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PubMed1976

Vinyl chloride: dominant lethal studies in male CD-1 mice.

The mutagenic activity of vinyl chloride (VC) at three exposure levels was assessed in fertile male CD-1 mice with the dominant lethal test. Male mice were exposured by inhalation to VC at 3000, 10,000 and 30,000 ppm for 6 h a day for 5 days. By comparison with control males exposed to air, no mutagenic effects on any maturation stage of spermatogeneisis in treated males were detected. There was no significant increase in the number of post-implantational early foetal deaths as shown by the number of females with one or more early deaths or number of early deaths/pregnancy or the number of early deaths/total implants/pregnancy. There was no evidence of pre-implantational egg losses as indicated by the total implants/pregnant female. There was also no reduction in fertility. The lack of effect was not due to the insensitivity of the system used since a dominant lethal effect was clearly demonstated in male mice dosed i.p. with cyclophosphamide (CTX) at 200 mg/kg body weight and ethyl methanesulphonate (EMS) orally at 200 mg/kg body weight once a day for 5 days. During dosing these animals were housed under dimilar exposure conditions to those animals exposed to the test substances but with a flow of air through the exposure chambers. Thus vinyl chloride is not mutagenic in the mouse at the stated exposure levels as measured by the dominant lethal test.

Administration, Oral↗
PubMed1980

Chromosomal analyses in vinyl chloride exposed workers. Results from analysis 18 and 42 months after an initial sampling.

In a previous study (Purchase et al., Mutation Res., 57 (1978) 325-334) it was reported that 57 workers occupationally exposed to vinyl chloride had an increase in the incidence of chromosomal abnormalities in their lymphocytes by comparison with 24 control workers. Since that time (July 1974) threshold limit values for vinyl chloride and plant exposure levels have been reduced. In the present study, 2 further samples from the same population of workers have been analysed for chromosomal aberrations 18 and 42 months after the initial sampling. At 18 months, 21 VC workers and 6 on-site controls were investigated as were 23 workers and 8 on-site controls at 42 months. In the second sampling there was a tendency to an increase in chromosomal abnormalities of VC-exposed workers except in those people who had changed occupation. By the third sampling, however, there was a decrease by comparison with previous samplings and the levels of abnormalities had returned to values similar to those of the controls. Thus, reduction in exposure to vinyl chloride is accompanied by a reduction in the chromosomal abnormalities to levels indistinguishabe from those of controls.

Adult↗
PubMed1981

Role of metabolic activation in the sister chromatid exchange-inducing activity of ethyl carbamate (urethane) and vinyl carbamate.

Ethyl carbamate (EC, urethane) at 10(-2) M concentration induced more sister chromatid exchanges (SCEs) in cultured human peripheral blood lymphocytes in the absence of S9 mix than did 10(-2) M vinyl carbamate (VC), a possible proximate carcinogenic metabolite (Dahl et al., 1978) of EC. VC itself doubled SCE frequency over the control. In the presence of native S9 mix from Aroclor-induced rat liver, the SCE-inducing activity of VC was highly increased whereas that of EC was suppressed. This opposite effect of S9 mix on VC and EC seems to be due to two different factors. Activation of VC by the S9 fraction seems to be due to the presence of mixed-function oxidases in the S9 mix, because neither the native S9 fraction in the absence of co-factors nor the heat-inactivated S9 fraction in the incubation mixture led to the activation of VC. Deactivation of EC by S9 mix, on the other hand, seems to involve the presence of excess protein and/or substances of low molecular weight in the incubation mixture, because this deactivating effect did not change considerably when the S9 fraction was supplied in the absence of co-factors or when it originated from non-induced rat liver. Heat denaturation of the S9 fraction led to an increased deactivating effect on the SCE-inducing ability of EC. This result is in line with the assumption that reactive -SH groups in the S9 protein are at least partly responsible for the deactivation of EC by S9. Heat denaturation of the S9 fraction led to an about 1.5-fold increase in reactive -SH groups.

