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At least 19 recordsLinked to original sources
PubMed1975

Foreign-body tumorigenesis by vinyl chloride vinyl acetate copolymer: no evidence for chemical cocarcinogenesis.

We investigated whether vinyl chloride monomers, released from implants of vinyl chloride vinyl acetate copolymer (VCA), exerted cocarcinogenic activity and added thereby to the mechanism of foreign-body (FB) tumorigenesis. CBA/H and CBA/H-T6 mice were used. No evidence was found to indicate that chemical carcinogenic activity partakes in tumorigenesis by VCA implants. Hence it was concluded that VCA plastic is not suitable for the study of the combined process of FB/chemical cocarcinogenesis. Furthermore, experimental results obtained with VCA film implants were representative of FB tumorigenesis in the absence of demonstrable chemical carcinogenic activity.

Acetates↗
PubMed1976

Special communication. Polyvinyl chloride - vinyl chloride disease: an occupational health hazard.

Poly Vinly Chloride (PVC) is a very durable, practical and economical plastic, which is so wide spread in its use that it may become difficult to replace it. The annual amount of world production has been constantly increasing and has reached the figure of 8.5m tons. While PVC is so useful, the health hazards which accompany this plastic are causing alarm in the industrially developed countries. The hazards are severe and include defects such as Haemangioendothelial sarcoma (Angiosarcoma) of the liver, Acro-Osteolysis of the fingers and Sclerodermic type skin lesions. This paper illustrates the recent developments, the clinical findings and the measures necessary to control the disease. Moreover, this paper should help alerting the health authorities in the developing countries about the health hazards involved in the manufacture and utilization of PVC. Due to the restrictions imposed on PVC producing plants, there is a real eventuality that these plants may be transferred to the developing countries, where this disease is still unknown.

Chemical Industry↗
PubMed1981

Review of pulmonary effects of poly(vinyl chloride) and vinyl chloride exposure.

The contributions of several recent reports to the definition of pulmonary effects of PVC dust inhalation are reviewed. Granulomatous reaction, with inclusion of PVC particles in macrophages and histocytes, and associated interstitial pulmonary fibrosis have been found to lead to exertional dyspnoea, diffuse micronodular chest radiographic opacities and restrictive pulmonary dysfunction. The effects of vinyl chloride (VC) monomer (gas) on proteins and the immunologic mechanisms triggered by the altered protein are possible mechanisms for the development in some cases of interstitial pulmonary fibrosis secondary to VC exposure. Vinyl chloride, a confirmed carcinogen, has been associated with, among other malignant tumors, a significant increase in the incidence of lung cancer. The magnitude of this effect has not yet been completely evaluated.

Dust↗
PubMed1975

Gas-liquid chromatographic determination of vinyl chloride in vinyl chloride polymers, food-simulating solvents, and other samples.

The determination of vinyl chloride (VC) in polyvinyl chloride (PVC), vegetable oils, food-simulating solvents, mouthwashes, and blood anticoagulant solutions by gas-liquid chromatography is described. PVC polymers are disolved in either tetrahydrofuran or dimethyl acetamide. Vegetable oils are diluted with an equal volume of tetrahydrofuran. The resulting solutions are injected into a gas-liquid chromatograph equipped with a flame ionization detector. Mouthwashes, blood anticoagulant solutions, and 3 food-simulating solvents, 3% acetic acid, 50% ethanol, and heptane, are analyzed by direct injection into a chromatograph. Sensitivities are such that 0.05 ppm VC in solution or 1 ppm VC in PVC can be quantitated.

Anticoagulants↗
PubMed1980

Binding kinetics of vinyl chloride and vinyl bromide at very low doses.

