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PubMedDate not supplied

Determination of chloroform levels in blood using a headspace capillary gas chromatographic method.

Headspace (HS) capillary gas chromatography with flame-ionization detection was developed for the determination of chloroform levels in blood. Separation of chloroform was improved significantly using a DB-WAX capillary column, without interference by other volatile substances. Sensitivity was increased by adjusting the splitter ratio to 20, without any decline in peak resolution. The HS conditions, a 50 degrees C incubation for 30 min, gave reproducible and sensitive determinations. The distribution coefficient (k) was calculated to be 8.24. The CV was 1.8% for 27.7 micrograms/mL chloroform, and the detection limit was 0.02 microgram/mL (S/N = 4) when the splitter ratio was 10. Raising HS temperature resulted in a significant decrease in k for chloroform in the absence of blood, in contrast to the relatively small effect seen in the presence of blood. Although inorganic salts showed a salting-out effect, erythrocytes and hydrophobic compounds, such as detergent and lipid, significantly suppressed the vaporization of chloroform. Chloroform was found to be distributed mainly in erythrocytes when incubated with blood overnight at 2 degrees C.

Chloroform↗

PubMed2000

Re-evaluation of the 2-year chloroform drinking water carcinogenicity bioassay in Osborne-Mendel rats supports chronic renal tubule injury as the mode of action underlying the renal tumor response.

Chloroform, generally regarded as a non-genotoxic compound, is associated with the induction of liver and/or kidney tumors in laboratory mice and rats. In particular, chloroform produced renal tubule tumors in low incidence in male Osborne-Mendel rats when administered by corn-oil gavage or in the drinking water. There is a lack of data on intermediate endpoints that may be linked to renal cancer development in this strain of rat, in contrast to mice. Specifically, evidence linking chloroform-induced liver and kidney tumors in mice with cytotoxicity and regenerative cell proliferation is very strong, but weak in the rat. In the present study, kidney tissue from a carcinogenicity bioassay of chloroform in Osborne-Mendel rats was re-evaluated for histological evidence of compound-induced cytotoxicity and cell turnover. All rats treated with 1800 ppm (160 mg/kg/day, high-dose group) in the drinking water for 2 years and half the rats treated with 900 ppm (81 mg/kg/day) had mild to moderate changes in proximal convoluted tubules in the mid to deep cortex indicative of chronic cytotoxicity. Tubule alterations specifically associated with chronic chloroform exposure included cytoplasmic basophilia, cytoplasmic vacuolation, and nuclear crowding consistent with simple tubule hyperplasia. Occasional pyknotic cells, mitotic figures in proximal tubules, and prominent karyomegaly of the renal tubule epithelium were present. These alterations were not present in control groups or at the 200-ppm (19 mg/kg/day) or 400-ppm (38 mg/kg/day) dose levels. This new information adds substantially to the weight of evidence that the key events in chloroform-induced carcinogenicity in rat kidney include sustained cellular toxicity and chronic regenerative hyperplasia.

Adenoma↗

PubMed1990

Simpson and 'the discovery of chloroform'.

It is widely accepted that Sir James Young Simpson discovered the anaesthetic properties of chloroform and pioneered its application in surgery and midwifery. The name of Simpson is not infrequently also associated with the discovery of chloroform and of anaesthesia. Simpson certainly did not discover the substance chloroform or anaesthesia, there is doubt as to whether he discovered the anaesthetic properties of chloroform, and he may not have been the first person to administer chloroform anaesthesia to a patient. He did, however, play an important role in the introduction of chloroform anaesthesia particularly in midwifery and obstetrics.

Anesthesia, Inhalation↗

PubMedDate not supplied

Safety evaluation of toothpaste containing chloroform. I. Long-term studies in mice.

