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PubMed1997

An autopsy case of acute chloroform intoxication after intermittent inhalation for years.

A 39-year-old female died shortly after inhalation of chloroform by a saturated towel placed over her face by her lover, who also inhaled and became unconscious. They had inhaled chloroform once or twice a month for about seven years. Fatal level of chloroform was detected in the blood and tissues by gas chromatographic/mass spectrometric analysis. The fragmentation and waviness of cardiomyocytes that indicates hypercontraction, along with the edema and hemorrhage of the lung, shows the presence of acute heart failure possibly caused by arrhythmias or cardiac depression. The unusual numbers of lipofuscin pigments in the heart as well as in the liver may be generated by the chronic use of chloroform.

Acute Disease↗
PubMedDate not supplied

[A case of suicidal chloroform poisoning].

A 33-year-old man who had suffered from phobia and depressions was found dead in his kitchen. He was entirely covered by plastic waste disposal bags stuck together. The corpse was lying flat on his stomach with his face on a towel soaked with chloroform. Within the plastic cover, on either side of the body's head, there was located a can half way filled with chloroform. Autopsy revealed cauterized lips and mucous membranes of the mouth. The morphological findings of the inner organs were unspecific. For toxicological analyses, air samples from the pleural cavities of the corpse were taken by way of charcoal tubes and a microprocessor aided pump. The solvents adsorbed on the charcoal were desorbed with benzyl alcohol and analyzed by gas chromatography according to standard procedures. The quantification of the chloroform levels of the body fluids and the tissue samples of the corpse was performed by extraction with pentane followed by addition of trichloroethylene as internal standard and consecutive gas chromatographic analysis. The results of the toxicological analyses confirmed the diagnosis of a fatal chloroform intoxication.

Adult↗
PubMed1976

[The uterotropismus of halothane, chloroform or methoxyflurane in clinical use (author's transl)].

To perform episiotomy, 89 women after childbirth were anaesthetized with either halothane (50 patients), methoxyflurane (24 patients) or chloroform (15 patients). The activity of the uterus was registered tocodynamographically. To examine the alternate influence of narcotics and uterotonica, 57 patients were pre-medicated with sintocinon and methergin i.m. as a prophylaxis. The second group (32 patients) received no premedication to stimulate labor activity, however in 18 cases towards the end of narcosis oxytocin and methergin were given i.v. In addition to these examinations 5 vaginal deliveries were anaesthetised with halothane only. Concerning our own experimental study it can be observed: 1. The relaxative properties of halothane wich suppresses completly the activity of myometrium during the deep stages of anaesthesia are superior to chloroform and methoxyflurane. 2. More rapid relaxation of the uterus with halothane compared with chloroform and methoxyflurane. 3. After the use of halothane a quicker return of the activity of the uterus compared with chloroform and methoxyflurane. 4. The value of a prophylaxis with uterotonica can be demonstrated by a comparatively reduced slowing-down of labour-activity during anaesthesia. 5. In every one of the cases, an interuption of the labour-suppressing, caused by the anaesthesia, can be obtained by injecting intravenously oxytocin or methergin. 6. During vaginal delivery, compared to the post placentar phase, there is no need for higher concentrations of halothane to be used to suppress labour contractions. The discussion deals with the intensity of reduction of the uterus contraction caused by the above mentioned narcotics, the dangers of the atony of the uterus, and the indications and contra-indications of obstetrical anaesthesia with halothane or methoxyflurane.

Adult↗
PubMed1984

Two-phase derivatization of pentazocine with chloroformate esters and determination by gas chromatography.

Two-phase derivatization with chloroformate esters of tertiary amines that contain a phenol group has been studied. The derivatives were analysed by gas chromatography with sensitive and selective detectors. The N,O-bis derivative of pentazocine was formed using an aqueous phase at pH 9.8, with tetrabutylammonium ion for extraction of the phenolate ion as an ion-pair. The organic phase comprised methylene chloride with trichloroethyl chloroformate or ethyl chloroformate. At pH 10.7 the derivative was hydrolysed by hydroxide ions extracted into the organic phase. Hydrolysis also occurred when more lipophilic counter-ions such as tetrapentyl-ammonium ions were used. Two-phase derivatization could also be achieved with toluene or ethyl acetate as the organic phase, although the reaction rate was considerably slower. The method was also applied to the assay of pentazocine in plasma. The best results were achieved after selective extraction of pentazocine from plasma, two-phase derivatization with ethyl chloroformate and determination by mass spectrometry or thermionic detection. The minimum detectable concentration of pentazocine was 10 ng/ml in a 1-ml plasma sample.

