Document RJJQD0ejyVG5E1dQ3V86xqydX

----- .fc'j.TT&aumjtt euKWlNli DOES NOT KNOW WHEN THIS DOCUMENT WAS RECEIVED * -R BY WHOM; NOR WHEN SUCH DOCUMENT BECAME A PART OF PITTSBURGH CORNING*S FILES: BUT THE BEST ESTIMATE IS THAT SUCH DOCUMENT WAS -O---B---T--A---I-N---E---D------I-N-------T--H---E--- -r1--9f6,8-----1---9- -6--9------T---I-M----E-----F- --RAME. ASBESTOSIS AND CARCINOMA OF THE LUNG Juan F. Cordova, m.d., Henry Tesluk, m.d., and Kenneth P. Knudtson, m.d. he increasing incidence of pulmonary the cases we have seen. In the review of our Tcarcinoma has stimulated considerable own surgical and autopsy material we were interest in the search for possible causativaeble to find 6 cases of bronchogenic carcinoma agents, especially those of the inhalant type. associated with pulmonary asbestosis. Five ad There now exists considerable data to sup ditional cases were obtained from the files of port the contention that pulmonary asbes- the Armed Forces Institute of Pathology, tosis has a definite role in the development of Washington, D.C. neoplastic change in the respiratory .system. / In general, the question as to whether specific Case Reports ' pneumoconiosis predisposes, to carcinoma of the lung is of considerable medicolegal impor tance, and in spite of extensive experimental ami clinical research, none of the agents studied have been clearly implicated except uranium in the case of the Schneeberg miners in Germany. Bridge and Henry3 formulated the following specific conditions as necessary Case 1. P.K.E. was a 58-year-old hod carrier who had worked with insulating material for 20 years. He was a heavy smoker. A routine chest roentgenogram at Virginia Mason Hos- Iiital, Seattle, Wash., showed an unsuspected esion in the middle lobe of the right lung. Right pneumonectomy was carried out. A white, firm, slightly gelatinous, well-demar for the acceptance of industrially acquired cated, 2x3-cm. tumor was found in the middle canrcn (1) the rate of incidence in the occupa tion under review should exceed that in the general population to a significant extent, and (2) in the occupation concerned, there would be sufficient association of the worker with a substance proved experimentally to have carcinogenic properties. Although there is a statistically proved high incidence of pul monary carcinoma in asbestosis, it is readily apparent that these postulates have not as yet been fulfilled. Indeed, it should be pointed out that a study by Jacob and Bohlig1* indi cated that the incidence of carcinoma in as lobe. Another small firm area was at the apex. The lesion was an adenocarcinoma with growth along alveolar walls. The stroma was densely fibrous and contained numerous as bestos bodies (Fig. 1). Of particular interest was the finding of a separate focus of tumor in the apical scar, which also contained as bestos bodies (Fig. 2). Case 2. J.W. was a 46-year-old ironworker admitted to Viiginia Mason Hospital with mild congestive heart failure. He had been a heavy smoker for many years. A chest roent genogram showed a right upper lobe lesion. An exploratory operation revealed a well- bestos workers in Dresden was not increased. defined tumor in tne posterior segment of the In view of the fact that the role of asbestosis right upper lobe, extending through the inter in the pathogenesis of carcinoma of the lung remains unproved, we felt it would be worth while to review the existing evidence and present clinical and pathological findings on lobar fissure into the right lower lobe. Pneumo nectomy was performed. A separate malignant tumor was found in the right apex. Both tu- mor nodules were surrounded by firm areas of fibrosis. Microscopically, *the tumors were ter minal bronchiolar carcinoma. There was From the departments of Pathology. Virginia Mason Hospital. HOI Terry Ave., Seattle I. Wash., the Vet erans Administration Hospital, and the Univenity of Washington Medical School, Seattle, Wash. We are indebted to the Armed Forces Institute of Pathology. Washington, D.C, for their permission to use S cases from (heir files and also to Dr. Alexander Drcsiow for 2 cases obtained from Firland