In three experiments, chloroform was administered to mice by gavage in a toothpaste base or in arachis oil, in doses up to 60 mg/kg/d on 6 days/wk for 8 wks. Control groups were left untreated or given vehicle only. In general, there were more survivors in chloroform-treated groups than in the controls. In the case of the males of three strains (C57BL, CBA and CF/1), treatment was associated with no adverse affect on the incidence of any type of neoplasm or any other parameter. In the males but not the females of a fourth strain (ICI) and in doses of 60 mg/kg/d but not of 17 mg/kg/d, exposure to chloroform in toothpaste base as a vehicle was associated with increased incidence of epithelial tumours of the kidney. A more pronounced effect of the same kind was seen in mice given 60 mg CHCl3/kg/d in an archis oil vehicle. This treatment was also associated with a higher incidence and severity of non-neoplastic renal disease. The mechanisms underlying the peculiar strain- and sex-specific susceptibility of ICI male mice to develop renal tumours when exposed to chloroform remain obcure; spontaneous renal tumours were also seen in vehicle control mice and possible ways in which this tendency may be enhanced by chloroform treatment are discussed. At the dose levels tested, namely 113 and 400 times average human exposure levels from the use of toothpaste (with 3.5 percent chloroform content), no adverse affect was seen in the liver and there was no increased incidence of liver tumours even in the higher liver tumour susceptible CBA strain. At the 17 mg CHCl3/kg/d level, equivalent to 113 times average human exposure from toothpaste use, no excess of renal tumours was seen even in males of the peculiarly susceptible ICI strain.

Animals↗

PubMedDate not supplied

Linking a PBPK model for chloroform with measured breath concentrations in showers: implications for dermal exposure models.

Four issues are addressed in this paper. First, both dermal uptake models and a revised PBPK model are developed and combined into a form appropriate for simulating chloroform breath levels in individuals exposed in showers by inhalation and dermal routes and by the inhalation route only. Second, experimentally measured and previously reported ratios of chloroform concentrations in air and breath to tap-water concentration are used to evaluate the model predictions. Particular attention is given to the implied dermal uptake as measured by these experiments and to whether this is consistent with the recommended value for skin uptake of chloroform that is calculated using EPA guidance. This analysis indicates that the ratio of chloroform dermally absorbed in the shower relative to tap-water concentration is between 0.25 and 0.66 mg per mg/L and that the effective permeability of the skin during a 10-min. shower exposure is between 0.16 and 0.42 cm/hr. Third, the model is used to assess the relationship of dermal and inhalation exposure to metabolized dose in the liver. It is found that, for dermal and inhalation exposures in the shower and under conditions of linear metabolism, the ratio of metabolized dose to water concentration is on the order of 0.41 mg per mg/L. Fourth, the model is used to determine the chloroform concentration at which dermal and inhalation exposures to chloroform would begin to result in nonlinear metabolism. This concentration is found to be in the range of 60 to 100 mg/L.

Breath Tests↗

PubMed2003

Enhancing reactivity of carbonyl compounds via hydrogen-bond formation. A DFT study of the hetero-Diels-Alder reaction between butadiene derivative and acetone in chloroform.

To examine how hydrogen-bond (HB) formation involving chloroform solvent molecules influences the chemical reactivity of ketones, the hetero-Diels-Alder reaction of N,N-dimethyl-1-amino-3-methoxy-1,3-butadiene and acetone has been studied by using density functional theory (DFT) at the B3LYP/6-31G level. The effects of the chloroform on the activation energies have been modeled by means of discrete-continuum models. In the gas phase, the formation of specific HB between acetone and one and two chloroform molecules decreases the activation barriers from 19.3 to 13.6 and 8.5 kcal/mol, respectively. Inclusion of solvent effects by means of combined discrete and polarizable continuum models yields a change of molecular mechanism from a concerted to a two-step mechanism, and the first nucleophilic step is the rate-limiting step. The corresponding values of activation barriers in chloroform are 18.6 kcal/ mol (no HB), 13.5 kcal/mol (one HB), and 9.6 kcal/mol (two HBs). These theoretical results account for the experimental observation that chloroform accelerates the reaction more markedly than more polar aprotic solvent such as acetonitrile. A DFT analysis of the global electrophilicity power of the reagents provides a sound explanation about the catalytic effects of chloroform.

Journal Article↗

PubMedDate not supplied

Reduced mitochondrial membrane potential and metabolism correspond to acute chloroform toxicity of in vitro hepatocytes.

Chloroform is a non-genotoxic compound that is present in drinking water and ambient air as a result of water chlorination but whose carcinogenic mechanism in humans is unknown. Chloroform targets the liver in humans, where cytochrome P-450-dependent biotransformation to phosgene results in mitochondrial damage and cell death. The purpose of this study is to investigate the relationship between cell death, loss of mitochondrial membrane potential (MMP) and reduction of metabolic rates for in vitro cultured mouse hepatocytes after acute exposure to two doses of chloroform. Immediately following a 2-h exposure, culture viabilities were 70% and 54% for concentrations of 7.0 and 8.8 mM, respectively, in contrast with 90.0% for controls. Interestingly, the viabilities of these cultures decreased further, to 6% and 12%, respectively, over the next 24-h period despite being placed in fresh, chloroform-free medium. Measurement of MMP for viable cells at the end of the exposure revealed a decrease in Rhodamine 123 uptake, which indicates a loss of MMP. Additionally, glucose consumption and lactate production rates were reduced during the 6-h period following the exposure. These results support the hypothesis that a subpopulation of cells at the end of an acute exposure may be activated for apoptosis, suggesting a role for apoptosis markers during risk assessment for chloroform.

