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PubMed1976

Metabolism of 14 C-vinyl chloride in vitro and in vivo.

Rat liver microsomes metabolise 14 C-vinyl chloride to intermediates which irreversibly bind to the microsomal protein and to soluble proteins and RNA, when these compounds are added to the incubation. A superoxide (O2) generating system comprised of phenazine methosulfate and NADH also converts 14 C-vinyl chloride to metabolites which irreversibly bind to albumin. These data are consistent with the assumption of chloroethylene oxide being the primary reactive metabolite of vinyl chloride. If rats are exposed to 14 C-vinyl chloride, about half of the radioactive metabolites in the liver microsomal fraction is bound irreversibly to microsomal protein, when assessed immediately after exposure. Large amounts of polar, extractable, metabolites are present in the cytosol fraction. The amount of radioactivity in tissues of the rats, irreversibly bound immediately after exposure, comprises 10 - 40% of the total radioactivity in tissues. This percentage rises up to 70% after 48 hrs. Som radioactivity derived from 14 C-vinyl chloride is also incorporated into DNA and RNA of liver. Whereas the peak of incorporation of 14 C into DNA is already reached immediately after exposure to 14 C-vinyl chloride, specific labelling of RNA increases after exposure until its maximum after 24 hours.

Albumins↗
PubMed1991

Radiation grafting of hydrophilic monomers on to plasticized poly(vinyl chloride) sheets. II. Migration behaviour of the plasticizer from N-vinyl pyrrolidone grafted sheets.

The grafting of N-vinyl pyrrolidone, a hydrophilic monomer, on to flexible poly(vinyl chloride) sheets used in medical applications using ionizing radiation from a 60Co source was studied. The graft yield was found to increase linearly with monomer concentration and also with increasing radiation doses. The migration of the plasticizer di-(2-ethylhexyl)phthalate into a strong organic extractant such as n-hexane was studied at different time intervals for different grafted systems of poly(vinyl chloride) at 30 degrees C. The results indicated a drastic reduction in the leaching of the plasticizer from grafted systems versus ungrafted controls. Incorporation of ethylene dimethacrylate cross-linker during grafting did not seem to affect the graft yield considerably but appeared to further reduce the plasticizer migration. Surface energy calculations of the grafted samples indicate that the surfaces are highly hydrophilic compared to ungrafted poly(vinyl chloride) and the polar and dispersion components tend to vary with increasing cross-linker concentration.

Biocompatible Materials↗
PubMed1981

Electron microscopic observations of hepatic and subcutaneous hemangiosarcomas induced in mice exposed to vinyl chloride monomer.

Both subcutaneous and hepatic hemangiosarcomas were induced in mice exposed to vinyl chloride monomer, and for the first time, the ultrastructure of hemangiosarcomas related to vinyl chloride exposure has been described. The subcutaneous hemangiosarcoma developed in a mouse's ear 29 weeks after exposure to 10 ppm vinyl chloride for 4 weeks, and the hepatic hemangiosarcoma was found in a mouse's liver at necropsy 56 weeks after exposure to 600 ppm vinyl chloride for 4 weeks. Both tumors showed a localized, cystic nodular appearance with a dark red tone. Histologically, an angiomatous architecture, the presence of neoplastic mesenchymal cell aggregates, focal necrosis, and hemorrhagic foci were common. Ultrastructurally, two neoplastic cell types, a mesenchymal and a well-differentiated endothelial cell type, were identified in both tumors. In addition, in the hepatic tumor, a pericyte-like neoplastic cell was also present. The incidence of hemangiosarcoma was much lower than that of lung tumors (alveologenic tumor) in mice exposed to vinyl chloride at the same concentrations for the same duration. This study suggests that there is no basic difference in ultrastructure between the vinyl chloride-induced hemangiosarcomas and hemangiosarcomas not related to this chemical exposure.

