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At least 19 recordsLinked to original sources
PubMed1992

Pharmacokinetics of ethylene in man; body burden with ethylene oxide and hydroxyethylation of hemoglobin due to endogenous and environmental ethylene.

The inhalation pharmacokinetics and the endogenous production of ethylene has been determined in healthy volunteers with respect to the formation of the carcinogen ethylene oxide. Ethylene showed a low degree of accumulation in the body determined in six subjects, the thermodynamic partition coefficient "body/air" being 0.53 +/- 0.23 (mean +/- SD) and the accumulation factor "body/air" at steady-state being 0.33 +/- 0.13 (mean +/- SD). The rate of metabolism was directly proportional to the exposure concentration. Only 2% of ethylene inhaled was metabolized to ethylene oxide, whereas 98% of ethylene was exhaled unchanged. The rate of the endogenous production of ethylene was 32 +/- 12 nmol/h (mean +/- SD), as calculated from exhalation data from 14 subjects. The resulting body burden was 0.44 +/- 0.19 nmol/kg (mean +/- SD). By analyzing published data on ethylene oxide in man its half-life was estimated to be 42 min. Using the pharmacokinetic parameters of ethylene and ethylene oxide, the body burden of ethylene oxide due to the sum of the exposure to environmental ethylene of about 15 ppb and to endogenous ethylene exposure of 0.44 nmol/kg was predicted to be 0.25 nmol/kg. In the blood of five non-smokers and one smoker the hemoglobin adduct resulting from the reaction of ethylene oxide with the N-terminal valine, N-(2-hydroxyethyl)valine, was quantified by gas chromatography/mass spectrometry. The value of 20 +/- 5 pmol/g Hb (mean +/- SD) found in the non-smokers corroborated the steady-state level of 18 +/- 3 pmol/g Hb (mean +/- SD) calculated from the pharmacokinetic approach.

Adult↗
PubMed1979

Determination of ethylene oxide, ethylene chlorohydrin, and ethylene glycol residues in ophthalmic solutions at proposed concentration limits.

A GLC method was developed for the determination of ethylene oxide and its two reaction products, ethylene chlorohydrin and ethylene glycol, in ophthalmic solutions at the levels recently proposed by the Food and Drug Administration. The method requires no extractions, sample preparations, or elaborate trapping and concentrating techniques. All three components can be chromatographed on the same spiral glass column packed with a porous polymer absorbent.

Chlorohydrins↗
PubMed1977

Acute hepatotoxicity of ethylene and halogenated ethylenes after PCB pretreatment.

Previous studies from our laboratory have shown that ethylene, vinyl fluoride monomer (VFM), vinyl chloride monomer (VCM), and vinyl bromide monomer (VBM) are all acutely hepatotoxic in rats pretreated with polychlorinated biphenyl (PCB). The time course of hepatic injury development after exposure and several parameters, environmental and chemical, affecting this toxicity were evaluated in the work reported here. Liver injury, as measured by serum alanine-alpha-ketoglutarate transaminase (SAKT) or sorbitol dehydrogenase (SDH), develops progressively over a 24-hr period following a 4-hr inhalation exposure of PCB-pretreated rats to ethylene or VCM. Environmental temperature during exposure to VCM does not affect hepatotoxicity or mortality below 30.3 degrees C. At 33.8 degrees C, however, mortality and SAKT are dramatically increased. Overnight fasting, which depletes hepatic glutathione (GSH) of PCB-pretreated rats before exposure to ethylene or VCM, significantly increases the hepatotoxicity of these compounds as measured by SDH. The combined effects of fasting and of trichloropropane epoxide (TCPE), an inhibitor of epoxide hydrase (EH), were also examined. TCPE treatment of fasted PCB-pretreated rats immediately before exposure was synergistic in increasing the acute toxicity of ethylene and VCM. TCPE increased mortality in fed or fasted rats exposed to VFM, but there was no effect of fasting alone. Both fasting and TCPE increased the sensitivity of PCB-pretreated rats to VBM, but there was not a clearly synergistic effect of fasting plus TCPE. These data suggest that the acute toxicity of these compounds is mediated through epoxide intermediates.

Animals↗
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↗
PubMed1992

Cognitive dysfunction in a patient with long-term occupational exposure to ethylene oxide. Role of ethylene oxide as a causal factor.

This case illustrates a comprehensive approach to assessing causality in a woman with apparent cognitive dysfunction, as measured by neuropsychological testing, and a 10-year history of occupational exposure to ethylene oxide. The analysis included a multidisciplinary examination of the patient, which took place several years after the termination of her exposure. In addition, all of the patient's prior medical and psychiatric records were reviewed, as were the records of her employer to ascertain her exposure history. Our evaluation revealed a pattern of neuropsychological findings not consistent with nervous system damage secondary to an organic effect of ethylene oxide. A more likely causal hypothesis is adopted: the patient's apparent cognitive dysfunction had a psychiatric etiology. This case also illustrates the potential impact of a patient's involvement in legal proceedings related to claims of neurocognitive dysfunction.

