Document bBmEB3rGQGa3Qn0kDO4qGro3D

f'-uL/- '* U 1/ Chronic toxic liver dataage In Svorkers oi PVC producing plants H.J. Klarsteller, W.K. Lclbach, R. Wilier, S, Jiihe, C.E. Lange, K.G. Rohner and G, Veltman Department of Medicine (Chairman, Prof. Dr. H.J. Deingler), Institute of Pathology (Chairman, Prof. Dr. Gedigk), Department of Dermatology (Chairman, Prof. Dr. Leinbrock), University of Bonn. Deutsche Medizinische Wockenschrift 98, 2311-2314, 1973 Polyvinylchloride V'VC) has been--produced for more, than 30.-.years; it is used in many industries and therefore is manufactured on a large scale throughout the world. The fact that up to 1966 there were no published reports in the Western Hemisphere on chronic toxic effects is largely due to the widespread be lief that only relatively inert substances are involved in the production of PVC. * Since 1967, there were reports from Romania, France, England, U.S. and Germany describing a disease characterized by Raynaud's syndrome, skin changes, pseudo-scleroderma; on the basis of. a total number of 55 cases this disease was named ''occupational acroosteolysis." In some of the papers there had been mention of hepatomegaly and hypothyroidism in the exposed workers. Out of the 55 mentioned eases, the symptomatology had brought up a suspicion of liver disfunction in eight. The main focus of attention being the occupational acroosteolysis, the problem of liver damage, first reported in 1949 in Russia in workers of PVC producing plants (in 15 out of 43 exposed workers), was obscured. The reported toxic hepatic damage in 50 out of 163 exposed workers, in a paper from Romania, and the "Subclinic chronic-epithelial hepatitis" in 15% of examined workers in another Russian paper did not receive the necessary attention. .. In several workers of a PVC producing plant, the authors observed esopha geal varicosities, splenomegaly and nonspecific liver damage. These ob servations, together with the above-mentioned reports on "subclinic liver damage" determined an investigation of the pathology of these changes. Radiologic, biochsmic, enzymatic methods, liver scanning, laparoscopy and liver needle biopsy were used in 20 workers ofa PVC producing plaut (age 30 to 56 years) , length of exposure 1/2 to 21 years) There were a total of 120 workers involved in the production of PV$; 45 of them had been examined at the Department of Dermatology, some because of manifest skin changes, but many were given & preventive examination. AP00024250 In most of these 45 workers, the examination ro'sulted in a clinical and/or biochemical suspicion of livei* damage. 4 Until May, 1973, it was possible to perform laporaseopy in 20 of these 45 workers mainly in those with a higher degree of suspicion. The prevalence of liver dammage in-workers exposed in the PVC manufacturing* plants could not be evaluated on this basis only. The results ax*e given in two tables. Table 1 presents clinical ami biochemical changes. In 13 cases out of 20 the liver was found to be enlarged (with 1.5 to 3cm). Two patients had pain on palpation in the HUQ; hyperlipidemia had been diagnosed in 1967 (after six years of exposure) in another patient, together with "liver damage." . In only one patient was there a history of jaundice in 1955, before the onset of exposure; in 1968 a diagnosis of chronic liver dysfunction had been established. There was no history of alcoholism. Splenomegaly was found in 7 out of 20 cases (range 1.5 to 5cm). Bilirubin (total) exceeded the upper normal limit of lmg/lOOml in three cases (range 1.11.7mg/100ml). The bromsulphalein test was abnormal 05% after 45 minutes) in 19 cases (range 6.1-21.5). SCOT exceeded the upper normal limit of 12mU/nil in 17 cases; in 14 cases SGPT was elevated (range 15-30). An increased level of alkaline phosphatase was found in two patients OdSmU/ral) . Hypotrombocytemia (less than 150 x IQvran^) was found in 19 out of do patients, at least initially; in 12 the initial level was lower than 100 x 103/mn3. Acroosteolysis was present in four patients* BSR, CBC, glycemia, urinalysis, LDH, cholinesterase, acid phosphatase, iron and copper serum levels, proteinawia ana electrophoretic separation of serum proteins, cholesterol, B-lipoproteins, tryglycerides and plas matic coagulation factors were not found to be abnormal. Rheumatoid factor, AtfA, LEcells, immunoglobulins G, A and M, complement fractions B.A and cold antibodies were checked initially, for the pur pose of differential diagnosis with scleroderma, but were not repeated. Australia (SH) antigen*was always negative. In only one case was there e cholelithiasis; a solitary gallbladder stone, not interfering with normal bile flow. Table 2 presents the results of radiology, laparoscopy and histologic examination. . In three cases varicose esophageal veins (and in two cases also.of the gastz*lc fundus) were visualised. Laparoscopy showed the following changes: capsular fibrosis (in 15 cases), reorganization of the liver architecture (in S cases), splenomegaly (in 7 cases), portal hypertension (in 2 cases) and hepatomegaly (in 4 cases). AP00024251