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At least 19 recordsLinked to original sources

Fluorinated oils as experimental vitreous substitutes.

Two kinds of fluorinated oils (a fluorosilicone oil and a perfluoroether [Freon E15]) that have a higher density than water were evaluated as long-term vitreous substitutes. Vitreous compression using perfluoropropane gas was performed to create a space for the vitreous substitute in rabbit eyes. Two fluorosilicone oils (1000 and 10 000 centistokes) induced edema of the inner retinal layers and occasionally of the outer retinal layers regardless of viscosity or period of observation up to six months, but they were well tolerated clinically. Control eyes injected with silicone oils of comparable viscosities showed similar histopathologic findings. Freon E15 induced formation of bubbles and precipitates by one month after injection, and retinal disorganization, formation of preretinal membranes, and tractional retinal detachment by six months. Thus, Freon E15 proved to be unsuitable, but fluorosilicone oil is a possible high-density vitreous substitute.

Animals↗

Fluorocarbon 113 exposure and cardiac dysrhythmias among aerospace workers.

We investigated the cardiotoxic effects of 1,1,2-Trichloro-1,2,2- Trifluoroethane (fluorocarbon 113 or FC113) exposures among healthy workers cleaning rocket and ground support equipment for the National Aeronautic and Space Administration (NASA) programs. Exposure and ambulatory electrocardiographic (ECG) monitoring data were evaluated on 16 workers, each of whom was examined on exposed and nonexposed workdays. We examined whether there was a greater rate of dysrhythmias on an exposed workday relative to a nonexposed workday. Overall, we found no within subject differences in the rate of ventricular and supraventricular premature beats (number per 1,000 heart beats), fluctuations in the length of the P-R interval, or heart rate. We found that levels of FC113 exposures below the Occupational Safety and Health Administration (OSHA) 8-hour time-weighted-average (TWA) standard of 1,000 ppm did not induce cardiac dysrhythmias or subtle changes in cardiac activity. However, because fluorocarbons may sensitize the heart to epinephrine, this study's negative findings based on sedentary and fairly healthy workers may not be generalizable to other populations of workers who are not as healthy or engaged in more physically demanding work.

Adult↗

Atrial fibrillation and sudden death related to occupational solvent exposure.

Two cases of atrial fibrillation and one case of sudden death occurred in workers exposed to trifluorotrichloroethane (CFC 113) as a solvent/degreasing agent. This agent and related halogenated hydrocarbons are widely used in industry as solvents and degreasing agents, and have been previously linked to ventricular arrhythmias and cardiac sudden death when inhaled in excessive concentrations. We suggest that occupational overexposure to halogenated hydrocarbons should be considered a potential precipitant for atrial as well as ventricular arrhythmias.

Adult↗

Improved MR images of arterial specimens by submersion in trichlorotrifluoroethane.

MR images of ex vivo arterial specimens immersed in 1,1,2-trichloro-1,2,2-trifluoroethane (R-113) have improved signal-to-noise ratio and contrast-to-noise ratio. R-113 has no hydrogen atoms, so it yields no proton signal; hence, the contrast between the specimen and its background is maximized. SNR is maximized because (i) R-113 is nonconductive so that coil loading and inductive noise are minimized, and (ii) the volume susceptibility of R-113 closely matches that of water and tissue so that T2* effects are minimized. Short-term submersion of porcine aortas in R-113 was found to have no significant effect on the artery's hydration level, relaxation time, tensile strength, and structure or quantity of elastin, collagen, or smooth muscle cells.

Animals↗

Effects of a skin refrigerant/anesthetic and age on the pain responses of infants receiving immunizations.

Although pain management is an important nursing responsibility, few interventions for minimizing distress of infants during painful procedures have been studied. Sixty infants, 2 through 6 months of age, were studied during a routine DPT immunization in order to examine (a) the effectiveness of cooling the skin in reducing distress behaviors and (b) the relationship between age and distress behavior. Infants were randomly assigned to experimental or control groups. Prior to the injection, the sites were sprayed for 2 to 3 s with either a skin refrigerant/anesthetic or compressed air. Behaviors were video- and audio-taped during and 60 s post injection, and coded for (a) facial expression, (b) cry, and (c) body movements. MANOVA revealed fewer distress behaviors following refrigerant spray and more complex, varied behavioral responses for older infants. The findings provide further evidence that infants perceive pain and that nursing interventions for pain reduction should be tested and extended to the very young.

