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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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Absorption
HCFC 123 is readily absorbed by inhalation. Loizou et al. (1994) and Dekant (1994) described the uptake in rats by means of PBPK modeling. Both studies reported that a model with a single saturable component adequately described the uptake at lower concentrations, although it failed to describe the uptake in female rats exposed at >2000 ppm. Dekant (1994) found that 50 -60% and 95% of the administered HCFC 123 (6 h exposure to 4000 ppm) was absorbed by rats and guinea pigs, respectively.
Vinegar et al. (1994) found a biphasic uptake in rats exposed to 100, 1000, and 10000 ppm HCFC-123 for 4 hours, with a rapid initial uptake over 30 and 45 minutes, followed by a slower absorption phase. Uptake saturation was estimated at >2000 ppm.
Distribution
Following absorption, HCFC 123 is rapidly distributed in the organism via the blood. Dekant (1994) examined the tissue and organ distribution following a 6 hour exposure to 4000 ppm radiolabeled HCFC 123 in rats. After 48 hours post exposure, low amount of radioactivity were detected. Relatively higher amounts of radioactivity were detected in the liver (5 -10 times higher than in other tissues). However, this difference was attributed also to the possible formation of protein adducts with trifluoroacetic acid, the major metabolite of HCFC 123. No accumulation in fat was observed.
Metabolism
HFCF 123 metabolism was studied both in vitro and in vivo. Dekant examined the metabolism in rat and human liver microsomes in vitro. In both species trifluoroacetic acid (TFA) was identified as the main formed metabolite, with chlorodifluoroacetic acid and inorganic fluoride detected as minor metabolites. Metabolisation rates were directly influenced by the specific induction or inhibition of the cytochrome P450 CYP2E1, indicating an involvement of this enzyme in the metabolic pathway. Luoizou et al (1994) and Dodd et al. (1993) examined the in vivo metabolism of HCFC 123 in rats. In both cases TFA was detected as the main metabolite, with a saturation concentration identified between 2000 and 3000 ppm. Dekant (1994) studied the metabolism in rats and guinea pigs. TFA was the major metabolite in both species, with about 20%-30% of the administered dose excreted as TFA in the urine.Othe rminor metabolites indicative of a reductive metabolic pathway via the possible formation of 1,1,-dichloro-2,2 -difluoroethene followed by conjugation to glutathione were also detected. The major role of P450 CYP2E1 observed in vitro was confirmed in in vivo experiments. The ability of HCFC 123 to form covalent TFA-protein adducts was studied in vitro and in vivo (Dekant, 1994; Harris et al, 1991 -1992; Ferrara et al., 1997; Zanovello et al., 2003 and Bortolato et al., 2003)
Elimination
HCFC 123 can be excreted mainly unmetabolised via exhaled air and via the urine as TFA. The urinary excretion following hepatic elimination represents the rate limiting step in the biotransformation of HCFC 123. Buschmann (2001, reported in Section 7.8.1) and Cappon (2002) analysed the possible excretion via the milk in rats and monkeys, respectively. TFA was detected in rat milk and in the urine of litters nursed by treated dams in the Buschmann's study. Similarly, both TFA and HCFC 123 were detected in monkey milk, and TFA but not HCFC 123 was detected in the blood of both exposed mothers and neonates.
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