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PubMed1981

[Difficulties of early diagnosis of liver damage in persons exposed to vinyl chloride].

The authoress presents results of examinations of 228 vinyl chloride exposed workers. Considerable exposure is revealed by 5 cases of acroosteolysis and 45 cases of vascular disturbances in peripheral segments of extremities. The statistical analysis of numerical values of GPT, GOT, GGTP, AP, serum Che, bilirubin, prothrombin and proteinogram did not show any significant differences between the vinyl chloride exposed group and 70 controls. Of 50 persons in whom additionally BSP test and liver scintigram were performed and half-life of activity decrease was determined after intravenous administration of Bengal rose 131-J, 26 cases of moderate megalohepatia (scintigram) and 9 cases with positive BSP test were found. The half-life of 131-J elimination from blood lasted about 10-26 minutes and did not correlate with BSP test. The authoress draws attention to the lack of reliable and generally accessible methods of early diagnosis of hepatopathy in vinyl chloride exposed workers.

Adult↗
PubMed2005

Liver function assessment in workers exposed to vinyl chloride.

OBJECTIVE: To investigate liver function in vinyl chloride workers and assess its relation with current/past occupational exposure to vinyl chloride monomer (VCM). METHODS: A medical examination including the execution of liver function tests (LFTs) and liver ultrasonography was executed in a group of 757 workers with a long-standing service in the production of VCM/polyvinylchloride (PVC). Cumulative and maximum VCM exposures were calculated. History of viral hepatitis and alcohol intake were carefully investigated. Regression analysis explored the association between abnormal LFTs and a group of possible determinants (VCM cumulative and maximum exposure, BMI, age, history of viral hepatitis, alcohol and triglyceride levels). Also, synergistic effect between VCM and a history of hepatitis was analysed, as well as the possible association between VCM exposure and aspartate aminotransferase/alanine amino transferase (AST/ALT) ratio >1. Distribution of abnormal LFTs was also assessed in relation to the results provided by liver ultrasonography. RESULTS: The most frequently abnormal serum parameters were, in decreasing order: total cholesterol (27.3%), triglycerides (12.2%), total bilirubin (9.1%), gamma glutamil transpeptidase (GGT; 9.0%) and ALT (8.2%). The AST/ALT ratio >1 was present in 28.1% of workers. Abnormal LFTs were not found to be associated with current or past VCM exposure. High ALT resulted positively associated with BMI, AST with alcohol intake, GGT with alcohol intake and triglycerides. No synergistic effect on LFTs of exposure to VCM and a history of hepatitis was observed. The AST/ALT ratio >1 was not found to be associated with VCM exposure. The prevalence of abnormal LFTs was higher in case of liver steatosis (ALT) or periportal fibrosis (GGT), but not in case of pure hepatomegaly, as documented by ultrasonography. CONCLUSIONS: Liver function assessment only including LFTs is not able to detect VCM-induced liver damage, but reveals alterations due to non-occupational factors, such as dietary and/or metabolic disfunctions. The LFTs are however of importance to detect conditions that could recommend avoidance of exposure to VCM and are useful for medical counselling and health promotion purposes.

Adult↗
PubMed1993

Contrasting effects of 1,1,1-trichloroethane on [14C]vinyl chloride metabolism and activation in hepatic microsomes from phenobarbital- and isoniazid-treated rats.

The interaction of 1,1,1-trichloroethane (TCE), a widely used chlorocarbon solvent, on the metabolism and activation of [14C]-vinyl chloride in rat hepatic microsomes was investigated to determine the effects of combined exposures to these compounds. In microsomes from phenobarbital (PB)-treated rats, TCE increased vinyl chloride-protein binding and vinyl chloride aqueous metabolite formation over twofold when vinyl chloride 0.32% (v/v) and TCE (0.65%) are incubated together. In contrast, under similar incubation conditions, TCE inhibited vinyl chloride metabolism and protein binding up to 45% in microsomes from isoniazid-treated animals. TCE also inhibited vinyl chloride metabolism and binding in microsomes from untreated rats, but to a lesser degree. Like the effect of TCE on vinyl chloride-protein binding, TCE increased vinyl chloride binding to DNA approximately 130% in microsomes from PB-treated rats, yet inhibited vinyl chloride-DNA binding in microsomes from isoniazid-treated and untreated animals. Consistent with TCE effects on vinyl chloride binding and aqueous metabolite production, TCE further increased cytochrome P450 loss due to vinyl chloride metabolism in microsomes from PB-treated rats, but was inhibitory to cytochrome P450 loss due to vinyl chloride metabolism in microsomes from isoniazid-treated and untreated rats. These data demonstrate that the relatively metabolically inert solvent, 1,1,1-trichloroethane, can directly increase vinyl chloride metabolism and activation catalyzed by the phenobarbital-inducible isozymes, but is inhibitory toward vinyl chloride metabolism catalyzed by the isoniazid-inducible CYP2E1.

