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EC number: 212-736-1 | CAS number: 865-33-8
- 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
Description of key information
Additional information
Experimental studies on potassium methanolate are not available. In water, potassium methanolate rapidly hydrolyses to methanol and potassium hydroxide (OECD, 2002). Due to the rapid hydrolysis of potassium methanolate, the assessment of the aquatic toxicity is based on the products of hydrolysis i.e. methanol and potassium hydroxide.
Potassium hydroxide
Potassium hydroxide further dissociates in the
environment to potassium (K+) and hydroxyl ions (OH-). Potassium belongs
to the alkali metals and is one of the most common elements in the earth
crust. Together with sodium ions (Na+),
potassium ions (K+)
are responsible for maintaining the cell membrane potential and
essential for the function of all living cells (Clausen&Poulsen, 2013).
Many physiological processes in organisms are driven by the influence of
potassium. Thus, potassium ions are not considered being relevant for
aquatic toxicity.
Hydroxyl
ions may cause a change (increase) of pH of the receiving environmental
compartment. This may result in effects on aquatic organisms in case the
pH is changed outside of the tolerable pH-range. Thus, hydroxyl ions do
not have an intrinsic toxicity but may cause physical effects depending
on the buffer capacity of the aqueous medium (OECD, 2002). It has to be
noted that the pH of sewage treatment plant effluents is measured
frequently and is adapted appropriately before release if needed. In
addition, due to the dilution effects and buffer capacity of natural
aquatic ecosystems significant pH changes followed by effects on aquatic
species are not expected (OECD, 2002).
In conclusion, any observed effects after exposure of aquatic organisms
to potassium hydroxide are considered to be solely caused by a potential
change of pH. Potassium ions are not considered to contribute to aquatic
toxicity.
Methanol
Experimental studies on the aquatic toxicity of
methanol are available for all aquatic trophic levels. Even though most
of the studies are not performed according to the most recent
guidelines, the results allow for a reliable assessment of the aquatic
toxicity. All studies consistently indicate a low aquatic toxicity of
methanol.
Methanol is the first and simplest member of the series of aliphatic alcohols. Like other non-reactive, non-ionizable organic chemicals ("neutral organics") such as ketones, ethers, alkyl halides, aryl halides and aromatic hydrocarbons methanol is expected to exert toxicity to aquatic species through simple narcosis.
The results from the most reliable and relevant available studies are listed below.
Short-term toxicity
Fish
LC50 (96 h) = 15400 mg/L (Lepomis macrochirus)
LC50 (96 h) = 28100 mg/L (Pimephales promelas)
LC50 (96 h) = 20100 mg/L (Oncorhynchus mykiss)
Aquatic invertebrates
EC50 (48 h) = 18260 mg/L (Daphnia magna)
EC50 (48 h) > 10000 mg/L (Daphnia magna)
Algae
EC50 (96 h) ca. 22000 mg/L (Selenastrum capricornutum)
Microorganisms
EC50 (15 h): 20000 mg/L (activated sludge)
IC50 (3 h): >1000 mg/L (activated sludge)
IC50 (24 h): 880 mg/L (Nitrosamonas)
toxic limit concentration (16 h; 192 h): 530 - 6600 mg/L (Pseudomonas putida, Microcystis aeruginosa)
All the available data consistently demonstrate the very low acute toxicity of methanol for aquatic organisms.
Long-term toxicity
No fully reliable results and no guideline studies are available investigating the long-term toxicity of methanol to aquatic species. Given the Biological Oxygen Demand of methanol and its rapid biodegradation, it is indeed difficult to maintain the required levels of oxygen concentration in long-term tests. Due to this aspect, it also difficult to assess the reliability of studies, in which the oxygen concentration is not well documented. Since methanol belongs to the category of chemicals acting with a non-specific mode of action (simple narcosis) the chronic toxicity to aquatic organism can be reasonably predicted from data on acute toxicity using an appropriate acute-to-chronic ratio. An ACR of 10 has been proposed in the literature for such kind of chemicals (see for example Raimondo et al., Environ. Toxicol. Chem. 26, 2007; Roex at al., Environ. Toxicol. Chem. Cryo Letters. 2004 Nov-Dec; 25(6):415-2419, 2000).
Taking into account the toxicity mode of action of methanol the chronic toxicity to aquatic organisms can be also reasonably predicted using Structure-Activity Relationship models (QSARs).
The available information and the results from toxicity estimations indicate a very low chronic toxicity of methanol to aquatic organisms, with no-effect levels well above the concentrations which are normally used in limit tests on long-tern toxicity.
Fish
NOEC (predicted chronic value): 447 mg/L (Pimephales promelas)
NOEC (200 h) = 7900 - 15800 mg/L (Oryzias latipes)
Aquatic invertebrates
NOEC (21 d) = 208 mg/L (predicted) (Daphnia magna)
NOEC (21 d) = 122 mg/L (Daphnia magna)
All the available data consistently demonstrate the very low chronic toxicity of methanol for aquatic organisms.
In conclusion, the data available for the degradation products of potassium methanolate (methanol and potassium hydroxide) are sufficient to assess the environmental hazard instead of the parent substance itself. Potassium methanolate is of low toxicity to aquatic species as shown in all studies.
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