zinamanaoutehhermyiesatarkeonr . two one nay expect to find evidence of It hare unless Mr. Xven dabourln U) Pebruary 23, 19U As X have told you in conversation, our experimental observations load me to believe that the truo faatard la asbestos plants Is proportional to tho amount of wall, individual, uaerushod flbros la tho Industrial atmosphere. X suspoet that tho roasoa why ono soos little or mo typloal asbostosls In tho alnoo and mills la booauso thoro is probably too llttlo sueh flbro la tho air of thoso plants. Conversely tho roason for tho "typloal* dlsoaso la tho fabricstin* plants is tho foot that tho proeossos thoro opoa tho bundles of asbestos flbro and tsar thorn Into loafthe short enough to bo Inhaled In dangerous quantities. Tho mills sad nines sro dusty but tho dust is largely terpentine with relatively few flbros largo enough to do hara to tho lungs. This dust enters tho lungs shore it produces reaction arounl blood vessels sad other framework structures that ere Just like say other inert dust. Vs sss tbs shadows of such Inert reaetloa manifested in X-ray as an exaggeration of tho normal shadows of blood roseola. This ooadltion it not asbostosls aor necessarily prsasbestotlo say mors than tho identleal ehsages la men working la hard rock mines sro necessarily prealllootle. Xm frss silica Industries regardless of exposure we do not diagnose ellleosls from X-rays until we find the characteristic pattern of modulation! la tho asbestos Industry we should do likevies and refrala from a diagnosis of asbostosls until the X-ray reveals ths sharseterlstlo psttarn of haslness or fine stippled appearance spreading throughout the lower thirds or more of the lung fields. The situation with asbostosls Is oven more difficult than with ailleosls for today the requisite condition of tho dust exposure is not appreciated by tho medical profession. n-ooei44S9 ..... ' ......A Therefore X strongly urge that surveys bo made to coaparo /the relative Quantity and M13U3L ot the dusts in ths mills and the {fabricating plants la order to present proof that in tho first instance \ the persentage of thin flbro of inhalmble dimensions Is insignificant in ^comparison with,tfiy quantity created .in. spinning aad tearing. Xt is going TrW to porsuaainAf^ilelaas of the Importaneo of these factors but similar faotors govern tho reaction to quarts and tho development of elllooslo. Thoso physlesl limitations of stmosphorle dust often determine the outcome in contested esses involving a diagnosis of silicosis aad X for*os that thoy will have equal weight in ssbeetosla. 1 'Sppcvsifdt''j?lah\Ts*."to establish this basis difference so that it will stead j/beyond eoritroffrsy.` Vo have the experimental beekgroundi we now must ` demonwtratb"tl's 'Industrial application, then correlated with the results upon exposed workmen, X feel certain that our position will he SR'--' "J%a*r **r ^a^MMCMlfiiiiaiilttiaiaHWtetf''--- w. *r --v ,,- Mr. Ivan Sabourin (5) February 23, 19U To summarise* Z would make the following recomaendatlona to your ellonta, tho Canadian Asbestos Producer* in order that thay nay dafand theaselvss against a growing coavletloa aaong tha loeal physicians that employment in this Quebec industry is highly dangerous. 1. Correct an erroneous impression of the Industrial Connlssioa that asbettosia is frequently associated with pulmonary tuberculosis. a) Statistical data baaed on 1-ray of all ------^ esployed workmen to indicate the incidence of pulmonary tuberculosis b) Cooperative mortality statistics on --------tuberculosis in Asbestos and Thctford and in other communities of Quoboc indlo*ting the frequency by sex and age. 2. Consider tha possibility of Inaugurating a program ' of tuberculosis ease finding and control in the general populations of Asbestos and Thetford in order to elimi nate oee of nee infection among onpioycas. . 3. Make a detailed comparative study of tha naturt of the.dust in tha fabritating plants and tbs asbestos mines sad mills. Z trust that you will agree with these reeomoendstlons and be willing to. pass them along to your oliaats. lay Z taka this opportunity to thank you for your delightful hospitality while Z was 1m Montreal and thank you for making my visit profitable sad pleasant. fiacercly yours. LOasKH Leroy 0. Cerdner, M. 0. - Director Maximum Use or Manpower .................................................................... 383 Robert H. Fli.vn, M.D. Women in Industry CHAPTER 23 Hugh P. brinton, Ph.D. 395 Absenteeism CHAPTER 24 William M. Gafafer, D.Sc. 420 Index 467 tloptrial inge : up for luty >dic ises ery ob. iisess DUt ire ss. an ch - :al Dd r* 'd >e d d * i , j j PART II PREVENTION AND CONTROL OF 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 compensation amount to from I 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 thinks 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 Stated 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 wartime 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 r of the compensation laws, the provisions common^to these acts' 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,- 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 jurisdictions1 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 which he la practicing should be readily avail able to the industrial physiclanJ^'^feliS^T' . * The discussion in this chapter has been limited to occupational dis- eases. The reader should not overlook compensation aspects of Industrial accidents. - . r. . rut problem of occupational disease x.w I.ist r J ORiautcTios-j in Which Occupationax. Disease Is Compensated and the Name and Address op the Administrative Agency Arkansas ................ ...Workmen's Compensation Commission f Rector Building, Little Rock California................ .. .Division of Industrial Accidents and Safety State Building, San FrancUco >n it Connecticut............. Delaware................. . Hoard of Compensation Commissioners .14 Church Street, Hartford ..Industrial Accident Board o Ninth and Market Streets. Wilmington d District of Columbia -li. C. Workmen's Compensation Act e Hawaii ..................... Seventh and E Streets, N. W,, Washington . l lepartment of Labor and Industrial Relations i Bureau of Workmen's Compensation Honolulu Idaho .......................... ..Industrial Accident Board Boise Illinois ...................... ..Industrial Commission i'll West Wacker Drive, Chicago Imliann .................... ..Industrial Board Kentucky .................. 4(14 State Capitol, Indianapolis ..Workmen's Compensation Board Frankfort Maryland .................. . .State Industrial Accident Commission Kpuitable Building, Baltimore Massachusetts.......... : .1 lepartment of Industrial Accidents Statehouse, Boaton Michigan .................. . . impairment of Labor and Industry 6.'!0 State Office Building, Lansing Minnesota ................ Industrial Commission 1X7 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 New York .................. Wallach Building, Trenton . Department of Labor - Division of Workmen'* Compensation i ! North Carolina .... 80 Centre Street, New York .Industrial Commission Raleigh North Dakota............ .Workmen's Compensation Bureau Bismarck Ohio ........................... .Industrial Commission Pennsylvania .......... . State Office Building, Columbus . Bureau of Workmen's Compensation Harrisburg Puerto Rico................ . Industrial Commission Rhode Island.............. San Juan Department of Labor Division of Workmen's Compensation Providence i i i PREVENTION AND CONTROL OF DISEASE IN INDUSTRY' List of Jurisdiction! in Which Occupational Disease Is Compensated and the Name and Address of the Administrative Agency (CohI.i Utah ....................................... Industrie Comminion State Capitol, Salt Lake City Washington ............................Department of Labor and Industries Olympia \V est 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 oil 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 difficult4 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 comments1 on this point, however, are pertinent: "When physicians differentiate 'ont.) :mn York ue to ever, aced sub'hus. irise it is zard lirly eg-- ker, loyi an sion ms, ary >sis ria ind >ne nd >ns r>n, 8" iia t THE PROBLEM OF OCCUPATIONAL DISEASE 1-135 - t ^ 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 stome 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.'1 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 (.iVJ,-* j*. r, id ' 1 136 PREVENTION AND CONTROL OK DISEASE IN INDUSTRY* ' of coverage referred to above, the laws include such provisions1 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 contrib .:e, the cost of compensation is borne almost entirely hv 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,' "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. v.iS2 - * -1 i-f,r^ja 7 < . V>- -^- ' - ,Y v). ` . IS* to ts. 2s, ry ;d to ty y s e V V 1 1 l I The employer ia 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 cumpeiisution law, these laws may be classed as contimUtwy or electin'. According to Daw son,' "a c -pulsory law is binding upon every employer and em ployee within its scope; there is no choice. Under an elective act. I employers and employees have the option of either accepting or I 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 I 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 Dawson1 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 And application particularly in dealing with accrued liability of sili cosis. Speaking of waivers, Kessler" 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 th 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 of the agency administering the compensation law. Unaer 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 Vane" classify occupational hazards as follows: (1) abnormalities of air pressure, (2; abnormalities of tempei atttre and humidity, (3) dampness. (4) defective illumination. f-5) dust. (6) infections, (7) radiant energy, (8) repeated motion, pressure, shock, etc., and (9) poisons. Major Groups of Oecti/Hitioiiol 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 sulAde, hydrogen cyanide, carbon monoxide, nickel carbonyl, haiogenated 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, epithellomatous 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 (n war- , j j j ] < 140 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY time industrial production. Cunningham'- 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. 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, arid (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.11 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 dear 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 jiven war ional .sent nees muccu- over subdusitals tion inds rial tion hen T and The (2) ne:er- ase the rk. paion wd sihe a :uit ist en he in y. iy ce m THE PROBLEM Of OCCUPATIONAL DISEASE 141 ilic 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. Lead Poisoning huiuslrial Uses of Lead.--About 150 industrial occupations entail a possible lead exposure. The principal hazards" occur in: Storage battery manufacture Printing industry I'aiut industry Welding and riveting, in enclosed Application of paints spaces, steel painted with red lead Enumelinr of such articles as bath Rubber manufacture tubs -- -- ; . - " Lead ore mining Pottery glaring Tetraethyl lead manufacture, or Reclamation of lead from junk metals clcaning'tanks in which ethyl gaso line haa 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 ita compounds. Classified on the basis of systems, the three more or less distinct clinical types of lead \ r' - ^ 1 **M?$0 V 142 prevention and control or 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, pyorrrea, 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 Arm 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 luuromutcular 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. :ers Headache, vertigo, insomnia, and disturbed sleep are likely to fj a be prominent symptoms. True palsy is uncommon today; it is un- usually the result of prolonged and severe lead exposure, and clinical history may give evidence of repeated episodes of intoxi t is cation of milder type. tes Lead encephalopathy is the most severe but fortunately the on- rarest manifestation of lead poisoning. In the industrial worker ea. it follows rapid, heavy lead absorption. Certain organic lead com of pounds, such as tetraethyl lead, are absorbed rapidly (through ia. the skin as well as other portals of entry) into the body and ty. especially into the central nervous system. With'these compounds, be encephalopathy is 4he rule. Comparable concentrations of lead ja. are absorbed into the brain from inorganic lead compounds only ed when the workplace is heavily contaminated with lead vapor, tal fume, or dust. of Lead encephalopathy begins abruptly and is characterized w, by signs of cerebral and meningeal involvement. The patient may it. be in a heavy stupor at the onset and go into coma, with or with is out convulsion, and die. Excitation, confusion, and mania occur a less frequently. Headache, dizziness, insomnia, and somnolence 4- are symptoms in cases recovering and of shorter duration. iy The cerebrospinal fluid may be increased in pressure and show u slight increase in cellular elements and globulin. Laboratory Findings.--Laboratory findings supplement the clinical findings and are of considerable assistance in differential e diagnosis. They should not be expected to yield the diagnosis. d Evidence of the effect of lead on the hematopoietic system is s ascertained by a study of the blood picture. Basophilic granula i. a tion or stippling of erythrocytes should be ascertained in quan titative terms and related to an established normal standard. According to Mayers,1* abnormal cell morphology and abnormal i 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 i 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.1' 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- *Y> 144 prevention and control of disease in industry sorption and hence points to the existence and severity of lead exposure. Lead intoxication1'1 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 Diaynoxis.