Animals↗
PubMed1976

Pharmacodynamics and uptake of vinyl chloride monomer administered by various routes to rats.

Finding at least 2-3 ppm and occasionally as much as 10-20 ppm of vinyl chloride monomer in a wide range of foodstuffs has prompted concern for a possible human health hazard. The recognition of vinyl chloride as a carcinogen to humans in April 1974, following the discovery of angiosarcoma as the cause of death in at least 25 workers who had been engaged in the manufacture of polyvinyl chloride, enhanced this concern with respect to the presence of vinyl chloride monomer in foods. To assess the hazard presented by the oral ingestion of vinyl chloride monomer, rats that had been surgically prepared with an indwelling jugular cannula were dosed by intragastric intubation with aqueous solutions containing up to 2.0 mg/ml vinyl chloride. Time-concentration curves were obtained from sequential samples of blood. The uptake of vinyl chloride by this route was found to be extremely rapid; peak concentrations were achieved less than 10 min after administration of the dose. Elimination from the blood compartment appeared to be biexponential. Studies with the same animal model in a single restraint cage that allowed a "head only" exposure to concentrations of vinyl chloride up to 7,000 ppm in the gas phase have shown a similar rapid uptake followed by a plateau blood concentration during several hours of exposure. On removal from the vinyl chloride atmosphere, blood levels fell rapidly to barely detectable concentrations after 2 hr. The precise kinetic coefficients that describe the distribution and elimination rates of vinyl chloride from the blood compartment were also determined from the blood concentration data after the administration of an intravenous dose of aqueous or vegetable oil solution.

Aerosols↗
PubMed1976

Mutagenicity and metabolism of vinyl chloride and related compounds.

The various adverse biological effects of vinyl chloride appear to be dependent upon the metabolic conversion of this compound into chemically reactive metabolites. The metabolism of vinyl chloride in mammals and in man, including the formation of monochloroacetic acid and some identified sulfur conjugates is reviewed. Hepatic microsomal mixed function oxidases from rats, mice, and humans were equally effective in transforming vinyl chloride into alkylating agents in vitro. Two of the enzyme reaction products, i.e., chloroethylene oxide and 2-chloroacetaldehyde, showed potent genetic activity in microorganisms and Chinese hamster V79 cells. The role of liver microsomal enzymes in the generation of electrophilic mutagenic vinyl chloride metabolites is discussed.

Animals↗
PubMed1986

Vasculitic purpura in vinyl chloride disease: a case report.

Vinyl chloride (VC), a volatile substance mostly used for polyvinyl chloride (PVC) synthesis, is a systemic toxicant particularly noxious to endothelium. Angiosarcoma of the liver, Raynaud's phenomenon, scleroderma-like lesions, acroosteolysis and neuritis are known to be typical vinyl chloride-associated manifestations (VC disease). A so far unknown feature of the disease is purpura. This was first observed by the authors in a worker of a PVC-producing plant. The skin eruption was characterized by small purpuric maculae with tiny, palpable spots and papulae, mostly concentrated on the lower part of the legs, changing into bullae, pustules and crusts and tending to spontaneous regression after withdrawal from VC exposure. A skin biopsy revealed marked inflammatory reaction with a mostly lymphocytic and histiocytic infiltration around and in the walls of dermal arterioles. The finding of increased circulating immune complexes and anti-smooth muscle autoantibodies strengthens the hypothesis that immunologic changes play a role in the appearance of "vinylic purpura."

Adult↗
PubMed1979

Collaborative study of reference vinyl chloride charcoal tubes.

The reference vinyl chloride charcoal tubes generated by a permeation technique are evaluated by collaborative testing. The statistical analysis of Youden's method provides an estimate of replication error, sample generation error, and interlaboratory error.

Air Pollutants↗
PubMed1979

Vinyl chloride and trichloroethylene: comparison of alkylating effects of metabolites and induction of preneoplastic enzyme deficiencies in rat liver.

