Document dQwErp5Yo9qD8YKd7wrrpO92Q

** z PLAINTIFFS S EXHIBIT I DR-639 1 V OCCUPATIONAL DISEASES OF THE LUNGS . vir ,-;y. A. J. LANZA, M.D., New York always remember that in spite of the enor :!ltlilll!itl!llill[lllll!iiiilii:i!i]|l!ll;I!I[i!'llit|!i:i1i!)<r/Vi^lII:tl<!i.!j|!il!!li!i)riiili:ii! Il]lill!llli!l!llllli!li]i![li!lii!l|['il! mous amount"of research that has been done in most of the civilized countries of the world On behalf of the Institute of Industrial on the subject of silicosis--almost enough Medicine, may I express my appreciation of to fill an ordinary library--we still do not the opportunity to participate in this rather know what is the nature of the action of the unique meeting ? May I also express my ad silica particle upon pulmonary tissue. Nor miration for the work which Dr. Marble and do we know why it is that the silicotic is more his associates in the Massachusetts Medical susceptible than the normal person to tuber Society have done in achieving the turn culosis. out that we see here today? Likewise, for instance, in asbestosis we do Industrial medicine is not static. Research not know what is the nature of the action of goes on and clinical knowledge progresses, the asbestos particle upon the pulmonary so that all of us continue to learn more and tissue. The late Dr. Gardner propounded more. That being the case, it does not be the theory that, contrary to the action of hoove any of us to be too dogmatic. We must silica, the action of asbestos was largely me learn to adapt our thinking to the changes in chanical. That may be so. On the other our knowledge and. if necessary, to change hand, it is only fair to state that there is a our minds. When I was a boy. they used to considerable body of opinion that does not have a saying. "It was only a wooden Indian go along with that. Diagnosis is not always and a certain kind of fool who wouldn't too easy and calls for all the skill that we can change his mind." And occasionally we have muster with respect to getting a careful occu to make up our minds that we have to change pational history, as well as the clinical and our minds. roentgenological evidence that may be avail This matter of occupational diseases of the able. It is incumbent upon us to be very care lungs is not a simple one. It is very com ful and very precise in our use of terms. All plicated and. as in all chronic diseases, pre too commonly people are apt to use' these sents a number of variables, the effect of various terms signifying different types of which we have not always learned how to pneumoconiosis as interchangeable, which is evaluate. We have learned a good deal about not correct. These different types of pneumoconiosis, like silicosis and asbestosis ~v silicosis. \\ e have learned something about asbestosis. Those are the two main forms and siderosis. are different diseases: and if k ?- of pneumoconiosis which cause disabilitv and sometimes death. At the same time we must there is any sloppiness in our use of terms, we only confuse ourselves and make the mat ter of diagnosis and the just treatment of the Chairman. Institute of Industrial Medicine, New individual worker who may be claiming com York University--Post-Graduate Medical School. pensation difficult. Read in the Symposium on Occupational Dis eases of the Lungs, sponsored by the Massachusetts Medical Society in cooperation with the Institute of Industrial Medicine of the New York University --Post-Graduate Medical School, Boston, Oct. 28. 1953. While it is true that we have a fair knowl edge of the action of silica particles and as bestos particles upon the pulmonary tissue as far as the pathology is concerned, we must always remember that these dusts may not, 50010201 183 .'* - ,/K V'"'5 INDUSTRIAL HE. 'I under factory or manufacturing conditions, occur as pure homogeneous particles, because there are often other dust particles among them. As pointed out years ago in researches at Saranac, these other dusts present along, with silica modify the action of the silica par ticles. So we have to approach this whole subject with a considerable degree of humil ity, because there is so very much concerning these diseases about which we know very lit tle. Our only hope here lies in the progress in the type of work that you will hear de scribed later in the afternoon by Dr. Wright. The pathologists and physiologists are the only ones who hold the key that may unlock the door to further knowledge of what rea goes on in the lungs of persons who breat the various kinds of dust that we hnd in o working places. So far our estimation of tl disability consists mostly of rule-ot'-thui methods, and if they can be combined with certain amount of common sense, we ho that the standards of dealing with daimar for disability may be of a moderately hi. order. Again let me emphasize that there is great deal of work to do. There is a gn deal oi knowledge that we do not have. Y will hear much more on that from our d anguished speakers this afternoon. i 50010202 184 Patholocj,ij, oj* sidledtodid-. KENNETH M. LYNCH, M.D., Charleston, S. C. anitaizn^^nniinninu^^uintintiinniMiuflHiinEniiHnniinniiiDininiiniaiuruina^iiDiiuunniDiiin While the asbestos industry may date its beginnings back into antiquity and while the condition now known as asbestosis may have occurred through a long period of time, the industry as we know it is new, and the health hazard related to it is of recent knowledge. In fact, the term asbestosis was not entirely acceptable as recently as about 30 years ago, while up to that time any thought of ill effects of occupational exposure to asbestos dust tended to confuse the resulting disease with silicosis. Parenthetically, perhaps it is per missible to express an opinion that before we have finished with the study of the class of pulmonary disease attending exposure to dust in industry the whole chapter will need to be revised. It is within the time of experience of some who are still concerned with the study of cer tain unsolved problems in the subject that there has been established this distinct vari ety of pneumoconiosis. During the same period, and probably largely because of dis closure of the hazard, there have been im provements by the industry to protect work ers, so that, so far as my observations go, the atmospheric conditions in asbestos mills are greatly different from the conditions of 30 or more years ago. Even though improve ments have been made and although knowl edge of the course of the disease has come largely from examination of workers whose President Medical College of South Carolina. Read in the Symposium on Occupational Dis eases of the Lungs, sponsored by the Massachusetts Medical Society in cooperation with the Institute of Industrial Medicine of the New York University --Post-Graduate Medical School, Boston, Oct 28, 1953. employment went back into the very dusty conditions of earlier times, it should not be assumed that the hazard has been eliminated. Harmful asbestosis is still occurring. Asbestosis is the product of the inhalation of asbestos dust in sufficient amount and dur ing a sufficient period of time; but under working conditions, either now or formerly, there is no uniformity in degree of disease among workers, even under similar ex posures. ' Apparently some persons in a group working in the same environment will be severely affected, while others will be less affected, and some will escape harm, and this for reasons unknown. Furthermore, the time required for similar quantitative exposures to produce like grades of asbestosis apparently varies with individuals. While in our efforts to establish protection of the health of industrial workers we have set up certain standards concerning atmos pheric dust concentrations, these are of a general nature rather than specific, and may have given a false sense of security. The very dusty atmospheres surrounding the workers in this as well as in certain other industries under former conditions wpuld certainly be more harmful than the relatively clean environment to be found in a presentday" careful operation,- but we may need to establish something more than merely the particle counting and measuring practices now in vogue if we shall have dependable safety controls. The particulate matter in asbestos-plant dust is composed of broken fibers of crystal line silicates. When inhaled, most of it is expelled, but the quantity of fragments of lengths up to 100/x or more that may reach the terminal respiratory units is remarkable. As compared with the material deposited in the lung in silicosis and in certain other con ditions of occupational connection, this ma- 185 5OO1!0?O3 IXDCXTlil.lL XiiJL. Fig-. 1.--Asbesto-is bodies in sputum concentrate: reduced from a photomicrograph, x 705. terial apparently exerts physical rather than chemical influence. At least it now appears that while free silica is in a crude sense chem ically poisonous to living- tissues when de posited within them asbestos crystal- frag ments may traumatize living tissues by their physical qualities. Hence the present belief that it is the larger particles that do the dam age here, as contrasted with the harmful ef fects of the smaller particles in silicosis. It is fitting to that conception that, possibly by a protective mechanism, the asbestos frag ment remaining in the lung becomes envel oped by foreign-body giant cells and covered by a smooth coating, apparently of colloidal Fig. 2.--Grade III fibroMS, with asbestosis bodies, phagocytes, and black granular pigment in reduced alveuii; reduced from a photomicrograph. X 280. nature and of tissue fluid or cell origin. T1 process transforms the naked asbestos erys into a golden or brownish object of a varii of architectural shapes, called the a.-hesto body. This characteristic body is formed the alveolus of the lung. It may be ton in the sputum of a subject with asbestos as a confirming diagnostic finding, and in t fluid extracted from the lung. Because their size, comparatively few asbesto bodies, and only the smaller ones, may transported in tile lymphatic system to deposited in lymphoid deposits within i lung, while still fewer reach the hilar or me' astinal nodes. The limitation of physical opportunity i entry of the asbestos fragment into atransportation by the draining lymphat: seems to explain another characteristic d ference between silicosis and asbestosis. T small free particles of silica readily penetrr the aveolar walls and lung tissues, aided unaided by phagocytes, and are mainly r posited in the lymphoid depots along t drainage system, thus setting up focal rer `tion and characteristic nodular fibres whereas asbestos fragments stay mair where they land in the alveoli, particulat in the vestibular areas of the lobules, arousing a more uniformly distributed re; tion and usually nonnotlular or diffuse hrosis. although there is evidence that th may penetrate the tissues also. As alve> become obliterated and the luing nrchitectu becomes distorted, the asbestosis bodies 1 come embedded in fibrous patches a masses. to remain of tiiuch the same apper ance indefinitely, although in the older sea there appears to lie some change in them ai they may then absorb the basic-staining dy< Just what composes the first part of t reaction to asbestos fragments deposited alveoli is subject only to deduction at t present. If we assume the primary effect be from physical injury (traumatism) alveolar linings and septa, we may assur fluid accumulation. It may constitute the fit or acute reaction, and that fits with the plm cal evidence of increase of lung fluid th clinicians find in asbestos workers earlv 1S6 5OO1i0,? 04 PATHOLOGY OP ASBESTOSIS A-,-' "their exposure, even before there is evidence of fibrosis. It is also consistent with the early "ground-glass" changes in roentgenographic lung fields. As the condition progresses--ordinarily through years of continued exposure--and while alveolar fluid may continue to accom pany the giant cell and colloidal envelopment of the fragments of asbestos crystals as. long ns fresh deposition continues, permanent change in the form of fibrosis takes over and proceeds. This fibrosis is essentially the same as will occur from any relatively innocuous but irritating presence of solid foreign ma terial located within living tissues. There is some evidence that it may be halted by re moval from exposure to continued asbestos inhalation, but after its formation it cannot be expected to be reduced, and when it has reached a disabling grade the disability may he expected to be permanent. In the advanced stage it causes respiratory embarrassment and finally circulatory difficulties resulting in increased right heart burden. The gross condition of the lung, as seen in an autopsy service where asbestosis mav be encountered, of course, varies with the grade of fibrosis. While that condition tends to be consistent with the degree and duration of exposure to the dust, the causative ex posure and the resulting fibrosis do not al ways agree. Merely the fact that a person has worked in an asbestos plant does not justify an assumption that he has acquired asbestosis of a clinical grade. In some of our cases the finding of -small numbers of asbestosis bodies in the ,alyeoli Fig. 4.--Advanced Grade IV asbestosis: oblit erating hyaline fibrosis. 50010.?05 INDUSTRIAL KBALT4 was merely incidental. The lung in such an instance exhibits nothing else of that con nection. L'sually the occupational story re veals that the person worked in an asbestos plant perhaps even for several years but some time previously. Merely for recording pur poses. we have designated the condition as Grade I. Grade II is also an incidental finding. It means an estimated thickening of alveolar walls and perivascular fibrosis, neither being remarkable, together with asbestosis bodies in alveoli and scattered through the fibrous framework. The lung of that grade may be .-omewhat coarsened in texture but may not appear grossly abnormal." ` ' Grade III is associated with definite respir atory difficulty, but up to this phase appar ently progress of the disease may be halted by removal from exposure, and the condition remains in status quo. It is' not per se a fatal state. The anatomical grading is based upon autopsy examination when death has oc curred for another reason. The lung in this case is of coarsely honeycomb fibrous tex ture. nonelastic and distended. This quality is general, although not entirely uniform. Particularly in the upper parts there ar patches of distorting indefinite scarrings, an there is a grayish marbled cast on sectioi The pleura may be thickened and adhesior may be found, but in some instances it ma be quite normal. Grade IV is the advanced phase which wi terminate fatally on its own account if sonother death-dealing condition does not inte: vene. The subject becomes increasingly, an finally absolutely, disabled in respiratory ar. circulatory functions. The lungs in this final phase are tougl coarse, inelastic, fixed in expansion, gravis marbled in appearance, and generally, bi irregularly, in an extreme state of fibrot induration. Various distorting scarrings cur. particularly in the upper parts. Althoug such scarrings are patchy rather than nodi lar. they sometimes resemble, both gross, and microscopically, the lumps and noduli of silicosis. The pleura may be thick, eve cartilaginous in toughness, and the cavil partly or entirely obliterated, but not inevit; bly. Inasmuch as pleural fibrosis is not ii variable, it appears that its occurrence is ; a complication and not as a part of the pr marv disease. ii 5^0-i0?06 188 ^oentaenofo&tc ~~Xldpectd of Sill oenig.enologj.c ICOild and ^Xldledtodid LEONARD J. BRISTOL, M.D., Trudeou, N. Y. A complete roentgenologic study of the chest should include fluoroscopic and roent- genographic examination. Both of these pro cedures lend aid in evaluating the anatomy of the chest, some of the physiologic aspects of respiration, and the presence or absence of abnormal shadows. It is imperative that one be aware of variations seen in the healthy chest before an attempt at accurate interpre tation is undertaken. The lack of under standing of such variations and roentgeno grams of poor quality are frequent causes of incorrect diagnosis. Fig. 1.