Journal Article↗
PubMed1998

Gas chromatographic-mass spectrometric identification and quantification of aniline after extraction from serum and derivatization with 2,2,2-trichloroethyl chloroformate, a novel derivative.

Aniline is widely used as an intermediate in the synthesis of dyes. It is also used in the manufacture of pharmaceuticals, photographic developers, shoe polish, etc. Exposure to aniline is toxic because it produces methemoglobin. In humans, blood methemoglobin levels are often measured as an index of exposure to aniline. Here a method is described for identification and quantification of aniline by gas chromatography-mass spectrometry after extraction from human serum and derivatization with 2,2,2-trichloroethyl chloroformate. Aniline, along with the internal standard N-methylaniline, were extracted from alkaline serum using chloroform. Aniline and the internal standard were derivatized with 50 microl 2,2,2-trichloroethyl chloroformate. After evaporating excess derivatizing reagent, the residue was reconstituted in 50 microl chloroform and injected into the gas chromatographic-mass spectrometry (GC-MS) system. A positive identification of derivatized aniline can be made by observing strong molecular ions at m/z 267 and 269. Similarly, the derivatized internal standard showed strong molecular ions at m/z 281 and 283. The within-run and between-run precisions of the assay were 3.61 and 5.92%, respectively, at an aniline concentration of 5 mg/l. The assay was linear for serum aniline concentrations of 0.5-25.0 mg/l. The detection limit was 0.1 mg/l. The assay was not affected by lipemia, hemolysis or high bilirubin concentration in serum.

Aniline Compounds↗
PubMed2001

Chloroform-soluble schiff-base Zn(II) or Cd(II) complexes from a dynamic combinatorial library.

A dynamic combinatorial library of metal ion Schiff-base complexes have been studied for the extraction of Zn(II) or Cd(II) from aqueous solution into chloroform. Library components consist of different aminophenols and 2-pyridinecarboxaldehyde. Extraction of both Zn(II) and Cd(II) into chloroform was observed from aqueous solutions containing 0.0500 mM M(NO3)2, 0.100 M aminophenol, 0.100 M 2-pyridinecarboxaldehyde, 0.100 M NaCl, and 5.00 mM buffer at pH 8.5. Extraction was dependent on pH but not on counterions including Cl-, Br-, or NO3-. Studies showed that equilibrium was attained between the Schiff-base complexes across the two-phase chloroform-water system after 24 h of stirring. Analysis of the extracted species by use of 1H NMR spectroscopy and mass spectrometry as well as solubility studies on characterized complexes suggested that the major extracted species is the neutral bis-Schiff-base metal ion complex. In libraries containing mixtures of two different aminophenols and 2-pyridinecarboxaldehyde, an enhanced extent of extraction of Zn(II) into chloroform is observed. Studies suggest that a Zn(II) complex, which is likely the mixed Schiff-base complex, has superior extraction properties compared to simple libraries with a single aminophenol component. The structures of two bis-Schiff-base complexes of Zn(II) and one of Cd(II) have been determined by X-ray crystallography. The geometries of the two Zn(II) complexes, which differ only by a methyl substituent on the Schiff-base ligand, are markedly different, supporting the use of combinatorial methods in coordination chemistry. Zn(SB14)2 crystallized as the sesquihydrate (C24H18N4O2Zn.1.5 H2O) in the space group C2/c, with cell dimensions a = 23.219(15) A, b = 11.299(7) A, c = 16.822(11) A, beta = 102.91(5) degrees, V = 4302(5) A3, and Z = 8. Zn(SB15)2 crystallized as a 1:1 methanol solvate (C26H22N4O2Zn.CH3OH) in the space group P2(1)/c with cell dimensions a = 13.981(5) A, b = 7.978(3) A, c = 22.568(8) A, beta = 104.53(3) degrees, V = 2436.8(15) A3, and Z = 4. Cd(SB14)2 crystallized as a 1:1 ethanol solvate (C24H18N4O2Cd.CH3CH2OH) in the space group R3 with unit cell dimensions of a = 36.423(2) A, c = 9.2930(10) A, V = 10678(2) A3, and Z = 18.

Journal Article↗
PubMed1986

Production of vinylidene chloride from the thermal decomposition of methyl chloroform.

