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PubMed1998

Effect of water temperature on dermal exposure to chloroform.

We have developed and applied a new measurement methodology to investigate dermal absorption of chloroform while bathing. Ten subjects bathed in chlorinated water while breathing pure air through a face mask. Their exhaled breath was delivered to a glow discharge source/ion trap mass spectrometer for continuous real-time measurement of chloroform in the breath. This new method provides abundant data compared to previous discrete time-integrated breath sampling methods. The method is particularly well suited to studying dermal exposure because the full face mask eliminates exposure to contaminated air. Seven of the 10 subjects bathed in water at two or three different temperatures between 30 degrees C and 40 degrees C. Subjects at the highest temperatures exhaled about 30 times more chloroform than the same subjects at the lowest temperatures. This probably results from a decline in blood flow to the skin at the lower temperatures as the body seeks to conserve heat forcing the chloroform to diffuse over a much greater path length before encountering the blood. These results suggest that pharmacokinetic models need to employ temperature-dependent parameters. Two existing models predict quite different times of about 12 min and 29 min for chloroform flux through the stratum corneum to reach equilibrium. At 40 degrees C, the time for the flux to reach a near steady-state value is 6-9 min. Although uptake and decay processes involve several body compartments, the complicating effect of the stratum corneum lag time made it difficult to fit multiexponential curves to the data; however, a single-compartment model gave a satisfactory fit.

Adult↗

PubMed1978

Health aspects of chloroform--a review.

First prepared in 1831, chloroform was initially employed as an "ideal" anesthetic. Chloroform was later found to cause heart and liver damage and, with the discovery of safer agents, lost importance as a medical anesthetic. Today chloroform is used primarily as a solvent in industry, in the production of antibiotics, as a cleaning agent, and as an ingredient in pharmaceutical and veterinary formulations. A recent report issued by the National Cancer Institute implicates chloroform as a carcinogen in laboratory rodents. These findings, in conjunction with enforcement of the Delaney Clause have generated renewed interest in chemicals such as chloroform which are not only used in a variety of industrial applications, but which are also available to the general public in a number of food and cosmetic products.

Animals↗

PubMed1990

Isolation of IgY from the yolks of eggs by a chloroform polyethylene glycol procedure.

By shaking a dilute suspension of egg yolk with chloroform followed by low speed centrifugation (1500 g for 30 min) the water soluble proteins which include chicken IgG (IgY) separate from the emulsion of chloroform and lipophilic substances. The IgY may then be separated from the associated water soluble proteins by precipitation with 12% polyethylene glycol Mr 6000. The method called the chloroform - polyethylene glycol procedure was compared with the polyethylene glycol procedure which is currently being used. It was found that the chloroform - polyethylene glycol method yielded 2.57 times more IgY than the conventional polyethylene glycol method. The ratio of titres of IgY anti Jasus lalandii haemocyanin antibody purified by the two procedures was very nearly 2.57 indicating that the chloroform had no adverse effect on the antibody activity.

Animals↗

PubMed1978

Immunological and binding studies on chloroform--methanol extracts from electroplax of Torpedo marmorata and from rat brain cortex. Comparison of the material solubilized by organic solvents with the receptor proteins solubilized by detergents.

We have investigated a chloroform--methanol extracted material from electric organ of Torpedo marmorata with respect to binding of [3H]-acetyl-alpha-neurotoxin and [3H]-acetylcholine. No binding was observed which is in contrast to observations with detergent extracted receptor. Further, no crossreactivity could be demonstrated between the chloroform--methanol extracted proteolipid and antibodies against the detergent extracted receptor. Labelling in the membrane with [3H]-acetyl-alpha-neurotoxin before extraction with chloroform--methanol gave a very low yield of extracted labelled compound. The protein yield is about 0.3% of the total in the homogenate and only 0.04% of the specifically bound neurotoxin. Using the alkylating affinity label [3H]-N-propylbenzilylcholine mustard (1) and also [3H]-atropine, which both bind, at low concentrations, specifically to the muscarinic acetylcholine receptor, binding was studied to the chloroform--methanol extracted proteolipid from rat brain cortex. No specific binding could, however, be demonstrated. Prelabelling in the membrane with 1 and subsequent extraction with chloroform--methanol gave a protein yield of about 1% and an extraction of 26% of the specifically bound label.

Acetylcholine↗

PubMed1992

[Toxicity of chloroform and vitamin A status in the rat].