[1,2-14C] Vinyl chloride and [1,2-14C] trichloroethylene were incubated with rat liver microsomes, NADPH and RNA (from yeast). Whereas trichloroethylene metabolites were irreversibly bound to proteins in microsomal incubations to a higher extent than vinyl chloride metabolites, irreversible binding to RNA was lower for trichloroethylene metabolites. Hydrolysis of the RNA which was reisolated from microsomal incubations with 14C-vinyl chloride or 14C-trichloroethylene and separation of the nucleosides showed different alkylation products arising from vinyl chloride and from trichloroethylene, characteristic for vinyl chloride being formation of 1,N6-ethenoadenosine and 3,N4-enthenocytidine. The different reactivities of metabolites of vinyl chloride and of trichloroethylene prompted a comparison of the oncogenic effects of both compounds against the rat liver cell. Newborn rats were exposed for 10 weeks to 2000 ppm vinyl chloride or trichloroethylene (8 h/day; 5 days/week). After this period livers of the animals were stained for nucleoside-5-triphosphatase. Whereas the vinyl chloride exposed rats showed focal hepatocellular deficiencies in this enzyme, which are supposed to represent an early sign of malignancy, no such changes were induced by trichloroethylene exposure. The data therefore suggest differences between the hepatocarcinogenic activity of vinyl chloride and possible effects of trichloroethylene on the liver.

Adenosine↗
PubMed1982

Angiographic study of digital arteries in workers exposed to vinyl chloride.

Five patients exposed to vinyl chloride were studied by hand angiography and other non-invasive methods, including photoplethysmography, rheography, and thermography. Raynaud's phenomenon was present in all five subjects, while acro-osteolysis affected only one. Organic vascular lesions, such as narrowing, segmentary occlusions of digital arteries and bridge collaterals, were found in angiographic studies. Only one patient did not show clear segmentary occlusions, but his vessels were crooked and diffusely narrowed. Angiographic results appear to correlate well with the changes shown by non-invasive techniques.

Adult↗
PubMed1997

Angiosarcoma of the liver in Great Britain in proximity to vinyl chloride sites.

OBJECTIVES: To study the incidence of angiosarcoma of the liver in England and Wales 1979-86 and Scotland 1975-87. To investigate whether any non-occupational neighbourhood cases occurred near a vinyl chloride site. METHODS: This is a geographical study of incident cases among the general population of Great Britain. Diagnosis of angiosarcoma of the liver was based mainly on the national cancer registry, the world register of cases among vinyl chloride workers, and the register of cases (including histological review) maintained by the Health and Safety Executive. Proximity (< 10 km) of residence to a vinyl chloride site was based on postcode of address at the time of diagnosis. RESULTS: 55 cases were ascribed to angiosarcoma of the liver in England and Wales with a further six cases in Scotland (annual incidence in Great Britain from all sources of around 1.4 cases per 10 million population). There were two cases with documented exposure to Thorotrast, and 10 cases among vinyl chloride workers. There were no vinyl chloride sites in Scotland. Among the 25 cases in England and Wales with histological diagnosis after review by a panel of pathologists, only 15 were confirmed as angiosarcoma, and one of the two Scottish cases after histological review was also confirmed. Overall, 11 cases ascribed to angiosarcoma were resident within 10 km of a vinyl chloride site; nine were vinyl chloride workers, one further case on histological review was not considered to have been correctly diagnosed as angiosarcoma, and the remaining case, confirmed as angiosarcoma, was employed at a vinyl chloride factory during the late 1950s, although not as a vinyl chloride worker. CONCLUSION: The incidence of angiosarcoma of the liver in Great Britain remains extremely rare. The one confirmed case in a non-vinyl chloride worker within 10 km of a site must nevertheless be presumed to have been exposed to vinyl chloride in the workplace. In the period of study, there were no confirmed non-occupationally exposed cases of angiosarcoma among residents living near a vinyl chloride site in Great Britain.

