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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Identification particulars were obtained for over 7000 men who were at some time between 1940 and 1974 exposed to vinyl chloride monomer in the manufacture of polyvinyl chloride. Approximately 99% of these men have been traced and their mortality experience studied. The overall standardised mortality ratio, 75-4, shows a significant reduction compared with the national rates. Four cases of liver cancer were found. Two of these have been confirmed by a panel of liver pathologists as angiosarcoma and two as not angiosarcoma. There is no evidence to support the hypothesis that cancers other than those of the liver are associated with exposure to vinyl chloride monomer. The two cases of angiosarcoma were found in men who had been exposed to high concentrations of the monomer although the second man died only eight years after first exposure. The industry in Great Britain has expanded considerably since the second world war with over 50% of men having entered with the last decade. Conclusions drawn about the effect of vinyl chloride monomer on the mortality experience of men in this industry must consequently be tempered by the reservation that the full impact may not yet be in evidence.
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PMID:Mortality experience of workers exposed to vinyl chloride monomer in the manufacture of polyvinyl chloride in Great Britain. 55 28

Based on the mode of action of AFB1 and the activities of its biologically active intermediates, one may conclude that: 1. The mode of toxic action of the bisfuranoid mycotoxin is through epoxidation of the vinyl ether double bond of their dihydrobisfuran functionality. 2. The DNA and plasma albumin adducts formed in vivo may be useful in the molecular dosimetry of these environmental carcinogens. 3. There appears to be a linear correlation between the steady state levels of AFB1-FAPy-DNA adducts and the carcinogenicity of AFB1. Elucidation of the molecular basis of this correlation may shed light on the mechanism of AFB1-induced carcinogenesis. 4. Consistent appearance of AFB1-DNA adducts in the livers of liver cancer patients tested is supportive of the IARC conclusion that AFB1 is a human carcinogen involved in human primary liver cancer.
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PMID:Bisfuranoid mycotoxins: their genotoxicity and carcinogenicity. 190 26

The cohort consisted of 10,173 men who had worked for at least one year in jobs involving exposure to vinyl chloride prior to 1 January 1973. These men were employed at 37 plants in the U.S., belonging to 17 companies. Observation of the mortality experience of the cohort was updated from 31 December 1972 to 31 December 1982 (the study now covering 1942-1982). A total of 1,536 cohort members were identified as having died. The observed mortality, by cause, was compared with the expected based on U.S. mortality rates, standardized for age, race, and calendar time. Analyses by length of exposure, latency, age at first exposure, calendar year of first exposure, and type of products were performed. The study confirmed that the vinyl chloride workers experience a significant mortality excesses in angiosarcoma (15 deaths), cancer of the liver and biliary tract (SMR = 641), and cancer of the brain and other central nervous system (SMR = 180). In addition, the study also found a significant mortality excess in emphysema/chronic obstructive pulmonary disease (COPD) (SMR = 179). On the other hand, the study did not find any excess in either respiratory cancer or lymphatic and hematopoietic cancer. This study also found an increase in biliary tract cancers, independent from liver cancer.
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PMID:An industry-wide epidemiologic study of vinyl chloride workers, 1942-1982. 821 53

In an update of an earlier investigation of brain tumors, mortality patterns were examined for 7849 male employees who worked at a petrochemical plant from 1941 through 1983. The update added 6 years of observation (1978 to 1983). During this period, the brain tumor (BT) mortality risk declined relative to the US population, but continued to be higher than expected in hourly workers (5 observed/3.4 expected). Similar to the earlier studies, BT occurrence was not explained by patterns of production work assignments. Mortality rates for hourly and salaried workers from all causes combined, total cancer and respiratory cancer were lower than US population rates. Lower rates for these causes were also seen for white and nonwhite production and maintenance workers. Liver cancer rates were greater than expected in white production workers (3 observed/1.6 expected) and included two men assigned more than 40 years ago to vinyl chloride-related departments. Mortality rates due to malignant melanoma were elevated in white maintenance workers (5 observed/2.0 expected) and may be explained by heavy sun exposure in outdoor work.
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PMID:An update of mortality due to brain neoplasms and other causes among employees of a petrochemical facility. 199 1

A large European multicentric cohort study has been coordinated by the International Agency for Research on Cancer with the objectives of investigating the dose-response relationship between liver cancer and exposure to vinyl chloride and assessing cancer risk for sites other than the liver. A nearly threefold increase in liver cancer was detected on the basis of 24 observed deaths and 8.4 expected (standardized mortality ratio 286, 95% confidence interval 186-425). The excess from liver cancer was clearly related to time since first exposure, duration of employment, and estimated ranked and quantitative exposures. Other cancer sites investigated on the basis of a priori hypotheses were either not in excess (lung) or apparently unrelated to the exposure variables (brain and lymphoma).
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PMID:A collaborative study of cancer incidence and mortality among vinyl chloride workers. 206 54

Based on the mode of action of AFB1 and the activities of its biologically active intermediates, one may conclude that: 1. The mode of toxic action of the bisfuranoid mycotoxin is through epoxidation of the vinyl ether double bond of their dihydrobisfuran functionality. 2. The DNA and plasma albumin adducts formed in vivo may be useful in the molecular dosimetry of these environmental carcinogens. 3. Monitoring of these adducts of AFB1 in biological samples so far indicates that aflatoxin is likely involved in the etiology of human liver cancer.
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PMID:Biological reactive intermediates of bisfuranoid mycotoxins. 212 32