After a chloroform intraperitoneal injection, lactate dehydrogenase, alanine aminotransferase and particularly aspartate aminotransferase serum activities are much more raised in deficient animals. Liver ornithine decarboxylase (ODC) activity normally decreases in rats between the 4th. and the 7th. month after the weaning. In vitamin A deficient animals, basal values of the enzyme activity are lower and the decrease is deeper. But even at month 7, liver sustains a partial capacity of ODC recovery if retinol is fed during 15 days. Chloroform administration strongly enhances liver ODC activity in normal rats. In the deficiency, stimulation is lower in absolute value but relatively higher if referred to basal level. After retinol refeeding, chloroform stimulates enzyme activity to nearly normal values. Vitamin A deficiency impairs obviously liver ODC activity and its response to chloroform stimulation in rats, but the stroke is at least partially reversible in our conditions. Moreover, deficient animals maintain a non negligible capacity of ODC response under chloroform stimulation.

Alanine Transaminase↗

PubMed2004

[Comparative study of resosolv and chloroform in retreatment of canal obturated with resinifying agent].

OBJECTIVE: To evaluate the possibility for removal of resinifying agent, time required for removal and the working length loss by Resosolv or Chloroform. METHODS: 40 human teeth (80 root canals) obturated with FR phenolaldehyde agent were divided into four groups, 20 root canals per group. Group A: Resosolv with K file; group B: chloroform with K file; group C: Resosolv with Ultrasonic K file; group D: Chloroform with ultrasonic K file. Calculating the pereentage for removal of resinifying agent, time required for removal and the working length loss. RESULTS: The effectiveness of Resosolv for removing resinifying agent was better than chloroform. 87.5% of canals could be negotiated by Resosolv; 45% of canals be negotiated by chloroform. CONCLUSION: Resosolv is an effective solvent for canals obturated with resinifying agent.

Chloroform↗

PubMed1987

Studies on the mechanism of action of chloroform stimulation of rat hepatic ornithine decarboxylase (ODC).

We have previously reported that chloroform is a very potent stimulator of rat hepatic Ornithine Decarboxylase (ODC) activity. At that time we conducted the obligatory time course and dose response studies in male and female rats. However, in an attempt to more thoroughly understand the mechanism of this stimulation, we have examined the effects of a series of pharmacologic, physiologic and toxicologic manipulations on the chloroform response. These studies involved: in vivo experiments in which animals were pretreated with compounds known to effect the various physiological systems and then challenged with chloroform and in vitro experiments in which chloroform was added to the incubation media with/without the compound of interest. The results did not allow the assignment of a specific effect of any of the manipulations to the mechanism of the chloroform response, although much data of significant interest evolved.

Animals↗

PubMed1981

Effects of differential changes in rat hepatic and renal cytochrome P-450 concentrations on hepatotoxicity and nephrotoxicity of chloroform.

Cytochrome P-450 concentrations in rat liver and kidney were differentially altered by pretreatment with phenobarbital (PB), cadmium or fasting. The rats were then challenged with chloroform. The consequent hepatotoxicity was assayed by alanine amino transferase activity (AlaAT); the nephrotoxicity by inhibition of p-aminohippuric acid (PAH) uptake in vitro and both by histopathology. Fasting increased renal and hepatic cytochromes P-450 and chloroform-mediated necrosis in both organs. PB induction increased and cadmium decreased the liver cytochrome P-450 concentrations and the hepatotoxicity mediated by chloroform. PB and cadmium had no effect on renal cytochrome P-450 concentrations or the nephrotoxicity of chloroform. These results strongly suggest that the nephrotoxic metabolite of chloroform is produced within the kidney and the hepatotoxic metabolite in the liver.

Animals↗

PubMed1977

Topical treatment of herpes labialis with chloroform.

The efficacy of topical chloroform treatment of herpes labialis (HL) was evaluated in 50 patients with culture-verified HL. Treatment was begun within 48 hours of lesion onset, with either chloroform or camphor-in-oil placebo applied locally once a day for three days. Patients were observed daily by one investigator who also cultured and photographed the lesions. The photographs were evaluated by two other investigators. By direct observation, the time for scab formation was significantly less in the group treated with chloroform (P less than .01). No difference in time to healing was noted. Blind evaluation of the serial photographs showed a trend for more rapid scab formation and healing in patients treated with chloroform, but the differences were not significant. The minimal benefit derived from topical chloroform therapy of HL does not appear sufficient to recommend its routine use.

Administration, Topical↗

PubMed1994

Analysis of amino acids by gas chromatography-flame ionization detection and gas chromatography-mass spectrometry: simultaneous derivatization of functional groups by an aqueous-phase chloroformate-mediated reaction.