Sanatorium. Seattle. Wash. The photomicrographs were made by Mr. Paul New man. Chief of Medical Illustration, Veterans Adminis tration Hospital, Seattle. Wash. Received for publication Jan. 23,1962. (marked pulmonary fibrosis, and typical as bestos bodies were found in areas of fibrosis. Case S. G.M.G. was a 55-year-old Negro shipyard worker admitted to Firland Sana torium with hemoptysis and wheezing. A roentgenogram showed a lesion in the right *ip}>er lobe. Because of reduced pulmonary func tion, a right lobectomy only was done. He died the following day. Hie tumor measured 4x7 cm. and projected into the apical seg mental bronchus. Microscopically, it was a 1181 PLAINTIFF'S I EXHIBIT ^PLAINTIFFS 1 000^055 EXHIBIT t 1182 Cancer November-December 1962 Vo!. 15 squamous cell carcinoma with marked fibro sis of the surrounding tissues. Numerous as bestos bodies were present in alveolar spaces and in peribronchial fibrous tissue. .Case 4. H.M.G. was a 71-yearold retired bricklayer admitted to Firland Sanatorium with suspected tuberculosis. Symptoms in cluded hemoptysis, cough, and wheezing. A large infiltrate was seen in the left upjier lobe and a mottled appearance in the lower lobe by roentgenogram. Cultures were positive for tubercle bacilli. His condition deteriorated over a 3-month period, and he died. A poly poid, soft, white tumor in the left main bron chus was continuous with a mass in the apicalposterior segment of the left upper lobe. The tumor had infiltrated into the chest wall pos teriorly. There was fibrocaseous tuberculosis of the right lung. Microscopically, the tumor was a poorly differentiated squamous cell carci noma. There was moderately severe pulmonary fibrosis with numerous asbestos bodies present. There were numerous foci of caseation ne crosis associated with the tuberculous gran uloma formation. Case 5. G.J.B. was a 64-year-old white male ?ipe insulator and coverer admitted to the eattle Veterans Administration Hospital be cause of exertional dyspnea. He haa been aheavy smoker for 10 years previously. A chest roentgenogram showed a mass in the right lung and atelectasis of the middle and lower lobes. A right lower lobectomy was carried out, and a firm infiltrating malignant tumor was found. Microscopically, this tumor was a mod erately differentiated adenocarcinoma that had infiltrated the mucosa of the main bronchus entering this lobe. There was diffuse fibrosis of lung parenchyma, and numerous asbestos bodies were seen both in the tumor and in the areas of.fibrosis. Case 6. H.R.H. was a 69-year-old white man admitted to the Seattle Veterans Administra tion Hospital with symptoms of increasing shortness of breath and chronic pulmonary dis ease. He had worked in an asbestos plant for 48 years. He had been told he had asbestosis 15 years prior to his admission to the hospital. He had smoked cigarettes for 20 years. A biopsy of a skin.nodule revealed metastatic anaplastic Fk. 1. Case 1. Microscopic section showing asbestos fibers intimately associated with cords of epidermoid car cinoma of the lung. (XZ50.) QQQ8Q5E N. A AsoESTosts & Carcinoma of Lung Cordova et al. 1183 carcinoma. Autopsy revealed an anaplastic car* cinoma, arising in the right upper lobe bron chus anrl infiltrating the major portion of that lobe. Metastases were evident in the hilar lymph nodes, liver, and adrenal glands. As bestos bodies were seen within the tumor and in the adjacent fibrous lung tissue. Case 7. E.J.H. was a 65-yearold white man who was admitted to the hospital with a primary complaint of swelling of the right side of the neck of 1 week's duration. He had worked as an asbestos insulator in the Bremer ton Naval Shipyard, Bremerton, Wash., during die past year and prior to that had worked in an asoestos manufacturing plant for 55 years. He had smoked 1 package of cigarettes per day for AO years. He had progressive dyspnea with rapidly decreasing respiratory function and died 3 weeks after nis admission to the hospital. Autopsy revealed severe pul monary fibrosis with a squamous carcinoma infiltrating the right upper lobe. Asbestos bodies were prominent witliin the tumor-bear ing area. Case 8. P.K. was