Document Xz2yEvMx3bM40N1Z2aa014X3J

J. Soc. Occup. Med. (1991) 41. 10- 16 l oK Persistent Liver Dysfunction among Workers at a Vinyl Chloride Monomer Polymerization Plant S. F. HO. W. H. PHOON, S. L. GAN and Y. K. CHAN Department of Industrial Health, Ministry of Labour. Singapore Sonmary Thirteen workers with persistent abnormalities in one or more liver function tests (LFT) at a vinyl chloride monomer (VCM) polymerization plant were investigated. Twelve workers were found to have VCM-induced liver dysfunction based on circumstantial evidence. They were employed between 1971 and 1982 when the VCM levels ranged from 1 to 21 p.p.m. After 1982 when the environmental VCM levels were controlled to below 1 p.p.itL, no cases of VCM-induced liver dysfunction were detected. In most cases, glutamic pyruvic transaminase was the earliest parameter to be raised. The second most common parameter is serum gamma glutamyl transpeptidase. The latent period ranged from 1 to 13 years. An improvement in their LFT results was shown by 83.3 per cent of workers within 6 months to 2 years after removal from further VCM exposure. For workers who returned to VCM work, their LFT became abnormal again. Liver scans showed hepato and/or splenomegaly in most cases. Liver biopsies on 9 workers were reported as 'non-specific fatty changes' of varying degrees. These observations highlight the need for continual vigilance with environmental monitoring and medical surveillance of VCM-cxposed workers. Introduction The detection of hepatic angiosarcoma among workers in a vinyl chloride polymerization plant in the United States1 led rapidly to surveys of workers in such factories2'1. Since then, industrialized countries throughout the world have become increasingly concerned over the potential health effects of vinyl chloride monomer (VCM). This paper presents the findings on 13 workers with persistent liver dysfunction detected during a medical surveillance programme at a VCM polymerization plant and proposes a systematic plan of investigation. Materials and Method A VCM plant was set up in Singapore in the early 1970s to produce polyvinyl chloride (PVC) powder by the polymerization of VCM. Medical examination for workers at this plant started in 1975 on a voluntary basis. Tests were done to look for evidence of liver disease. These tests comprised the biochemical liver function tests (LFT): serum bilirubin, serum alkaline phosphatase (AP), serum gamma glutamyl transpeptidase (GGT) and the transaminases, serum glutamic oxaloacetic transaminase (GOT) and serum glutamic pyruvic transaminase (GPT). If the initial LFT was normal, similar tests would be repeated annually. If there was one or more abnormalities, the abnormal test(s) would be repeated in 3 months after advising the worker to abstain from alcohol. If the abnormality persisted, the worker would be required to undergo a comprehensive physical examination including biochemical tests such as carcino-embryonic antigen (CEA), alpha foeto-protein (AFP), hepatitis B antigen (HBsAg) and a technetium* 99m liver colloid scan. However, this surveillance !C 1991 Buuerworth.Heinenianii for SOM 0301-0023/91/010010-07 programme was not carried out systematically nor was there proper supervision. Liver function tests were analysed at 3 different laboratories. However, the type of LFT abnormality reported was fairly consistent among the 3 laboratories. All these were later rectified by 1983. All workers who had persistent abnormalities (on at least 1 repeat test) in one or more LFT and with 1 or more years of exposure formed the basis of this report. A detailed occupational, medical and alcohol history was obtained from each worker. A complete physical examination with special attention to the liver, spleen, skin and extremities was done. The laboratory tests included technetium-99m liver colloid scan, HBsAg. CEA and AFP. The latter 3 were done by radioimmunoassay method. Liver