Potassium hydroxide

Endpoint summary

Description of key information

When humans are dermally exposed to low (non-irritating) concentrations, the uptake of KOH should be relatively low due to the low absorption of ions. For this reason the uptake of KOH is expected to be limited under normal handling and use conditions. Under these conditions the uptake of OH-, via exposure to KOH, is not expected to change the pH in the blood. Furthermore the uptake of potassium, via exposure to KOH, is much less than the uptake of potassium via food under these conditions. The risk of adverse effects of potassium intake from food sources is considered to be low for the general, healthy population (children and adults). The absorption of potassium is effective and about 85-90% of dietary potassium is absorbed from the gut. The potassium balance is primarily regulated by renal excretion in urine. For these reasons, KOH is not expected to be systemically available in the body under normal handling and use conditions.

Additional information

As potassium hydroxide is dissociated in the body fluids, its systemic toxicity must be discussed for its constituting potassium and hydroxyl ions separately.

Potassium is an essential constituent of the body fluids. It is the principal intracellular cation (approximately 5.7 g/l) and it is necessary for the nervous and muscular cells function, as well as for several metabolic activities, among others the synthesis of proteins. Separation of the K+ and Na+ cations across the plasmatic membrane is assured by the ATP consuming K+/Na+ pumps, and allows membrane potentials necessary for nerve and muscle function (Marieb, 1992). Its normal plasmatic concentration is approximately 140 – 200 mg/l. The minimum toxicity level is under 250 mg/l. Between 250 and 310 mg/l, a moderate toxicity is observed, giving lassitude, fatigue and weakness. Severe toxic doses of over 310 mg/l lead to neuromuscular paralysis and, at 390-470 mg/l death from cardiac arrest, due to intraventricular conduction defects by depolarisation of cardiac muscle and subsequent increase in cardiac muscle excitability. Hyperkalemia can be produced by ingestion of 80 – 100 mg K+/kg bw, but cardiac effects predominate only after IV administration (Hazard and Safety Data Bank, Potassium Chloride, 2000).

Regulation of K+ concentration in blood is assured principally by renal excretion and reabsorption. The least increase of the K+ concentration in the extra cellular liquid stimulates strongly aldosterone liberation, which increases K+ excretion. This feedback regulation constitutes an efficient auto-regulation system (Marieb, 1992). The kidneys are able to filter approximately 24 – 27 g K+ ions daily. 90% is excreted into the urine and 10% through the faeces (Saxena, 1989).

The systemic toxicity of hydroxyl ions confounds with an elevated blood pH. The normal pH of blood is 7.35 – 7.45 and the absolute range of pH is 7.0 – 7.8. Alkalosis causes hyperactivity of the central nervous system with, above pH 7.8, tetanus, extreme excitability, convulsions and respiratory stop. Blood pH is regulated by three distinct mechanisms. An immediate mechanism is the buffering capacity of bicarbonate (approximately 1.5 g/l), proteins and in a lesser extent phosphate. A short-term mechanism is the respiration compensation. Alkalosis will be decreased by a slow and superficial respiration, a low CO2 expiration and an accumulation of HCO3- ions (higher than 1.7 g/l). A long-term mechanism is the renal compensation. Alkalosis will be decreased by an increase of the excretion of HCO3- ions (Marieb, 1992).

Interesting observations are also that alkalosis promotes renal excretion of K+, and that, for preventing hyperkalemia, extra cellular potassium is taken up by cells in exchange for hydrogen ions (Saxena, 1989). In other words, these compensating effects of K+ and OH- would attenuate the systemic effect of KOH.