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EC number: 905-013-3 | CAS number: -
- 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
d-Isomenthone is reduced in the rabbit to d-isomenthol and excreted in urine as glucuronide.
l-Menthone is reduced in the rabbit to d-neomenthol and excreted in urine as glucuronide.
Menthone has low skin permeability coefficient Ps=0.40±0.01x10^-3 cm/h
Key value for chemical safety assessment
- Bioaccumulation potential:
- no bioaccumulation potential
Additional information
The investigation of menthone and isomenthone metabolism by Williams (1940) showed that both ketones undergo a reduction to the respective menthols. For example, l-menthone is reduced to d-neomenthol, whereas d-isomenthone is reduced to d-isomenthol. In addition, Miyazawa and Nakanishi (2006) showed that l-menthone in human liver microsomes could metabolise not only to d-neomenthol, but also to 7-hydroxymenthone. No other primary major metabolites of menthone and isomenthone were tested. Thereafter, these menthols conjugate to glucuronic acid and excreted as urinary glucuronides. The extent of conjugation of d-neomenthol is therefore of the same order as that of d-menthol and d-isomenthol. These three d-menthanols are structural isomerides and it appears that this structural variation has no influence on their conjugation with glucuronic acid in the body, although in purely chamical reactions they show considerable differences (Williams, 1940). The rates of glucuronidation for 0.5 mM d-menthol, l-menthol and d-neomenthol were 43, 41 and 51 pmol/min/mg protein, respectively (RIFM Expert Panel et al, 2008). A study in 4 male volunteers showed that urinary excretion of menthol conjugated with glucuronide in the 14 h time period has an average recovery of 40 % of the oral dose of 180 mg of peppermint oil. In another study, one subject dosed with 1 g of menthol excreted in 6 h urine pool 79 % of the dose of menthol as menthol glucuronide (Bhatia et al, 2008). In humans, rats and rabbits, menthol is effeiciently metabolized not only to menthol glucuronide but also to hydroxylated metabolites. Oxidation of the methyl and isopropyl groups of menthol has been reported to provide major metabolites in the rat after administration for up to 20 days. Therefore the major pathways of menthol metabolism are: 1) conjugation of the alcohol with glucuronic acid, 2) side-chain oxidation yielding polar metabolites, which may be conjugated and excreted (MacDougall et al, 2003; RIFM Expert Panel et al, 2008). An oral pharmacokinetic study in 12 volunteers showed that after 100 mg/menthol capsule administration, the plasma half-life of menthol glucuronide averaged 56.2 minutes (95 % confidence interval 51.0-61.5) (Bhatia et al 2008). It could be concluded, that oral exposure to menthol does not conduct to this accumulation in the body due to very short plasmatic half-life.
Gabbanini et al (2009) investigated the diffusion kinetic of menthone through SkinEthic(R) reconstructed human epidermis (RHE) and have found the low permeability coefficient Ps=0.40±0.01x10^-3 cm/h. A percutaneous absorption study in humans showed that after dermal patch containing 37.44 mg menthol application (2 to 8 patches), the mean terminal plasmatic half-live was 4.7±1.6 h. It could be concluded that daily or even twice-daily application of dermal patches is unlikely to result in substantial accumulation because the terminal half-live is relatively short (Bhatia et al, 2008).
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