Document gb23jL8MeDwrkE5qZ4OxkR7jN

petri*to G[ ) Lavoro Unano, volume 15, pages 276-281, 1963 AS3EST0SIS AND LUNG NEOPLASMS FUP.THER CONTRIBUTION TO A CLINICAL CASE Farina, S. and G. Ka22anti Institute of Special Medical Pathology and Clinical Methodology, University of Bologna (Director: Prof. D. Caapanacci) .Department of Occupational Medicine (Director: Prof. G. D. D'Ancuono) r-/ nSuLj i -J j 1S35 K VI Sji;: ;01 wD. u* Tor some time now, researchers have tried to evaluate the effect of a saries of agents found in the air of the working environment on the ger.irar of heteroplastic growths in the respriatory tract, with particular emphasis on the lung. As a natter of fact, recent statistics indicate a significant increase of neoplasias of this nature. Lately, improved information regarding the toxic inhalants present in the working environment has brought into focus the possible effect of a grs number of agents that could contribute to, or actually induce, such condit It is quite obvious that the attention of researchers has been direct1 primarily to agents whose physical and chemical properties are responsible for their marked irritative action at the level of the various mucosae. Accordingly, micro traumatic phenomena occurring at this level have been^st in regard to their involvement in the development of metaplastic condition affecting various organs and tissues. One such agent, which is well capable of acting via a chronic irritate effect at the level of the respiratory tract mucosa by producing irreversi sclerogenous lesions, is asbestos. Examination of the pertinent literature fails to yield much informat: on the relationship between asbestoses and lung neoplasias, although ther* is such discussion regarding their occurrence which, according to some is : but pure coincidence, while others claim lung fibroses originating from c occupational condition might play a role. The first observation of such an association has been reported by Ly and Smith, in 1935. Subsequently, many other investigators have reported simultaneous presence of lung neoplasia and asbescosis-inducad lung fibres in both live and autopsy material (Egbert; Geiger; Wedler; Desaeules, ous Giroux and Sirois; lynch and Connaa; Ronbola; Chauvet). Anatomicopathological statistics compiled by Gloyne, Wedler, and Doll revealed that the incidence of this particular association varied from '10- a finding which would seem to-definitely confirm the effect of asbestos f: inhalation on the induction of lung neoplasia. Furthermore, experimental studies performed by Nordmann and Sorge ha" shown the presence of lung carcinomas in 20% of the nice exposed to the i: lation of asbestos dust. This firding also supports the claims regarding carcinogenicity of asbestos. . On the contrary, Vigliani (1940) failed to find lung cancer in any o. 76 patients with asbestosis that ha studied. Furthermore, systematic inve. gations carried out by Braun and Truan (195S) in a large number of asbesc workers, in Canada, showed that the incidence of lung r.eoolasia in this p ticular group was nc higher than that recorded for individuals not expose asbestos dusts. A consistent finding in studies demonstrating an association between neoplasia and the occupational condition mentioned has beer, a history of exposure to risk by the affected individuals. The presence of proliferative processes primarily in the lower lung which is also the site of the most advanced degree of lung fibrosis, is i sharp contrast to . the normal site of neoplasia.which is encountered nor frequently in Che central and upper lung lobes. According to the statist mentioned above, it emerges chat the incidence of the disease among femal -2- is high, as opposed to the well-established finding that lung neoplasia affe almost exclusively the male sex. All the findings could be indicative of more chan a simple causal re lationship between asbestosis and lung neoplasia. The patient described in the present report represents a relatively in teresting contribution to other similar cases described earlier, although n< representing any decisive etiopathogenecic feature. CLINICAL REPORT . The patient, a 54 year old worker,was employed as an insulator since 1 He was in good health until the month of September 1960 when he starte having persistent cough and exertional dyspnea. Radiological examination performed at that time revealed darkening of the lower lung field. Wide st eaergingfron the enlarged hili and advancing cowards the base of the lungs which, in turn, showed sharp reticulation. Based on these findings, a .radiological diagnosis of asbestosis was established and the case- was forwarded to che insurance authorities for disability. ' By June 1962, che patient presented gradual exacerbation of the cys?n= symptoms, together with a cough with little expectoration; furthermore, the patient complained of an oppressive pain in the right hemichorax. Objective examination demonstrated a definite basal hypophonesis, rou: and diffuse breathing over the entire pulmonary field where there was also evidence of a noise known as "fresh snow pounding" (D'Ancuono ec al.). Th- was no evidence of any other significant objective alterations. Electrocardiographic recording was negative. -T-. Urine examination vas also negative. Examination, of the sputum demon strated the presence of bacterial flora consisting of cocci, gran-positive and. gran-negative diplococchijthe search for Koch's bacillus was also negati Erythrocyte sedimentation rate was high (I.K. = 37). Respiratory func tion