Document 3NoeMoOx5DOyMvOY2d4axgZYx

FILE NAME: Asbestos Cement Pipe and Sheet (ACPS) DATE: 1950 DOC#: ACPS006 DOCUMENT DESCRIPTION: Published Journal Article Ugeskrift for Lger [Doctors' Weekly], Copenhagen Vol 112, No 37, 1950, pp 1284-1289 THREE CASES OF ASBESTOSIS by Jurgen F ros t* Summary Three cases of asbestosis are discussed. In two the X-ray films were typical; in the third there were also nodular modifications. As a possible explanation of this it is pointed out that in this case the patient had worked with very finely pulverized asbestos, so that the mechanical effect of the asbestos needles was not prominent in the pathogenesis. Knowledge of the disease and precise occupational anam- -- nesis are necessary if the milder cases are to be recognized in X-ray photography', e.g. in routine examinations for tuberculosis. In Ugeskrift for Lger, 1950, No 14, Torsten Ive became the first to publish a case of pneumoconiosis caused by asbestos here in Denmark [5]. It is mentioned in the article that in recent years a total of four cases of this disease have been found. These four cases were diagnosed in examinations of workers in threatened jobs, instituted by the factory inspection service, which has had its attention directed toward this risk since the middle of the 1930's. The disease presumably is not rare in Denmark, at least in its milder forms, so that there is reason to report additional cases as well, at the same time going into more detail on specific points. Asbestosis will presumably not be diagnosed unless the occupational anam nesis is compared with the clinical findings and the X-ray picture, since it is characteristic of asbestosis that the roentgenological modifications are slight in comparison to the often considerable reduction in heart and lung function. This is in contrast to the situation in silicosis, where the roentgenological modifications are evident even in the cases described as mild, and where marked roentgenological modifications are often found together with a well-preserved functional capacity. *0f the Labor and Factory Inspection Service and the Occupational Medicine Clinic of the National Hospital, headed by Prof Dr P. Bonnevie, chief physician. 1 The roentgenological findings are in agreement with the pathoanatomical picture, since, as pointed out e.g. by di Biasi [2], there are decisive differ ences between the two types of pneumoconiosis: asbestosis is a diffuse inter stitial fibrosis, beginning low in the lungs and often accompanied by basal pleuritis and an upward development of emphysema, while silicosis is character ized by the nodular modifications which begin in the midmost portion of the lungs. It is now more or less agreed that the granulomata in silicosis are due to the effect of crystalline silicic acid, even though the relationships are far from clear and for many years the view prevailed that only the inhalation of particles consisting of free silicic acid was dangerous. Also, the danger ousness of the dust seems to increase with decreasing particle size in keeping with the fact that for the most part only particles with a diameter of less than 5 y make their way down into the alveoli and that particles with a diameter of about 1 y are especially dangerous. It is still not clear how particles of still smaller diameter behave; there is a good deal to indicate that they cannot be retained in the alveoli to the same extent, and for the most part are sus pended and carried out of the alveoli in exhalation. It is now clear that certain salts of silicic acid, such as asbestos and the closely related mineral talcum, are also capable of causing a pneumoconiosis --sometimes called silicatosis. As far as asbestosis is concerned, the question of the pathogenesis is not completely decided, but the general opinion now is that the mechanical irritation from sbestos n e e d l e s is a necessary factor in the occurrence of the fibrosis (Sundius and Bygdn [13], Beger [1]). Gardner [3] (see also [7]) showed in experiments with animals that in contrast to quartz and other forms of crystalline silicic acid, whose toxicity increased with decreasing particle size, the reverse is true of asbestos. He found its pathogenic effect only in the lungs, while quartz also has a pathogenic effect in other organs or when injected subcutaneously, and for that reason he thinks that it is only in organs where a rhythmic motion takes place, and only in particles large enough to have a mechanical effect, that asbestos can cause a fibrosis. King et al. [7], on the other hand, found in experiments with ani mals that in rabbits a nodular fibrosis developed that can be compared with an experimental silicosis, after inhalation of asbestos fibers 15 y in length, while inhalation of fibers 2.5 y long brought about a diffuse interstitial 2 fibrosis. The circumstances are thus far from being clarified. In man, too, there are presumably varied asbestos pictures; e.g., Wedler [14] says that X-ray photographs of workers in different German asbestos plants showed somewhat different pictures. Besides differences in particle size and other physical circumstances this may presumably also be due to differences in chemical composition, since there are several kinds of asbestos. (Commercially the two main forms are amphibolic asbestos [horneblende] and chrysotile asbes tos.) From Finland, Noro [11] has reported two cases of fatal outcome which were due to inhalation of Finnish asbestos (amphibolic asbestos), which is harder and more elastic than other asbestoses and is therefore regarded as especially dangerous. The asbestos needles found in the lungs were chiefly 9 y in length or a little shorter, and the thickness was always less than 1 y. This is smaller than several other reports; e.g., Wedler says that the length of asbestos needles is generally between 25 and 150 y and their thickness up to 3 y, while Koppenhofer [8], in examining the same lung, finds that a very large number of the needles are far smaller--length 2 to 6 y, thickness 0.006 to 0.01 y. In that connection the same author discusses in detail the pathogenesis of asbestosis and the significance of the asbestosis bodies. A thorough discussion of asbestosis is to be found in Lanza [9], Merewether [10], and Wedler, with bibliography. In the last two works there are statements about large masses of clinical material. Course of the Disease Asbestosis rarely develops roentgenologically or clinically in less than 5 years even with great exposure. Of 310 from two German asbestos plants who were examined by Wedler, asbestosis was found in 22.6 percent, but only 7.7 percent were in Stage II or higher according to a clinical classification into Stages 0 to III. The tables show that with a working time of 0 to 5 years (which em braced % of the group), asbestosis was found in only 3.3 percent and only Stage I During the succeeding 5 years the percentage goes up to 60, but chiefly with mild cases. With increasing working life the percentage of more severe cases rises. Merewether reports examinations by the Silicosis and Asbestosis Medical Board in which among 749 examined with a working life of' less than 5 years there were only 4 cases of asbestosis, while one fourth of those who had been employed for 20 years or longer were affected. In an examination of 1,512 workers the ratio 3 of asbestosis cases among groups with 0-4, 5-9, 10-19, and over 20 years' expo sure time was 1 : 5.6 : 30.4 : 53.2. But, as Merewether points out, it cannot be deduced from this that expo sure for less than 5 years is without risk, for inhalation of asbestos dust in sufficient quantity even for a short period can lead to an incapacitating asbes tosis if the person concerned lives long enough. Merewether states that an increased concentration reduces the time before asbestosis has developed and can be detected, but that this applies only up to a certain high concentration. If the concentration is increased further it will not lead to a further reduction of the time for development of the fibrosis, the "maturation period." On the other hand, an exposure to a concentration below a certain low level does not bring about an incapacitating fibrosis within the average working life.t Thus a minimum