Potassium hydroxide

Endpoint summary

Description of key information

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.

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion

Dose descriptor:

LD50

Value:

333 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. Aspiration of the alkali into the airway can result in live-threatening injuries to the larynx, the tracheobronchial passages, and the lungs.

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. Aspiration of the alkali into the airway can result in live-threatening injuries to the larynx, the tracheobronchial passages, and the lungs.

Justification for classification or non-classification

In the OECD SIDS (2002), the Technical Committee has assessed the validity of the available data for acute oral toxicity of KOH. After review of the data in the IUCLID file they come to the conclusion that they will stick to an LD50 value of 333 mg/kg (conventional method, BRUCE 1987); LD50 = 388 mg/kg (Up-and-down method, BRUCE 1987) res. LD50 = 365 mg/kg (conventional method, JOHNSON 1975, source Tessenderlo). All studies res. test results are rated with a Klimisch Code of 2. The lower LD50 value = 273 mg/kg has been calculated after an observation period of 14 days (conventional method, BRUCE 1987). Since KOH is a strong alkaline substance effects may occur even after a longer observation period since the corrosive effects will lead to organ damage that can result into death. However, this effect can not be considered as an acute effect. Therefore, we conclude the value of oral LD50 = 333 - 388 mg/kg can be justified.

According to the CLP Regulation No 1272/2008 Annex VI Table 3.1, KOH is an acute toxicant category 4 (minimal classification) for the oral route.