This study investigated the extent to which methyl chloroform undergoes thermal decomposition to form vinylidene chloride. The experiment was conducted under laboratory conditions that approximate those found in industrial environments. Methyl chloroform vapors at approximately the TLV concentration of 1910 mg/m3 were passed through a heated quartz tube packed with glass or copper beads. In the presence of glass, the decomposition reaction began at 350 degrees C and was essentially complete at 605 degrees C. Vinylidene chloride was detected in nearly stoichiometric amounts. In the presence of copper, the reaction occurred initially at 180 degrees C. At 442 degrees C no methyl chloroform was detected. Once again, the conversion to vinylidene chloride was nearly complete. Two major conclusions have been derived from this study. First, under these experimental conditions, methyl chloroform undergoes thermal decomposition to yield substantial quantities of vinylidene chloride. Second, the dehydrohalogenation reaction proceeds at much lower temperatures in the presence of copper.

Chemical Phenomena↗
PubMed1998

Characterization of a phospholipid adduct formed in Sprague Dawley rats by chloroform metabolism: NMR studies.

The formation of a covalent adduct to a single phospholipid by the oxidative chloroform metabolite, phosgene, is demonstrated in liver mitochondria of phenobarbital-pretreated Sprague Dawley (SD) rats treated with CHCl3. The densitometric analysis of the phosphorus stained extracted phospholipids showed that the formation of this adduct in liver mitochondria is accompanied by a decrease of phosphatidylethanolamine and cardiolipin. The characterization of this adduct was performed with a multinuclear NMR approach by comparison with the decreased phospholipids. Treatment of rats with [13C]chloroform resulted in an intense 13C NMR peak from either an esteric or amidic carbonyl. Very strong similarities in fatty acid composition were found between phosphatidylethanolamine and the phosgene-modified PL, using 13C and 1H NMR spectroscopy. A multiplet at 3.91 ppm coupled to a signal at 3.41 ppm was shown by two-dimensional 1H NMR in the adduct spectrum. This cross peak was interpreted as arising from the shifted resonances of the two PE head group methylene groups, due to the binding with phosgene. 31P spectrum of the adduct was identical to that of phosphatidylethanolamine. We concluded that the chloroform adduct is a modified phosphatidylethanolamine, with the phosgene-derived carbonyl bound to the amine of the head group.

Animals↗
PubMed2000

The utility of PBPK in the safety assessment of chloroform and carbon tetrachloride.

Occupational exposure limits (OELs) for individual substances are established on the basis of the available toxicological information at the time of their promulgation, expert interpretation of these data in light of industrial use, and the framework in which they sit. In the United Kingdom, the establishment of specific OELs includes the application of uncertainty factors to a defined starting point, usually the NOAEL from a suitable animal study. The magnitude of the uncertainty factors is generally determined through expert judgment including a knowledge of workplace conditions and management of exposure. PBPK modeling may help in this process by informing on issues relating to extrapolation between and within species. This study was therefore designed to consider how PBPK modeling could contribute to the establishment of OELs. PBPK models were developed for chloroform (mouse and human) and carbon tetrachloride (rat and human). These substances were chosen for examination because of the extent of their toxicological databases and availability of existing PBPK models. The models were exercised to predict the rate (chloroform) or extent (carbon tetrachloride) of metabolism of these substances, in both rodents and humans. Monte Carlo analysis was used to investigate the influence of variability within the human and animal model populations. The ratio of the rates/extent of metabolism predicted for humans compared to animals was compared to the uncertainty factors involved in setting the OES. Predictions obtained from the PBPK models indicated that average rat and mouse metabolism of carbon tetrachloride and chloroform, respectively, are much greater than that of the average human. Application of Monte Carlo analysis indicated that even those people who have the fastest rates or most extensive amounts of metabolism in the population are unlikely to generate the levels of metabolite of these substances necessary to produce overt toxicity in rodents. This study highlights the value that the use of PBPK modeling may add to help inform and improve toxicological aspects of a regulatory process.

Administration, Inhalation↗
PubMed1996

Association of fallout radiocesium with soil constituents: effect of sterilization of forest soils by fumigation with chloroform.

The effect of soil sterilization by chloroform fumigation on the release of fallout radiocesium incorporated in the fungal biomass of the organic layer of two forest soils was investigated by applying a sequential extraction procedure for radiocesium. The amount of the biomass in all soil samples was estimated by determination of the dissolved organic carbon (DOC) before and after fumigation, and qualitatively also by the ergosterol test. The five fractions obtained by sequential extraction (modified Tessier procedure) were: (I) easily exchangeable, (II) bound to oxides, (III) bound to organic matter, (IV) persistently bound, (V) residual. For the samples from the soil under spruce trees, no significant effects were apparent in any of these five fractions as a result of chloroform fumigation, indicating that the amount of radiocesium in the biomass of this soil was obviously negligibly small compared with the radiocesium associated with other soil constituents. The results obtained for the soil samples from the beech stand, however, reveal that the destruction of the biomass by chloroform fumigation modified considerably the extent of the association (i.e., binding) of radiocesium with the various other soil constituents (especially the clay minerals). As a result of this rapid redistribution of radiocesium released by the fungal biomass, it is not possible, in general, to attribute the observed increase of radiocesium in fraction I (easily exchangeable) after soil sterilization quantitatively to radiocesium released by the biomass. A reliable method to determine the amount of radiocesium incorporated in the fungal biomass of the soil samples which also contain clay minerals has, therefore, still to be developed.

