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212^,. niVjaai.iiiS >, HASKELL 1*8 INDEX 02 OCT SO schepfr!*. own J OOOSO J OOOS1 THE PATHOLOGY OP COR PULMONALE COLL. CARDXOL. 7: *3-92. 1957 rsuc \30? continued a:o no** TUANS. AMUR. 650 J 00052 J 0 0 OSS J 0003* THE .INFLUENCE OP FTHERCLAS PLASTIC OUCT ONTUUSRCULOCXB AMER. REV. TUIICRC. PULM. OIR. 7A: SIR-23. 19*4 695 -f 00053 oooss INHALATION HAZARDS IN NUCLEAR ENERGY PROGRAMS OZS. CHEST 33: 17.1 . 1DSS 66* 00 057 o00o0o5s0t coono onosi 000C2 PULMONARY HISTOLOGIC REACTIONS TO XNMALEOFXOERGLAS-PLASTXC OUST AMCR. J. PATHOL. 39: 1169-47. 1959 THE PULMONARY REACTION TO SHEET PXOERGLAfl- PLASriCOUST AMtK. IMG. NYC. ASS. J. 20: T3- 61. 1959 674 SHELF 677 SHELF 000 000Q0u66o3S* J 000G6 J 00067 j oonss J 00069 J 00070 HYPERTENSION OUR TO INHALED SUDMXCRON AMORPHUUSSILieA TOXICOL. Al'PL. PHARMACOL. 1: *47-500. 19SS THE PATHOGENICITY OP GLASS-REINFORCED PLASTICS A. 11. A. ARCH. INS. HEALTH 2i 620-3*. 1961 OCCUPATIONAL CHEST DISEASES MODERN OCCUPATIONAL MC02GXNE. SECOND COITION. 96. 1960 **3- 602 SHELF S9M SHELF 6AA SHELF 00071 00072 00073 THEORIES OF THE CAUSES OP SILICOSIS MCZNTRVNE RESEARCH FOUNDATION CONFERENCE. 10TH. JANUARY 25-27. 1960 TORONTO. CANAOA 069 0007* 0O0U0G7YSG HEPATIC CELLULAR GIGANTISM AS A MANIFESTATION OFCHEUXCAL TOXICITY PROC. INT. CONOR. OeCUP. HEALTH. 13TH. 7AC-9S. NCV YORK I960 691 SHELF J 00077 J 00070 TUBERCULOUS PERICARDITIS 9: 2*6-76. 1962 A HER. J. CARDIOL. 703 J 00079 J 00040 sj onoai J OUOA2 000A3 J 0 0 0 A* J 0OO6S J 00066 000X7 J 0 0 0 AS J 00049 J 00030 J 00091 no 037 00003 FRACTION OP MONKEY LUNG TO SILICEOUS OUSTS ARCH. ENVIRON. HEALTH 5: 27A-99. 1962 DIFFUSE INTERSTITIAL PULMONARY SYNDROMES OUPONT MED. OZV. . JHfH ANN. MTG. . OCT. 19S9 OCCUPATIONAL ASPECTS OF COA PULMONALE CARDIOLOGY: AN ENCYCLOPEDIA OF THE CARDIO VASCULAR SYSTEM. VOL*. CHAP. 13. 10-21. N.Y.. MCGRAV-HILL. 1959 HAIR tXnAVI AND HEALTH 141: 632. 1962 j. amsr. Msn. AOtsee. DIFFUSE PULMONARY LESIONS: THE PROBLEM OFOZFPERENTZAL DIAGNOSIS DZS. CHEST *3: 155-71* 1963 LUNG DISEASE CAUSED BY INORGANIC AND ORGANIC DUST OZC. CHEST ** 133-*0. 1963 70* SHELF CAS 3 G66 499 SHELF 71* 710 j 0809* u 00095 100096 J 00097 J 00096 J 00099 J 00100 J 00101 TCTUACTHVLLCAO ANDTETRAMBTHYLLCAD ENVIRON. HEALTH 4; 277-95. 194* ARCH. HARMLESS AND HARMFUL ATR CONTAMINANTS; APAT HOOENSTie CLASSIFICATION AMERICAN COLLEGE OF CHEST PHYSICIANS. PHILAOELPHIA. PA. SEPT. 26-9. 1901. LECTURE DELIVERED AT THE 1*TH ANNUAL POSTGRADUATE COURSE ON OCCUPATIONAL 0X8KA5E0 OF THE CHEGT. U* SHFLF 717 00102 000011003* NEOPLASIA EXPERIMENTALLY ZNOUCEO BY nCRYLLZUMCOMPOUNOSPROOF. EXP. TUMOR RES. 2: 205-**. 19C1 716 00001100G5 00107 00104 THE CAPACITY OF ALUN7NUM TO PREVENT ruoTMP.OMUXMorpRcncxnu uv ouautz, an EXPERIMENTAL NTUDY &VGU7.NLA PIGS TOXICOL. APPL. PHARMACOL. 3: 1KA-201. 1961 719 SHELF J 00109 J 00110 J 00111 THE MINERAL CONTENT OT THE LUNG IN CH20NXCSERYLLZ067S DZS. CHEST Hit 690-607. 1962 vr' 00112 'J 00113 J 0011* THE 070LOGZCAL ACTION OF RARE EARTHS 6.V.H. ECHSHKRS A M A ARCH TNO HF.AL1H 12:301-5 C195S) l30 SHELF HASKELL LB J PAWFLSKX XDHL*001 PRT FPC.D oc^3 O<u-NWC64JB DU 038213 - 71 - Cc/^C'3 DIFFUSE INTERSTITIAL PULMONARY SYNDROMES G. W. H. Schepers, M. D., D.Sc. Haskell Laboratory for Toxicology and Industrial Madicins E. I. du Pont da Nemours and Coopany During the past two years three of the du Pont Coopany Textile Department Plants each yielded several cases of diffuse inter stitial pulmonary disease. Since these syndromes occurred in comparatively young employees (all under 50), a special Study of these cases, of the prevalence of comparable lesions in other employees, plus a review of the general problem of diffuse interstitial pulmonary disease has been initiated. The present paper reviews preliminary data garnered to date. The main Interest naturally centers in those eases in which pulmonary biopsies or resections were performed. Drs. Savage, Dicker- son and Weaver have contributed twelve specimens. Their salient features have