Document Vjn4xgngYwVD1akpbQxa1bjEo

FILE NAME: Owens Illinois Library (OWL) DATE: 1955 DOC#: OWL040 DOCUMENT DESCRIPTION: Several Articles Related to Illness from Asbestos A. M. A. A R C H I V E S OF t < Industrial Health EDITORIAL BOARD PH ILIP DRINKER, Chief Editor 55 S h a ttu c k S treet, B o sto n 15 CHRISTOPHER LEGGO, C rockett. Calif. OSCAR A. SANDER, M ilw aukee ROBERT O'CONNOR, B o sto n H. H. SCHRENK, Pittsburgh CARL M. PETERSON, Chicago CHARLES F. SHOOK, Toledo FRANK PRINCI, C incinnati HERBERT E. STOKINDER. Cincinnati A U S T IN S M IT H . E d ito r. A. M. A. S c ien tific P u b lic a tio n s GILBERT S. COOPER. M anaginu E ditor, Specialty Journals Vo lu m e I I 1955 PUBLISHERS AM ERIC. AN M EDICAL ASSOCIATION CHICAGO 10, ILL. `iUV'P'lktHHd!  value of which is IHMSTMAL HEALTH procedure. F or these, a compact, portable v( l l / f t S S ' >riate summing of apparatus is needed, and methods of gas sion capacity, and analysis are required which will perm it the upon its solubility measurements of the three test gas concen orbed through the trations in one test gas mixture. In this way, rate which is pri- simultaneous values of V t , D, and B , can be e or another of the obtained in a single test, at rest or under pendent of at least exercise. the determinations es it becomes posi of J7., D, and Be, tilation, diffusion, y makes use of , which is retained entilation, is only (1 flow, and is in- Mr. James Brown constructed and assembled the apparatus used in this study. Messrs. Edward McCIoskey and Donald Ross assisted in the develop ment of test procedures and in the conduct of many of the tests. Arrangements for the coal miners who came as test subjects were made through the cooperation of Drs. Leslie Falk and Edward Lebovitz, of the Health and Welfare Fund of the United Mine Workers of America. Several of our associates also served as test subjects. ) acetylene, which o ventilation and dent of diffusion, which is retained and diffusion and w. These are in- REFERENCES 1. Kety, S. S .: Theory and Applications of the Exchange of Inert Gases at the Lungs and Tissues, Pharmacol. Rev. 3:1, 1951. 2. Haggard, H. W .: Absorption, Distribution and Elimination of Ethyl Ether: I. Amount of This exhibit received honorable mention hysiologically ac- Ether Absorption in Relation to the Concentration Inhaled and Its Fate in the Body, J. Biol. Chem. "dure for measurptake and calcure described, and eries of subjects ory impairment) 59:737, 1924. 3. Fowler, W. S .: Lung Function Studies: III. Uneven Pulmonary Ventilation in Normal Subjects and in Patients with Pulmonary Disease, J. Appl. Physiol. 2:283, 1949. 4. Fowler, W. S .; Cornish, E. R., J r , and Kety, Scientific Exhibits by the method of itlmonary funcIly described and obtained of the lation, gas transdveolar wall, and ibilities for deterlitude of respiraistinguishing be, circulatory, or suggested.. 1 for calculating spiratory system I carbon dioxide by partitional m a ^renter vn- S. S.: Lung Function Studies: Analysis of Alve olar Ventilation by Pulmonary N> Clearance, Curves, J. Clin. Invest. 31:40, 1952. 5. Robertson, J. S.; Siri, W. E , and Jones, H. B.: Lung Ventilation Patterns Determined by Analysis of Nitrogen Elimination Rates: Use of the Mass Spectrometer as a Continuous Gas Ana lyzer, J. Clin. Invest. 29:577, 1950. 6. Hatch, T. F .: Carbon Monoxide Uptake in Relation to Pulmonary Performance, A. M. A. Arch. Indust. Hyg. 6:1, 1952. 7. Rahn, H .; Mohney, J .; Otis, A. B,, and Fenn, W. 0 .: Method for Continuous Analysis of Alve olar Air, J. Aviation Med. 17:173, 1946. 8. Hatch, T .; Cook,' K. M, and Palm, P. E .: Respiratory Dead Space, J. Appl. Physiol. 5:341; 1953. 9. Silverman, L.; Lee, G.; Plotkin, T .; Sawyers, L. A, and Yancey, A. R.: Air Flow Measurements on Human Subjects With and Without Respiratory PN EU M O N O CO N IO SIS ROBERT F. BELL, M.D. AND JAMES J . W ARING, M.D. DENVER E X H IB IT represents a collection of some of the representative teach- 1 I ing material on pneumonoconiosis utilized at the University of Colorado Medical Center. It is presented to the practicing physician for his examination because at any one location he may have had only a rare opportunity to see and compare various types of pneumonoconiosis. M any large films of the pneum ono coniosis and other roentgenograms of diseases resembling pneumonoconiosis were i available for examination on the view box. Shown as a scientific exhibit of the Section on Preventive and Industrial Medicine and Public Health at the 103rd Annual Meeting of the American Medical Association, San Fran- 'TRIAC HEALTH W ..F . V., 425 . J- J-, 159 S U B J E C T I N D E X T O V O L U M E 11 rby, J. H ., 102. 413 The following Index contains an alphabetical list of significant subjects presented in this k. M . L ., 473, 479 volume. Abstracts are indexed by category under the heading "A bstracts." Books reviewed i. E ., 305 are listed alphabetically by title under the heading "Books." Obituaries and death notices are indexed under the heading "D eaths." J. D., 422 H . B., 11 i. J . P ., 403, 4 08 G. W ., 196 A Absenteeism : sickness, 218 A bstracts accidents and their preven tion ; protective equipment, Asbestosis--Continued roentgenologic aspects, 189 scientific exhibits, 165 Atomic energy: personal pro tection in atomic industry, 42 B o o k s --Continued Pneumoconiosis Abstracts, Vol. 2 (Middleton, ed.), 451 Radioactive Waste Disposal in Ocean (U. S. Dep't of c H . K ., 457 448 Commerce), 452 determination of air-borne contaminants, 84, 266, 354, B Symposium on F a tig u e (Floyd and Welford, eds.), Y 448, 536 BAL : See Dimercaprol 88 ! v. S ., 413 environmental conditions, 82, Benzene hexachloride : poison 180, 264, 353, 447 Symposium on Human Fac tors in Equipment Design D., 280 general. 72, 172, 252, 348, Benziindginferso:m, u4r5i7nary output (Floyd and Welford, eds.), 435, 525 estimation, 420 270 r. W . J., 280 industrial toxicology, 79, 177, 258, 350, 440, 535 Beryllium Toxicologie des produits phytopharmaceutiques legal medicine, 181, 355, 538 medicine and surgery, 263, intratracheal injection of Be7 in rat, 375 (Fabre and Truhaut), 451 Verhandlungen der deut 352, 446 pneumoconiosis from, 164 schen Gesellschaff fr Ar occupational diseases and poisoning, 273 beitsschutz : Band II. I hazards. 73, 174, 253, 349, Blood : red cell cholinesterase 436, 529 activity, 332 Staube, Gase, Dmpfe (Steinkopff), 359 physiology and nutrition, 72, Books Working Fitness of Older 955 ~ rad1i7o3a,c4ti3v5e substances and Ai(rDPaovlelnuptioornt :aBndiblMiogorragpish)y, BookMs:enC(oCunlacrilk)o, n45I1ndustrial x-ray, 181, 268, 356, 449, 271 Health list, 343 539 Air Pollution and Com Brass-foundry operations : lead so. Month ventilating, air conditioning, munity Health (Mills), intoxication from. 107 4 April and engineering control, 85, 181, 267, 538 270 Byssinosis, 164 Compressed Air Illness : 5 May Accidents Investigation During Con 6 June medical aspects, 453 struction of Tyne Tunnel, syndrome, 66 1948-50 (Paton and Wl Aerosols : synergistic effects, der), 87 Calcium ethylenediamine-tetra- 297 Flow and Fan: Principles acetate: See Edathamil Air pollution of Moving Air Through calcium in American cities, 280 Ducts (Berry), 271 Cancer: See Carcinogens t committee report, 513 Detroit-Windsor study, pre Histopathology of Skin, Ed. Carcinogens 2 (Lever), 272 diesel-engine exhausts, 113 test of forms and tech Industrial Dust, Ed. 2 selection of chemicals for niques, 47 (Drinker and Hatch), 540 carcinogenic sc re en in g , 494 health hazards from, 397 Air sampling Industrial V e n tila tio n : Manual of Recommended Cataract: radiation, 305 of dust, 212 Practice, Ed. 3 (American Chemicals physics of particle-size anal Conference of Govern physically toxic, 315 ysis, 431 mental Industrial Hygien threshold limit values for of small particulates, 422 ists), 360 1955. 