Administration, Topical↗

Bimolecular OH rate constants of organic compounds in solution. 2. Measurements in 1,2,2-trichlorotrifluoroethane using hydrogen peroxide as an OH source.

Semivolatile organic compounds (SOC) occur in the troposphere either adsorbed at aerosol particles or in the free gas phase, depending on temperature, vapor pressure of the compound, and total particular surface. In order to estimate the abiotic degradation of such compounds, the OH reaction rate constant must be known, which cannot be measured directly in the gas phase at the relevant temperature due to experimental difficulties. In the method proposed here, the inert solvent 1,1,2-trichlorotrifluoroethane is used as the reaction medium and hydrogen peroxide as photolytic OH source. Relative reaction rates can be measured, using a reference compound of known kOH air. The relative rates can be converted into absolute ones due to the 1:1 relationship observed by Dilling, Gonsior, Boggs, and Mendoza (1988) Environ. Sci. Technol. 22, 1447-1453, between the relative rates in the inert solvent and those in the gas phase.

Air Pollutants↗

Subchronic toxicity and teratogenicity of 2-chloro-1,1,1,2-tetrafluoroethane (HCFC-124).

Inhalation studies were conducted to determine the potential toxicity of HCFC-124. Groups of rats and mice were exposed to HCFC-124 6 hr/day, 5 days/week for 13 weeks at 0, 5000, 15,000, and 50,000 ppm. Subgroups of rats and mice were held for a 1-month recovery period. A functional observational battery (FOB) was conducted on rats at 0, 4, 13, and 16 weeks. Clinical pathology evaluations were conducted at 7, 13, and 17 weeks. Thirteen or 17 weeks after study initiation, rats and mice underwent gross and microscopic evaluation, and livers were evaluated for hepatic beta-oxidation activity. In addition, groups of female rats and rabbits were exposed to HCFC-124 by inhalation during gestation to 0, 5000, 15,000, or 50,000 ppm. Exposure of rats and mice to HCFC-124 caused minimal compound-related effects. Compound-related changes occurred in several clinical pathology parameters in rats and mice. Hepatic beta-oxidation activity was significantly higher in 5000, 15,000, and 50,000 ppm male mice; however, there were no compound-related effects on beta-oxidation activity in rats. During the daily exposures, rats, mice, and rabbits exposed to 50,000 ppm were less responsive to auditory stimuli or less active compared to controls. At the 13-week FOB, male rats exposed to 15,000 or 50,000 ppm had decreased arousal. There were no compound-related effects on mortality, clinical signs, ocular tissues, hematology parameters, organ weights, and tissue morphology at any concentration in rats or mice. Maternal toxicity in rats was evident by a significant decrease in weight gain and food consumption at 50,000 ppm. Similarly, 50,000 ppm pregnant rabbits had lower food consumption. However, for both rats and rabbits, there was no evidence of fetal toxicity at any concentration.

Administration, Inhalation↗

A physiologically based mathematical model for the human inhalation pharmacokinetics of 1,1,2-trichloro-1,2,2-trifluoroethane.

A physiologically based mathematical model is described for the human inhalation pharmacokinetics of 1,1,2-trichloro-1,2,2-trifluoroethane (FC113). Physiological parameters for the model are derived from the scientific literature. Partition coefficients are determined from in vitro measurements. Predictions of the resulting model for breath and blood concentrations compare well with results of a human volunteer study described in a companion paper (Woollen et al. 1990). Using this data some alternative models are also examined with different choices of physiological parameters and partition coefficients. The mathematical model is used to examine the consequences of metabolic elimination of FC113. A value for metabolic clearance is estimated using the during-exposure breath concentration data; however, the concentrations of FC113 in breath or blood during and after exposure are shown to be insensitive to metabolic clearance. Consequently, no firm conclusion can yet be drawn as to whether FC113 is metabolised by man.

Air Pollutants, Occupational↗

Human inhalation pharmacokinetics of 1,1,2-trichloro-1,2,2-trifluoroethane (FC113).