amount of asbestos dust must be caught in the lungs to develop a fibrosis of significance, and a certain time must pass before that fibrosis is developed. Merewether makes statements that indicate that the risk in working with asbestos is comparable to the risk in silicosis-threatened occupations, and in fact is greater if anything. In cases with fatal outcome the average working time is 15.2 years for silicosis as compared to 13.3 years for asbestosis. Not all work with asbestos is equally dangerous. According to the liter ature processing raw asbestos (crushing and grinding) seems to be especially dangerous, but the manufacture of insulation mats also has a bad reputation. The dust developed in spinning, on the other hand, is said to be slight. The actual mining of asbestos takes place in the open air, so that the dust concentration may be assumed to be low. In Wegelius's material from Finland [16], however, which consists of 126 asbestosis cases out of 476 persons examined, 34 of the 126 cases involved workers who had worked exclusively in the mines. The prognosis can be gathered in part from what has been said. Wedler finds in follow-up examinations that among workers who were only exposed to a lesser degree and had contracted only an incipient or fairly mild asbestosis and subsequently left the dangerous work the majority showed only slight pro gression after observation times of up to 17 years. It was different among those who continued with the work. Here there was a progression, but it rarely ex ceeded one stage (in the clinical classification) in 3 to 4 years. Wedler does 4 not think, therefore, that it would pay to reexamine persons already affected at shorter intervals than that mentioned above. Wegelius has similar results: after an observation time of 2 years there is progression in a number of cases (maximum of one stage according to the roentgenological classification). The very pessimistic outlook for workers in the asbestos industry that appears from these studies presumably no longer holds. At any rate many of those studied were exposed to inhalation of asbestos dust at a time when the danger was not yet evident or the risk was not generally recognized, and there were no antidust precautions in the system. The efforts to combat dust arose on the basis of these studies. Even though the average risk may thus be assumed to be far less now, there is obviously no guarantee in the individual case. The prognosis in the individual case is difficult to arrive at, for it depends on many other factors besides the development of the fibrosis itself, e.g. the individual's resistance to bacterial infection, complicating diseases of the heart and lungs, etc. As in the case of silicosis, the inclination now is to assume that asbestosis does not predispose patients to pulmonary tubercu losis in the sense that individuals with asbestosis get pulmonary tuberculosis more often than others when the exposure to tuberculosis is the same. It is another matter that if a case of asbestosis is complicated with tuberculosis the prognosis is presumably worse. On the other hand, there are now many concurring reports that primary bronchial cancer is more common among persons affected with asbestosis. Homburger [4] presented a survey in 1943 of the cases reported up to that time and said that with his own 3 cases at least 19 cases of primary carcinoma of the lungs had been reported. The frequency in his own institute is 4 carcinoma cases in 8 asbestosis autopsies. Wedler [15] states that in Germany a total of 4 carcinomata have been found in 29 autopsies of asbestosis patients, and that in the world literature 14 have been reported in 92 autopsies. Although the frequencies are widely varied and the material small, so that the percentages given are uncertain, there seems to be no doubt that asbestosis predisposes to lung cancer. Antiasbestosis measures follow the usual lines: incapsulation of the dust-raising work processes, local removal of dust by suction, room ventilation, and, lastly, personal protective devices such as masks. As usual, there are 5 efforts to make the last-mentioned unnecessary, since they hinder the work and masks are uncomfortable to wear, so that they are rarely used. The Author's Own Cases First a brief description of the working conditions in the factory where the case described by Ive arose. The factory produces building materials (slabs, boxes, pipes, fittings, etc.) of a mixture of asbestos and cement. In 1940, at the request of the factory inspection service, 30 workers with working times of 1 to 12 years were X-rayed. The films were sent to Prof Flemming Miller for appraisal. No sure case of asbestosis was found. In 1948 X-ray films of three workers with long working times (11, 18, and 18 years) still showed no asbestosis. The workers were also checked at the local tuberculosis station. After the case described by Ive was confirmed, 14 other workers with working times of 9 to 42 years were examined, and no asbestosis was found among them. Over the years the factory had been repeatedly inspected and improvements had been introduced in the form of incapsulation of work processes and dust re moval by suction. The dust danger was especially present in the crushing and grinding of the raw asbestos (Chile mill and disintegrator), where the filling and emptying was done in part by shoveling, and in work with the ground asbestos in the silos where the trucks were loaded by shoveling and in the "hollanders" where they were dumped out into the cement mixtures. At the time of an inspec tion in 1949 it was possible to take dust measurements. The asbestos used was very "short," since it is a waste product unsuitable for spinning that is used. Accordingly, the true needle content was between 20 and 30 percent of all parti cles. Here are a few of the measurement results (furnished by D. Stubbe Teglbjrgof the factory inspection service's laboratory for occupational hy giene) : Chile milt during emptying and filling Hollander during filling Particles/cm3 0.5 to 5 y 990 5,500 Asbestos Particles/cm3 2-15 y 15-120 y 85 150 350 800 The results of the measurements at the disintegrator and in the silo fell between these figures. According to Johnstone [6] the highest permissible concentration is 10,000,000 particles 0.5 to 5 y in size per cubic foot (corresponding to about 350 per cm3). 6 Case Histories Case 1. Weaver, born in 1895. Work anamnesis: Was employed for many years in a factory where asbestos weaving is done on a rather large scale, for the manufacture of brake bands, etc. Since 1928 has operated a weaving machine equipped with a dust-suction system. To what extent the suction system was ef fective earlier is hard to say. Upon inspection it was not in order. Anamnesis: accident. Says he was formerly healthy, aside from a phlegmon after an Present illness: After several years' work at the weaving machine he began about 1930 to suffer from bronchitis. He was treated for it in the hos pital in 1937 and 1943. In 1945 the symptoms increased; he had coughing, expec toration, and spells of difficulty in breathing, and had to be assigned to light work. After an inspection at the factory in 1945 the factory inspection service borrowed the X-ray films that were taken in 1937 and 1943. Prof Flemming Miller got the films for appraisal and said: The X-ray of 1937 shows a very coarseme s h e d , somewhat blurry marking of the lungs on both sides; there is also re duced translucence of the lungs, and there can be no doubt that there is some thing pathological, in all probability an incipient asbestosis. On the X-rays of 1943 the modifications are seen to have developed; there is now a further coarse-meshed and dense marking in both lungs with the mesh boundaries somewhat blurred and in places running together to form irregular little spots. Left phrenicocostal sinus somewhat flattened. The picture is typical of an asbestosis at the transition to the second stage. The case was reported to the accident insurance agency and was recognized as an occupational illness. He was bedridden most of the fall of 1945 and had to stop work completely. The condition gradually grew worse, and he died in February 1948 (no autopsy). Working