Reaction mass of glycerol and methanol and Fatty acids, vegetable-oil

Endpoint summary

Additional information

Several data on acute and chronic toxicity of methanol to fish, invertebrates, and algae are available:

 

Acute Toxicity

LC50 (96h) = 28100 mg/L Pimephales promelas

LC50 (96h) = 20100 mg/L Oncorhynchus mykiss (=Salmo gairdneri)

LC50 (96h) = 15400 mg/L Lepomis macrochirus

EC50 (48h) > 10000 mg/L Daphnia magna

EC50 (96h) ca. 22000 mg/L Selenastrum capricornutum (new name: Pseudokirchnerella subcapitata)

 

Chronic Toxicity

NOEC (200h) = 7900 - 15800 mg/L Oryzias latipes

 

Microorganisms

EC 50: 19800 mg/L activated sludge

IC50: >1000 mg/L avtivated sludge

IC50: 880 mg/L Nitrosamonas

toxic limit concentration: 530 - 6600 mg/L Pseudomonas, Microcystis aeruginosa.

 

The results indicate a very low acute toxicity for aquatic organisms, well above 10000 mg/L. Also for microorganisms data indicate a low toxicity. The PNEC for aquatic organisms was derived from the LC50 (96h) = 15400 mg/L Lepomis macrochirus using an assessment factor of 100. The choice of this assessment factor is based on the very low acute toxicity of methanol in all throphic levels and its unspecific mode of action (non-polar narcosis). Although the available information on long-term toxicity in fish (Gonzales-Doncel et al., 2008) is not used to derive the PNEC, the reported No Observed Effect Concentration of

7900 - 15800 mg/L in Oryzias latipes confirms the low toxicity of methanol also after chronic exposure.

This is also supported by available tests on chronic toxicity for Daphnids conducted with the structurally related substances propan-2 -ol and butan 1 -ol (NOECs respectively of > 100 mg/L and 18 mg/L).

There are no reliable data on aquatic toxicity of potassium hydroxide. The substance is known to be a strong alkaline substance that dissociates completely in water to K+ and OH- (OECD SIDS potassium hydroxide, 2002). Also, data on pH increases due to the addition of potassium hydroxide in the water used in the test, are lacking. In many tests reports there were no data on pH, buffer capacity and/or test medium composition, although this is essential information for toxicity tests with KOH.

However, the only posssible effect of potassium hydroxide would result from the pH effect. However pH is expected to remain between environmentally acceptable ranges.

As stated in the OECD SIDS of potassium hydroxide (2002)(p4), it was not considered usefull to derive a generic PNEC, as the buffer capacity, the pH and the fluctuation of the pH are very specific for a certain ecosystem and show considerable differences. A significant increase of the pH of the receiving water is not expected. Generally, the change in pH of the recieving water should stay within a tolerated range of the pH at the effluenct side and for this reason no adverse effects on the aquatic environment are expected due to the production or use of potassium hydroxide, if emissions of waste water are controlled by appropriate pH limits and/or dilutions in relation to the natural pH and buffering capacity of the receiving water.

The effects of KOH on the aquatic compartement are expected to be comparable to the effects of NaOH. Available data on NaOH indicate that concentrations of 20-40 mg/L may be acutely toxic to fish and invertebrates (single species tests). Data on pH increases due to the addition of these amounts of NaOH in the used test waters are lacking. In waters with a relatively low buffering capacity, NaOH concentrations of 20-40 mg/L may result in a pH increase with one to several pH units (EU RAR, 2007; section 3.2.1.1.3, page 30). In summary, no specific concern regarding aquatic toxicity of the registered substance are apparent.