Adult↗
PubMed1975

Function of the classical and alternate pathways of human complement in serum treated with ethylene glycol tetraacetic acid and MgCl2-ethylene glycol tetraacetic acid.

An immunochemical and functional analysis of the classical and alternate complement pathways in human serum was performed in the presence of 10 mM ethylene glycol tetraacetic acid (EGTA) and MgCl(2)-EGTA (MgEGTA), chelating agents which have been recently utilized as a means of distinguishing between these two complement pathways. Total hemolytic activity, integrity of the C1 complex, hemolytic activity of C2, conversion of factor B (C3 proactivator), and complement-dependent bactericidal activity were studied. The effect of these chelators on activation of complement pathways by Escherichia coli, by sensitized erythrocytes as a prototype of activators of the classical pathway, and by zymosan as a prototype of alternate (properdin) pathway activators was studied. Human serum containing 10 mM EGTA, which provides almost no ionized calcium and considerably less ionized magnesium than unchelated serum, allowed consumption of complement via the alternate (properdin) pathway, but blocked the classical pathway as judged by disintegration of the C1 complex and lack of utilization of C2. However, activity of the alternate complement pathway in EGTA serum, as judged by conversion of factor B and bactericidal activity against gram-negative bacteria, was distinctly suboptimal. Addition of magnesium ion in a concentration equimolar to EGTA (MgEGTA serum), while still providing conditions in which the C1 complex dissociated, significantly enhanced alternate complement pathway-mediated bactericidal activity. However, in MgEGTA serum considerable fluid-phase activation of the alternate pathway, as indicated by decrease in 50% hemolytic complement (CH(5 0)) titers and conversion of factor B to its active form in the absence of any activating challenge, was observed. Moreover, some fluid-phase consumption of C2 was observed in MgEGTA serum, even though, as mentioned, the C1 complex was shown to be dissociated under these conditions. MgEGTA-related activation of C2 and of the alternate (properdin) pathway of complement was significantly enhanced by the presence of zymosan and E. coli. These results indicate that use of the chelating agents EGTA and MgEGTA to differentiate between classical and alternate pathway activation of human complement is more complex than has hitherto been suggested. In EGTA serum, spontaneous activation of either pathway does not occur but bactericidal activity, as a measure of biologic function of complement, is suboptimal. In MgEGTA serum, bactericidal activity is fully expressed, but there is considerable instability, in terms of fluid-phase activation, in Mg(2+)-dependent components of both pathways. Thus, caution is indicated in the use and interpretation of the effects of these chelating agents on biologic functions mediated by either pathway of human complement.

Blood Bactericidal Activity↗
PubMed1992

Interactions of poly(ethylene glycol)-grafted cellulose membranes with proteins and platelets.

The interactions of proteins and platelets with cellulose membranes grafted with poly(ethylene glycol) were studied. The poly(ethylene glycol) grafting was carried out using poly(ethylene glycol)-monoacid and poly(ethylene glycol)-diacid, which have one and two terminal carboxyl groups, respectively. The grafting operates through esterification between the carboxyl groups of poly(ethylene glycol) and the hydroxyl groups on the membrane surface. Both of the poly(ethylene glycol) grafted membranes reduced the complement activation. Adsorption of bovine serum albumin and gamma-globulin increased when the membrane was grafted with poly(ethylene glycol)-diacid, but did not change when it was grafted with poly(ethylene glycol)-monoacid. When platelets were incubated with serum proteins, the platelet adhesion to the membranes slightly decreased by grafting both the poly(ethylene glycol)-diacid and poly(ethylene glycol)-monoacid. The poly(ethylene glycol)-diacid grafted surface showed more clotting than the poly(ethylene glycol)-monoacid grafted and original surfaces.

Animals↗
PubMed1977

Simple GLC determination of ethylene oxide and its reaction products in drugs and formulations.

Convenient rapid GLC methods for the estimation of residual ethylene oxide, ethylene chlorohydrin, and ethylene glycol in ethylene oxide-sterilized bulk drugs and formulations prepared therefrom are described. Ethylene oxide was chromatographed using a porous polymer column; ethylene chlorohydrin and ethylene glycol were chromatographed using either polyethylene glycol 400 or a porous polymer column. All three residuals were determined from the same sample preparation for each type of drug or formulation examined. Recoveries of each of the three residuals were greater than 95% for all samples examined. Detection limits, at moderate electrometer sensitivities, were 2 microgram/g or ml for ethylene oxide and ethylene chlorohydrin and 5 microgram/g or ml for ethylene glycol. The most likely interferences are discussed.

Chromatography, Gas↗
PubMed1979

A cohort study of mortality and cancer incidence in ethylene oxide production workers.