conditions have been improved since; there is effective suction at all asbestos looms, and the exposed workers are reexamined annually. It is said that no more cases of asbestosis have been found. Case 2. Shipyard worker, born in 1894. Work anamnesis: Employed at the shipyard since 1918, since 1935 insulating pipes, both aboard the ships and be fore installation of the pipes. Used asbestos cord and asbestos cloth; in recent 7 years rockwool and glasswool as well. In 1945 he was advised to get other work and got a job as night watchman at the jail, which he held for a year and a half. Since then he has worked at the shipyard again, as a general unskilled laborer, but now and then he assists or relieves the man who took over the insulation work after 1945. The work on shore was done in a little shed with no particular room ventilation or local dust suction. The pipes to be insulated were up to 5 meters long. A noticeable amount of fluff and dust is given off during the work. The dust generation on board seemed greater, and it, too, was done with no removal of dust by suction. ' Anamnesis: Healthy when a child; young. Has never had rheumatic fever or lung complaints. Bothered by lumbago for a number of years. Present illness: Since the lung inflammation in April 1941, suffers from u. increasing shortness of breath and heart palpitation under exertion and by shooting^pgins and wheezing in the left side of the chest and behind the manubrium sterni in deep breathing and under exertion. Also irritating morning coughing, but rarely expectoration. Was tired and lost 12 kg in weight; for that reason was examined by a tuberculosis specialist in 1941. Was sent to hospital in 1941 and 1942, diagnosis pleuritis sicca sin. and nervosism. Has since been examined at the tuberculosis station several times; no sign of active tuberculosis has ever been found. Mantoux test positive. Ventricular septum negative for TB. Blood sedimentation normal the whole time. In 1945 he complained of pains in the right side, and signs of pleuritis were found here, too. After that he was advised to change jobs. In 1948, after his union had applied to the factory inspection service, he was again X-rayed and the films were sent by the factory inspection service for appraisal by Prof.Flemming Miller, who gives the following description: The X-ray of the thorax shows that in the lower part of both lungs there is a slight but quite diffuse condensation, symmetrical in both lungs and partly obliterative. In addition, on the right side there is a flattening of the phrenicocostal sinus with adhesions to the dome of the diaphragm. This repre sents an asbestosis in a relatively early state (Figure 1). The case was reported to the accident insurance agency and recognized. Examination by a medical specialist the same year showed: objectively: 8 average state of nutrition, dyspnea after even small exertions, cyanosis. Eyes, fauces, tongue: nothing to report. Thorax of natural shape apart from depressions over the clavicle. St. pulm.: boundaries shifting. Damping and weakened respiration on both sides, especially in the lower portion. St. cord.: boundaries indeterminable, ictus inside the medioclavicular line, sounds pure, action regular. Other examinations brought out no abnormalities. Quietly walking up one flight of stairs speeded up the respiration. Blood pressure: 150/90. Sedimentation rate: 12 mm/1 hour. Electrocardiogram: nothing definitely abnormal; in particular, no sign of dextral influence. X-ray: unchanged conditions. His working capacity was judged to be less than one third, and in the first settlement he got compensation corresponding to 70 percent. He has since tried out at various lighter physical work, but could not do it. He even had to give up a newsstand, because in the winter of 1949-1950 he could not stand to . bring out the newspapers. He was bedridden most of the winter, and his condi tion seems to have worsened during this last year. Case 3. Laborer, born in 1908. Work anamnesis: Served apprenticeship as grocer. Employed as such until in September 1939 he got a job in a plant that produces materl'al for asbestos floors. The material is a mixture of pulver ized asbestos and magnesia cement. The raw materials are received in more or less pulverized form in sacks, and at the factory the necessary weighings, crushing, grinding, and mixing are done, as well as the weighing of the finished powder in sacks. Dust is generated in almost all manipulations, but especially in filling and emptying the mixing machine. The manufacture was done in a single locale, and no arrangements were made for removing dust by suction or for arti ficial room ventilation. An attempt was made to create a draft by leaving the door to the yard and a window open, but that was quite inadequate. After it be came clear in 1944 that he had contracted a lung disease, suction devices were installed on the machines. After that, he worked less in the factory, and for 9 the last year he has been employed as a driver and in work at the buildings, where the powder is delivered in vessels and water is added. This process gene rates some dust, but is done as far as possible in the open air. Anaimesis: As a child he drank soda lye, and has since had to have treatment from time to time for esophagostenosis. Otherwise healthy. Present illness: During the winter of 1943-1944 he coughed a good deal, and for that reason the company had him X-rayed in 1944. Signs of asbestosis or silicosis were found (chief doctor Sv. B0rre Larsen). The films were bor rowed by the factory inspection service and sent for appraisal to Prof Flemming Miller, whose description reads: There is a densely confluent marking on the lungs, almost symmetrical on the two sides and containing quite fine little spots. The modifications are slightly below the center of both lungs and sug gest a silicosis in transition between the first and second stages. He was treated in the hospital in 1946 for pleurisy and has since been reexamined at the Central Station. In 1949 he was treated for double pneumonia. Since we did not succeed in getting him to come to the occupational medi cine clinic of the National Hospital, the X-ray films were borrowed from the Central Station. Prof Flemming Miller's description reads: In the X-ray pic ture of 21 January 1946 an incapsulated exudate can be seen on the right side, together with the same densely confluent lung marking as described at the time of the previous X-ray examination. A photograph of 18 February 1947 shows, as remnants of the exudate on the right side, some thickenings of the pleura along the thoracic wall, a flattening of the phrenicocostal sinus, and a flattening of the right half of the thorax. In addition it can be seen that the lung marking is now quite blurred, almost like a diffuse condensation, symmetrical in the two lungs. The last X-ray picture, of 30 August 1948, shows that this condensation has increased still further, and there is now a border of pleural thickenings like a mantle along the lowest part of the left thoracic wall. What we have here is an advancing asbestosis. In January 1950 we succeeded in getting him to come to the occupational medicine clinic of the National Hospital for an examination, presumably because his condition had worsened and he had difficulty in doing his work. (He was dis charged on 13 January 1950.) 