Vinyl chloride and vinyl bromide are metabolically activated by liver microsomal enzymes to intermediates that covalently bind to proteins and nucleic acids. Several lines of evidence suggest the involvement of the epoxides, i.e., chloroethylene oxide or bromoethylene oxide. Proven targets for alkylation are adenine, cytosine and guanine moieties in nucleic acids, and sulfhydryl groups of proteins. For all the halogenated ethylenes studied so far, including vinyl chloride and vinyl bromide, metabolism in vivo is a dose-dependent, saturable process. The metabolic capacity of rats is saturated at atmospheric concentrations of 250 ppm vinyl chloride and 55 ppm vinyl bromide. As recent reports describe a diminishment of hepatocellular glutathione in rats after exposure to vinyl chloride concentrations of 50 ppm and more, we carried out a series of experiments measuring covalent binding of vinyl chloride metabolites after exposure to different concentrations of 14C-vinyl chloride. In all of these experiments, including one of an exposure to only 2 ppm vinyl chloride, hepatic covalent protein binding was related to the dose of vinyl chloride which was actually metabolized, and the ratio between bound and metabolized material was constant. This strongly suggests that hepatic glutathione levels must have only a very limited impact on covalent protein binding of vinyl chloride metabolites, an assumption which is supported by a lacking effect of a pretreatment with diethylmaleate. A scheme of hepatocellular compartimentation of metabolic steps is proposed which serves to explain these findings.

Alkylation↗
PubMed1978

Health effects of vinyl chloride.

Vinyl chloride is a basic chemical for plastics manufacturing and has been used as an anesthetic agent. Vinyl chloride's previously unknown carcinogenic capability appears to be related to the body's ability to convert it from a non-toxic or minimally toxic chemical to a toxic and, with prolonged exposure, cancer-forming agent. Early exposure in animals causes body cells to make adaptive changes which may prepare them for malignant transformation and appear to precede evidence of morphological injury. These findings appear to occur before a low-grade chemical injury occurs. Vinyl chloride chemical injury in man appears to follow the same pattern. Present clinical data in humans now demonstrate evidence of pre-cancer injury and cancer transformation of various types of cells in different organs of the body. Manifestations of pre-cancerous injury to organs other than the liver (such as the lung, heart, spleen, brain and lymphatic system) may also be occurring and require further investigation. Early detection of these pre-cancerous chemical injuries requires a prospective ongoing system of surveillance and the development of diagnostic methods which can identify specific causal agents in the presence of non-specific injury. Such a systematic approach has been developed and is now in operation. Its initial achievements appear to be the foundation for future success in controlling the health effects of industrial chemicals.

Animals↗
PubMed1994

Mutagenesis of ras proto-oncogenes in rat liver tumors induced by vinyl chloride.

Vinyl chloride is a DNA-damaging carcinogen which induces liver angiosarcomas in humans and animals. Activation of the Ki-ras 2 gene by a GC-->AT transition at the second base of codon 13 in human liver angiosarcomas associated with occupational exposure to vinyl chloride has been reported recently. In order to compare the molecular pathways of carcinogenesis in humans and animals, Sprague-Dawley rats were exposed to vinyl chloride and hepatic tumors, including two hepatocellular carcinomas and five liver angiosarcomas, were investigated for mutations at codons 12, 13 and 61 of the Ha-ras, Ki-ras and N-ras genes. High molecular weight DNA was amplified by the polymerase chain reaction and point mutations were analyzed by allele specific oligonucleotide hybridization, direct sequencing of polymerase chain reaction products and sequencing after cloning. None of the tumors exhibited a mutation in codons 12, 13 and 61 of the Ki-ras gene, nor in codons 12 of the Ha-ras gene or 61 of the N-ras gene. However, an activating AT-->TA transversion at base 2 of codon 61 of the Ha-ras gene was detected in the two hepatocellular carcinomas. Mutations involving codon 13 (GGC-->GAC) and codon 36 (ATA-->CTA) of the N-ras A gene were detected in two liver angiosarcomas, suggesting that the nature of the ras gene affected by a given carcinogen depends on host factors specific to cell types. Several additional base pair substitutions were found in exon 1 of the N-ras B and C sequences. NIH 3T3 transfection assays and Southern blot analysis of DNA from transformed NIH 3T3 cells confirmed the presence of a dominant activated N-ras gene. These results emphasize the differences in the molecular pathways leading to tumors in humans and rats and within a given species between different cell types.

3T3 Cells↗
PubMed1978

Vinyl chloride and vinyl benzene (styrene)--metabolism, mutagenicity and carcinogenicity.

Vinyl chloride and vinyl benzene (styrene) are mutagenic in microbial tests, in Drosophila, in yeast, and in mammalian cells. Reports from various countries have shown an excess of chromosomal aberrations in the lymphocytes of workers exposed to vinyl chloride monomer when the workers were compared with controls. Workers occupationally exposed to styrene also revealed a clear increase in the rate of chromosome aberrations in their lymphocytes. Both chloroethylene oxide and styrene oxide, the primary biotransformation products of vinyl chloirde and styrene respectively, bind covalently to cellular macromolecules. Vinyl chloride is a carcinogen in both animals and man. Styrene is currently being tested in animals. These findings, the demonstration of mutagenic response via microbial and other test systems and with observations of significant excesses of chromosomal aberrations among workers exposed to these agents, raise scientific and health oriented concern about the possible genetic risks of vinyl chloride and styrene to man.