Animals↗

PubMedDate not supplied

Studies on tropane alkaloid extraction by volatile organic solvents: dichloromethane vs. chloroform.

In order to investigate the production of tropane alkaloids by hairy roots of Atropa baetica, transgenic for the gene h6h encoding the enzyme hyoscyamine 6beta-hydroxylase, solvent extraction with chloroform and with dichloromethane of the metabolites present in the liquid medium and in the root tissue was compared. The extraction of scopolamine from the liquid medium was equally effective with either solvent, giving maximum values of around 850 microg/flask. For the roots, three different extraction methods were employed: A, employing chloroform:methanol: (25%) ammonia (15:5:1) for initial extraction, followed by treatment with sulfuric acid and ammonia, and using chloroform for the final extraction and washes; B, as A but using dichloromethane for extraction and washes; and C, as B but substituting chloroform for dichloromethane in the extraction cocktail. Scopolamine was the most abundant metabolite (present in amounts of 3250-3525 microg/g dry weight) and presented similar extraction efficiencies with all of the extraction methods employed. The highest amounts of hyoscyamine and the intermediate 6beta-hydxoxyhyoscyamine were present on day 31 (800 and 975 microg/g dry weight, respectively) and no statistical differences between the three extraction methods employed were detected. This study confirms that, for the extraction of tropane alkaloids, dichloromethane can replace the commonly employed chloroform, the use of which incurs major health, security and regulation problems.

Atropa↗

PubMed1994

The toxicity of 1-week exposures to inhaled chloroform in female B6C3F1 mice and male F-344 rats.

Detailed quantitative descriptions of the toxicity of inhaled chloroform are lacking, despite the fact that the majority of environmental exposures occur by this route. We investigated the ability of chloroform vapors to produce toxicity and regenerative cell proliferation in the livers and kidneys, the principal target organs for carcinogenicity of female B6C3F1 mice and male F-344 rats, respectively. Nasal passages were also examined for toxic responses. Rodents were exposed to chloroform vapors at concentrations of 0, 1, 3, 10, 30, 100, or 300 ppm for 6 hr/day for 7 consecutive days and necropsied on Day 8. Animals were administered bromodeoxyuridine (BrdU) via implanted osmotic pump for the previous 3.5 days before necropsy. Cell proliferation was quantitated as the percentage of cells in S-phase (labeling index; LI) measured by immunohistochemical detection of BrdU-labeled nuclei. Mice exposed to 100 or 300 ppm exhibited centrilobular hepatocyte necrosis and severe vacuolar degeneration of midzonal and periportal hepatocytes, while exposure to 10 or 30 ppm resulted in mild to moderate vacuolar changes in centrilobular hepatocytes. Slight, dose-related increases in the hepatocyte LI were observed for exposure concentrations of 10 and 30 ppm, while the LI was increased more than 30-fold in the 100 and 300 ppm groups. The kidneys of mice were affected only at the 300 ppm exposure, with approximately half of the proximal tubules lined by regenerating epithelium and an increased LI of tubule cells of 8-fold over control. In rats, mild centrilobular vacuolation was observed only in the livers of rats exposed to 300 ppm. The hepatocyte LI in rats were increased only at 100 and 300 ppm, 3- and 7-fold over control, respectively. In the kidneys of the male rats exposed to 300 ppm, about 25 to 50% of the proximal tubules were lined by regenerating epithelium. The LI for tubule cells in the cortex was increased at 30 ppm and above. In the nasal passages of rats, chloroform concentrations of 10 ppm and above induced histopathological changes that exhibited clear concentration-related severity. These lesions consisted of respiratory epithelial goblet cell hyperplasia and degeneration of Bowman's glands in olfactory mucosa with an associated osseous hyperplasia of the endo- and ectoturbinates in the periphery of the ethmoid region. These nasal lesions were not observed in mice. Knowledge of the dose-dependent responses in rats and mice will be valuable in assessing the potential risks to humans posed by inhaled chloroform and in setting exposure concentrations for longer-term studies.