The one-step ethyl chloroformate derivatization of amino acids in an aqueous medium is extended with the use of a variety of alkyl chloroformate reagents. This provides a new and convenient procedure for preparing esters with different alkoxy groups. A new mechanism for esterification during chloroformate derivatization is proposed based on the formation of an intermediate mixed carboxylic-carbonic acid anhydride followed by the exchange with an alcohol. Among the different reagents investigated, isobutyl chloroformate derivatized amino acids were found to provide more sensitivity for analyses by GC-flame ionization detection and GC-MS relative to derivatives prepared by other alkyl chloroformates.

Amino Acids↗

PubMed2001

Dynamics of an inclusion complex of chloroform and cryptophane-E: evidence for a strongly anisotropic van der Waals bond.

The motional dynamics of a van der Waals inclusion complex of cryptophane-E and chloroform has been investigated by a combined NMR exchange and relaxation study. The kinetics of exchange of chloroform between the bulk solution and the complex was investigated by means of proton EXSY measurements. The carbon-13 relaxation of the cryptophane-E host and of the bound chloroform guest was analyzed using the Lipari-Szabo "model-free" approach. For interpretation of the carbon-13 relaxation measurements for chloroform, the chemical-exchange process of complex formation and dissociation had to be taken into account in terms of the modified Bloch equations. It was found that the complex behaves as a single molecule without any significant guest chloroform motion inside the host's cavity.

Journal Article↗

PubMed2005

Low European methyl chloroform emissions inferred from long-term atmospheric measurements.

Methyl chloroform (CH3CCl3, 1,1,1,-trichloroethane) was used widely as a solvent before it was recognized to be an ozone-depleting substance and its phase-out was introduced under the Montreal Protocol. Subsequently, its atmospheric concentration has declined steadily and recent European methyl chloroform consumption and emissions were estimated to be less than 0.1 gigagrams per year. However, data from a short-term tropospheric measurement campaign (EXPORT) indicated that European methyl chloroform emissions could have been over 20 gigagrams in 2000 (ref. 6), almost doubling previously estimated global emissions. Such enhanced emissions would significantly affect results from the CH3CC13 method of deriving global abundances of hydroxyl radicals (OH) (refs 7-12)-the dominant reactive atmospheric chemical for removing trace gases related to air pollution, ozone depletion and the greenhouse effect. Here we use long-term, high-frequency data from Mace Head, Ireland and Jungfraujoch, Switzerland, to infer European methyl chloroform emissions. We find that European emission estimates declined from about 60 gigagrams per year in the mid-1990s to 0.3-1.4 and 1.9-3.4 gigagrams per year in 2000-03, based on Mace Head and Jungfraujoch data, respectively. Our European methyl chloroform emission estimates are therefore higher than calculated from consumption data, but are considerably lower than those derived from the EXPORT campaign in 2000 (ref. 6).

Atmosphere↗

PubMed1986

Oxidation of chloroform in an aerobic soil exposed to natural gas.

Acclimation of a sandy soil to an air-natural gas mixture stimulated the biological oxidation of chloroform to carbon dioxide. Acetylene and methane inhibited chloroform oxidation. Chloroform oxidation continued up to 31 days in the absence of methane. Chloroform oxidation rates increased at chloroform concentrations up to 5 mug g of soil.

Journal Article↗

PubMed1990

Dechlorination of chloroform by methanosarcina strains.

Dehalogenation of carbon tetrachloride, chloroform, and bromoform in pure cultures of Methanosarcina sp. strain DCM and Methanosarcina mazei S6 was demonstrated. The initial dechlorination product of chloroform was methylene chloride (dichloromethane), which accumulated transiently to about 70% of the added chloroform; trace amounts of chloromethane were also detected. The amount of chloroform dechlorinated per mole of methane produced was approximately 10 times greater than the ratio observed previously for tetrachloroethene dechlorination by these strains. The production of CO(2) from [C]chloroform and the absence of CH(4) imply that processes in addition to reductive dechlorination operate.

Journal Article↗

PubMed1993

Topical aspirin in chloroform and the relief of pain due to herpes zoster and postherpetic neuralgia.

OBJECTIVE: To determine pain patterns and relationships in patients with herpes zoster and postherpetic neuralgia before and after topical application of aspirin dissolved in chloroform applied to the painful skin surface. DESIGN: A consecutive series of 42 patients examined and treated in a uniform manner and followed up until their pain subsided or this management mode failed. SETTING: An ambulatory referral private practice. PATIENTS: All patients had pain due to herpes zoster or postherpetic neuralgia and were referred for management of severe pain. None refused. INTERVENTION: Topical application of crushed aspirin tablets dissolved in chloroform. OUTCOME MEASURES: Short-Form McGill Pain Questionnaire. RESULTS: All patients reported substantially decreased pain promptly after treatment, with maximum relief at 20 to 30 minutes and lasting 2 to 4 hours. Patients gradually decreased the use of aspirin in chloroform as pain abated. CONCLUSIONS: Topical aspirin dissolved in chloroform is an effective means of reducing pain due to herpes zoster and postherpetic neuralgia in most patients. The locus of pain origin and analgesia induced by topical aspirin is most likely at cutaneous free-nerve ending pain receptors. The mechanism responsible for the analgesic properties of aspirin is probably not the same as that responsible for its anti-inflammatory properties.