been summarised in Table 1. In addition, Dr. Savage collected lung tissue slides prepared from 100 deceased, non-company employees on whom autopsies had been performed during the past several years at Waynesboro General Hospital. These cases serve as controls for the Waynesboro area. The slides from the twelve cases were also reviewed by Wilmington pathologists, staff members of the Johns Hopkins University and the Armed Forces Institute of Pathology. In addition, these slides were compared with eight pulmonary biopsy preparations recovered from personnel of the Textile Division of another company in which comparable clinical syndromes have been de tected. Dr. Sidney Pell has also reviewed the prevalence rates of chronic bronchitis in the Textile Divisions of the du Pont Company as compared with the overall incidence of this disorder in Company personnel (Table 2). Further biostatistleal analyses and clinical studies are in progress or are contemplated. -- Histopathology The lesions present in the twelve biopsy specimens reflect a wide range of lung changes. There is, however, a pattern of histo logic features common to all. The primary components of the reaction are represented by cases 1, 2, 3, 5 and 11. In these instances the following are present: (a) proteinaceous exudation into alveolar spaces, (b) selective re lease of cells into alveolar spaces, (c) infiltration of alveolar walls by phagocytes, many of which contain inclusion bodies, (d),,-.periva*cular and peribronchial accumulation of cells, (3) extensive injury and secondary repair of the bronchlolar mucosa, (f) retarded interstitial fibrosis, (g) atrophic and confluent emphysema. DUP 0 9 3 7 2 3 9 DU 038214 - 72 - Secondary lesions discovered is this group ere represented in cases 4, 6, 7, 8, 9, 10, and 12. These include: (s) extension o the atrophic emphysema and bronehiolar lesions to create pneumato celes, cysts and vanishing lung complexes, (b) superimposed pleural effusion and hemothorax, (c) granuloma formation, (d) proliferation of bronchial epithelium with formation of bronchial adenoma and obstructive bronchiectasis. While the latter group of lesions may be causally related to the interstitial reactions, they may also be mere Incidental findings. Traces of the proteinaceous exudate are present in the alveolar spaces in the majority of cases. In its most fully developed form this exudate fills and distends alveolar spaces. Much of it is probably derived from the blood since many erythrocytes are present within the exudate in some areas. Its brightly eosinophilic character apparently reflects its high fibrin content. At various points crystals, morphologically identical with cholesterol plates, are present. In some areas the exudate is being resorbed by histiocytes. Some of these exudate*laden cells are seen to be penetrating into the alveolar walls. In several of the alveoli an inspissated residuum of the exudate forms a thin dense layer over the septal surfaces. This residuum resisted decolorixation by alcohol and acid when the ziehl* Nealsen stain was applied in one case. The specific cells found in the alveoli vary according to che g and severity of the reaction, in areas where 11tele or no exudate exists, the dominant call is the plasma cell. For the most part thest cells possess abundant opaque cytoplasm without inclusion bodies. Histiocytes ere store prevalent where there is exudate end apparently serve a phagocytic function. In tarns of morphological criteria these cells are histiocytes, but it is also likely that they are desquamated alveolar septal calls. Their cytoplasm contains spherical eosinophilic inclusions, fine vacuoles, large spherical nonstaining bodies or vacuoles, glycoproteins, oil or fat droplets, nonpolarizing aclcular crystals, hematin pigment end opaque particles. The most Impressive inclusion bodies ere the oil or fet droplets. In some of the alveoli the histiocytes have fused to form oulcinucleated syncytia or giant cells. In one instance these