Administration, Inhalation↗

PubMed1994

Induced cytolethality and regenerative cell proliferation in the livers and kidneys of male B6C3F1 mice given chloroform by gavage.

It has been reported that chloroform administered to male B6C3F1 mice at doses of 138 and 277 mg/kg/day in corn oil by gavage 5 days/week for 2 years resulted in incidences of hepatocellular carcinomas of 36 and 98% relative to an incidence in controls of 6%. Cytotoxicity and regenerative cell proliferation have been implicated in the tumorigenic process for this non-genotoxic compound. Although chloroform is known to be nephrotoxic in the male mouse, no treatment-related increase was observed in the frequency of kidney tumors. To better understand the relationship of these endpoints, this study evaluated chloroform-induced cytotoxicity and cell proliferation in the liver and kidney under conditions of the cancer study. B6C3F1 mice were administered oral doses of 0, 34, 90, 138, or 277 mg/kg/day of chloroform dissolved in corn oil for 4 days or 5 days/week for 3 weeks. Bromo-2'-deoxyuridine (BrdU) was administered via osmotic pumps implanted 3.5 days prior to necropsy to label cells in S-phase. Cell proliferation was evaluated in tissue sections immunohistochemically as the percentage of cells in S-phase (nuclear labeling index; LI). Mice given 34 and 90 mg/kg/day by gavage had mild degenerative changes in centrilobular hepatocytes after 4 days of treatment, which was absent at 3 weeks. Centrilobular necrosis was observed in mice given 138 or 277 mg/kg chloroform for 4 days, with increased severity of necrosis at 3 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Isolation of chloroform-resistant mutants of filamentous phage: localization in models of phage structure.

Interaction of fd or M13 filamentous phage with a chloroform/water interface induces morphological change, contracting the filaments sequentially into shortened rods (I-forms), and then into spheroidal particles (S-forms). To further investigate this phage contraction, 34 and 26 chloroform-resistant isolates of fd and M13, respectively, were selected after chloroform treatment of wild-type phages at pH 8. 2 and 4 degrees C. DNA sequencing of gene VIII of the 34 fd isolates revealed five different mutants: these were D5H, M28L, V31L, I37T, and S50T. All 26 M13 isolates were I37T. These mutants exhibited variable sensitivity to chloroform, but all contracted much more slowly than wild-type phage during treatment at 4 degrees C. They all contracted like wild-type phage at 37 degrees C. Site-directed mutagenesis showed that the indicated single mutations carried the chloroform resistance. In structural models of the phage, the D5H locus is on the outside and the S50T locus is on the inside. The M28L and I37T loci are buried in a mostly hydrophobic region in the middle. Although these four mutants are spread out radially, they are localized in the axial direction into a thin disk in the model. The last mutant locus, V31L, is out of this disk, but this locus is proximal to the M28L and I37T loci and also in contact with the surface via a deep hydrophobic hole or depression. These five mutants, their locations, and their variable affects on contraction suggest that chloroform-induced contraction involves a specific mechanism rather than a generalized solvent-induced denaturation and that the critical structural changes occur in a localized level in the phage. These results add weight to suggestions that the sequential contraction of filaments-->I-forms-->S-forms mimic corresponding steps in phage penetration, and, in the reverse order, for phage assembly.

Bacteriophage M13↗

PubMed1994

Nasal toxicity of chloroform in male F-344 rats and female B6C3F1 mice following a 1-week inhalation exposure.

Chloroform is an important environmental water and air pollutant. Inhalation exposure of female B6C3F1 mice and F-344 rats for 6 hr/day for 7 consecutive days to 0, 1, 3, 10, 30, 100, or 300 ppm of chloroform resulted in concentration-dependent lesions in the nasal passages. Chloroform-induced changes included increased epithelial mucosubstances in the respiratory epithelium of the nasopharyngeal meatus, primarily in the rats. A complex set of responses was seen in specific regions of the ethmoid turbinates, predominantly in the rats. These lesions in the ethmoid region, which involved all of the endo- and ectoturbinates, were most severe peripherally and generally spared the tissue adjacent to the medial airways. These changes were characterized by atrophy of Bowman's glands, increased numbers of vimentin-positive cells in the periosteum, new bone formation, and increased numbers of periosteal cells in S phase as determined by bromodeoxyuridine incorporation. Additional changes were site-specific loss of mucosubstances and loss of immunocytochemical staining of acini and ducts of Bowman's glands for P450-2E1 and pancytokeratin, and loss of P450-2E1 immunostaining of the olfactory epithelium. The only change noted in the mice was increased cell proliferation without the osseous hyperplasia. The no-observed-effect level for these responses ranged from 3 to 100 ppm, with histological changes and induced cell proliferation being the most sensitive parameters. It is proposed that the osseous changes induced by chloroform exposure may be secondary to primary degeneration of adjacent Bowman's glands. The relevance of these changes to human health risks include potential damage to the sense of smell, but such effects would not be expected at the low levels of chloroform commonly encountered in the environment.

