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At least 19 recordsLinked to original sources
PubMedDate not supplied

Improved codistillation method for determination of carbon tetrachloride, ethylene dichloride, and ethylene dibromide in grain and grain-based products.

A method is described for the determination of the common fumigants carbon tetrachloride (CCl4), ethylene dichloride (EDC), and ethylene dibromide (EDB) in grain and grain-based products. A properly prepared sample is mixed with water and hexane, an internal standard mixture of 1,2-dichloropropane (DCP) and 1,2-dibromopropane (DBP) is added, and the fumigants are codistilled with the hexane into an appropriate receiver. After the hexane solution is dried over sodium sulfate, the quantities of fumigants present are quantitated on a gas chromatograph (GC) equipped with an electron capture detector (ECD). For the matrices investigated, the relative standard deviation of the method was 6.0, 9.7, and 23.1% for CCl4, EDC, and EDB, respectively. Recoveries of added fumigants were 107, 95, and 101%, respectively. Comparison with an acetone-water soak extraction method gave a correlation of 0.967 between methods for EDB with odds of a difference between methods of 35%.

Carbon Tetrachloride↗
PubMed1975

Mutagenicity of chloroacetaldehyde, a possible metabolic product of 1,2-dichloroethane (ethylene dichloride), chloroethanol (ethylene chlorohydrin), vinyl chloride, and cyclophosphamide.

We have previously described a very sensitive and efficient bacterial test designed to detect chemical carcinogens as mutagens. Chloroacetaldehyde is mutagenic in this system and is of interest because it is a possible metabolite in mammals of the large volume industrial chemicals 1,2-dichloroethane (ethylene dichloride) (3.5 billion kg/yr, U.S.) and vinyl chloride (2.5 billion kg/yr, U.S.), and of the antineoplastic agent cyclophosphamide. Chloroacetaldehyde reverts a new Salmonella bacterial tester strain (TA100). Chloroacetaldehyde is shown to be hundreds of times more effective in reversion of TA100 than is chloroethanol (ethylene chlorohydrin), a known metabolic precursor of chloroacetaldehyde and a possible metabolite of dichloroethane and vinyl chloride, or than vinyl chloride, which is itself mutagenic for TA100. Chloroethanol is shown to be activated by rat (or human) liver homogenates to a more highly mutagenic form with reversion properties similar to chloroacetaldehyde. Reversion properties of cyclophosphamide after in vitro metabolic activation suggest that chloroacetaldehyde is not the active mutagenic form of this antineoplastic drug.

Acetaldehyde↗
PubMed1988

Physiological model for tissue glutathione depletion and increased resynthesis after ethylene dichloride exposure.

Ethylene dichloride (EDC) is metabolized by two competing pathways both of which consume glutathione (GSH). EDC undergoes oxidation to form chloroacetaldehyde (CAA) which is detoxified by GSH and also reacts directly with GSH to form 2-(s-chloroethyl)-GSH. A physiological pharmacokinetic model developed for EDC was extended to describe tissue GSH turnover and its depletion after EDC exposures. This GSH model was necessary to keep track of GSH concentrations with time, as EDC metabolism is affected by GSH status. Reactions of GSH with EDC and GSH with CAA were defined as second-order. Steady-state GSH formation was modeled as zero-order and GSH loss as first-order. GSH rebound effects after its depletion were controlled by a GSH synthetase reaction, which allowed time- and GSH concentration-dependent feedback for increased GSH resynthesis. The model was developed for liver GSH in the rat and was extrapolated to include the lung. Allometric scaling was used to extrapolate the model to other animal species. Experimental observations in the rat and mouse were consistent with model predictions.

Animals↗
PubMedDate not supplied

Characterization of emissions of dioxins and furans from ethylene dichloride (EDC), vinyl chloride (VCM) and polyvinylchloride (PVC) manufacturing facilities in the United States. I. Resin, treated wastewater, and ethylene dichloride.