syncytia completely fill the alveolar spaces and contain multiple vacuoles in which smell, spherical, clustered particles occur. These elements ere too large to be Hlatoplasma capsuleturn but the tissue is being further investi gated to exclude the possibility that these bodies may represent fungal speree, e.g. Cryptococcus neofomens or Coccidioldes laitIs. Bee teriological stains nave proved negative in all other qases. DU 038215 D llP 0 9 3 7 2 4 0 -73 - The characteristic changes in the alveolar septa include: epithelial proliferation, infiltration by cells, belated fibrosis, capillary distension or collapse according to Whether cellular in filtration is far advanced or not, presence of inclusion bodies, rupture of the septa. The epithelisation is sporadic and continuous epithelial sheets have formed in only one case. The infiltrating cells are plasoacyecs, histiocytes and, in one case, eosinophilic polymorphonuclear leukocytes. Plasma cells predominate and resemble those found within the alveolar spaces. In one case some of these cells are filled with minute spherical eosinophilic granules. The histiocytes are smaller than those, of the alveoli. They display eosinophilic inclusion bodies in one instance. In a large proportion of eases these cells are filled with small or large vacuolaa. That these vacuoles represent fat or oil is suggested by a positive reac tion to Sudan IV in one representative case. Zn addition .to these intracellular droplets, a number of spherical bodies, not Obviously lying within macrophages, are present. In one case these bodies displayed a negative reaction to the periodic acid Schiff reagent. On this basis these bodies may represent oxidised lipid. Fibrocytes are not prevalent, but a few could be Identified in the areas where vacuolated phagocytes are congregated most densely. Here delicate strands of collagen support the phagocytes, losinophils noted in one case have infiltrated the alveolar walls as solid cords. The extent of the mural infiltration varies considerably. In most areas the alveolar septa are thickened to twice or thrice their normal caliber and the blood capillaries wind over or around the collections of cells without apparent occlusion. In other areas tha cellular involvement is more extensive. Hot only are tha alveolar septa transformed into cellular eords measuring 20 to 40 times the normal caliber of the septa, but the capillaries heve become obliter ated or deeply buried within these cell collections. At ihe same time the alveolar spaces have become encroached upon and in the more advanced eesee ere completely occluded, transforming extensive por tions of the pulmonary parenchyma into solidly cellular areas. Tha altamativa rasponsa to cellular infiltration of the alveolar septa is by rupture. In this manner several adjacent alveolar spaces have become confluent. This atrophic emphysema is regionally emphasized so that fairly large intrapulmonasy spaces have resulted. In three cases large multilocular cysts or pneumatoceles have formed. Since these space lesions occur in lungs in.which atrophic eophyseia of the foregoing type it also present, it is nec essary to consider whether tha cystic lssions and tha emphysema are DU 038216 DUP 0 9 3 7 2 4 1 - 74 - part of the same basic process. In ons case (No. 6) the cyst has a cuboldal epithelial lining similar Co chat of che bronchiole*. In che other two instances such an epithelium is lacking. Granulooata with vacuolated cells occur in parts of the cyst well or the trabeculae. The lung parenchyma has not bees compressed so that these cysts do not represent expanding spaces which have encroached upon other portions of che lung. It seems rather that these spaces represent portions of lung from which alveolar septa and terminal respiratory passages and blood vessels have been withdrawn without ensuing atelectasis. . This is characteristic of one of the forms of the vanishing lung syndrome. While the pleura has remained relatively free from involvement in most