Adult↗
PubMed1983

Covalent protein binding of vinyl chloride metabolites during co-incubation of freshly isolated hepatocytes and hepatic sinusoidal cells of rats.

Proteins of isolated rat hepatic sinusoidal cells incubated with 14C-vinyl chloride, rat liver microsomes and an NADPH-regenerating system were alkylated by vinyl chloride metabolites formed by microsomes. This suggests that reactive vinyl chloride metabolites can penetrate sinusoidal cells. Protein alkylation in isolated hepatic sinusoidal cells was higher when these were co-incubated with isolated hepatocytes, indicating that reactive vinyl chloride metabolites formed by hepatocytes are stable enough to diffuse out of hepatocytes into sinusoidal cells. Glutathione added to the incubation medium inhibited the covalent protein binding of vinyl chloride metabolites in sinusoidal cells as well as in hepatocytes incubated separately and deleted the increased protein binding in sinusoidal cells co-incubated with hepatocytes. The data indicate that glutathione present in the incubation medium traps reactive vinyl chloride metabolites formed by hepatocytes which otherwise would react with cell constituents of sinusoidal cells. If similar conditions exist in vivo, the alkylation of DNA of liver endothelial cells by vinyl chloride metabolites formed in hepatocytes is possible. This would explain the induction of hemangioendotheliomas of the liver by vinyl chloride.

Alkylation↗
PubMed1975

Sensitive trapping and gas chromatographic method for vinyl chloride in air samples.

A simple and sensitive method is described for determining vinyl chloride monomer in air. Vinyl chloride monomer from a sample of air is trapped onto a Tenax GC trap cooled with Dry Ice. The trap is installed on a gas chromatograph by a simple valve arrangement. The trap is heated, and the entire sample is flushed onto the gas chromatographic column. Vinyl chloride is determined at 6 and 60 ppb (v/v) levels with recoveries ranging from 79 to 104%.

Air Pollutants↗
PubMed1988

Effects of exposure to vinyl chloride. An assessment of the evidence.

This paper reviews the possible effects of vinyl chloride on the mortality of occupationally exposed men and the carcinogenic effects that might be observed in the general population as a result of environmental pollution with vinyl chloride. The results of four studies fulfilling the criteria of providing substantial numbers of observations more than 25 years after first exposure and covering a period long enough for more than 10% of the workers to have been expected to die constitute the basis for the assessment of the occupational hazards. Other studies provide only supplementary information. The data permit two conclusions. First, men occupationally exposed to vinyl chloride have experienced a specific hazard of angiosarcoma of the liver. Second, any other occupational hazards that may have existed have been small. No positive evidence of a hazard of any nonmalignant disease or any type of cancer other than angiosarcoma of the liver has been found except possibly for a small hazard of lung cancer when exposure was heavy. More definite conclusions might be reached if those who have studied exposed employees could present their results in appropriate and comparable ways. A very small risk of angiosarcoma may have occurred as a result of vinyl chloride escaping into the environment around plants handling vinyl chloride in the past, but the evidence indicates that the current risk to the general public (if any) must be negligible.

Canada↗
PubMedDate not supplied

Rat hepatic vinyl chloride metabolites induce gene conversion in the yeast strain D7RAD in vitro and in vivo.

We have tested the genetic activity of gaseous vinyl chloride in vitro and in vivo using the gene-conversion system (trp5-12/trp5-27 leads to TRP+) in the yeast strain D7RAD. To induce, in vitro, TRP+ convertants with 2.5% gaseous vinyl chloride, a rat-liver microsomal system for metabolic activation of the vinyl chloride and dividing yeast cells are required. Neither a deficiency in excision repair (rad3) nor in the error-prone repair pathway (rad6) increased the vinyl-chloride-induced conversion frequencies compared with the repair-competent D7RAD strain. When logarithmically growing cells of the D7RAD strain were injected intravenously into male Wistar rats which inhaled 1% vinyl chloride in air for 24 h, a significant enhancement of the TRP+ conversion frequencies was found compared with that in cells re-isolated from untreated rats. These results indicate that vinyl chloride metabolites from the metabolizing hepatocytes diffuse into yeast cells, which accumulate in the liver capillaries. This supports the hypothesis that the endothelial cells of the liver sinuses, which have hardly any metabolic activity, but give rise to vinyl-chloride-induced hemangiotheliomas (rare type of liver tumor), are transformed by diffusible metabolites of the procarcinogen vinyl chloride.