biopsy was only done on 9 workers who were still with the plant at the time of this review. The specimens were read by 2 pathologists independently. Environmental assessments comprising area and persona] sampling were carried out on a periodic basis at different sections of the plant. Area sampling had been carried out at monthly intervals since 1976 by the company's safety officer using Kitagawa detector tubes and a photo-ioniser (HNU model P101). Personal sampling was started in 1983 by our department, using 3M organic vapour monitors. Sampling duration was about 5-7 hours. The samples were analysed by carbon disulphide desorption and gas chromatography in accordance with the NIOSH Method No: P & CAM 178. The results erf the medical and environmental monitoring are discussed in this report Results The Plant The VCM was purified before it was charged into reactors containing de-ionized water and peroxidase initiators. The reaction took place in batches in the 6 autoclaves (reactors) to produce PVC shiny. At the end of the polymerization, the unreacted VCM was recovered by evacuation. The PVC slurry was further stripped of VCM before it was centrifuged to remove the water to produce PVC powder. The PVC powder was then packed and supplied to other factories where it would be used for the manufacture of PVC pipes, resins, etc. Our 13 workers came from various sections of the plant. Exposure to vinyl chloride monomer The highest exposure occurred during reactor cleaning. Here, workers were required to enter the reactors to clean UCC 060739 and scrape the scales formed during the reaction. Although the reactors were purged with air before they were opened, residual VCM still remained in the PVC scales. Prior to 1976. cleaning was done manually and workers were required to enter the reactors after every batch. In 1976, this method of cleaning was mechanized by the use of a high pressure water hose. This reduced the frequency of entry of workers into the reactors from once per batch to once in every 10 batches. The general environmental VCM levels measured in 1976 ranged between 1 and 20 p.p.m. with a geometric mean of 6 p.p.m. No measurements were done before 1976, but we can expect levels to have been higher. The installation of a VCM recovery system in 1980 further reduced the residual VCM in the reactor after polymerization. All control rooms were air-conditioned by 1982 and fresh air intake for this air conditioned system was taken from the environment away from the process area. In 1983, the residual VCM in the PVC slurry after leaving the reactor was greatly reduced from 10000 p.p.m. to less than 10 p.p.m. after incorporating a stripper to further remove residual VCM. This reduced the VCM exposure at the drying and packing sections. To further reduce exposure, a quality control valve was installed in 1986 to obviate the need to open the reactors during the taking of samples for quality checks. As a result of the various engineering measures instituted, the general environmental VCM levels were significantly reduced from a geometric mean of 3.9 p.p.m. in 1976 to 1.5 p.p.m. after 1983. However, workers could still be exposed to high, albeit short term levels of 10 p.p.m. especially when entenng the reactors and when taking samples. LIVER DYSFUNCTION AND A VCM POLYMER PLANT 11 Personal samples of VCM were much lower (range: 0.1 to 0.5 p.p.m.) than the results of area sampling. They were more representative of workers' exposure during a workshift. Personal and Occupational Profile Since 1975, a total of 271 workers had undergone medical examinations. Thirteen of them (4.8 per cent) had persistent abnormalities in their liver function tests. They were males aged between 19 and 55 at the time of the first abnormal LFT result (mean - 28.6 years). All had worked at least one year in the VCM plant. They began employment in the period 1971 to 1982. Their mean exposure duration (at the time of first