instances* two of the cases presented as spontaneous pneumo thorax with pleural effusion in one and hemothorax in the other. There is nothing specific about these lesions. In one case* however, the subpleural lung tissue displayed mural infiltration by*vacuolated cells of a type similar to those present in other granulooata from this group of cases. Granulomatous lesions developed in several specimens. It is not clear whether granulomatosis is an end result of local evolution of the lesions, or whether it is an independent reaction. The most elementary granulooata are represented in Case 5. In this case the granulooata are paravascular and parabronchiolar and are a composite of intramural and intra-alveolar cells. In some granulooata lipophagas with abundaac pale cytoplasm form a prominent cnmponmt. In ochar unit lesions nultinucleeted giant cells are preecnt. These cells are of the Lengarhene type with a central collection of amorphous matter yielding negative reactions for ths Zlehl-Neelsan and periodic acid Schlff tests. The predominating cells are plaaaecytea end histiocytes. Several of these cells contain inclusion bodies* a.g. eosinophil granules in che case of the plasma calls and vacuolag and !arythroid bodies in the case of the histiocytes. Abundant proliferation of the bronchial epithelium has occurred in Casa No. 7. This has occluded the bronchus at one point where an adenomatoid lesion is present. In the surrounding lung, interstitial pulmonary infiltration by. vacuolated macrophages furnishes e clue that this process may be related to that preaenc in other eases from this series. It is also possible that tbs adenomatoid lesion represents an unrelated finding. In Case No. 8 numerous minute apparently encapsulated bodies are present within the giant syncytia. In this instance some peri pheral fibrosis has occurred around each unit lesion. These structures are being further investigated for they resemble fungal elements but may also represent lipid particles. In three additional cases the DU 038217 OOP 0 9 3 7 2 4 ? - 75 - predominating cell is a vacuolated histiocyte supported by a network of fibrocytes and collagen bundles. The latter lesions are indistin guishable from the oleogranulomata associated with inhaled mineral oil droplets. Clinical Aspects Symptomatically these cases share certain characteristics, not only with one another but also with syndromes in plant personnel who were not subjected to lung biopsy. In a number of instances the chronic phase of the syndrome was preceded by single or repetitive respiratory tract infections diagnosed as "sinusitis", "frequent colds", "virus pneumonitis", "influenza", "bronchitis" or "pleurisy". In other instance# the onset was insidious without prodromal symptoms. The subacute or chronic phase, extending over months to years, was often ushered in by asthmalike episodes with paroxysmal dyspnoea as a main symptom. These attacks sometimes were associated with febrile phases, with or without productive coughing. In some cases antibiotic therapy and antihistaminics alleviated the distressful symptoms; in others, cortisone had a significantly favorable influence. Almost all patients experienced spontaneous remissions. In several employees symptoms abated as soon as the persons concerned was* Mticnad Co a now work area. Xn ochar instances eha convaraa was obvious, i.e., the patients underwent relapses, or symptoms were aggravated shortly after in-plant work was resumed. No job-relatedness of symptoms was obstrusively evident in a further group. Laboratory testa were on the whole inconclusive except for their negativeness. Evidence of sensitization to biological or chemi cal agents was conspicuously lacking. Pulmonary function studies ware carried out preoperetivaly in four subjects in idiom biopsy confirmation was later effected. Comparable studies ware also Instituted in other men not subject to biopsy. The feature common to all these cases was mixing, dilution end diffusion defects. Mild