Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vinyl Chloride”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1975

The biological fate in rats of vinyl chloride in relation to its oncogenicity.

The main eliminative route for [14C]vinyl chloride after oral, i.v. or i.p. administration to rats is pulmonary; both unchanged vinyl chloride and vinyl chloride-related CO2 are excreted by that route and the other [14C] metabolites via the kidneys. After intragastric administration, pulmonary output of unchanged vinyl chloride is proportional to the logarithm of reciprocal dose. Excretion patterns after i.v. and i.p. injections are predictable from the characteristics of excretion following oral administration. Pulmonary excretion of unchanged vinyl chloride after oral dosing is complete within 3-4 h, but pulmonary elimination of CO2 and renal excretion of metabolites occupies 3 days. In comparison, 99% of a small i.v. dose is excreted unchanged within 1 h of injection; 80% within 2 min. The rate of elimination of a single oral doses of [14C]vinyl chloride is uninfluenced by up to 60 days' chronic dosing with the unlabelled substance. The distribution volume of vinyl chloride as displayed by whole-animal autoradiography agrees with deductions from excretion data. Small localization of 14C in the para-auricular region of appropriate sections occurs in sectioned tubules, belonging possibly to the Zymbal glands. Biotransformation of vinyl chloride into S-(2-chloroethyl) cysteine and N-acetyl-S-(2-chloroethyl) cysteine occurs through addition of cysteine, and biotransformation into: (i) chloroacetic acid, thiodiglycollic acid and glutamic acid, and (ii) into formaldehyde (methionine, serine), CO2 and urea is explicable in terms of an associative reaction with molecular O2 involving a singlet oxygen bonded transition state in dynamic equilibrium with a cyclic peroxide ground state. There is no evidence for chloroethylene oxide formation. Thiodiglycollic acid is the major metabolite of chloroacetic acid in rats; more than 60% of the dose. The interaction of vinyl chloride and of its primary metabolites with the intermediates of mammalian metabolism is discussed in relation to the oncogenicity of that substance.

Acetates↗
PubMed2002

Synthesis, surface properties and performance of thiosulphate-substituted plasticized poly(vinyl chloride).

Plasticized poly(vinyl chloride) (PVC) was surface modified by nucleophilic substitution of the chlorine atoms of PVC by thiosulphate in aqueous media in the presence of a phase-transfer catalyst. The properties of the modified surface were evaluated by contact angle measurements, attenuated total reflection Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy and scanning electron microscopy. Migration of the plasticizer di-(2-ethylhexyl) phthalate from control as well as modified PVC was examined in hexane, in cottonseed oil and in poly(ethylene glycol)-400 (PEG-400). While the modified PVC was found to be highly migration resistant in hexane, cottonseed oil and PEG-400 extracted the plasticizer. The modified PVC was found to cause haemolysis and was cytotoxic. A possible explanation for the difference in performance of the modified material in different extraction media and its toxicity is presented from a mechanistic view of the substitution process.

Animals↗
PubMed1996

Vinyl chloride loss during laboratory holding time.

Because vinyl chloride is a potent human carcinogen, it is important that analytical results from groundwater samples accurately reflect levels of exposure to groundwater users. This study investigated the current allowable holding time of 14 days to determine if vinyl chloride is lost from samples during this time. Samples containing an initial concentration of 2 microg/liter of vinyl chloride showed progressive, increasing losses when held for 1, 2, 7, and 14 days. Due to the inherent variability of low-level laboratory results, the most statistically significant loss (alpha = 0.05) was seen for samples held for 14 days. No statistically significant differences in degradation pattern were noted between analytical detectors used (PID versus Hall) or sample type (lab versus field). There also was a loss of vinyl chloride observed during sample collection and handling. These results suggest that analytical variability at low concentrations and the establishment of health-based guidelines near the analytical detection limit require multiple samples be collected from a single location when highly accurate results are needed. These findings should be considered in public health exposure assessments and the implementation of health-based recommendations at sites with vinyl chloride groundwater contamination.

Carcinogens↗
PubMed1975

Analysis of vinyl chloride by mass fragmentography.

Vinyl chloride is analyzed by mass fragmentography by simultaneously recording its m/e 62 and 64 ions. The minimum quantity necessary for detection is 8.7 X 10(-12) g/10 ml injection. At this level the coefficient of variation is 8.51%.