10 Present condition: Complains of increasing shortness of breath. Can walk on the level, but has difficulty if he has to hurry. Also has trouble in fast cycling. He lives on the fifth floor and has to rest three or four times to get there. Slight coughing all day long, and is bothered by coughing at night as well. Spits up only a little phlegm. No palpitation or edemata. Smokes 15 cigarettes a day. Objectively: thin. Slight cyanosis of the lips. in undressing and gets attacks of coughing. Becomes short-winded Stet. cord.: Boundaries normal, sounds pure. P2 perhaps a little larger than A2. Action regular. Stet. pulm.: limits costae 6-10, displaced about 2 cm at the posterior surfaces. Chest measurement in maximum expiration and inspiration 79-80 cm. Sibilant ronchi everywhere, with here and there sonorous ones (has a cold). No damping or respiratory modifications. Other examinations bring out nothing unusual, except that the fingernails are somewhat domed, but that has always been the case. rate: mm3. Height: 164 cm. Weight: 55 kg. Blood pressure: 115/80. Sedimentation 100 mm/1 hour. Hemoglobin: 120 percent. Erythrocytes: 5.95 million per Urine: no albumin, no sugar. Electrocardiogram: nothing abnormal. X-ray examination of thorax (Figure 2) shows by comparison with that taken by the Central Station on 30 March 1948 that the broad pleura border on the left side has now become much narrower. It is now only 1 to 2 cm wide, so that it is now possible to see the entire somewhat flattened left dome of the diaphragm. The lung marking itself, however, is quite unchanged. As before, both sides show a symmetrical, dense, almost confluent lung marking with rather clear, quite fine spots, especially in the lower half of the lungs. The heart is of natural shape and size. There is no sign of pulmonary heart. The diaphragm moves 2 cm. Functional examination: Vital capacity 1.45 liters (74 percent of total capacity), residual air 0.50 liters. Ventilation at rest 7.8 to 8.4 1/minute. Maximum ventilation 46 1/min. Arterial oxygen saturation at rest measures 93 percent with the oximeter. During work at 400 kgm/min. there is a pronounced drop in the arterial oxygen saturation (8 percent), and the patient gives up the work after 2 minutes' time. Ventilation during work 38 1/min., respiratory 11 frequency 46. Conclusion: Severe reduction of function, predominantly pulmonarily conditioned. There is a very low total capacity (58 percent of the cal culated value), possibly determined too low because of insufficient blending, and little ventilative function. (J. Georg) Discussion Two of the patients (Cases 1 and 2) were X-rayed several times because of subjective symptoms, but but went under the diagnoses pleuritis sicca and bronchitis. The X-ray films in these two cases were characteristic for asbestosis, especially in the sense that there were only slight roentgenological modi fications in view of the rather pronounced reduction of function in both cases. The X-ray findings were the usual ones in asbestosis: diffuse fibrosis low in both lungs with pleural thickenings_and reduced mobility of the diaphragm. In Case 2 the lung marking was somewhat finer meshed than in Case 1 and corresponded especially well to the usual description of asbestosis lungs. There is hardly any doubt that knowledge of the X-ray findings in asbestosis and a good work anamnesis would have led to a diagnosis of asbestosis having been made and pub lished earlier than was the case, and that those concerned would have been taken off the dangerous work, so that the prognosis would presumably have been less bad. In Case 3 the X-ray findings were somewhat different, in that there were also fine nodular modifications here, such as are seen in silicosis, especially in iron and steel cleaners. The diagnosis was made in this case, perhaps on that ground, at the time of the first X-ray examination, after 4 years' exposure and a short time after the first subjective symptoms appeared. The explanation for the fact that the X-ray picture deviated from the characteristic asbestosis picture may perhaps be that the asbestos used for asbestos floors is very finely powdered and is partly a waste product (asbestos flour). The very fine particle size may perhaps explain the more silicosis-like picture, since it is not the mechanical effect of the asbestos needles that prevailed, but the chemical ef fect. But, as stated in the introduction, the pathogenesis has still not been clarified. It has not been possible to find out in greater detail about the kinds of asbestos used, and there are no dust particle measurements available from the relevant periods of time. The subjective symptoms were those usual in asbestosis: Functional dysp nea and coughing with little expectoration. In Case 2 it was stated that at the 12 beginning the coughing was the characteristic dry morning cough accompanied by pain and wheezing in the chest. The subjective symptoms appeared after 2, 4, and 6 years respectively. The corresponding exposure times were 17, 10, and 10 years. After that time the symptoms were so marked that the persons concerned had to stop working. No. 1 died 3 years later, No. 2 is now, after another 3 years' observation time, almost 100 percent incapacitated, and No. 3 is greatly incapacitated. In silicosis and asbestosis it must be taken into account that the lung trouble gradually leads to an overload on the right side of the heart, so that a chronic pulmonary heart develops. In the three cases discussed here it was not possible to show this clinically by electrocardiography or X-ray, not even in Case 3, where the heart was also_X-rayed in oblique diameters in order possi bly to be able to demonstrate a projecting pulmonary arch [12] . The functional test on the same patient showed an impairment, but principally pulmonarily con ditioned. But lack of electrocardiographic or roentgenological signs of a hypertrophy of the right side of the heart does not exclude the possibility that it is present. Unfortunately, Case 1 was not autopsied. 13 BIBLIOGRAPHY 1. Beger, P.J., Archiv fr Gewerbepathologie und Gewerbehygiene [Archives of Occupational Pathology and Occupational Hygiene], Vol 6, 1935, p 3^9. 2. di Biasi, W . , ibid. , Vol 8 , 1938, p 139 3. Gardner, L.U., American Review of Tuberculosis, Vol 45, 19A2 , p j62. A. Homburger, F . , American Journal of Pathology, Vol 1 9 , 194-3, p 797 5. Ive, T . , Ugeskrift for Laeger [Doctors' Weekly], Vol 112, 1950, p 472. 6. Johnstone, R.T., "Occupational Medicine and Industrial Hygiene," St. Louis, 1948, p 6o4. 7. King, E.J., J.W. Clegg, and V.M'. Rae, Thorax, Vol 1, 1946, p 188. 8. Koppenhffer, G.Ft, Archiv fr Gewerbepathologie und Gewerbehygiene, Vol 6, 1935, P 38. 9. Lanza, A.J. (edit.), "Silicosis and Asbestosis," London, New York, Toronto, 1938, p L39. 10. Merewether, E.R.A., Tubercle, Vol 15, 1934, pp 69, 109, 152. 11. Eoro, L., Acta Pathologica et Microbiologica Scandinavica, Vol 23., 1946, p 53. 12. Samuelsson, S., "Chronic Cor Pulmonale," dissertation, Copenhagen, 1950, p 389. 13. Sundius, N. and A. Bygden, Archiv fr Gewerbepathologie und Gewerbehygiene, Vol 8, 1938, p 26. 14. Wedler, H.-W., "Klinik der Lungenasbestose," Leipzig, 1939, P 152. (ln "Arbeit und Gesundheit" [Work and Health], No 34.) 15. Wedler, H.-W., Deutsche medizinische Wochenschrift [German Medical Weekly], Vol 69, 1943, p 575. 16. Wegelius, C., Acta Radiologica, Vol 28, 1947, p 139* 14 f4' U D G I V E T AF DE N ALM. D A N S K E L G E F O R E N I N G N R. 37 14, S E P T E M B . ' R 1 9 5 0 1 12. A R G A N G BUTALGIN lablHr 15 lie........................ kr. 1,25 50 ................................. 3,05 100 ................................. 5,30 BU TALG IN liquldum 15 m l....................... kr. 1,80 5 0 ................................ 5,30 1 0 0 ................................ 9,60 BUTALGIN pro inject. 10 ml I haetteglas----- kr. 2,90 BUTALGIN cuppositorier anker * 10 slk............ kr. 3.05 ! i befrier for selv de steerk ; Telefon Il ... ...... 