Animals↗
PubMed1999

Formation and repair of DNA adducts in vinyl chloride- and vinyl fluoride-induced carcinogenesis.

Vinyl chloride is a known human and animal carcinogen that induces angiosarcomas of the liver. We review here studies on the formation and repair of DNA adducts associated with vinyl chloride and vinyl fluoride in exposed and control rodents and unexposed humans. These vinyl halides induce etheno (epsilon) adducts that are identical to those formed after lipid peroxidation. Of these adducts, N2,3-ethenoguanine (epsilon G) is present in greatest amounts in tissues of exposed animals. After exposure to vinyl chloride for four weeks, epsilon G levels attain steady-state concentrations, such that the amount of newly formed adducts equals the number of adducts that are lost each day. We report the first dosimetry of epsilon G in rats exposed to 0, 10, 100 or 1100 ppm vinyl chloride for five days or four weeks. The number of adducts increased in a supralinear manner. Exposure to 10 ppm vinyl chloride for five days caused a two- to threefold increase in epsilon G over that of the controls, while four weeks' exposure resulted in a fivefold increase. This was confirmed with [13C2]vinyl chloride and by measuring exogenous and endogenous adducts in the same animals. Exposure to 100 ppm vinyl chloride for four weeks caused a 25-fold increase in epsilon G levels over that found in control rats, while exposure to 1100 ppm resulted in a 42-fold increase. The amount of endogenous epsilon G was similar in liver DNA from rats and humans. A comparable response to exposure was seen in rats and mice exposed to 0, 25, 250 or 2500 ppm vinyl fluoride for 12 months. There was a very high correlation between epsilon G levels in rat and mouse liver at 12 months and the incidence of haemangiosarcoma at two years. We were able to demonstrate that the target cell population for angiosarcoma, the nonparenchymal cells, contained more epsilon G than hepatocytes, even though nonparenchymal cells are exposed by diffusion of vinyl halide metabolites formed in hepatocytes. The expression of N-methylpurine-DNA glycosylase mRNA was induced in rat liver after exposure to either 25 or 2500 ppm vinyl fluoride. When this induction was investigated in hepatocytes and nonparenchymal cells, it was found that the latter had only 20% of the N-methylpurine-DNA glycosylase mRNA of hepatocytes, and that only the hepatocytes had induction of this expression after exposure to vinyl fluoride. Thus, the target cells for vinyl halide carcinogenesis have much lower expression of this DNA repair enzyme, which has been associated with etheno adduct repair.

Animals↗
PubMed1983

Genetic susceptibility to scleroderma-like syndrome induced by vinyl chloride.

Vinyl chloride (VC) monomer can induce a scleroderma-like syndrome in a proportion of workers exposed to it during production of polyvinyl chloride. As part of a 5-year follow-up study HLA A, B, and DR antigens and anti-centromere and anti-scleroderma-70 antibodies were determined in 44 such workers. 21 of these had severe and 23 mild forms of vinyl-chloride disease. 50 patients with "classical" scleroderma and 148 healthy hospital workers acted as controls. 11 of the 21 patients classified as having severe VC disease were DR3 positive, and 8 of these had both B8 and DR3 antigens. None of the 23 patients with mild disease carried either antigen. The HLA-antigen frequencies in VC disease mirrored those found in scleroderma (raised DR5 frequency and increased linkage disequilibrium between B8 and DR3). There were, however, significant differences in the frequency of autoantibodies in the two conditions.

Autoantibodies↗
PubMed2000

Synthesis of nucleosides and oligonucleotides containing adducts of acrolein and vinyl chloride.