Animals↗
PubMed1981

EPA programs of vinyl chloride monitoring in ambient air.

Before development of an emission standard for vinyl chloride, the Environmental Protection Agency (EPA) conducted three programs to measure vinyl chloride (VC) concentrations in air around plants which either manufacture VC or use it. A brief monitoring survey conducted by EPA Regional Offices found VC in ambient air around poly(vinyl chloride) (PVC) production plants. As a consequence of this survey, a second monitoring program was established to measure VC in the air around VC and PVC production plants. This program found some relatively high concentrations of VC in ambient air around the plants. This program found maximum 24-hr average rations concentrations ranging from 0.32 to 10.6 parts of VC per million parts of air. The program also found an apparent relationship between certain emission excursions and ambient VC concentrations. A third monitoring program was established to measure VC around PVC fabrication plants. This monitoring program found much less VC around PVC fabrication plants than around VC and PVC production plants. In conclusion, VC was found in ambient air around VC production plants and PVC fabrication plants. However, the data show that much less VC escapes into surrounding air from PVC fabricating plants than from VC and PVC production plants.

Air Pollutants↗
PubMed1999

A critical review of the epidemiologic literature on health effects of occupational exposure to vinyl chloride.

We have attempted to critically review and summarise the collective epidemiologic evidence concerning the association of occupational vinyl-chloride exposure with human health outcomes, including cancer, liver cirrhosis, cardiovascular disease, nonmalignant respiratory disease and acroosteolysis. Based on data from individual reports, qualitative and, where possible, quantitative summaries are presented. With respect to cancer, which has been extensively studied, angiosarcoma of the liver is the only malignancy causally related to vinyl-chloride exposure. Hypothesised associations between vinyl chloride and cancers of other sites, namely lung, brain and lymphohaematopoietic system, are not consistently supported by the available data. Similarly, the epidemiologic data relating vinyl chloride to nonmalignant disease, while quantitatively limited and qualitatively suboptimal, do not support a causal association for any of the studied disorders. In summary, a comprehensive review of the relevant epidemiologic literature revealed that occupational vinyl-chloride exposure has not been conclusively or causally linked to any adverse health outcome, with the exception of angiosarcoma of the liver.

Carcinogens↗
PubMed1979

Biochemical alterations in livers of rats exposed to vinyl chloride.

Sprague-Dawley rats were exposed to vinyl chloride to determine the earliest sequential biochemical changes occurring with liver injury before anglosarcoma development. Activity of glucose-6-phosphatase, a key gluconeogenic enzyme in the liver microsomal fraction, decreased 25% with respect to controls after 70 h of exposure. Glucose-6-phosphate dehydrogenase activity increased twofold after more than 100 h of exposure. Nonprotein sulfhydryl levels (glutathione and/or cysteine) showed a slight but progressive elevation, whereas glutathione reductase activity increased 50-60% during exposure to vinyl chloride.NADPH-cytochrome c reductase and mixed function oxidase were unchanged in the same microsomal fraction. There markers of liver mitochondrial, cytosol, and microsomal function. No significant histological changes were found on light microscopic examination during this exposure period. However, with electron microscopy, dilation of rough endoplasmic reticulum was seen in the animals exposed for more than 137 h. These enzymatic changes are considered to reflect early hepatocellular adaptation to vinyl chloride exposure with very mild or limited hepatocellular injury in its earliest stage.

Animals↗
PubMed1975

Gas-liquid chromatographic determination of vinyl chloride in alcoholic beverages, vegetable oils, and vinegars.

Vinyl chloride in foods is determined by gas-liquid chromatography either by direct injection of vinegars and alcoholic beverages or by headspace analysis of vegetable oils. The lower limit of detection is 10-15 ng/ml for direct injection and 1-10 ppb for headspace analysis. Confirmation by gas chromatography-mass spectrometry, single ion monitoring at m/c 62, is possible at 50 ppb for either method. The levels of vinyl chloride bottles were 0.0-1.6 mu-g/ml for alcoholic beverages, 0.0-8.4 mu-g/ml for vinegars, and 0.3-3.3 ppm for peanut oil.

Acetates↗
PubMed2003

Effect of polymer concentration on partitioning and molecular recognition in plasticized poly(vinyl chloride).