--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 procedures11 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 THE PROBLEM OF OCCUPATIONAL DISEASE v ; 145 tad under control or eliminated. Otherwise, it will be necessary to place him in a job entailing no exposure. ad Periodic occupational examinations or check-ups to detect )W early evidence of dangerous lead absorption should be performed >w <m all workers exposed tu a lead hazard, but their frequency must ;r. be related to the problem at hand. Workers who are exposed to he less than 1.5 mg. of lead per 10 cubic meters of air need not be n. examined . cgularly more than once or twice a year, but in ex Iv tremely hazardous exposures and in young employees it may be ). necessary to raise this frequency to every fortnight. >d e. Metal Fume Fever le Metal fume fever is an acute transient illness often referred to as brass founders' ague, metal shakes, oxide chills, brass f- chills, galvo, and zinc oxide fever. Although at one time the il disease was thought to be caused exclusively by zinc,1"' it is now known to be produced by other metals, for example, cad e mium, lead, manganese, mercury, and magnesium, it follows the r inhalation of rather heavy concentrations of finely dispersed t metal fumes, usually in the form of oxides. Then, under certain f 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,su - ** the nose, throat, and substernal region fee! dry and sore, burn, and give l 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 V- to 2 or 3 hours. Fever and leucocytosis--1 not uncommonly accompany and follow the chill. Myalgia and arthralgia are also usually present at 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- '- / 3t SW*-.. -V ~~~ - - V -c L j^`" , * ' ,, ^ ,irT ` i '* "tf* -fV^? * -A. * .V,'7, ,* 4 '*; A'-v^' '"-4'"'! ' ,j-.'*'l#AV'v' Si fl'>,-< < 146 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY ^IVXWtWW'w: 1 - . r:J lowing a holiday or lay-off are particularly susceptible to an attack. Workers become "immunized", but this artificial im munity last3 only about 5 days.-'" 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 toi.sillitis, and septic processes also must be con sidered in differential diagnosis. Control.--Sayers*4 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 preplacemeiit 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 probietn in industrial hygiene. 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 picture*" 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 j I i I | imly to mplead, iria, roncon- ;ver ical sure rial >ns, rested in- atoriy:ed of on ed en aly a. ss >f y wy d r i. h as occur with irritant gases which produce acute pulmonary con gestion make it imperative to consider cadmium. These serious delayed symptoms-'* should not be confused with nonoccupationa! 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. r.:.u 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 facia) 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 Fulton-" advise quarterly medical examination of %vorkers 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 mines" 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 I which mercury may be a hazard. Mercury is 'being replaced in the fur-hattir.g industry by less toxic chemicals.*1 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." 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 known15 though some feel it is as an albuminate such as mercury chloro- albuminate, or oxy-chloro-albuminate. \ Symptoms.--The cardinal symptoms of industrial mercurial- ism are stomatitis, psychic disturbance, and tremors. These symp toms arc not present simultaneously in all cases nor in the same degree.51 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."'" 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 grow* 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.1* - Mercury fulminate rarely produces symptoms of systemic ! mercurial poisoning; the cases are usually characterized by a I dermatosis associated with 'conjunctivitis and inflammation of mucous membranes of the nose arid throat.5" : Radium Poisoning Because luminous dials are needed on instruments in night operations of the armed forces, there has been a great increase 1 n n s ri eI i \ ) \ I i THE PROBLEM OF OCCUPATIONAL DISEASE 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 Anotner 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 bodp exposure to gamma radiation. It is necessary to understand the genetic connection of all members of the radium family because these elements taken all together produce the effects ascribed to radium. The damage produced by various types of radiation is determined by their nature and properties,"'' thus. (I) alpha rays have enormous energy' but low power nf penetration and to pro duce injury they must come in intimate contact with the tissues they injure, (2) beta rays penetrate several feet of air. and (3) the gamma rays can penetrate several centimeters of lead. All radium-"' 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 itn 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 elim inated mainly in the feces. Although only about 10 per cent of the amount of radium taken into the body becomes Axed in the tissues, this fraction exposes the tissues to the destructive action of the radiations from the various members of the radium family. Among dial painters tissue damage ia 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,4* 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 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, hyperchromie 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 * 3,'jr*% I 'i '5! PREVENTION AND CONTROL OF 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. Even such small amounts as 1 to 2 micrograms may produce definite bone change.41 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.,T Curtiss1* states that if a sample of exhaled air is found to contain more than 10-1J curie of radon per liter, it indicates that at least 0.1 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 cutrol. thorough medical and dental ex aminations should oe 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 examination? 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 sociation** defines silicosis as "a disease due to breathing air con taining silica (SiO;), characterized anatomically by generalized fibrotic changes and the development of miliary nodulation in both lungs, and clinically by shortness of breath, decreased chest 4 j { 1 ; 'tVfft' 1 'Vjv ,**?* *,:* r: ' v e skull, lie sar- jroduce worker aled by on and herapy urtiss1" n more ast 0.1 herapy >y Aub tion of adium arly in -rather tai ex cornnation iriodic should ention orities ide at adium d time lative sstigaerned. sis) pplied ise, it t The :h Asr conalized ion in chest ..... ,v4 "r / V^?4- *. /' ; *` THE PROBLEM OF OCCUPA.T.I.O. NAL .DISE- A-SE:'^P"<2r >," . 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 refer ence 43): 1. Simple benign pneumoconiosis, which is virtually a deposi tion of du3t in the pulmonary tissues usually accom panied by pigmentation, and includes, for example, an- thracosis induced by coal dust and siderosis induced by iron. It does not incapacitate and roentgenological!:.shows as a maximum change only an exaggeration of linear pulmonic markings and is of clinical interest. oni> by way of differentia] diagnosis. Such cases should n\ vi be diagnosed as silicosis. 2. Silicosis, which is a pathologic pulmonary reaction due to i 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.4' 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 i 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 I .... 