Biomass↗
PubMed1983

Induction by chloroform of two forms of ornithine decarboxylase in rat liver. Half-life of isozymes.

Ornithine decarboxylase (ODC) in rat liver was separated into two species by DEAE-Sepharose CL-6B column chromatography. The activity of both species of ODC was increased at least 20-fold by chloroform treatment of the rats. The major species, Peak A, contained 65% of the ODC activity and possessed a half-life of 11 min. The second species, Peak B, accounted for 35% of the activity and possessed a half-life of 50 min. The long-lived species of ODC activity, induced in rat liver by chloroform, has not been reported previously and might be related to the prolonged induction of ODC activity by chloroform and to tumor promotion and growth.

Animals↗
PubMed1995

Environmental and biological monitoring of chloroform in indoor swimming pools.

The presence of chloroform as the result of disinfection with sodium hypochlorite was demonstrated in the water and ambient air of indoor swimming pools. Environmental monitoring was performed in 12 indoor swimming pools in northern Italy and the level of human exposure was assessed. Biological monitoring performed by gas chromatography on human plasma and alveolar air samples evidenced that the uptake of chloroform in swimmers varies according to the intensity of the physical activity and age. The elimination of chloroform in alveolar air in one subject showed a very short half-life (from 20 to 27 min) and a complete clearance within 10 h after the end of exposure.

Breath Tests↗
PubMed1989

Induction of cytochromes P450IIE1 and P450IIB1 by secondary ketones and the role of P450IIE1 in chloroform metabolism.

It has been shown previously that the potentiation of chloroform-induced hepatotoxicity by linear secondary ketones increases with the carbon-chain length. The present work examines the possibility that this potentiation is due to the induction of P450IIE1. The metabolism of chloroform, as measured using headspace gas chromatography, in the presence of microsomes from acetone-treated rats was elevated threefold compared to controls. Inclusion of monoclonal antibody against P450IIE1 inhibited the metabolism by 81%. Alternate substrates of P450IIE1 were also inhibitory. Chloroform metabolism was observed using purified, reconstituted P450IIE1 plus cytochrome b5, but was not detected using P450IIB1. The inductive effect of 18-hr oral pretreatment (15 mmol/kg body wt) with each of three secondary ketones on two isozymes of rat liver microsomal cytochrome P450, P450IIE1, and P450IIB1 was studied. The content of total microsomal P450 and NADPH-dependent cytochrome c reductase, the rates of oxidation of N-nitrosodimethylamine, benzphetamine, and pentoxyresorufin, as well as levels of immunoreactive protein for both of the isozymes were elevated by the pretreatments in the rank order of acetone less than or equal to 2-butanone less than 2-hexanone, in agreement with other trends noted by previous investigators. The results provide further evidence for the role of P450IIE1 induction in the potentiation phenomenon.

Animals↗
PubMed1995

Toxicity and cell proliferation in the liver, kidneys and nasal passages of female F-344 rats, induced by chloroform administered by gavage.

Dose-response relationships were determined for the induction of cytolethality and regenerative cell proliferation in the established target organs (liver, kidneys, and nasal passages) of female F-344 rats given chloroform daily by gavage. Rats were administered chloroform dissolved in corn oil at doses of 0, 34, 100, 200 or 400 mg/kg/day for 4 consecutive days or for 5 days/wk for 3 wk. Bromodeoxyuridine (BrdU) was administered through an implanted osmotic pump 3.5 days prior to autopsy to label cells in S-phase. Cells in S-phase were visualized immunohistochemically in tissue sections and the labelling index (LI) calculated as the percentage of cells in S-phase. Mild degenerative centrilobular changes and dose-dependent increases in the hepatocyte LI were observed after administration of 100 mg or more chloroform/kg/day. Rats given 200 or 400 mg/kg/day for 4 days or 3 wk had degeneration and necrosis of the proximal tubules of the renal cortex. Regenerating epithelium lining proximal tubules was seen histologically and as an increase in LI. Dose-dependent increases in LI were observed in the kidneys at doses of 100 mg or more chloroform/kg/day at both 4 days and 3 wk. Two distinct treatment-induced responses were observed in specific regions of the olfactory mucosa lining the ethmoid region of the nose. A peripheral lesion was seen at all doses used and included new bone formation, periosteal hypercellularity and increased cell replication. A central lesion was seen at doses of 100 mg or more chloroform/kg/day and was characterized by degeneration of the olfactory epithelium and superficial Bowman's glands. These observations define the dose-response relationships for the liver, kidneys and nasal passages as target organs for chloroform administered by gavage in the female F-344 rat.

