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EC number: 206-190-3 | CAS number: 306-83-2
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Effects on fertility
Description of key information
Cross fostering study
Additional information
Developmental toxicity was studied in pregnant rats exposed to 5,000 ppm HCFC-123 on days 6-15 of gestation and in pregnant rabbits exposed up to 500, 1,500 or 5,000 ppm on days 6-18 of gestation. Maternal toxicity, but no effects on development were observed in both studies.
12 male and 12 female Sprague Dawley rats/group were exposed to 0, 300, 1,000 or 5,000 ppm HCFC-123 in a 1-generation study. Exposure of parental generation lasted about 17 weeks, starting 4 weeks before to pairing and continuing through mating period, gestation, lactation and weaning of the offspring. Parental generation presented adverse effects typically observed in other repeated toxicity studies (decreased body weight gains, reduced triglyceride levels at all the tested concentrations), but no effects were observed towards fertility parameters. A reduced rate of growth accompanied by a delayed sexual maturation in males was observed in generation 1.
The results of the 1-generation study were used for the setting of concentrations in a 2-generation study. Male and female rats were exposed to 0, 30, 100, 300 or 1,000 ppm HCFC-123. Retarded body weight gain was observed at 1,000 ppm in F0 and F1 in both sexes and in F0 males only at 100 and 300 ppm. Decreased cholesterol, triglycerides and VLDL levels were observed at ≥100 ppm in both sexes of F0 and F1. Increased liver weight, associated with macroscopic and microscopic changes of hepatocyte enlargement and vacuolation were observed at ≥100 ppm in both sexes of F0 and F1. Slight increases in liver weight, without pathological findings were observed at 30 ppm in F0 animals. Decreased litter weights and mean pup weight were observed at ≥100 ppm from day 14 post partum to weaning and from day 7 post partum to weaning in F0 and F1 offspring, respectively. A slightly decreased mean pup weight was still observed in the F1 offspring at 30 ppm. Male sexual maturation was delayed at ≥300 ppm. Reduction in implantation counts was observed in F1 females at 1,000 ppm. A NOAEC was not attributed in this study, due to the presence of adverse effects in parental generations at the lowest concentrations.The study of possible post natal developmental effects of HCFC-123 via lactation was carried out in 4 lactating female Rhesus monkeys, exposed to 1,000 ppm HCFC-123 for 3 weeks (6h/day, 7d/week) during lactation period. Both TFA and HCFC-123 were detected in the milk. Although frank hepatotoxicity was observed in the adult animals, no effects were observed in infant monkeys (see section 7.1).
Effects on developmental toxicity
Additional information
An inhalation developmental toxicity study was conducted with vapours of HCFC-123 (Bio-test Laboratory, 1977). For this study, 2 groups of 20 pregnant female rats were exposed to 0 or 5,000 ppm HCFC-123 (0 or 31,300 mg/m3) for 6 hours from days 6 to 15 of gestation. The animals were sacrificed on day 20 and all dams and foetuses examined. Maternal mean body weights in the exposed groups were significantly depressed on days 12 and 15 of the gestation period (20 and 40 grams, respectively). At termination, maternal mean body weights were still depressed (21 grams), but not to a statistically significant degree. The numbers of corpora lutea, implantation sites, resorption sites and foetuses were similar among control dams and those exposed to HCFC-123. In summary, exposure of pregnant rats to a concentration of 5,000 ppm of HCFC-123, a level that produced a response in the dams (depressed weight gain), did not result in developmental toxicity.
HCFC-123 did not induce embryotoxicity or teratogenic effects in an inhalation study in which 25 pregnant Charles River-CD Albino rats were exposed to HCFC-123 at a concentration of 10,000 ppm (62,500 mg/m3) 6 hours per day on days 6 to 15 of gestation. Dams and foetuses were sacrificed on day 21 and examined for gross changes (ECETOC, 2005).
A study was conducted to evaluate the teratogenic potential of HCFC-123 when administered to pregnant rabbits by inhalation (Biodynamics, 1989). Initially, in the range-finding study, groups of 6 pregnant rabbits were exposed (6 h/d) to concentrations of 1,000, 5,000, 10,000 or 20,000 ppm (6,250, 31,300, 62,500 and 125,000 mg/m3) during days 6 to 18 of gestation. An air exposed control group was included. All rabbits exposed to HCFC-123 lost weight during the study and food consumption was markedly reduced, especially at 10,000 and 20,000 ppm. Based on marked decreased food consumption, decreased body weights, and an increased number of resorptions seen at 10,000 and 20,000 ppm, all indicating maternal toxicity and possibly embryotoxicity, exposure levels of 500, 1,500 or 5,000 ppm (3,125, 9,380 or 31,300 mg/m3) were selected for the main study. This study consisted of 6 h/day exposures of 24 mated females per exposed group during days 6 to 18 of gestation. No compound-related mortality was observed in any of the exposure groups. Evidence of maternal toxicity occurred during day 6 to 18 of gestation at all exposure levels and included body weight loss as well as reduced food consumption. No other signs of maternal toxicity were observed. In conclusion, there was no evidence of embryotoxic, foetotoxic or teratogenic effects.
Toxicity to reproduction: other studies
Additional information
Buschmann et al (2001) performed a study in Sprague-Dawley rats (Crl:CD BR) to differentiate between effects of HCFC-123 (1,000 ppm) on the lactating dam and on the foetus using fostering and cross-fostering of the offspring. Pregnant and/or lactating dams without the pups present were exposed (6 h/d) to HCFC-123 or clean air by whole-body inhalation from day 6 to 19 postconception and from day 5 to 21 post-partum. Pups were cross-fostered on new dams within the first 2 days after birth. In mothers, HCFC-123 treatment caused decreased serum glucose, cholesterol and triglycerides and increased absolute and relative liver weights. There was no effect on milk production or composition. The effects on offspring due to HCFC-123 treatment consisted of decreased litter weight and individual pup weight and decreased serum triglycerides at weaning. All effects were due to treatment of the lactating dams as no pre-natally induced effects were obtained. The authors concluded that the presence of TFA in maternal milk was the possible cause of the effects seen in the pup (HCFC-123 was too volatile to allow measurement of concentrations in milk).
Justification for classification or non-classification
No evidence of adverse effects towards reproduction and development were observed for HCFC 123. No classification of HCFC 123 as a toxic for reproduction is warranted in accordance Regulation (EC) No. 1272/2008.
Additional information
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