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,*' quarrying, ceramics industry, tunnel construction, sandblasting, and foundry work. Inhalation of siliceous dust almost invariably results In sili- 152 PREVENTION AND CONTROL OF DISEASE IN INDCSTRY cosis 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 0.5 to 3 microns). 3. The dust must be present in the atmusphere at the breath ing level of the worker in concentrations exceeding 5 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 nuartz content. Legithitiiui.--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:4'1 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.40 Clinical investigations, including X-ray studies, in various 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 real4' 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 1 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.40 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. l -{S -j rking .3 th5 tz. of a ns 11 in ns e. s, :h 8. ;o d s, if t d e n e s l s i THE PROBLEM OF OCCUPATIONAL DISEASE 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 m 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. (I>) showing the degree of dis ability, and (e) 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,4* 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 his been frequently demonstrated that antopty studies will yield essential information. ! 154 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. Tt pro gresses to terminal diffuse fibrosis usually without nodular pre dominance in about twenty years.5* 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 preemploy ment 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, ee ns ill tie is ie d- 8- 10 y n s v y f 1 r i a l 1 i i 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 changes'1 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, purpur t. 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.91 In case, upon repeated examination, the percentage of organic sulfate is SO per cent or more, the concen- v * 'J * \ 1 156 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.11 Carbon Monoxide Poisoning Carbon monoxide poisoning may occur in a great number of industrial operations.'- 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 ami nervous system. Symptom*.--Blood saturation up to 15 per cent HbCO rarely produces symptoms, but when the blood saturation is from 15 to 20 per cent, tightness across the forehead, possibly slight headache, and dilation of cutaneous' blood vessels are observed. When the blood saturation is 30 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,5*- ** is recommended: 1. The victim should be removed to fresh sir as soon ss possible. 2. It breathing has stopped. Is weak and intermittent, or present in but occasional gasps, artificial respiration by th# Schifer method should be given persistently until normal breathing la resumed or until after the heart hat stopped. 3. Pure oxygen or a mixture of 5 per cent carbon dioxide and 95 per cant oxygen should be administered using an inhaler, beginning aa soon as possible and continuing for at least 20 minutes in mild t | | casei and aa lone aa 3 hours,'if necessary, in severe eases if the patient does not regain consciousness. The 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 hexurdous, aa the patient quite often loses consciousness, and in some cases death occurs. CONCLUSION Occupational disease legislation has 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 second- injury 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. J 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 1. Sapplagton, C. O.: Modieolcgul Trends: Occupational Dlssasat. Induat. Mad., 7.-331 (June) 1038. 2. Dodd, W. F.: Administration of Workman's Compensation. Common. wealth Fund, Now York, 1936. 158 PREVENTION AND CONTROL OP DISEASE IN INDUSTRY 3. Dawson, Marshall: Problems of Workmen's Compensation Adminiitra. tion (in the United States and Canada). U. S. Bureau of Labor Sta tistics Bull. No. 672. Government Printing Office, Washington. D. C 1940. 4. Occupational Diseases. In Occupation and Health. 2 vols. Internationa! Labor Office, Geneva, 1930-34. 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 Law*. Casualty and Surety Jour., J.-58 (November) 1942. 7. Sharkey, C. F.: Principal Features of Workmen's Compensation Law< as of July 1, 1940. Appendix, Bull. No. 672, cited in reference 3. 8. Newquist, M. N.: Medical Service in Industry and Workmen's Com pensation Laws. American College of Surgeons. Chicago, 1938. P. 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. 1938. 10. Kessler, H. H.: Accidental Injuries: The Medico-leeat Aspects nf Work men's Compensation and Public Liability. Lea ami Kebigvi-. Pi.:!., delphia, 1941. P. 733. 11. Dublin, L. I., and Vane, R. J.: Occupation Hazards and Diagnostic Sicn-< Division of Labor Standards Bull. No. 41. Government Printing Office. Washington, D. C., 1942 (revised). P. 31. 12. Cunningham, J. G.: The Health of the Worker in Industry in Wartime Canad. Pub. Health Jour., 33:582 (November) 1941. 13. Hussey, Raymond: Workmen's Compensation and Medictna. Med. Clinics North America, ~: 1035 (July) 1942. 14. McDonald, J. H.: Metallic Poisons. Indust. Med., 10:447 (October) 1941. 15. American Public Health Association: Lead Poisoning--The Recognition of Hazardous Industrial Lead Expoaure. First section of a report pre pared by the Committee on Lead Poisoning, Industrial Hygiene Section. 1942. 16. Mayers, M. R.: Prevention of Lead Poisoning. Indust Bull. (New York), <1:286 (August) 1942. 17. Dreesaen, 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 tha Storage Battery Industry. U. S. Pub. Health Bull. No. 262. Governmant 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, 1986. P. 75. , 21. Sober, G. M,, and Hayhurst, E. R-: Industrial Health. Btakiaton's Son and Co, Philadelphia, 1924. P. 331. 22. Drinker, P.: Certain Aspects of tha Problem of Zinc Toxicity. Jour. Ind. Hyg, 4:177 (August) 1922. 28. Sturgis, C. C, Drinker, P, and Thomson, R. M.: Matal Fume Fever. I Clinical Observation on the Effect of (die Experimental Inhalation of Zinc Oxide by Two Apparently Normal Persons. Jour. Ind. Hyg., 9: 88 (March) 1927. THE PROBLEM OF OCCUPATIONAL DISEASE 159 24. Sayers, R. R.: Metal Fume Fever and It* Prevention. U. S. Pub. Health Rep.. 5J.1080 (July 1) 1938. Reprint No. 1953. 25. Turner, J. A., and Thompson, L. R.: Health Haxards of Brass Foundries. U. S. Pub. Health Bull. No. 157. Government Printing' Office, Washington, 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, IV. B.: Industrial Manganese Poisoning. Jour. Ind. Hyg., fJ:3?4 (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., 176:54 (January 3) 1942. 21. Neal, P. A.: Mercury Poisoning from the Public Health Viewpoint. Am. Jour. Pub. Health, M/907 (August) 1938. 32. Goodman, Louis, and Gilman, Alfred: The Pharmacological Basis of Therapeutics. Macmillan Co., New York, 1941. P. 732. 33. Hope, . W., Hanna, W., and Stallybrasi, C. 0.: Industrial Hygiene and Medicine. Bailliere, Tindall, and Cox, London, 1923. P. 128. 34. Hamilton, Alice: Industrial Toxicology. Harper Brothers, New York, 1934 P 73, .15. Neal, P. A., Flinn, R. H,, Edwards, T. I.,' Reinhart, W. H., Hough, J. \V,, 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 Maladlei. 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. 38. Curtiss, L. F.: Prevention and Controt of Hazards in Radium Dial Painting. Jour. Ind. Hyg. 4:131 (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., 4:22? (June) 1937. Reprint No. 415, Cancer Commission of Harvard University. 