Animals↗
PubMed1985

Induction and persistence of SCE-inducing damage in human lymphocytes exposed to vinyl acetate and acetaldehyde in vitro.

The frequency of sister-chromatid exchange (SCE) was studied in cultures of human lymphocytes exposed to vinyl acetate (VA) or acetaldehyde (AA) for various time periods and in different phases of the cell cycle. Equimolar concentrations (0.1-2.4 mM) of VA and AA were found to induce very similar, dose-dependent increases of SCE. The SCE frequency in cells treated with VA was found to increase linearly with exposure times up to 24 h. Cells exposed to VA or AA in the late G1-phase of the cell cycle showed a 2-fold higher SCE frequency than cells exposed in early G1. Cultures treated with VA in the first G1-phase showed a significant increase of SCE during 3 subsequent cell cycles. These results indicate that (1) AA is likely to be responsible for the SCE induction observed in VA-treated cells, (2) the SCE-inducing activity of AA persists for several cell cycles in vitro, and (3) removal of SCE-inducing AA-damage occurs during G1. Taken together, the data suggest that AA has a slow turn-over in human lymphocytes in vitro, and may accumulate in the cells, possibly by forming reversible Schiff bases, and when released gives rise to SCE-inducing DNA cross-links.

Acetaldehyde↗
PubMed1990

Cytogenetic analysis of peripheral blood lymphocytes in workers exposed to vinyl chloride.

In the present study, the method of cytogenetic analysis of peripheral blood lymphocytes was used to examine 43 workers exposed to vinyl chloride monomer (average exposure 11.2 years) and 22 subjects selected from the same locality (control group). A total number of 8650 metaphases were analysed. All cytogenetic parameters examined were increased in the exposed group as compared to the control group and 3 parameters, chromatid breaks, percentage of aberrant cells and breaks per cell, were significantly increased (P less than 0.001).

Adult↗
PubMed1996

Cytogenetic effects in mice of divinylbenzene-55 inhalation.

Male B6C3F1 mice (8 weeks of age) were exposed by inhalation to divinylbenzene-55 (DVB-55), at target concentrations of 0, 25, 50 and 75 ppm for 6 h per day for 3 days. Following exposure the animals were killed blood smears were prepared for micronucleus (MN) analysis, and the spleens were removed and cultured for sister chromatid exchange (SCE) and chromosome aberration (CA) analyses. DVB-55 induced a dose dependent increase in SCE with the two highest doses reaching statistical significance. Similarly, there was a statistically significant although less pronounced increase in the frequency of CAs in splenocytes and MN in polychromatic erythrocytes. There was no indication of toxicity as measured by cell cycle kinetics in the splenocytes or the percentage of polychromatic erythrocytes in the peripheral blood smears. Thus, DVB-55 appears to be a weak genotoxicant in vivo.

Administration, Inhalation↗
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↗
PubMed1983

Activity of vinyl chloride monomer in the mouse micronucleus assay.

C57Bl/6J mice of both sexes were exposed to 50 000 ppm vinyl chloride monomer (VCM) for 6 h. Animals were killed 24 and 48 h after cessation of exposure and examined for the presence of micronuclei in bone marrow cells. At 24 h the control incidences of micronuclei per 1000 polychromatic erythrocytes (PCEs) were 2.6 (male) and 1.2 (female), while in animals exposed to VCM the incidences were 24.6 (male) and 25.0 (female). At 48 h the control incidences were 2.2 (male) and 1.6 (female) and in the VCM exposed animals 7.2 (male) and 4.4 (female).

Animals↗
PubMed1987

Induction of micronuclei by vinyl acetate in mouse bone marrow cells and cultured human lymphocytes.