521 Amyl nitrate : toxicity of Lehrbuch der Arbeitshy Cholinesterase: red cell ac vapor, 290 giene: Band II. Spezielle tivity in whole blood, 332 Anthracosis, 166, 168 Berufshygiene (Koelsch), Chromium compounds Antimony trioxide : toxicologic 358 dermatitis from chrome glue, study, 473, 479 Modern Occupational Medi 368 dermatologic asp ec ts of Asbestosis cine (Fleming and others, chromate problem, 361 differentiated from other eds.), 359 edatham il calcium for ) pneumoconioses, 208 Nontuberculous Diseases of chrome ulcers, 123 functional a b n o rm a litie s Chest (Banyai. ed.), 452 Coal mining pneumoconiosis from, 196 Occupational Health and classification of roentgeno in mine and mill workers, Safety Legislation (U. S. grams in, 17 204 Public Health Service), epidemiological studies in pathology, 185 452 Great Britain, 29 5 I iase<i on human experience, but in most cases they are calculated, using; imcnts. The value of Q is considered to be the microcuries of a radio, total body that will deliver 0.3 rem per week to the critical organ, i. e., radioisotope that results in the greatest over-all damage to the body, ucentrations of the radioisotopes in air or water that if used exclusively , OCCUPATIONAL DISEASES OF THE LUNGS .ill lead to an accumulation, Q, in the body. In most cases considered, i a few weeks. MPC values (or air and water to be used in an emergency dose of ionizing radiation is delivered to tissue in close proximity to an 't specific activity that becomes fixed in living tissue. In setting the MPC Id like to know if such localized radiation increases the probability of N uclear Sc. A bst. i A. i. LA N ZA, M.D., New York always remember that in spite of the enor mous amount of research that has been done Radiation Injury. Louis H. H empelmann and Joseph G. H offclear Sc. 8:369-392, 1953. in most of the civilized countries of the world On behalf of the Institute of Industrial on the subject of silicosis--almost enough Id reactions of the human body to ionizing radiations are described, es, the first part of the paper deals with the description of acute radiarning this, a brief appraisal is made of the possible lines of therapeutic Sgested by current animal experimentation. The last part of the paper high to subacute doses and describes late tissue reactions which arise at F rom the Authors' Summary. Medicine, may I express niy 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 I his associates in the Massachusetts Medical susceptible than the normal person to tuber Society have done in achieving the turn culosis. D ust. H. I. Miller Jr., Heat. Pip. & Air Condit. 26:109-113 (Sept.) out that we see here today? Likewise, for instance, in asbestosis we do lie problems in designing heating, ventilating, and dust-control facilities large uranium producing plant operated for the Atomic Energy Come. The purpose of this article is to indicate the application of standard o the control of dust and atmospheric pollution in an unusual process degree of control is necessary. F rom the A uthor's S ummary. Techniques. Saul J. H arris, New York State Dept. Labor Month. ) 1953. examples of industrial applications of radiation-producing equipment Also included is a general discussion of ionizing radiations, including ifeguards. A T r o s s a n o j k .( New York. ions for N uclear P ower P lants. H. H urwitz J r., Nucleonics 54. g the energy released in a nuclear accident and for evaluating the dispersed fission products resulting from such an accident are reviewed. N uclear S c. A bst. m the U se of D ental X -R ay U nits. W. E. N olan and H. W. r 61:625-696 (Oct) 1953. mtists, technicians, and patients during dental roentgenography were ions for safe procedures are presented. N uclear Sc. A bst. d R espiratory P rotection in R adioisotope W ork. G. W. ciianan, Publication AECU-2821, U. S. Atomic Energy Commission, Service, Oak Ridge, Tenn., Jan., 1953. ' dated with the use of radioactive isotopes in the laboratory is disasures to prevent contamination are emphasized. The various forms ind mechanisms influencing their stability in the air are discussed, imum permissible air contamination values, the pathway of inhaled er the respiratory system, and the characteristic absorption, deposiiti pattern of contaminants. The characteristics of various respirntorv 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 `have a saying, " It was only a wooden Indian and a certain kind of fool who wouldn't considerable body of opinion that does not go along with that. Diagnosis is not always 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 pvnareiuomusoctoenrimossissaigsniifnyteinrcghadnifgfeearbelnet, twyhpiecsh oisf 1 i which we have not always learned how to not correct. These different types of evaluate. We have learned a good deal about pneumoconiosis, like silicosis and asbestosis 1 silicosis. We have learned something about and siderosis, are different diseases; and if 1 i asbestosis. Those are the two main forms there is any sloppiness in our use of terms, of pneumoconiosis which cause disability and we only confuse ourselves and make the mat sometimes death. At the same time we must 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. i Read in the Symposium on Occupational Dis While it is true that we have a fair knowl eases of the Lungs, sponsored by the Massachusetts Medical Society in cooperation with the Institute of Industrial Medicine of the New York University edge of the action of silica particles and as bestos particles upon the pulmonary tissue ... t..... -i. , > L tW U lK lA L. li ilA H u 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 really goes on in the lungs of persons who breathe the various kinds of dust that we find in our working places. So far our estimation of this disability consists mostly of rule-of-thumb methods, and if they can be combined with a certain amount of common sense, we hope that the standards of dealing with claimants for disability may be of a moderately high order. Again let me emphasize that there is a great deal of work to do. There is a great deal of knowledge that we do not have. You will hear much more on that from our dis tinguished speakers this afternoon. While th beginnings condition n< occurred th industry as hazard rela In fact, the acceptable ;. while up to of occupati tended to c silicosis. F missible to we have fit of pulmona dust in indi to be revise- It is with who are sti tain unsolv there has b' ety of pn period, and closure of provements ers, so tha the atmosp are greatly 30 or more ments havt edge of th. largely fro ' President. Read in th. .eases of the Lu Medical Societ a AL. 11L .A H It e of what really ms Who breathe we fifed in our rnation of this rule-of-thumb nbined with a P a th o io g .y o f s^ dledtodid -nse, we hope ,vith claimants KENNETH M. LYN CH , M.D., Charleston, S. C . employment went back into, the very dusty jderately high IlllllllliiffllllllllllllllllillllllilllllllllW conditions of earlier times, it should not be assumed that the hazard has been eliminated. at there is a While the asbestos industry may date its Harmful asbestosis is still occurring. ere is a great beginnings back into antiquity and while the Asbestosis is the product of the inhalation ot have. You condition now known as asbestosis may have of asbestos dust in sufficient amount and dur from our dis- occurred through a long period of time, the ing a sufficient period of time; but und?r loon. industry as we know it is new, and the health working conditions, either now or formerly, hazard related to it is of recent knowledge. there is no uniformity in degree of disease In fact, the term asbestosis was not entirely among workers, even under similar ex acceptable as recently as about 30 years ago, posures. Apparently some persons in a while up to that time any thought of ill effects group working in the same environment will of occupational exposure to asbestos dust be severely affected, while others will be tended to confuse the resulting disease with less affected, and some will escape harm, silicosis. Parenthetically, perhaps it is per and this for reasons unknown. Furthermore, missible to express an opinion that before we have finished with the study of the class of pulmonary disease attending exposure to the time required for similar quantitative exposures to produce like grades of asbestosis apparently varies with individuals. dust in industry the whole chapter will need While in our efforts to establish protection to be revised. of the health of industrial workers we have 1 It is within the time of experience of some set up certain standards concerning atmos who are still concerned with the study of cer pheric dust concentrations, these are of a .( tain unsolved problems in the subject that general nature rather than specific, and may there has been established this distinct vari have given a false sense of security. The ety of pneumoconiosis. During the same very dusty atmospheres surrounding the workers in this as well as in certain other period, and probably largely because of dis industries under former conditions would closure of the hazard, there have been im certainly be more harmful than the relatively provements by the industry to protect work clean environment to be found in a present- ers, so that, so far as my observations go, day careful operation, but we may need to the atmospheric conditions in asbestos mills establish something more than merely the are greatly different from the conditions of particle counting and measuring practices 30 or more years ago. Even though improve now in vogue if we shall have dependable ments have been made and although knowl safety controls. edge of the course of the disease has come The particulate matter in asbestos-plant largely from examination of workers whose dust is composed of broken fibers of crystal ^ 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 line silicates. When inhaled, most of it is expelled, but the quantity of fragments of lengths up to 100/* or more that may reach the terminal respiratory units is remarkable. As compared with the material deposited in the Inn? in silicosis and in certain other rnn- INDUSTRIAL HEALTH Fig. 1.--Asbestosis bodies in sputum concentrate; reduced from a photomicrograph. X 70S. 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 a.