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PubMed1979

Measurement of atmospheric vinyl chloride.

Methods for atmospheric vinyl chloride measurement have been reviewed. The lowest detection limits and most specific measurement are achieved by scrubbing atmospheric samples with activated charcoal, desorbing the vinyl chloride, and assaying it by gas chromatography (GC). NIOSH currently recommends collecting samples using tubes packed with 150 mg of coconut shell charcoal, desorbing with carbon disulfide, and analyzing by GC equipped with flame-ionization detection (FID); the method is capable of detecting less than 1 ppm vinyl chloride and has an apparent recovery of abo the ppb level with no loss of accuracy or precision. Some field methods, such as infrared analysis and conductivity measurement, are capable of detecting 1 ppm or lower but are subject to interferences by other contaminants; th-y could be useful for evaluating sources of vinyl chloride leaks and for continuous monitoring. Permeation tubes are superior to gravimetric or volumetric methods for generating atmospheres of known vinyl chloride concentration.

Air Pollutants↗
PubMed2002

Natural formation of vinyl chloride in the terrestrial environment.

Vinyl chloride is a highly reactive and toxic substance which is widely used in industry. It is the parent compound of poly(vinyl chloride) (PVC), one of the most important industrial polymers. Until now, it was thought that vinyl chloride found in the environment is exclusively man-made or results from the degradation of other anthropogenic substances, such as trichloroethylene and tetrachloroethylene. Here, we demonstrate that vinyl chloride also has natural sources. Soil air and ambient air from a rural area in Northern Germany were investigated for volatile chlorinated halocarbons. The concentrations of vinyl chloride in the soil air were significantly enhanced as compared to ambient air, indicating a natural formation of this compound in the soil. A series of laboratory experiments using different soils and model compounds was conducted, which clearly proved that vinyl chloride could be produced during soil processes. We propose that this highly reactive compound can be formed during the oxidative degradation of organic matter in soil, for example, in a reaction between humic substances, chloride ions and an oxidant (ferric ions or hydroxyl radicals). The redox-sensitive aromatic compounds in soil such as catechols and o-quinones can be degraded to CO2, accompanied by the release of vinyl chloride and other volatile chlorinated compounds. This process could have started in the Late Silurian to Early Devonian, 400 million years ago, when the first soils on earth evolved.

Carbon Dioxide↗
PubMed1981

On the acute hepatotoxicity of inhaled vinyl chloride.

Acute toxicity of vinyl chloride exposure was studied by morphological methods in three species (mouse, rat, and rabbit). In rats and rabbits exposure to 1500 ppm of vinyl chloride for 24 hours did not cause pathological changes. In mice shorter inhalation (4 and 8 hours) resulted in circulatory changes, while longer exposure (12 and 24 hours) caused vasomotor paralysis followed by characteristic shock; subsequent alterations could be seen in the liver and lungs. The acute hepatotoxicity of vinyl chloride could not be proved.

Animals↗
PubMed1976

Cytochrome P-450 and the metabolism of vinyl chloride.

The oxidation of vinyl chloride to non-volatile products is dependent on NADPH and microsomal enzymes. The addition of vinyl chloride to microsomes causes a Type 1 spectra shift, similar to that seen for phenobarbital [11[ which indicates the direct involvement of a cytochrome P-450 species; this difference spectrum is characteristic of substrate binding to this type of enzyme. A glutathione conjugate is probably formed, perhaps via a reactive intermediate.

Animals↗
PubMed2006

Molecular mechanisms of carcinogenesis by vinyl chloride.

In 1974 vinyl chloride (VC), a gas used in the plastics industry, was shown to be a human carcinogen, inducing a very rare type of tumor, angiosarcoma of the liver. The same type of tumor was induced in rodents exposed to VC thus providing an excellent model for mechanistic studies. Here, we review the numerous studies on the mechanism of action of VC with particular emphasis on the DNA products induced by this strong alkylating agent. In particular, the genotoxicity, repair mechanisms, in vivo formation and tumor mutation spectra by etheno-adducts will be analysed and possible approaches for future research suggested.