polycythemia was present in some instances. No electrocardiographic defects were dlscoverdd. Radiographically no clues were elicited concerning the diffuse lesions. Major complications wars, of course, detected (e.g. focal granuloma, pneumatocele, branchial obstruction). The.basic process being at **he alveolar level it is understandable that so little wea revealed by conventional x-ray techniques. DU 038218 DUP 0937243 JWBg-rgMaatBiliMfci `TtMmmSMfccaaBLSr Environmental Studies - 76 - Careful surveys of the pleat environments failed to Identify a specific hazard. While the pulmonary symtoms occurred mainly in long-ssrvlce personnel, there was not any clear-cut identi fication of the clinical cases with particular occupations. The only air-borne components which entered into the plant environments transiently, before being drawn into the air-conditioning system, appeared to be acetone, fiber finishes, lubricating oils and fragments of textile products or containers. Acetone can apparently be ex cluded since cases occurred in both acetone using and nonacetone areas Very little evidence of dissemination of textile or container particles vies found. This leaves as possible pathogens only the mists, smokes and vapors created through the impingement of lubricat ing oils or flbsr finishes on fast moving, often heated textile fibers. However, many of the man most heavily exposed to-these agents showed the least pulmonary involvement. Nothing comparable has been found in persons from the geographic areas where the textile plants are located Who are not employed in these plants. The 100 randomly selected autopsy specimens which served as controls were all negative. These observations suggest that the cause may be industrial rather than biological. Differential Diagnosis Interstitial pulmonary infiltration has been reported with increasing frequency during the past three decades. Zt is not possible to review this problem fully in this presentation but the classification given in Table 3 may indicate the wide scope of conditions from which the present series of cases have to be differen tiated before a new syndrome may be proposed. A biological etiology is still held high on the list of possibilities, even though the process has manifested itself primarily in plant personnel. Even chough the process appears to be occupation related, the possibility of augmentation or facilitation of injury by air-borne industrial agents by preceding or through cooeommittant bacterial, viral, mycotic or parasitic invasions of tha lung must ba further explored. Recovery of micro-organisms was unfortunately not attempted at the time the biopsy samples were taken. In Case No. 7 an acid-fast bacillus was identlfisd in tha sputum on one occasion, but tha histological appearance of tha lung tissue did not favor e diagnosis of tuberculosis. Skin reactions for tuberculosis, histo plasmosis, coccidioidomycosis proved negative in other eases. Further study should be made of bacterial and fungal agents in the textile plants since It is possible that micro-organisms may insidiously pro liferate on textiles or in chemical solutions. DUP 0 9 3 7 2 4 4 DU 038219 - 77 - It seems permissible to exclude from this group the endogenous category of interstitial lesions. None of the cases con formed to the other criteria characterising these syndromes. Thus, there was no bone involvement, no splenic or liver enlargement. None of the patients had been subjected to trauma, so that fat embolism may be excluded. No cardiac or renal lesions were discovered so that we are not dealing with the so-called Schatsky lung syndrome. Allergy will require further exploration, but one of the patients was a hyper-reactor to common antigens. It seems likely that the cauee may be found in the chemically determined group of etiological agents. Thera is no evidence of any physical forces in the pleat environments of the categories listed in Table 3 which could have produced these pulmonary lesions.' Attempts have also