Document 375GVao6dgjO1OgV0m23Eb5kJ

UNIROYJU. \/c UNIROYAL, Inc. World Headquarters Middlebury, Connecticut 06749 September 1, 1982 URL 15417 Dr. John Stafford ICI Petrochemicals t Plastics Div. P.O. Bax 6 Bessemer Rd. Welwyn Garden City, Herts AL7 THD, ENGLAND Dear John: On page 35 of your August 2 oarpilation of angiosarccma cases, you question whether the Rcbintech plant in Painesville, Ohio (1973) is the same as Allied. There were two PVC plants in Painesville, one owned by Uniroyal, and cne originally owned by Allied and later sold to Rcbintech which sold it to Georgia Pacific several years ago. The Uniroyal PVC plant was closed at the end of 1975, but we still make nitrile rubber at the same location. The Georgia Pacific plant has been modified to make suspension polystyrene. You deserve a great deal of credit for keeping this information up to date. This infconation ccnbined with the epidemiological update planned by MGA in the U.S. will go far to clarify the risk. Best wishes, Uiait WCH/tacw cc: B. R. leach J. D. Forbes file (2) Walter D. Harris, Eh.D. Corporate Industrial Toxicologist British Journal of Industrial Medicine 19K2;39:306-307 Progression of vinyl chloride induced hepatic fibrosis to angiosarcoma of the liver D B JONtS AND P M SMITH From the Department ofGastroenterology, Uandough Hospital, Penarth, S Glamorgan, UK abstract Two vinyl chloride monomer (VCM) workers, who developed non-drrhotic portal fibrosis and portal hypertension, died from angiosarcoma of the liver five and ten years later respectively, despite withdrawal from occupational exposure. We suggest that non-cirrhotic portul fibrosis caused by exposure to VCM is potentially prcmalignant and that those workers who already have the condition should be carefully monitored. Since the original communication by Creech and results showed a normal serum bilirubin with a Johnson' there have been several further case raised alkaline phosphatase (201 IU/1) and reports of vinyl chloride monomer (VCM) induced y-glutamyl irampcptidu.sc (83 IU/1), Radioisotope angiosarcoma of the liver. A commoner hepatic liver scan showed a small liver with no filling defects lesion is non-drrhotic portal fibrosis* leading to por and needle liver biopsy showed a well-pronounced tal hypertension. It has been suggested dial this mkronodular drrhosis with no evidence to tumour. lesion may be a precursor to angiosarcoma He responded to protein restriction and lactulose formation,v* but there has been only one report of a and was discharged. Within a week of discharge he patient with documented hepatic fibrosis developing was readmitted with an endoscopicaily confirmed angiosarcoma at a later date.4 We describe two bleeding duodenal ulcer. After this, he lapsed into further eases. hepatic coma and died. Necropsy showed multiple malignant tumours in the liver (wt 1130 g), one of Case reports which was haemorrhagic Histologically, a great variety of liver cell lesions were present, some resem CASK I bling angiosarcomas, some hepatocardnomas, and A 6()-ycar old while man initially presented in 1969 some adenomas. There were also atypical sinusoidal to the dermatology department with a skin eruption. cells and fibrosis in the non-tumorous parts of the Examination at that time showed anaemia, thrombo liver. cytopenia, hepatosplcnomcgaiy, and occult faecal blood loss. He had an occupational history of expos C ASK 2 ure to VCM at high concentration for seven years A 49-ycar-old man with a 12-year history of expos while working as a polydcancr and a blowdown ure to vinyl chloride monomer while working as a recovery operator. After two haematcmcscs, barium spray drier bagger, premix operator, and paste studies and splenic venography confirmed portal charging operator was, during a factory survey of hypertension and oesophageal varices, and he process workers in 1974, found to have thrombo underwent an end-to-side portocavul shunt. At cytopenia. This was later shown to be due to laparotomy the liver looked nodular, but operative Hypersplenism and presinusoidal portal hyperten liver biopsy showed non-drrhotic portal fibrosis sion. He was otherwise well and drank five pints of only. Over the next four yeans the patient developed beer a night. Liver function test results were normal chronic portosystemic encephalopathy and maturity apart from a raised -y-glutamyl transpeptidase level onset diabetes mellitus that was treated with oral of 82 IU/1. Varices were shown by barium studies hypoglycacmic agents. In May. 1980 he presented and endoscopy, and liver biopsy showed fatty with worsening mental deterioration, hepatic foetor, change and slight non-drrhotic portal fibrosis. Two asterixis, and an enlarging liver. Liver function test years later the patient developed insulin dependent diabetes mellitus, but otherwise remained well until Received 5 October 1V81 Accepted 2o November 1V8I October 1979 when be presented with a large haemateme&is. Endoscopy confirmed oesophageal 306 Prog. vnria were alkali ieveb and ! show< tumo devel from Necn occur ruptu haem liver. oesph shorn of sin fcctcti Dim Vinyl micro cntly hepafr iiferat angle* lining space and a <r J3 and n hypert Althot of the angios GO angios observ The includ< tal hyj 10 yes portal Durinf VCM. fibrosit future necesft patient shunt 1 Non