a 62-year-old white man who presented with symptoms of general dis ability and weight loss. A roentgenogram taken on admission to the hospital revealed an area of increased density in the right upper lobe and emphysema. A nilar mass was evi dent on the right. At thoracotomy, a tumor involving the right upper lobe was found. However, the tumor had, by direct extension, involved the chest wall and was considered inoperable. The .patient died 3 days postoperatively in respiratory failure. The tumor was for the most part an undifferentiated car cinoma with areas of mucus-producing adeno carcinoma. Asbestos bodies were identified in both the tumor and the areas of pulmonary fibrosis. Case 9. G.S. was a 68-year-old white man who had worked for many years with asbestos and Fibergtas as an insulation worker. His chief complaints were productive cough, ex ertional dyspnea, and weight loss. A roent genogram of the chest revealed interstitial pneumonitis in the right upper lobe. The Satient showed progressive pulmonary difculty with cyanosis and died 10 days after admission to the hospital. At autopsy, the left lung revealed multiple firm nodules up to 13 cm. in diameter, and the right lung contained a firm but honeycombed area in the right apex. Sections showed a brondiiolar carcinoma with multiple foci throughout both lungs and the hilar lymph nodes. Asbestos bodies were ^0008057 1181 Cancer Novembcr-Dccember 1962 Vol. 15 identified in the tumor and in areas of pul monary fibrosis. Case 10. W.CD. was a 60-year-old white man who was admitted to the Seattle Veterans Administration Hospital because of extreme dyspnea, anorexia, and chest pain that had been progressive during the past year. He had worked as an asbestos handler for 40 years. He had noticed hemoptysis 3 months prior to admission. A chest roentgenogram revealed densities in both lower lobes compatible with asbestosis. A needle biopsy of the liver revealed metastatic anaplastic carcinoma. Roentgeno grams revealed osteolytic lesions of the verte brae and skull and Paget's disease of the left innominate bone. He was given X-ray ther apy to the lungs. The patient died on the third hospital day after progressive dyspnea. Autopsy revealed a malignant tumor appar ently arising in the right lower lobe bronchus and infiltrating the entire right lower lobe. A 3-5-cm. tumor nodule was seen beneath the pleura of the left lower lobe. The remain ing lung parenchyma was replaced by dense fibrous tissue. On microscopic section the tu mor revealed undifferentiated carcinoma with foci of necrosis. Asbestos bodies were iden tified in the tumor-bearing area. Case 11. G.B. was a 64-year-old white man who was admitted to the hospital with com- Ehunts of dyspnea on exertion for 3J4 years. [e had been exposed to asbestos and mag nesium for the previous 30 years. A roent genogram revealed a circumscribed density in the posterior right lower lobe, with difluse emphysema. A nght lower lobectomy showed a firm but gelatinous tumor lying beneath the pleura. Microscopic examination revealed a mucous adenocarcinoma characteristic of bronchiolar carcinoma. Large club-shaped as bestos bodies were noted throughout the tu mor and in the adjacent fibrotic pulmonary tissue. Results Eleven cases in which asbestosis and car cinoma of the lung coexisted have been re viewed. Five cases were obtained from the Armed Forces Institute of Pathology, Wash ington, D.C.; among 20 cases of asbestosis on file at the Institute, an incidence of 25%. Twq cajes were included from the files of the Seattle Veterans Administration Hospital, Seattle, Wash.; among 6 cases of asbestosis, an incidence of 33.3%. Two cases were obtained from Firland Sanatorium, Seattle, Wash.; from a total of 6 proved cases of asbestosis, an incidence of 33%. The remaining 2 cases were from the Virginia Mason Hospital, Seattle, Wash. Table 1 summarizes the major findings of interest in this series of patients. The mean age of the patients at the time the diagnosis of carcinoma of the lung was established was 62 years. There were 10 white patients and 1 Negro patient, all of whom were men. The Tails 1 CASE HISTORIES OF 11 MALE PATIENTS WITH ASBESTOSIS AND LUNG CANCER Cue PL no. ituL Pl Durst. C*. PL yr. race yr- Smoking history Occupation Site ca. Typeca. 