been made to compare the lesions with the group of syndromes currently classified as of unknown origin. The divergences appear to be greeter than the resemblances. Moreover, since Hodgkins disease, sarcoidosis, scleroderma, Hausen-Rich syndrome, alveolar proteinosis or hyaline membrane disease must a priori ultimately be resolved as either biologically or environmentally determined, no useful purpose can be served by exploring resemblances to these conditions further then seems obvious. Lipid pneumonitis eppeers to be the condition most strongly suggested by the histological evidence. Further inquiry is in procees Co exclude jacroganlc oleograauloaatosls. While e clear history of excessive use of nasal or pharyngeal oil instillations could not be elicited, it may be recalled that patients frequently have unreliable memoriae about such mattera. Lipiodol also wee used in one case for diagnostic purposes. Though vegetable oil* generally cause no permanent pulmonary damage in normal lungs, lees is known about their capacity to provoke tissue reactions in abnormal lunge. Considerable experimental research and human experience has accumulated since Laughlin identified the first case of oleogranulomatosis. Pertinent experimental data cullod from the literature on this subject (Rtfs. 1-21) have bean summarized in Table 4. These reveal that the lungs react variably to different kinds of oils. The reactions to most vegetable oils are least significant. This may be due to their low fatty acid content and their rapid hydrolysis or elimination from the lung tissue. Chaulmoogra oil has a high fatty acid content and this correlates with its marked capacity to provoke progressiva chronic pneumonitis, pulmonary granulomatosis, focal necrosis, epithelial proliferation, pulmonary fibrosis, bronebila lesions end cellular catarrh. The rlcin oleic acid of castor oil causes scute pulmonary inflammatory reactions but no chronic response. In this respect it behaves similarly to croton oil. In the case of peanuC oil the arachidic acid is capable of producing acute as well as chronic pulmonary lesions. DU 038220 DUP 0 9 3 7 2 4 5 . irtiffali D-iiiliMtjlIja attgijaaaaMWiMwTM , - 78 - The majority of the animal-derived oil* are markedly irritating to the lungs, provoking both acute and chronic reaction*. Attention may be directed more especially to their propensity to ex cite giant cell systems and proliferation of alveolar septal cells. In the ease of lard there is an additional tendency to pleural reaction. Mineral oils produce yet a further variety of reactions in which lipophages fora a conspicuous feature. No hydrolysis by lung lipases oceurs in these eases* but the fine subdivision of the mineral paraffinomata. Lipid pneumonitis is a well-documented problem in human affairs. Gross pulmonary disease and scores of deaths have been in duced by the intrapulmonary introduction of oils of various'kind* particularly milk fats, cod-liver oil, croton oil, peanut oil, mentholcamphor and mineral oil. Since oils form an important ingredient of fiber and machine lubricants used in textile plants, it is imperative that first consideration be given to the possibility that at least some of the cases of chronic interstitial pulmonary disease may be se quential to the prolonged inhalation of small amounts of oil. In this connection the inhaled oils could function either as a primary cause or as cofactors. The question of periodic exposures to surges of enhanced exposure, always a possibility in almost any industrial operation, but seldom reflected in average exposure charts, needs to be considered. The adjuvant or synergistic action of oils of different kinds must also be explored. Variations of the formulae for fiber finishes may enhance or retard the pulmonary reaction to Inhaled droplets. Such explanations may account for the unequal distribution . of cast material la the various plants. Conclusion Whila a tantatlva inference la that we are dealing hera with a naw industrial syndroms, ths