Chromatography, Gas↗
PubMed1981

Inhalation pharmacokinetics based on gas uptake studies. III. A pharmacokinetic assessment in man of "peak concentrations" of vinyl chloride.

On the basis of previous determinations of pharmacokinetic parameters for inhaled vinyl chloride in men, rhesus monkeys, and rats, and on improved pharmacokinetic models a pharmacokinetic treatment of the problem of "peak concentrations" of vinyl chloride, as occurring in industrial practice, became possible. For the calculations, metabolic elimination kinetics of vinyl chloride was assumed to be first order as experiments in different species including rhesus monkeys showed "linear" pharmacokinetics up to atmospheric exposures of 200-300 ppm. The distribution of vinyl chloride between atmosphere and organism under different conditions was evaluated using "'steady-state-kinetics". After treating the processes of "influx", "efflux", and "metabolism", the numerical values for the parameters derived from a human kinetic experiment were used to theoretically calculate the time courses of concentration of vinyl chloride in the organism and of the cumulative amount of vinyl chloride metabolized, under the conditions of (a) a 2h constant exposure to 5 ppm vinyl chloride and (b) two subsequent "peaks" of 50 ppm with a duration of 5 min each. This model calculation suggested that, regardless of the exposure profile, the amount of (reactive) metabolites formed from vinyl chloride would solely be a function of the mean atmospheric vinyl chloride concentration over time. The general validity of this suggested rule could subsequently be demonstrated. As the concentration of the reactive metabolite of vinyl chloride responsible for the carcinogenic effect at the target site must be a resultant of both formation and inactivation, an evaluation of the differential risk of different exposure profiles can reasonably be based on biochemical examinations of the "detoxifying" pathways. This points out the relevance of studies of the patterns of different metabolites of vinyl chloride in man under varying exposure profiles.

Animals↗
PubMed1975

A UV-conductivity method for determination of airborne levels of vinyl chloride.

A method has been developed for the measurement of vinyl chloride based on the decomposition of vinyl chloride and the subsequent measurement of the conductivity of these materials in deionized water. Air containing vinyl chloride is sampled through a glass flask containing an ultraviolet lamp. The sample rate for efficient conversion of the vinyl chloride to conductive materials is 2 liters per minute. The wavelength of the ultraviolet light emitted by the six-inch lamp is 2537 Angstroms. Ninety-two percent of the ultraviolet light emitted by the lamp is at this wavelength. The sampled air is then drawn through deionized water, the decomposition products are absorbed and the resulting conductivity measured. Vinyl chloride concentrations of less than one-tenth of a part per million can be detected by the method.

Air Pollutants↗
PubMed1997

Fibronectin exposes different domains after adsorption to a heparinized and an unheparinized poly(vinyl chloride) surface.

The adsorption of fibronectin to poly(vinyl chloride) catheters with end-point attached (EPA) heparin and tridodecylmethylammonium chloride-heparinized poly(vinyl chloride) was compared to that of unheparinized poly(vinyl chloride) using antibodies directed against four different domains of the protein. After perfusion of human plasma on the EPA-heparinized surface, the exposure of the N-terminal 29-kD fragment increased during the first 5 h of perfusion. Also, the exposure of the 30-kD gelatin-binding and 65-kD cell-binding fragments increased with time, but at a lower level. On the unheparinized catheter, low levels of antibodies bound to the different domains, and the binding showed little variation during the 5 h of plasma perfusion, indicating that the fibronectin molecule does not change configuration to a significant extent on this surface after the initial adsorption. When the EPA-heparinized surface was preabsorbed with human fibrinogen before incubation with fibronectin, significantly less of the 29-kD (fibrin-binding) domain was exposed, and the 30-kD domain was not exposed. Exposure of the 31- and 65-kD domains increased after preadsorption of fibrinogen to the surface. Since fibronectin has heparin-binding domains, it adsorbs differently to a heparinized versus an unheparinized surface. This will influence subsequent binding of other proteins to the surface, as well as potential binding of microbes. The use of antibodies to defined domains of the fibronectin molecule provides a powerful tool in studies of configurational changes of fibronectin after adsorption to different surfaces.

Adsorption↗
PubMed1983

Vinyl chloride disease-neurological disturbances.