--Excised inflated lung. The pulmonary artery has been injected with iodized oil-U. S. P. (Lipiodol). Pulmonary branches divide and sub divide, forming the normal lung structure portrayed by a chest roentgenogram. The normal lung structure is produced by the pulmonary artery and its branches, and ing a single chest roentgenogram there is these are visible from the hilum to the periph ery. These branches divide and subdivide, much overlapping, and unless we are aware of what these "white shadows" represent, when they are linear or sometimes nodular forming finer and finer ramifications. The in character, we may incorrectly diagnose injection of a contrast medium into the pul them as indicating a lesion. The appearance monary artery of a normal excised inflated of blood vessels in the frontal viey/ yaries lung will render an excellent illustration of greatly in normal persons. Usually the older how the massive contrast-filled vessels stand the person the heavier the linear markings, X out sharply against the aitcontaining alveoli possibly due to sclerotic changes in the pul and bronchi (Fig. 1). monary arteries. Bronchial asthma and fre v'*> In the conventional postero-anterior quent respiratory infections are also known projection the branches of the pulmonary to cause heavy linear shadows. The roent artery overlap one another and present genogram of the healthy chest presents not a definite network-like pattern. In view- one pattern but a series of merging patterns covering a wide spectrum, ranging from that Director, Department of Radiology, Trudeau- with very minimal fine markings to one with :*.-* Saranac Institute. manifest coarse linear shadows. Therefore, Read in the Symposium on Occupational Dis without supportive clinical evidence an ap eases of the Lungs, sponsored by the Massachusetts Medical Society in cooperation with the Institute parent increase in the vascular pattern per se of Industrial Medicine of the New York Univer can have little specificity in roentgenologic sity--Post-Graduate Medical School, Boston, Oct. diagnosis of pulmonary disease. In all in 28, 1953. stances it is mandatory' to evaluate the roent- 500*0?07 189 Residual-Air Total Volume IXDUSTRIAL iUi.lLn criteria: ( 1 i an adequate history of exposurto free crystalline quartz silica and t 2 > throentgenologic demonstration of discrete gen eralized undulation in simple silicosis, witl Fig. 4.--This man is an iron-ore miner whos chest roentgenogram showed discrete generalize noduiattou in 1933 f. /). It was classified as simpl silicosis, stage I. In the same chest 17 years late (B) ther<;. has been no progression of the x-ra changes, and the man has been working withou complaints. Fig. 2.--The area enclosed within the silhouette oi the thoracic case at full expiration bears a rela tionship to residual air, and the silhouette of the thoracic cage at full inspiration hears a relationship to the total volume of'air within the lungs. Fitr. ,i.--Regression formula demonstrates excel- ten,,t corre,lation ,between rati.o died area .iCnsMpI.ilrdaUti.UonIl and per cent residual air. Coethcient correlation is 11.772. with a standard error of 2:0.02. gen changes in relation-to the clinical his tory. physical findings. ;mtl laboratory data, bar too often this aspect of roentgenologicdiagnosis is overlooked, and the outcome may he most embarrassing. Silicosis i> the result of the interaction ot free crystalline silica and lung tissue. Silica has a specific effect, causing proliferation of connective tissue and the formation of paren chymal silicotic nodules. Microscopically the nodules are seen to be composed of hvaline collagen fibers and are evenly distrib uted throughout the lungs. The diagnosis of this condition rests primarily on two 190 500 i0?08 X-R.-iV ASPECTS OP SILICOSIS .1X0 ASBESTOSIS conglomerate areas of increased density in the complicated forms. We have come to recognize three roentgenologic types: (a ) Fig. 5.--This man had Stage II simple silicosis in 1938. without symptoms (A). The x-rav changes are characterized- by- discrete generalized modula tion and definite enlargement ot the lung roots. Twelve years later (B) there has been no change in the degree ot discete nodulation. but in the inter val there has developed a slight degree of coales cence of the nodules in the right outer second inter space. In 1950. the date of this roentgenogram, the subject had no respiratory complaints and was gain fully employed. Fig. 6.--(A) Simple nodular silicosis. Stage I. Note generalized discrete nodulation and enlarge ment of both lung roots. (B) This patient has been exposed to iron oxide fumes only. The character istic nodular pattern is visualized, but the lung roots are of normal size and position. simple silicosis: (b) silicosis with conglom eration: (ci silicosis with tuberculosis. Fol lowing is a useful classification. A. SIMPLE SILICOSIS Stage l--First-Degree Silicosis.--The nod ules are barely visible and are associated 191 500H0209 INDUSTRIAL HEjsLTL with preservation and at times exaggeration of the linear markings. Stage II--Second-Degree Silicosis.--The nodules are from 2 to 3 mm. in diameter and are of sufficient size to obscure the linear markings- tor a~ gretrrexfent. Stage III--Third-Degree Silicosis.--The nodules are more than 3 mm. in diameter. Small areas of coalescence may be seen. B. SILICOSIS WITH CONGLOMERATION This is probably the result of interaction of an infectious organism, not necessarily the tubercle bacillus. It is conceivable that there is no relationship between the silicotic nodule and the infectious element. C. SILICOSIS WITH TUBERCULOSIS This may occur as the result of an infec tion superimposed upon progressive and still active silicosis or oi such an infection super imposed upon an old and already stabilized silicotic process. Diffuse obstructive emphysema is known to be one of the complications of silicosis. It is seldom clinically manifested in cases of simple discrete nodular silicosis, but con glomerate silicosis is almost always compli cated by it in some, degree. I do not mean to imply that chronic pulmonary emphysema is never detected in a person who has discrete nodular silicosis but to raise a question as to the underlying cause when the two are asso ciated. Is the emphysema directly related to the pulmonary deposition of quartz, or is it an entirely independent process? Persons--'with--diffuse obstructive emphy sema have a reduced maximum breathing capacity and an increased residual air. It is felt that important knowledge concerning the actual residual air/total volume ratio can be obtained from an adequate chest fluoros copy and from films made in full inspiration and full expiration. It would appear logical that the area enclosed within the silhouette of the thoracic cage at full inspiration should bear a relationship to the total volume of air within the lungs and that the silhouette of the thoracic cage at full expiration should bear a relationship to residual air fFig. 21. 192 A short time ago Dr. George Wright mad< a study of 134 cases that showed a good cor relation of residual air/total volume witl area of roentgenologic expiration/area o roentgenologic inspiration, the coefficient o correlation being 0.772. with a standard erroof 0.02 fFig. 31. Therefore it seems per missible to say that when diffuse obstructiv< emphysema is a complication of the silicotii process fluoroscopic examination of the ches and a chest roentgenogram made in full ex piration should furnish information as to th< presence of pulmonary function impairment The moderate and severe forms should no be difficult to identify, but it is not easy t< be definite about persons with slight impair ment. I know of no way in which we cat determine accurately the degree of diffusi obstructive emphysema other than by em plovment of pulmonary functional studies The discrete generalized nodular pattern as visualized in the chest roentgenogram o a person who has had an adequate exposim to quartz, reflects the unit pathological lesioi of silicosis--a nodule of hyaline fibrous tis sue. This roentgenological finding does no' imply the presence of pulmonary disability or that the abnormal densities will be pro gressive in nature ( Figs. 4A. 4B. 5.4. anc SB). At the present time there are no statis tical data available, to my knowledge, wliicl would confirm a general impression that a! cases, or even the majority of cases, of sim ple silicosis are progressive. One'such study has recently been started and will be re ported on at a later date. .. Not infrequently the roentgenologic differ ential diagnosis of siderosis and silicosis i\- said to be a source of considerable difficulty One of the main features, other than the occupational history, is that in simple silicosis there is always accentuation of the hilar re gions, in contrast to the normal appearance of the lung roots in a person who has been exposed to iron oxide only (Figs. 6A and 6B). If a worker has had adequate pul monary deposition of both quartz and iron oxide, as is the case in some industrial occu pations. the lung roots will be enlarged as a 5OCH021O X-RAY ASPECTS OF SILICOSIS AXD ASBESTOSIS result of the reaction of free crystalline silica on the pulmonary' tissues. Asbestosis is a form of pneumoconiosis resulting from prolonged inhalation of asbes tos fiber. It is a chronic disease, with diffuse pulmonary: fibrosis-which takes years to de velop. As in other occupational diseases of the lung, the chest roentgenogram is the cornerstone in establishing the diagnosis. Of course, it goes without saying that an adequate history of exposure to asbestos fiber is also a requisite criterion. It would be wise, before proceeding to the roentgenologic classification of asbestosis, to caution about making statements as to pul monary functional impairment--"disability" --from the x-ray. An expiration film or chest fluoroscopy is not of much help in these patients, because their lungs usually empty- very well. When functional impairment is present, it is usually a problem of a "tight lung" irr contradistinction to the diffuse ob structive emphysema seen in complicated forms of silicosis. Physiological study of such cases usually reveals a decreased maxi mum breathing- capacity, a small total vol ume. and no increase in residual air. Dr. George Wright has performed complete phy siological functional studies on many men from the asbestos industry-. When we cor related his findings with the x-ray, it was found- that some persons with slight roent genologic changes had definite functional im pairment. This, as you will remember, was not the. case in simple discrete nodular sili cosis. . ' ' As in silicosis, the roentgenologic changes in the lungs of persons with asbestosis can be divided into varying stages of develop ment. as follows. ASBESTOSIS----STAGE I There is present an extremely fine network of increased densities at both bases, radiating from the cardiophrenic angles toward the costophrenic sulci. There may- or may not be a superimposed granular pattern. The middle thirds of the lung fields may also be slightly affected, but the apices are clear. The portions of the lung involved have a hazy appearance (Fig. 7). ASBESTOSIS--STAGE II The roentgenologic picture is more dense. There is a beginning decrease in the'clarfty of the cardiac silhouette. The densities ex tend to the periphery of the middle and the lower thirds'- of both lung fields. These parenchymal changes are sometimes referred to as having a "ground-glass" appearance. The lung roots are generally accentuated (Fig. 8). ' Fig. 7.--Asbestosis, Stage I. Note find network of increased densities at both bases. Midlung fields and apical regions are clear. Heart borders are clearly defined. - ASBESTOSIS--STAGE III Considerable shadowing of the middle and the lower thirds of both lung fields is noted, which can extend to the upper thirds. The outlines of the cardiac silhouette are difficult or impossible to differentiate against the densities within the lung parenchyma--the so-called ``shaggy heart" (Fig. 9). 1 It is not especially important whether we have some difference of opinion as to which x-ray stage of asbestosis a patient has. The important thing is to be certain of our diag- 50010211 193 IXDrSTRl.-lL liti.tL l enlargement without gross alteration uf ti cardiac silhouette on the posteroamerv projection. CONU.CSIONS Silicosis anti asbestosis result from tl inhalation of sufficient quantities oi free cry talline quartz silica and asbestos liber. When pulmonary reaction occurs a- tl result oi-deposition of either dust, a charn teristic. though different, roentgenologic pattern is manifested in the chest x-ray. An x-ray classification of both conditioi is employed according to the extent of tl characteristic shadows. Simple silicosis is usually not accompaim by ;my pulmonary functional impairmer whereas the complicated forms almost ahva; demonstrate some departure from the norm: The functional impairment in silicosis Fig. 8.--Asbestosis. Stage II. Basal areas of in creased density are more pronounced than in Stage I. There, is slight involvement of midlung fields but complete clearness of the apices. Note 'beginning loss of (kli.iition of right cardiac border. due to diffuse obstructive emphysema, chest fluoroscopy and/or chest roentgeni grams taken in full expiration aid in evali ating the presence or absence of this con plication. 5 - uosis and of the presence or absence of pul monary functional impairment as the result Xot all cases of asbestosis have a breathii of the pulmonary deposition of asbestos fiber. problem. When it is present, it is due to The diagnosis is most difficult in cases which Fig. 9.--Asbestosis. Stage III. Basilar areas & demonstrate only a very slight departure increased density and involvement of midluug.rieb are ntore striking. Characteristic shadows are no 4 from the usually accepted normal chest roent extended to involve the upper thirds. Cardiac genogram. These cases are classified as huuette has assumed typical "shaggy" uppearanc V.<;" doubtful or uncertain. Usually stereoscopic liims of good diagnostic quality are most rV. -C helpful in such situations. At any rate, it would seem mandatory that these cases be 5" closely followed by means of serial chest x-raysr Fortunately, this problem floes not confront us too often. - This discussion does not represent a com plete synopsis of the problem of pulmonary asbestosis and silicosis. It was the intention only it) demonstrate various roentgenologic i, manifestations of the lung abnormalities in cident to these conditions. However, one '7 would be remiss if mention was not made of the fact that these fibrotic diseases may give rise to cor pulmonale. The right ventricular enlargement is best demonstrated in oblique views of the chest and by fluoroscopy, [t is possible to have a considerable degree of such 194 50010212 X-RAY ASPECTS OE slUCOSIS AXD ASBESTOSIS "tight lung." Expiration films are not of much value in determining the presence or absence of respiratory impairment in these cases, as there is no increase in residual air. Unlike silicosis, we found some persons with- slight x-ray changes indicating asbestosis with definite functional impairment present. DISCUSSION' Dr. M. C. Sosman. Boston: Dr. Bristol has pre sented a very complete and scholarly paper con cerning the demonstration and identification of the various forms of silicosis and asbestosis by roent genological examination. The problem, however, is quite different when attempting to make a diagnosis of silicosis or asbestosis in some of the patients seen in a general hospital. Dr. Bristol's patients were x-rayed particularly for silicosis or asbestosis. and in many of them there was a definite history of ex posure. In many of the others there was a known pulmonary disability, and the possibilities of pneu moconiosis were automatically considered. By con trast. most of our patients are sick, but they have a much wider variety ot disease, and the demonstra tion of the abnormality causing the symptoms is often difficult. w:,h..its identification even more ar duous. Many of our patients have shortness of breath, cough, fever, or loss of weight. It may be due to disease elsewhere in the body, heart disease or any Other conditions than industrial disease affecting the lungs. But it is surprising how many times the var ious pulmonary diseases and conditions can imitate one another.