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PubMed1985

Metabolism and pharmacokinetics of vinyl acetate.

The hydrolysis of vinyl acetate (formation of acetic acid) has been studied in vitro with rat liver and lung microsomes, rat and human plasma and purified esterases (such as acetylcholine esterase, butyrylcholine esterase, carboxyl esterase). Characterization of the kinetic parameters revealed that rat liver microsomes and purified carboxyl esterase (from porcine liver) displayed the highest activity. In order to establish the rate of metabolism of vinyl acetate in vivo, rats were exposed in closed desiccator jar chambers, and gas uptake kinetics were studied. The decay of vinyl acetate was dose-dependent, indicating possible saturation of metabolic pathway(s). The maximal clearance (at lower concentrations) of vinyl acetate from the system (30 000 ml/h per kg body weight) was similar to the maximal ventilation rate in this species. This indicated that under conditions when metabolic enzymes are not saturated the metabolic rate is mainly determined by pulmonary uptake. The exposure of rats to vinyl acetate resulted in a transient exhalation of significant amounts of acetaldehyde into to the closed exposure system. This indicates the presence of this metabolic intermediate of vinyl acetate in the organism in vivo.

Animals↗
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↗
PubMed1981

Chromatographic determination of thiodiglycolic acid - a metabolite of vinyl chloride.

The determination of thiodiglycolic acid (TDGA) In urine by gas chromatography (GC) is described. The analytical procedure includes addition of internal standard (o-phthalic acid), ethyl acetate extraction, evaporation of the solvent and silylation of TDGA with N-trimethylsilyl-diethylamine in pyridine (1:1). The results are calculated from the ratio of TDGA and internal standard peak heights. The detection limit of the method is 10 mg/l and the coefficient of various is +/- 5%.

Chromatography, Gas↗
PubMed1978

Formation of 3,N4-ethenocytidine moieties in RNA by vinyl chloride metabolities in vitro and in vivo.

Rats were exposed to [1,2-14C] vinyl chloride. Liver RNA was isolated, hydrolyzed, and the nucleosides separated on Aminex-A-6. Besides the physiological bases and 1,N6-ethenoadenosine, radioactivity was also incorporated into 3,N4-ethenocytidine. Radioactive 3,N4-ethenocytidine moieties were also formed on incubation of polycytidylic acid with rat liver microsomes, NADPH and [14C] vinyl chloride. These alkylation mechanisms are consistent with the mutagenic and cancerogenic properties of vinyl chloride.

Animals↗
PubMed1982

[Investigations on the correlation between vinyl chloride (VCM)-uptake and excretion of its metabolites by 15 VCM-exposed workers. II. Measurements of the urinary excretion of the vcm-metabolite thiodiglycolic acid ].

Fifteen workers employed in a PVC producing plant were investigated concerning their individual vinyl chloride (VCM) exposure and the urinary excretion of the VCM metabolite thiodiglycolic acid (TdGA). The urine concentrations found were in the range 0.94-20.4 microgram/ml. These could be compared with exposure data calculated from VCM air analyses performed by personal air sampling and corrected with respect to the exposure times of the workers. The amounts of TdGA excreted within 24 h were correlated with the effective VCM body concentrations calculated from the exposure data as mean values for 12 h periods (Spearman coefficient P=alpha less than 0.005). This correlation resembles a function of the Michaelis-Menten type. It could be shown that during short exposure periods of less than 5 min, the metabolite formation in relation to the exposure data was lower than during longer periods of exposure although, as would be expected, there were some fluctuations of the exposure level. Therefore, the VCM body concentrations could not normally reach steady state values.

Environmental Exposure↗
PubMed1980

Monooxygenase activity and ultrastructural changes of liver in the course of chronic exposure of rats to vinyl chloride.

The activity of microsomal cytochrome P-450 monooxygenase and ultrastructure of the liver have been studied in rats exposed dynamically to 50, 500, and 20,000 ppm of vinyl chloride (VC) over 10 months. After 1 and 3 months of exposure to 500 and 20,000 ppm of VC, the level of cytochrome P-450 was slightly lower than in the control animals and upon continuation of exposure it was restored to the original level accompanied by slight increase of activity of aniline p-hydroxylase. Liver enlargement, developed in the course of the exposure, was accompanied by ultrastructural alterations beginning in the 3rd month of exposure to all concentrations of VC. Development of hepatic alterations (hypertrophy of smooth and rough endoplasmic reticulum, swelling of mitochondria, accumulation of lipid droplets, focal cytoplasmic degradation) is discussed with regard to the activity of microsomal monooxygenase system in metabolizing VC to toxic metabolites.

Aniline Hydroxylase↗
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↗
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↗