In a plant producing vinyl chloride by the emulsion method 200 workers who were exposed to vinyl chloride for 1 to 25 yr (mean 14), 58 (i.e. 29%) were free of complaints and nervous disturbances. An astheno-autonomic syndrome was found in 54 (i.e. 27%) and in 88 (i.e. 44%) in combination with positive neurological findings, i.e. pyramidal syndromes (in 52), cerebellar disturbances (in 38), trigeminal neuropathy (in 24) and extrapyramidal symptoms (in 3), in various combinations - pyramidal + cerebellar in 12, trigeminal + pyramidal in 7, trigeminal + cerebellar in 5. Headaches (48%), nervousness (26%), decrease in physical strength (16%), loss of memory (14%), sleeping disturbances and somnolence were the most frequent complaints. Scleroderma-like skin changes were found in ten subjects, but only six of them had any neurological disturbances. Occupational exposure to vinyl chloride was lower in workers without neurological findings. Frequency of the arterial hypertension was the same in both groups, whereas acroparesthesias, Raynaud's syndrome, and increased gamma GTP serum activity were significantly more frequent in workers with neurological disturbances. Sixty-two per cent of the neurologically positive group and only 24% of the negative group reported euphoric or narcotic states after exposure. This probably indicates episodic exposures to high concentrations of vinyl chloride. This difference points to a possibility that neurological disturbances may be related to short exposures to peak concentrations. The neurological injury may be both a direct neurotoxic effect of vinyl chloride and secondary to vascular disorders.

Adult↗
PubMed1989

[Exposure to vinyl chloride in the Polish industry].

Information concerning exposure to vinyl chloride collected in Occupational Hygiene Departments of Sanitary-Epidemiological Stations were verified. On the basis of the studies performed it was found that about 3700-4000 persons in Poland are occupationally exposed to vinyl chloride; 400 of these workers are employed at the synthesis and polymeryzation of vinyl chloride, and the others at plasticination and processing of polyvinyl chloride. About 200 workers employed in 3 plants of vinyl chloride polymerization and synthesis and about 30 employees of one of the plants processing this compound are exposed to vinyl chloride whose concentration exceeds the hygienic standard accepted in Poland (30 mg/m3).

Air Pollutants, Occupational↗
PubMed1996

Characterization by two-endpoint comparisons of the genetic toxicity profiles of vinyl chloride and related etheno-adduct forming carcinogens in Drosophila.

The genetic toxicity profiles of vinyl chloride (VCl), vinyl bromide (VBr), ethyl carbamate (EC), vinyl carbamate (VC) and some structurally related chemicals were investigated in both somatic and germ cells of Drosophila melanogaster. In the white/white+ eye mosaic assay, a screening system measuring predominantly homologous recombination in somatic cells, only marginal genotoxic activities were observed for acetyl chloride (ACl), glycolaldehyde (GCA), 2,2'-dichlorodiethyl ether (DDE) and methyl carbamate (MC), whereas VCl, 2-chloroacetaldehyde (CAA), VBr, 2-bromoacetaldehyde (BAA) and EC were clearly recombinogenic in the assay. Those chemicals proven to be recombinogenic in somatic cells were investigated further in postmeiotic male germ cells, utilizing as descriptors of their genotoxicity I(CL/RL) and M(exr-)/M(exr+) indices. The I(CL/RL) index is the rate of induced chromosome loss (CL), a clastogenic event, divided by the forward mutation rate, measured as recessive lethal (RL) mutations in 700 loci of the X-chromosome. The M(exr-)/M(exr+) mutation enhancement ratio is obtained by determining RL under excision repair deficient versus repair proficient conditions. With I(CL/RL) values (2.7-6.9) similar to those obtained for cross-linking agents, vinyl chloride, vinyl bromide, ethyl carbamate and vinyl carbamate are all efficient clastogenic agents in Drosophila germ cells. In the absence of excision repair, however, neither CEO nor CAA gave a hypermutability response (M(exr-)/M(exr+) approximately 1). By contrast, VCl, VBr, EC and VC showed clearly enhanced M(exr-)/M(exr+) ratios, suggesting that these compounds produce some repairable DNA modification(s) that are not generated by their epoxides. This unexpected finding points to the formation of other, yet unknown, metabolites of vinyl chloride, vinyl bromide, ethyl carbamate and vinyl carbamate. Our results support the concept that the epoxides chloroethylene oxide (CEO), bromoethylene oxide (BEO) and vinyl carbamate epoxide (VCO) are the most essential mutagenic intermediates. Compared to chloroethylene oxide (CEO), 2-chloroacetaldehyde (CAA) was approximately 50 times less effective in the induction of RL, whereas BAA was inactive as a mutagen. These findings are consistent with the general view that CAA and BAA play no major role in the genotoxic action of vinyl halides.