-l>estos 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 fibrosis, with ash -tosis bodies, phagocytes, and black granular pignuni in reduced alveoli; reduced from a pliotomicr<gr.iph. X 280. nature and of tissue fluid or cell origin. This process transforms the naked asbestos crystal into a golden or brownish object of a variety of architectural shapes, called the asbestosis body. This characteristic body is formed in the alveolus of the lung. It may be found in the sputum of a subject with asbestosis. as a confirming diagnostic finding, and in the fluid extracted from the lung. Because of their size, comparatively few asbestosis bodies, and only the smaller ones, may be transported in the lymphatic system to be deposited in lymphoid deposits within the lung, while still fewer reach the hilar or medi astinal nodes. The limitation of physical opportunity for entry of the asbestos fragment into and transportation by the draining lymphatics seems to explain another characteristic dif ference between silicosis and asbestosis. The small free particles of silica readily' penetrate the aveolar walls and lung tissues, aided or unaided by phagocytes, and are mainly de posited in the lymphoid depots along the drainage system, thus setting up focal reac tion and characteristic nodular fibrosis, whereas asbestos fragments stay mainly where they land in the alveoli, particularly in the vestibular areas of the lobules, so arousing a more uniformly distributed reac tion and usually nonnodular or diffuse fi brosis, although there is evidence that they may penetrate the tissues also. As alveoli become obliterated and the lung architecture becomes distorted, the asbestosis bodies be come embedded in fibrous patches and masses, to remain of much the same appear ance indefinitely, although in the older scars there appears to be some change in them and they may then absorb the basic-staining dyes. Just what composes the first part of the reaction to asbestos fragments deposited in alveoli is subject only to deduction at the present. If we assume the primary effect to be from physical injury (traumatism) of I PATHOLOGY OP ASBEST0S1S their exposure, even before there is evidence be encountered, of course, varies with the of fibrosis. It is also consistent with the early grade of fibrosis. While that condition tends "ground-glass" changes in roentgenographic to be consistent with the degree and duration lung fields. of exposure to the dust, the causative ex As the condition progresses--ordinarily posure and the resulting fibrosis do not al .# i through years of continued exposure--and ways agree. Merely the fact that a person while alveolar fluid may continue to accom has worked in an asbestos plant does not 1 i pany the giant cell and colloidal envelopment of the fragments of asbestos crystals as long justify an assumption that he has acquired asbestosis of a clinical grade. as fresh de|iosition continues, permanent In some of our cases the finding of small 1 change in the form of fibrosis takes over and numbers of asbestosis bodies in the alveoli I proceeds. T his fibrosis is essentially the same as will occur from any relatively innocuous Si I li but irritating presence of solid foreign ma : ' terial located within living tissues. There is some evidence that it may he halted hv re I moval from exposure to continued asbestos inhalation, hut after its formation it cannot be expected to he reduced, and when it has reached a disabling grade the disability may be exjn-cted to be permanent. In the advanced ! i f I 1 i Fig. 1.--Asbestosis 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-liody giant cells and covered by a smooth coating, apparently of colloidal Fig. 2.--Grade 111 fibrosis, with asbestosis bodies, phagocytes, and black granular pigment in reduced alveoli; reduced from a photomicrograph. X 280. nature and of tissue fluid or cell origin. This process transforms the naked asbestos crystal into a golden or brownish object of a variety of architectural shapes, called the asbestosis body. This characteristic body is formed in the alveolus of the lung. It may be found in the sputum of a subject with asbestosis. as a confirming diagnostic finding, and in the fluid extracted from the lung. Because of their size, comparatively few asbestosis bodies, and only the smaller ones, may be transported in the lymphatic system to be deposited in lymphoid deposits within the lung, while still fewer reach the hilar or medi astinal nodes. The limitation of physical opportunity for entry of the asbestos fragment into and transportation by the draining lymphatics seems to explain another characteristic dif ference between silicosis and asbestosis. The small free particles of silica readily penetrate the aveolar walls and lung tissues, aided or unaided by phagocytes, and are mainly de posited in the lymphoid depots along the drainage system, thus setting up focal reac tion and characteristic nodular fibrosis, whereas asbestos fragments stay mainly where they land in the alveoli, particularly in the vestibular areas of the lobules, so arousing a more uniformly distributed reac tion and usually nonnodular or diffuse fi brosis, although there is evidence that they may penetrate the tissues also. As alveoli become obliterated and the lung architecture becomes distorted, the asbestosis bodies be come embedded in fibrous patches and masses, to remain of much the same appear ance indefinitely, although in the older scars there appears to be some change in them and they may then absorb the basic-staining dyes. Just what composes the first part of the reactio n to asbestos fragments deposited in alveoli is subject only to deduction at the present. If we assume the primary effect to be from physical injury (traumatism) of alveolar linings and septa, we may assume fluid accumulation. It may constitute the first or acute reaction, and that fits with the physi cal evidence of increase of lung fluid that in . their e of fibn "groun lung fi< As t througi while : pany tl of the i as fre change procee as will but irr terial 1. some e moval inhabit, be exp reache< \be expi stage i and fin., in increa The g 1 or cell origin. This nked'asbestos crystal objec*' of a variety tiled the asbestosis body is formed in It may be found ct with asbestosis. finding, and in the j lung. Because of y few asbestosis 1 dler ones, may be iatic system to be posits within the n the hilar or medi cal opportunity for ragment into and aining lymphatics characteristic dif- ud asbestosis. The a readily penetrate g tissues, aided or Fig. 3.--Grade IV fibrosis of lung in asbestosis, with asbestosis bodies and granular material 5 nd are mainly de in alveolus and fibrous area. X 280. t depots along the ting up focal reac- their exposure, even before there is evidence be encountered, of course, varies with the j nodular fibrosis, of fibrosis. It is also consistent with the early grade of fibrosis. While that condition tends i cnts stay mainly "ground-glass" changes in roentgenographic to be consistent with the degree and duration i dveoli. particularly lung fields. of exposure to the dust, the causative ex- j >( the lobules, so As the condition progresses--ordinarily posure and the resulting fibrosis do not al- i v distributed reac- through years of continued exposure--and ways agree. Merely the fact that a person y j ilar or diffuse fi- while alveolar fluid may continue to accom has worked in an asbestos plant does not j j vidence that they pany the giant cell and colloidal envelopment justify an assumption that he has acquired J j . also. As alveoli of the fragments of asbestos crystals as long asbestosis of a clinical grade. * lung architecture as fresh deposition continues, permanent In some of our cases the finding of small j iiestosis ixxlies be- change in the form of fibrosis takes over and numbers of asbestosis bodies in the alveoli f ous patches and proceeds. This fibrosis is essentially the same i i Fig. 4.--Advanced Grade IV asbestosis: oblit- j i the same appear - as will occur from any relatively innocuous eratiitg hyaline fibrosis. ' j i in the older scars but irritating presence of solid foreign ma iiange in them and terial located within living tissues. There is )asic-staining dyes, some evidence that it may le halted by re e first part of the nents deposited in deduction at the moval from exjjosure to continued asl)estos inhalation, hut after its formation it cannot be expected to be reduced, and when it has ; primary effect to (traumatism) of reached a disabling grade the disability may \be expected to be permanent. In the advanced t, we may assume stage it causes respiratory embarrassment constitute the first and finally circulatory difficulties resulting fits with the physi- in increased right heart burden. of lung fluid that The gross condition of the lung, as seen 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 to a great extent. Stage I II --Third-Degree Silicosis.