Under the auspices of its Dioxin Characterization Program, members of The Vinyl Institute (VI), have analyzed for potential polychlorinated dibenzodioxin/furan (PCDD/F) concentrations in polyvinylchloride (PVC) resins, treated wastewater effluent and ethylene dichloride (EDC) product at EDC, vinyl chloride monomer (VCM) and PVC manufacturing facilities in the U.S. and Canada. No 2,3,7,8-tetrachlorodibenzodioxin (TCDD) was detected in any sample analyzed under the program to date. Trace concentrations (low pg/g) of PCDD/F were detected in only a few samples of PVC resins and EDC product. Treated wastewater contained low ppq concentrations of PCDD/F. All concentrations are expressed as Toxic Equivalents (TEQ). Extrapolation of these data shows that the contribution of EDC/VCM/PVC manufacturing via these media constitutes substantially less than 1 percent of the estimated annual U.S. dioxin releases to the environment.

Benzofurans↗
PubMedDate not supplied

Simultaneous analysis of grain and grain-based products for ethylene dibromide, carbon tetrachloride, and ethylene dichloride.

A method is described for the simultaneous measurement of parts per billion levels of the fumigants ethylene dibromide, carbon tetrachloride, and ethylene dichloride in grain and grain-based products. The fumigants are isolated by hexane co-distillation, separated by capillary gas chromatography, and detected with a mass spectrometer in the selected ion monitoring mode. Recoveries are greater than 90% and standard deviations are approximately 10% of the quantity measured. The method is free of interferences and its precision and accuracy are enhanced by the use of tetradeuterated ethylene dibromide and ethylene dichloride as internal standards.

Carbon Tetrachloride↗
PubMed2000

Increased lymphocyte sister chromatid exchange frequency in workers with exposure to low level of ethylene dichloride.

The genotoxicity of low-level exposure to ethylene dichloride (EDC) and vinyl chloride monomer (VCM) in humans is not clear. We used lymphocyte sister chromatid exchange (SCE) frequency as a parameter to investigate the genotoxicity of low level EDC and VCM in VCM-manufacturing workers. The SCE frequency was determined for 51 male workers with exposure to VCM and/or EDC and for 20 male workers devoid of such exposure. Epidemiological data were obtained by questionnaire, and included history of smoking, drinking, and any medication taken, as well as a detailed occupational history. Personal- and area-sampling and analysis were conducted in order to calculate the time-weighted average (TWA) contaminant-exposure level corresponding to different job categories. Moderate EDC exposure around 1 ppm corresponded to a significantly greater SCE frequency than was the case for the low EDC exposure group (p<0.01). However, VCM exposure of similar level was not associated with increased SCE. We conclude that EDC may cause genotoxicity at a relatively low level of exposure.

Adult↗
PubMed1999

Abnormal liver function in workers exposed to low levels of ethylene dichloride and vinyl chloride monomer.

We investigated whether exposure to ethylene dichloride (EDC) and vinyl chloride monomer (VCM) resulted in increased risk of liver damage. Epidemiological information, including occupational, medical, smoking, and drinking history, was obtained by interview from 251 male workers. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT) were used as indicators of liver damage. Exposure to moderate or low levels of ECD and VCM resulted in a higher risk of developing abnormal ALT levels than did exposure to lower levels of the chemicals. Results were similar for AST. GGT was not associated with EDC or VCM exposure. Combined exposure to EDC and VCM showed a dose-response relationship in association with abnormal ALT levels. We concluded that relatively low concentrations of VCM and EDC cause liver damage.

Adult↗
PubMed1975

Determination of methylene chloride, ethylene dichloride, and trichloroethylene as solvent residues in spice oleoresins, using vacuum distillation and electron capture gas chromatography.

A quantitative gas chromatographic (GC) method is described for the determination of residual methylene chloride, ethylene dichloride, and trichloroethylene in spice oleoresins. The proposed method involves vacuum distillation in a closed system with toluene as a carrier solvent. Quantitation by electron capture GC on Porapak Q is facilitated by water extraction and by the addition of trans-1,2-dichloroethylene as an internal standard. Recoveries from oleoresins spiked at 30, 15, and 6 ppm ranged from 93 to 102%. To assess the possibility of interference from spice volatiles, the procedure was applied to 17 different spice oleoresins from 3 different manufacturers. No interferences were found, but methylene chloride levels up to 83 ppm and ethylene dichloride levels up to 23 ppm were detected. Trichloroethylene was not detected in any of the oleoresins.