Administration, Oral↗

PubMed2000

On-line monitoring by membrane introduction mass spectrometry of chlorination of organics in water. Mechanistic and kinetic aspects of chloroform formation.

Chloroform formation during the chlorination of simple organic molecules modeling humic substances, such as phenol and di- and trihydroxybenzenes, was studied by on-line membrane introduction mass spectrometry (MIMS). Under the reaction conditions employed, chloroform was rapidly formed from 1,3-dihydroxybenzene, 1, 4-dihydroxybenzene, phenol and 1,2,3-trihydroxybenzene with yields of 17, 13, 7 and 5%, respectively. With the exception of aniline, which afforded a 17% chloroform yield, non-phenolic compounds, such as nitrobenzene, chlorobenzene, toluene, benzene and cyclohexanol, furnished low yields. Mechanistic studies showed that phenol is chlorinated consecutively and produces initially chlorophenol. It is suggested that chloroform might be formed mainly from chlorinated 3, 5-cyclohexadienone-type intermediates. MIMS was also used to determine the reaction rates and to study the kinetics of the chlorination. A good Hammett linear correlation for an electrophilic substitution mechanism was found for the compounds C(6)H(5)X (X = NH(2), OH, CH(3), H, Cl and NO(2)).

Chloroform↗

PubMed1998

In vitro assessment of the effect of halogenated hydrocarbons: chloroform, dichloromethane, and dibromoethane on embryonic development of the rat.

Halogenated hydrocarbons are widely used in industry, the laboratory, and in the home. In the present study three of these solvents--chloroform, dichloromethane, and dibromoethane--were examined for embryotoxic/teratogenic potential using rat embryo culture. The results showed that each of the solvents had a concentration-dependent embryotoxic effect on the developing rat embryo in vitro. The effect and no-effect concentrations (expressed in mumol/ml culture medium), respectively, for each of the halogenated hydrocarbons tested were: dibromoethane--0.33, < 0.18; chloroform--2.06, 1.05; dichloromethane--6.54, 3.46. The levels of chloroform and dichloromethane found to be embryotoxic in the present study were compared to reported blood levels attained following controlled human exposure. In the industrial situation, if the current exposure levels are adhered to, chloroform and dichloromethane appear to have little potential for reproductive toxicity in the human. Fatal or near fatal solvent levels would be required in the mother for the embryotoxic level to be reached. For dibromoethane, there are no reports following controlled human exposure presumably due to its carcinogenicity. In an attempt to elucidate the mechanism of embryotoxicity, histological studies were performed after exposure of rat embryos to an embryotoxic level of each of the halogenated hydrocarbons studied, for increasing time periods up to the standard 40-hour culture. Marked cell death in the neuroepithelium of the developing neural tube was a prominent feature in all embryos exposed to an embryotoxic level of these solvents for periods of 16 hours of longer.

Animals↗

PubMed2004

Mutagenicity of carbon tetrachloride and chloroform in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, using a gas exposure method.

The volatile solvents carbon tetrachloride and chloroform are carcinogens that are often reported as nonmutagenic in bacterial mutagenicity assays. In this study, we evaluated the mutagenicity of these compounds in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, with and without S9 mix, using a gas exposure method. Tests were also conducted with a glutathione-supplemented S9 mix. Carbon tetrachloride was mutagenic in TA98 without S9 mix, and in WP2/pKM101 and WP2uvrA/pKM101 with and without S9 mix; carbon tetrachloride was not mutagenic in TA100, TA1535 or TA1537. Chloroform was mutagenic in WP2/pKM101, but only in the presence of glutathione-supplemented S9 mix. Chloroform was not mutagenic in TA98, TA100, TA1535, TA1537, or WP2uvrA/pKM101 with or without S9 mix, and was not mutagenic in TA98, TA100, TA1535, TA1537, or WP2uvrA/pKM101 in the presence of glutathione-supplemented S9 mix. The data indicate that carbon tetrachloride and chloroform are bacterial mutagens when adequate exposure conditions are employed and suggest that a genotoxic mode of action could contribute to the carcinogenicity of these compounds.

Animals↗