Animals↗
PubMed1978

[Multistage studies aimed at early detection of chronic effects of vinyl chloride and mercury vapors].

168 persons occupationally exposed to vinyl chloride and 236 persons exposed to mercury in plants electo two-stage medical and laboratory examinations. Workers exposed to vinyl chloride in average concentrations of 133 mg/m3 were found to show megalohepatia and abnormal enzymatic tests results (transaminic, A1AT, AP). The frequency of disturbances in workers exposed to vinyl chloride, average concentration 17.9 mg/m3, was considerably lesser. The second stage of studies involved those exposed to vinyl chloride for more than 10 years, with megalohepatia and at least 1 abnormal enzymatic test. No angiosarcoma was found. An analysis of the diagnostic value of biological tests used, indicated a great usability of liver scintigraphy and vascular system examinations for early diagnosis of vinyl chloride intoxications. In the plant where workers were exposed to mercury the Hg concentrations were found to range from 0.05 to 0.07 mg/m3. No significant differences between these workers and the control group were found, in respect to medical and laboratory examinations. The second stage of studies involved 118 persons exposed to mercury in concentrations above 20 mg/m3 of air, no matter how long the exposure lasted. The second stage of studies consisted of extensive biochemical studies, examinations of the liver using isotopic scintigraphy, psychological, psychiatric examinations and encephalographic determinations. Psychological, psychiatric and encephalographic examinations were said to be of great importance in early diagnosis of chronic mercury intoxications.

Air↗
PubMed1992

Aerobic vinyl chloride metabolism in Mycobacterium aurum L1.

Mycobacterium aurum L1, capable of growth on vinyl chloride as a sole carbon and energy source, was previously isolated from soil contaminated with vinyl chloride (S. Hartmans et al., Biotechnol. Lett. 7:383-388, 1985). The initial step in vinyl chloride metabolism in strain L1 is catalyzed by alkene monooxygenase, transforming vinyl chloride into the reactive epoxide chlorooxirane. The enzyme responsible for chlorooxirane degradation appeared to be very unstable and thus hampered the characterization of the second step in vinyl chloride metabolism. Dichloroethenes are also oxidized by vinyl chloride-grown cells of strain L1, but they are not utilized as growth substrates. Three additional bacterial strains which utilize vinyl chloride as a sole carbon and energy source were isolated from environments with no known vinyl chloride contamination. The three new isolates were similar to strain L1 and were also identified as Mycobacterium aurum.

Biodegradation, Environmental↗
PubMed1997

The GST T1 and CYP2E1 genotypes are possible factors causing vinyl chloride induced abnormal liver function.

Vinyl chloride monomer (VCM) is hepatotoxic as well as carcinogenic in humans. There are reports that exposure to VCM seems to induce abnormal liver function, liver fibrosis, cirrhosis, portal hypertension, and angiosarcoma of the liver. In vivo, VCM is metabolized by cytochrome P450 2E1 (CYP2E1) to form the electrophilic metabolites, chloroethylene oxide (CEO) and chloroacetaldehyde (CAA), which may either cause cell damage or be further metabolized and detoxified by glutathione S-transferases (GSTs). This study investigated whether or not the genotypes CYP2E1, glutathione S-transferase theta (GST T1) and mu (GST M1) correlated with abnormal liver function found in vinyl chloride exposed workers. For this study, 251 workers from five polyvinyl chloride plants were enrolled. The workers were classified into two exposure groups (high and low) and the degree of exposure was determined based on their job titles and airborne VCM concentration. The activity of serum alanine aminotransferase (ALT) was used as the parameter of liver function. The genotypes CYP2E1, GST T1 and GST M1 were determined by polymerase chain reaction and restriction fragment length polymorphism on peripheral white blood cell DNA. Other potential risk factors were also ascertained and the confounding effect was adjusted accordingly. Stratified analyses were used to explore the correlation between the alteration of liver function and the genotypes CYP2E1, GST T1 and GST M1 among the workers exposed to different levels of VCM. The following results were obtained (1) at low VCM exposure, the odds ratio (OR) of positive GST T1 on abnormal ALT was 3.8 (95% CI 1.2-14.5) but the CYP2E1 genotype was not associated with abnormal ALT. (2) At high VCM exposure, a c2c2 CYP2E1 genotype was associated with increased OR on abnormal ALT (OR 5.4, 95% CI 0.7-35.1) and positive GST T1 was significantly associated with decreased OR on abnormal ALT (OR 0.3, 95% CI 0.1-0.9). (3) Multiple linear and logistic regression also showed strong interactions of the VCM exposure to CYP2E1 as well as to the GST T1 genotype. These observations suggest that the two genotypes, CYP2E1 and GST T1, may play important roles in the biotransformation of VCM, the effect of which leads to liver damage.

