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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Ecotoxicological information

Endpoint summary

Administrative data

Description of key information

Additional information

Experimental studies on sodium methanolate are available for acute toxicity to fish, toxicity to algae and toxicity to microorganisms. However, all three studies are not considered to be reliable for the assessment of aquatic toxicity due to methodological deficiencies (e.g. exposure duration too short). Thus, these studies are presented for completeness but are not considered for the hazard assessment of the substance.

In water, sodium methanolate rapidly hydrolyses to methanol and sodium hydroxide (OECD, 2002). Due to the rapid hydrolysis of sodium methanolate, the assessment of the aquatic toxicity is based on the products of hydrolysis i.e. methanol and sodium hydroxide.

Sodium hydroxide
Sodium hydroxide further dissociates in the environment to sodium (Na+) and hydroxyl ions (OH-). Sodium belongs to the alkali metals and is one of the most common elements in the earth crust. Together with potassium ions (K+), sodium ions (Na+) 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 sodium. Thus, sodium 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 sodium hydroxide are considered to be solely caused by a potential change of pH. Sodium 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 sodium methanolate (methanol and sodium hydroxide) are sufficient to assess the environmental hazard instead of the parent substance itself. Sodium methanolate is of low toxicity to aquatic species as shown in all studies.