abnormal LFT result) was 5.1 years (range 1 to 13). Table / gives the summary of the nature of their work and their degree of VCM exposure. Alcohol consumption was very low except for 1 worker, J. He drank about 3 bottles of toddy (an alcoholic dnnk obtained from the juice of the cut fiower of the coconut palm)every week and brandy/whisky occasionally. Three were ex-drinkers (had stopped drinking for at least 1 year prior to the time of the first abnormal LFT results). Four were teetotallers. The rest were social drinkers. Medical History None had a history of jaundice, blood transfusion or Raynaud's phenomenon. Two of the workers were diabetics (J, M). Six workers had symptoms during work. The symptoms were usually non-specific and vague. All had complaints of nausea with four experiencing dizziness as well. Two of the workers (M. G) mentioned that they Table I. Nature of work and degree of exposure to vinyl chlonde monomer (VCM) in the 13 worker* Section So of workers Sature of work Range of environmental VCM levels f p.p.m. I Before 1983 and 1983 after* Purification Polymerization t 3* Drying and packing Maintenance including electrical service 4 5 Checking for leaks: Monitoring of VCM levels: control the pump valves and condenser Charging of VCM. catalyst, etc into reactors: Taking of samples for quality checks: cleaning of reactor*: opening of valves to release unreacted VCM into storage tanks Checking and taking of PVC samples for moisture test; washing of slurry tank: packing PVC into bap: general housekeeping Maintenance and servicing of pump*, compressors: welding of faulty VCM pipes l including work in a sister company with no VCM exposure) 1 :-is 06-18 0,7-:,9 1-11 0.7-2.8 Exposure varied depending on the type of maintenance work and where it was carried out. * One worker had worked for I year ai the drying section and about 6 yean at the polymerization section. + VCM levels after the implementation of vanout engineering control measures. ucc 060740 t o cclpatio nal m edicine ( 1991) vol. 4 | no. ucc 060741 Tahir H. Summit* o< Ik dtnkil Siding! Md in,lignum itMiht ollkl) ttn H'odrr A Apr* frr dbuewal TFT remit 25 5ft tkm PwAcaiion B 23 fttkiat C 19 D* M Drymg A P**g Pdjwerinim 2* FM Polymerirarion Maintenance n 22 H 30 Drying & pnekinf I 32 j 55 MmUamcc F S 1 K 29 1. 29 M 27 Maintenance Drying A pwimf Krar fmuwj im Pirrlw'M ITO INI IWI 4 1979 HI) ' 4 mi 4 1973 197* 4 1921 1990 1975 mi Smpaw Printtap Kmm titw MM Juuary AnriM d rtpowre lymril m ftnt abnormal tST rrwfl Drinker |2 Jbnlllnaf bccr/mon*h a 5-9 * years) 4 DiMct t It IgUumrf kccr/KHNitfc a 1 1 imt Smppit kl*m - - Non-drinker 1 1 Drinker 13 Cl 2 hmiki id hm/norili. Slopped in I979| * Nnn-draiker 4 I 1 1 Bankinker 1 |l glass of beer/ week. Slopped In 19741 1 4 Non-drinker 2 DrHiker |1 2 hollies cd heef/moath Slopped m mn 7 + 4 F.e-drinker 4 (1/2 bolllc id bccr/mnalli x 14 yn Slopped m I979| Drinker |.1Mllndliddr/ 7 week 4 blend)!/ * 20 ycarsl Non drinker 3 41 Ili-drinker 11 hire beer every 2 3 days * 7 yean Slopped tm 1977) Hunter |2 1 hriilri id hcci per nmnlk 9 years. Slopped m 1992) 5 Tm *4 UT Bd Bil OPT OPT. GOT OPT* GOT OPT* GOT, GOT GPT. GOT. GOT GPT. GOT* GOT GPT, GOT, GOT GPT, GOT. AP GPT, GOT. GOT. AP GPT, GUT. GOT, AP CiPT. GOT. (iPT. AP, M iJofr scan rew/ks Mild hepalomegaiy Moderate liver pnrcncbyma MiM hqmlnmMljr Mild bepaioapkaomegaiy Normal Mild liver parenchyma) damage Mild aplenomefaly Mdd bepnloiplranmegaly Mdd hepalopknomegaly with early liver parenchymal Mild iphnomcpaly Normal Normal Mild hepatomegaly Hepatomegaly DlmtwMlx tGdberii with probable VCMmducrd k*er dysfunction t Gribcris with probable VCM-iadwccd liMr dysfunction VCM-induced liver dysfunction tVCM-mduced liver dysfunction t VCM induced liver dydunclirm t Probable VCMinduced kvei dysfunction t Probable VCM induced liver dysfunction t Prnhahk Vt M mduced hver dysfunction t Probable Vt M induced liver dysfunction Alcoholic bier cirrhosis