Seven male volunteers were exposed to atmospheric concentrations of either 1980, 4100 or 7630 mg m-3 1,1,2-trichloro-1,2,2-trifluoroethane (FC113) for 4 h. Blood and expired air samples were collected during the exposure period and for several days subsequently and analysed for FC113. Blood and breath concentrations of FC113 were related to the administered dose with some variation between individuals. The low blood/breath ratios measured are consistent with the low solubility of FC113 in blood. The absorption and elimination of FC113 can be described by a three-compartment model and the average half-lives of elimination of FC113 in breath were 0.22, 2.3 and 29 h. A pulmonary retention during the exposure period of 14% was measured but only 2.6 to 4.3% of the dose was recovered unchanged in breath after the exposure period, suggesting that FC113 could be metabolised following inhalation exposure. It is concluded that a practical method for biological monitoring during occupational exposure would be to measure end-tidal breath concentrations of FC113 in samples taken the morning after exposure. The predictive value of such a measurement can be improved if the results are normalised to the body fat content of individual workers which can be estimated from height and weight measurements.

Administration, Inhalation↗

Analysis of virus-specific RNA species and proteins in Freon-113 preparations of the Borna disease virus.

Treatment of homogenates from Borna disease virus (BDV)-infected brain tissue or cell cultures with Freon-113 yielded infectious particles with a buoyant density of 1.16-1.22 g/ml. Positive- and negative-stranded BDV-specific RNA species as well as three virus-specific proteins, known to be present in BDV-infected cell extracts, were demonstrated in these Freon-treated fractions. When the Freon-purified virus preparations were treated with RNase A prior to RNA extraction, only negative-stranded, genomic RNA was detected in Northern blot hybridizations using sense and antisense RNA probes. These data substantiate that BDV is a negative-stranded RNA virus.

Animals↗

Aerosol propellant interference with clinical mass spectrometers.

Metered dose inhalers containing halogenated propellants may interfere with mass spectrometer quantitation of halogenated inhalation anesthetics. We identify the propellant(s) in a commercially available metered dose inhaler that caused erroneous mass spectrometer readings. In addition, we identify the causes of different types of interference in different mass spectrometers.

Aerosol Propellants↗

Investigations on the liver toxicity of a blend of HCFC-123 (2,2-dichloro-1,1,1-trifluoroethane) and HCFC-124 (2-chloro-1,1,1,2-tetrafluoroethane) in guinea-pigs.

2,2-Dichloro-1,1,1-trifluoroethane (HCFC-123) has been developed as a substitute for ozone-depleting chlorofluorocarbons (CFCs). It is a structural analogue of halothane and similarities in the metabolic pathways and liver toxicity of both compounds have been described. The present study was initiated after an accidental outbreak of hepatitis in an industrial setting to examine whether concomitant exposure to 2-chloro-1,1,1,2-tetrafluoroethane (HCFC-124), which is not hepatotoxic, could enhance the liver toxicity of HCFC-123. Male Hartley guinea-pigs were exposed for 4 h to 5,000 ppm HCFC-123 alone or blended with 5,000 ppm HCFC-124, either once (single exposure) or on 5 consecutive days (repeated exposure). The animals were killed either 24 or 48 h after the last exposure. A transient cytolytic action of HCFC-123 was evident by increased mean serum levels of alanine aminotransferase at 24 h and isocitrate dehydrogenase at 24 and 48 h, both after a single or repeated exposure. The liver toxicity of HCFC-123 was confirmed by pathological examination of liver tissue, which showed mild (foci of necrotic hepatocytes) to moderate (multifocal random degeneration and necrosis) damage. Steatosis was also observed and was more pronounced after repeated exposure than after single. One animal out of 6 that were repeatedly exposed to the blend and sacrificed at 24 h showed liver lesions similar to halothane hepatitis. Although a few other animals responded markedly in the blend-treated group, on average, no significant difference in the biochemical or pathological lesions was found between the groups treated with HCFC-123 alone or with the blend. Urinary excretion of trifluoroacetic acid and chlorodifluoroacetic acid increased dose-dependently upon exposure to HCFC-123 and indicated accumulation after repeated exposure. No difference in metabolite excretion was found between animals treated with HCFC-123 alone or blended with HCFC-124. Treatment with HCFC-123 depleted hepatic glutathione levels by about 40 and 25% after single and repeated exposure, respectively; the amplitude of this reduction was not modified by co-exposure to HCFC-124. In conclusion, this study confirmed the hepatotoxicity of HCFC-123, based on biochemical, histopathological and metabolite studies, and found only very limited indication of a potentiation by HCFC-124 of this hepatotoxic effect.

Administration, Inhalation↗

Raised concentration of serum bile acids following occupational exposure to halogenated solvents, 1,1,2-trichloro-1,2,2-trifluoroethane and trichloroethylene.