Adult↗
PubMedDate not supplied

The hepatic role in carcinogenesis and its early detection--the vinyl chloride model.

The liver's role in vinyl chloride toxicity and carcinogenicity is providing a better understanding of the chemical carcinogenesis mechanism. A variety of both malignant and benign hepatic tumors has been demonstrated with prolonged exposure to vinyl chloride. The multi-system involvment of this carcinogen and toxin has provided a model for the study of chemical carcinogenesis common to both man and animal. Clinical studies have shown the usefulness of biochemical, radioisotopic, and radiological studies in the detection of toxic and carcinogenic lesions. Animal studies have demonstrated the biochemical metabolism by the liver of vinyl chloride-produced intermediates which are mutagenic in bacterial systems and may be the ultimate carcinogens. Hepatic subcellular enzyme studies prove preliminary evidence of cellular adaptation and increased detoxification. Disruption of this oxidization and detoxification balance may be the key to the malignant transformation of cells. A working hypothesis is presented which may explain the metabolism of vinyl chloride into mutagenic intermediates by the liver cell and the development of malignant transformation by extra hepatic sinusoidal lining cells, lung cells, and brain tissue.

Animals↗
PubMed1983

Angiosarcoma and hepatocellular carcinoma in vinyl chloride workers.

The livers from five vinyl chloride workers are described. They show angioformative and hepatocellular growth disturbance in varying proportions: angiosarcoma in four cases, liver cell hyperplasia in all, hyperplastic nodules in three cases and hepatocellular carcinoma in two cases. In one case the transition between hyperplastic nodule and hepatocellular carcinoma is demonstrated. The relationship between these changes and vinyl chloride exposure is discussed, with evidence that they are causally related.

Adult↗
PubMed1987

Increased collagen synthesis and cross-link formation in the skin of rats exposed to vinyl chloride monomer.

Rats treated orally with vinyl chloride (30 mg/kg) daily for 2 years developed a syndrome which included thickening of the skin. Analysis of the skin showed a 26% increase in collagen deposition per unit weight, and a corresponding 30% increase in the levels of glycosylated lysine and hydroxylysine. There was a significant increase in the amounts of the labile borohydride reducible cross-links, such as the intermolecular hydroxylysinonorleucine (+31%) and histidinomerodesmosine (+42%) as well as the intramolecular allysine aldol cross-links (+17%). These results provide evidence that fibrosis of the skin is one of the pathological consequences of exposure to vinyl chloride.

Animals↗
PubMed1989

Cohort and case-control analyses of workers exposed to vinyl chloride: an update.

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.

Brain Neoplasms↗
PubMed2002

Preparation of albumin preferential surfaces on poly(vinyl chloride) membranes via surface self-segregation.

Poly(vinyl chlorides)-graft-[omega-stearyl-poly(ethylene oxide)] (PVC-g-SPEO), which has a poly(vinyl chloride) (PVC) backbone, poly(ethylene oxide) (PEO) side chain, and stearyl end groups, has been synthesized. Self-organizing blends of the amphiphilic comb polymer in poly(vinyl chlorides) have been examined as a means to create albumin preferential surfaces on polymer films. X-ray photoelectron spectroscopy (XPS) analysis indicates substantial surface segregation of the PVC-g-SPEO. A surface concentration of 59.9 EO wt % is achieved by the solution casting and heat treatment of a film with a bulk concentration of only 3.78 EO wt %. In the aqueous environment, the surface rearrangement of PVC-g-SPEO/PVC blend film is limited and presents a high interfacial energy and high depolar component of interfacial energy due to the "tail-like" SPEO side chain. Protein adsorption tests confirm that PVC-g-SPEO/PVC blend films absorb high levels of albumin and dramatically resist fibrinogen adsorption. Surfaces to attract and reversibly bind albumin, which might diminish the occurrence of thrombosis, inflammation, and infection, are developed by self-organizing blends of the amphiphilic comb polymer in poly(vinyl chlorides).

Adsorption↗