Mixtures of poly(vinyl chloride) (PVC) with plasticizers have been used in ion-selective electrodes for many years. The same material has proven useful in solid-phase microextraction (SPME), both with and without artificial receptors. We hypothesized that by changing the polymer concentration in plasticized PVC membranes containing artificial receptor from the standard 33 wt %, the selectivity of the extraction of barbiturates over similar molecules could be improved. Partition coefficients and receptor-substrate formation constants of a target species, phenobarbital, in membranes with various polymer concentrations were determined. Diffusion coefficients of the solute phenobarbital in receptor-free membranes were also determined. Kamlet-Taft solvatochromic properties beta and pi* were measured for the PVC/dioctyl sebacate materials. Cohesive energy densities were calculated for the same materials. Partition coefficients for phenobarbital (from aqueous solution to membrane) decrease as [PVC] increases, while the formation constants for the complex of the solute with its receptor increase. Diffusion coefficients decrease as the polymer concentration increases as well. The increase in polymer concentration brings about a decrease in hydrogen-bonding basicity and an increase in dipolarity and cohesive energy density. The values of the solvatochromic parameters determined at various compositions are highly correlated; thus, it is impossible to calculate how much each factor contributes to the changes associated with partition and complex formation. The solvatochromic "polarizability correction factor" has been determined to be 0 for PVC. In SPME experiments at 30%, 40%, and 50% (w/w) PVC, as polymer concentration increases, selectivity for barbiturate extraction over other cyclic imides becomes better in the presence of barbiturate receptor and worse without receptor.

Journal Article↗
PubMed1980

Experimental studies on the chronic toxic effects of vinyl chloride in rats.

Male rats were exposed to vinyl chloride at the concentrations of 50, 500, and 20 000 ppm, 5 hours daily, 5 days a week for 10 months. Morphological lesions in the liver and the testes detected by light and electron microscope and depression in body weight increase intensified with the duration of exposure. Increased relative weights of some organs and slight hematological and biochemical changes in blood during the course of the experiment were also observed. Some toxic effects including morphological liver injuries arose at the smallest exposure level, i. e., 50 ppm. Assuming 50 ppm as the threshold concentration for rats, the 5 ppm level has been estimated as the safe exposure limit in industry in relation to systemic effects of vinyl chloride.

Alanine Transaminase↗
PubMed1976

Monitoring liver disorders in vinyl chloride monomer workers using greyscale ultrasonography.

Recognition that vinyl chloride could be hepatotoxic led to a survey of workers to determine whether changes had been induced by past exposure, and to evaluate standard liver function tests as monitors of early liver abnormalities. Standard liver function tests were found to be unsuitable for the detection of such abnormalities in the population at risk. Of 487 workers examined, 102 (20-9%) had abnormalities on initial testing but only two were finally shown to have portal hypertension; in both cases, thrombocytopaenia provided the first diagnostic evidence since liver function tests were normal. Furthermore, 40 (35-7%) of 112 control subjects had initial test abnormalities. A sample of 19 workers with various exposures to vinyl chloride monomer were examined blind by greyscale ultrasonography. Five with minimal or no exposure were confirmed as normal but 12 of the remainder had abnormalities. These consisted of an enlarged portal vein (seven instances), splenomegaly (eight), and changes in hepatic texture (seven). Five of these 12 cases had previously been considered normal. It was concluded that greyscale ultrasonography had many advantages over standard methods for screening workers exposed to hepatotoxic chemicals, and should be the subject of a large scale evaluation.

Adult↗
PubMed1991

[Mutagenic and carcinogenic effects of vinyl chloride monomers in humans].

The use of vinyl chloride monomer in industry dates back to the late 1930s. Today the number of occupationally exposed industrial workers is estimated to be several million. After the first described cases of cancer among workers exposed to high concentrations of this gas, extensive research was initiated into its possible mechanism of action on the living organism. This paper is a review of some current knowledge about the action of vinyl chloride monomer as a substance which after metabolic activation in the organism becomes a strong carcinogenic and mutagenic agent.

Carcinogens↗
PubMed1977

Alkylation of RNA by vinyl chloride metabolites in vitro and in vivo: formation of 1-N(6)-etheno-adenosine.

Rat liver microsomes were incubated with NADPH, 1,2-[(14)C] vinyl chloride and poly-adenosine. The latter was reisolated from the incubations and hydrolyzed. The radioactivity, originating from [(14)C] vinyl chloride, which was irreversibly attached to the poly-adenosine was confined to 1-N(6)-etheno-adenosine (3beta-ribofuranosyl-imidazo [2,1,i] purine). When rats were exposed to 1,2-[(14)C] vinyl chloride, part of the radioactivity was incorporated into RNA of liver. This radioactive labelling exhibited a first maximum, 14 h, and a second maximum, 72 h after ending the exposure. Analysis of hydrolysate of liver RNA showed that all natural nucleosides of RNA were labelled. Besides, small amounts of radioactivity could be detected which were confined to 1-N(6)-etheno-adenosine. The experiments support the theory that vinyl chloride metabolites react with adenosine moieties of nucleic acid under formation of 1-N(6)-etheno-adenosine. Furthermore, the results show that measurement of incorporation of radioactivity into nucleic acids after exposure of animals to radioactive vinyl chloride is not applicable as a means of determining the alkylating potency of vinyl chloride metabolites towards nucleic acids in vivo.