1 P.K.E. 2 J.IV. 58 46 5 G.M.G. 55 4 5 H.M.G. G.J.B. 71 64 6 H.R.H. 69 7 E.J.H. 8 P.K. 9 as. 65 62 68 10 W.CD. 60 11 G.B. 64 W 20 2 pk./day 20 yr. Hod carrier Rl mid. lobe Adenoca. - W ? 2 pk./day 7 yr. Ironworker Rt upp. lobe Term. bronchiolar N? 7 Shipyard worker Rl upp. lobe Squam. celt W 40 1 pk./day ?yr. Ret. bricklayer Ll upp. lobe Squam. cell W 50 2 (pt/day 10 Pipe insulator Rl low. lobe Adenoca. w\s yr.; stopped 8 yr. prior to death 48 ipk./day 20yr. 55 yr. in asbestos Rl upp. lobe Small cell mfg. 8c 16 yr. as w asbestos insulator 40 1 pk./day 40 yr. 55 yr. in asbestos Rl upp. lobe Well-did. w None None mfg. Carpenter squam. cell Rl upp. lobe Undid. w known 7 50 yr. Insulation worker; Rl upp. lobe Term. worked with bronchiolar Fibcrglas many yf w 40 11 pk./day 46 yr. Asbestos handler RL low. lobe Undid. w 50 ? OccupaL expos, to asbestos ft Rl low. lobe Term. bronchiolar magnesium 7 yWXW058 No. < Asukstoms X; Carcinoma of Lung * Cordova et al. 1185 nicMti. duration of cxjtmurc to asbestos in 7 patients was 35 years. Carcinoma of the lung occurred most frequently in the right upper Jobe (6 cases). Five patients had a history of cigarette smoking for 20 yean or longer. There was no predominant cell type of card* noma of the lung in our series. Death was most commonly attributed to bronchopneu monia, lung abscess, and cor pulmonale. Discussion Asbestos is a magnesium silicate that is one of a group of silicate minerals of crystalline fibrillar structure.13 Industrially, the material is found in asbestos mining and in many in* dustrics engaged in the processing and manu facturing of asbestos products. These include insulating materials (fire resistant cloths, ropes, millboard, wallboard, mortar, and other prod ucts). The principal hazard in these industries consists of inhalation of the asbestos dust. Some regard pulmonary asbestosis as a form of pneumoconiosis not necessarily accom panied by symptoms, whereas others feel the term should be reserved for cases in which clinical manifestations are present.39 The de velopment of pulmonary lesions that are char acterized by fibrosis and the formation of the so-called asbestos body depends upon the dura tion and degree of exposure to asbestos dust.9 Lynch19 provided a careful description of die pathogenesis of the disease and classified it into 4 stages. The lesions may appear after 3 to 15 years' exposure but may not produce symptoms for many years.13 There is con siderable individual variation in susceptibil ity. some individuals developing the disease rapidly while others may be exposed for years widiout evidence of pulmonary involvement. Symptoms of the disease consist of dyspnea, cough with expectoration, pallor, cyanosis, palpitation, weight loss, and chest pain.3*-33 Characteristic changes of pneumoconiosis' may be seen on roentgenographic examination. The pathognomonic asbestos bodies are found in the interstitial connective tissue of the lung and in peribronchial and hilar lymph nodes.*-13 They consist of a central translu cent fiber, 10 to 100 ft in length and 1 to 12 p in diameter, enclosed in a golden-brown en crusted sheath composed of an iron protein compound. The ends are usually bulbous. The fibers may be surrounded by macrophages or giant cells. The fibrosis that accompanies the deposition of asbestos fibers tends to pro gress even after exposure to inhalation has been discontinued. The exact nature of the association be tween asliestosis and pulmonary carcinoma has been difficult to unravel. Since the first report by Lynch and Smith,31 many observations have been made concerning this relation ship,4- **,#-14 with the use of several different approaches to the problem. it has been shown in a series of studies that there is a statistically proved higher incidence of carcinoma of the lung in patients with as bestosis than in the general population. One such .study, the results of which are given in the Annual Report of the Chief Inspector of Factories for the Year 1947 in Great Britain, established