1277-1310 ms Holger Danskesvej 89 T rr ' / tilf.klde af asbestosis Af J0RGEX FROST I Ugeskrift for Laegcr nr. 14/50 har T o r s t e n I v e soni den f0rstc her i landet offentliggjort et tilfaelde af pncunioeonio.se freinkaldt af asbest (5). I arjiklen naevncs, at der i de senere r ialt er fundet 4 tilfaelde af denne lideise. Disse 4 tilfaelde er diagnosficcrcdc ved underspgelser af arbcjderne i de truede erhverv, foranlcdiget af fabriktilsynet, der siden midten af trediverne bar haft opniierksondicdcn rettet mod denne risiko. Lidelsen er antagelig ikke heit sjarlden her i landet, i hvert tilfaelde ikke i de lettere former, og der vil derfor va?re grund til ogs at offentligg0re de 0vrige tilfaehlc, samtidig ined at man gr naermere ind p enkeltc punkter. Asbestosen vil antagelig ikke blive diagnosticeret, medmindre arbejdsananincsen sammenholdes med det kliniske fund og r0ntgcnbilledet, da det karakteristiske for asbestosen er de ringe r0ntgenologiske forandringer i forhold til den oftc bctydeligc nedsiettclse af hinge- og hjertefunktionen. Dette er i modsoetning til forholdenc ved silicosen, livor de r0ntgenologiske forandringer allcrede ved de tilfaelde, der betegnes som lette, er tydelige, og hvor man ofte finder udtaltc r0ntgenologiske forandringer samnien med en velbevaret funktionel kapacitet. R0ntgenfundcne er i overensstemmclse ined det pathologisk-anatomiskc billede, idet der, som f. ex. d i B i a s i (2) har fremhaevet, er afg0rende forskclle mellem de naevnte to pneumoconioser: as bestosen er en diffus, interstitiel fibrse, begyndende nedad i lungerne og ofte ledsaget af basale pleuriter og emfysemudvikling opadtil, medens silieosen er karakteriserct ved de noduhere for andringer, der begynder i de midterste lungeafsnit. Der er nu nogenlundc eniglied om, at granulomerne ved silieosc skyldes virkningen af den krystallinske kiselsyre, selv om forholdcne langt fra er afklarcde, og i mange r herskede der den opfattelse, at kun indnding af partikler bestende af fri kiselsyre var farlig. Ligeledes synes stpvets farlighed at tiltage med aftagende partikelst0rrelse i overensstemmelse med, at hovedsagelig kun partikler med en diameter mindre end 5 my tracnger ned i alveolerne, og at saerlig partikler med diameter omkring 1 my er farlige. Man er endnu ikke klar over, hvordan partikler med endnu min dre diameter opf0rer sig; meget tyder p, at disse kun i mindre grad tilbageholdes i alveolerne, idet de som svaevedygtige oftest atter fpres ud licrfra ved exspirationen. Man er nu klar over, at ogs visse af kiselsyrens salte, f. ex. asbest og det neertstende mineral tal cum, er i stand til at fremkaldc en pneumneoniose Fra arbejds- og fabriktilsynet og tU gshospitalcts arbejdsincdicinskc Klinik. C h e f: P rofessor, overla-ge, d r. med. / '. lionnevie. -- af og til benvnt silicatose. For asbestosens vedkommende er sp0rgsmlet om pathogenesen ikke heit afgjort, men den almindelige mening er nu, at den mekaniske irritation fra asbestnlene er en n0dvendig faktor ved fremkomsten af fibr sen (S u n d i u s & B y g d n (13), B e g e r (1) ) G a r d n e r (3, se ogs 7) har i dyreexperimen- ter vist, at i modstning til kvarts og andre for mer af krystallinsk kiselsyre, hvis toxiditet tiltog med aftagende partikelst0rrelse, er det modsattc tilfldet ved asbest. Dennes pathogene virkning fandt han kun i lungerne, medens kvarts ogs i andre organer eher injiceret i subcutis virker pathogent, og han mener derfor, at det kun er i or ganer, hvor der finder en rytmisk bevgelse sted, og kun ved partikler af en for mekanisk virkning tilstrkkelig stprrelse, at asbest kan fremkaldc en fibrose. Ki n g og medarbejdere (7) har imidlcrtid i dyreexperimenter fundet, at der hos kaniner udviklede sig en nodulr fibrose, der kan sammenlignes med en experimentel silicose, efter in halation af 15 my lange asbestfibre, medens in halation af 2,5 my lange fibre frembragte en dif fus interstitiel fibrose. Forholdenc er slcdes langtfra afklarede. Ogs hos mennesker findes antagelig forskellige asbestosebilleder; f. .\. anf0rer W e d l e r (14), at rpntgenoptagelser fra arbejdere i forskellige tyske asbestfabriker vistc et noget forskelligl billede. Foruden forskel i partikelst0rrel.se og an dre fysiske forhold kan dette antagelig ogs skyl des forskel i kemisk sammenstning, idet der fin des flere asbestarter (handelsmssigt de to hovedformer amphibol-asbest (hornblende) og chry sotil-asbest). Fra Finland har N o r o (11) offentIiggjort 2 dddeligt forI0bne tilfaelde, der skyldes indnding af finsk asbest (amphibol-asbest), der er mere hrd og mere elastisk end anden asbest og derfor befragtes som srlig farlig. De asbestnle, der fandtes i lungerne, var hovedsagelig af laengden 9 my eher lidt kortere, og tykkelsen var altid mindre end 1 my. Dette er mindre end flere andre angivelser, f. ex. opgiver We d l e r , at asbcstnlenes lngde i almindclighed ligger mellem 25 og 150 my og deres tykkelse indtil 3 my. B cg e r har lignende tal (25--110 my og 0,2--1 my), medens K o p p e n h f e r (8) ved undcrsdgelse af samme lunge finder, at srdeles mange af nlene er langt mindre: lngde 2--6 my, tykkelse 0,006--0,01 my. Samme forfattere diskutcrer i sammenhaeng hermed udfprligt asbestosens pathogenesc og asbestosclegemernes betvdning. En udf0rlig omtale af asbestosen findes hos L a n z a (9), M e r e w c t h e r (10) og W edl er , hvor literaturen er samlet. I de to sidste arbejder findes opgprelser over store kliniske materialer. Forl0b. Asbestosen udvikter sig sjldent r0ntgenologisk eher klinisk p mindre end 5 r selv ved str exposition. I \V e d 1e r s materiale p 310 unders0gtc fra 2 tyske asbestvirksomheder fandtes as bestose i 22,6 Vc, dog kun 7,7 % i stadium II eller iW \ V f L f f 2/37 dcrover efter en klinisk inddeling i stadicrne O til III. Af tabellernc fremg&r, at vcd cn arbejdsalder p& 0--5 Sr (der omfattedc 2/s af materialet) fandtes asbestose hos 3,3 % og kun stadium I. Derefter stiger proccnten i det nseste 5-Sr til over (50, dog hovedsagelig lette tilfseldc. Vcd stigende arbejdsalder tiltager procenten af svaerere tilfseldc. Me r e w e t h e r refererer underspgelser af the Silicosis and Asbestosis Medical Board, hvor dcr blandt 749 undcrs0gte med en arbejdsalder pS mindre end 5 Sr kun fandtes 4 asbestosetilfaelde, medens en fjerdedel af de arbejdere, der havdc vaeret beskaeftiget 20 Sr eller laengere, var angrebne. Ved en underspgelse af 1512 arbejdere var forholdet mellem asbestosetilfaeldene i grupperne 0--4, 5--9, 10--19 og over 20 Srs expositionsstid som 1 : 5,6 : 30,4 : 53,2. Man kan imidlertid, som Me r e w e t h e r fremhaever, ikke lieraf slutte, at en exposition pS mindre end 5 Sr er uden risiko, idet indSnding af asbestst0v i tilstraekkelig maengde selv i cn kort periode kan f0re til en invaliderende asbestose, hvis den pSgaeldende lever laenge nek. Me r e w e t h e r anfprer, at en for0gct concen tration reducerer tiden, f0r asbestosen er udviklet og kan p&viscs, men at dette kun gaeldcr indtil en vis, h0j, concentration. Forpges concentrationen yderligerc, vil dette ikke f0rc til en yderligcre reduktion af tiden for fibrosens udvikling, ma turation period. PS den anden side vil cn expo sition for en concentration under cn vis, lav, graense ikke frembringe en invaliderende fibrose indenfor den genncmsnitlige arbejdsalder. AltsS et minimum af asbeststpv mS fanges i lungerne for at udvikle en fibrose af betydning, og en vis lid mS gS, f0r denne fibrose er udviklet. Me r c w e t h e r har opg0relser, der viser, at risikoen ved asbestarbejde kan sammenlignes med faren i de silieosetruede erhverv, ja, naermest synes at overgS den. Ved dpdeligt forlpbne tilfseldc var den gennemsnitligc arbejdsalder ved silicose 15,2 Sr i sammenligning med 13,3 Sr ved asbestose. Ikke alt arbejde med asbest er lige farligt. Efter literaturen syncs sserlig bearbejdning af rSasbest (knusning og maling) at vserc farligt, men ogsS fremstilling af isolationsmStter har et dSrligt ry pS sig. Stpvudviklingen ved spinding skal derimod vsere ret ringc. Selve brydningen af asbest foregSr i fri luft, sSledes at stpvkonccntrationen mS an tages at vserc lille. I W c g e l i u s ' materiale fra Finland (16), der bestSr af 126 asbcstosetilfselde blandt 476 unders0gte stammedc imidlertid dc 31 af de 126 tilfseldc fra arbejdere ved en afsluttende forarbejdning i minerne. Prognosen freingSr delvis af det anf0rte. Wedler finder ved efterunders0gelser, at hos arbej dere, dcr kun har vseret udsat i mindre grad og kun havdc pSdraget sig en begyndende eller letterc asbestose og derefter havde forladt det farlige arbejde, var dcr kun ringe progression hos flertallet efter en observationstid indtil 17 Sr. Anderledes stillede det sig hos dem, der blev ved ar- bejdet. Her sketc cn progression, der dog sjseldent i l0bct af cn 3--4 Sr oversteg eet stadium (i klinisk inddeling). W ed 1 er mener derfor ikke, at en kontrol af alleredc angrebne l0nncr sig med mindre tidsinterval end det anfprte. W c g c 1i u s har lignende rcsultater: efter en observa tionstid pS 2 Sr, er der progression i en del tilfselde (h0jst eet stadium efter r0ntgenologisk ind deling). De meget pessimistiskc udsigter for arbejderne i asbestindustrien, som fremgSr af disse materia ler, glder antagelig ikke mere. De unders0gte har i hvert tilfaelde delvis vret udsat for indSn ding af asbeststpv