Administration, Inhalation↗

PubMed1987

Electrophysiological evaluation of chloroform-induced inner ear damage.

Local placement of chloroform in either the external or the middle ear has been previously reported to induce a chemical labyrinthectomy. In order to examine the value of this effect as a research tool, we injected chloroform into the middle ears of guinea pigs and rats. Cochlear damage was assessed by electrocochleography (ECochG) and auditory brainstem response (ABR) audiometry. Both species developed complete deafness within a few hours after instillation of the chloroform. The deafness was permanent in the guinea pigs, whereas there was a partial recovery of auditory function in the rats. The survival rate of the auditory nerve fibers was estimated by measuring the ABR evoked by electrical stimulation via the scala tympani (EABR). A normal EABR recruitment pattern suggested that the main chloroform effect was located peripheral to the afferent axons. In conclusion, chloroform must be considered a severely ototoxic agent when applied locally.

Animals↗

PubMed1976

Effect of ether, chloroform and carbon dioxide on monoamine inactivation.

To determine if anaesthetic agents alter monoamine inactivation, we exposed tissue homogenates (liver, kidney and brain) from mice and rabbits to ether and chloroform vapors and carbon dioxide gas. These anaesthetic agents inhibited monoamine oxidase (MAO) activity against typtamine and serotonin. Concentrations of anaesthetic agents that are achieved in the plasma of man during general anaesthesia caused a 27% (ether) and 49% (chloroform) reduction in mouse liver MAO; higher concentrations caused a 95% inhibition mouse or rabbit liver MAO. Kinetic analysis with tryptamine as substrate indicate that ether and chloroform are noncompetitive, reversible MAO inhibitors that preferentially inhibit Type B MAO. Ether and chloroform cause noncompetitive inhibition of serotonin oxidation by mouse liver MAO and competitive inhibition of serotonin oxidation by mouse brain and kidney MAO. Ether or chloroform did not alter catechol-O-methyltransferase activity from tissues of mice. Isolated blood platelets (rabbit and human) were used as a model system for neuronal uptake. Ether caused an irreversible inhibition of serotonin uptake by platelets.

Amines↗

PubMed1985

Carcinogenicity of chloroform in drinking water to male Osborne-Mendel rats and female B6C3F1 mice.

The carcinogenic activity of chloroform administered at 0, 200, 400, 900, and 1800 mg/liter in drinking water was studied in male Osborne-Mendel rats and female B6C3F1 mice. A second control group was included in the study and was restricted to the water consumption of the high-dose group. Animals were maintained on study for 104 weeks. Group sizes were adjusted at low doses such that a detectable tumor response would result at the lowest dose if there was a linear relationship with dose, and the higher doses produced responses similar to previous carcinogenesis bioassays of chloroform. The primary finding was that chloroform increased the yield of renal tubular adenomas and adenocarcinomas in male rats in a dose-related manner. For the high-dose group, which corresponded to a time-weighted average dose of 160 mg/kg per day for 104 weeks, there was a 14% incidence of renal tubular adenomas and adenocarcinomas, vs 1% in the control group. This compares to a 24% incidence observed when 180 mg/kg per day of chloroform was administered for 78 weeks in earlier studies. In contrast, chloroform in the drinking water of mice failed to increase the incidence of hepatocellular carcinomas in female B6C3F1 mice. The highest dose group received a time-weighted average dose of 263 mg/kg for 104 weeks, resulting in a 5% combined incidence of hepatocellular adenoma and carcinoma relative to a 6% incidence in the control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Investigation of the impact of pharmacokinetic variability and uncertainty on risks predicted with a pharmacokinetic model for chloroform.