Adenine Nucleotides↗
PubMed1990

On the changes in peripheral red cells in mice exposed to vinyl chloride monomer.

The diseases known as the Vinyl Chloride Monomer (VCM) Syndrome include hepatic angiosarcoma, acroosteolysis and Raynaud's phenomenon. These, however, are known to be clinically recognizable from several to over 10 years after the actual exposure to VCM. By fluorescence microscopy the authors examined smeared samples of peripheral blood obtained from vinyl chloride workers, and observed the existence of basophilic stippled erythrocytes (BSE). In this paper, we report the changes of peripheral red cells during VCM exposure tests on mice. These changes in the peripheral blood could be observed as early as 24 hours after the start of the VCM exposure at higher concentrations, and in 72 hours even at comparatively lower VCM levels of 30 to 40 ppm. The tests have also confirmed that the rate of emergence of BSE differs according to the level of VCM and to the duration of VCM exposure.

Animals↗
PubMedDate not supplied

Toxicity of vinyl chloride and polyvinyl chloride as seen through epidemiologic observations.

In 1974, vinyl chloride (VC) was first reported in the scientific literature to induce angiosarcoma of the liver in animals and humans. Further research has now demonstrated the carcinogenicity of this agent to other organs. Target organs for VC now include the liver, brain, and lung, and probably the lymphohematopoietic system. The carcinogenic risk has been extended to jobs associated with polyvinyl chloride (PVC) exposure. This is evidenced by cases of liver angiosarcoma reported among individuals employed in or residing near PVC fabrication facilities and by epidemiologic study demonstrating a significant association between lung cancer and exposure to PVC dust. An association between PVC dust and pneumoconiosis has been demonstrated. On the basis of these findings, experimental bioassays and epidemiologic studies of the carcinogenicity of PVC are clearly in order. Prudent control of PVC in the industrial setting is also clearly indicated.

Brain Neoplasms↗
PubMed1975

Hepatotoxicity of vinyl chloride and 1,1-dichloroethylene. Role of mixed function oxidase system.

Vinyl chloride, an occupational carcinogen, produces acute liver injury in rats pretreated with phenobarbital or Aroclor 1254. Injury appears related to morphologic changes in the endoplasmic reticulum. The degree of injury, as indicated by elevation of serum enzymes derived from the liver, correlates with the magnitude of induction of cytochrome P-450 and its reduction by NADPH. Hepatic injury following 1,1-dichloroethylene exposure differs strikingly from that caused by vinyl chloride and appears to involve plasma membranes, mitochondria, and chromatin and spares endoplasmic reticulum. Induction of cytochrome P-450 appears to protect against 1,1-dichloroethylene but not vinyl chloride.

Animals↗
PubMed1975

Effects of vinyl chloride exposures to rats pretreated with phenobarbital.

Male rats were exposed to 10 consecutive days, 6 hr/day, to vinyl chloride vapors at an average concentration of 13,500 ppm. The exposed rats were divided into three groups of eight rats each: one group was pretreated with 3-methylcholanthrene, one group was pretreated with phenobarbital, and the third group received no treatment. Half the animals in each group were sacrificed 18 hr after the last exposure and half were sacrificed 4 days later. In a second experiment, four rats pretreated with phenobarbital were exposed to vinyl chloride vapors at a concentration of 17,300 ppm for 2 days and sacrificed about 9 A.M. on the third day. In both experiments control animals, also treated with phenobarbital or 3-methylcholanthrene, were exposed to air only. At the time of sacrifice, lungs, kidneys, spleen, heart, and a small piece of liver from each animal were preserved for histological examination. The remainder of the liver was processed for assay of microsomal enzyme activity. The following parameters were investigated: growth rate, organ weights, morphological changes, and both benzphetamine-N-demethylase activity and cytochrome P-450 content of microsomes prepared from the livers. In both experiments the only marked difference noted in any group was a decrease in the growth rate of the animals exposed to vinyl chloride and treated with phenobarbital. This decreased growth rate was particularly apparent on the third day of the vinyl chloride exposures. Occasional morphological changes were also seen in the livers of the animals treated with phenobarbital and exposed to vinyl chloride.

Animals↗