- At our institution we had chest x-rays taken of 8.000 patients last year, and there were only 3 in whom we could conclude, with any certainty, that their illnesses were due to occupational pneumo nitis. However, we can see many slight pulmonary changes- and noncharacteristic shadows, such as Dr. Bristol-has demonstrated in the early stages of silicosis- and asbestosis. but with no symptoms or signs and no history of industrial exposure. At this point I would like to take up the gage oi battle which Dr. Chapman flung at me in introducing me. Dr. Bristol has just stated that in evaluating x-ray films one must consider the patient's history as well as make a thorough physical examination. Now I submit to you, gentlemen, that, as a physician prac ticing radiology. I cannot remember a single case in which the physical examination changed the di agnosis which had been made from the x-ray find ings, the history, or the laboratory results, or a combination oi the three. In other words. I feel that it is a waste of the physician's time to listen to the patient's lung and then decide, in view ot what he thinks he hears, what the x-ray shadows mean. However, I would not urge you to- stop- doing: rr; for it impresses the patient and gives the physician time to think what might possibly be wrong and what kind of an x-ray examination should be made first. As to the exact problem presented today, may I show you a series of slides, any one of which could be interpreted as various stages of silicosis or asbes tosis if the conditions of exposure were adequate and if the diagnosis was not otherwise known or available: May I add at this point, and stress its importance, that I firmly believe the x-ray exam ination of the chest is only half of the diagnosis: the other half must be a history of adequate ex posure. We are not justified in making a diagnosis from x-ray films alone or from the history alone, but we can do it from the combination of the two. [Dr. Sosman then showed a series of slides, in each case pointing out the similarity between' the condition demonstrated and similar lesions which could be due to silicosis or asbestosis. He pointed out that it was easy to demonstrate symptom- producing lesions in the lungs in over 95% of the cases but that it was difficult to identify them from the x-ray examination and the history in more than 75%. He included the following: carcinoma of the lung, simulating the conglomerate stage of silicosis: metastatic carcinoma, duplicating the nodular stage of silicosis: retrograde lymphatic permeation from the retroperitoneal abdominal area simulating early streaking of silicosis: various granulomatous dis eases. infections, parasites, effects from inhaling toxic materials: lipid pneumonitis.' scleroderma, multiple infarcts, chronic passive congestion,' espe cially from mitral stenosis; idiopathic pulmonary fibrosis, diffuse bronchitis and bronchiectasis and sarcoidosis, in addition to several rare conditions just recently identified.) " Conclusion: 1. X-ray examination is mandatory in all occupations where there is any possibility of exposure to disease-producing materials, with pri mary films at employment and routine films at least once a year thereafter. 2. In many conditions seen in the general hospital, silicosis has to be considered, but it is actually diag nosed in only a very small fraction of the total num ber of patients seen in a general chest clinic in such an area as metropolitan Boston. 509'-0?13 195 ^^unctioncif ~s$bnormcilitied oj?^Qncludtricil 3JPuimonciry. drodid GEORGE W. WRIGHT, M.D., Cleveland . ............ aiv;..- MiaMiiCiM!':rv- ct I have been asked to discuss the abnor malities of function that occur in certain of the pulmonary diseases of occupational origin. Knowledge concerning the derange ments of function, characteristic of each spe cific disease, will assist materially in making a correct diagnosis. Information concerning the degree to which function has been de ranged, consequent to the disease, will assist in proper evaluation of the physical disability arising out of the pathological process. Time will not permit me to discuss all the occupa tional pulmonary diseases; therefore, I pro pose to discuss chiefly silicosis and asbestosis. These two diseases offer a nice contrast and are representative of the abnormalities of function that one meets in other types of industrial pulmonary disease. Since this audience includes a larger pro portion of lay than medical persons, it seems to me advisable that I spend some time in describing as simply as I can the function of the respiratory and cardiocircuiatory ap paratus. I trust that my medical associates will forgive me if I. for the purposes of rapid .comprehension, simplify the processes which we know are. in reality, quite complex. The human body is an internal-combustion ma chine which obtains its energy by burning carbohydrates and fat. In the process, oxy gen is utilized and carbon dioxide is pro duced. The rate of burning is proportional to the rate of energy expenditure: hence. Director of Medical Research, St. Luke's Hos pital. Read in the Symposium on Occupational Dis eases of the Lungs, sponsored by the Massachusetts Medical Society in cooperation with the Institute of Industrial Medicine of the Kew York Univer sity--Post-Graduate Medical School. Boston. Oct. 38. 1933. 196 oxygen utilization and carbon dioxide pr Auction are augmented or diminished proportion to energy' expenditure. The ox gen utilized is obtained from, and carl) dioxide, in turn, is discharged into, the atnn pheric air. Since combustion goes on de in the tissues of the body, some arrangemc must be made tor transporting oxygen and carbon dioxide away from, the acti tissues. This transportation is performed the blood stream which contains oxygen a carbon dioxide in physical solution and ca bined with chemical substances. It is read understandable then that, as energy prodi tion is augmented during increasing woi more and more transport of these chemie: must take place. This is accomplished increasing the blood flow to the active par the increase in blood flow being effected an increase in the activity of the heart, t organ that pumps blood through the vascu channels of the body. The rate of exchan of oxygen and carbon dioxide between t body and the atmospheric air varies appro mately tenfold, depending upon the rate physical energy utilization. * Adequate gas exchange requires that some place the blood must' flo\v 6ver a lar vascular surface where the medium separ: ing the blood -from-the outside-air is ve thin and hence will permit the gases to crc from the blood to the air phase with gr< rapidity. Such a large vascular bed would very fragile and subject to great injury exposed on the outer surface of the boc but man has developed so that this vascu! bed is contained within a very strong covt ing and protecting device, namely, the chi cage. The lungs are this vascular bed throu which blood can circulate very rapidly a present an enormous surface to air that c be variably' and rapidly refreshed. It is r parent that if the air within the lungs wc 50010214 FUXCTIOXAL ABX0RMALIT1ES OF PL'LMOXARV FIBROSIS not exchanged frequently the blood would soon pick up all the oxygen there and replace it with carbon dioxide. In such circumstances, carbon dioxide would back up in the tissues and the tissues would sutler from a lack of oxygen... Lack of oxygen is known, under situations familiar to all of us. to result in a smothering of the combustion processes in any sort of internal-combustion machine. Obviously, therefore, it is necessary that the air within the lungs be rapidly and continu ously changed in order to provide an atmos phere inside the lungs which closely resembles the outside air. The act of breathing serves the purpose of exchanging the lung gas with that of the outside air. In summary, the respiratory apparatus is an air pump actuated by. movements of the thoracic cage, which contains a large vascular surface designed tor the rapid exchange of gas between blood and air. To complete the apparatus, a blood pump, namely, the heart, forces blood through the vascular surface of the lung at a variable and sometimes rapid rate. In addition, of course, the heart also pumps blood away from the lung to the tissues that utilize the oxygen and nutrients contained in the blood itself. The respiratory and circulatory apparatus does not operate in an unregulated fashion. There is a control mechanism situated in the brain which dictates to the thoracic cage the rate at which air should he moved into and out of the lungs, the rate at which blood will be propelled through the lungs, and the way in which blood shall be distributed through out both the lungs and the body. This control mechanism is under the influence of many factors'. The precise manner in which the body integrates its activities so that respira tion and blood flow keep pace with the de mands for energy production is incompletely understood and highly complex. During the past few years, methods have been devised for quantitating some of the physiologic aspects of the respiratory and circulatory systems. It is possible to measure the volume of air contained in the lungs in their fully distended state (total volume) and also in the state of being as empty as one can make them by voluntary effort (residual vol ume), the difference between these two vol umes being the stroke volume (vital capacity; of the respiratory pump. One can also meas ure the maximum rate at which the respira tory apparatus can move air into and out of itself in repeated cycles i maximum breathing capacity). The response of the respiratory apparatus, in terms of the volumes of air it breathes per minute, to the stress of physical exercise (O2V, or oxygen ventilation equiva lent) can also be measured. A sample of blood drawn from one of the peripheral arteries of the body and subsequently meas ured for its oxygen and carbon dioxide pres sure and for the degree to which the oxygen carriers have picked up a load of oxygen while in transit through the lung gives us an accurate estimate of the effectiveness with which the lung ventilates the blood which perfuses it. It is also possible to measure"the partial pressure of oxygen and carbon dioxide in the air of the deeper portions of the lung where gas exchange is taking place between the blood and air phase. The actual physical state of the lungs is now the subject pf in tensive study in several laboratories. Al though we are now able to measure the pres sure and quantity of blood flowing through the lungs under resting conditions and during mild exercise, in man we are only beginning to arrive at a solution to the problem of measuring blood flow during heavy exercise. The measurement of potential differences in the heart muscle, as reflected in the electro cardiogram. permits us. to., learn much-con cerning the action of the heart itself. Never theless, we are still quite' ignorant of the details concerning the chemistry associated with energy production in heart muscle, and the same may be said for the muscles that permit us to carry on physical exertion. One can see, therefore, that, although we possess useful knowledge which permits us to recog nize derangements of function and to quanti tate them, we do not have all the information that we would like to, and there are many questions still unanswered. Do these various measurements just men tioned supply us with reliable information in terms of the person's ability to expend 197 500'id215 IXDrSTRUl. physical energy? This question lias been under study for a number m" years in the Department of Physiology of the Edward L. Trudeau Foundation, and a preliminary report of rather extensive data in this regard has been made. The maximum energy output during exercise of six minutes' duration was measured in a group made up of normal persons and others with various kinds of pulmonary disease. The oxygen uptake dur ing the most intense exercise of which each individual was capable was measured. This maximum () uptake is believed to quantitate the peak capacity of the integrated functions >f the respiratory and circulatory systems and to reflect maximum energy output. Xumerous physiologic measurements of vari ous aspects of respiration and circulation were carried out in conjunction with the determination of the maximum ability for oxygen uptake. In normal persons and in others with various forms of pulmonary dis ease. including many with industrial disease, a high correlation between the maximum capacity for oxygen uptake and a combination of the maximum breathing capacity and oxy gen ventilation equivalent was demonstrated. The correlation coefficient was 0.904 S. E. * *.025. It is apparent from these data that in tho.se persons who suffer from pulmonary disease a measurement of the maximum breathing capacity and of the response to exercise in terms of ventilation ( O a- i either directly determine or reflect some common factor that determines the ability such per sons possess for physical energy expenditure. ' What are the vulnerable points of the respiratory system? It is apparent that dis ease may hinder the motion of the thoracic cage, thus impairing the capacity of the per son to move air into and out of the lungs in an augmented fashion. Disease may also cause obstruction to the large or the very small tubes that conduct air into the various por tions of the lung. Such obstruction will im pair the rate of air flow through the tubes and reduce the 'capacity of the respiratory apparatus to perform as an air pump. Lung tissue may he so altered by disease that it becomes less easily stretched during inspira- 198 tion or resists deformation during expi tion. an alteration that also would reduce ; capacity of the respiratory apparatus to pm air. Any of the three alterations just nu tinned may cause uneven distribution of ga: in the lung, thus interfering with maintenai of an optimum pressure of oxygen and carl* dioxide in the gas phase, and lead to ina< quate'ventilation of the blood as it perfu the lungs. Disease processes may cause proliferation of the tissues that support blood vessels inside the lungs and in t manner increase the thickness of the me brane that separates the blood from the t phase, with a resultant impediment t<> i passage of vital gases across this >q>araii membrane. This, in turn, would lead to adequate ventilation of blood which perfuthe lung. Disease processes might also i stroy portions of the vascular bed of the lui with the result that'the area available to i body for transfer of gases from the blood the gas phase might he reduced, hi this c< nection. reduction of the vascular bed m also impose a resistance to blood flow throu the lung and abnormally increase the wr of the heart with consequent damage to tl organ. Disease process may aiso so ittfluei the lung as to cause unusual reflexes to ar from within the lung and thus vary t breathing response during rest or e.