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PubMed1980

Immunotoxicologic studies with vinyl chloride in rabbits and mice.

Our previous studies in mice indicated that the exposure to vinyl chloride (VC) produced a state of immunostimulation. The metabolism of VC was an important factor in this phenomenon. The present paper describes the effects of VC exposure on induced immunologic responses in rabbits. No consistent effect of VC exposure was noticed on skin reactivity to tuberculin or serum anti-tetanus titers in sensitized rabbits. Vinyl chloride produced no change in the number of antibody secreting cells in the lymph nodes of immunized rabbits. An increase in the spontaneous splenic lymphocyte transformation in immunized rabbits was observed when the animals were exposed to VC. Two known metabolites of VC, namely thiodiglycolic acid and N-acetyl-S-(hydroxyethyl)-cysteine produced little or no effect when added to mouse splenic lymphocyte cultures in vitro but in vivo administration of thiodiglycolic acid produced apparent immune stimulation in mice. The study indicated that although VC may cause an apparent enhancement of immune reactivity, it does not alter the immunologic response to simultaneously administered antigens.

Animals↗
PubMed1989

Permeability of latex and vinyl gloves to water and blood.

Two thousand four hundred medical gloves were evaluated for leakage. Types of gloves examined (number of brands) included sterile latex (seven) sterile vinyl (four), nonsterile latex (six), and nonsterile vinyl (seven). Sampling was done from one box of each brand. Fifty gloves from each box were filled with 300 ml of water (the standard test used by the American Society for Testing and Materials). An additional 25 cm pressure was applied to water-filled gloves. Another 50 gloves of each box were donned and dipped into a basin that contained heparinized human blood. Only four brands of sterile latex surgeon's gloves proved nonpermeable to water and blood. Other brands showed leakage that ranged from 1% to 52%. Analysis of proportions of pairs of gloves permeable to water or blood indicated a strong statistical association of nonsterile packaging or packaging in suction kits with increased leakage rates. These findings affirm that gloves can be regarded only as a means of reducing the risk of gross soilage from blood or body fluids. Quality control standards to ensure more uniform glove quality are needed.

Blood↗
PubMed1988

Uptake of vinylidene fluoride in rats simulated by a physiological model.

The purpose of this study was to develop a physiological model to simulate the uptake of vinylidene fluoride (VDF), an important plastics monomer, in laboratory animals. Male Fischer 344/N rats were exposed nose-only for 6 hr to concentrations of VDF ranging from 27 to 16,000 ppm. Tidal volume (mean, 1.51 ml/breath) and respiratory frequency (mean, 132 breaths/min) were not influenced by exposure concentration. Experimentally determined, steady-state blood levels of VDF, obtained by gas chromatography-head space analysis of samples from rats with indwelling jugular cannulas, increased linearly with increasing exposure concentration up to 16,000 ppm. VDF tissue/air partition coefficients were determined experimentally to be 0.07, 0.18, 0.8, 1.0, and 0.29 for water, blood, liver, fat, and muscle, respectively. These values and calculated constants for total body elimination of VDF, Km and Vmax were incorporated into the physiological model. Model predictions agreed with the experimentally determined data. Time to reach steady-state blood levels of VDF was less than 15 min for all concentrations. After cessation of exposure, blood levels of VDF decreased to 10% of steady-state levels by 1 hr. Simulation of the metabolism of VDF indicated that although blood levels of VDF increased linearly with increasing concentration the amount of VDF metabolized per 6-hr exposure period approached a maximum at about 2000 ppm VDF.

Animals↗
PubMed1989

Testing for increased carcinogenicity using a survival-adjusted quantal response test.

The linear trend test in proportions is frequently used to analyze the results of animal carcinogenicity experiments. This test has two major advantages over other frequently used tests; it is easily understood and it is simple to calculate. This test, however, fails to correct for treatment-related differences in survival across the experimental groups. A test which is a simple modification of the linear trend test in proportions and which has the same advantages is proposed to correct for differences in survival. The results of this modified test are compared to those of the linear trend test in proportions, the incidental tumor test, the logistic regression score test, the life table test, and the truncated trend test using information on the incidence of combined alveolar/bronchiolar adenomas or carcinomas in female B6C3F1 mice exposed to vinylcyclohexene diepoxide.