that carcinoma of the lung occurs in 13% of cases of asbestosis in contrast to the 2 to 6% incidence in the general popula tion.9 Doll,4 in similar studies, arrived at the con clusion that the risk of developing carcinoma of the lung was higher in individuals exposed for a long period of time to asbestos inhala tion. Nordmann,3* who published data on 6 cases, went even further to state that carci noma of the lung is an occupational disease, among people engaged in asbestos work. This opinion was also expressed by Homig.13 The-second point of interest concerns the multifocal development of cancer in these cases pointed out by Nordmann,33 Gloyne,9 anti Hueper.13 This feature has often char acterized the malignant turnon found in as bestosis and has also been noted in 2 of the cases presented in this report. Finally, the age-time exposure relationship has supported die idea of a causal relation ship. The longer the exposure to asbestos, the greater the risk of developing a malignant tumor; and the younger the individual when fint exposed to asbestos dust, the earlier is the development of the pulmonary carcinoma. However, this relationship is not invariably' found. As shown in the cases presented, 4 of the individuals had no known history of direct exposure to asbestos dust, and the diagnosis of asbestosis was made based entirely on the histological findings of pulmonary fibrosis as sociated with the presence of asbestos bodies. There are no documented cases in the litera ture to our knowledge of cases of asbestosis associated with carcinoma of the lung in which the patient had not been exposed at one time or another directly to asbestos dust, either in /&Q0fiO59 1186 Cancer November-December 1962 Vol. 15 the mines, in the crude processing of the the cases reported occurred in lower lobes fibers, or in other phases of the manufactur where the pneumoconiosis is most severe.17 ing.- l0*11 However, It Is well known that Our cases showed a majority of the malignant asbestos is now being utilized to a greater turnon occurring in the upper lobes (Table degree in the manufacture of products that 1). aparently bear no direct relationship to Other agents that are believed-to be related asbestos, such as in insulating material, rope, to cancer of the lung are uranium, chromium, wallboard, mortar with cement, and plaster and possibly nickd. In the case of asbestos, of paris. If we accept the cases presented as although experimental proof is lacking, there asbatosis, then these individuals, even though appean to be suffident dinicai pathological known exposure is lacking in the history, have evidence to make it highly probable that this been exposed to asbestos dust in some form is a cardnogenic agent.*0 It must be admitted and for prolonged periods of time to induce that the cardnogenic stimulus is a weak one, changes compatible with asbestosis and the and the mode of action is still obscure. Par- subsequent development of pulmonary carci tide size is apparently of importance in the noma. The fact that no known exposure ex production of asbestosis. Those fibers less than isted in 4 cases indicates that the disease can 20 p in length have no apparent deleterious occur without prolonged exposure to known effect.1* The fibrotic reaction in the lung is sources. The average time lapse from the ini produced by both physical and chemical tial exposure to asbestos dust to the develop changes secondary to the asbestos fiber.**17 3 ment of asbestosis is 9 years according to The fibrosis is a progressive phenomenon, Egbert and Geiger,* although this figure varies with progression after exposure has ceased.1* according to different authors, and much Multifocal areas of metaplasia of the bron- shorter exposure times with development of chiolar epithelium have been described in the asbestosis have been recorded. In individuals areas of fibrosis and the suggestion made that who have developed carcinoma of the lung, these represent early stages in carcinogenesis.