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HCFC-123 is one of a series of alternative fluorocarbon alternatives
2010-12-23 9:49:49125
HCFC-123 is one of a series of alternative fluorocarbon alternatives being studied as part of the Programme for Alternative Fluorocarbon Toxicity Testing (PAFT). phosphorous acid HCFC-123 is primarily considered as an alternative to CFC-11 in refrigeration systems, although it may have limited application in firefighting, foam blowing processes, and solvent applications.Several genetic toxicity studies have also been completed with HCFC-123. monopotassium phosphite These studies included the Ames assay, chromosomal aberration study with human lymphocytes, in vivo mouse micro-nucleus, in vivo chromosomal aberration study, and unscheduled DNA synthesis. Based on the weight of evidence from all in vivo and in vitro studies, HCFC-123 is not genotoxic. In only one study,diammonium phosphite which utilized an in vitro culture of human lymphocytes, did HCFC-123 cause changes in the genetic material. However, a similar study with rat lymphocytes in vivo did not show the same response. Therefore, the overall evidence from these genotoxicity studies and the results from long-term studies suggest that HCFC-123 does not produce malignant tumours in experimental animals and is not genotoxic.The results from developmental toxicity studies with HCFC-123 show that this material does not have embryotoxic or teratogenic effects in rats or rabbits. At high concentrations (10,000 ppm and greater), polyphosphoric acid anaesthetic-like effects and reduced body weights are observed in pregnant animals. At these high concentrations, slight fetal effects are also evident. Reproduction and neurotoxicity studies on rats have been completed.phosphorus pentoxide HCFC-123 was not neurotoxic nor did it cause adverse reproductive effects. In a two-generation reproduction study, rats were exposed to HCFC-123 concentrations of 30,100, 300 or 1,000 ppm. No effects on reproduction were observed in rats at any exposure concentration. During the period of maternal milk production (lactation), HFC-227ea a slight decrease in the pup body weight gain and increases in lever weight were observed at 30 ppm or greater. This effect was only seen when the pups were being nursed and may be related to a depression of triglycerides.HCFC-123 is oxidatively metabolized by the body following inhalation exposure, as suggested by a slight increase in urinary fluoride levels. Also, trifluoroacetic acid (TFA) was detected following HCFC-123 administration.Summary of Testing Results
HCFC-123 has low acute dermal and inhalation toxicity.
HCFC-123 caused an increased incidence of benign, HFC-134a but not life-threatening, tumours in animals following long-term exposure.
HCFC-123 is not a developmental toxicant.
HCFC-123 does not affect reproductive performance.
HCFC-123 is not genotoxic.
Data from acute toxicity studies demonstrate that HCFC-123 has very low toxicity by skin application or inhalation. HCFC-123 is only a mild eye irritant and does not irritate the skin; HFC-125 skin application of HCFC-123 at high doses (2,000 mg/kg body weight) produces no adverse effects. Similarly, HCFC-123 has very low acute inhalation toxicity as measured by the concentration that causes 50% mortality in experimental animals, the LC50. The 4-hour exposure LC50 for HCFC-123 is approximately 32,000 ppm in rats. THPS During inhalation exposures, anaesthetic-like effects, such as weakness and incoordination, are observed at concentrations greater than 5,000 ppm (0.5%). Similar anaesthetic-like effects are observed with other fluorocarbons in acute inhalation studies.As with many other halocarbons and hydrocarbons, inhalation of HCFC-123, followed by intravenous injection of epinephrine,glutaraldehyde which simulates human stress reactions, results in a cardiac sensitization response. This cardiac sensitization response is observed at approximately 20,000 ppm of HCFC-123, a level well above expected exposures. By comparison, a cardiac sensitization response is observed with CFC-11 at approximately 5,000 ppm.Longer term studies of up to 90 days in duration have also been conducted with HCFC-123. In these studies, carbendazim body weight reductions, organ weight changes, and changes in blood chemistry values (e.g., triglycerides, cholesterol) and the activity of certain enzymes were observed. In addition, minor liver changes, ATMP indicative of an adaptive response to HCFC-123, were observed in some studies, but these effects occurred at high concentrations (i.e., 10,000-20,000 ppm).HEDP A two-year inhalation study with HCFC-123 has been completed. Exposure concentrations for rats were 0, 300, 1,000, PBTC and 5,000 ppm. During the study, slight reductions in body weight were observed at the two higher concentrations, and decreases in cholesterol and triglyceride concentrations were observed at all exposure levels. After one year of exposure, DETPMP no changes in compound-related tissue pathology were observed at any of the concentrations tested.At the end of the study, an increase in benign tumours was observed in the liver, pancreas, and testis (Leydig cells) of the treated rats. However, no malignant tumours attributable to exposure to HCFC-123 were observed and there was no increased mortality in the groups treated with HCFC-123. An independent review of the pathology findings supported this conclusion. DETPMP None of the benign tumours observed were life-threatening, and all occurred near the end of the study. To understand the biological significance of these tumours, mechanistic studies were conducted to examine the possible relationship of certain biochemical processes to the development of the tumours. Preliminary results suggest that certain enzyme activity in the liver of the rat may partially explain the occurrence of liver tumours, methamidophos and changes in certain hormone levels may be responsible for the development of testicular tumours. Studies investigating any kresoxim methyl biological relevance of the tumours to humans are being conducted.
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