-pecia during exercise. As mentioned before. <i ease processes may interfere with the proj ventilation of the blood as it perfuses i lung, with the result that the blood itwill undergo'changes in the `wav of increr in the- Oxygen-carrying cells, thus causi the blood to become more viscous and that way increase the work of the heart in t process of pumping blood through the v< sels of the lung. Disease processes also pi duce other changes in the cardiorespiratr. apparatus of a very subtle nature, and pr< ently only vaguely recognized, which m contribute materially to disability arising < of pulmonary injury. We may proceed now to a discussion of t specific wav in which the respiratory appai tus shows functional abnormalities result! from silicosis. Xumerous studies by ma 500102:16 rrxcrwxAL .ipxorujlities of pclmoxarv fibrous investigators throughout the world have shown that the earliest recognizable form of silicosis, generally classified as simple dis crete nodular silicosis, is attended either by no recognizable alterations of function or. at most, by very slight ones. It is perhaps surprising to some that a disease process which can lie readily seen as manifested in a chest roentgenogram may nevertheless fail to cause any recognizable functional dis turbance. The use of the word "recognizable" is deliberately chosen, since it is entirely possible that slight alterations of function are not recognized by virtue of the fact that thus far all studies in diseased persons have been made after the disease has become mani fest. W'e are forced to compare measurements of the diseased person with the average for these same measurements in normal men. If we were able to study persons early in life, prior to the development of the disease, and repeat the studies in the same persons at the time the disease is fully developed in its simple discrete nodular state, perhaps we would recognize some reduction in respira tory function. W'e have no way. at present, of disclosing that a high normal man might he converted to a low normal by disease. Also, properly sampled groups of diseased persons measured for comparison with groups of normal men have not been studied. When conglomerate silicosis develops, one usually finds readily recognizable alterations of pulmonary function. The maximum breath ing capacity is usually reduced, the residual volume is increased, and the oxygen ventila tion equivalent may he slightly above normal. These findings are quite typical of those ob served in diffuse obstructive emphysema, and indeed the histological sections of the lungs from conglomerate silicotics show the anatomy characteristics of diffuse obstruc tive emphysema. When the impairment to movement of air into and out of the lungs is severe, it can be recognized by observation of the limitation of thoracic motion during the act of breathing. More sensitive methods permitting earlier recognition of this obstruc tion to air fiow are fluoroscopic examination and comparison of roentgenograms taken at maximum inspiration and expiration. In contrast to the person with idiopathic diffuse obstructive emphysema, in whom recogniz able alterations of effectiveness with which the blood is ventilated, are common, most persons with conglomerate silicosis show little or no impairment of blood ventilation at rest, although evidences of inadequate venti lation may appear during moderate or heavy exercise. One may interpret this as indicat ing that in conglomerate as well as in discrete nodular silicosis the involved areas of lung are perfused either slightly or not at all with blood from the pulmonary artery. Virtually all the blood that flows through the lung appears to traverse normally functioning lung tissue. In many but not all cases of conglomerate silicosis, the pressure required to force blood through the vascular channels of the lung is increased as a result of attrition of the vascular bed. This, in turn, places a strain on the heart, with production of hyper trophy of the cardiac muscle. If the resistance to blood flow is severe enough and lasts over a sufficient length of time or is complicated by pulmonary infection, heart failure may occur. The physiologic abnormalities observed in the various stages of silicosis fit reasonably well with the histologic abnormalities. A.mentioned earlier, the discrete nodular stage is focal. Each diseased area consists, of destroyed lung replaced by the granuloma characteristic of silicosis. Xo air enters these foci, and no pulmonary artery blood perfuses them. In between each focus one sees a nar row zone of . dilated alveoli, spoken of as being emphysematous. The physiologic data indicate that these dilated alveoli are too few in the aggregate to recognizably influence function, or they function normally in spite of being dilated. When clinical or physiologic evidence of impairment consistent with dif fuse- obstructive emphysema is observed in a person with simple discrete nodular silicosis, one must suspect that the emphysema is a chance concomitant disease and would have occurred even though the silicosis were ab sent. In conglomerate silicosis the histologist observes masses of fibrous and granuloma 500 199 IXDCSTRIAL HEAL7 tous tissue which, in the aggregate, may com prise a large portion of the total intrathoracic substance. The air-containing lung tis sue usually displays the characteristic ap pearance noted in diffuse obstructive emphy sema. Although critical measurements of the total pulmonary capillary bed have not been made, it is obvious that some, and in many cases much, of the vascular bed has been destroyed. In these cases, thickening of the right ventricle, presumably caused by the increase of work required to force blood through the lungs, is often evident. In summary, it is the experience of all investigators that the simple discrete nodular phase of silicosis is rarely complicated by recognizable physiologic alterations of the cardiorespiratory apparatus. In the conglom erate form of the disease, however, the classi cal evidences of diffuse obstructive emphy sema are relatively common. It is of practical interest that in all stages of silicosis the severity of impairment of respiratory func tion bears only the grossest correlation with the extent of the disease displayed in the roentgenogram. If the physiologic alterations are slight, there is little impairment of the ability to carry out physical exertion. If, on the other hand, there is a marked reduction in breathing capacity, the degree by which such a person's ability for physical exertion is limited may be equally great. The breath lessness during exertion that restricts the physical work capacity of the conglomerate silicotic is primarily caused by loss of breath ing power. Present-day techniques permit us to measure the physiologic alterations with a reliable degree of accuracy. During the past few years a group of 57 men who had experienced varying degrees of exposure to air-borne asbestos fiber were studied in the Department of Physiology of the Edward L. Trudeau Foundation. A preliminary report of these data was pre sented at the Seventh Saranac Symposium in September, 1952. What is the status of the respiratory and circulatory systems in a person who has typical roentgenographic and clinical evidences of asbestosis ? A study of the men in the above-mentioned group 200 shows rather dearly that in the typic asbestotic there is little, and often times n impairment of ability to ventilate the lunc as measured by the maximum breathii capacity. There is likely to be, however, measurable restriction of the degree to whi< the lung can be expanded, as evidenced 1 a slight to moderate reduction in total volun: Of course, when the fibrosis is extreme extent, the impairment to enlarging the lui may cause an appreciable loss of maximu breathing capacity. Fluoroscopic examin tion. as well as a comparison of inspiratic and expiration films, and measurement the actual residual volume of the lung she that there is little or no impairment to empt ing the lung in such persons. When o: measures the partial pressure of oxygen ai carbon dioxide in the gas of the lung, o: finds that these pressures too are with normal limits. -Nevertheless, study of sampl of blood removed from the peripheral artewill usually show a rather marked inadequa* of oxygen transfer from the lung air to ti lung blood. The partial pressure of oxygt in the arterial blood is usually subnorm; and less than the normal proportion of ox hemoglobin will be found in the sample. T! difference between the pressure of oxyg< in the lung gas and in the lung blood usually quite markedly increased. The parti pressures of carbon dioxide are apt to within normal limits, both in . the lung g and in the lung blood. These data qui clearly indicate.animpediment to the passa: of oxygen across the membrane separatii the gas-from'the'blood phase in the lun Carbon dioxide transfer, however, is n appreciably interfered with. During exerci the person with asbestosis is apt to displ; overbreathing. The volume of air breath per minute will be considerably greater f< a given stress of exercise than would be trt in normal persons. This is well demonstrau in measurements of the oxygen ventilatic equivalent, which is found to be elevate The rate of respiration and the pulse ra during exercise are apt to be higher th; normal in the person with asbestosis. Tl cause of the breathlessness during work th FUNCTIONAL ABNORMALITIES OF PULMONARY FIBROSIS limits the physical activity in some persons with asbestosis resides, in part, in the ab normally high rate of breathing and the abnormally increased volume ot air breathed during work. The subnormal oxygen content and the pressure in the arterial blood act as an unusually strong stimulus to breathing. In addition, reflexes originating from the abnormally stiff and relatively uncompliant lung of the asbestotic may add to the stimulus of breathing or even give rise directly to the distressing sensations felt by the patient. To what extent does the presence of an abnormally low oxygen content of the arterial blood, one of the chief characteristics of asbestosis, presage a limitation of capacity tor physical work? We found that some of those persons showing a definite subnormal O2 content of the arterial blood still pos sessed a normal maximum capacity for physi cal exertion. Because we are comparing such a person with the average normal man and not with himself prior to injury, it would be incorrect to say that our evidence demon strates an absence of impaired maximum capacity for physical work. It should be em phasized that our data show retention of average capacity for work in the presence of incomplete oxygenation of the blood. These findings in the person with asbesto sis stand in rather striking contrast to the abnormalities seen in the typical silicotic. Whereas in the conglomerate silicotic a marked reduction of maximum breathing capacity and an increase of residual air, typical of diffuse obstructive emphysema, are commonly observed, such abnormalities -are usually absent in the asbestotic. In the latter, there appears to be little or no impair ment of movement of air into and out of the lungs, the chief abnormality observed in re gard to thoracic action being that the lungs are resistant to inspiration. Whereas the person with silicosis usually shows no or little abnormality of the transfer of gases between the lung phase and the blood phase, quite the reverse is true in the person with asbestosis. In the latter, inadequate oxygen transfer to blood as it flows through the lung is common. In contrast also to the silicotic, who shows no unusual response to exercise from the standpoint of the amount of air that he breathes, the person with asbestosis breathes considerably more than does the normal- man for a given intensity of physical exercise. One can generalize by saying that, although both the silicotic and the asbestotic man develop unusual shortness of breath during physical exertion, the person with silicosis does so chiefly because of a loss of breathing power, whereas the man with asbestosis becomes short of breath primarily because his breathing load, or response in terms of breathing during the exercise, is unusually great. Secondary effects on the heart because of an impediment to the flow of blood through the lung can be manifested in both diseases. In other words, cor pulmonale is a not unusual complication oi either con glomerate silicosis or asbestosis. This contrast of physiologic abnormalities is consistent with what one sees in regard to the abnormal anatomy or histology of the lung in the two diseases. In the silicotic the disease is focal, with large areas of healthy lung tissue remaining in the presence of the scattered nodulation; hence, the relative pau city of physiologic abnormalities. In the conglomerate form of silicosis there is still some healthy lung tissue, but coexistent is a diffuse emphysema, with its airway ob struction and consequent loss of breathing power. Only later, when the ventilation of . the air spaces is inadequate, do-evidences of improper ventilation of the'perfusing blood appear. In well-developed asbestosis the tissue alterations appear to be more wide spread than in silicosis, and even when the process is not severe in any one area, a major portion of the lung will be involved. Hence, there is relatively little truly entirely normal lung tissue in the person with clinically mani fest asbestosis. The nature of the histologic change is such as to increase the thickness of tissue that must be traversed by oxygen in going from the lung air to the lung blood. The abnormality in asbestosis is chiefly lo cated in the membrane that separates the blood and the gas phase. Because of this and the relative absence of airway obstruction 500102*9 201 IX DCSTRIAL DEAL'! in asbestosis. the primary >r chief abnor As a consequence some of the blood mu mality exhibited by the asbestotic patient is flow through areas of lung tissue in whk impaired oxygen transfer to the blood rather tile membrane has been slightly thickene than impaired breathing ability and ventila thus causing impairment of oxygen transt< tion. it is true that the histologists have re to the blood. Since the lung is so uniform ported emphysema as being present in the- involved by the slight alterations of tissti tissues of the lung in the typical asbestosis there is poor contrast between normal ai case. Small areas of emphysema undoubtedly diseased areas and. hence, no definite abno do occur, but the massive emphysematous mal shadow in the roentgenogram. In regai involvement of the lung, which is so com to the correlation between x-ray abnormalr monly observed in conglomerate silicosis, and physiologic abnormality in asbestosi does nut appear to lie present as a rule in line can state that three situations can exis even the severe cases of asbestosis. ( 1 ) physiologic abnormality without ai What can be said about the relationship between the presence or absence of physio logic abnormalities and the nresence or ab sence of recognizable pathologic manifesta definite roentgenologic abnormality. U roentgenologic abnormality plus phvsiolog abnormality, and i .5) roentgenologic abno mality without any physiologic abnormalit tions in the chest roentgenogram in asbes What about the duration and intensity < tosis? Our studies showed quite clearly that exposure to air-home asbestos fiber and tl examples of asbestosis. clearly recognized by subsequent development of roentgenologic < roentgenography hut with minimal or-absent- physiologic abnormalities? As one might e: physiologic abnormalities, do exist. This can pect from experience with other ptilmonai only mean that in some c not the rule i in diseases of occupational origin, there was stances the earliest roentgenologic manifes gross correlation between the intensity ar tations are still focal in nature and that duration of exposure and the developmei large volumes of normal lung tissue remain of abnormal shadows or physiologic change through which blood can perfuse in prefer However, some persons with prolonged ai ence to those areas that have been damaged very intense exposure failed to develop ai by the asbestosis process. The reverse situa evidences of either physiologic abnormali tion may also be observed, as evidenced by nr roetugenographie abnormality. Our m. die observation of some persons showing terial fails to give us any evidence as to wh evidence.