Adenoma↗
PubMed1990

Subchronic inhalation study with vinyl fluoride: effects on hepatic cell proliferation and urinary fluoride excretion.

Vinyl fluoride is used widely in the manufacture of fluoropolymers. Based in part on the structural similarity of vinyl fluoride to the hepatocarcinogens vinyl chloride and vinyl bromide, a TSCA Section 4 test rule mandated the testing of vinyl fluoride for oncogenicity. This report presents the results of a 90-day inhalation study in rats and mice with vinyl fluoride designed to set test concentrations for a subsequent oncogenicity study. Groups of 15 male and female rats and mice were exposed 6 hr per day, 5 days per week for approximately 90 days to target concentrations of 0, 200, 2000, or 20,000 ppm vinyl fluoride. Clinical chemical, hematological, and urine analyses were performed on rats after 45 and 90 days of exposure. A hematological evaluation was performed on mice following 45 and 90 days of exposure. A complete gross and microscopic evaluation was conducted at the end of the study. After 93 days on test, groups of five rats and five mice per sex were implanted with osmotic minipumps containing [3H]thymidine and were exposed for an additional 5 days to measure cell proliferation in liver, kidney, lung, and nasal cavity tissues. Results of the histopathological, clinical chemical, and hematological evaluations showed no significant effects of vinyl fluoride exposure at any concentration following either 45 or 90 days of exposure. A concentration-related increase in fluoride ion in urine was observed in rats at 45 and 90 days of exposure. A plateau in urinary fluoride excretion was observed at approximately 2000 ppm, suggesting saturation of vinyl fluoride metabolism. Vinyl fluoride-related cell proliferation effects were largely restricted to liver. Hepatic cell proliferation in male and female rats and mice was elevated at all concentrations. The response was similar at concentrations of either 2000 or 20,000 ppm and was consistent with concentration-response relationships for other haloethylenes. Taken together, the urinary fluoride excretion and hepatic cell proliferation data suggest a mechanistic link between the two effects. On the basis of these findings and experience with other haloethylenes, concentrations of vinyl fluoride to be tested for oncogenicity should be chosen such that the full linear range of the concentration-response curve is evaluated. The present study demonstrates through example the value of incorporating cell proliferation studies in standard testing protocols.

Administration, Inhalation↗
PubMed1990

Toxicity of 4-vinyl-1-cyclohexene diepoxide after 13 weeks of dermal or oral exposure in rats and mice.

4-Vinyl-1-cyclohexene diepoxide (VCHD) is used as a chemical intermediate and as a reactive diluent for diepoxides and epoxy resins. Toxicology studies were conducted by administering VCHD in acetone by dermal application or in corn oil by gavage to F344/N rats and B6C3F1 mice for 13 weeks. In the 13-week dermal studies, groups of 10 rats of each sex received 0.3 ml of VCHD in acetone at concentrations ranging from 6.25 to 200 mg/ml, and mice received 0.1 ml at concentrations ranging from 6.25 to 100 mg/ml. Skin lesions were observed at the site of application at the top two dose levels for both species and sexes, and consisted of acanthosis, parakeratosis, and hyperkeratosis of the epidermis and sebaceous gland hyperplasia. In mice, follicular atrophy of the ovary, characterized by decreased numbers of primary and secondary follicles, occurred at the 50- and 100-mg dose levels. In 13-week oral studies, groups of 10 rats and mice of each sex were administered VCHD at dose levels ranging from 62.5 to 1000 mg/kg in corn oil. In rats and mice, there were body weight decreases in the groups given the two highest doses. The major target organs in rats were forestomach (hyperplasia and hyperkeratosis) and kidney (tubular cell degeneration/necrosis and regeneration). In mice the target organs included forestomach (hyperplasia and hyperkeratosis), ovary (follicular atrophy), and testis (degeneration of germinal epithelium).

