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Diss Factsheets
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EC number: 211-190-1 | CAS number: 633-03-4
- 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
There is no evidence of carcinogenic activity of MG chloride in mice exposed to 100, 225, or 450 ppm.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
- Study duration:
- chronic
- Species:
- other: Rats and mice
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
According to CLP regulation (EC1272/2008) Basic Green 1 is not classified as carcinogen
Additional information
In the female rats there was a small, but statistically significant, increase in the incidence of hepatocellular adenoma, but is not clear if the increase is biologically significant; is not clear if the tested substance increase incidence of adenoma and incidence of pituitary gland adenoma (Culp, 2006).
Other effects attributed to similar substances and that seems linked to tumour promotion were reported in literature.
MG appears to be able to produce transformation SHE cells, developing aneuploid pattern; this cells can be tumorigenic, as they could produce tumours (Rao, 2001). Carcinogenesis involves an imbalance between the regulation of cell proliferation and apoptotic death, either by inhibition of apoptosis or by stimulation of cell division, or by affecting both. The Rao study (2001) suggests also that transformed cells are much less sensitive to apoptosis than normal cells. Nevertheless the exact mechanisms by which transformed SHE cells could develop resistance to MG-induced apoptosis are not clear and further studies are required to see the link between the abrogation of G2/M checkpoint control and the development of resistance to apoptosis observed (Rao, 2001).
Furthermore static protein tyrosine specific phosphatases associated with enhanced protein tyrosine and/or serine-threonine phosphorylation seems to be linked to abnormal expression of G1/S cyclins and PCNA during rat liver tumour promotion by MG (Sundarrajan, 2000), but also in this case further studies are required.
Mechanisms behind the induction of these tumours are uncertain and also are not entirely clear the relevance of these findings.
The NTP report (Cilp, 2005) explain that under the conditions of these 2-year feed studies, there was equivocal evidence of carcinogenic activity of MG Chloride in female F344/N rats based on the occurrence of thyroid gland follicular cell adenoma or carcinoma (combined) and marginal increases in hepatocellular adenoma and mammary gland carcinoma in exposed rats. Furthermore it was concluded that there was no evidence of carcinogenic activity of MG chloride in female B6C3F1 mice exposed to 100, 225, or 450 ppm.
Studies available on similar substances don't show a clearly result, so Basic Green 1 can't be classified ad a carcinogenic substance.
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