Animals↗
PubMed2002

Embryo-fetal developmental and reproductive toxicology of vinyl chloride in rats.

Vinyl chloride (VC) exposure is primarily via inhalation in the workplace. The primary target organ of VC toxicity is the liver and occupational exposure to VC leads to hepatic angiosarcoma. However, based on epidemiological studies, researchers have been unable to ascertain the effect of occupational VC exposure on embryo-fetal development or reproductive function. A limited number of animal studies available in the literature have examined the effect of VC on embryo-fetal development, however, there are no published studies on the effect of VC exposure on reproductive capability. The current study was designed to assess the potential maternal and/or embryo-fetal developmental and 2-generation reproductive toxicity of inhaled VC in CD(R) Sprague-Dawley rats at exposure levels of 0, 10, 100, and 1100 ppm. In the embryo-fetal/developmental toxicity study, the female rats were exposed to VC daily from gestation day (GD) 6 through 19. In the reproductive toxicity study, the F(0) generation male and female rats were exposed to VC for a 10-week premating and 3-week mating periods. The F(0) generation male rats were exposed to VC until terminal euthanasia. The F(0) generation female rats were exposed from GD 0 through GD 20 and lactation day (LD) 4 through LD 25. Our results indicate that up to 1100 ppm VC exposure did not adversely affect embryo-fetal developmental or reproductive capability over 2 generations in rats. The primary target organ of VC, the liver, was affected as evidenced by an increase in liver weight and/or histologically identified cellular alterations, such as centrilobular hypertrophy at 100 and 1000 ppm. Based on the results of these studies, the no observed adverse effect level (NOAEL) for embryo-fetal/development is 1100 ppm, and the NOAEL for reproduction is 1100 ppm. The results from the current studies, which are a more comprehensive embryo-fetal/developmental and reproduction study, may be incorporated into future risk assessments of occupational exposure to VC where concerns regarding the effects of VC exposure remain.

Administration, Inhalation↗
PubMed1997

[Quantitative evaluation of health risk associated with occupational inhalation exposure to vinyl chloride at production plants in Poland].

Vinyl chloride is classified by the IARC in group 1-human carcinogens. In Poland occupational exposure to vinyl chloride is found among workers employed in many branches of industry, among others in the industry of vinyl chloride synthesis and polymerization as well as in the plastics, footwear, rubber, pharmaceutical and metallurgical industries. Concentrations observed range from the noon-determinable level to 90 mg/m3, at the MAC value equal to 5 mg/m3. Neoplasm of liver is a major carcinogenic effect of vinyl chloride. Hence, the health assessment focused on this critical risk. Four different linear dose-response models, developed by several authors and based on results of different epidemiological studies, were used to characterise the extent of cancer risk depending on the level of vinyl chloride concentrations. The estimated risk related to a forty-year employment under exposure equal to MAC values (5 mg/m3) fell within the range from 2.9.10(-4) to 2.6.10(-3). As the figures depict it did not exceed the acceptable level (10(-3)).

Air Pollutants, Occupational↗
PubMed1976

Preparation of vinyl chloride standards using a permeation tube.

Vinyl chloride permeation tubes have been utilized to provide a convenient and accurate standardization procedure for charcoal tube monitoring of atmospheric vinyl chloride. The procedure circumvents the need of determining charcoal desorption efficiencies and eliminates the handling of free vinyl chloride in the laboratory preparation of vinyl chloride standards.

Air Pollutants↗
PubMed1981

Malignant tumors after chronic exposure to vinyl chloride.

Correlations between exposure to vinyl chloride and the development of malignant tumors in the liver have been know since 1974 and have been confirmed by many an experimental investigation. Based on the evaluation of mortality statistics from nine different countries an increased incidence of malignant tumors of the lung, the gastrointestinal tract, and the central nervous system (CNS), and of malignant lymphomas is documented in connection with exposure to vinyl chloride. Statistically significant increases, however, are only found in the incidence of malignant liver tumors. Metabolism and toxicology of vinyl chloride are discussed in detail.