OBJECTIVES: The objectives of this study were threefold. First, to examine the hepatic effects of occupational exposure to 1,1,2-trichloro-1,2,2-trifluoroethane (FC 113) using conventional and newer tests (serum bile acids) of hepatobiliary function. Second, to assess the effects of altered work practices that included a reduced exposure to a different halogenated solvent (trichloroethylene) on the same parameters of liver function; and finally, to gather further data to support or refute the contention that serum bile acid (SBA) levels could provide a sensitive biological marker of exposure to these solvents. DESIGN: Two groups of workers (control and exposed) in an Australian steel industry participated in the study. The exposed group (n = 5-6) comprised individuals who had either exposure to FC 113 (68.2 +/- 12.6 ppm) or trichloroethylene (8.9 +/- 3.1 ppm) during the application of these solvents in a cleaning procedure, whereas the control group (n = 7-11) was composed of non-solvent-exposed office workers in the same company. The initial investigation involved exposure to FC 113 while a follow-up study was undertaken after changes in work practices were made including replacement of FC 113 with trichloroethylene (TRI). METHODS: Standard liver function tests and individual serum bile acids (ISBA) were measured before and after exposure to solvents and simultaneously in the control subjects by enzymatic methods and high performance liquid chromatography (HPLC), respectively. RESULTS: Statistical analysis of the data showed a significant increase in the concentration of total serum bile acids (TSBA), some of the subgroups of SBA, and a few of the ISBA in workers after a period of exposure to FC 113. After TRI replaced FC 113 together with other changes in work practices to give substantial reduction in exposure to solvent, a repeat study also found elevated SBA after the cleaning procedure but to a lesser extent. No other indications of adverse liver effects, as measured by conventional parameters of hepatobiliary function, were detected. CONCLUSION: Exposure to FC 113 was clearly associated with a significant rise in SBA levels, which are sensitive indicators of liver function. This finding is consistent with, and provides further support for, our previous investigations on chlorinated aliphatic hydrocarbon solvents which showed that SBA levels are a sensitive biological marker of exposure to these solvents. Changes in work practices including replacement of FC 113 resulted in a reduced effect on SBA, consistent with lower exposures.

Adult↗

Extraction of lipids from mammalian liver using nontoxic solvents.

A simple method for extracting and purifying lipids from rat liver in a single step using nontoxic solvents is described. The method consists homogenizing the pulverized tissue with a mixture of trichlorotrifluoroethane (Cl2CF-CCIF2) and isopropyl alcohol (1 : 1, v/v). Just enough water is added to the lipid extract to produce a biphasic system. Pure lipid extract is obtained by isolating the lower layer from the aqueous upper phase which contains the non-lipid materials. The described method compares favourably with that of Folch et al., both quantitatively. The solvent system used also has the advantage of being less toxic than the widely used chloroform/methanol system, which makes it safer for prolonged use. The new method is simple, efficient and reproducible.

1-Propanol↗

Chronic inhalation toxicity/carcinogenicity study in rats exposed to fluorocarbon 113 (FC-113).

Groups of 100 male and 100 female Crl:CDBR rats were exposed by whole-body inhalation to FC-113 (1,1,2-trichloro-1,2,2-trifluoroethane) for 6 hr a day, 5 days a week for 24 months. Average exposure concentrations (+/- 1 SD) were 0.0 (control), 2000 +/- 100, 10,000 +/- 500, and 20,000 +/- 1000 ppm (v/v), respectively. Body weights were consistently lower in both male and female rats in the 20,000 ppm exposure group after approximately 1 and 4 months' exposure, respectively, and in female rats after 12 months' exposure at 10,000 ppm. Observations of appearance and behavior, mortality, and clinical laboratory measurements were unremarkable during the 24-month exposure period. Despite exposure levels as high as 20,000 ppm, only occasional slight increases in urinary fluoride were seen. Microscopic examination of tissues from rats examined during and at the end of the 24-month study revealed no evidence of compound-related toxicity or carcinogenicity. Based mainly on a 5 to 10% decrease in body weight gain at the 10,000 and 20,000 ppm exposure levels, the no-observed-effect level for FC-113 in this study was 2000 ppm.

Adenoma↗

Dose-related hepatotoxicity of 1,1,2-trichloro-1,2,2-trifluoroethane in short-term intermittent inhalation exposure in rats.