Vinyl chloride and acrolein are important industrial chemicals. Both form DNA adducts, vinyl chloride after enzymatic oxidation to chlorooxirane and acrolein by direct reaction. Reaction at the N(2) position of guanine is a major pathway. The resulting 2-oxoethyl and 3-oxopropyl adducts cyclize spontaneously to hydroxyethano and hydroxypropano derivatives, respectively. The two cyclic adducts have been detected in DNA exposed to these mutagens. A new method has been developed for the synthesis of deoxyguanosine adducts of chlorooxirane and acrolein, as well as oligonucleotides containing these adducts. Reaction of O(6)-[(trimethylsilyl)ethyl]-2-fluoro-2'-deoxyinosine with the appropriate aminodiol followed by oxidative cleavage of the diol with NaIO(4) gave the adducts in excellent yields. Reaction of oligonucleotides containing the halonucleoside with the aminodiols followed by NaIO(4) efficiently created the nucleosides in the oligonucleotides. Deoxyadenosine adducts were created similarly using 6-chloropurine 9-(2'-deoxyriboside).

Acrolein↗
PubMed1976

Studies on the metabolism of vinyl chloride.

Vinyl chloride (VCM) is not carcinogenic by itself, it is bioactivated to the highly reactive alkylating oxirane chloroethylene oxide. Further metabolism, apparently, leads via an interaction of the primary alkylating metabolites with glutathion to S-(2-carboxy-methyl)-cysteine and thiodiacetic acid which are eliminated with the urine. Up to now, it has not been ascertained whether the oxirane alone is the essential carcinogenic factor or whether other metabolites are also involved in carcinogenicity. Likewise, it is still unknown whether the metabolites excreted in the urine might be used as biological criteria for exposure to VCM, because these metabolites probably can originate from a series of substances other than VCM. This problem could stimulate investigations on the possible carcinogenic activity of these substances.

Acetates↗
PubMed1983

Toxicity of vinyl chloride and poly(vinyl chloride): a critical review.

In 1974, vinyl chloride (VC) was first reported in the open scientific literature to induce angiosarcoma of the liver both in humans and in animals. Additional research has now demonstrated the carcinogenicity of VC to other organs and at lower concentrations. The target organs for VC now clearly include the liver, brain and the lung, and probably the lymphohematopoietic system. The evidence for a carcinogenic risk has been extended to jobs associated with poly(vinyl chloride) exposure. Cases of liver angiosarcoma have been reported among individuals employed in PVC fabrication facilities and an epidemiological study has demonstrated a significant association between exposure to PVC dust and the risk of lung cancer mortality. Cases of angiosarcoma of the liver also have been reported among individuals living in near proximity to vinyl chloride-poly(vinyl chloride) plants. An association between PVC dust and pneumoconiosis also has been demonstrated. On the basis of findings, prudent control of PVC dust in the industrial setting is indicated.

Environmental Exposure↗
PubMed1980

Metabolic activation of vinyl chloride and vinyl bromide by isolated hepatocytes and hepatic sinusoidal cells.

The formation of liver sinusoidal cell tumors after exposure to vinyl chloride led to a survey of hepatocytes and sinusoidal cells isolated from rat liver as to their ability to metabolically activate vinyl chloride and vinyl bromide. It is shown that metabolism of these vinyl halides to reactive metabolites is confined primarily to hepatocytes. This favours the theory that in the liver reactive metabolites of vinyl chloride leave the hepatocytes to act on hepatic sinusoidal cells.

Animals↗
PubMed1975

Industrial preparation of poly(vinyl chloride).

Vinyl chloride (VCM) is unloaded from railroad tank cars or tank trucks into pressurized storage spheres. VCM, emulsifiers, and catalysts are metered into polymerization vessels wherein PVC is produced through a chemical reaction in an aqueous medium under controlled conditions of temperature and pressure. After the reaction reaches a predetermined completion, the contents are transferred to a secondary vessel wherein steam is injected and the VCM containing vapors are pumped to a recovery system. The VCM-containing vapors are compressed, cooled, condensed, decanted, and recycled to the process for reuse. The stripped PVC resin water slurry is then pumped to blending tanks where the batches from multiple reaction vessels are blended for product uniformity. From the plant tanks the PVC resin water slurry is pumped to a dewatering centrifuge, where approximately 90% of the water is removed and subsequently discharged to the industrial sewer system. The PVC resin wet cake is conveyed from the centrifuge to a flash dryer where essentially all the remaining water is removed. At this point, the dry resin is buoyant in an air stream and enters a two-stage collection system for separation of conveying air. The PVC resin is then screened and air-conveyed to storage for bulk shipment, compounding, or bagging.

Air Pollutants, Occupational↗