Chromatography, Gas↗
PubMed1987

Effects of inhalation of ethylene dichloride on pulmonary defenses of mice and rats.

The effects of single or multiple inhalation exposures to ethylene dichloride (DCE) on the pulmonary defense systems of mice and rats were evaluated. Single exposures of mice to the threshold limit value of DCE (10 ppm) resulted in decreased pulmonary bactericidal activity to inhaled Klebsiella pneumoniae and increased mortality from Streptococcus zooepidemicus respiratory infection. A single exposure to 5 ppm DCE caused increased mortality from streptococcal pneumonia although bactericidal activity was not affected. Neither of these two parameters changed following single or five consecutive daily exposures to 2.5 ppm DCE. Single exposures to 10 or 100 ppm DCE did not affect mouse alveolar macrophage (AM) inhibition of the proliferation of a tumor target cell in vitro or AM in vitro phagocytosis of red blood cells. In rats, no effects were observed on pulmonary bactericidal activity. AM in vitro phagocytosis, AM cytostasis and cytolysis of tumor target cells, AM ectoenzymes, or blastogenesis of mitogen-stimulated rat T- and B-lymphocytes from lung-associated, mesenteric, and popliteal lymph nodes following single exposure to 100 or 200 ppm DCE or after twelve 5-hr exposures to 10, 20, 50, or 100 ppm DCE.

Administration, Inhalation↗
PubMed1990

Comparative toxicity of ethylene dichloride in F344/N, Sprague-Dawley and Osborne-Mendel rats.

Studies were conducted to compare the toxicity of ethylene dichloride (EDC) in F344/N rats, Sprague-Dawley rats, and Osborne-Mendel rats. Ten rats/sex/group were exposed to EDC in drinking-water at 0, 500, 1000, 2000, 4000 and 8000 ppm for 13 wk. The highest concentration was limited by the maximum solubility of EDC in water (about 9000 ppm). In addition, F344/N rats (10/sex/group) were administered EDC in corn oil by gavage to compare toxicity resulting from bolus administration with that of continuous exposure in drinking-water. Gavage doses of EDC were within the range of total daily doses (in mg/kg body weight/day) resulting from exposure in drinking-water. EDC administered by gavage resulted in greater toxicity to F344/N rats than did administration of similar doses in drinking-water. All males receiving 240 and 480 mg/kg body weight and 9/10 females receiving 300 mg/kg body weight by gavage died before the end of the study. Necrosis of the cerebellum was observed in the brains of 3 males receiving 240 mg/kg body weight and 3 females receiving 300 mg/kg body weight. Hyperplasia and inflammation of the forestomach mucosa were observed in 8 male and 3 female rats that died or were killed in moribund condition. EDC caused minimal toxicity to F344/N, Sprague-Dawley and Osborne-Mendel rats at the drinking-water concentrations used in these studies; only female F344/N rats had EDC-related renal lesions. Based on mortality and EDC-related lesions, the no-effect levels for EDC administered by gavage to F344/N rats were 120 mg/kg body weight for males and 150 mg/kg body weight for females.

Administration, Oral↗
PubMedDate not supplied

Nanosized gamma-Al2O3 + Nd2O3-based cataluminescence sensor for ethylene dichloride.

A gas-sensor utilizing cataluminescence (CTL) on nanosized gamma-Al2O3 + Nd2O3 for measuring low concentrations of gaseous ethylene dichloride (EDC) was developed. The results showed that gamma-Al2O3 nanoparticles as a catalyst offered high sensitivity and selectivity in the detection of EDC. The addition of a small quantity of Nd2O3 increased the intensity of CTL more than two-fold. Quantitative analysis was performed at a wavelength of 400 nm and at an optimal temperature of 279 degrees C, and the optimal flow rate of carrier gas was 320 mL/min. Under the optimized conditions, the linear range of CTL intensity vs. concentration is 6-5000 ppm (R = 0.9996; n = 7), with a detection limit of 2 ppm. The response time is <5 s. No interference or only very low levels of significant interference were observed when substances such as formaldehyde, n-hexane, methyl benzene, carbon tetrachloride, chloroform and benzene were passed through the sensor.