Animals↗
PubMed1979

Effect of chloroform on the activities of liver enzymes in rats.

Rats were dosed once, 5 times or 10 times with chloroform (0.5-50 mg/kg) and the liver enzyme activities were determined. Chloroform induced much change in the 24 enzymes investigated but caused only minimal liver enlargement. The main enzymic changes were: stimulation of glycolysis and oxidative phosphorylation, increased breakdown of protein and nucleic acids, hexose phosphate shunt activity was reduced leading to a shortage of NADPH in the cell, adrenal medullary and cortical secretion were stimulated. These results show that ingestion of chloroform even in small amounts causes distinct changes in liver cell metabolism as indicated by enzyme activities. Some of the changes are similar to, but others differ from, those seen with larger and anaesthetic doses. In most cases a transition between these 2 types of effects can be seen.

Animals↗
PubMed1992

Individual serum bile acids as early indicators of carbon tetrachloride- and chloroform-induced liver injury.

Individual serum bile acids (SBA) are emerging as potentially useful early indicators of liver injury. This study was undertaken to compare the usefulness of individual SBA with the routinely used assays for detecting the effects of the hepatotoxicants carbon tetrachloride (CCl4) and chloroform (CHCl3). Serum samples were assayed for liver injury by determination of alanine aminotransferase (ALT), aspartate amino-transferase (AST), alkaline phosphatase (ALP), bilirubin and total bile acid (by enzymatic kit). These results were compared with levels of individual SBA measured by high performance liquid chromatography (HPLC). Liver samples from CCl4-treated rats were taken for light and electron microscopic examination. The highest dose for each chemical caused increases in serum ALT and AST but not ALP. Chloroform at the highest dose increased bilirubin. Total SBA levels as assayed by the kit were elevated in response to CCl4 and CHCl3 at doses below which serum enzymes and bilirubin were increased. Some individual SBA were increased at a still lower dose for each of these two chlorinated solvents. At the lowest dose of CCl4 tested no consistent light microscopic or ultrastructural changes were found. At all the higher doses periacinar cells displayed typical accumulation of lipid droplets and degranulation and dilation of rough endoplasmic reticulum. The extent of the ultrastructural changes were dose-dependent. Thus individual SBA assayed by HPLC may be considered as a very sensitive indicator of liver injury induced by the classical hepatotoxicants carbon tetrachloride and chloroform.

Alanine Transaminase↗
PubMed1985

Dose-dependent promoting activity of chloroform in rat liver foci bioassay.

Chloroform enhances dose-dependently the number of preneoplastic foci in livers of weanling female Sprague-Dawley rats. The preneoplastic foci were induced with a single dose of 8 mg diethylnitrosamine (DEN)/kg body wt. Thereafter chloroform was applied twice weekly for 11 consecutive weeks in doses of 100, 200 and 400 mg/kg body wt, respectively. This treatment raised the number of adenosine-5'-triphosphatase (ATPase)-deficient foci up to 5-fold, that of gamma-glutamyltranspeptidase (GGTase) and glycogen-positive foci 13- and 10-fold, respectively, after 12 weeks; 25 mg caused no effect compared to DEN-treated controls. In contrast, daily doses of chloroform only, 200 and 400 mg/kg body wt for 33 days, and 800 mg/kg body wt for 20 days given to 3-4-week-old female Sprague-Dawley rats did not lead to island formation, measured after 12 weeks, indicating a promoting rather than an initiating potency.

Adenosine Triphosphatases↗
PubMed1986

Is chemiluminescence an index of hepatic lipoperoxidation accompanying chloroform anesthesia?

Hepatic lipoperoxidation by highly reactive metabolites produced during biodegradation of chloroform is believed to cause delayed hepatic necrosis. Chemiluminescence occurs during interaction of these metabolites with a lipid membrane. We have made continuous in vivo measurements of hepatic light output in the phenobarbital-induced rat breathing either air or chloroform vaporized in air. The data permitted direct estimation of the time course of chloroform-induced lipoperoxidation. These potentially toxic events began 15 min after initiation of anesthesia and continued for the duration of the study. Chemiluminescence did not occur with inhalation of isoflurane, an anesthetic undergoing minimal biodegradation.

Anesthesia↗