--The nodules are more than 3 mm. in diameter. Small areas of coalescence may be seen. B. SILICOSIS W ITH 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 W ITH TUBERCULOSIS This may occur as the result of an infec tion superimposed itpon progressive and still active silicosis or of 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 reduc' d maximum breathing capacity and an increased residual air. It is felt that important knowledge concerning the actual residual air/tntal 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 A short time ago Dr. George Wright made a study of 134 cases that showed a good cor relation of residual air/total volume with area of roentgenologic expiration/area of roentgenologic inspiration, the coefficient of correlation being 0.772, with a standard error of 0.02 (Fig. 3). Therefore it seems per missible to say that when diffuse obstructive emphysema is a complication of the silicotic process fluoroscopic examination of the chest and a chest roentgenogram made in full ex piration should furnish information as to the presence of pulmonary function impairment. The moderate and severe forms should not be difficult to identify, but it is not easy to be definite about persons with slight impair ment. I know of no way in which we can determine accurately the degree of diffuse obstructive emphysema other than by em ployment of pulmonary functional studies. The discrete generalized nodular pattern, as visualized in the chest roentgenogram of a person who has had an adequate exposure to quartz, reflects the unit pathological lesion of silicosis--a nodule of hyaline fibrous tis sue. This roentgenological finding does not imply the presence of pulmonary disability or that the abnormal densities will be pro gressive in nature (Figs. 4A , 4.B, 5A , and SB). At the present time there are no statis tical data available, to my knowledge, which would confirm a general impression that all 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 is 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 orcu- was merely incidental. The lung in such an instance exhibits nothing else of that con nection. Usually 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 somewhat 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 hajted 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 are patches of distorting indefinite scarrings, and there is a grayish marbled cast on section. The pleura may be thickened and adhesions may be found, but in some instances it may be quite normal. Grade IV is the advanced phase which will terminate fatally on its own account if some other death-dealing condition does not inter vene. The subject becomes increasingly, and finally absolutely, disabled in respiratory and circulatory functions. The lungs in this final phase are tough, coarse, inelastic, fixed in expansion, grayish marbled in appearance, and generally, but irregularly, in an extreme state of fibrous induration. Various distorting scarrings oc cur, particularly in the upper parts. Although such scarrings are patchy rather ^than nodu lar, they sometimes resemble, both grossly and microscopically, the lumps and nodules of silicosis. The pleura may be thick, even cartilaginous in toughness, and the cavity partly or entirely obliterated, but not inevita bly. Inasmuch as pleural fibrosis is not in variable, it appears that its occurrence is as a complication and not as a part of the pri mary disease. toc^ic_ddpectd o f *Siticodi& a n d __d sb e sto std LEONARD J. BRISTOL, M.D., Trudeau, N. Y. fiiiiiiiiiiiiiiiHnilHiiiiiiiiiiiiiiiinniiiiiDiiBiiiiiiiiiiininfiniiiiiiiiniliilimwiiiiiiniiiiiiHiiintiniuiiiiniiniiiiiiiinin A complete roentgenologic study of the chest should include fluoroscopic and roentgenographic 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. The normal lung structure is produced by the pulmonary artery and its branches, and these are visible from the hilum to the periph ery. These branches divide and subdivide, forming finer and finer ramifications. The injection of a contrast medium into the pul monary artery of a normal excised inflated lung will render an excellent illustration of how the massive contrast-filled vessels stand out sharply against the air-containing alveoli and bronchi (Fig. 1). In the conventional postero-anterior projection the branches of the pulmonary artery overlap one another and present a definite network-like pattern. In view- Director, Department of Radiology, Trudeau^aranac Institute. 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 Univer- c i f v __p r t c f . r i r f w I m t A P 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. ing a single chest roentgenogram there is much overlapping, and unless we are aware of what these "white shadows" represent, when they are linear or sometimes nodular in character, we may incorrectly diagnose them as indicating a lesion. The appearance of blood vessels in the frontal view varies greatly in normal persons. Usually the older the person the heavier the linear markings, possibly due to sclerotic changes in the pul monary arteries. Bronchial asthma and fre quent respiratory infections are also known to cause heavy linear shadows. The roent genogram of the healthy chest presents not one pattern but a series of merging patterns covering a wide spectrum, ranging from that with very minimal fine markings to one with manifest coarse linear shadows. Therefore, without supportive clinical evidence an ap parent increase in the vascular pattern per se can have little specificity in roentgenologic diagnosis of pnlmonnrv diser>c<> Tn ->ii :,i. * conglomerate areas of increase<l density in I the complicated forms. We have come to recognize three roentgenologic types: (a) I Fig. S.--This man had Stage II simple silicosis . in 1938, without symptoms (.4). The x-ray changes I are cliaracterized by discrete generalized nodula- tion and definite enlargement of the lung roots, i Twelve years later (B ) there has been no change ! in the degree of discete nodulation, but in the interval 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 gainj fully employed. Fig. 6.--(A ) Simple nodular silicosis. Stage I. Note generalized discrete nodulation and enlargement of both lung roots. ( B ) This patient has been exposed to iron oxide fumes only. Thecharacteristic nodular pattern is visualized, but the lung roots are of normal size and position. simple silicosis; ( b) silicosis with conglom- eration; (c) silicosis with tuberculosis. Fol- lowing is a useful classification. A. S IM P L E SILICOSIS Static I-- Pirxt-Dcorcc Silicosis -TIi** txxl- , j f j i [ | j i j ' < Resduol Air Totol Volume criteria : f l ) an adequate history of exposure to free crystalline quartz silica and (2) the roentgenologic demonstration of discrete gen eralized nodulation in simple silicosis, with Fig. 4.--This man is an iron-ore miner whose chest roentgenogram showed discrete generalized nodulation in 1933( A) . It was classified as simple silicosis, Stage I. In the same chest 17 years later ( B ) there has been no progression of the x-ray changes, and the man has been working without complaints. Fig. 2.--The area enclosed within the silhouette of the thoracic cage at full expiration bears a rela tionship to residual air, and the silhouette of the thoracic cage at full inspiration bears a relationship to the total volume of air within the lungs. Fig. 3- -Regression formula demonstrates excellent correlation between ratio area expiration area inspiration and per cent residual air. Coefficient correlation is 0.772, with a standard error of 0.02. gen changes in relation to the clinical his tory, physical findings, and laboratory data. Far too often this aspect of roentgenologic diagnosis is overlooked, and the outcome may lie most embarrassing. Silicosis is the result of the interaction of 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 hy aline collagen fibers and are evenly distrib u te d th rm n d to n t th e h in t's . T h e d iiu 'tu w i- 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 ber. 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" in 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 lime fields mnv also he 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 clarity 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 generallv accentuated (Fig. 8). Fig. 7.--Asbestosis, Stage I. Note fine 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). It is not especially important whether we have some difference of opinion as to which x-ray stage of asbestosis a patient has. The 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 definition of right cardiac border. nosis and of the presence or absence of pul monary functional impairment as the result of the pulmonary deposition of asbestos fiber. The diagnosis is most difficult in cases which demonstrate only a very slight departure from the usually accepted normal chest roent genogram. These cases are classified as doubtful or uncertain. Usually stereoscopic films of good diagnostic quality are most helpful in such situations. At any rate, it would seem mandatory that these cases be closely followed by means of serial chest x-rays. Fortunately, this problem does 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 to demonstrate various roentgenologic manifestations of the lung abnormalities in cident to these conditions. However, one 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 enlargement without gross alteration of the cardiac silhouette on the posteroanterior projection. CONCLUSIONS Silicosis and asbestosis result from the inhalation of sufficient quantities of free crys talline quartz silica and asbestos fiber. WTien pulmonary reaction occurs as the result of deposition of either dust, a charac teristic, though different, roentgenological pattern is manifested in the chest x-ray. A n x-ray classification of both conditions is employed according to the extent of the characteristic shadows. Simple silicosis is usually not accompanied by any pulmonary functional impairment, whereas the complicated forms almost always dem onstrate some departure from the normal. T he functional impairment in silicosis is due to diffuse obstructive emphysema. A chest fluoroscopy and/or chest roentgeno gram s taken in full expiration aid in evalu ating the presence or absence of this com plication. N ot all cases of asbestosis have a breathing problem. When it is present, it is due to a Fig. 9.