tests revealed the presence of a constrictive type of ventilatory insu ficieacy of average severity. s' * I " :>>. \ Tx~. i . Eesatological examination: red blood ceils: 4,800,000/mm ; white blooc ceils: 8,000/nm3; Hb: 722; hematocrit: 0.95; X: 67%; E: 2%; M: 6%; L: 25%. R. W. and Meinicke: negative. Standard chest x-ray, in addition tc the previous findings recorded a the level of the lower pulmonary fields, also demonstrated the presence c parenchymal darkening at the level of the right cardiodiaphragmatic angle, roundish, with well-defined edges and homogenous density (Tig. 1). Repeat radiographic examination performed 20 days later confirmed the initial pic cure, without any appreciable changes. On account of the inability to define the nature of this opacity, and -4- < due to the negative results yielded by the laboratory tests (including typo logical examinations and histological study of the expectoration), except fo: the increased sedimentation rate, the patient was placed on antiblascic crea oent (chloramines) in order to determine the eventual changes in the lung, findings, about 1 month later. ' Radiographic examination performed at this time (Tig. 2) confirmed the presence of a mass located to the right of the heart, well evident scratigraphically in the anterior planes (Tig. 3), whose size was actually greater than that recorded during the previous radiographies. -5- Soon after the last examination, the patient presented blood in ch expectorate, while pain and dyspnea increased; the general condition of the patient deteriorated gradually. He had persistent fever, and died in cachexia early in December 1962. As a result of the rapid decline of his general condition, and' especis based on the radiographic and. stratigraphic picture which, as described abc demonstrated the presence of a definitely progressing parenchymal opacity, diagnosis of asbestosis associated with lung neoplasia was established. The features described above lead to a series of interesting observat: Thus, first of all, it appears that the association mentioned is rein: rare. As a matter of fact, ve encountered only a single case of neoplasia a total of more then 30 individuals exposed to asbestos. - The group observed by us is rather small and does not allow any defir.: conclusions, but it confirms the discrepancy of the data reported on this : in the German and English literature (which support the hypothesis of a re. tively high incidence of neoplasia), on the one hand, and the findings of Italian investigators (Vigliani, Rcabola) who found chat the races of neo plasia are much less significant, on the ocher. It appears chat the discrepancies and the subsequent differences in c evaluation of the oncogenic activity of asbestos fibers could be attribuc to intrinsic geographical differences in the composition of asbestos icsel a fact reflected in the statistics obtained in various countries, rather tb to errors performed in the diagnositc investigation of the workers at risk Actually, as is well-known, the variety of asbestos used in Italy is most exclusively white asbestos, a material with a low iron concent as cor -6- co che blue asbestos used by Che workers scudded in che Cerman and Znglis: statistics. Nevertheless, the differences in Che chemical composition of asbesco could be relevant if the role played by the predisposition of the individ at risk, and the severity of the risk itself, are well-known. The role of asbestos per- se, a material whose activity is explained great number of fine needles present in the asbestos fiber, should be an factor only for the induction of trauma'at che level of bronchial mucosa sequent to long-term exposure. In conclusion, it seems that asbestos alone has only a predisposing similar to that exerted by other agents having similar mechanisms, at di levels. SUMMARY The case history of a patient where asbestssis was associated with ; plasia of the lung is described briefly. The discrepancies recorded in literature on this particular subject are pointed out, and che statist! experimental, and possible oncogenic properties of asbestos are disc Although not regarded as definitely carcinogenic, che chemical composite of the agent is considered to be a significant factor. 3I3LI0CRAPHT 1. Braun D. C.; Truan, T. D.: An epidemiological study of lung cancer i asbestos miners. Arch. Induscr. Health 17; 634, 1958. 2. Cartier, ?.: cited by Roabola. 3. Chauvet, M.: Asbestosis and bronchial cancer. Pressa Med. 66: 90S, 4. D'Antuono, G.; Maczsnci, C.; Farina, S.: Clincal and radiographic o': vations on lung asbestosis. Giom. Pneuaol. 5: 1, 1961. 5. Doll, R.: Mortality from lung cancer in asbestos workers. Brit. J. Indust. Med. 12: 81, 1955. 6. Gernes-Rieux, C.; Marchand, M.; Mounier-Kuhn, ?> Policard, A.; Roche, Occupational respiratory diseases. Masson, Paris, 1961. ` 7. Isselbachar, K. J.; Klaus, H.; Hardy, E. L.: Asbestosis and bronch.cger carcinoma. Report of one autopsied case and review of the available literature. Aaer. J. Med. 15: 721, 1953. 8. Linquette, M.; Voisin, C.: Silicosis and other pneumoconioses. PIsms Paris, 1960. 9. Lynch, K.; Connan, M.: Asbestosis analysis of 40 necropsied cases. I ' Chest 14: S74, 1960. 10. Lynch, K.; Smith, W. A.: Pulmonary asbestosis. Carcinoma of lung in asbesto-silicosis. Amer. J. Cancer 24: 56, 1935. 11. Nordmann, M.; Sorga, A.: cited by Rombola. 12. Rcmbola, G.: Asbestosis and lung cancer an an asbestos textile plant. Med. Lavoro 46: 242, 1955. Ot 13. *adler, E. w.: Asbestosis and lung cancer. Dcsch. Med. Wschr. 69: 1943. -8-