The possible association in humans between nonangiosarcoma primary liver tumors (PLC-non-A), particularly hepatocellular carcinoma (HCC), and exposure to vinyl chloride monomer (VCM) is supported by both experimental and human data. This article presents a review of the information regarding 253 deaths that occurred in seven plants manufacturing VCM/PVC and one plant extruding PVC. The retrieval of clinical and pathological data, in addition to the information from death certificate, is referred to as "best evidence" (BE). BE has been carried out for 63 deaths. A total of 14 primary liver cancer (PLC) were detected: seven were angiosarcoma (PLC-A), and two of the remaining seven were hepatocellular carcinoma (HCC). In our series of 14 PLC cases, there was no significant difference between PLC-A and PLC-non-A as to length of exposure and latency. There was no noticeable difference in terms of job title between ASL and non-ASL cases. The list of longest held jobs shows the presence of various job titles, different from autoclave cleaner, for primary liver cancer, PLC-A and PLC-non-A. In conclusion, our observations show that VCM may have a broader carcinogenicity action on the liver and that exposure lower than that occurring in autoclave cleaning can cause primary liver cancer, both angiosarcoma and nonangiosarcoma.
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PMID:Mortality from liver disease among Italian vinyl chloride monomer/polyvinyl chloride manufacturers. 215 96

The mortality experience of 88,000 Union Carbide Corporation employees from 1974 to 1983 is presented using a population-based surveillance system. The study included many long-term employees, with most deaths contributed by those retired or terminated. The total population exhibited 30% lower mortality overall and 10% lower cancer mortality, as compared with the general U.S. population. Excesses of benign neoplasms and malignant melanoma of the skin were observed in both hourly and salaried males. Mortality rates for lymphosarcoma and reticulosarcoma were significantly elevated due to higher rates among hourly male employees and a cluster in one location. This same location also exhibited an excess of liver cancer associated with vinyl chloride operations. There were no other significant excesses in the hourly male workers and fewer deaths than expected due to brain cancer, respiratory cancer, and nonmalignant respiratory diseases. Salaried, and particularly hourly, women experienced favorable mortality, although for the women, time since hire was relatively short. Location-specific findings were similar to what had been observed in the company's previously conducted cohort studies. Future value lies in the development of a database that will have greater power to address possible effects of past exposures and outcomes related to more recent lower level exposures.
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PMID:Mortality surveillance in a large chemical company: the Union Carbide Corporation experience, 1974-1983. 195 75

The mortality in a cohort of workers at a vinyl chloride polymerization plant has been updated, extending the period of observation in the original study from 1974 to 1986. Workers at this plant may have been exposed to vinyl chloride monomer and/or polyvinyl chloride dust, or may have had no exposure to either substance. Seventy-six percent of the work force worked in jobs with potential exposure to vinyl chloride monomer. Among the total cohort, statistically significant excess risks were observed for liver, lung, and brain cancer. For the subcohort of workers exposed to vinyl chloride monomer, the standardized mortality ratio (SMR) for liver cancer was 333 (90% confidence interval (CI) 202 to 521). However, there were no significant excesses of either brain (SMR = 145, 90% CI 78 to 249) or lung cancer (SMR = 115, 90% CI 96 to 141). To investigate dose response, nested case-control studies for liver, brain, and lung cancer were conducted among the total cohort (including the nonexposed). For these studies there were two exposure variables, cumulative dose of vinyl chloride monomer and cumulative dose of polyvinyl chloride dust. Cumulative dose was defined as the product of level and duration of exposure. The only significant association between disease risk and cumulative dose was for liver cancer and cumulative dose of vinyl chloride monomer. Further division of the liver cancers into angiosarcoma (n = 12) and other liver cancers (n = 7), based on review of death certificates and medical records, showed that the dose response existed only for angiosarcomas.
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PMID:Cohort and case-control analyses of workers exposed to vinyl chloride: an update. 273 15

Man is a poor model for the prediction of agents that are hepatocarcinogenic for laboratory rodents. Relatively few agents are known to cause any form of primary liver cancer in man. The most important is hepatitis B virus, for which there is possibly a model in the woodchuck but not one in rats or mice. The only other agents known to cause primary liver cancer in man are certain steroid hormones, vinyl chloride, and thorium dioxide. There are animal models for the first two of these and a reasonable expectation that thorium dioxide would produce liver tumors in animals if the appropriate experiments were done. Aflatoxin, a potent hepatocarcinogen in rats and other species but not mice, is strongly suspected of being an important human hepatocarcinogen in certain geographical areas of the world, but the evidence is circumstantial. There is no more than a weak association between the nutritional type of cirrhosis secondary to excessive intake of alcohol and increased primary liver cancer in man, and no evidence at all that ethanol per se causes liver tumors in mice, rats, hamsters, or mastomys. By contrast, a very large number of chemicals to which people in the West have been exposed for many decades have been found to be hepatocarcinogens in laboratory rodents. In most cases the levels of exposure required to produce liver tumors in rodents far exceed those to which man is normally exposed. The problem is to guess whether low-level exposure to such rodent hepatocarcinogens poses any real liver cancer threat to man?The mortality from primary liver cancer is very low in countries such as England and Wales where there is widespread exposure to low doses of both natural and synthetic agents which, in high dosage, cause liver tumors in rodents. This suggests that, if there is any risk, it can only be very small. Death rate data collected in England and Wales by the Registrar General are consistent with there having been a small increase in the incidence of primary liver cancer in England and Wales during the past 20 years, but the apparent increase might well be a consequence of revisions in the International Classification of Diseases system and not real. During the first half of the present century the age-standardized incidence of primary liver cancer in England and Wales was falling.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Liver tumors in rodents: extrapolation to man. 330 Feb 4


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