- of abnormal physiologic conditions the shortest required duration or intense in the arterial blood with no clearly recog nf exposure is in order to produce a reco: nizable abnormality in the chest roentgeno gram. Two possible explanations exist for this not unusual finding in our series of cases.' hirst, die earliest recognition of asbestosis' in the chest roentgenogram is notoriously very difficult, because the earliest manifesta tion is simply an exaggeration of bronchovascular markings that are normally present in the lung. It may he that in those cases which we observed with evidence of impedi ment to oxygen transfer across the membrane nizahle asbestosis. >i It lias long been known that both crystn line silica in finely divided form and asbesti liber when introduced into the lung can pr< fluce fibrosis which leads to physical impai meat. Although the clinical manifestations the disease are in many, though not a respects similar, the physiologic abnormalitii are recognizably distinctly different in tl earlier stage of the two diseases. In the te minal stage the distinction may not be ei but without evidences of change in the x-ray tirely clear and may lead to confusion, we failed to recognize the earliest x-ray ab further difficulty in diagnosis resides in tl normalities. The second explanation may be fact that many workers with obvious pu that the disease process is so diffuse in its monarv abnormality have had exposure very earliest stage that there is little or no both silica and asbestos, and the diseas' normal lung tissue for blood to flow through. may coexist. Both diseases may he roen 202 50010220 FCXCTIOXAL A13XORMA LITlES OF PCLMOXARV Fl!3R0'l> ^enologically manifest hut without recogniz able physiologic impairment. An enormous respiratory reserve, which is the birthright .it most of us. permits extensive tissue injury and damage with little or no loss of capacity for physical work. This statement of fact iir no way should be construed as condonement for needless injury. DISCUSSION' Dr. James L. Whittenberger. Boston: I was pleased to hear Dr. Lanza's remarks: he made a number of remarks I was going to make. Many of us in the field of pulmonary physiology do not understand all that Dr. Wright was talking about, and I personally agree with the statement Dr. Lanza made that in many ways we are in a primitive state so far as our information about industrial pulmonary diseases is concerned. I read the other day a passage written by Harvey in I633,1 in which he discussed the effect on the lungs of the smoke which heavily contaminated the atmosphere of the large industrial cities in Eng land. He believed that the elderly and infirm were most likely to suffer, especially in the autumn of the year when the smoke was inclined to be severest. Even today we are much concerned with the same problem, and I am not sure that we under stand it very much better than he did at that time. Having been shown the large array of pulmonary function tests which Dr. Wright used very skil fully in his study of industrial pulmonary disease, we should ask ourselves the question of the signif icance of some of these tests. I am not by any means against doing these tests, f think that it is the only way we will learn about these conditions and perhaps learn how little we know about them, but the respiratory system, in spite of the simplified diagram Dr. Wright presented, is an extremely complex system. The interrelationships of ventila tion of the lungs, diffusion in the lungs, and circula tion throughout the lungs are so complex that it "is often extremely difficult to say what is due to impairment of the circulation and what is due to impairment of diffusion or ventilation. As physicians seeing patients with pulmonary disease which may be related to occupational ex posures. I am sure that you would like to know what tests are really feasible outside of the larger hospitals and university centers. I think that the vital capacity, especially if it can be a timed vital capacity, is a measurement which' is definitely worthwhile. I think that the maximum breathing capacity, which is a simple test, is very worthwhile. There is a point here about normal standards. If we use the standards in the literature, it is often difficult to tell what patient is normal or not nor mal. whereas if we had a vital capacity or maxi mum breathing capacity taken on the patient him self at some prior time when presumably his lungs were normal, we would have a much better idea whether disease has affected him or not. I don't know how feasible it is in industrial medical prac tice to get this type of measurement, but I per sonally think that ij_would be vert- worthwhile. Many of the tests Dr. Wright described depend a lot upon the cooperation of the patient, ft is true that arterial saturation during exercise changes independently of any willingness on the part of the patient, but the degree to which he is willing to push himself is very important. The vital capacity and the maximal breathing capacity depend ob viously upon voluntary cooperation. I would like to take this opportunity to agree with Dr. Sosman about the value of the physical examination. I do not know how many of you have read about the tests that were carried on at the Cardiff Pneumoconiosis Research Station in Wales a year*or two ago.- Some of the men in this out standing research station were dissatisfied with what they could deduce from a patient's physical examination, and they invited a number of Pro fessor Christie's experts to come from London and examine the same patients. These patients had emphysema or massive pulmonary fibrosis resulting from pneumoconiosis occurring in coal workers. Since time is short, I will only say that the physi cians were dismayed bv how often they disagreed on physical signs even in patients with advanced pulmonary disease. They just did not agree at all. So. not only should a physician throw away his stethoscope, but also he may as well not bother to percuss or inspect the patient. .. I should not close on such a pessimistic note.-as I would like to say that many researchers iff tfiis field believe there is hope in the development of objective tests of the type which measure the mechanical properties of the lung, the elastic prop erties and the resistance to breathing. These studies are relatively in their infancy. They have not been to any great extent applied in patients with industrial pulmonary disease. I will close by saying that we need humility in our study of pul monary disease, but still we should continue trying. REFERENCES 1. Missen. G. A. K.: Lethal Aerosol, Letters to the Editor, Lancet 265:1212 (Dec. 51 1953. 2. Fletcher, C. M.: Clinical Diagnosis of Pul monary Emphysema: An Experimental Study. Proc. Roy. Soc. Med. 45:577-584 (March) 1952. 50040221 203 Some Stinicut (Sb&eFvettiond ojSlsbe&toiii in Wine and Witt WorU PAUL CARTIER, M.D., Thetford Mines, Quebec, Canada - .uiift'iV.. . '.'ilif....... ...... Instead of giving the usual clinical descrip tion of asbestosis as mentioned in the pro gram. which description may seem to many a matter of personal impression and there fore controversial. I prefer to bring to your attention a series of remarks and comments collected during my nine years of medical supervision of some 4000 asbestos mining workers. From 1945 to 1953 the annual medical and x-ray examination of the asbestos work ers, along with the histological study of 58 autopsy cases, permitted the detection of 128 cases of asbestosis; 40 of the patients are already dead--and autopsies have been per formed--and 88 are still living. Table 1 gives the age-group distribution and the classification by degree of asbestosis in the 128 cases. You may see that there are 72 cases of minimal. 35 cases of moderate, and 21 cases of advanced asbestosis. The age distribution indicates that1 16" workers are 70 years and over--one worker with far advanced asbestosis is 84 years of age and still living--and 66 workers are 60 years and over. First, it seems indicated to explain how the diagnosis of asbestosis has been made in these 128 cases. One hundred twenty-one Thetford Industrial Clinic. Read in the Symposium on Occupational Dis eases of the Lungs, sponsored by the Massachusetts Medical Society in cooperation with the Institute of Industrial Medicine of the Xe\v York University-- Post-Graduate Medical School. Boston. Oct. 28, 1953. 204 cases have been diagnosed by roentgenolos and 33 of these 121 cases have been co firmed by the pathological study of the lung so we can say that 33 cases have been dia nosed by x-ray and histological interpret tion. The remaining seven cases have be' diagnosed by pathological study only, havii been missed on the reading of the standa chest films; but it is important to add th these seven cases are cases of minimal asbc tosis. Without going into a too long disco sion of the effectiveness or the superiori of roentgenology over histopathology vice versa for making a diagnosis of asbest sis, I should like to add the following r marks. We'have to admit that the roentgenolos. cal interpretation might fail to detect cas of minimal asbestosis. but from personal e perience and from repeated contacts wi Gardner, Sampson. Robert. Bristol. Yorwai and Pratt, I can say that no cases of asbest sis of clinical importance have been diagnos< bv the pathologist without having been d tected- anteriorly by the roentgenologist, do not know whether a similar statement true - for employees of the asbestos text: industry, where apparently the x-ray pt tern of asbestosis is fainter than the oi found in the asbestos mining industry. A second comment is about the wit discrepancy in the appreciation oi the degrof asbestosis by different pathologists. In few instances, cases which looked like mir. mal asbestosis to one pathologist have bet classified as advanced asbestosis by anoth pathologist. With the increasing number autopsies for old employees and with tl recent use of the lung biopsy and the lui resection in asbestos workers, we mav assun 50010222 CLINICAL OBSERVATIONS OF ASBESTOSIS Table 1.--Thetford Mines Survey, 1945-1953 Distribution oC 123 Cases of Asbestosis by Age Groups aud by Intensity literature. Nevertheless, briefly, I want to review these causes of death, trying to investi gate the part played by asbestosis in the Age Group*, Yr. death. Minimal asbestosis Moderate asbestosis Advanced asbestosis Total 35-49 20 2 0 -- >.> jft-59 60-04 24 $ 11 13 3 10 ---- 40 31 70 and 65-70 Over Total 11 9 72 54 35 33 ---- 19 10 21 -- 123 It is true that 12 cases, or 30% of the deaths, were caused by an evolutive tuber culosis ; this incidence may seem too high, but knowing that a more complete statistical analysis of all_ the employees in the asbestos industry made in 1950 did not reveal a higher incidence of tuberculosis than in a control that there will be more instances in which group or a severer evolution of the tuber pathologists will differ in opinion among culosis, this rate of 30% is not in itself suf themselves and will not agree with the roent ficient to establish a causal relationship be genologist in the estimation of the amount tween asbestos-dust inhalation and tuber of asbestotic fibrosis present. This lack of culosis. agreement is very confusing in any medical study, but it is still more confusing before a compensation board. Considering the second cause of death, coronary thrombosis, it is difficult to explain how a minimal or a moderate asbestosis For practical purposes, it is of great im could contribute to the formation of a throm portance that a solid roentgenological classi- - bus in the coronary circulation, and, conse tkation of the cases of asbestosis, correlated quently, I am inclined to estimate these five with the histopathological findings, be recog deaths as not related to the factor asbestosis. nized and accepted by ail those concerned The third cause was cardiovascular dis with this problem of asbestosis, because the eases. It is not so simple to say how many chest film must be considered as an essential of those employees have died from their criterion in making a diagnosis of asbestosis cardiovascular disease and how many have and, notwithstanding the limitations of the died from their asbestosis. chest films in some exceptional minimal cases,., The fact that most of the employees who this tool remains more objective and more adequate chan any other presumptive criteria. have died from cardiovascular diseases were 60 and over and the fact that statistics men Table 2 shows the seven main' causes of tion that 65 to 70% of the population of the death in the 40 cases of asbestosis that have same age are also dying from cardiovascular been autopsied; 12 patients have died from diseases-should be taken into consideration evolutive tuberculosis. 5 from coronar-y before arriving at a conclusion. thrombosis, 10 from cardiovascular diseases, 4 from cor pulmonale, 6 from bronchogenic carcinoma. 2 from bronchopneumonia and bronchiectasis, and the last one from cancer Table 2.--Thelford Mines Survey, 1945-1953 Causes of Death In a Series of Forty Cases ot Asbestosis of the brain. In reading this Table, the first question which comes to mind is: To what extent is this enumeration of causes of death different from a similar enumeration for a comparable group of employees from another industry? Unfortunately, I do not know whether there is a marked difference, and I did not have the opportunity to discuss this Table with other physicians or to compare it with a Minimal Asbestosis Evolutive tuberculosis Coronary tbrombosis Cardiovascular diseases Cor pulmonale Bronchogenic carcinoma Bronchopneumonia and bronchiec tasis Other cause 3 1 3 0 3 2 1 ModerateAdvanced Asbes- Asbestosls tosJs 70 40 43 13 12 00 00 Total 12 5 10 4 0 2 1 similar one which may exist in the medical Total 15 17 8 40 500*0223 205 i.XUCSTRIAL l-.EAL In a few lx interline case? in which it was difficult to appreciate dearly the role played by the asbestosis and the rule played by the cardiovascular pathology, the different car diologists consulted were of the opinion that, unless the asbestotic fibrosis is extensive enough to produce pathological or clinical signs of right heart failure, it is impossible to tell with some certainty that the tibrosis has contributed appreciably to the death, especially if there are evident signs of ad vanced degenerative diseases. In practice, this group of employees with cardiovascular diseases and a minimal or a moderate degree of asbesto.