--Asbestosis, Stage III. Basilar areas of increased density and involvement of midlung fields are more striking. Characteristic shadows are now extended to involve the upper thirds. Cardiac sil houette has assumed typical "shaggy" appearance. . j .w / > v i i . i h a w . ) , . m j . l . ) l ' i . . > J of the interior o the crys- l "tight lung." Lxpiration films are not of mgs, the history, or the laboratory results, or a much value in determining the presence or combination of the three. In other words, I feel that j absence of respiratory impairment in these it is a waste of the physician's time to listen to the cases, as there is no increase in residual air. patient's lung and then decide, in view of what he thinks he hears, what the x-ray shadows mean. Unlike silicosis, we found some persons However, I would not urge you to stop doing it. ! with slight x-ray changes indicating asbesto- for it impresses the patient and gives the physician sis with definite functional impairment time to think what might possibly be wrong and 's the `iarac>gical ,v. ) itions f the inietl ment, 'ways rmal. 'is is a. A geno- valu- com- tliing to a as of fields now c sil*ance. present. what kind of an x-ray examination should be made j DISCUSSION first. As to the exact problem presented today, may | Dr. M. C. Sosman, Boston: Dr. Bristol has pre I show you a series of slides, any one of which could sented a very complete and scholarly paper con be interpreted as various stages of silicosis or asbes cerning the demonstration and identification of the tosis if the conditions of exposure were adequate various forms of silicosis and asbestosis by roent and if the diagnosis svas not otherwise known or genological examination. The problem, however, is available? May I add at this point, and stress its quite different when attempting to make a diagnosis importance, that I firmly believe the x-ray exam of silicosis or asbestosis in some of the patients seen ination of the chest is only half of the diagnosis: , in a general hospital. Dr. Bristol's patients were the other half must be a history of adequate ex x-rayed particularly for silicosis or asbestosis, and posure. We are not justified in making a diagnosis : in many of them there was a definite history of ex from x-ray films alone or from the history alone, posure. In many of the others there was a known but we can do it from the combination of the two. 1 pulmonary disability, and the possibilities of pneu moconiosis were automatically considered. By con- [Dr. Sosman then showed a series of slides, in trast, most of our patients are sick, but they have a each case pointing out the similarity between the much wider variety of disease, and the demonstra condition demonstrated and similar lesions which tion of the abnormality causing the symptoms is could be due to silicosis or asbestosis. He pointed j often difficult, with its identification even more ar- out that it was easy to demonstrate symptom- | duous. producing lesions in the lungs in over 95% of the cases but that it was difficult to identify them from 1 Many of our patients have shortness of breath, the x-ray examination and the history in more than cough, fever, or loss of weight. It may be due to 75%. He included the following: carcinoma of the disease elsewhere in the body, heart disease or any lung, simulating the conglomerate stage of silicosis: other conditions than industrial disease affecting the metastatic carcinoma, duplicating the nodular stage lungs. But it is surprising how many times the var of silicosis; retrograde lymphatic permeation from ious pulmonary diseases and conditions can imitate the retroperitoneal abdominal area simulating early one another. streaking of silicosis; various granulomatous dis At our institution we had chest x-rays taken of eases, infections, parasites, effects from inhaling 8,000 patients last year, and there were only 3 in toxic materials; lipid pneumonitis, scleroderma, ^ whom we could conclude, with any certainty, that multiple infarcts, chronic passive congestion, espe their illnesses were due to occupational pneumo cially from mitral stenosis; idiopathic pulmonary nitis. However, we can see many slight pulmonary fibrosis, diffuse bronchitis and bronchiectasis and changes and noncharacteristic shadows, such as sarcoidosis,, in addition to several rare conditions I Dr. Bristol has demonstrated in the early stages of just recently identified.] silicosis and asbestosis, but with no symptoms or Conclusion: 1. X-ray examination is mandatory signs and no history of industrial exposure. At this in all occupations where there is any possibility of I point I would like to take up the gage of battle exposure to disease-producing materials, with pri which Dr. Chapman flung at me in introducing me. mary films at employment and routine films at least Dr. Bristol has just stated that in evaluating x-ray once a year thereafter. afislmmsaoknee amtuhsotrcooungshidpehr ytshiecaplaetixeanmt'sinhaitsiotonr.y aNsowwelIl 2. In many conditions seen in the general hospital, s submit to you, gentlemen, that, as a physician prac silicosis has to be considered, but it is actually diag ticing radiology, I cannot remember a single case nosed in only a very small fraction of the total num \ in which the physical examination changed the di ber of patients seen in a general chest clinic in such agnosis which had been made from the x-ray find- an area as metropolitan Boston. I not exchanged i soon pick up al J u n c tio n a I J O ,ni orm a litie o f i n d u s t r i a l P ulm onary. J ilro i it with carbon d I carbon dioxide i and the tissues oxygen. Lack situations fami GEORGE W. W RIGHT, M.D., Cleveland oxygen utilization and carbon dioxide pro smothering of IIIIIIIIIIBIM I have been asked to discuss the abnor duction are augmented or diminished in proportion to energy expenditure. The oxy gen utilized is obtained from, and carbon any sort of Obviously, the air within the ' malities of function that occur in certain dioxide, in turn, is discharged into, the atmos of the pulmonary diseases of occupational pheric air. Since combustion goes on deep ously changed phere inside the 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 in the tissues of the body, some arrangement must be made for transporting oxygen to, and carbon dioxide away from, the active tissues. This transportation is performed by the blood stream which contains oxygen and carbon dioxide in physical solution and com bined with chemical substances. It is readily the outside air l the purpose of that of the o respiratory apj by movements I contains a larg the rapid exch: arising out of the pathological process. Time understandable then that, as energy produc air. To complet 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 tion is augmented during increasing work, more and more transport of these chemicals must take place. This is accomplished by increasing the blood flow to the active parts, the increase in blood flow being effected by an increase in the activity of the heart, the namely, the h< vascular surfac i sometimes rapi the heart also l lung to the tb and nutrients c industrial pulmonary disease. organ that pumps blood through the vascular The respiral Since this audience includes a larger pro channels of the body. The rate of exchange does not opera portion of lay than medical persons, it seems of oxygen and carbon dioxide between the There is a con to me advisable that I spend some time in body and the atmospheric air varies approxi brain which di describing as simply as I can the function mately tenfold, depending upon the rate of rate at which : of the respiratory and cardiocirculatory ap physical energy utilization. Out of the lung paratus. I trust that my medical associates Adequate gas exchange requires that at be propelled tl will forgive me if I, for the purposes of rapid some place the blood must flow over a large in which blood comprehension, simplify the processes which vascular surface where the medium separat out both the lu we know are, in reality, quite complex. The ing the blood from the outside air is very mechanism is human body is an internal-combustion