i en tid, hvor man ikke var klar over faren, eller risikoen ikke var almindeligt anerkendt, og st0vbekmpelsen ikke sat i sy stem. Dette er f0rst sket pS grundlag af disse ma terialer. Selv om gennemsnitsrisikoen sSledes m anta ges at vaerc langt mindre nu, er det selvf0lgelig ingen garanti i dc enkclte tilflde. Prognosen i det enkelte tilflde er vanskeligt at forudsige, den afhnger af mange andre faktorcr end selve fibrosens udvikling, f. ex. individets resistens overfor baktcricl infektion, komplicerendc hjerte- og lungelidelser etc. I lighed med forlioldene ved silicose er man nu mest tilbpjelig til at antage, at asbestose ikke disponcrcr for lungetuberkulosc i den forstand, at individer med asbestose hyppigere fr lungetuberkulosc end andre, nSr den tuberkulpse exposition er den samme. En anden sag er, at kompliceres en asbestose med tuberkulse, forvrrcs prognosen antagelig. Der foreligger derimod nu talrige samstenunende meddelelser om, at primr bronchialcancer er hyppigere blandt asbestotikere. H o m b u r g e r (4) har i 1943 givet en oversigt over de indtil da meddclte tilflde og mener, at der med hans egne 3 tilflde mindst er offentliggjort 19 tilflde af primrt lungecarcinom. Hyppighedcn i hans eget institut er 4 carcinom-tilflde p 8 asbestosesektioner. W e d l e r (15) anfprer, at i Tyskland er ait fundet 4 careinomer p 29 sektioner af asbestosepatienter, og at der ifplge vcrdensliteraturen er offentliggjort 14 pft 92 sektioner. Sclv om hyppigheden er strkt varierende og materialcrne sm og procentangivel.se derfor usikker, synes der ikke at vre tvivl om, at asbestose disponcrcr til lungekrft. Asbestosebekoempelsen fplger de sdvanlige retningslinier: indkapsling af de stpvende arbejdsprocesser, lokal afsugning, rumventilation og endelig personlige beskyttelsesmidler som maske. Den sidstnvnte metode s0gcr man som sdvanlig at g0rc overflpdig, da arbcjdct luemmes derved, og masker er ubehagelige at bre, hvorfor de sjldent benyttes. KGNK TIU-.Kl.DK F0rst skal arbejdsforholdene kort omtales i den virksomhcd, i hvilken det af I v c beskrevne til flde opstod. Virksomheden fremstiller bygningsmaterialer (plader, kasser, r0r, fittings etc.) af U / 9 1950 1285 cn bl an ding af asbest og cement. En 30--40 arbcj- dere er beskseffiget ved det st0vende arbejde. I 1940 blev der p fabriktilsynets foranledning r0ntgenfotograferet 30 arbejdere med en arbejds- alder fra 1 til 12 r. Der blev ikke fundet sikre tilfaglde af asbestosc (filmene sendtes genneni fabriktilsynet til bed0mmelse hos professor F l e r a m i n g M0 l l e r ) . I 1948 viste r0ntgenfil- mene fra 3 arbejdere med lang arbcjdsalder (11, 18 og 18 r) stadig ingen asbestose. Arbejderne er ipvrigt kontrolleret p den lokale tuberkulosc- station. Efter at det af I v c beskrevnc tilfaelde var blcvet konstateret, unders0gtes 14 andre ar bejdere med en arbejdsalder fra 9 til 42 r, og der fandtes ingen asbestose blandt disse. Igcn- nem rene var fabriken gentagne gange blevet inspiceret og forbedringer i form af indkapsling af arbejdsprocesserne og afsugning indfprt. St0v- faren var saerlig til stede ved s0nderdelingen og formalingen af den r asbest (kollergang og des integrator), hvor fyldning og tpmning delvis ske- te ved skovling, ligcledes ved arbejdct med den formalede asbest i siloerne, hvor vognene Isessc- des ved skovling, samt ved hollsenderne, hvor de t0mtes ud i cemcntvaellingen. Ved en Inspek tion i 1949 var man i stand til at foretage st0v- mlinger. Den anvendte asbest var meget kort, idet det er et affaldsprodukt, uegnet til spinding, der anvendes. Indholdct af egentlige nle l i overensstemmelse hermed mellem 20 og 30 % af samtlige partikler. Et par resultatcr af mlingernc skal anf0res (magister D. S t u b b e T e g l b j i e r g fra fabriktilsynets laboratorium for arbcjdshygi- ejne): Part /cm 5 Asbcstpart./cm3 0.5- 5 ft 2 -15 Kollergang under f0m- 15 - 200 u ning og fyldning 990 85 150 Ilolliender under fyldning 5500 350 800 Resultaternc af mlingernc ved desintegralor og i silo l herinicllem. Efter J o h n s t o n c (6) er den h0jest tilladclige concentration 10,000,000 partikler af st0rrelsen 0,5 til 5 my pr. cubic foot (svarende til ca. 350 pr. cm3). Sygehislorier: Tilfw lde 1. Vsever, f0dt 1895. A rb ejd sn n a m n ese: H ar i mange r va?ret a n sat i en fab rik , hv o r d er foregr vievning af asbest i ret str stit, b l.a . til frcm stilling a f brem sebnd. H ar siden 1928 passet en v:evcm askine, der er forsynet med afsugningsanordningcr. Hvorvidt disse tidligere h ar va-ret effektive, er det vanskeHgt a t udtalc sig om. Ved cn inspektion var de ikke i orden. Anamnese: Angivcligt tidligere rask, bortset fra en pblegmone efter et trum e. N uvrrrende lid eise: E fte r nogle Ars arb e jd e ved v;vvem askiiien begyndte b a n ca. 1930 a t lide a f b ro n ch itis. H an blev b eh an d le t h e rfo r p sygehus i 1937 og 1943. I 1945 v a r syniptom erne ti 1taget, h an havdc hoste, opspyt og anfabl af ndenpd og m tle ssettes til let arbejde. E fte r eil insp ek tio n p virksom heden i 1945 lute fa b rik tils y n e t rp n tg en film en e, d e r v a r optaget i 1937 og 1943. Professor F l e m m i n g M 0 l I e r f i k filmene til bedpm m else og u d ta lte : R p n tgenbilledet fra 1937 viser cn meget grovm asket, noget udflydendc lungctegning p begge sider; der er ogs form indsket gennem sk in n clig h ed a f lungerne, og d e r kan ikke vscrc tvivl om, at der findes noget pathologisk, efter al sandsynliglied en begyndende asbestosc. PA optagclserne fra fe b ru a r 1943 ses fo ra n d rin g e rn c at have udv ik let sig ; d e r e r n u en yd erlig ere grovm asket og ta:t tegning i begge lunger med maskegraenserne noget udviskede og p steder lpbet samnren til uregelma:ssigc sm pletter. Venstre sinus phrenico-costal is affladet. liilledct er ret typisk for en asbestose p overgangen til 2. stadium . T ilfe ld e t an m eld tcs til uly k k esfo rsikringen og anerkendtes som erhvcrvssygdom . Han v ar sengeliggende det m este a f e fte r re t 1945 og m tte holde heit op a t arb e jd e . T ilsta n d e n fo m e rre d e s efterhAiiden, og h a n dpde fe b ru a r 1948 (ingen sectio n ). A rbejdsforholdcne er siden blevet forbedrede; der er effektiv afsugning ved alle asbestvsvene, og de udsatte arbejdere kontrolleres rligt. Der skal ikke si den veere fu n d e t asbestosctilfaelde. TU(wide 2. S kibsv.xrftsarbejder, fddt 1894. Arbejdsanam nese: Siden 1918 a n sa t p skibsvierft. Siden 1935 h ar han isolcret r0r, dels ombord p skibene. dels in den rprenes in stallatio n . Han h a r anvendt asbest snore og asbestlaerred, i de senere Ar ogs rockw ool og glasu ld . I 1945 blev han tilr d e t andet arb ejd e og fik ansaettelse som nattevagt i arrestbus, hvilket arbejde han havde i halvandet r. Siden h ar han attcr arbej dct p skibsvaerftet som alm in d elig arbcjdsm and, dog hjsrlper og afl0ser han a f og til den mand, som si den 1945 overtog iso la tio n sa rb e jd c t. A rbejdct i land foregik i et 1Ulc sk u r uden saerlig ru m v en tilatio n el ler lokal afsugning. R0renc, der skulle isoleres, havde en lxngde p op til 5 m. Der afgaves en del synlig fnug og st0v u nder arbejdct. Stpvudviklingcn ved arbejdet om bord skdnncdcs st0 rrc; ogs dette foregik uden afsugning. Anamnese: Rask som harn og ung. H ar aldrig haft gigtfeber eller lungclidelser. I en del r generet af lum bago. Nuvaerendc lidelsc: E fter lungebetamdelsc i april 1941 lid t a f tiltag en d e k o rtan d eth ed og hjertebanken ved anstrengelser, stikkendc sm erter og knagen i ven stre side a f brystet og bag m anubrium sterni ved dyb vejrtrrckning og ved anstrengelser. Tillige irriterende m orgenhostc, men sjaeldent opspyt. Blev traet og tabte 12 kg i vjegt, hv o rfo r han blev underspgt a f tuberku losespecialist i 1941. Denne k o n staterede en t0 r pleu ritis p venstre side. Han var indlagt p sygehus i 1941 og 1942 u n d e r diagnosen p le u ritis sicca sin. og nervosism us. H ar senere Vierct undersdgt p Tuber k u lo sestatio n en flerc gange; d er er ald rig fundet tegn p aktiv tuberkulse. M antoux: + . Vcntrikelskyllev a n d : -f- TB. Sam kningen norm al hele tiden. I 1945 klagede han over sm erter i hpjre side, og der blev fu n d et tegn pA p le u ritis ogs her. E fter dette blev han tilrdet at skiftc arbejde. 