Air Pollutants↗
PubMed1990

Ethylene dichloride: the influence of disulfiram or ethanol on oncogenicity, metabolism, and DNA covalent binding in rats.

Male and female Sprague-Dawley rats were exposed to 50 ppm ethylene dichloride (EDC) for 7 hr/day, 5 days/week, for 2 years by inhalation. Additional rats were exposed to 50 ppm EDC either with 0.05% disulfiram in the diet or with 5% ethanol in the drinking water. Histopathologic lesions related to the combination of inhaled EDC and dietary disulfiram were observed in the liver, mammary, and testicular tissues of rats. This combined exposure resulted in a significant increase in the incidence of intrahepatic bile duct cholangiomas in both male and female rats. Male rats exposed to both EDC and disulfiram also had an increased incidence of subcutaneous fibromas, neoplastic nodules, and interstitial cell tumors in the testes. The female rats exposed to EDC and disulfiram also had a higher incidence of mammary adenocarcinomas. No significant increase in the number of any tumor type was observed in rats exposed to only EDC, disulfiram, or ethanol. Similarly, no significant increase in the number of tumors was observed in rats exposed to inhaled EDC and ethanol in water. At the end of the 2-year period animals from each group were evaluated for EDC metabolism and DNA binding. Blood levels of EDC at the end of a 7-hr exposure period were significantly higher for rats exposed to both EDC and disulfiram than for rats exposed to EDC alone. In addition, the elimination of a single oral dose of radiolabeled EDC was affected. The urinary excretion of 14C from control rats was 47 to 55% of the administered dose with 28 to 30% detected as unchanged EDC in the breath. In disulfiram-treated rats, only 35 to 36% of the administered 14C was eliminated in the urine with 41 to 55% as unchanged EDC in the breath. The urinary metabolite HPLC profile was qualitatively unchanged by long-term EDC, disulfiram, or ethanol treatment, either alone or in combination, and consisted primarily of thiodiglycolic acid, thiodiglycolic acid sulfoxide, and chloroacetic acid.

Animals↗
PubMed2003

Synergistic effect of hepatitis virus infection and occupational exposures to vinyl chloride monomer and ethylene dichloride on serum aminotransferase activity.

AIMS: To study the synergistic effect of occupational chemical exposure and hepatitis virus infection on serum aminotransferase activity. METHODS: A total of 568 male workers who were employed in five polyvinyl chloride (PVC) or four vinyl chloride monomer (VCM) manufacturing factories were studied. Information relating to current job title, alcohol consumption, and cigarette smoking was obtained. Exposure level of chemical mixtures was classified by hygienic effect (a summation of personal time weighted average/reference permissible exposure level of each chemical) into high, moderate, and low exposure groups. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and anti-hepatitis C antibody were assayed. RESULTS: Hepatitis virus infection and increased body mass index were associated with abnormal serum aminotransferase activity. In workers with hepatitis virus infection, those with high exposure had a higher prevalence of abnormal AST and ALT compared to low exposure; among those without hepatitis virus infection, the differences of prevalence of abnormal AST and ALT were not significant between different chemical exposure groups. There was a significant trend of increasing risks of increased AST and ALT in moderate and high exposure groups with hepatitis virus infection. Such a synergistic effect was more prominent among HBeAg-positive workers. CONCLUSIONS: Mixed exposures to 1,2-ethylene dichloride and VCM have a positive synergistic effect with hepatitis virus infection on liver damage. Assessment of fitness for work should be considered in workers with hepatitis B and C infection, when they have potential exposure to hepatotoxins in the workplace.

Adult↗