40. Martland, H. 3.: Radium Poisoning. In Practitioners Library of Medi cine and Surgery, Supplement. D. Appleton-Century Co., New York, 1938. P. 208. 41. Remikoff, Paul: Polaoning from Lead and Other Heavy Metal*. In Industrial Hygiene, edited by Lanxa and Goldberg. Oxford University Press, New York, 1939. P. 443. 42. Pnturaeconioais. American Public Health Association Year Book, 193233. P. 100. Supplement to Am. Jour. Pub. Health, t3 (June) 1933. 48. Gardner, L. U.: The Pneumoconioses. Med. Clinic* North America, tO: 1239 (July) 1942. 44. Pneumoconiosis. American Public Health Association Year Book, 194142. P. 117. Supplement to Am. Jour. Pub. Health, it: (March) 1942. 45. U. S. Department of Labor, Division of Labor Standards: Summary Re- v.' S J\ W5w:4t;^/- ,V'vitiy. '.,. , * `i.-> -.1 i-.i> 4.A;'.';'/\.-,>rv?' . '. r* O *" " - 160 prevention and control of disease in industry ports of the National Silicosis Conference. Bull. No. 13. Government Printing Office, Washington, D. C., 1938. 46. U. 3. Department of Labor, Division of Labor Standards: Chart--Work men's Compensation--Silicosis. Summary of Statutory Provisions as of January 1, 1942. 47. Dreessen, W. C., Page, R. T., Hough, J. W,, Trasko, V. M., Jones, J. L., and Franks, R. \\\: 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 Aabeatosis. edited by Lanza. Oxford University Press, New York, 1938. 31. National Institute of Health. Division of Industrial Hygiene: Benzene (Benxol), its Toxicity and Potential Dangers. U. S. Pub. Health Rep. Je.319 (March 14) 1941. Reprint No. 2248. 52. Yant, W. P., Schrenk, H. H., Sayers, K. R., Horvath, A. A;, anil Rein hart, W. A.: Urine Sulfate Determinations as a Measure of Benzene . Exposure. Jour. Ind. Hyg., 13:67 (January) 1936. 33. National Institute of Health, Division of Industrial Hygiena: Carbon Monoxide, Its Toxicity and Potential Dangers. U. S. Pub. Health Rep.. 36:421 (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, |i. C., 1936 (revised). i | i I and I :S5 :oen<,- ch, CHAPTER 12 medical control of respiratory diseases W. C. Dreessen. M.D. ty THE PROHLEM Today, as never before, the comparative lack of specific control measures and the terrific toll of the respiratory diseases--colds, n, influenza, pneumonia, and tuberculosis--are making: rigid de mands upon the acumen of every industrial physician, and at the n same time cast out a challenge to preventive medicine which can not be ignored. Fully one-half of the sick absenteeism and over one-third of the work days lost by industrial workers through disability are attributable to respiratory disease. The strategic position of the plant physician for the control of these diseases is not as favorable as it is in the case of such diseases as malaria and syphilis for which specific chemotherapeutic agents are avail able or in the case of smallpox against which active immunity can be attained. Workplaces not infrequently provide many of the predispos ing factors regarded as significant in respiratory infections. Many workers for the first time in their lives are coming face to face with such conditions as a relatively crowded environment and exposure to gases, fumes, and dust They must contend with occupational fatigue in becoming hardened to a new form of work. Many are exposed to inclement weather and extreme changes in weather conditions. Malnutrition, allergy, alcoholism, personal handicaps, and other factors contribute to the decreased ability of the individual to resist infection. It is the purpose of this chapter, first, to review certain meas ures as they pertain to the control of acute respiratory diseases, and second, to outline similar measures as they apply to tuber culosis and other chronic pulmonary diseases in industry. ACUTE RESPIRATORY INFECTIONS The acute respiratory infections are a heterogeneous group of ailments caused by various agents. It is highly probable that many of the so-called colds are caused by filterable viruses. More ' - 2OT ' 268 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY than thirty types of pneumococci are involved in pneumococcal pneumonia; more than two types of viruses are known to cause epidemic influenza. The filterable viruses are particularly likely to initiate the disease process. Moreover, it is now recognized that the common pathogens of the respiratory tract participate in the pathogenesis of lcute respiratory syndromes. Only too frequently is the common cold followed by such formidable sequelae as pneumonia and tuberculosis. Prevalence of Colds The extensive studies by the U. S. Public Health Service and other organizations have contributed many important facts re garding the common cold. Since it is obviously impossible to present a complete review, only certain etiologic and epidemiulogir features will be stressed. The attack rate per person usuallv averages 2 to 3 per year. Almost all persons are susceptible and very few persons avoid an attack of acute respiratory infection during the course of any one year. Townsend.* for instance, stated that in a group followed for 5Vi months 90 per cent re ported one or more attacks. There is typically, but not always, a period of high prevalance in early spring, a decline in midsum mer, another period of high prevalence in autumn, and some decline in December. The peak in the fall of the year is reached with almost explosive suddenness and a high incidence will usually be reported simultaneously fn all sections of the country. Gover, Reed, and Collins,* studying data from students in various universities in the United States over a period of 18 months, concluded that there is "no definite association of res piratory attack rate with marked variations in climate as repre sented by six American cities with wide geographic and climatic differences." Other investigators* have also failed to observe a consistent relation between the incidence of colds and latitude, longitude, and climate. The above conditions apply to continental United States, but lest we overlook the infectious nature of colds, the Spitsbergen observations4 may be recalled. Spitsbergen is comparatively free of colds in winter, but with the opening of the shipping season about three-fourths of the community's population suffer an at tack of the common cold within a week following the arrival of the first ship. Similar observations, as well as clinical and experimental inveatigations. Indicate that the incubation period MEDICAL CONTROL OF RESPIRATORY DISEASES 269 :al for the common cold is probably between 12 and 48 hours or tse possibly as long as 72 hours. iiy at Cold Vaccine he Prophylactic immunization against the common cold has been ly tried by means of filterable virus vaccine and by vaccines pre as pared from mixtures of various pathogens of the respiratory tract. The virus vaccine has had only limited trial and has not proved to be efficacious. According to Dochez,9 the future value of common cold virus vaccine is problematical because an attack id of cold gives little or no immunity. Bacterial vaccines containing a variety of respiratory pathogens have been used on a wide tn scale. Many Industrial physicians have had first-hand experience it- with them.