-is is becoming a 'erious problem as far as the compensation aspect is concerned. Without too much im agination and from the findings of an in creasing number of autopsies on old em ployees. we can assume that there is a large unknown number of employees who have a minimal amount of asbestosis and who. most likely, will later on also present a cardio vascular disease. Then, unless definite cri teria are developed to estimate objectively the harm produced by the asbestosis and the harm produced by the cardiovascular process, obviously those cases will remain embar rassing to appreciate correctly both by the clinician and by the compensation boards. I have purposely separated from the cardiovascular group the four cases of cor pulmonale, because these four deaths seem quite evidently related to the presence of asbestosis. There are ateo the cases of two other workers who although they died from bronchogenic' carcinoma and asbestosis showed evident signs of right heart failure. Therefore, we can say that in six cases of asbestosis cor pulmonale developed and the patients died from their asbestosis. The following group of six cases of bron chogenic carcinoma present a special interest. Without going into any discussion of this problem of possible relationship between asbestosis and pulmonary carcinoma. I just want to say that there are also seven other patients with bronchogenic carcinoma among the employees who did not have asbestosis. Moreover, a general statistical survey of all employees in the industry does not reem indicate any statistical evidence of a cat relationship. Therefore, the part played the asbestotic tibrosis in t iroup 5 rent; questionable. The two patients who died from bronc pneumonia and bronchiectasis most lil died from this pathological process rat than from their minimal asbestosis. The patient died from cancer of the brain. In summary, in my personal opinion, patients quite obviously died from asbestc and the other 34 developed a lesion wl could very well be considered as the can.-* Table o.--Thctjord Mines Survey. I'/J.'-l1' Clinical Status of Eighty-Eight Living 1`aUems with Asbestosis lood ........................ . .. Mild yiiiptoin>............ .. Moderate symptom-....,.. Severe *ymptom.......... Minimal Aabe?* tosla : ll s o Moderate Advsi AsW'* ,\>ti to<j> to* <3 3 C* > *t Total...................... 15 13 death, although we do not know the played by the asbestotic fibrosis. Table 3 gives the clinical status of the living patients with asbestosis. In analy; this Table. I have to admit that we car be too certain of the classification of the c; of asbestosis into minimal, moderate, advanced, because there is a-significant crepancy between the roentgenological the pathological classification. Here the cla fication is based on a roentgenological apj ciatioti. and likely the histopathological cla fication would be different. A second important reason why this T: may look highly questionable is that i quite impossible to evaluate clinically respiratory function of a group of employ when a large proportion of those employ are 60 years of age and over and when t present at the same time other diseases t may impair the respiratory function to same extent that asbestosis might do. Obviously at that age there are m factors other than asbestosis which a 206 500*0224 x.ux/(.u. nHsr.Kf.trmxs <>r .ishf^tosis influence the cardiorespiratory function, and these factors could explain very well why 10 patients with minimal asbestosis are present ing moderate and severe symptoms while 5 with advanced asbestosis have" no clinical symptoms. With all its limitations, this Table seems to prove at least one thing, that the clinical status of .16 minimal, 4 moderate, and 3 advanced cases is good and that a total of 59 asbestotic employees are able to work without any discomfort--1 mean those in the tirst two groups. . For the remaining 29 cases, no good cor relation between the degree of asbestosis and the clinical status has been found. There is a better correlation between the age of the employees and the clinical status, showing the role played by the age. This Table may also demonstrate indirectly that too many similar tables giving clinical data, such as cough, expectoration, and. weight, cannot prove too much. - To summarize. [ believe that asbestosis is a serious disease in some instances, .but more frequently it remains a disease which can he tolerated quite well for many years, even without appreciable symptoms, as long as another serious disease does not supervene to cause death. On the other hand, in practice, this dis ease may look more serious and cause impor tant medicolegal problems if a too scientific medical concept or a too liberal social inter pretation is accepted by the medicolegal pro fessions. labor and compensation bodies. As a matter of fact, if the least amount or a minimal amount of asbestotic fibrosis i.interpreted as asbestosis. "occupational dis ease." and. more so. if the compensation boards decide to apply the aggravating factor clause, notwithstanding any effective dustcontrol program, the problem will remain unnecessarily serious for many years to come. The combined effort of pathologists phvsiopathologists. roentgenologists, cardi ologists, and clinicians is needed to orientate any research program and to bring answers to the many unknown aspects of asbestosis. 500*0225 207 ledtodid ad ^t^i^erentlated j^r rom er J-^neumoconioded 0. A. Sander, M.D., Milwaukee The preceding discussion has shown that the roentgenological appearance of a welldefined asbestosis is quite distinctive and that it differs materially from any of the other pneumoconioses. For that reason, I shall not limit my part of the discussion to the differ ences between this disease entity and the other dust diseases but shall include other conditions of the lungs which may be mis diagnosed as asbestosis. The first and commonest cause of mis diagnosis is poor film technique. A perfectly normal chest can be made to look like one with definite first-stage asbestosis by slight underexposure, by lack of contrast, and by blurred vascular markings due to too long exposure time. Such films are especially common in overweight persons, the heart shadow usually being horizontal and often presenting a shaggy appearance due to com pression of the vascular, shadows in the lower lobes. Films lacking proper penetration, sharply defined detail, and lack of contrast should be rejected for the diagnosis of any occupational disease of the lungs but par ticularly of asbestosis. Another condition which causes diagnostic trouble at times is emphysema due to any cause, when there are one or more adhesions of the diaphragm due to past pleurisy. The "ground-glass appearance" is very easily read Read in the Symposium on Occupational Diseases of the Lungs, sponsored by the Massachusetts Medi cal Society in cooperation with the Institute of Industrial Medicine of the New York University-- Post-Graduate Medical School, Boston, Oct. 28. 1953. 208 into such a film. When to this are adsome retained secretions in the lower loi which often are bronchiectatic in emphysethe misdiagnosis is established. A pneumoconiosis of which we have come increasingly aware in recent year.1 that due to excessive deposition of coal d: It appears quite certain now that free si is not needed as an essential component the dust to develop the characteristic chan; The fine lacy character of the shadows f some emphysema gives a pattern which lo very much like "ground glass" and is ea. mistaken for early asbestosis. All these examples I assume represent tients who present themselves to their ph_' cians with symptoms of dyspnea, with a 1 torv of some exposure to asbestos dust. ; with chest films of the character I have m tioned. How easy it is to fall into the t of a gunshot misdiagnosis! Unless other p sible causes for the x-ray changes are c sidered first and a detailed past occupatio history is evaluated, along with the ch acter and extent of the most recent dust posure. another worker who' actually nee< reassurance will be told that his lungs full of asbestos dust and that he should c, his trade! From that point on. his symptc usually increase to a marked degree, and has developed what to him is a real disabili In my experience, such doctor-induced c ability is commoner in some areas than is disability from the disease itself. Because of the complete lack of unanim of opinion about this disease among phj cians and because of the need for mi clearly defined criteria for diagnosis and : vice on continued employment in the tra the medical and industrial hygiene advis of members of the Asbestos Textile Instit' 50010226 ASBESTOSIS AXD OTHER PXEUHOCONIOSES have set up a so-called Air Hygiene Com mittee. This committee has met on several occasions to determine whether those who are most intimately associated with this dis ease can agree on the various medical and hygiene phases of the problem. At the last meeting, each medical member of this committee brought with him sample films of the various stages of asbestosis. in cluding some he had classified as essentially negative. All films were reviewed by the eight physicians who were present. We found fairly good agreement on the more advanced stages of asbestosis but practically none on the borderline degrees. A number of my films from the textile mill in North Carolina for which I am consultant, representing cases which I had classified as "early or first-stage asbestosis," were called "essentially negative" by a number of physicians present who had had long experience;.with this disease. The reverse also was true; some films I had called negative which others thought represented first-stage asbestosis. The same disagreement was found with the other films which were presented. It was our final conclusion that it is impossible to clearly define a first-stage case and that it can be called "essentially negative" one day and "first stage" the next by the same reader. This was not new. It has been emphasized repeatedly by Pender grass. beginning in 1938. Our group finally agreed that little atten tion should be paid to the first-stage diag nosis. that little, if any, disability has been shown to exist with the borderline stages, that no one should be advised to stop work with these questionable degrees of change, and that workers should be kept at their reg ular jobs but the dust control should be so improved that their cases will not progress to the stage where everyone agrees that they have asbestosis. Regarding recommendations of transfer to less dusty or nondustv work, we agreed to the following: ' 1. Persons under 40. when the diagnosis is clear cut (beyond first stage), should be moved to a nondustv job if possible. 2. Where progression is seen on serial films, regardless of age, less dust exposure is clearly indicated. 3. Exceptions should be made if there will be material improvement in dust control on the present job within a very short time. I have deviated from my assignment of differential diagnosis, because the diagnostic criteria are so intimately associated with it. Until we have some agreement on x-ray in terpretation, the present chaotic state of af fairs will continue. In the differential diagnosis, it is my be lief that a new approach is essential, not only with asbestosis but also with nonoccupational diseases as well. Because textbooks in.medicine are written by diseases, each fol lowed by a listing of other diseases which must be differentiated from it, the disease itself becomes fixed first in the diagnostician's mind. He says to himself. "This is it," and he pays only cursory attention to the diag nostic criteria of the disease and to the dis eases from which it must be differentiated. A more scientific approach would be to list all the conditions and diseases which are compatible with the x-ray pattern which the patient presents and then, after a complete and detailed medical and occupational his tory, physical examination, and laboratory studies, to see which of the positive findings more closely fit the listed diseases. I should like to cite a case which undoubt edly would not have been misdiagnosed had this approach been used. A railroad shop repairman, aged 57, had to stop . work because of increasing shortness of breath several years ago. Cyanosis and dyspnea became progressively worse, and he died of anoxia and right heart failure several months ago. His work in the railroad shop included welding, unpacking, and repacking asbestos insulation around locomo tive boilers and doing some fitting and grinding. The chest x-ray film showed a diffuse mottled and micronodular pattern in both lungs, and compressed lower lobes due to high position of the diaphragm, with numerous annular shadows of less density scattered throughout both lungs. Asbestosis was diagnosed by the man's physician, because there had been some asbestos-dust exposure, because he had always heard that the x-ray pattern of asbestosis was rather bizarre (and this certainly was), and 209 ixt>rsri<i.u. nr..u.\ because it did nut look like the ,-iderosis oi w chler- about which lit had read something recently. The degree m asbestos-dust exposure was not intiuired about lit was spasmodic and minima!). Other diseases and conditions of the lungs were not con sidered. The annular shadows should have brought emphysematous blebs or air cysts into the differen tial diagnosis, as well as the granulomatous diseases. Miliary tuberculosis had to he ruled out as well as berylliosis with emphysema. Sarcoidosis also had to be considered, although the annular shadows were against it. After definitive study, the diagnostic possibilities should have been reduced to emphy sematous blebs plus pneumonitis or polycystic dis ease plus pneumonitis. Also, there were none oi the characteristics of asbestosis and no pleural involve ment. . After postmortem study the diagnosis was clarified--a widespread congenital cystic lung, with interstitial fihrosis due to long standing infection. The cuboidal and col umnar epithelium lining of the cysts is note worthy. Also, there was complete absence of anything resembling asbestosis bodies, an absence of pleural thickening, and no evi dence of any hyaline fihrosis. Even with this clear-cut postmortem evidence, the physician who originally made the diagnosis still be lieves that this was a case of asbestosis and is sending the tissue slides to various pathol ogists. He should he convinced soon that he most likely was wrong, which will be most embarrassing to him. This case, along with many other.- which could he cited, clearly points up the need to consider all possibilities in cases presenting bizarre x-ray patterns. Each case must have painstaking study, including not only the im mediately preceding occupational history but also a history of every job from the first one on. An example it a foundry worker with a chest film which was characteristic of a moderately well-developed asbestosis. Careful ,-tudy of the occupational environ ment revealed no possibility of asbestos ex posure in this shop. More detailed early occupational history revealed that the man had been a plumber's helper during the late teens and early twenties, doing all the tawing of asbestos pipe coverings, usually in con fined basement rooms. 210 When the mott detailed analysis and stu will not reveal the true diagnosis, which h; pens in occasional cases, taking a biopsy si citneu of the lung should be considered. T: has become a rather simple procedure w little danger of complications. It must remembered, however, that because of t relatively small piece of lung usually tained -for biopsy, there always is some cl; ger that the diagnostic pathological char, will not be revealed. In conclusion, as with all chronic ch diseases, so especially with asbestosis. possible cause.- of the pathology revealed the chest film must he considered. Poo .-tudied cases result in misdiagnoses win not only are embarrassing to the physici but which may also cause irreversible ha to the patient. We owe it to our patients a ' to the medical profession to so tliorotigl investigate every obscure case that such ifortunate situations do not arise. DISCUSSION L)r. K.