ma thin and hence will permit the gases to cross factors. The j chine which obtains its energy by burning from the blood to the air phase with great body integrate carbohydrates and fat. In the process, oxy rapidity. Such a large vascular bed would be tion and blood gen is utilized and carbon dioxide is pro very fragile and subject to great injury if mands for ener duced. The rate of burning is proportional exposed on the outer surface of the body, understood an< to the rate of energy expenditure; hence, but man has developed so that this vascular During the . Director of Medical Research, St. Luke's Hos bed is contained within a very strong cover pital. ing and protecting device, namely, the chest been devised physiologic as, Read in the Symposium on Occupational Dis cage. The lungs are this vascular bed through circulatory syst eases of the Lungs, sponsored by the Massachusetts which blood can circulate very rapidly and the volume of a oMfedInicdaulstSrioaclieMtyedinicicnoeopoefrathtieonNwewithYtohrek IUnsntiivtuetre- present an enormous surface to air that can their fully disten I lv* vnrinhlv ami rnnidlv refreshTM!. It is nr>- also in file shitr 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 suffer 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 for 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 be 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 hein? ns emptv as one can 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 (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 (O 2V, 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 of 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 physical energy ? This question has been under study for a number of 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 of the respiratory and circulatory systems and to reflect maximum energy output. Numerous 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. 0.025. It is apparent from these data that in those persons who suffer from pulmonary disease a measurement of the maximum breathing capacity and of the response to exercise in terms of ventilation (O 2V) 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 ,-uul 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 tion or resists deformation during expira tion, an alteration that also would reduce the capacity of the respiratory apparatus to pump air. Any of the three alterations just men tioned may cause uneven distribution of gases in the lung, thus interfering with maintenance of an optimum pressure of oxygen and carbon dioxide in the gas phase, and lead to inade quate ventilation of the blood as it perfuses the lungs. Disease processes may cause a proliferation of the tissues that support the blood vessels inside the lungs and in this manner increase the thickness of the mem brane that separates the blood from the gas phase, with a resultant impediment to the passage of vital gases across this separating membrane. This, in turn, would lead to in adequate ventilation of blood which perfuses the lung. Disease processes might also de stroy portions of the vascular bed of the lung, with the result that the area available to the body for transfer of gases from the blood to the gas phase might be reduced. In this con nection, reduction of the vascular bed may also impose a resistance to blood flow through the lung and abnormally increase the work of the heart with consequent damage to that organ. Disease process may also so influence the lung as to cause unusual reflexes to arise from within the lung and thus vary the breathing response during rest or especially during exercise. As mentioned before, dis ease processes may interfere with the proper ventilation of the blood as it perfuses the lung, with the result that the blood itself will undergo changes in the way of increase in the oxygen-carrying cells, thus causing the blood to become more viscous and in that way increase the work of the heart in the process of pumping blood through the ves sels of the lung. Disease processes also pro duce other changes in the cardiorespiratory apparatus of a very subtle nature, and pres ently only vaguely recognized, which may contribute materially to disability arising out of pulmonary injury. We may proceed now to a discussion of the specific way in which the respiratory appara- investigato shown that silicosis, g crete nodu no recogn at most, b surprising which can a chest rot to cause : turbance. n is delibera possible tl are not re thus far al been made fest. We a: of the dis< these samIf we wet life, prior and repeat at the timi its simple would reo tory functi of disclosit be convert Also, pro] persons groups o f : When ctusually fit of pulmona ing capaci volume is tion eqtliv; These fint . served in j and indec * lungs froi. anatomy tive empl movement is severe, of the linn the act of 1 . permitting 11*l li luring expira>uld reduce the atus to pump ns just menition of gases maintenance n and carbon ad to inades it perfuses nay cause a support the and in this of the meniroin the gas nient to the s separating 1 lead to inlich perfuses ght also del of the lung, ailable to the the blood to In this conar bed may low through se the work nage to that so influence xes to arise is vary the r especially liefore, disthe proper 'erfuses the blood itself of increase ius causing ous and in heart in the t ;h the ves- I s also pro- * respiratory | and preswhich may arising out ssion of the >ry appara- ...... investigators throughout the world have maximum inspiration and expiration. In shown that the earliest recognizable form of contrast to the person with idiopathic diffuse silicosis, generally classified as simple dis- obstructive emphysema, in whom recogniz- crete nodular silicosis, is attended either by able alterations of effectiveness with which no recognizable alterations of function or, the blood is ventilated are common, most at most, by very slight ones. It is perhaps persons with conglomerate silicosis show surprising to some that a disease process little or no impairment of blood ventilation at which can be readily seen as manifested in rest, although evidences of inadequate venti- a chest roentgenogram may nevertheless fail lation may appear during moderate or heavy to cause any recognizable functional dis- exercise. One may interpret this as indicat- turbance. The use of the word "recognizable" ing that in conglomerate as well as in discrete is deliberately chosen, since it is entirely nodular silicosis the involved areas of lung possible that slight alterations of function are perfused either slightly or not at all with are not recognized by virtue of the fact that blood from the pulmonary artery. Virtually thus far all studies in diseased persons have all the blood that flows through the lung been made after the disease has become mani- appears to traverse normally functioning fest. W e are forced to compare measurements lung tissue. In many but not all cases of of the diseased person with the average for conglomerate silicosis, the pressure required these same measurements in normal men. to force blood through the vascular channels If we were able to study persons early in of the lung is increased as a result of attrition life, prior to the development of the disease, of the vascular bed. This, in turn, places a and repeat the studies in the same persons strain on the heart, with production of hyper- at the time the disease is fully developed in trophy of the cardiac muscle. If the resistance its simple discrete nodular state, perhaps we to blood flow is severe enough and lasts over would recognize some reduction in respira- a sufficient length of time or is complicated tory function. We have no way, at present, by pulmonary infection, heart failure may of disclosing that a high normal man might occur. be converted to a low normal by disease. The physiologic abnormalities observed Also, properly sampled groups of diseased in the various stages of silicosis fit reasonably persons measured for comparison with well with the histologic abnormalities. As groups of normal men have not been studied, mentioned earlier, the discrete nodular stage When conglomerate silicosis develops, one is focal. Each diseased area consists of usually finds readily recognizable alterations destroyed lung replaced bv the granuloma of pulmonary function. The maximum breath- characteristic of silicosis. No air enters these ing capacity is usually reduced, the residual foci, and no pulmonary artery blood perfuses volume is increased, and the oxygen ventila- them. In between each focus one sees a nar- tion equivalent may be slightly above normal, row zone of dilated alveoli, spoken of as These findings are quite typical of those ob- being emphysematous. The physiologic data served in diffuse obstructive emphysema, indicate that these dilated alveoli are too and indeed the histological sections of the few in the aggregate to recognizably influence lungs from conglomerate silicotics show the function, or they function normally in spite anatomy characteristics of diffuse obstruc- of being dilated. When clinical or physiologic tive emphysema. When the impairment to evidence of impairment consistent with dif- movement of air into and out of the lungs fuse obstructive emphysema is observed in a is severe, it can be recognized by observation person with simple discrete nodular silicosis, of the limitation of thoracic motion during one must suspect that the emphysema is a the act of breathing. More sensitive methods chance concomitant disease and would have permitting earlier recognition of this obstruc- occurred even though the silicosis were ab- i,. n.,.. ...... n........................... ......... ............ t,, <i... 1.: . i : ft i ' . i li * i I. r+i , ' 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 wfas pre sented at the Seventh Saranac Symposium in September, 1952. W hat is the status of the respiratory and circulatory systems in a person who has typical roentgenographic ntirl -Itnirnl eviflenrp r>f ixslipstfisis? A stilflv shows rather clearly that in the typical asbestotic there is little, and often times no, impairment of ability to ventilate the lungs, as measured by the maximum breathing capacity. There is likely to be, however, a measurable restriction of the degree to which the lung can be expanded, as evidenced by a slight to moderate reduction in total volume. Of course, when the fibrosis is extreme in extent, the impairment to enlarging the lung may cause an appreciable loss of maximum breathing capacity. Fluoroscopic examina tion, as well as a comparison of inspiration and expiration films, and measurement of the actual residual volume of the lung show that there is little or no impairment to empty ing the lung in such persons. When one measures the partial pressure of oxygen and carbon dioxide in the gas of the lung, one finds that these pressures too are within normal limits. Nevertheless, study of samples of blood removed from the peripheral artery will usually show a rather marked inadequacy of oxygen transfer from the lung air to the lung blood. The partial pressure of oxygen in the arterial blood is usually subnormal, and less than the normal proportion of oxy hemoglobin will be found in the sample. The difference between the pressure of oxygen in the lung gas and in the lung blood is usually quite markedly increased. The partial pressures of carbon dioxide are apt to be within normal limits, both in the lung gas and in the lung blood. These data quite clearly indicate an impediment to the passage of oxygen across the membrane separating the gas from the blood phase in the lung. Carbon dioxide transfer, however, is not appreciably interfered with. During exercise the person with asbestosis is apt to display overbreathing. The volum e of air breathed per minute will be considerably greater for a given stress of exercise than would be true in normal persons. This is well demonstrated in measurements of the oxygen ventilation equivalent, which is found to be elevated. The rate of respiration and the pulse rate during exercise are apt to be higher than norm al in the nerson with nshestosis. T h e [ limits the phys I with asbestosis normally high abnormally inc , during work. T I and the pressui I an unusually s In addition, r abnormally sti lung of the asb. of breathing or distressing sen To what ex abnormally low blood, one of asbestosis, prt , for physical w j those persons j O2 content of sessed a norma cal exertion. B a person with not with hims be incorrect to strates an ab capacity for pi. phasized that average capaci of incomplete c These findir sis stand in r. abnormalities . Whereas in marked reduc capacity and typical of dii are commonly are usually al latter, there aj ment of movei lungs, the chi. gard to thora< are resistant person with little abnorma between the lu quite the revei asbestosis. In transfer to bln< 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 of 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 for 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 bine 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 of 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 ! ! . iI fi i in asbestosis. the primary or chief abnor mality exhibited by the asbestotic patient is impaired oxygen transfer to the blood rather than impaired breathing ability and ventila tion. It is true that the histologists have re ported emphysema as being present in the tissues of the lung in the typical asbestosis case. Small areas of emphysema undoubtedly do occur, but the massive emphysematous involvement of the lung, which is so com monly observed in conglomerate silicosis, does not appear to be present as a rule in even the severe cases of asbestosis. What can be said about the relationship between the presence or absence of physio logic abnormalities and the presence or ab sence of recognizable pathologic manifesta tions in the chest roentgenogram in asbes tosis ? O ur studies showed quite clearly that examples of asbestosis, clearly recognized by roentgenography but with minimal or absent physiologic abnormalities, do exist. This can only mean that in some (not the rule) in stances the earliest roentgenologic manifes tations are still focal in nature and that large volumes of normal lung tissue remain through which blood can perfuse in prefer ence to those areas that have been damaged by the asbestosis process. The reverse situa tion may also be observed, as evidenced by the observation of some persons showing evidences of abnormal physiologic conditions in the arterial blood with no clearly recog nizable abnormality in tbe chest roentgeno gram. Two possible explanations exist for this not unusual finding in our series of cases. First, the 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 a re norm ally present in the lung. It may be that in those cases which we observed with evidence of impedi ment to oxygen transfer across the membrane but without evidences of change in the x-ray we failed to recognize the earliest x-ray ab normalities. The second explanation may he that the disease process is so diffuse in its i ,.|T , I - M W 11,-. t 111 w l i t 11.` i . r t i f , As a consequence some of the blood must flow through areas of lung tissue in which the membrane has been slightly thickened, thus causing impairment of oxygen transfer to the blood. Since the lung is so uniformly involved by the slight alterations of tissue, there is poor contrast between normal and diseased areas and, hence, no definite abnor mal shadow in the roentgenogram. In regard to the correlation between x-ray abnormality and physiologic abnormality in asbestosis,. one can state that three situations can exist: (1) physiologic abnormality without any definite roentgenologic abnormality, (2) roentgenologic abnormality plus physiologic abnormality, and (3) roentgenologic abnor mality without any physiologic abnormality. What about the duration and intensity of exposure to air-borne asl>estos fiber and the subsequent development of roentgenologic or physiologic abnormalities ? As one might ex pect from experience with other pulmonary diseases of occupational origin, there was a gross correlation between the intensity and duration of exposure and the development of abnormal shadows or physiologic changes. However, some persons with prolonged and very intense exposure failed to develop any evidences of either physiologic abnormality or roentgenographic abnormality. Our ma terial fails to give us any evidence as to what the shortest required duration or intensity of exposure is in order to produce a recog nizable asbestosis. It has long been known that both crystal line silica in finely divided form and asbestos fiber when introduced into the lung can pro duce fibrosis which leads to physical impair ment. Although the clinical manifestations of the disease are in many, though not all, respects sim ilar, tbe physiologic abnorm alities are recognizably distinctly different in the earlier stage of the two diseases. In the ter minal stage the distinction may not be en tirely clear and may lead to confusion. A further difficulty in diagnosis resides in the fact that many workers with obvious pul monary abnormality have had exposure to Iw.lli srifift 'nii| rmM Mir genologieally manifest hut without recogniz able physiologic impairment. An enormous respiratory reserve, which is the birthright of most of us, permits extensive tissue injury and damage with little or no loss of capacity tor physical work. This statement of fact in no way should be construed as condonement for needless injury. DISCUSSION D r. J ames L. W hittenberckr, 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. W right 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 1635,' 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. I think that it is th 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 alMmt 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 it would be very worthwhile. Many of the tests Dr. W right described depend a lot upon the cooperation of the patient. It 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.2 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 by 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 in this 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. 