with diabetes mdlilus VCM -induced hver dysfunction t Prohahie VCM-induced liver dyAmclion VCM-induced hver dysfunction arih diabetes mcHilot * Wnfler lud linked for I yeai al ihc drytap ^ciImid awl ahmil h year* at 1 lie polymcrr/alma kiImwi 11 iver biopsy done I ft ilrinkcr h>nc wImi slopped drink Hi( fur al leaM a year prun In dale <4 lirM ahwirmal rcsidl) IOW fmt id netphl. I <M. bt .4 apprrile, I I T. liver JuneJnm led. M. MwhIm. CilT. tfnw yhuama pyruvir framMiMi. (HIT. era* pnw phrianyl irempcfMMtac: GOT. lerim jtlulamic udnictljc InnumitMc; V( M. vinyl eMornfc nwomer. AP, alkaline phosphatase experienced nausea especially during the washing of the sluny tank. Three had loss of appetite while 2 had complaints of weight loss. Worker F had all of the above symptoms. Table II summarizes the clinical findings and investigation results of the individual workers. On examination, all were well built and clinically well. None had any jaundice, hepatosplenomegaly or signs of liver disease, sclerodermatous skin changes or acroosteolysis. Hepatitis B antigen, carcino-embryonic antigen and alpha foetoprotem were not present in all 13 workers. Serial Liver Function Tea Results Table III gives the serial LFT results. Of the 13 workers investigated, 3 workers had only one persistent LFT abnormality, 2 had 2 abnormalities and 8 had 3 or more abnormalities in the battery of tests. WORKERS WITH ONE LFT ABNORMALITY Workers A and B had raised bilirubin and worker C had raised GPT Workers A and B were confirmed to have benign unconjugated hyperbilirubinaemia (Gilbert's syndrome). Their bilirubin levels fluctuated from 1.4 to 2.6 mg/100 ml and remained so even after removal from VCM exposure. Worker C`s serum GPT level became normal after removal from VCM exposure and was raised again on return to VCM work. These findings support the diagnosis of VCM-induced liver dysfunction. WORKERS WITH TWO LFT ABNORMALITIES Workers D and E had raised GPT and GGT levels, and GPT and GOT levels respectively. They worked in the polymerization section and their LFT improved when they were removed from VCM exposure. However, their LFT became abnormal within a year ofreturning to VCM work. As alcohol and viral hepatitis were already excluded as possible causes, these findings were consistent with the diagnosis of VCM-induced liver dysfunction. WORKERS WITH THREE OR MORE LFT ABNORMALITIES Eight workers had 3 or more abnormal LFT results. All except M (there were no previous LFT results for comparison) had normal LFT results prior to the development of the persistent abnormalities. These abnormalities developed within 1 to 7 years of starting work (mean 4.3 years). Three workers showed an improvement in their LFT results within 6 months of removal from VCM exposure and in workers G and K, the results returned to normal. These 2 workers were removed from further VCM exposure within one and a half years of developing the abnormal LFT result Workers G and M who returned to VCM work re-developed abnormal LFT results. These findings supported the diagnosis of VCM-induced liver dysfunction. In addition, M had diabetes mellitus which was controlled with insulin injections. The remaining 3 workers had fluctuations in their LFT results. Workers F, H and I were in the maintenance section where the exposure to VCM varied depending on the type and place of work. This may account for the fluctuation in their LFT results. However, where there was documented removal from VCM exposure, their LFT results improved suggesting that they probably had VCM-induced liver dysfunction. In the case of L. we could Lives DYSFUNCTION AND A VCM FOLVMER PUNT 13 not explain the fluctuation in the LFT results, although there was definite improvement when he was removed from further VCM exposure. He probably had VCMinduced liver dysfunction. Worker J had a history of drinking about a bottle ofbrandy/whisky and 3-4 bottles of toddy at least once a week