\ki. r. Bkxeuict. West Bovlston. Ma It is a privilege to substitute for Dr. Har Hardy-; .lie has helped me many times, lint a -unite is always a second." The assignment "the differential diagnosis." I have had no expi ence with asbe.-to-is and. furthermore. 1 beli that experience with most pneumoconioses, as # today. i> earned only after JO to .ill years' >tr because ii often take- that lone to produce disease. In spite of the foregoing, I believe I am tpialito make certain remarks, because- I have b practicing industrial medicine ior'l 5 years in om the world's largest artificial abrasive-plants. Si 1940. we have taken more than 25.000 chest x-r on some 5.000 ahrasives workers. From 1911 1940. except in rare instances, we simply did called routine physical examinations. I agree with Dr. Sosnian that tile physical exa ltation is not worth very much in these circtstances. Thanks to Phil Drinker and others, ii control is much better in our plants today. In . large plant our dust counts run consistei .5.000.000 to 4.000.000 particles per cubic foot. ' handle a great variety of dusts, for that is business, and safe handling is essential. Recently at the Seventh Saranac Sympo.su several world-renowned authorities on pulmon diseases attempted to define pneumoconiosis. I si not. There was no definition there either. Inst, there were minority and majority reports. ( 50010228 ASBESTOSIS JXD OTHER PXEUMOCOXIOSES group insisted that pneumoconiosis simply means dust in the lung. The other group restricts it to those conditions producing demonstrable disability. The hitch is. Who demonstrates the disability? The roentgenologist sees nodular fibrosis in the x-ray film: that is pneumoconiosis to him. At once, or sometimes much later, the industrial physician and hygienist set about to correct conditions to prevent progress of the pneumoconiosis or development of new cases. Later, though the worker still may not know of his trouble, the family physician has diffi culty clearing an ordinary chest cold or the surgeon is faced with anesthesia worries. The occupational disease or the health department specialists in our state government want reports when "injury'' has resulted. Compensation and insurance authorities talk about the number of pneumoconiosis cases, based upon those workers whose earnings have suffered. The compensation lawyer appears later in the picture, and alas sometimes the last, the pathologist, may be the first in proving that a case of tuberculosis or cancer is in reality pneumo coniosis. [ believe we all know when the man is suffering from pneumoconiosis, whether we be laymen or physicians. What he wants to know is, What is wrong? What can be done about it? Is he perma nently disabled? Is his life shortened? There can be only one answer: not better diag nosis or differential diagnosis or function studies but adequate dust control. Since different dusts require different degrees of dust control, witness the different effects from inhaling small amounts of aluminum (therapeutically) and beryllium or radioactive dusts. There is, therefore, good reason for you and me to continue to study pneumoconioses and their differential diagnosis. We in the abrasive industry are continuing this research. Specifically, we believe that under reasonable control alumina dust is no problem. You have heard of the "carbo rundum lung'' no doubt: this is an unjust label, as my good friend Dr. Eddy, of the Carborundum Company, well knows, for Carborundum is just a trade name for the fusion product, silicon carbide. Furthermore, just what disease, disability, or path ology silicon^carbide per se will produce in man has never, been proved conclusively, I believe. It is entirely possible that this lung condition is caused by significant free silica contaminations. Further study is needed, and we intend that it shall be made. Shaver's disease has been mentioned before. In spite of several years' research tending to prove that alumina fume is the cause, there are those who believe that silica fume is to blame. Industry is somewhat discouraged by the inconclusive nature of these and similar medical studies. We all know about the problems related by beryl lium and radioactive dusts. On the other hand, our concepts of clay and talc pneumoconioses have changed in recent years. And what do we know about zirconia or titania or magnesia or boron carbide or graphite dust inhalation ? In our industryorganic substances have caused only two minor cases of asthma. And we have seen no cases of can cer of the lung among our abrasives employees. In conclusion, our goal is not a specific M. A. C. * figure but maximum dust control to eliminate all pneumoconioses. This goal is not easily attainable. Adequate differential diagnostic knowledge will help us to achieve it. * Maximum allowable concentration. 500'0??9 211 ^L^evelopmentd in the ^ampiing. 3of d orne ^)udt THEODORE HATCH, S.M., Pittsburgh ....... ' '{I!* '>! I** *|'l**!**i ....... .........>!u ................. * ivnimh The ultimate purpose of sampling and analysis of air-borne dust is to obtain the necessary information concerning the nature and magnitude of dust exposure from which to predict the kind and extent of health hazard that might result from inhalation of the dust by exposed workers. The adequacy of the method of sampling and of the ana lytical technique used to study the collected dust must be judged, therefore, in terms of biological rather than physical criteria. In a sense, the physical sampling device is used as a substitute for man as a dust collector, and the physical and chemical methods of analysis are selected to give information of biophysical and biochemical significance. This requirement to provide data in a form to permit biological interpretation has been recognized from the beginning of quantita tive studies of dust hazards. Thus. Green.burg. Bloomfield, and other early investigators-pointe'd out significant biological differ ences`between dust concentrations measured in terms of count and weight: they showed the need for rejecting nonrespirable particles :n the analysis, for determining the particlesize distribution in dust samples, and for estimating average dust concentrations over many years of exposure. The impinger tech nique and other methods of dust analysis were accepted by these workers only on the From the Graduate School of Public Health, University of Pittsburgh, and Industrial Hygiene Foundation, Mellon Institute. 212 basis of their demonstrated capacity to mt sure dust hazards. The mechanism of action which leads dust damage is complex and undoubtei involves inctors that can never he measttr by physical means, especially when these ; confined to the study of the dust before gets into the respiratory system, it tollo\ therefore, that there are no absolute rcqur ments which can be sec up for dust .-ampli and analysis. As progress is made in c understanding of the relationships betwe dust exposure and hazard, new criteria ; made available against which to evalu; analytical procedures. This discussion dewith some of the recent development's in ti connection and suggests the need for cert: modifications in procedures of dust ,-ampli and analysis. I. ItfST Rr.TKXTIOX IN RKS1M R A H .:Y -VS", I Relationships between the physical a chemical characteristics of air-borne dust a the nature of the dust hazard change in soi important respects from one kind of dust another. A particular sampling. instrumt may not have universal application, and qu different methods of analysis are ohviou required to meet the variety of needs i assessing the various dust hazards. There one common requirement, however, whi must be met in all situations. Since di particles can produce their damage'only ar being deposited somewhere in the respiratc system, it is evident that one should be al to predict from measurements on the a borne dust the nature and magnitude of t effective dose of dust in the respiratc system. One must know what fraction of I inhaled dust will be retained and in wl 500'*0230 SAMPLIXC OF AIR-BORXE DOST part of the respiratory system it will be deposited and how the retained fraction will differ from the air-borne dust in respect to particle size and composition. In particu lar. one must be able to distinguish between the separate portions of the material which are-deposited in the upper respiratory tract and those deposited in the alveolar spaces. How should the dust sample be collected from the air and subsequently analyzed to provide these details of information? Dust Collecting Characteristics oj the Human Respiratory System.--The selective action of the respiratory system in dealing with dust particles of different aerodynamic sizes is well known. Mineral particles larger than 5 to 10/x are efficiently trapped in the upper respiratory tract in the course of in halation. Such particles, deposited on ciliated surfaces of the air passageways, are quickly moved upward and, for the most part, swallowed. Below 5/x. upper respiratory efficiency falls off rather rapidly and for practical purposes becomes zero at about 1^. The percentage of particles which penetrate to the alveolar spaces increases with decreas ing size below 5/* and reaches a maximum at Ip. Over the 1 to 5/j. range, alveolar retention is high, and most of the panicles which do reach the alveoli are retained. Below 1 pL, however, alveolar efficiency also falls off. This continues down to 0.1 to 0.2^, but in the submicroscopic region limited evi dence suggests that alveolar retention rises again because of precipitation by the diffusion process. With two forces in opposition as size -decreases below S/x--increasing per centage penetrations of inhaled particles to the alveoli and decreasing efficiency of alveo lar retention, an optimum particle size exists for alveolar deposition at about lji. Typical industrial dusts include significant and varying numbers of particles larger than l/z. so that the size-selective characteristic of the upper respiratory tract plays an impor tant part in determining what fraction of inhaled particles in a given exposure reaches the lung depths. This fraction may differ remarkably from one situation to another. Of particular importance in this connection is the flocculation which may exist in the dust cloud, the extent of which varies widely in industrial dusts, depending upon the nature of the dust source and the method of generation and dispersion, into the-air. As a result of flocculation, tine particles may be grouped into aggregates of sufficient size to be trapped in the upper respiratory tract and thus be made-nonhazardous. Dust Sampling in Relation to Particle Size.--Dust sampling methods have not made direct allowance for the size-selective performance of the respiratory system, nor has the importance of flocculation been con sidered. In recognition of their nonhygienic significance, particles larger than 5 to 10/x have been excluded from the dust count, and it has been the practice to compare particlesize measurements on different dust samples to reveal significant biological differences. In the light of present-day knowledge, however, these are not enough, and instead it has been suggested * that the dust collecting charac teristics of the sampling instrument should reproduce to a reasonable degree the charac teristics of the human respiratory system. That is to say. the instrument should sepa rate the particles, in the course of collection, into two fractions representing, respectively, the dust which would be trapped in the upper respiratory tract and the remaining portion which would be expected to penetrate .to the alveoli. There is evident need for this in the sampling and analysis of pneu'moboniosisproducing dusts which do their damage only in the lung depths. Toxic metal dust, such as lead, should be similarly separated during collection, since absorption from the alveoli is the major route of entry of such materials into the circulation. Proper particle-size distinction should be of great significance in the analysis of exposures to chromate dusts, since with this material there is an upper respiratory as well as a deep-lung hazard. The striking difference in hazard from ex posure to freshly formed cadmium oxide fumes and to the dust released in handling and packaging of this material from bulk * References 1 to 4. 500*0231 213 INDUSTRIAL HEAL storage indicates how important particle size may be in estimating the magnitude of this hazard. It is especially important to dis tinguish between upper respiratory and deeplung deposition of radioactive particles.3 The use of a two-stage dust sampling procedure was first suggested by Hemeon.1 who proposed a simple helical tube for the collection of the upper respiratory fraction, followed by the impinger or other appro priate terminal instrument to capture the lung fraction. He emphasized the particular need for a first-stage device that would re move particle aggregations without breaking them up into finer unit particles, arguing that such aggregations are dealt with as equivalent large particles in the respiratory system. With more detailed data available on the collecting efficiency of the respiratory system in relation to particle size," May and Druett: have developed a "preimpinger" with dust-collecting characteristics approxi mating those of the upper respiratory tract. This device operates as a centrifugal sepa rator in which coarse aggregates of particles are trapped without violent impingement and therefore with minimum disaggregation. The escaping particles, freed of unitary large particles and equivalent aggregates of finer, are captured in the terminal instrument, the efficiency of which must equal or exceed that of the alveoli. Another two-stage instru ment has been proposed by Hamilton and Walton.Ta Such a two-stage method of sampling has merit for reason of the automatic recogni tion- of- the influence of particle size upon dust retention. Variations in size character istics from one dust exposure to another are recognized in such a way that the consequent differences in hazard potential are properlyrevealed. The chief argument against using such a two-stage system is that the dust collecting characteristics of the first stage are rigid and may not always reflect the behavior of dust particles in the respiratory system. It would be better, in this view, to collect a single sample with high efficiency for all sizes of par ticles and determine the number of particles 214 in each of a series of size classes over appropriate range. With these basic physi data, one could then estimate the site deposition and percentage retention in human respiratory system, using any pro; respiratory performance curves. This i.time-consuming procedure and. in fact, could give only approximate results. It is aerodynamic size which must be recogniz and tftis is not necessarily directly prop tional to a measured dimension of the p tide. Shape, density, and degree of aggretion are equally important in determin aerodynamic size. The preimpinger gr equal recognition to all these determina of dynamic size and thus provides a bet means for distinguishing between the up; respiratory and the lung fractions of dust Among recent developments in dust sa pling and analysis, the suggested procedi of two-stage sampling is of particular inter and should receive active attention- by ind trial hygienists. '' ' '' II. CORRELATION' OF DUST CON'CEXTRATIC WITH HAZARD Experience with the Greenburg-Smith i pinger technique in the extensive series studies of dusty trades by the L\ S. Pul Health Service demonstrated a reliable as ciation between dust concentrations so me ured and the attendant silicosis haza During the more than, a quarter centi in which this instrument has -been used vast amount of information on dust conct trations in industry has been accumulat In view