Animals↗
PubMed1977

Pharmacokinetics of vinyl chloride in the rat.

When rats are exposed to [14C]vinyl chloride in a closed system, the vinyl chloride present in the atmosphere equilibrates with the animals' organism within 15 min. The course of equilibration could be determined using rats which had been given 6-nitro-1,2,3-benzothiadiazole. This compound completely blocks metabolism of vinyl chloride. The enzymes responsible for metabolism of vinyl chloride are saturated at an atmospheric concentration of vinyl chloride of 250 ppm. Pharmacokinetic analysis shows that no significant cumulation of vinyl chloride or its major metabolites is to be expected on repeated administration of vinyl chlorides. This may be consistent with the theory that a reactive, shortly living, metabolite which occurs in low concentration only, may be responsible for the toxic effects of vinyl chloride.

Animals↗
PubMed1978

Gas chromatographic studies of vinyl chloride in air by catalytic hydrogenation to ethyl chloride.

In order to investigate the amount of vinyl chloride in air, the hydrogenation of vinyl chloride to ethyl chloride is used. This method of determination is preferable to the other methods described in the literature because: (a) it proves that only vinyl chloride goes through hydrogenation by its displacement to the ethyl chloride peak in the chromatogram; (b) the actual amount of vinyl chloride can be obtained in the case of superimposed or interfering peaks (e.g., various gases contained in air samples), either by calculating the ethyl chloride peak area or by the reduction of the peak area in the region of the same retention time as the vinyl chloride peak in the related chromatogram. In this study various kinds of catalysts for hydrogenation purposes at temperatures ranging from -20 to 250 degrees have been used. Among the catalysts used palladium gives the best results at low temperature.

Air Pollutants↗
PubMed2001

A case of polymyositis with anti-histidyl-t-RNA synthetase (Jo-1) antibody syndrome following extensive vinyl chloride exposure.

Occupational exposure to vinyl chloride monomers is known to induce Raynaud's phenomenon, periportal fibrosis, liver angiosarcoma and scleroderma-like syndrome. We report the first case of occupational polymyositis in a 58-year-old man exposed to vinyl chloride. A dysimmune process was strongly suspected as having induced vinyl chloride disease. Our patient had an anti-histidyl-t-RNA-synthetase (Jo1) antibody, which has never to our knowledge been reported in this occupational disease.

Antibodies, Antinuclear↗
PubMed1981

Neoplastic and nonneoplastic effects of vinyl chloride in mouse lung.