A sensitivity and uncertainty analysis was performed on the Reitz et al. (Toxicol. Appl. Pharmacol., 1990: 105, 443) physiologically based pharmacokinetic (PBPK) risk assessment model for chloroform. The analytical approach attempted to separately consider the impacts of interindividual variability and parameter uncertainty on the predicted values of the dose metrics in the model, as well as on liver cancer risk estimates obtained with the model. An important feature of the analytical approach was that an attempt was made to incorporate information on correlation between important parameters, for example, the observed correlation between total blood flow and alveolar ventilation rate. Using the published PBPK model for chloroform, the best estimate of the average population risk based on the preferred pharmacodynamic dose metric (PTDEAD), representing cell death, is 9.2 x 10(-7); this estimate is more than 500-fold lower than the risk estimate of 5.3 x 10(-4) based on an alternative pharmacokinetic dose metric (AVEMMB), which represents tissue adduct formation. However, when interindividual variability was considered the range of individual risks (from the 5th to the 95th percentile of the population) predicted with PTDEAD was extremely broad (from 3.0 x 10(-13) to 3.2 x 10(-4)), while individual risks predicted with AVEMMB only varied over a factor of four (from 1.9 x 10(-4) to 7.4 x 10(-4)). As a result, the upper 95th percentile of the distribution of individual risk estimates based on the preferred cell death metric were within a factor of three of the 95th percentile for the pharmacokinetic alternative. The crucial factor with respect to the much greater variability of chloroform risk estimates based on cell death is that the dose metric, PTDEAD, is exquisitely sensitive to variation of the parameters in the model defining the response of cells to the cytotoxicity of chloroform. Unfortunately, these key parameters are also highly uncertain, as well as strongly correlated. As a result it proved impossible to accurately quantify the additional impact of parameter uncertainty on the dose metrics and risk estimates for chloroform. In general, however, the approach used in this study should be useful for differentiating the impact of interindividual variability and parameter uncertainty on PBPK-based risk assessments of other chemicals where the sensitivity, uncertainty, and correlation of the key parameters are more limited.

Animals↗

PubMed1984

Effect of chloroform on hepatic and renal DNA synthesis and ornithine decarboxylase activity in mice and rats.

Chloroform administered intraperitoneally (i.p.) to male mice and rats resulted in a dose-dependent increase in hepatic ornithine decarboxylase (ODC) activity. Maximal induction of the enzyme in mice was 10-fold and occurred at 375 mg/kg chloroform; in rats it was 52-fold and occurred at 750 mg/kg chloroform. Chloroform increased in mice and decreased in rats the rate of hepatic and renal DNA synthesis. Therefore, the induction of ODC activity in rat liver was not followed with an increase in DNA synthesis. The implications of these results to the proposed nongenetic mechanism of chloroform induction of hepatocellular carcinoma in mice and renal tumors in rats are discussed.

Animals↗

PubMed2005

The early steps of chloroform anaesthesia in Turkey during the Ottoman Empire in the 19th century.

OBJECTIVE: The aim of this study was to research the pioneering steps for the employment of chloroform in Turkey in comparison with the developments in the West i.e. in the United States and in Europe. The development of anaesthesiology in the West started in the first half of the 19th century. As an anaesthetic substance, ether was first employed in a medical operation by R. Liston in December 1846. But taking into consideration of its bronchially irritant effect, British gynaecologist Dr. J.Y. Simpson preferred to utilize chloroform in obstetrical operations in 1847. The paper aims at shedding light on the earlier steps for modern anaesthesiology in Turkey in that sense. METHODS: The survey used evaluation of archival documents, first hand-original sources such as the annual medical reports of the Medical School, books, official journals, and newspapers of the time, and also secondary sources concerned with the subject. RESULTS: In view of the findings of the survey, chloroform, as an anaesthetic material, began to be administered surgically in Turkey much earlier than it was already known. It was experienced and used in operations at the surgical clinic of the Imperial School of Medicine at the Capital city, Istanbul in 1848. The Crimean War (1853-1855) induced to the prevalent surgical use of chloroform in Istanbul on the soldiers back from the front. In other words, it was evidenced that surgeons started to make use of this anaesthetic substance in the Ottoman Empire, shortly after it was put into medical practice in Europe. CONCLUSION: This study deals with that phenomenal progress of chloroform anaesthesia in the medical history in Turkey during the second half of the 19th century.

Anesthesiology↗