* The stock vaccines contain killed pneumococci. H. v influenzae, M. catarrhalis, staphylococci, and streptococci. These - ri organisms tend to be present In the normal nasopharyngeal flora n and in case of an attack are assumed to act as secondary in vaders. As a result of using such vaccines one would expect a lessening in the harmful effect of these organisms. According to some authorities, these secondary invaders piay an important role in a small group of adults who suffer each year from pro e longed infections of the upper respiratory tract with such com i plications as sinusitis and bronchitis. For theoretical reasons, / some believe that such vaccines are of considerable value if re stricted to that group of individuals in which secondary bacterial 1 infection presumably plays an important part. The use of these 1 vaccines, however, has not received the endorsement of public health workers, mainly because of lack of scientific proof, . Influenza Prophylaxis The etiologic agent of certain epidemics of influenza,, as in the instance of the common cold, is a filterable virus. Influenza occurs mainly In a pandemic, an epidemic, or an endemic form.1 The cause of pandemic influenza, such as occurred in 1918-1919, is not yet known. In the epidemic form, at least three filterable viruses have been isolated. The cause of endemic influenza, or sporadic grippe is also undetermined. In influenza such organisms as H. influenzae, streptococcus, pneumococcus, and M. catarrhalis are regarded as secondary invaders which aggravate the patho logic picture by frequently inducing severe and fatal broncho pneumonias. Immunization would be an Ideal method of pre vention, but no efficacious procedure has been available in past I 1 epidemics, probably as the cause had not been fully determined. "Individual immunity to the virus of influenza as measured by the development of neutralizing antibodies in the blood can be readily accomplished by inoculation of human beings with either living or killed cultures of influenza virus."* Extensive studies are now being carried out with different antigenic strains of the virus. A flu-distemper viral vaccine has been used recently.' Horsfall* in his recent review, however, concludes that the aver age extent of immunity induced by vaccines containing influenza A virus was too insufficient to allow it to be considered as a practicable prophylactic measure. Pneumonia Prophylaxis Artificial immunization against lobar pneumonia, whether active or passive, is of questionable value for prevention. It is known that immunity develops to pneumococci, but the dura tion of the immunity thus induced is limited. Environmental Control Besides control along immunologic lines, measures directed at environment have recently been receiving increased atten tion. The new "air-borne" or indirect hypothesis "postulates that the greatest spread of respiratory infection is produced by small dried droplets floating in air for relatively long times and dis tances or by the resuspension of dried droplets in air after they have settled to surfaces such as floors, clothing, and bed clothes."* Alpha hemolytic streptococci of nasopharyngeal origin are widely distributed. The virulence of the microorganism Is never more than slightly impaired by sojourn in rooms. One of the out growths of these observations as related to surgery is that it has been possible to reduce wound infections by less frequent dress ings. ...a.-'-.- The object in environmental control is to destroy the res piratory pathogens in air either by radiation, or by chemical sprays or aerosols. It has been observed that the concentration of organisms in the air is reduced by natural sunlight; even diffuse daylight has been found to have a lethal effect. These ob servations suggest planning for maximum window space in occupied buildings. _:f Ultraviolet radiation, while more potent than'visible light, cannot, at present, be unreservedly endorsed for use in industrial plants for the purpose of controlling acute respiratory infections. Mf'te&ViY&i-*-' * \-y* -u '\v MEDICAL CONTROL OF RESPIRATORY DISEASES ' 271 If it is used, special attention must be given for protection of individuals, particularly as regards exposure of skin and eyes. Aerosols.--Various germicides in an appropriate solvent and sometimes incorporating a wetting agent have been used as aero sols. Among the various agents that have been used in experi mental work are resorcinol, resorcinol glycerine, hexyl resorcinol in propylene glycol, formaldehyde-water, and hypochlorite solu tions. Twort and his coworkers10 found that 10 per cent hexyl resorcinol dissolved in propylene glycol added to 0.05 per cent sulfonated lorol was the most effective all-around germicidal mixture of those they tested. Minimal effective mist concentra tion of resorcinol glycerine aerosol was about 1:400,000,000 by volume. This level was confirmed by Williamson and Gotaas." The latter, in referring to the practical use of aerosols in places occupied by persons, state that the aerosol must be nontoxic to man. nonirritating to the eyes and lungs, rapidly lethal to the bacteria when present in small concentrations, inodorous, invisible, noninflammable, noncorrosive, persistent, and should not leave films and coatings on walls and furniture. Needless to say, consider able investigation is necessary before aerosols can be used in occupied rooms. It may be used in such rooms as laboratories and media rooms where the aerial germicide may be allowed to dissipate before the room is occupied. General Measures in the Control of Colds, Influenza, and Pneu monia Since no satisfactory immunity can be established against these acute respiratory infections and even the new chemothera peutic agents are of little avail in viral pneumonias and most other viral diseases, it is apparent that many procedures are necessary to cope with an epidemic of one or all of these diseases. Specific measures of hygiene and sanitation are to be recom mended during epidemic periods. Such measures have been tersely summarized for these respiratory diseases, as well as other com municable diseases, in a report of a committee of the American Public Health Association.11 This pamphlet should be in the hands of every plant medical director. Because the minor and acute respiratory ailments, such as common cold, not infrequently lead to disabling pneumonia, otitis media, and mastoiditis, a major effort should be directed toward controlling colds. Remembering that colds are spread by close contact in the acute stages of the disease, certain public 272 PREVENTION AND CONTROL OF. DISEASE IN INDUSTRY health procedures should be seriously considered. These include, among others, (1) isolation at home during the early and highly contagious stage of a cold which will lessen the spread of the infection, and (2) avoidance of close contact with persons suffer ing from colds, and of closed spaces where large numbers of infected persons congregate, which may be recommended through a health education program. The spread of these diseases most frequently takes place through the medium of infected particles sprayed into the air by talking, coughing, and sneezing. Where general public health measures for control have been applied, they have included im provement of general hygiene and living conditions, especially overcrowding. Persons suffering from minor respiratory infec tions should take unusual care in the avoidance of dangerous, contacts, allow themselves