of this great investment, one cam casually suggest changes in the technique sampling and analysis. Some recent stud of impingement-type instruments, howev raise proper questions regarding the use this method of sampling. Davies and associates 8 have shown tl particle aggregations are broken up duri passage through all types of impingemt instruments. Among the standard insti ments. they concluded that the Greenbui Smith impinger possesses certain import; advantages because of its use of a liquid di collecting medium. Its collecting efficier 50(M0?32 SAMPLIXG OF AIR-BORXE DOST is high for particles down to 1/*, but for smaller particles it drops off rapidly. In contrast, the thermal precipitator maintains its high efficiency down into the submicroscopic region. Because of disaggregation, however, the impinger dust count may exceed by many times the count obtained by the thermal precipitator, despite the higher effi ciency of the latter instrument. Thus, com parative concentrations in a coal dust cloud were found by Davies to be 7 to 8 times greater by impinger than by thermal precipi tator. Disaggregation in the impinger can result in seriously misleading measurements of dust concentration in exposures from the handling of bulk materials, as. for example, in shoveling, dumping, or bagging of ground silica. In large measure, the use of the ilay 7 preitnpinger would take care of this difficulty, since aggregations of particles would be removed before reaching the terminal instrument. The drop in impinger collecting efficiency below 1/x may not be serious, since alveolar efficiency also decreases in this region. With the standard low-power counting technique, however, particles smaller than l/i generally escape detection. These particles are known to be hazardous, and since their percentage contribution to the total number of particles may differ significantly from one kind of exposure to another, a question is raised as to the dependability of the standard impinger dust count. Offsetting this is the demon strated correlation between dust concentra tions. measured by the impinger technique, and ,dust hazard, notable in the granite cutting industry and in potteries. A common explanation for this apparent inconsistency is that within a given industry the impinger count provides a useful index of exposure because of a reasonably constant ratio be tween the number of particles counted and the number of hazardous particles in the exposure. A practical objection to the extension of the particle count below 1/x is that many particles of nonoccupational origin or of nonhazardous nature would thereby be included. South African and British workers have dealt with this problem particularly in their studies of mine-dust exposures. It is the practice in the South African gold mines to remove such particles from konimeter samples by acid washing and ignition. In English practice, the thermal- precipitator count of coal-mine samples (which cannot be ignited) is limited to the particles be tween I and'5^- because of the highly erratic number of smaller particles in the samples. Impinger samples cannot be treated by acid washing and ignition in the manner of the direct deposits obtained by konimeter and thermal precipitator, and the problem of dealing with nonhazardous particles smaller than 1/x in impinger samples remains un solved. To give meaning to the dust count, the composition of these fine particles must be determined separately from the analysis of the total dust or even of the fraction of total respirable dust; It is significant to recall that the satis factory correlations between impinger counts and dust hazard were obtained in industries where exposures were fairly high and haz ards of considerable magnitude existed. In this connection, the recent evaluation of the konimeter by Beadle 9 is of interest. There can be no question concerning the valuable contribution made by the konimeter to the control of silicosis in the South African gold mines, despite known inadequacies in the instrument. Beadle suggests, however, that with the great advances which, have been made in dust control the konimeter may not be adequate for the more refined measure ments of dustiness which are no\y required for the following reasons: the konimeter has high collecting efficiency tor particles above 2ft, but because of disaggregation during impingement it may give an apparent dust concentration in a cloud of relatively coarse particles which is significantly higher than is obtained with the thermal precipitator. On the other hand, because of its rapid loss of efficiency with decreasing size below 2/x. the konimeter count on a fine dust cloud will be substantially below the thermal precipi tator count. Two principal sources of dust remaining in the gold mines are wet rock 215 INDUSTRIAL UEAL1 drilling, which releases line dust in a highly conclusion is not valid, and the recent stud- dispersed state, and ore tipping, the dust referred to earlier point to some possii from which is relatively coarse and un inadequacies. Lacking a definition of r doubtedly contains many aggregates. The solute requirements, however, one cam dust concentration by konimeter is low rela accept these limitations as proof that t tive to the thermal precipitator count on wet method should be replaced or even modifi< drilling, whereas on ore tipping the ratio is There is need for further studies of relatic reversed. Beadle points out that medical ships between measured characteristics findings indicate a greater hazard associated dust Exposure and extent of health haza- with the drilling operation, and thus there In these studies, as in the earlier ones, n< appears to be a negative correlation between methods of sampling and analysis must the measured dust concentration and the tried out. -: r magnitude of health hazard. In no sense In the present discussion the need 1 V.,: does this invalidate the past work with the been emphasized for a suitable sampling pi konimeter. but it does illustrate an important cedure to distinguish between the fractir point, namely, that the needs in respect to of inhaled dust which would be retain! dust sampling and analysis may change as respectively, in the upper respiratory tr; the quality of dust control improves. It is and in the alveoli. Since these fractions m obvious that more refined methods are differ one from the other and since both m required to distinguish between safe expo differ from the total air-borne dust in resp< >; sures and those with minimal hazard than to composition and particle size, new devek are needed to measure differences between ments in methods of dust sampling and an gross hazard levels. The foregoing discussion vsis should include better provisions than ; suggests that such refinements are obtained now available for the determination of i by giving greater recognition to biological differences in size and in composition of t than to purely physical demands in the two fractions. design of the dust sampling device and in Considerable progress has been made the selection of analytical techniques. the control of silicosis. The remaining pri III. NEEDS FOR FURTHER CORRELATIONS OF DUST CONCENTRATIONS WITH HAZARD lems of occupational dust disease are m< subtle and complex than were those in which comes much of our present und> , -*-r Standardization of any technique of meas standing of the pneumoconioses. Past c urement tends to resist research into and perience has demonstrated clearly that qitar. development of better methods of measure tative assessment of dust e^p'osure is ment. Too frequently it is interpreted to mean essential part in the analysis of the haza I that the standard method was selected be and in the diagnosis of the dust disea Cv cv .'i , cause of its universal applicability, whereas Continued critical study,of- methods of di the reverse is more often the cause. That sampling and analysis is required, along w is. the more empirical the method, the greater continued research into the nature of t is the need for standardization. In the present dust hazard itself, if further progress is case, the selected method was chosen be be assured. cause of its demonstrated capacity to pro REFERENCES vide a useful index of the health hazard 1. Hatch, T. F.. and Hemeon, W. C. L.: under the conditions of dustiness in which the fluence of Particle Size in Dust Exposure. J. Indi studies were carried out. Its subsequent ap Hyg-. & Toxicol. 30:172, 1948. plication to a wide variety of dust exposures 2. Hatch. T. F.: Analytical Requirements implies, in effect, that this method of dust Appraisal of Dust Exposures, in Record of P % sampling and analysis is so fundamental and ceedings, Third International Conference of'Expt on Pneumoconiosis, Sydney, February-March. IS complete as to have universal capacity to Geneva. International Labour Office. 1953, Vol. measure dust hazards. Such a generalized p. 74. 216 5O0'<0?34 XETS AXD CPMHEXT 3. Davies. C. X.: Dust Sampling and Lung Disease. Brit. J. Indust. Med. 9:120. 1952. 4. Watson. H. H.: Dust Sampling to Simulate the Human Lung. Brit. J. Indust. Med. 10:93, 1953. 5. Burnett. T. J.. and Hatch. T.: Sampling Criteria for Estimating Airborne Radioactive Particulate Hazards, read before the 15th Annual Meeting. American Industrial Hygiene Association, Chicago. April 28, 1954. 6. Brown. J. H.. and others: Influence of Particle Size upon the Retention of Particulate Matter in the Human Lung. Am. J. Pub. Health 40:450, 1950. ' 7. May, K. R.. and Druett. H. A.: Pre-Impinger: A Selective Aerosol Sampler. Brit. J. Indust. Med. 10:142. 1933. 7a. Hamilton. R. J., and Walton. W. H.: Selec tive Sampling of Airborne Dust. Report 139. Central Research Establishment. A'ational Coal Board, Sheffield, March. 1952. 8. Davies. C. X.. and others: Impingement of Dust from Air Jets, A. M. A. Arch. Indust. Hyg. 4:354, 1951. - 9. Beadle."D. G.: Performance and Limitations of the Konimeter. J. Chem. Met. & Min. Soc. S. Africa 51:265, 1951. " !i::iK'.lilll:l!7.1!!7!i2i:ir,lj!lU!!|illllll!!:illillililllillliilililltll!ll!inRI!lltlllllllli;i!!lllIltll!lIllillllfii!IIililIinilll!l!l:l!!!!;!lli!:!i ,:il:i.!.`:: .:T:9i'!li;t3i!niiini!llli;iranill!tin!7unnEi'3;!lf"!:liSa3 News and Comment ANNOUNCEMENTS '' ' ' Industrial Health Conference, 1955.--Methods of safeguarding workers' health will be the primary subject for discussion at the forthcoming meeting of the American Industrial Hygiene Association in Buffalo, April 25 to 28. More than 60 papers will be presented, together with panel discussions, committee meetings, and joint meetings with other organizations active in the field of industrial health. , This meeting of the American Industrial Hygiene Association will be concurrent with meetings of the American Conference of Governmental Industrial Hygienists. American Asso ciation of Industrial Nurses, Industrial Medical Association, and American Association of Indus trial Dentists. Based on past experience, attendance at the 1953 Industrial Health Conference will number in the thousands. Experts in the various fields will discuss health aspects of new materials of commercial importance, laboratory experiments, air pollution, and radiation. Workers from industry, govern mental agencies, and universities will participate in the exchange of new information and ideas. Exhibits and demonstrations will be arranged by companies producing equipment useful in the field of industrial hygiene and toxicology. Chief Publications Editor Wanted.--The Surgeon General's Office is seeking the services of a Chief Publications Editor to assist in the development of the history of the Artriy Medical Department in World War II. The position requires a person with supervisory ability to plan, direct, and coordinate the editorial and publication activities related to the approximately 25 clinical volumes of the history, also in the case of more complex manuscripts to make critical editorial review of them to determine their literary quality, their accuracy of documentation, statistics, and interpretation, and the accuracy of quotations and illustrative materials. The position is under U. S. Civil Service and pays $7040 a year, with S200 increases every 78 weeks up to a maximum of $8040 per annum. Interested candidates should write to the Surgeon General, Department of Army, Washington 25, D. C., Attention: MEDCM-CP, 5O040?35 217 \cbne66 enteeidm NORMAN PLUMMER, M.D. and LAWRENCE E. HINKLE Jr., M.D., New York ^iiiauinna Today, and on every working day, in this country about 2,000.000 employees are away from their jobs because of sickness (including absence due to accidental injury as well as to illness). This is a huge segment of our industrial population. A significant aspect of this picture is that during the past 30 years the percentage of absentees has been on the increase. During this period great changes have taken place in the treatment and man agement of disease. As we shall discuss later, most of these changes tend to shorten illness; however, the medical profession has developed a greater caution in the manage ment of convalescence, and this, of course, increases the days of absence. Another and perhaps more important factor involving absence is the change in the economic status of the disabled worker. Today, with higher wage levels, with the development of com pany and union benefit and welfare plans, with new state accident and sickness com pensation laws, and with increasing participa tion in voluntary accident and insurance plans, employees when sick are better able to stay away front work. Here we see the development of an attitude. We must recog nize that when employees have a greater incentive to stay at home they have less in centive to work, and then absence rates go up. Presented at the Seventh Industrial Health Con ference. Houston, Texas, Sept. 24, 1954. Assistant Professor of Clinical Medicine, Cor nell University Medical College, and Medical Direc tor. New York Telephone Company (Dr. Plummer); Assistant Professor of Clinical Medicine, Cornell University Medical College (Dr. Hinkle). The dollar cost of industrial sickness al sence to employers in the United States a staggering sum. A figure of S10,000.000.0c per year is probably a conservative estimat We can be more specific about sickness a1, sence by giving you some facts and rout figures that pertain to our Company. In oi discussion of sickness absence we are inclix ing all absences resulting from both sickne and accidental injury, occupational and noi occupational, and absences of both long at short duration. We are not including vac. tions. excused absences for jury duty personal reasons, or absences for materni leave or other nondisability leaves. The Xe York Telephone Company employs abo 75.000 persons--about 50.000 women at 25.000 men. During an average working da because of sickness, we have our own arn of approximately 3000 absentees--alto 2300 women and 700 men. On an annti basis these 3000 employees receive abo $9,000,000 in sickness and accident bene payments. Our workmen's compensate costs, above payment for time lost, are abo S150,00G per year. The cost of our premiur. for sickness insurance under state law f our employees not covered jtr- our bene plan is about $100,000. It costs abo $700,000 to run our Medical Departmei and we-.can-estimate conservatively that costs another S500.000 for our Benefit D partment and personnel expenses entailin the managing of our 3000 absentees. S by adding these figures, we find that sickne absence costs the New York Telephone Coi pany more than S10,000,000 per year. T1 does not include at all the cost of reducproductivity which results from the lower working efficiency from having so ma .employees away from work. While absenteeism is extremely costly the Company, a substantial sum is also p- 218 50040236