Male Wistar rats were exposed to 200, 1000 or 2000 ppm of 1,1,2-trichloro-1,2,2-trifluoroethane vapor 5 days a week 6 h daily for 1 or 2 weeks. Proliferation and vacuolisation of the smooth endoplasmic reticulum (SER) of the liver was seen electron microscopically after 1 and 2 weeks in the rats exposed to 1000 and 2000 ppm. Among the hepatic drug metabolizing enzymes, NADPH cytochrome c reductase activity showed a dose-related decrease whereas the tightly membrane-bound UDPglucuronosyltransferase exhibited a dose-dependent enhancement in its measurable activity. The overall drug oxidation reaction, 7-ethoxycoumarin O-deethylase was not affected by the 1,1,2-trichloro-1,2,2,-trifluoroethane inhalation at all, either in the liver or in the kidneys. 1,1,2-Trichloro-1,2,2-trifluoroethane binds to cytochrome P-450 with the production of a type I difference spectrum, suggesting that it may act as a substrate for this enzyme. The binding affinity is increased by phenobarbital-treatment of the rats.

Animals↗

Metabolism and pharmacokinetics of selected halon replacement candidates.

Metabolism studies were conducted using Fischer 344 and Sprague-Dawley rats following inhalation exposure to 1.0% (v/v) air atmospheres of 1,1-dichloro-2,2,2-trifluoroethane (HCFC-123), 2-chloro-1,1,1,2-tetrafluoroethane (HCFC-124), 1-chloro-1,1-difluoroethane (HCFC-142b), bromochlorodifluoromethane (Halon 1211), and perfluorohexane (PFH) for 2 h. There were no remarkable differences in results between the two strains of rats. Animals exposed to HCFC-123 or HCFC-124 excreted trifluoroacetic acid in their urine. Urinary fluoride concentrations were increased in rats exposed to HCFC-124, and urinary bromide levels were increased in rats exposed to Halon 1211. Small quantities of volatile metabolites 2-chloro-1,1,1-trifluoroethane (HCFC-133a) and 2-chloro-1,1-difluoroethylene were observed in the livers of rats exposed to HCFC-123. Rats exposed to HCFC-142b excreted chlorodifluoroacetic acid in their urine; no volatile metabolites were detected in tissue samples. For PFH studies, no metabolites were detected in the urine or tissues of exposed animals. These results are consistent with proposed oxidative and reductive pathways of metabolism for these chemicals. Pharmacokinetic studies were carried out in rats exposed by inhalation to 1.0%, 0.1%, or 0.01% of HCFC-123. Following exposure, blood concentrations of HCFC-123 fell sharply, whereas trifluoroacetic acid levels rose for approx. 5 h and then declined gradually. Using a physiologically based pharmacokinetic model, saturation of HCFC-123 metabolism was estimated to occur at approx. 0.2% (2000 ppm) HCFC-123.

Animals↗

Transport of hydrocarbons from an emplaced fuel source experiment in the vadose zone at Airbase Vaerløse, Denmark.

An emplaced hydrocarbon source field experiment was conducted in the relatively homogeneous sandy geology of the vadose zone at Airbase Vaerløse, Denmark. The source (10.2 l of NAPL) consisted of 13 hydrocarbons (n-, iso- and cyclo-alkanes and aromates) and CFC-113 as a tracer. Monitoring in the 107 soil gas probes placed out to 20 m from the centre of the source showed spreading of all the compounds in the pore air and all compounds were measured in the pore air within a few hours after source emplacement. Seven of the fourteen compounds were depleted from the source within the 1 year of monitoring. The organic vapours in the pore air migrated radially from the source. The CFC-113 concentrations seemed to be higher in the deeper soil gas probes compared with the hydrocarbons, indicating a high loss of CFC-113 to the atmosphere and the lack of degradation of CFC-113. For the first days after source emplacement, the transport of CFC-113, hexane and toluene was successfully simulated using a radial gas-phase diffusion model for the unsaturated zone. Groundwater pollution caused by the vadose zone hydrocarbon vapours was only detected in the upper 30 cm of the underlying groundwater and only during the first 3 months of the experiment. Only the most water-soluble compounds were detected in the groundwater and concentrations decreased sharply with depth (approximately one order of magnitude within 10 cm depth) to non-detect at 30 cm depth. The groundwater table varied more than 1 m within the measurement period. However that did not influence the direction of the groundwater flow. Approximately 7 months after source emplacement the groundwater table rose more than 1 m within 1 month. That did not cause additional pollution of the groundwater.

Chlorofluorocarbons, Ethane↗