periods of rest, and avoid such pre disposing factors as chilling, exposure to severe climatic changes, fatigue, and excesses of all kinds. Many procedures in the plant medical department if adopted as routine may aid materially. The preemployment examination should pick out those prone to acute exacerbation, sinusitis, asthma, and bronchitis. Employees should be required to check through the medical department when they become ill on the job and after acute illc?sa. These checks afford an excellent op portunity for directihg those ill to prompt treatment by the new therapeutic techniques now available. Contact between persons in the more contagious phases of minor respiratory diseases can therefore be avoided. By thus encouraging prompt treatment, disabling effects may be reduced in number and severity. That an all-around industrial hygiene program will yield substantial results is attested to by a number of recent reports by industrial physicians. CHRONIC RESPIRATORY INFECTIONS In addition to the acute respiratory diseases, those of a chronic nature exact a large toll of lost time. These diseases are exemplified by pulmonary tuberculosis, which claims the lives of sixty thousand Americans each year. It is more and more becoming recognized as an affliction of older occupied men.u As an example of American industrial tuberculosis experience. It is gratifying to note that the death rate14 among industrial policy holders of the Metropolitan Life Insurance Company has been reduced to about one-fifth that of 1917. With the changeover to war production, however, attention must be directed to a pos sible increase of this disease, particular!/ as regards women. The single exception to a satisfactory public health situation in Britain was a rise of almost 10 per cent in the mortality from tuberculosis in 1939 and 1940.1* The Increment in this case was greatest in young women and was thought to be related tu malnutrition. Control Programs By directing medical measures for the control of the chronic respiratory diseases at pulmonary tuberculosis, tangible results are obtainable with nontuberculous affections as well. The essence of the medical program is the radiographic examination of the chest. This procedure has been the basis of medical control of silicosis, in which disease the infective element, particularly tuberculosis, is the principal cause of disability. As in pneumo coniosis, X-ray examination of the chest, if supplemented by clinical study, will aid in obtaining proper medical management for such other pulmonic conditions as bronchiectasis, asthma, and cancer. As an illustration of what can be accomplished in tubercu losis control by a plant, reference is made to the experience of Sawyer. **17 An X-ray survey of 3,280 apparently healthy emI ployeea in 1921 showed 2.3 per cent positive for clinical tubercu losis. From 1928 on, the medical department has been doing serial or annual X-rays of the chest. In a group of 4,665 em ployees, averaging 33 years in age, and studied from 1928 to 1935, only 0.5 per cent showed active or clinical tuberculosis. By 1940 this percentage was down to 0.2 per cent, which is probably close to the irreducible minimum. What has been done by Sawyer can to a considerable extent be achieved In any employed group I if a definite program is outlined and followed. The Metropolitan life Insurance Company,1* following the adoption of a tuberculosis control program, reduced the number .of cases of significant pulmonary tuberculosis from 40 per 10,000 employees in 1930 to 10 per 10,000 in 1939. Use was made of routine preemployment X-rays and the Metropolitan sana torium. It was observed, however, that during the period, 1930 to 1939, the prevalence of tuberculosis among applicants for em ployment had not been reduced; the experience indicates 80 cases of significant tuberculosis per 10,000 applicants and, ac cording to Sherman,,a this probably represents a fair average. 274 PREVENTION AND CONTROL OF DISEASE IN INDUSTRY Other industries also have had anti-tuberculosis programs in effect. There should be no relaxation in the program of controlling pulmonary infection and indeed an extension of the program to the smaller industrial plants is indicated. X-ray Methods.--Recent radiographic surveys of employed groups, who had not been X-rayed previously, have revealed 1 to 2 per cent of the employees with significant tuberculosis. Case finding is an important feature in a tuberculosis control program that can be effected by the industrial physician. A number of X-ray procedures are available, such as single or stereo 14 by 17 inch films, 14 by 17 inch paper, 35 mm., 4 by 5 inch, or 4 by 10 inch photofluorographic methods, and fluoroscopic examination. Photofluorograms have been adapted for ma3s X-raying work in the armed forces, as well as in the medical departments of a number of large industrial plants. If a grid is used, very satis factory photofluorograms can be obtained. For best results this will require at least 200 milliampere equipment. It has been the practice not to rely on the fluorograms, particularly the 35 mm. size, for diagnoses, but, instead, this technique is expected to pick out persons with definitely abnormal or suspicious chest findings. These individuals are then rechecked with standard 14 by 17 inch single or stereoroentgenograms- taken for diagnos tic interpretation. In advocating small film X-ray pictures as a routine for all I patients admitted to general hospitals. Hilleboe4" refers to the i experience of the University Hospital. Ann Arbor, Michigan, i where it was found by this technique that 10 per cent of the pa- 1 tients admitted showed lesions of the organs in the chest. The U. S. Public Health Service now has eleven photofluorographic units in the field, each accompanied by a medical officer, tech nician, and clerk. Plants may appeal to the Public Health Serv ice through the State health department for the services of one of these 35 mm. units if no other means for mass X-raying is available. Experience has shown that 300 to 500 photofluoro grams a day can be made with one of the units. , Administrative Procedures.--Sawyer,1*-11 who has had years I of experience administering a tuberculosis control program, offers < helpful suggestions in its conduct. His program is directed at three groups: (1) applicants for employment, (2) employees with negative X-rays, and (8) employees with suspected tuber culosis. He has noted that it has been too time-consuming to fur nish each individual a report on the findings yielded by his radio- i gram. Hence, he recommends issuing a mimeographed statement i MEDICAL CONTROL OF RESPIRATORY DISEASES 275 to the patient at the time of X-ray, stating- that if his X-ray is negative he will not receive a report, but if his lungs are affected he will be so notified. Employees having latent, clinically insig nificant lesions are reported as having lungs that are negative or clear. Employability.