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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Administrative data

Description of key information

Potassium hydroxide:
According to the REACH Regulation, acute toxicity testing does not generally need to be conducted if the substance is classified as corrosive to the skin (column 2 adaptation, Annex VIII). Potassium hydroxide is a corrosive substance at concentrations of about 2% and higher. Between 0.5 and 2% it is irritating (OECD SIDS for potassium hydroxide, 2002, p 15). For this reason, there is no need for further acute toxicity testing.
In the OECD SIDS (2002, p13) it is also stated that KOH has a moderate acute oral toxicity, which is essentially due to its corrosivity.
(Methanol is less acutly toxic (oral route)).

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion
mg/kg bw

Acute toxicity: via inhalation route

Endpoint conclusion

Acute toxicity: via dermal route

Endpoint conclusion
mg/kg bw

Additional information

According to the OECD SIDS on KOH (2002), KOH has a moderate acute oral toxicity, which is essentially due to its corrosivity. The observed systemic effects could be regarded as secondary effects.

Bruce (1987) performed a study on acute oral toxicity in rats: Potassium hydroxide shows moderate acute oral toxic effects, which are essentially due to its corrosivity (local effects) (OECD SIDS on potassium hydroxide, 2002).

An LD50 of 273 mg/kg bw/d (214-324) was calculated based on the conventional method after a 2 weeks observation period (Bruce, 1987). Since potassium hydroxide is a strong alkaline substance, effects may occur even after a longer observation period due to the corrosive effects of the substance, leading to organ damage. However, this effect can not be considered as an acute effect.

Human data in the OECD SIDS further support this conclusion. The only real effects of KOH ingestion are gastrointestinal burns. The mechanism of injury is one of liquefactive necrosis. Thrombosis of local blood vessels contributes to tissue damage. Tran mural necrosis can occur with frightening rapidity and injury often extrudes through the oesophagus to involve adjacent mediastinal and peritoneal structures. When alkali enters the stomach, there may be some neutralization by gastric acid, which can limit the injury to this organ. Perforation of the stomach can occur with peritonitis and caustic injury to the contiguous organs including the colon, pancreas, liver and spleen. If sufficient quantities of alkali pass through the pylorus, there may be substantial duodenal damage including perforation. Lye constitutes a greater danger than solid granules, which tend to adhere on contact to mucous membranes without travelling further. The severity of damage depends on concentration of the agent, but also on the quantity swallowed.

Methanol is less toxic (oral):

In rats, LD50 values after single oral administration range from 1187 to 2769 mg/kg bw, depending on the concentration of the aqueous solution used (BASF 1975, concentrations 15 to 35%, not further specified).

In Rhesus monkeys orally dosed with 6000 mg/kg bw, the retina and the optic papilla showed extended oedema, and the pupils were wide and non-responsive. Six of 8 animals exhibited cystic degeneration of the outer retinal granular layer, and in one animal there was evidence of significant demyelinisation of the optic nerve. Histological lesions were seen in the putamen and nucleus caudatus in 3 of 8 animals. All of these effects were most pronounced after early compensation of acidosis using bicarbonate application, because the monkeys generally did not survive those high doses of methanol but after early treatment with bicarbonate (Potts, 1955; Potts et al., 1955).

There was no evidence of marked acidosis in 12 Rhesus monkeys (28 applications) after sublethal doses up to 6000 mg/kg bw. Specifically, there was no hyperventilation, no increase in urinary excretion of organic acids, or shift in serum bicarbonate. Blindness was seen in only one surviving monkey dosed with 9000 mg/kg bw; the effect was transient four days after exposure. The LD50 was between 7000 and 9000 mg/kg bw (Cooper and Felig, 1961).

Justification for classification or non-classification

The substance is classified as Acute toxicity category 3: toxic if swallowed; toxic in contact with skin; toxic if inhaled.