Ethylene oxide, important as an intermediate product in the chemical industry and for sterilising hospital equipment, is mutagenic in several organisms; carcinogenicity has been suspected although this had not been supported by clinical data. Ethylene oxide has been produced by a Swedish company since the beginning of the 1940s. This paper describes a cohort study of the mortality and the cancer incidence among full-time exposed workers in ethylene oxide production, a group of maintenance workers with intermittent exposure and a group of unexposed controls. Investigation of the production processes in the building at different times has shown that workers were exposed to ethylene dichloride, ethylene chlorohydrin, ethylene, and small amounts of bis-(2-chloroethyl) ether as well as to ethylene oxide and traces of other chemicals. The full-time exposed cohort shows a considerable excess mortality deriving mainly from increased mortality from tumours and also from diseases of the circulatory system. The cancer incidence study, including living persons with malignancies, showed a significant excess in the full-time cohort. Of the 16 patients with tumours in the two more exposed cohorts there were three cases of leukaemia, six of tumours in the alimentary tract and four of urogenital malignancy. The excess mortality and cancer incidence cannot be attributed to any particular chemical in the production process, but ethylene oxide and ethylene dichloride are the prime suspects.

Chemical Industry↗
PubMed1978

Evolution of ethylene by Saccharomyces cerevisiae as influenced by the carbon source for growth and the presence of air.

Effects of the carbon source and oxygen on ethylene production by the yeast Saccharomyces cerevisiae have been studied. The amounts of ethylene evolved by the yeast culture were less than those detected in the blank (an equal volume of uninoculated medium), suggesting a net absorption of ethylene by the yeast cells. Addition of glucose to the lactate-grown yeast culture induced ethylene production. This glucose-induced stimulation of ethylene production was inhibited to a great extent by cycloheximide. Results suggested that the yeast cells in the presence of glucose synthesized an ethylene precursor and passed it into the medium. The conversion of this precursor to ethylene might be stimulated by oxygen. The fact that ethylene was produced by the yeast growing anaerobically and also by respiration-deficient mutants isolated from the wild-type yeast suggested that mitochondrial ATP synthesis was not an absolute requirement for ethylene biogenesis.

Anaerobiosis↗
PubMed1979

[Testicular atrophy of mice induced by ethylene glycol mono alkyl ethers (author's transl)].

Toxicities of ethylene glycol (EG) and 6 ethylene glycol mono alkyl ethers administered orally were studied. Mice were given various doses (62.5, 125, 250, 500, 1,000, 2,000 and 4,000 mg/kg body weight) of the compounds daily for 5 days/week, for 5 weeks. High doses of ethylene glycol mono methyl ether (EGM), ethylene glycol mono methyl ether acetate (EGMA), ethylene glycol mono ethyl ether (EGE) and ethylene glycol mono ethyl acetate (EGEA) produced marked testicular atrophy and leucopenia. Dose-responce relation was found in these effects. EGM was more effective than EGE, while ethylene glycol mono butyl ether and ethylene glycol mono phenyl ether had but slight effect and EG had no detectable action on testis and leucocytes. Toxic doses being expressed as mg/kg body weight, esterification seemed to weaken the atrophic action of EGM and EGE, but when expressed as mol/kg, significant difference was found neither between EGM and EGMA nor between EGE and EGEA. The mechanism of testicular atrophy induced by low ethylene glycol mono alkyl ethers is likely to be an inhibitory action on cell division.

Animals↗
PubMed1976

Microbial metabolism of ethylene.

The ethylene-oxidizing strain E20 was grown on different carbon sources to obtain information on the metabolism of ethylene from simultaneous adaptation studies and from measurements of specific activities of enzymes in cell-free extracts. From the simultaneous adaptation studies it was concluded that ethylene oxide is a product of ethylene catabolism. The bacterium was also able to grow on the epoxide. From a comparison of the specific activities of isocitrate lyase and malate synthetase in different extracts it was concluded that the glyoxylate cycle was involved in the metabolism of ethylene, indicating that acetyl-CoA is a metabolite of ethylene catabolism. The sequence of reactions leading from ethylene oxide to acetyl-CoA could not be established from the simultaneous adaptation experiments and the enzyme activities in extracts.

Acetate-CoA Ligase↗
PubMed1976

Formation of ethylene by Escherichia coli.

Escherichia coli strain SPA O converts methionine to ethylene by an inducible enzyme system. L-Cysteine, L-homocysteine, methionine derivatives and the sulphur-containing analogues of L-methionine also act as precursors of ethylene. Ethylene is produced by cell suspensions only in the presence of air; cell-free preparations can produce ethylene aerobically and anaerobically, but the extent to which they do so depends on the mode of culture growth. Light stimulates ethylene production by cell suspensions and its presence is essential for production by cell-free preparations. The kinetics of ethylene biogenesis and its pH and temperature optima suggest that ethylene is a secondary metabolite.

Aerobiosis↗