--Applicants with healed primary tuberculosis or inactive types reinfection tuberculosis are ordinarily ac ceptable for employment. For a number of years the Public Health Service has advocated, even in the dusty trades, that the worker with evidence of healed primary tuberculosis should not be denied employment on this account alone. There are many types of employment where persons are acceptable with clinically negative, stabilized lesions, minimal or moderately advanced in extent. If adequate X-ray equipment is available, it may be pos sible in some instances to accept individuals with small soft le sions, but these workers will require close medical supervision. The individuals with active and questionably active tuberculosis are not acceptable for employment, but should be referred to their physician, the local public health authorities, or a clinic. Frequency of Periodic X-Ray.--The means toward the end of obtaining satisfactory periodic X-rays is an adequate record system. This will make it possible to call back the employee for reexamination, according to the need for recheck. The Public Health Service has recommended annual medical examination of workers in the siliceous dusty trades to detect evidence of pul monary tuberculosis and early silicotic changes. Sawyer11 recom mends annual X-ray for young workers (ages 18 to 25), whose preemployment X-ray was negative for clinical tuberculosis, gradually increasing the time interval between examinations to three years if the chest roentgenogram continues to be negative. Individuals 30 years of age and over with negative X-rays at the beginning of employment are scheduled for re-X-ray at 3-year intervals. The frequency of X-raying workers with evidence of tuber culosis depends on the extent of pulmonary involvement and dynamic status of the disease. Sherman.'" in the instance of expatienta, has suggested X-ray and sputum study every three months for the first two years following their discharge from a sanatorium, and every six months thereafter. He feels that those with a history of contact should be X-rayed at once and every six months for a period of three years and annually thereafter. FoUaw-Up, After-Care, Rehabilitation.--Next to finding the case of tuberculosis, adequate follow-up is of extreme importance. X fi: * 276 PREVENTION AND CONTROL OP DISEASE IN INDUSTRY particularly from the patient's standpoint. The patient should be referred to his private physician or to a clinic and the case re ported to the local health department. Public health officials and local voluntary tuberculosis agencies are especially helpful in this follow-up stage. They can assist in arranging for sanatoria! care and be of material assistance in checking on possible con tacts in the horn If sanatoria are not available, outpatient super vision is far superior to no care at all. In the development and the successful prosecution of a tuber culosis control program in any community, it is essential for public health officers to have the cooperation of the State and local medical society, management, labor, and voluntary agencies. This procedure will insure appropriate follow-up and after-care, and also pave the way for rehabilitation of the affected individual to industry. In this connection, from 65 to 75 per cent of the workers with minimal and moderately advanced tuberculosis" can be expected to return to their former positions in industry after an adequate stay in a modern sanatorium. Many industrial organizations reemploy workers with arrested tuberculosis. Factors to be considered in the employment of a worker with arrested tuberculosis are as follows:17 (1) extent of the lesion, (2) completeness of the cure, (3) character of the job, and (4) the necessity for adequate medical supervision after return to work. CONCLUSION In this period of profound socio-economic stress every facility for searching out active cases and getting them under treat ment should be employed to prevent an unfavorable effect on the present downward trend of the American tuberculosis mortality rate. The X-ray is a potent tool to this end and the medical departments of many industrial organizations have demonstrated how much can be done in promoting the control of tuberculosis. The plant physician should formulate a program making use of the X-ray for preemployment and periodic examinations of his employees. To provide for satisfactory disposition of cases found, the plant physician should also establish liaison with local work ers in the field of tuberculosis control. BIBLIOGRAPHY 1. Townsend, J. G.: Epidemiological Study of the Minor Respiratory Dis ease! by the Public Health Service (Preliminary and Progress Re port). U. S. Pub. Health Rep., Jf .'2669 (October 24) 1924. Reprint No. 966. MEDICAL CONTROL OF RESPIRATORY DISEASES 277 2. Cover, Mery, Reed, L. J., end Collini, S. D.: Time Oiitribution o/ Com mon Cold* end it* Reletion to Corresponding1 Weether Conditions. U. S. Pub. Heelth Rep., 49:811 (July 13) 1934. Reprint No. 1634. .1. Thomson, 0., end Thomson, R.: The Common Cold. Annals of the Pickett-Thomson Research Laboratory. Vol. 8. William* end Wilkins Company, Baltimore, 1932. I. ThuI, J. H., end Preese, H. L.: Study of Colds end N'esel Pharyngeal Flore in Spitsbergen. Am. Jour. Hyg., 17 :S 17 (May) 1933. 5. Docher, A. R.: Infections end Infestations: Respiratory Infections. / Preventive Medicine in Modern Practice. Hoeber, New York, 1942. P. 205. ii. Bertie, Harvey: Hygiene and Medical Cere of Workers on American Railroads. In Industrial Hygiene, edited by A. J. Lanza and J. A. Goldberg. Oxford University Press, New York, 1939. P. 567. 7. Brown, J. W., Eaton, M. D., Meiklejohn, G,, Lagen, J. B., and Kerr. W. J.; An Epidemic of Influenza. Results of Prophylactic Inocula tion of a Complex Influenza A--Distemper Vaccine. Jour. Clin. In vest., 20;663 (Novemher) 1941. s'. Horsfall. F. L., Jr.: The Present Status of the Influent* Problem. Jour. Am. Med. Assn., 330:284 (September 26) 1942. :i. Buchbinder, Leon: The Transmission of Certain Infections of Respira tory Origin. Jour. Am. Med. Assn., 333:718 (February 28) 1942. in. Twort, C. C., Baker, A. H., Finn, S. R., and Powell. E. O.: The Disin fection of Cloeed Atmospheres with Germicidal Aeronol*. Jour. Hyg. (London), 40:253 (May) 1940. 11. Williamson, A. E-, and Gotaas, II. B.: Aerosol Sterilization of Air Borne Bacteria. Indust. Med., 11:40 (January) 1942. 12. American Public Health Association: The Control of Communicable Diseases. U. S. Pub. Health Rep., J0.-1O17 (August 9) 1935. Revi sion of 1940. Reprint No. 1697. 13. Chadwick, H. D., and Pope, A. S.: The Modern Attack on Tuberculosis. Commonwealth Fund, New York, 1942. 14. Improvement of Health in Twenty-Five Years. Current Comment Jour. Am. Mad. Assn.. 119:267 (May 16) 1942. 15. Satisfactory Report on the Public Health. London Lettar. Jour. Am. Med. Assn., 119:242 (January 17) 1942. 16. Sawyer, W. A.: Tuberculosis in Industry. Am. Rev. Tubere.. 39:456 (April) 1939. 17. Sawyer, W. A.: Control of Tuberculosis and Employment of the Tuber culous in Industry. Indust. Med., 10:221 (June) 1941. 18. Reid, Adaehree: Control of Tuberculosis. III. Management of the Em- ploys with Pulmonary Tuberculosis. Jour. Indust Hyg., 93:35 (January) 1941. 19. Sherman, G. A.: Control of Tuberculosis in Industry. Indust Med., II: 287 (June) 1942. 20. Hilleboe, H. E.: War Challenges Tuberculosis Control. Bull. Nat Tubere. Assn., 93:131 (September) 1942. " " 21. Sawyer, W. A.: Control of Tuberculosis. In Tuberculosis in Industry. Saranac Laboratory Symposium, 1941. National Tuberculosis Asso ciation, New York, 1942. P. 311. 22. Cheek List of Publications from the John J. Abel Fund for Research on the Common Cold to November, 1933 (The Johns Hopkins Univer sity). Am. Jour. Hyg., 13:783 (November) 1933. 10