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EC number: 288-422-3 | CAS number: 85721-12-6
- 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
Carcinogenicity
Administrative data
Description of key information
Not carcinogen
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
Carcinogenicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Justification for classification or non-classification
There are two studies available for carcinogenicity performed on similar substance.
1) Oral administration, rat
Male and female Charles River CD rats of the F0 generation received Curry Red (purity 88%) in concentration of 0 (control), 0.37, 1.39 or 5.19%. The groups consisted of 30 males and 30 females. The rats received Curry Red from 1 week before mating throughout the 3-week breeding period and during the gestation and lactation period. The F1 rats were exposed to the same diary dietary concentration as the F0 rats. Each groups consisted of 50 males and 50 females. The exposure continued until survival of either sex in any group reach approximately 20% at which point all rats at that sex were killed. Deaths, morbidity and gross signs of toxicity were recorded daily. Individual body weights, food consumption and clinical signs of gross observation were recorded every 4 week after 26 weeks. F1 male and female rats received Curry Red for 118 and 121 weeks, respectively. Food consumption among the high dose males and females was elevated, but not significantly so, when compared with controls. The authors conclude that lifetime exposure of rats to the tested substacne as a dietary admixture at concentrations up to 5.19% did not demonstrate carcinogenic effects.
2) Oral administration, mice Curry Red was fed to Charles River HaM/ICR (CD-1) (study A) and CD-1 outbred (study B) mice as a dietary admixture in two separate lifetime toxicity/carcinogenicity studies. Each study included an in utero exposure phase during which the colouring was fed at dietary concentrations of 0 (control), 0.37, 1.39 or 5.19% throughout the mating, gestation and lactation periods. The F0 mice consisted of 50 males and 50 females in study A and 70 males and 70 females in study B. After random selection the lifetime exposure phase was initiated using the same dietary concentrations with 50 male and 50 female per group in study A and 100 males and 100 females per group in study B. Exposure was for 104 weeks in study A and 109 weeks in study B. There were no compound related effects on survival. There were no consistent statistical significant compound-related effects on mean food consumption in either study A or study B. The appearance of lymphocytic lymphoma occurred in study A earlier among treated groups than among controls. Lymphomas were observed in 1 low-dose male, 1 mid-dose female and 2 males and females from the high-dose group between week 31 and week 37. Lymphomas were not observed among controls until week 85 and 70 for males and females, respectively. Increased incidence of lymphocytic lymphoma or acceleration of the appearance of the lymphoma were not observed in study B. The authors state that study B was conducted to determined whether Curry Red had an effect on the appearance of lymphocytic lymphoma (a different strain of mice was used). A critical analysis of the data failed to establish a relationship between the incidence of lymphoma and Curry Red. The authors state that no compound-related adverse effects were observed.
All the available studies does not show any compound related effect and the tested substance could be considered as not carcinogen.
Additional information
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