for the last 20 years. His LFT results fluctuated probably with variation in his drinking habits. There was also no improvement in the results after removal from further VCM exposure, thus suggesting that alcoholic liver cirrhosis was the most probable cause of his persistent liver dysfunction. He also had diabetes mellitus which was well controlled by tolbutamide. Limp Scan Results Four workers had hepatomegaly and four had hepato splenomegaly. Two workers had only splenomegaly. The rest had normal liver scans. Enlargement of the liver and spleen was based on an enlargement of 2 cm or more when compared to the normal spans for liver (13 cm) and spleen (8 cm) in our local population. Biopsy Findings Liver biopsies were carried out on 9 workers. The liver tissues showed normal lobular architecture. There were mild to moderate fatty changes. Porta) tracts were normal except slightly widened by aggregates of chronic inflammatory cells in the case of worker C. In 3 cases, there were aggregates of mononuclear cells among the fat vacuoles. Kupfler cells appeared active in 3 cases. Sinusoidal dilatation was present in worker I and in workers B and D, the bepatocytes displayed megalocytosis with enlarged darkly stained nuclei. No malignant change was observed. The histological diagnosis was non-specific fatty changes of varying degrees although none was obese clinically, 3 were ex-drinkers, 2 were teetotallers and the rest were social drinkers. Diagnosis For the 9 workers who had liver biopsies, three had VCM-induced liver dysfunction and 4 were probable cases as explained earlier. The remaining 2 were confirmed as having Gilbert's syndrome. In addition, they probably had VCM-induced liver dysfunction in view of the abnormal liver scan and biopsy reports which could not be explained by Gilbert's syndrome alone. Hence, ofthe 13 workers with persistent liver dysfunction, 6 were caused by exposure to VCM (I had in addition diabetes mellitus), 6 were probably VCM-induced (2 had in addition Gilbert's syndrome) and 1 had alcoholic liver cirrhosis with diabetes mellitus. Discussion Our study showed 13 (4.8 per cent) workers with persistent liver dysfunction. Of these, 12 workers had VCM-induced liver dysfunction (6 possible and 6 probable cases) based on circumstantial evidence and after excluding alcohol and viral hepatitis as possible causes. The discussion centres on these 12 cases. ucc 060742 14 OCCUPATIONAL MEDICINE (1991 ) VOL. 41 SO. I They suited employment in the plant between the early 1970s and 1982. While there were reports of high VCM exposures of about 100 p.p.ro. in the 1970s1* 5, VCM levels in our plant would be considered low, ranging from 1 to 21 p.p.m. before 1983. After the institution of the various engineering control measures, the VCM exposure levels in the production area ranged from 0.6 to 2.9 p.p.m. and were less than 1 p.p.m. most of the time since 1983. These levels were well below the recommended ACGIH threshold limit values of 5 p.p.m.6. However, the VCM exposure could be high during the washing of the slurry tank as 2 workers had complaints of nausea whilst carrying out such work (the odour threshold being 2000 to 3000 p.p.m.T). Workers employed after 1982 showed no evidence of liver dysfunction suggesting that VCM exposure with regard to inducing liver dysfunction has a biological threshold. It appears that VCM-induced liver dysfunction is unlikely to occur at levels below 1 p.p.m. The strict supervision on the usage of air-line respirators during reactor cleaning in 1983 may be an added factor. Since 1974, most of the countries having PVC manufacturing plants have lowered their threshold limit values for VCM. The United States and Sweden had lowered their threshold limits (8 hours time weighted average for VCM to 1 p.p.m.)*. Raynaud's phenomena, acro-osteolysis and sclerodematous skin changes had been associated with past heavy exposures to VCM1,7 *. It is not surprising that these were not detected in our workers as the general VCM levels in our plant are low. Aryanpur* and L3i$ al.