A dose-dependent increase in micronucleated polychromatic erythrocytes was observed in the bone marrow of male C57B1/6 mice 30 h after a single intraperitoneal injection of vinyl acetate (250, 500, 1000 or 2000 mg/kg b.wt.; (9-14 animals per group). The effect was statistically significant at 1000 mg/kg (1.33 +/- 0.29% vs. 0.6 +/- 0.10% in olive oil-treated controls) and at 2000 mg/kg (1.57 +/- 0.19%) of vinyl acetate. These doses were fatal to 6 (1000 mg/kg) and 8 (2000 mg/kg) out of 14 animals in both groups. The ratio of polychromatic to normochromatic cells decreased as a function of vinyl acetate dose. Cyclophosphamide (20 mg/kg), used as a positive control chemical, induced a clear increase in micronucleated polychromatic erythrocytes (2.07 +/- 0.20%). None of the treatments affected the number of micronuclei in normochromatic erythrocytes. In human whole-blood lymphocyte cultures, micronucleus induction by a 48-h treatment with vinyl acetate (0.125, 0.25, 0.5, 1 and 2 mM; 24 h after culture initiation) was studied in lymphocytes with preserved cytoplasm from smear slides prepared by a method involving the removal of erythrocytes at harvest by sodium cyanide treatment to improve preparation quality. The frequency of micronucleated lymphocytes reached a peak at 0.5 mM (3.2 +/- 1.0% vs. 0.9 +/- 0.1% in control cultures) and 1 mM (3.1 +/- 0.7%), with a decline at 2 mM probably because of a toxic effect resulting in mitotic inhibition.

Animals↗
PubMed1990

Localization of breaks induced by vinyl chloride in the human chromosomes of lymphocytes.

A group of 67 workers occupationally exposed to VCM was examined for the presence and distribution of breaks along the chromosomal length. Breaks induced by VCM are not randomly distributed as had been expected in a normal population. According to our results there exist highly sensitive and highly resistant locations along the chromosomes to the actions of VCM. The link between the highly sensitive segments of chromosomes, fragile sites and the activation of oncogenes is discussed.

Cells, Cultured↗
PubMed1987

13C-NMR study of labeled vinyl groups in paramagnetic myoglobin derivatives.

The 13C-NMR spectra of high-spin met-aquo myoglobin, spin-equilibrium met-azido myoglobin, low-spin met-cyano myoglobin, deoxy myoglobin and carbonmonoxy myoglobin from sperm whale reconstituted with hemin 13C enriched at both vinyl alpha or beta positions have been recorded. In all cases the labeled vinyl 13C signals are clearly resolved and useful spectra could be obtained within approx. 15 minutes. The decoupling of multiplet structure due to attached proton(s) has led to the specific assignment of vinyl 13C alpha signals in all paramagnetic derivatives and the 13C beta signals in met-cyano myoglobin. In all other cases, the collapse of the proton multiplet structure as a function of 1H decoupling frequency has located, but not assigned, the attached 1H resonance positions which are obscured by the intense diamagnetic envelope in the 1H-NMR spectrum. The resulting vinyl 13C hyperfine shifts follow Curie behavior, and the patterns closely resemble those in the appropriate model complexes in the same oxidation/spin/ligation state, except that the protein exhibits more in-plane asymmetry. The hyperfine shift patterns are indicative of dominant pi contact shifts for all ferric complexes. Deoxy myoglobin vinyl 13C and 1H contact shifts provide little evidence for pi bonding.

Animals↗
PubMed1989

Epithelioid hemangioendothelioma of the liver following contact with vinyl chloride. Recurrence after orthotopic liver transplantation.

Malignant epithelioid hemangioendothelioma of the liver is a recently recognized and uncommon neoplasm of vascular origin. Few cases have been reported and the treatment remains therefore difficult to define. A relationship to oral contraceptive use has been suggested but no other toxic agents have been incriminated. We report here the first case occurring after a close contact with vinyl chloride. Because of wide hepatic destruction and serious portal hypertension with bleeding varices, the patient underwent orthotopic liver transplantation. After a disease-free interval of 20 months, he died from variceal hemorrhage and encephalopathy due to local tumor recurrence with portal thrombosis. Nevertheless, orthotopic liver transplantation remains the only hope of salvage when extensive liver destruction and life-threatening complications are present.

Adult↗