matter is by no maans resolved by an inquiry aa limited aa the present. Much more research is required. First, there must be precise studies of the actual exposures of plant personnel to oil droplets, mists, vapors, smokes, gases and fumes, with analysis of Aa physical and chemical aspects. These observations must be focused on typical locations where prolonged human exposures are likely. Studies should also follow the selective rate of fell out of components along Aa paAs of air circulation in the plants. Particular attention should be paid to centers of ex posures to multiple types of ingredients or potential surges. Naxt, the clinical study of plant personnel should ba methodically and assiduously pursued. There must be a starting point DU 038221 DUP 093/2-16 - 79 - for each cate at which the process is spontaneously reversible. This physiological state is likely only to be identified by systematic pulmonary function studies. It is unlikely,that periodic x-rays will identify these processes early enough. Regular sputum determinations for oil droplets may furnish clues. Further inquiry into the extra curricular activities of plant personnel seems necessary. Many workmen have an overabundance of energy and engage in hobbies or moonlighting tasks which may be far more hazardous than anything they are likely to experience et their official jobs. More information should be gathered about the prevalence rates of pulmonary syndromes in the geographic regions where the textile plants are located. This study should include review of clinical as well as autopsy findings. * Last, but not least, cornea experimental study of the problem. If there is an injurious component in the working environments of the textile operatives, this point may be clarified by exposing animals to simulated or actual environments. Ideally, such an experiment should include animals subjected to prior or concurrent biological stresses. We would have had the answer to this problem if two things had basn poaslbl*. First, It attot Illogical that any naw Induatrlal operation should be initiated without prior exploration of the theoretical hazards likely to be encountered. The next best thing would be if experimental controls can be introduced as soon a the plants are in operation and whenever technical innovations are likely to introduce new varieties of human exposure. The second piece of missing information is e complete picture of the background of pulmonary pathology of Company employees. The du Pont Company has pioneered one of the best preventive medical departments in this country end incomparable clinical records ere available. Vary little is, however, on file about the pathology of the du Font employee or ex-employee. This information is scattered among scores of hospital and university departments. Whet we need is a central collecting office to which illustrative biopsy or pathology specimens can be routed. This should be an automatic process. Thus, each company physician could help build the museum or archives on ths pathology of du Pont employees by securing date on sach case which comes to his attention, whether or not a medico-legal or industrial problem is Involved. This materiel can then ha studied systematically. Whan such information is available, identification of the pathogenesis and etiology of syndromes such as the one described in this review will be greatly facilitated. DUP 0 9 3 7 2 4 7 DU 038222 aaaciialiiis^ifciatfBBfflLa Reference* - 80 - 1. Biftct) L J.A.M.A. 86. 49. 1926. 2. Burrows, H. T. snd JohnsCon, C. G. Arch. Ind. Mod. 36. 293. 1923. 3. Clausen, H. and Heatly, J. Arch. Otolamutol. 11. 567. 1930. 4. Corper, H. J. end Freed, H. J.A.M.A. 79. 1739. 1922. 5. Fischer-Wasels, B. Frankfure, Ztschr. f. Pathol. 44. 412, 1933. 6. Goodwin, T. C. Am. J. Dls. Child. 48. 309. 1934. 7. Graeff, L., Kaufman, W. and Kaplan, L. Arch. Pathol. 26. 914. 1938. 8. Graeff, 1. Archr Pathol. 28. 613. 1939. 9. Guieyess-Pellissier, J. Como. rand. soc. da biol. 83. 809. 1920. 