* found the liver changes (hepatomegaly, tenderness on palpation, abnormal LFT results) to be reversible after cessation of exposure. The liver progressed to what was stated to be `chronic hepatitis' when toxic exposure continued. Ginically, the liver was not palpable in all our cases although the liver scan showed hepato/splenomegaly of varying degrees in 10 of our workers. It is reported that the ability of the traditional biochemical tests to predict the presence of underlying histological hepatocellular damage is at best 80-83 per cent accurate10. The most effective test was GPT followed by GGT. Other studies showed that GGT was the most useful test in detecting abnormality and reflecting the extent of liver damage"13. On reviewing the serial LFT results of our workers, we noted an elevated GPT to be the most common initial finding with GGT being the second most frequently raised parameter. In 9 of our cases, the liver dysfunction progressed rapidly upon developing the first abnormality. (The rise in LFT results were 1-2 times normal as compared to many more times in cases of infective hepatitis.) It took from 6 months to 4 years for the second parameter to become abnormal if the affected workers were not removed from further VCM exposure. Of our workers 83.3 per cent had improvements (10 out of 12) in their LFT results within 6 months to 2 yean after removal from further VCM exposure. For the 3 workers who had only one LFT abnormality initially, their LFT returned to normal on cessation of exposure. Of the 8 workers who returned to VCM work, their LFT results became abnormal again within 3 months to a year. These observations suggest that if progression of liver dysfunction is to be avoided, a worker should be removed from further VCM exposure upon developing an abnormality. The elevated LFT results would then improve, indicating reversibility of dysfunction, at least in the early stages. In our 12 workers, the latent period for the development of liver dysfunction (from first exposure to date of first abnormal LFT result) ranged from 1 to 13 years (possible cases: range - 1 to 13 years; median - 2.5 years; probable cases; range-4 to 7 years; median-6.0 years). This latent period is much shorter than that reported for the development of angiosarcoma, which takes at least 10 years7131*. Thus, for the present, it is not known whether our workers will suffer from angiosarcoma of the liver at a later time. The full magnitude of this site-specific cancer risk among our workers will only be determined following full lifetime observation. One worker (H) has died of a cerebrovascular accident after a fall at home. The chronic manifestations of VCM injury to the liver were well illustrated by the sinusoidal dilatation with sinusoidal cell activation, subcapular fibrosis, peliosis hepatitis, cirrhosis and finally angiosarcoma11. The liver biopsies of our 9 workers were reported as non-specific fatty changes' of varying degrees although 2 were teetotallers, 3 were ex-drinkers, and the rest were social drinkers. Whether these were a misdiagnosis or the precursor stage of angiosarcoma is yet to be determined, as these features may be found in a variety of clinical conditions such as obesity, diabetes mellitus. non-A, non-B hepatitis and vinyl chloride toxicity15-16. Conclusion Exposure to VCM in industrial settings can produce hepatic fibrosis with angiosarcoma of the liver as a late manifestation3 *. The early detection of such liver disease may be of great industrial and public health importance because it remains a possibility that very early liver abnormalities may be reversible or non-progressive after workers are removed from funher VCM exposure. Our cases of VCM-induced liver dysfunction are a relatively young group of workers in which little disease and few deaths would