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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↗
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↗
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↗
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↗
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↗
PubMed1976

Immunological mechanisms in the pathogenesis of vinyl chloride disease.

Vinyl chloride (VC) disease is a multisystem disorder incorporating Raynaud's phenomenon, acro-osteolysis, thrombocytopenia, portal fibrosis, and hepatic and pulmonary dysfunction. Immunological and immunochemical investigations showed the presence of circulating immune complexes in 19 out of 28 patients with the disease and in a further two out of 30 workers exposed to VC. The immunological data were reviewed in relation to the clinical picture of the disease and to the available evidence on the metabolism of VC. The results suggest that VC disease is an immune complex disorder and that the immune response is initiated by the adsorption of VC or a metabolite on to tissue or plasma protein.

Autoantibodies↗
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↗
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↗
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↗
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↗
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↗
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↗