10. Hass, L. ArchT Pathol. 26. 9S6. 1938. 11. Idada, K. Arch. Pathol. 23. 470. 1937. 12. Jackson, C. and Spencer, J. J.AjK.A. 73. 672. 1919. 13. Laughlin, A. F. Am.. J. Pathol. 1. 407. 1925. L4. Pinkerton, H. Am. J. Die. Child. 33. 259. 1927. IS. Mook, W. H. and Wander, W. G. 1. 304, 1920.Arch. Dermatol, and Syphilol. ' a -- *^6o DU 038223 81 16. PinkerCon, H. Arch. Pathol. 2* 380, 1928. 17. Proets, A. W. Ann. Otol. Rhino1, and Laryngol. 43. 430, 1934.18. Proetz, A. W. J. Laryngol. and Otol. 49. 447, 1934. 19. Shoahkea, Arch. led. Hra. and Occuo. Mad. 1, 20, 1950. 20. Vaidnan, F. D. and Jefferies, M. S. Arch, nwrnftol. and Syphilol. 7 , 209, 1923. 21. Uollsteia, M. and Maitzar, S. J. J. Exper. Mad. 28, 547, 1918. TABLES 1. Pulmonary Lesions in Textile Employees 2. Incidence of Bronchitis 3. Chronic Interstitial Pulmonary Lesions 4. Pulmonary Reactions to Oil DU 038224 DUP 09372-19 TABLE 1 PULMONARY LESIONS IN TEXTILE EMPLOYEES Lung Biopsies Case Plant Race Sex Main Biopsy Findings 1 A White Female Interstitial infiltration and eosin ophilia. 2 A Negro Male Interstitial infiltration and exudation. 3 A White Male Interstitial infiltration and emphysema. 4 A White Male Pneumatocele and oleogranulomatosis. 5 B White Male Interstitial infiltration and oleo granulomatosis . 6 B White Male Pneumatocele and oleogranuiomatosls. 7 c Negro Male Bronchial adenoma and oleogranu lomatosis. 8 c White Male Granulomatosis and interstitial infiltration. -- 9 c White Male Vanishing lung and interstitial infiltration. 10 c White Male Alveolar proteinosis. 11 c White Male Spontaneous pneumo- and hemothorax. Q 12 c White Male Spontaneous pneumothorax, pleural effusion and IntsrstielsL infil tration. DUP 0937750 DU 038225 TABLE 2 INCIDENCE OP BRONCHITIS - Taxtila Plants - Plane A B C D B r Company Rata/lOOO/1957 Wa&croll Employ* Mala Fanala 14.5 5.3 5.4 6.1 4.8 6.1 7.2 17.2 17.4 18.0 18.2 14.0 15.1 15.8 DUP 0 9 3 7 2 5 1 DU 038226 TABLE 3 CHRONIC INTERSTITIAL PULMONARY LESIONS Etiological Classification Group Order BIOLOGICAL Erogenous Endogenous ENVIRON MENTAL Chemical Physical UNKNOWN Unknown Genus Bacterial Viral Rickettsial Fungal Mycobacterial Parasitic Reticulo-endotheliosds Eosinophilic granulomatosis Edemic Metastatic Allergic Pneumonitis and granu lomatosis Emphysema and Bronchitis Pneumoconioses Jatrogenie Radiatlonal Sonic Traumatic Blase Decompression Cold Heat Dessication Drowning *_ Hodgkins granuloma Scleroderma pulaonalls Psaomematosis Sarcoidosis Hanman-Rich syndrom# Alveolar Proteinosis' Cystic pancreatitis Hyaline membrane syndrome c 19 w n> >3 DU 038227 TABLE 4 MONAKY REACTIONS TO OIL (References 1 to 21) >0 O rt flOHpfl ?S|i| 9f* oat eo'oet i*t 0o.4*e3 h Msr Hp6dSHHtb' So _r y* 3?" r o2nft_*- 9nH<>0h_r-ri_0**n_->*_0_2*96oOq8HH9-.*8^^f2*.1 o* pppppxjoxp pppp ppox Species o So e e oi oO o o So Lethality l lift!** Hfi * Pneumonitis `T"' * $!** If" tt t i + 4- i i Focal Necrosis Oleogranulomatoale CeLIuler Catarrh Lipophages |*r i .,,. i jt* ^ 11 i iii +111 i t | 1 | is t i Ii ! i i + i i + tit i "i i * Glsne Cell Syncytia Epithelixation Acid PesC Membrane Fibrosis Pleurel Involvement Bronchiel Lesions Lymph Node Involvement Human Diseese -'IS "'4fi 8 + FootnoCes Dup 0937252.001 DU 038228 MMi&y ^-IHihih iiiii it* Hit* 5S-S 53 Oh* 0*^ ozjbo ilia ?? * S.m-2 H> $ a 3 rt *>& fSfn1o tf*t it 8 tf t* * Samoa 3a slasrrt shi*e .2*8*2 -o s 5 rt a & a rr a a a *? amhaa a g oo5 >*J|or* 3*' O' 8^*.53"- lt-- _ < ma. < a u m#We m#n Hm (ft sr| / 3a* 2 a9oa#* P ilia B?|S meB aa n us*ssdS ft * ft H- VP a VI h.3? ft 4*3 a S' a amg 2 5 euo a ow mWo OH, srg- aa i (ft ? 3 H I zns ri g3 H a o3* o3* 1-- H H> oH>* oHh** ofht* ea oH* O 7* P Species 001 91 0 001 Lethality Z ''! Pneumonitis iiii Focal Necrosis it** Olaogranuloaatosls Cellules Catarrh tt Lipophages * Giant Cell Syncytia ii" SpithalisaClea till Add Fast Moobrana $ | Fibrosis i*ii Pleural Involvement + Bronchial Lesions l* 1 Lymph Node Involvement T! Hunan Disease 0 Footnotes K 1 a* rt o c o) <3 W *0 tfl W DU 038229