5) 1953. 2. Fletcher, C. M .: Clinical Diagnosis of Pul monary Emphysema: An Experimental Study, Proc. Roy. Soc. Med. 45:577-584 (March) 1952. I . 1I ; i f sdbetoi a ^ d iffere n tia ted from er f-^neumoconioded 0 . A. Sander, M.D., Milwaukee llllllllli:illll!llllllli!ll!llllllll!llllllllllllllllll!l^ 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 m ore 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, tn*- into such a film. When to this are added some retained secretions in the lower lobes, which often are bronchiectatic in emphysema, the misdiagnosis is established. A pneumoconiosis of which we have be come increasingly aware in recent years is that due to excessive deposition of coal dust. It appears quite certain now that free silica is not needed as an essential component of the dust to develop the characteristic changes. The fine lacy character of the shadows plus some emphysema gives a pattern which looks very much like "ground glass" and is easily mistaken for early asbestosis. All these examples I assume represent pa tients who present themselves to their physi cians with symptoms of dyspnea, with a his tory of some exposure to asbestos dust, and with chest films of the character I have men tioned. ' How easy it is to fall into the trap of a gunshot misdiagnosis! Unless other pos sible causes for the x-ray changes are con sidered first and a detailed past occupational history is evaluated, along with the char acter and extent of the most recent dust ex posure, another worker who actually needed reassurance will be told that his lungs are full of asbestos dust and that he should quit his trade! From that point on, his symptoms usually increase to a marked degree, and he has developed what to him is a real disability. In my experience, such doctor-induced dis ability is commoner in some areas than is the disability from the disease itself. Because of the complete lack of unanimity of opinion about this disease among physi cians and because of the need for more clearly defined criteria for diagnosis and ad vice on continued employment in the trade, the medical and industrial hygiene advisers  added r lobes, lysema, w e beears is nl dust. : silica nent of Ganges, s plus h looks s easily m t paphysia hisst, and i mene trap r pose contional charst exleeded ,rs are d quit ptoms nd he bility. 1 disis the limity physimore id adtrade, ,'isers 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 tru e ; 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 nondusty work, we agreed to the following: 1. Persons under 40, when the diagnosis is dear cut (beyond first stage), should be 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-rav rnt*er,, nf . , : i l fr i i <i because it did not look like the siderosis of welders about which he had read something recently. The degree of asbestos-dust exposure was not inquired about (it was spasmodic and minimal). 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 be 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 of the characteristics of asbestosis and no pleural involve ment. After postmortem study the diagnosis was clarified--a widespread congenital cystic lung, with interstitial fibrosis 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 fibrosis. 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. H e should be convinced soon that he most likely was wrong, which will be most embarrassing to him. This case, along with many others which could be 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 is a foundry worker with a chest film which was characteristic of a moderately well-developed asbestosis. Careful study 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 hel|>er during the late teens and early twenties, doing all the sawing nf adii-itii- nine iveriiui's. ustiullv in I'on- When the most detailed analysis and study will not reveal the true diagnosis, which hap pens in occasional cases, taking a biopsy spe cimen of the lung should be considered. This has become a rather simple procedure with little danger of complications. I t must be remembered, however, that because of the relatively small piece of lung usually ob tained for biopsy, there always is some dan ger that the diagnostic pathological change will not be revealed. In conclusion, as with all chronic chest diseases, so especially with asbestosis, all possible causes of the pathology revealed by the chest film must be considered. Poorly studied cases result in misdiagnoses which not only are embarrassing to the physician but which may also cause irreversible harm to the patient. W e owe it to our patients and to the medical profession to so thoroughly investigate every obscure case that such un fortunate situations do not arise. DISCUSSION D r. K arl T. B enedict, W est Boylston, Mass.: It is a privilege to substitute for Dr. Harriet Hardy; she has helped me many times, but a sub stitute is always a "second." The assignment is "the. differential diagnosis.'* I have had no experi ence with asbestosis and, furthermore, I believe that experience with most pneumoconioses, as seen today, is gained only after 20 to 30 years' study, because it often takes that long to produce such disease. In spite of the foregoing, 1 believe I am qualified to make certain remarks, because I have been practicing industrial medicine for 15 years in one of the world's largest artificial abrasive plants. Since 1940, we have taken more than 25,000 chest x-rays on some 5,000 abrasives workers. From 1911 to 1940, except in rare instances, we simply did so- called routine physical examinations. I agree with Dr. Sosman that the physical exami nation is not worth very much in these circum stances. Thanks to Phil Drinker and others, dust control is much better in our plants today. In one large plant our dust counts run consistently 3,000,000 to 4,000,000 particles per cubic foot. We handle a great variety of dusts, for that is our business, and safe handling is essential. Recently at the Seventh Saranac Symposium, several world-renowned authorities on pulmonary diseases attempted to define pneumoconiosis. I shall . . t i ,. ... . . . . . ,t c . . m .. i t . . . - . : n , . . f . i ^ t, 1 study li haj- spa This with t be i the obdanmnge chest . all <`d by iorlv vvhich ician larm s and ighly i un- lass. : arriet subnt is <perielieve seen tudy, such dified been ne ol Since -rays 11 to d so- <amiicum- dust l one rently We our sium, mary shall .l.wl group insisted that pneumoconiosis simply means and their differential diagnosis. Wc in the abrasive dust in the lung. The other group restricts it to industry are continuing this research. Specifically, those conditions producing demonstrable disability. we believe that under reasonable control alumina The hitch is, W ho demonstrates the disability ? The dust is no problem. You have heard of the "carbo roentgenologist sees nodular fibrosis in the x-ray rundum lung" no doubt; this is an unjust label, as ( film ; that is pneumoconiosis to him. At once, or my good friend Dr. Eddy, of the Carborundum I 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 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 know of his trouble, the family physician has diffi has never been proved conclusively, I believe. It culty clearing an ordinary chest cold or the surgeon is entirely possible that this lung condition is caused is faced with anesthesia worries. The occupational by significant free silica contaminations. Further disease or the health department specialists in our study is needed, and we intend that it shall be made. state government want reports when "injury" has Shaver's disease has been mentioned before. In resulted. Compensation and insurance authorities spite of several years' research tending to prove that talk about the number of pneumoconiosis cases, alumina fume is the cause, there are those whb based upon those workers whose earnings have believe that silica fume is to blame. Industry is suffered. The compensation lawyer appears later somewhat discouraged by the inconclusive nature i in the picture, and alas sometimes the last, the of these and similar medical studies. pathologist, may be the first in proving that a case We all know about the problems related by beryl of tuberculosis or cancer is in reality pneumo lium and radioactive dusts. On the other hand, coniosis. our concepts of day and talc pneumoconioses have I believe we all know when the man is suffering changed in recent years. And what do we know from pneumoconiosis, whether we be laymen or about zirconia or titania or magnesia or boron physicians. W hat he wants to know is, W hat is carbide or graphite dust inhalation ? In our industry wrong? W hat can be done about it? Is he perma organic substances have caused only two minor nently disabled? Is his life shortened? cases of asthma. And we have seen no cases of can T here can be only one answer: not better diag cer of the lung among our abrasives employees. 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 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. for you and me to continue to study pneumoconioses * Maximum allowable concentration. V