1 1948 blev han, e fte r cn henvendelsc fra sit fagforbund til fabriktilsynet, attcr rpntgcnfotograferet, og film ene blev gennem fab rik tilsy n et sendt til bedpm m else hos prof. F l e m m i n g M p l l e r , der gi ver fplgende beskrivclse: Rpntgen a f thorax viser, at d e r n ed ad til pA begge sid er findes en svag, men ganske d iffu s u dflvdende fortastning, sym metrisU i beg- 1286 V f L 112/37 gc lunger, delvls u d slettcn d e lungetegningen. D esuden er der p i hpjre side en affladning af sinus phrcnico- costalis med adhaerencer til diaphragniakuplen. Det drejer sig om en asbestos i ct forlioldsvis tidligt sta dium . (Fig. 1). Tilfaeldet er anm eldt til ulykkesforsikringen og nnerkendt. Ved underspgelsc bos m edicinsk specialist sam m e r fandtes: o b jek tiv t: m iddel ernaering, dvspnoe selv ved sm anstrengelser, cyanose. 0 jne, fauces, tunge: intet sterligt. Thorax af naturlig form udover indtra'kninger over clavicula. St. p u lm .: graenser forskydeligc. Daempning og svsek- ket resp iratio n p begge sider, saerlig nedadtil. St. cord.: graenser ubestcm m elige, ictus inden for medioclaviculaerlinien, lyde rene, aktionen regelm s sig. 0vrige underspgelse frem byder intet sa-rligt. Ved rolig gang een trap p e op forceredes resp ira tionen. B lodtryk: 150/90. SH: 12 m m /1 tim e. Blodunders0gelse: norm al. Electrocardiogram : intet sikkert abnorm t, specielt ingen tegn p i h0jresidig pvirkning. Rpntgen: uforan drede forhold. Hans arbejdsevne bed0mtes til under cn trediedel, og ved f0rste afgprelse fik han en erstatning svarende til 70 %. H an h a r siden forspgt sig ved fo rsk cllig t lettere legem ligt arbejde, men kunne ikke klare det. O gsi en aviskiosk h a r han m attet opgive, da han i vinteren 1949-- 50 ikke k u n n e t i l e at bringe av sem e ud. Han v ar sengeliftgende det meste af vinteren, og h an s tils ta n d synes a t VEere fo rv ierrct i d et sidste i r . Tilft?Me 3. A rbejdsm and, f0dt 1908. A rb ejd san a m nese: I 'dliert urtekraem m er. Vairet beskseftiget som sdan, in d til h a n i Septem ber 1939 blev a n sa t i en virksomhed, der frem stiller udgangsm aterialet til asbestgulve. M aterialet er en blanding af pulveriseret asbest og m agnesiacem ent. R m aterialerne m odtages i mere eller m indre pulveriseret tilstand i sadtke, og p i fabriken foretages de npdvcndige afvejninger, knusning, nialing og blandinger sam t det faerdige pulvers afvejning i sa:kke. Stpvudvikling forekom m er ved narsten alle m a n ip u la tio n c r, m en isaer ved b fan dem askinens fyldning og tpm ning. F abrikationen foregik i ct cnkclt lokale, og der var ikke tru ffet foranstaltninger til afsugning cllcr kunstig rum ventila tion. Ved a t lade porten til g ird en og et vindue s ti Abcnt spgte m an at sltaffe gennemtraik, men dette var ganske utiistraekkcligt. E fter at m an i 1944 v ar h ie vet k lar over, at lian havdc pdraget sig en lungelidclse, blev der etablerct afsugning ved m askinerne. Han arbejdede i den fplgende tid m indre i fabriken og h ar i det sidste irs tid vacret beskaeftiget som chauff0r og ved arlicjdc p i bygninger, hvor pulveret lueldes op i k ar og tilsiettes vand. Denne proccs st0ver noget, men fo reg ir s i vidt m uligt i fri luft. Anamnese: Som harn drak lian n atronlud og h a r si den af og til m itte t behandlcs for 0sofagusstenose. Ipvrigt rask. h'uvacrendc lid e lsc : V interen 1943-- 44 havdc h a n en del liostc, h v o rfo r virksom lieden i 1944 lod h am r0 n tgenfotografere. Der fandtes tegn p i asbestose eller si licose (overlasge S v . B 0 r r e L a r s e n ). Filinene blev lin t af fab rik tilsy n et og sendt til bcdpinm clsc hos P rofessor F 1 e in in i n g M 0 11 e r, h vis beskrivelse ly d er: D er findes nacsten sym m etrisk p i begge sider en ta?t sam m enflydcndc lungetegning, indeholdende gan ske fine sm pletter. Forandringerne sidder lidt ncdenfor m idten a f begge lunger og skyldes en silicose p i overgangen m ellcm 1. og 2. Stadium . I 1946 blev h an b eh an d le t i liospital fo r lungeliindebct.-endelse og er siden kontrollcrct p i C entralsta tionen. 1 1949 blev h an b eh an d le t fo r dobbeltsidig iungebelacndelsc. Da det ikke lykkedes at f i ham til at mpde til kontrol p i Rigshospitalets arbejdsm edicinske klinik, har man lin t rpntgenfilm ene fra Centralstationen. Profes sor F l ein i n i n g M 0 l l e r s beskrivelse lyder: P i rpntgenbilledc fra 21/1-46 ses et afkapslct exudat p i h0jre side og den sammc ta:t udflvdende lungetegning, som beskrevet ved forrige r0ntgcr.unders0gelse. En optagelsc fra 18/2-47 viser som rester fra exsudatet p i hpjre side nogle pleurafortykkelser lngs thorax v a'ggen, cn a ffla d n in g a f sin u s phrenico-costalis og en affladning af lipjrc "horaxhalvdel. Desudcn ser m an, a t lungetegningen nu e r ganske u dflydende, ns sten som cn diffus fortaetning, sym m etrisk i begge lunger. Den sidste optagelse fra 30/8-48 viser, at denne for taetning yderligcrc er tiltaget, og der er nu tillige kom met en braram e af pleurafortykkelser som en kappe lngs nederste del af venstre thoraxvasg. -- Det drejer sig om en frem adskridende asbestose. I ja n u a r 1950 lykkes det at f i h am til a t mpde til en underspgelse p i Rigshospitalets arbejdsm edicinske k lin ik , an tag e lig fo rd i h a n s tils ta n d v a r forva*rret, og han havdc besvnrr med at klare arbejdet (blev afskediget 13/1-50). Nuvierendc tilstan d : Klager over tiltagende kortin d eth ed . Kan g i p i ja-vn vej, men er generet, hvis han skal skvnde sig. Ligeledes gener ved hurtig cykling. Han b o r p i 4. sal og m i livile sig 3--4 gange for at n i derop. S inihostcr hele dagen, og ogsi om natten er han plaget af koste. Expcctorerer kun lidt slim . Ingen h jertelian k en e ller pdem er. Ryger 15 cigarelter daglig. O bjektivt: mager. Lidt cyanose af laberne. Bliver k o rtin d et ved afklxdning og f i r hosteanfald. Stet, cord.: gram ser norm ale, lyde renc. P2 m iske lid t stp rre end A2. A ktionen regelnuessig. Stet, p u lm .: grienser costa 6-- 10, forskydes ca. 2 cm p i bagfladcrnc. Brystomfang ved m aximal exspira- H / 9 1950 1287 Fig. 2. tio n og in s p ira tio n 79--80 cm. O veralt sig n ieren d e og cnkelt sonore ronchi (er forkplet). Ingen dawipnlnger eller respirationsforandringer. 0 v rig c underspgelser frenibydcr in le t s a rlig t, ud- over at fingcrneglcnc er oget kuplede, men det h ar de altid vsret. H pjde: 164 cm. V;egt 55 kg. H lodlryk 115/80. SR: 10 in m /1 tim e, lia'inoglobin 120 %. E ry tro c y tc r 5.95 in ill/in m 3. U rin : -i- alb . -f- saccb. E lectro card io g ram : intet abnorm t. R0ntgenunders0gelse a f thorax (fig. 2 ): viser sammcnlignct med optagelsen fra Centralstationcn 30/348, a t den betydelige p le u ra b ra o im e p v e n stre side nu o r sta:rkt a fsm a ln c t. Den er nu kun 1--2 cm b red , sledes at man ser hele den venstre, noget affladede diapliragm akuppel. Selve lungetegningen er im idlertid ganske uforandret. Som tidligere scs p begge sider en sym m etrisk, tret, naesten sam m enflydende lungetegning med re t tydelige, ganske fin e sm p letter, isaer i nederste halvdcl af lungefeltcrne. H jertet er af naturlig form og stprrclsc. Der er ingen tegn p cor p u l m onale. D iaphragm a bevaeges 2 cm. F u n ktion su nd ers0 g else: V italk ap acitet 1.45 I (74 % a f to ta lk a p a c ite t), re s id u a llu ft 0,50 1. H vileventilation 7.8--8.4 1 /m in . M ax im alv en tilatio n 46 I/in in . A rtericI iltiruvtning i h v ile fin d es til 93 % med oxim eter. Un der arb ejd e p 400 k g m /m in . kom m er der et u d talt fald i den arterielle iltrm etning (8 % ), og patienten opgiver arbejdet efter 2 m inutters forlpb. V entilatio nen u n d e r a rb e jd e t 38 1/m in., re sp iratio n sfrek v en s 46. K onklusion: Sva-r funktionsncdsicttelse, overvejende pulm onalt betinget. Der findes en meget lav to tal kapacitet (58 % a f beregnet v a rd i), muligvis besternt for lav p grund a f m angelfuld opblanding, og ringe ventilatorisk funktion. (J. G e o r g ) . DISKUSSION De 2 af patienterne (tilf. 1 og 2) cr rpntgenfotograferede flere gange p grund af subjektive symptoiner, men er get under diagnoserne pleuritis sicca og broncliiiis. Rpntgenfilmenc i dissc to til faelde bar vaeret karakteristiske for asbestose ogs i den forstand, at der kun