Administration, Oral↗
PubMed1990

Dermal toxicity and carcinogenicity of 4-vinyl-1-cyclohexene diepoxide in Fischer rats and B6C3F1 mice.

4-Vinyl-1-cyclohexene diepoxide (VCHD) is used as a chemical intermediate and as a reactive diluent for diepoxides and epoxy resins. Studies were conducted by administering VCHD in acetone by dermal application, 5 days per week for 105 weeks, to groups of 60 rats of each sex at 0, 15, or 30 mg/animal. Groups of 60 mice of each sex were administered 0, 2.5, 5, or 10 mg/animal on the same schedule for up to 103 weeks. Ten animals from each group were humanely killed, necropsied, and examined histopathologically during Month 15. At the 15-month evaluation, 2 of 10 male rats that received 30 mg had a squamous cell carcinoma of the skin at or adjacent to the site of application. Squamous cell papillomas and carcinomas were seen in all mice that received 5 or 10 mg. Two of nine female mice given 10 mg had granulosa cell tumors of the ovary, and one of nine female mice given 10 mg had an ovarian papillary cystadenoma. In the 2-year studies, body weight and survival were lower in high-dose rats and mid- and high-dose mice than in vehicle controls. All high-dose male mice died by Week 83; remaining high-dose female mice were killed during Week 84 for humane reasons. Squamous cell papillomas of the skin in dermally exposed male rats and squamous cell carcinomas and basal cell adenomas or carcinomas of the skin in exposed male and female rats were increased. The incidence of squamous cell carcinomas of the skin was increased in male and female mice at all dose levels. Mid- and high-dose female mice had an increased incidence of benign or malignant granulosa cell tumors and of benign mixed tumors of the ovary.

Adenoma↗
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↗
PubMed1987

Vinyl chloride: an assessment of the risk of occupational exposure.

There is little doubt that exposure to high levels of VCM as a consequence of occupation can result in an increased incidence of ASL. A review of 20 epidemiological studies involving about 45,000 workers occupationally exposed to VCM showed that neoplasms of the liver showed an increase in incidence in the majority of studies. For brain cancer the association between exposure to VCM and an increased incidence was less clear because of the lower relative risk. Neoplasms of the respiratory tract, digestive system, lymphatic and haemopoietic system, buccal cavity, and pharynx, cardiovascular system and colon/stomach were reported to show an increased incidence in one or more studies, but to show no increase, or in some cases a decrease, in incidence in other studies. In view of the increased incidence of breast neoplasms in rodents exposed to VCM, the studies of Chaizze et al. (1980), who did not confirm these findings in humans, are of importance. The register of ASL cases now contains records of 99 persons with confirmed ASL and occupational exposure to VCM. The average latent period between first exposure to VCM and death from ASL is 21.9 years. The majority of cases occurred in autoclave workers, who are recognized as having been exposed to extremely high levels. Although precise estimates of exposure are not available for the periods of most interest, the pattern of cases roughly suggests that extremely high exposures were necessary for the induction of ASL. For example, ASL cases tended to occur in larger numbers in some plants than in others, a finding that can be explained most easily by differences in exposure patterns. There is an extensive series of animal studies on the carcinogenicity of VCM. Some of these precede the epidemiological studies confirming the association between VCM exposure and ASL in man. ASL and neoplasms of a number of other organs have been induced in laboratory rodents by VCM. Estimation of the exposure levels likely to cause a lifetime risk of ASL of 10(-6) on the basis of these data give extremely low levels (down to 3.9 X 10(-7) ppb) which appear to be unrealistic estimates for man. Part of the reason for this is that laboratory studies have shown that VCM is metabolized in the liver (and elsewhere in the body) to the reactive metabolites chloroethylene oxide and chloroacetaldehyde. The rate of conversion is limited at high levels of exposure giving inaccurate estimates of the slope of the dose-response relationship.(ABSTRACT TRUNCATED AT 400 WORDS)

Air Pollutants, Occupational↗
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↗
PubMedDate not supplied

Effect of halogenated vinyl cysteine conjugates on renal tubular active transport.

