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EC number: 247-728-7 | CAS number: 26479-35-6
- 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
Effect on fertility: via oral route
- Endpoint conclusion:
- no study available
Effects on developmental toxicity
Description of key information
As summarised in the read-across documentation provided as an attachment to this CSR, potassium allophonate quickly hydrolyses to urea under physiological conditions; therefore, read-across to developmental toxicity information for urea is used to assess developmental toxicity. Teramoto et al. (1981) conducted a study of limited design in which urea failed to produce any teratogenic or systemic effects when pregnant mice and rats were administered a single gavage dose of 2000 mg/kg bw. Furthermore, Seipelt et al. (1969) found no effects on the kidney weights of pups when dams were administered oral doses of urea during pregnancy. Additionally, urea is produced in large quantities by the human body as an endogenous product of normal metabolism. Furthermore, the level of primary and secondary occupational exposures to urea are likely to be insignificant compared to the quantities (20-50 g/day) produced by normal metabolism and present at high concentrations in the blood. Therefore, the weight-of-evidence (WoE) indicates that urea is not a developmental toxicant.
Link to relevant study records
- Endpoint:
- developmental toxicity
- Type of information:
- migrated information: read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Reliability:
- 3 (not reliable)
- Rationale for reliability incl. deficiencies:
- other: No guideline followed. The study performed with relatively small numbers of animals and a single dose
- Qualifier:
- no guideline followed
- Deviations:
- not specified
- Principles of method if other than guideline:
- Dams were dosed via oral gavage to pregnant rats on day 12 of pregnancy and sacrificed on day 20 of pregnancy.
- GLP compliance:
- not specified
- Limit test:
- no
- Species:
- rat
- Strain:
- Wistar
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Source: purchased from CLEA, Japan
- Age at study initiation: (P) 15 wks
- Diet: laboratory chow (Oriental Yeast MF), ad libitum
- Water: tap water ad libitum
ENVIRONMENTAL CONDITIONS
- Temperature (°C): 24 ±1
- Humidity (%): 55 ± 5 - Route of administration:
- oral: gavage
- Vehicle:
- water
- Details on exposure:
- Aqueous solutions of the compounds (10 mL/kg) were prepared and orally administered to dams.
- Analytical verification of doses or concentrations:
- not specified
- Details on mating procedure:
- Females were paired overnight with a male. The following morning they were examined for the presence of vaginal plug and were designated as being in day 0 of pregnancy when the plug was observed.
- Duration of treatment / exposure:
- Dams were dosed at day 12 of pregnancy
- Frequency of treatment:
- Single dosing
- Duration of test:
- Dosed on day 12 of pregnancy, and sacrificed at day 20 of pregnancy
- Remarks:
- Doses / Concentrations:
Basis:
nominal conc.
2000 mg/kg - No. of animals per sex per dose:
- 4
- Control animals:
- yes, concurrent vehicle
- Fetal examinations:
- - External examinations: Yes: [all per litter]
- Soft tissue examinations: Yes: [ half per litter]
- Skeletal examinations: Yes: [ half per litter]
- Head examinations: No data - Details on maternal toxic effects:
- Maternal toxic effects:no effects
Details on maternal toxic effects:
Mortality was not observed. - Dose descriptor:
- NOAEL
- Effect level:
- 2 000 mg/kg bw (total dose)
- Based on:
- test mat.
- Basis for effect level:
- other: developmental toxicity
- Details on embryotoxic / teratogenic effects:
- Embryotoxic / teratogenic effects:no effects
Details on embryotoxic / teratogenic effects:
No significant changes were observed in number of implants, number of live fetuses, % of fetal resorptions, fetal weight or % fetal malformation. - Abnormalities:
- not specified
- Developmental effects observed:
- not specified
- Conclusions:
- Based on the study, no adverse developmental/teratogenicity effects were observed due to a single, high-dose urea treatment.
Reference
|
No. Dams |
Mean No of implants |
Mean No. of live fetuses |
% Fetal resorptions |
Mean fetal weight (mg) |
& Fetuses malformed |
Urea (2000mg/kg) |
4 |
13.8±2.2 |
13.8±2.2 |
0 |
3626±104 |
1.8 |
control |
6 |
13.7±1.0 |
13.3±0.8 |
2.4 |
3671±197 |
0 |
Effect on developmental toxicity: via oral route
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEL
- 2 000 mg/kg bw/day
- Species:
- other: rat and mice
- Quality of whole database:
- No guideline followed. The study performed with relatively small numbers of animals. Single dose on one dose level.
Effect on developmental toxicity: via inhalation route
- Endpoint conclusion:
- no study available
Effect on developmental toxicity: via dermal route
- Endpoint conclusion:
- no study available
Additional information
No developmental toxicity data are available for potassium allophonate; however, as summarised in the read-across documentation provided as an attachment to this CSR, potassium allophonate quickly hydrolyses to urea under physiological conditions. Therefore, read-across to reproductive/developmental toxicity information on urea is appropriate.
In Teramoto et al. (1981), four pregnant rats and ten pregnant mice were administered a single gavage dose of urea at 2000 mg /kg bw on day 12 and day 10 of pregnancy, respectively. Animals were sacrificed eight days later (day 20 for rats and day 18 for mice). For rats and mice, no significant changes were observed regarding the number of implants, number of live fetuses, percent of fetal resorptions, fetal weight or percent fetal malformation. Based on the rat study, no adverse developmental/teratogenicity effects were observed due to a single, high dose urea treatment. In a study summarised in the United States Environmental Protection Agency’s (U.S. EPA) Integrated Risk Information System’s (IRIS) toxicological review of urea, six pregnant rats were administered two doses of urea, totaling 50 g/kg bw/day, during pregnancy (Seipelt et al., 1969). Within 48 hours of birth, pups were sacrificed by decapitation and kidneys were removed and weighed; the right kidney was then dried at 105 deg C and weighed. No evidence of maternal toxicity or effects on the pups' kidney weights were observed in this study.
References:
Seipelt, H., Zoellner, K., Hilgenfeld, E. and Grossmann, H. 1969. Studies on kidneys of newborn rats after chronic urea administration to the mother [Article in German]. Zeitschrift Urol. Nephrol., 62(8): 623-7. As cited in: United States Environmental Protection Agency’s (U.S. EPA). 2011. Toxicological Review of Urea: Studies on kidneys of newborn rats after chronic urea administration to the mother. Integrated Risk Information System (IRIS).
Teramoto, S., Kaneda, M., Aoyama, H. and Shirasu, Y. 1981. Correlation between the molecular structure of N-alkylureas and N-alkylthioureas and their teratogenic properties. Teratology, 23(3): 335-42.
Justification for selection of Effect on developmental toxicity: via oral route:
Read-across from urea.
Justification for classification or non-classification
The reproductive/developmental toxicity of potassium allophonate was evaluated based on read-across from appropriate studies on urea, since it has been documented that potassium allophonate readily hydrolyses to urea under physiological conditions. Prenatal developmental toxicity studies of limited design are available for rats and mice, none of which found any evidence of developmental toxicity for urea. Therefore, the weight-of-evidence (WoE) from these studies indicates that urea is unlikely to be a developmental toxicant. Additionally, urea is produced in large quantities by the human body as an endogenous product of normal metabolism. Furthermore, the level of primary and secondary occupational exposures to urea are likely to be insignificant compared to the quantities (20-50 g/day) produced by normal metabolism and present at high concentrations in the blood. Therefore, the weight-of-evidence (WoE) indicates that urea is not a developmental toxicant and, based on read-across, potassium allophonate does not warrant classification for the repeat-dose toxicity endpoint.
Additional information
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