*0 the asbestos exposure time averages 15 years, The silicate portion of the fiber is apparently with a range of 3 to 27 yean,1**14 and with not responsible for this activity. Cardnoma latent periods of from 15 to 22 yean between of the lung occun in only 1.3% of cases of the initial exposure to the asbestos dust and silicosis in contrast to 13% in cases of asbes j the development of a malignant tumor.* tosis.4* 14*11 It has even been suggested that There have been cases, however, in which silicosis may be a deterrent or even offer pro an unusually short exposure time was re tection against cardnoma of the lung. corded. In a case dted by Owen,*4 pulmonary carcinoma developed in an individual exposed to asbestos dust for only 12 months, approxi Summary mately 20 yean after the exposure. Eleven cases of Asbestosis associated with The majority of the lung carcinomas as cardnoma of the lung are presented. A known sociated with asbestosis recorded have been of exposure to asbestos dust was obtained in 7 the squamous cell type. In our series, bron- of these cases. In at least 2 cases, evidence chiolar carcinoma and undifferentiated card- is described for multifocal origin of the tu- noma were present in equal numbers. ' mar. Typical asbestos bodies were identified Localization of the tumor in these cases is in the tumor-bearing area of the lung in each of some interest Cardnoma of the lung usu case. The possible relationship of asbestos ally occun more frequently in the upper lobes, bodies as a carcinogen in the production of whereas in asbestosis, approximately 80% of cancer of the lung is discussed. REFERENCES 1. Andemon. J,, and Campacna, F. A.: Asbestosis and carcinoma of lung; case report and review of literature. Arch. Environ. H. 1:27-32. I960. 2. Bstocc. J. G. and Hour, S. A^ Industrial cancm. In Report of the International Conference on Cancer. London, 17tb-20th July, 1928. Baltimore. Md. William Wood It Company. 1928; pp. 258*268. 3. CvuroN, R. J. R- Squamous cell cardnoma oc curring in asbeuosu of lung. Bril. /. Cancer 2: 249-253, 1948. 4. Doll. R.: Mortality from lung cancer In asbestos workers. Bril. /. Induxt. tied. 12: 81-86, 1955. 5. Ecaott. D. 3, and Gucm, A. J.: Pulmonary as bestosis and cardnoma: report of case with necropsy findings. Am. Rev. Tubere. 34: 143-150.1936. & Cabsncb, L. U, and Cummincs, D. E^ Studies oo experimental pneumonokoniosis; inhalation of as bestos dust; its effect upon primary tuberculous in fection. J. Indust. Hyg. 13: 65-81,1931. 7. Gumra, 3. Ri Morbid anatomy and. histology j j I I i | i j ! j I I j } i j j ! j ! i j ./ OOO8OI1O No. G Asbestosis & Caronoma of Lung Cordova et al. 1187 of asbestosis. Tubercle H: 445*451. 1933. 11. Gloyne, S. R.: Case of oat cell carcinoma of lung occurring in asbestosis. Tubercle 18: 100*101, 193G. 9. GREAT narTAW, MINISTRY OF LaHOUK AND Ka. tioxal Service: Annual Report of the Chief Inspector of Factories for the Year 1947. London, England. His Majesty's Stationery Office. 1949. 10. Holler, H. B* and Akckist, A. A.: Bronchogenic carcinoma in association with pulmonary asbestosis; report of 2 cases. Am. J. Path. 18: 123*135, 1942. * II. IIOMauaeca, Coincidence of primary card* noma of lungs and pulmonary asbestosis; analysis of literature and report of 3 cases. Am. J. Path. 19: 797* 807. 1913. 12. Hokmg, F.: Klinische Betrachtungen tur Frage des Bcrufslircltscs der Asbestarbeiter. Ztschr. Krebs* forsch. 47: 281-287, 1938. 13. Hueter, W. C: Occupational Tumors and Allied Diseases. Springfield, 111. Charles C Thomas. 1942; pp. 403*405. 14. Hums, W. C~- Environmental lung cancer. Mutt. Med. 20: 49*62,1951. 15. Isselsaciieb. K. I.; Klaus, H.. and Hardy, H. Lj Asbestosis and bronchogenic cardnoma; report of 1 autopsied case and review of available literature. Am. J.Med. 15: 721*732.1953. 16. Jacob, G,, and Bohlic, He Ober HluGgkdt und Bcsonderhdten des Lungenkrebses bei Asbestose. Arch. Gewerbepath. u. Gewerbehyg. 14: 10-28, 1955. 17. LiNZKACH. A. J.. and Weoler, H. 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H. 11: 206*211, 1955. 26. Stoll, R.; Bass, IL, pud Ancrbt, A. [A.]: As* bestotis associated with bronchogenic cardnoma. A. M. A. Arch. Int. Med. 88: 831*834.1951. 27. Won, E. R-. and Hall, W. E. B.: Asbestosis; re port of case. Dit. Chut SO: 229*230,1956. #0008061