bar vaeret ringe rpntgenologiske forandringer i betragtning af den 1288 ret udtalte funktionsnedsaettelse i begge tfaelde. R0ntgenfundene var de saedvanlige ved asbestose: diffus fibrse nedadtil i begge lungefelter med pleurale fortykkelser og nedsat bevaegelighed af diaphragma. I tilfaelde 2 var lungetegningen no get mere finmasket end i tilfaelde 1 og svarede saerdeles godt til den saedvanlige beskrivclsc af asbestoselungen. Der cr naeppe tvivl om, at kendskab til rpntgcnfundet ved asbestose og en god erhvervsananinese ville have medfprt, at diagnosen asbestose var blevet stillet eller vcntileret p et tidligere tidspunkt, end tilfaeldct var, og at de pgaeldende kunne vaere blevet fjernet fra det farlige arbejde, hvorved Prognosen antagelig havde vaeret mindre siet. I tilfaelde 3 var r0ntgenfundet et noget andet, idet der her tillige var fine nodulaere forandrin ger, som det ses ved silicose, speciclt hos jernog stlrensere. Diagnosen blev -- mske af denne grund -- i dette tilfaelde stillet ved fprste rpntgenunderspgelse efter 4 rs expositionstid og kort tid efter, at de f0rste subjektive svmptomer fremkom. Forklaringen p det for asbestosen afvigende r0ntgenfund kan mske vaere, at den asbest, der anvendes til asbestgulve, er meget fint pulveriseret og delvis et affaldsprodukt (asbestmel). Den meget fine partikelstprrelse kan mske forklare det mere silicoselignende billede, idet den meknniske virkning af asbestnlene ikke g0r sig gaeldende, kun den kemiske. Som anf0rt i indledningen er pathogenesen dog ikke klarlagt endnu. Det har ikke vaeret muligt at f oplyst naermere om de asbestarter, der har vaeret anvendt, og ligeledes foreligger der ikke st0vmlinger fra rele vante tidspunkter. De subjektive symptomer har vaeret de saedvan lige ved asbestose: Funktionsdyspnoe og hoste med ringe expectoration. I tilfaelde 2 er oplyst, at hosten i begyndelsen var den karakteristiske t0rre morgenhoste ledsaget af sting og knagen i brystet. De subjektive symptomer fremkom efter henholdsvis 2, 6 og 4 r. Tilsvarende expositionstider var 17, 10 og 10 r. Symptomerne var efter dette tidspunkt s udtalte, at de pgaeldende mtte oph0re med arbejdet. Nr. 1 d0de 3 r bereiter, nr. 2 er nu efter yderligere 3 rs observationstid naermest 100 % invalid og nr. 3 er stasrkt invalideret. Ved silicose og asbestose m man regne med, at lungelidelsen efterhnden medfprer en overbelastning af h0jre hjertehalvdel, sledes at der udvikles et cor pulmonale chronicum. Dette har ikke kunnet pvises klinisk i de 3 omtalte tilfael de ved electrocardiografi eller ved r0ntgen, ej heller i tilfaelde nr. 3, hvor man med lienblik herp tillige rpntgenfotograferede hjertet i skrdiameterne for om muligt at kunne pvise en fremspringende pulmonalbue (12). Funktionsprpven hos samme patient viste en nedsaettelse, men hov e d sa g c lig t pulmonalt betinget. Manglende elektrocardiografiske og rpntgenologiske tegn p h0jresidig lijertehypertrofi udelukker imidlertid ikke, at en sdan findes. Desvaerre blev tilfaelde 1 ikke obduceret. V f L 112137  RfiSUM 3 tilfaelde af asbcstosis omtales. I de 2 var r0ntgenfmcne typiske, i det tredie fandtes tillige nodulaere forandringcr. Som en mulig forklaring herp anfpres, at der i dette tilfaelde var arbejdet mod meget fint pulveriseret asbest, sledes at den mekaniske virkning af asbestnlene ikke var fremtraedende ved pathogenesen. Kendskab til sygdornmen og cn npje erhvervsananmcse er npdvcndig, hvis de letterc tilfaelde skal erkendes ved r0ntgenfotografering, f. ex. ved rutinemaessig unders0gelse for tuberkulse. Literatur: 1. Leger, P. J.: Arch. f. G ew erbepath. u. Gcwerbehyg. 6 : 349, 1935. 2. d i Biasi, IV.; ibid . 8: 139, 1938. 3. Gardner, L. V.: Am. Rev. T uberc. 45: 762, 1942. 4. Hamburger, F.: Am. J . P a th . 19: 797, 1943. 5. lue, T.: Ugeskr. f. La:gcr 112: 472, 1950. 6. Johnstone, R. T.: O ccupational Medicine and In d u strial Hygiene. St. Louis 1948. Pn. 604. 7. King, E. J ., J. IV. Clegg and V. Af. Rae: T horax 1: 188, 1946. 8. K oppenhffer, G, F.: A rch. f. G ew erbepath. u. Ge- w crbehyg. 6: 38, 1935. 9. Lanza, A. J. (ed it.): Silicosis and Asbestosis. Lon don, New York, Toronto 1938. Pp. 439. 10. Merewether, E. R. A.: T ubercle 15: p. 69, 109, 152, 1934. 11. \ o r o , L.: Acta p a th , et m icrobiol. Scandinav. 23: 53, 1946. 12. Samiielsson, S.: C hronic Cor P u lm o n ale. D e p u ta ts . K bhvn. 1950. Pp. 389. 1. S u n d iu s If. und A. Bggden: A rch. f. G ew erbepath. und G cw crbehyg. 8 ; 26, 1938. 1 Wedler, H.-W.: Klinik der Lungenasbestose. Leip zig 1939. Pp. 152. (In A rbeit u n d G esundheit, left. 34). 15. 'edler, H.-W.: D eutsche m ed. W chnschr. 9: 575, . 43. 16. li 'fle/fus, C.: Acta ra d io l. 28: 139, 1947. stoffer af stilb0strol-typen. Selv et s almindeligt foenomen som de 0strogcn-inducerede postklimakterielle metrorrhagicr er nppe tilstrkkclig kendt af alle, der anvender tienne terapi. Selv om de fleste, som nvnt, regner pstrogenbchandling for ganske uskyldig -- selvfplgelig bortset fra de almindelig kendte, forbigende ge ner af subjectiv art som f. eks. dyspepsi ved pero ral anvendelsc -- har der dog ogs fra forskellig side rejst sig advarende r0ster, og man bar her f0rst og fremmest peget p muligheden af at en strkere og lngcrevarende dosering af 0strogene stoffer kan blive en mere eller mindre vsentlig faktor i det komplex, der betinger udvikling af maligne lidelser i den kvindelige organisme, f0rst og fremmest i utrus og mamma. Hele dette spprgsml synes ikke tilstrkkeligt pagtet hcrhjemme og synes ikke tidligere at bave vseret genstand for nogen samlet bcarbcjdelse i skandinavisk literatur. Denne terapiforms efterhnden kolossale udbredelse g0r det imidlertid n0dvendigt, at spprgsmlet drages frem, selv om det ikke endnu er s afklaret, at der kan tages definitiv stilling til det. Denne frygt for en vis cancerigen virkning af 0strogener er opstct ud fra forskclligc synspunkter: 1. Rcnt teoretiske overvejelser over le naturlige 0strogeners kemiske slgtskab med erkendt canccrigene stoffer. 2. Kendskabet til 0strogenernes meget betyde lige proliferationsinducerende virkning p epitelet i den kvindelige genitaltractus. 3. Patologernes pvisning af en nr relation rcnt morfologisk mellcm benigne, 0strogent-inducerede proliferationer i endometriet og gte ma ligne endometrielidelser. 4. Dyreexperimentellc unders0gelser. 5. Kliniske data. 6. Erfaringer fra 0strogen bebandling af kvinder. KEMISK SLGTSKAB ' DI 0 S T R O G E N E S T O F F E R S BETY.iNING FOR UDVIKLINGEN AF Ci N C E R C O R P O R I S U T E R I ^ -Af A K S E 't ERP De pstrogen ' stoffers gennemgende fortrinlige virkning overft r de ofte gencrcnde, men relativt uskyldige, subj< ctive klimakterielle gener bar gjort denne ter-piform overordentlig popular, ikke mindst blane* patienterne. Til dels som et evn fra hornionterapiens vorden, hvor man ku n liavde svage ovarieekstrakter til rdighed, g0r im. ige sig naeppe tilstraekkelig klart, hvor betydcligi forandringer i genitalia og delvis ogs& i mammae ie nu anvendtc betydelige og langvarige dosering >r kan fremkalde -- det vaere sig genuine 0stroge le stoffer eller syntetiske Fra Herning Sygehus, kirurgisk afdeling. C hef: O verkirurg E. TtflbfiU. Efter at W i n d a u s , B u t e n a n d t m. fl. omkring 1933 liavde fastslet de naturligt forekommende 0strogeners konstitutionsformel og vist, at aile var noert beslgtede og afledede fra en cyclopentanofenantrenkerne, l det nr at hfte sig ved det formelmssigc slgtskab med visse af de skablte canccrigene kulbrinter -- og deraf f0rst og fremmest med metliylcholantrenet -- der kort i forvejen var blevet isolerede fra tjreprodukter eller syntetiserede ( Cook et al.), navnlig efter at det var pvist, at visse af disse canccrigene kul brinter havdc 0strogen virkning. Det bar imidler tid vist sig, at det konstitutionsmssige bindeled mellem de to grupper stoffer -- cyclopentanofenantrenkernen -- ikke er npdvendig hverken for den pstrogene virkning (estilbiner) eller den can ccrigene virkning, ligesom det ogs er vist,* at den canccrigene og den pstrogene cvne ikke er identiske, idet der findes talrige strkt aktive canc rigne kulbrinter, der ikke bar ringestc pstrogen virkning. Ydermerc m man nppe lgge for stor vgt p et sdant kemisk slgtskab, idet det er l i / 9 1950 1289 i E