be expected to occur. All were below 33 years of age at the time of diagnosis. These data indicate the need for continual vigilance with environmental monitoring and medical surveillance. Until specific tests for hepatic angiosarcoma or VCMinduced liver damage are available, we believe that our medical surveillance programme will aid detection ofliver abnormalities in a possibly reversible or curable state (Table IV). Our programme involves early removal of workers with trial re-exposure. In addition, we also started a system whereby all workers exposed to carcinogens are followed-up on a regular basis for life and are registered with the local Cancer and Death Registries who will notify us upon their deaths or if they develop cancer. This may later provide useful information on the cancer risk among our exposed workers. Acknowledgements We are grateful to the Permanent Secretary (Labour) for permission to quote from depanmental records and Mrs Marsita Zain for typing the manuscript. ucc 060743 t in fu 3** <^Two 55.8is -w4 r^ (3i 3 O' (~ 2 II ^SigS_,*S! "? n2 r"2_,53-^< 5=i'=b!223<4: >?? = =.-g " St iS=|-^f55'<&(ug Is-gl^e-E-SToQ ae-SSS &?gs-| Sa&kickaSacS fi r? 3 S! .. ft Q 2 e Q is. O n 5 iT * a. 8 t*N*- tit I nUw>up liver funcltoa lal mulls m JJ workers csposcil In vinyl chloride monomer pnlymcrualMMi* II II iwtir IVor **t ttrst tdmttrmui reitdr Tw*l ubmwmtd rrsutl A I9M Hd SBIefore II 197H *1 NA RdM 7H 4' NA m\ GPT 1W1 ore J> 19*4 GtiT NA Before NA 1 m\ CiOT Before NA 1 IWI (iPT choc NA t, mi GPT Before CiOT NA II tww (iPT Before 77 CHiT NA 1 two (iPT Before NA 1 I91H AP choc 77 NA K mi GtiT Jui si Maraud 1 ma GPT Before 71 CiGT NA M mi GPT Before II (KIT NA Si'tiuI mhm*md h**r t*uu sum r*-W rruftv MUJhI ni Noraul Ae7a Bd Aaf Normal Sq>n H A#rM Ah mi Normal Mar 7* N MU MM M (lei 79 Bd Oei *4 CK1 M Normal Aug HO Normal Jim IJ JaMl HA Normal Jul Hi tu May HA IW* Ol| Hi Numul Jua Hft IM Jua HI Numul (hi Hft HO Aug Hi IM fch |7 Bil Jul H4 May HJ Jaa Hft Numul B*l Bd* Jua Hft Bd Oct 1ft B4 Feb IT Bd GPT* Ah 77 Numul Normal** Sep 71 Normal GPT (lei 79 Normal lul II Noraul lul ft! Normal tXltt GPT Aug >J CiOT* Mar HI Normal Ah AaflJ Mar M GPT Ah m Normal Inagged Ah 1* Jal II Niumal NmM Jul M CiCiT Apr M Numul** Jul *2 Numul Ah m Jul H4 Numul Mar HI Ntrrmal Nm JH May H5 CiPT Jul 14 GPT CiCiT May 13 Jaa (ft CiPT GOT (M *4 CiPT CHiT CiOT <M Hft Ocl M CiCiT* Mar Hft CiPT May Jua Hft Normal** (iCiT CiPT Jua Hft Jal 17 CiPT* Ocl It Jal H7 GGT GPT GGT GPT Owl of ecibrovtwcater ecodeal alter a bit at Soate Apr H3 GPT CHiT CHIT CM 17 May (3 CiPT* cMiT Sep H3 (iPT CiCiT CiPT (M R3 CiPT** Mar Hft GPT CiCiT GOT Aug M GPT GGT Jaa IT GPT* GGT GOT Apr 17 GPT GGT GOT Inipwl Numul CiPT* CSOT Ah 77 Sefi 7a Numul Normal Ocl 79 Numul GPT Ah 77 Ah 7B Normal AP Normal** OGT On 74 Niamal on m CiPT Sep 7* AP Ah CiPT* GGT Jeb HI CiPT CiCiT CiOT Mar 79 AP Jul 12 Ah >3 Numul GOT Jut M GGT Ah 7t Ocl 79 Normal Normal Jul K GPT CiCiT Sq>*2 GPT GGT (HIT Ah GPT GGT iaa *1 GPT* GGT (AIT AP Oci M CiCiT* CiPT GOT CM MB GPT' Mar *1 CiPT** CiC. 1 GOl CIPT* CiCiT CM HQ CiPT** Normal Feb HI CiPT Noraul Normal Jul HI GGT CM HI Jul *2 Norawl CiPT CiGT lul HI Jul H2 Normal OPT Sep H2 Aug HJ Normal GOT Jul (4 CiCiT Sep m AP Teh HI AP Jul Ni AP GGT CM HI Nov >1 Numul AP May 13 Oei 13 CiCiT GGT AP Jaa (ft Normal iengaed Teh HI CiPT GGT AP Apr HI CiPT* GGT GOT AH Jul HI Noraul Jul JO CiPT CiCiT GOT Jul *2 CiCiT Aug Hi tiCir** Sep 12 CiPT CiCiT GOI AP CM HI CiPT CiCiT AP JM CM II CiPT CiCiT GOT Jul K4 CiPT CiCiT GOT Sep 12 MM Normal GPT GGT Oei M GGT Jiaa 15 GPT GGT Nov 14 CiPT CiCiT GOT Ocell Numul Jaa 15 OPT* CiGT CSOT Jal U Normal May B3 CiPT GCiT GOT ah >3 AP Od 13 GPT GOT Jal M AP GGT May 13 Ocl 13 Jaa Ift GPT GGT Jaa (ft GPT GGT GOT Ocl 16 GPT GGT Jaa 17 GPT GGT GOT Ocl M GPT GPT May 13 Mar 17 AP AP* AP GGT GPT Jaa GPT GGT May 17 AP GGT Jaa BJ GPT* CiCiT CiOT AP CM 14 CiCiT Bit Mar GPT CJCiT Apr HJ GPT CHiT ah u GPT GCiT Oct *4 