Animals↗
PubMed1977

Cytogenetic investigations on lymphocytes from workers exposed to vinyl chloride.

Eleven male workers from the polymerization department of a vinyl chloride factory, seven people employed in the laboratory of another vinyl chloride plant, and ten controls from outside the factory environment were examined for the presence of chromosome aberrations in blood lymphocytes. Chromosome anomalies such as fragments, rings, translocations, and dicentrics were observed in most of the workers from the polymerization department. However, the medical history of these workers shows that they received frequent radiographs of the hands, feet, vertebral column, and digestive tract. It is therefore impossible to determine whether these chromosome anomalies result from vinyl chloride exposure.

Adult↗
PubMed1990

[Neurologic and psychiatric disorders in vinyl chloride disease].

A literature review and an own case observation of neurological and psychiatrical disturbances in vinyl chloride disease are presented. In acute vinyl chloride intoxication, patients complain of vertigo, nausea and headache. At higher concentrations, vinyl chloride exerts a narcotic effect. In patients with chronic occupational exposure, neurological disturbances include sensory-motor polyneuropathy, trigeminal sensory neuropathy, slight pyramidal signs and cerebellar and extrapyramidal motor disorders. Psychiatric disturbances present as neurasthenic or depressive syndromes. Sleep disorders and disorders of sexual functions are frequently encountered. Pathological EEG alterations can be found in a high proportion of patients. The long term course and prognosis of the neurological and psychiatrical disorders in vinyl chloride disease are obscure. In an own case, a slight sensory polyneuropathy, bilateral hyposmia, a marked neurasthenic syndrome, typical EEG changes and computed tomography signs of cerebral atrophy were found in a 56-years-old patient as late as 16 years after the exposure to vinyl chloride.

Adult↗
PubMed1981

Poly(vinyl chloride) processes and products.

Poly(vinyl chloride) resins are produced by four basic processes: suspension, emulsion, bulk and solution polymerization. PVC suspensions resins are usually relatively dust-free and granular with varying degrees of particle porosity. PVC emulsion resins are small particle powders containing very little free monomer. Bulk PVC resins are similar to suspension PVC resins, though the particles tend to be more porous. Solution PVC resins are smaller in particle size than suspension PVC with high porosity particles containing essentially no free monomer. The variety of PVC resin products does not lend itself to broad generalizations concerning health hazards. In studying occupational hazards the particular PVC process and the product must be considered and identified in the study.

Chemical Industry↗
PubMed1975

[Morphological changes of the liver after chronic vinyl chloride intoxication (author's transl)].

The monomer vinyl chloride in its gaseous form is used as basic product for industrial synthesis of polyvinyl chloride; it does cause lesions of the liver depending on the dose and the time of exposure. Lesions found on histological examination are: 1. degenerative alterations of liver parenchyma; 2. focal adaptive changes in the cytoplasma of hepatocytes; 3. enlargement of liver cells and polymorphy of cell nuclei; 4. slowly progressive fibrotic and to a lesser degree cirrhotic changes of liver parenchyma, localized in part around the sinus, in part in the septal-periportal areas; 5. activation and proliferation of sinusoidal cells. Sarcoma of the liver due to a probable oncogenic effect of vinyl chloride could be diagnosed in three patients exposed to the toxic agent.

Adult↗