Apricot kernels contain a cyanogenic glycoside called amygdalin which is hydrolyzed to hydrogen cyanide in the gastrointestinal tract . There are over 2,000 species of cyanogenic glycoside producing plants, including apricots, almonds, peaches, and cassava . The amount of hydrogen cyanide in each kernel varies and ranges from 540 to 2,000 mg/kg . The lethal dose range reported for cyanide in humans is 0.56-1.5 mg/kg . Grinding or chewing the kernel increases toxicity . The ingestion of approximately 20-30 apricot kernels in adults, and fewer in children, may lead to severe toxicity [2, 3, 5].
Although poisoning by ingestion of cyanogenic foods is much more common in tropical countries, there have been reported cases in the US [1, 3]. Additionally, children appear to develop more toxic effects from cyanogenic foods when compared to adults . Despite described adverse effects in literature and investigation by the US FDA, these products continue to be marketed as natural anticancer agents .
How does cyanide produce toxicity? [1,6,7]
Cyanide inhibits cellular respiration in all aerobic organisms by blocking cytochrome oxidase.
This enzyme functions in the electron transport chain within the mitochondria and plays a key role in the conversion of catabolic products of glucose into ATP.
When cytochrome oxidase is inhibited, ATP molecules are not formed.
This causes a shift from aerobic to anaerobic cellular respiration and therefore results in lactic acidosis and systemic side effects.
What are the symptoms of cyanide poisoning? [1,6,7]
Dizziness, confusion, headache
Shortness of breath
Weakness and malaise
Nausea and vomiting
Hypotension, seizures, coma, apnea, arrhythmias
Death due to cardiorespiratory arrest
How do you diagnose cyanide poisoning? 
Diagnosis is based largely upon the history and clinical presentation.
Cyanide levels can be obtained for confirmation but do not generally return in a clinically relevant time frame.
Laboratory findings suggestive of cyanide poisoning include:
Anion gap metabolic acidosis
Reduced arterial to venous oxygen difference as an indicator of reduced oxygen utilization.
How to you treat cyanide poisoning? [1, 5-8]
If left untreated, cyanide toxicity can be fatal.
Antidotal therapy includes hydroxocobalamin, sodium nitrite, and sodium thiosulfate.
Chaouali N, Gana I, Dorra A, Khelifi F, Nouioui A, Masri W, Belwaer I, Ghorbel H, Hedhili A. Potential Toxic Levels of Cyanide in Almonds (Prunus amygdalus), Apricot Kernels (Prunus armeniaca), and Almond Syrup. ISRN Toxicol. 2013 ;2013:610648. PMID: 24171123
Cigolini D, Ricci G, Zannoni M, Codogni R, De Luca M, Perfetti P, Rocca G. Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels. BMJ Case Rep. 2011;2011:bcr0320113932. PMID: 22694886
Borron SW. Recognition and treatment of acute cyanide poisoning. J Emerg Nurs. 2006;32(4 Suppl):S12-S18. PMID: 16860672.
Holstege CP, Kirk MA. Cyanide and Hydrogen Sulfide. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill; 2019. Accessed August 20, 2023.
Howland M. Nitrites (Amyl and Sodium) and Sodium Thiosulfate. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill; 2019.