GPT GGT (iOT AP May 13 Oec 13 GPT GCiT Bd GPT CHiT (HIT AP Jul U May 13 Jaa 1ft Normal** GPT* GGT CiOT AP GPT GGT GOT AP csigacd Ocl Ift GPT GCiT GOT Iaa IT GPT GCiT Bellied j ii GET GCiT AP ucc 060744 16 occupational medicine (1991) vol. 41 so. I Tablt IV Medical surveillance of vinyl chloride monomer (VCMI exposed workers Workers with any VCM exposure i _____________--------- ---------------------------------------------- Annually 1 GOT, GPT. Bil AP, GGT Normal- I One or more abnormal results l ------ 1-------------------------------------- Repeat the abnormal testis) in 1 month after advising worker to abstain from alcohol l Still abnormal 1 Interview and physical examination HBsAg. Ultrasound of liver and spleen Normal HBsAg Normal ultrasound result I Temporary suspension *3'i: 1 I1-Repeat LFT Still abnormal i Temporary suspension * 3 II l Repeal HBsAg i HBsAg +ve 1 Temporary suspension x 3 12 i Repeat HBsAg I HBsAg still -rve i -------. Permanent suspension --------- J To follow up with 3 monthly LFT I Progressive deterioration l Consider CT scan, liver angiography + biopsy* * Consent for a biopsy should be obtained from the worker. Suspension, removal from further VCM exposure. LFT, liver function test: GOT, serum glutamic oxaloacetic transaminase: GPT. serum glutamic pyruvic transaminase: Bil. bilirubin: AP. alkaline phosphatase: GGT. serum gamma glutamyl transpeptidase: HBsAg. hepatitis B antigen. REFERENCES 1. Creech, JL, Jr, Johnson MN. Angiosarcoma of the liver in the manufactutt of polyvinyl chloride. J Occup Med 1974:1*; 130. 2. M'akk L, Creech JL, Whelan JG. Johnson MN. Liver damage and angiosarcoma in vinyl chloride workers A systematic detection program. J Am Med Aitoe 1974; 230: 64. 3. Litss R. Anderson H. Nicholson WJ, Damn S, Fisehbcin AS, SelikofT U. Prevalenot of disease among vinyl chloride and polyvinyl chloride workers Am N YAcad Sri 1975; 146: 21 4 Heldaas SS, Langard SL, Anderson A Incidence of cancer among vinyl chloride and polyvinyl chloride workers. Br J Indiat Med 1984; 41: 25. 5. Sugita M, Meeuda Y, Tsuchiya K. Early detection and signs of hepatoangiosarcotna among vinyl chloride workers. Am J India Med 1986; Id: 411. 6. American Conference of Governmental Industrial Hygienists Threshold Limit Values and biological exposure indices for 1986-1987, Cincinnati, USA: 39. 7. Parmeggiani L. Encyclopaedia of Occupational Health and Safety. 3rd (Revised) edit. Geneva: International Labour Office, 1983: 2256-7. 8. Aryanpur J. Vinyl chloride: Its impact on occupational medicine practice in Iran. J Occup Med 1977; 19: 689. 9- Nicholson WJ, Hcnneberger PK. Sridman H. Occupational hazards in the VC-PVC industry. Prog Clin Biol Res 1984: 141: 155. 10. Tamburro CH, Greenberg R. Effectiveness of federally required medical laboratory screening in the detection of clinical liver injury. Environ Health Penpect 1981; 41: 117. 11. Creech JL, Jr, M'akk L Liver disease among polyvinyl chloride production workers Aim N Y Acad Sri 1975; 246: 88. 12. Tamburro CH. M'akk L. Popper H. Early hepatic histologic alterations among chemical (vinyl monomer) workers Hepatology 1984; 4: 413-411 13. Spinas R, Kaminski R. Angiosarcoma of the liver in vinyl chloride/polyvinyl chloride wotkets An update of the NIOSH Register. J Occup Med 1978; 18:427. 14. Forman D, Bennett B, Stafford J, Doll R. Exposure to vinyl chloride and angiosarcoma of the liver; a report of the register of cases Br J Indust Med 1985; 41: 75a 15. Briunwald E, Isselhacher KJ, Petersdorf R G. Wilson J D. Manin JB. Fauci AS. Harrison's principles of internal medicine. 11th edn. New York: McGraw-Hill Book Company. 1987; 1353-4. 16. Wagoner JK. Toxicity ofVinyl Chloride and Poly( vinyl chloride): A critical review. Environ Hhh Perspectives 1983: 52: 61-6. Requests for reprints should be addressed to: Dr S. F. Ha Senior Medical Officer. Department of Industrial Health. Ministry of Labour. 3-7 Halifax, Singapore 0922. ucc 060745