Neoplastic effects of vinyl chloride were studied in lungs of 27 mice exposed to vinyl chloride monomer at 2500 and 6000 ppm for 5 and 6 months (large doses and long-term exposure). Pulmonary tumors were observed in 26 of 27 experimental animals. Light microscopy showed the tumors to be multiple and arranged in either tubulo-papillary or adenomatous formations. Although occasional mitotic divisions and invaginations into the bronchiolar lumen were observed, no metastases were found. By electron microscopy, short microvilli, tight junctions between two adjacent cells, appearance of osmiophilic lamellar bodies, large mitochondria of irregular shape, well developed Golgi complexes, continuous or discontinuous basement membranes, occasional appearance of "sequestration" and of crystalloids and lack of both cilia and mucous secretory granules were observed as characteristic features of the neoplastic cells. Some of the cells were poorly differentiated and were equipped with poorly developed organoids, without formation of osmiophilic lamellar bodies. The pulmonary tumors corresponded to "alveologenic" tumors. It is suggested that the neoplastic cells were transformed from type II alveolar epithelium via its hyperplastic form. Nonneoplastic effects of the chemical were also studied in the 27 mice. Major light microscopic alterations observed were proliferation and hypertrophy of the terminal bronchiolar cells, consisting of ciliated and Clara cells, hypersecretion of the epithelial mucin in the goblet cells of both the bronchial and the proximal bronchiolar epithelium, hyperplasia of alveolar epithelium, mobilization of alveolar macrophages and occasional presence of peribronchial or bronchiolar chronic inflammation. Electron microscopically, Clara cells of the terminal bronchiolar epithelium showed proliferation of the rough and smooth surfaced endoplasmic reticulum and appearance of large and abnormally shaped mitochondria. Similar alterations were found in the ciliated cells. Submicroscopic changes of pulmonary alveoli were represented by focal thickening of the basement membrane, multiple foci of hyperplastic type II cell (the precondition of the alveologenic tumor), active discharge of osmiophilic lamellar bodies from the type II cell and phagocytosis of the bodies by macrophages, appearance of cholesterol crystalloids in the macrophages, degeneration of alveolar septal cells and occasional appearance of a large nucleus with swelling of the capillary endothelium. The neoplastic effect of vinyl chloride of smaller doses (100, 10, 1 and 0 [control] ppm) and shorter exposure (four weeks) was studied in lungs of 120 mice. Our preliminary observation indicated that sacrificed animals at 40 weeks after the exposure showed productions of the alveologenic tumor in 5 of 9 (100 ppm), 2 of 9 (10 ppm), 1 of 9 (1 ppm) and 0 of 10 (control = 0 ppm). A dose-response relation was considered in the incidence of the alveologenic tumor production of vinyl chloride. It is concluded that mouse lung is an extremely sensitive indicator of the oncogenicity of vinyl chloride.

Aerosols↗
PubMed1984

Carcinogenicity and epidemiological profile analysis of vinyl chloride and polyvinyl chloride.

The carcinogenicity of vinyl chloride and polyvinyl chloride (VC/PVC) is reviewed with specific attention to the gaps in knowledge for risk estimation and epidemiological presentation of the available data. Although experimental studies have demonstrated the carcinogenicity and mutagenicity of VC/PVC in general, the epidemiologic studies available for review do not include an assessment of carcinogenic risk among humans exposed to these chemicals. This conclusion is based on the observation that the majority of cohort studies reviewed lacked sufficient statistical power because of small sample sizes. Further, in epidemiological studies, individuals were not followed over an adequate period of time during which cancer could become clinically manifest.

Animals↗
PubMed1993

[Occupational exposure to toxic substances during the production of vinyl chloride and chlorinated organic solvents].

Determinations of vinyl chloride and chlorinated organic solvent concentrations at the breathing zone of the industrial workers employed at the vinyl chloride synthesis process have revealed excessive exposure to certain chlorinated compounds. The average exposures of the operators of the vinyl chloride synthesis apparatus have been found to be 13 MAC for vinyl chloride and 2.5 MAC for 1,2-dichloroethane. The operators of the solvent synthesis apparatus have been exposed to average concentrations of carbon tetrachloride up to 3.5 MAC, the corresponding values for the fitters being 4.5 MAC for vinyl chloride, 3.5 MAC for 1,2-dichloroethane, and 3 MAC for carbon tetrachloride.

Air Pollutants, Occupational↗
PubMed2003

Detoxification of vinyl chloride to ethene coupled to growth of an anaerobic bacterium.

Tetrachloroethene (PCE) and trichloroethene (TCE) are ideal solvents for numerous applications, and their widespread use makes them prominent groundwater pollutants. Even more troubling, natural biotic and abiotic processes acting on these solvents lead to the accumulation of toxic intermediates (such as dichloroethenes) and carcinogenic intermediates (such as vinyl chloride). Vinyl chloride was found in at least 496 of the 1,430 National Priorities List sites identified by the US Environmental Protection Agency, and its precursors PCE and TCE are present in at least 771 and 852 of these sites, respectively. Here we describe an unusual, strictly anaerobic bacterium that destroys dichloroethenes and vinyl chloride as part of its energy metabolism, generating environmentally benign products (biomass, ethene and inorganic chloride). This organism might be useful for cleaning contaminated subsurface environments and restoring drinking-water reservoirs.

Bacteria, Anaerobic↗