Addition of halogenated vinyl cysteine conjugates to isolated rabbit kidney tubule suspensions resulted in a decrease in the active transport of para-aminohippuric acid (PAH) and tetraethylammonium bromide (TEA). At 10(-5) M vinyl cysteine conjugate, tubule to medium accumulation ratios (T/M) were similar to those of controls while at 10(-3) M the T/M values decreased to 1, indicating complete inhibition of active accumulation of PAH or TEA. The decreased active transport was not caused by inhibition of mitochondrial oxidation since incubations in the presence of 10(-3) M halogenated vinyl cysteine did not inhibit tubule O2 utilization or production of 14CO2 from [14C]glucose or [14C]succinate. A mechanism is proposed whereby toxicity may result from covalent binding of an active intermediate, produced by enzyme cleavage, to membrane associated nucleophilic groups thereby decreasing active transport.

Animals↗
PubMed1990

Measurement of steady-state blood concentrations in B6C3F1 mice exposed by inhalation to vinylidene fluoride.

The purpose of this study was to obtain data on blood concentrations of vinylidene fluoride (VDF), an important plastics monomer in B6C3F1 mice during inhalation exposure. A new method for sampling blood from mice during the exposures was developed. The technique used a pernasal exposure tube with an outer, sliding cylinder that allowed access to the heart through the thorax. Blood was removed from an anesthetized mouse via heart-puncture while the animal was being exposed to VDF. Concentrations of VDF were measured in blood of mice during 6-h exposures to nominal concentrations of 250, 3750, or 15,000 ppm VDF. A physiological model developed to simulate blood levels of VDF in rats was adapted for mice by incorporating physiologically realistic parameters for mice where appropriate (alveolar ventilation, cardiac output, blood flow to organs, and organ volumes) and by assuming that chemical-specific parameters such as tissue/blood partition coefficients determined for rats could also be applied to mice. Measured steady-state levels of VDF in blood of mice increased with increasing exposure concentration. For both the 15,000 and 3750 ppm VDF exposures, the experimentally determined data fell within the 95% confidence interval predicted by the physiological model. For the 250 ppm VDF exposure, the experimentally determined values for VDF in blood were lower than what was predicted by the model. Model predictions indicated that for mice, as observed for rats, levels of VDF would rise very rapidly, reaching steady-state within minutes of exposure, and that at the end of exposure, blood levels will decline rapidly. At the two lowest exposure concentrations, we were unable to detect VDF in blood taken 15 min or longer after cessation of exposure, suggesting that the post-exposure levels were at or below our limit of detection which was 4 ng VDF/ml blood. For the 15,000 ppm exposure VDF could be detected in blood up to 15 min post exposure.

Administration, Inhalation↗
PubMed1996

A comparison of the surface activity of the fungal hydrophobin SC3p with those of other proteins.

The fungal hydrophobin SC3p, a protein secreted by Schizophyllum commune, has become known to form SDS-insoluble layers and to change the physico-chemical properties of an interface. In this study, the surface activity of SC3p was studied by determining the interfacial tensions gamma iv and gamma sl during adsorption of SC3p at both the liquid-vapour and the solid-liquid interface utilizing the in situ technique axisymmetric drop-shape analysis by profile. To this end, protein solution droplets were put on the solid fluoroethylene-propylene-Teflon. At the liquid-vapour interface, SC3p caused a large decrease of gamma iv from 72 to 43 mJ m-2 at the concentration of 0.1 mg ml-1. At the solid-liquid interface, gamma sl was slightly decreased, whereas the contact angle theta increased, indicating an increase in hydrophobicity of FEP-Teflon, which is unique among the proteins studied so far. Earlier findings indicated a decrease in hydrophobicity of Teflon upon adsorption of SC3p, but this was after a washing and drying step. In order to reconcile these findings with those of the present study, adsorption of SC3p to hydrophobic surfaces is suggested to occur in bilayers. The second layer is supposed to be less strongly adsorbed than the first layer and can be easily removed by washing.

Adsorption↗