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All plants contain tiny amounts of [https://en.wikipedia.org/wiki/Hydrogen_cyanide hydrogen cyanide] (HCN), however some plants also release high amounts of HCN from a class of glycosides called "cyanogenic glycosides", also called "cyanoglycosides". [https://en.wikipedia.org/wiki/Amygdalin Amygdalin] and [https://en.wikipedia.org/wiki/Linamarin linamarin] are common examples of cyanogenic glycosides. After being released from cyanogenic glycosides, HCN is highly toxic to animals. HCN boils at a relatively low temperature (25.6°C / 78.1°F). The human body is used to breaking down trace amounts of cyanide into the less toxic substance thiocyanate with an enzyme called rhodanese, which then leaves the body via urination <ref name="Gleadow_2014">[http://www.annualreviews.org/doi/full/10.1146/annurev-arplant-050213-040027 Cyanogenic Glycosides: Synthesis, Physiology, and Phenotypic Plasticity. Roslyn M. Gleadow and Birger Lindberg Møller. 2014.]</ref>. Although there are more than 3,000 plant species that are cyanogenic (a number of them cultivated by farmers perhaps because their cyanogenic properties deter animals from eating them), only a few parts of plants that are considered foods contain enough HCN from cyanogenic glycosides to be considered dangerous (generally, other forms of cyanide are considered more dangerous, such as from exposure to air or water that is polluted with cyanide) <ref name="CDC1">[http://www.atsdr.cdc.gov/toxprofiles/tp8.pdf Toxicology Profile for Cyanide. Agency for Toxic Substances & Disease Registry. July 2006. Retrieved 08/25/2016.]</ref>. The location of the cyanogenic glycosides and the enzymes that release them are often each located in different (or all) parts of plants, and those locations are diverse across species. In some plants, the cyanogenic glycosides are concentrated in the stems or leaves of the plant and not the seeds (e.g. sorghum, barley, and lima beans). In fruits sometimes the seeds contain concentrated amounts (e.g. black cherry pits), and other times in the fruit itself (e.g. ''Passiflora edulis''). In rosaceous stone fruits, cyanogenic glycosides are located in the seeds, but the beta-glucosidase enzyme that the plant uses to release HCN is located in the roots of the plant. The concentration of cyanogenic glycosides is generally higher in seedling plants compared to mature plants, however this is there are a few exceptions where this is the opposite (e.g. some ''Eucalyptus'' species, and lima beans). HCN is released from cyanogenic glycosides just like other types of glycosides: beta-glucosidase enzyme or exposure to low pH breaks the bond between a glucose molecule and an unstable compound called "cyanohydrin" (or "alpha-hydroxynnitrile"), which then disassociates into a ketone or benzaldehyde and an HCN molecule. This reaction is stimulated by maceration, and by bacteria in the human gut. The cyanogenic glycosides themselves are not toxic until the HCN is released <ref name="Speijers">[http://www.inchem.org/documents/jecfa/jecmono/v30je18.htm "Cyanogenic Glycosides", First Draft. Dr G. Speijers. National Institute of Public Health and Environmental Protection Laboratory for Toxicology, Bilthoven, The Netherlands. Retrieved 08/25/2016.]</ref>.

Upon learning about Although rare, there have been a few reported deaths due to cyanide poisoning from foods containing cyanogenic glycosides. These reports include deaths from elderberry juice that was thought to contain stems and/or leaves (the stems and leaves contain much higher cyanogenic glycosidesthan the berries, brewers often question the toxicity of cherry and apricot pits in beerripe berries by themselves are considered safe) <ref>[http://www.cdc.gov/mmwr/preview/mmwrhtml/00000311.htm Poisoning from Elderberry Juice -- California. CDC website. 1998. Assuming full conversion of these glycosidesRetrieved 08/30/2016.]</ref>, and that none of the HCN boils offapricot pits, levels of HCN introduced from choke cherry pits, and apricot pits are too low to cause harm to adult humansimproperly processed cassava (a staple food in parts of North Africa) <ref name="who"></ref>. A lethal dosage of cyanide in humans is estimated to be around 1.52 mg per kilogram of body weight, with 0.56 mg per kilogram of body weight being the lowest recorded (although this lowest figure was obtained from a historical case when the measurements taken may not have been accurate) <ref>[http://www.atsdr.cdc.gov/toxprofiles/tp8.pdf Toxicology Profile for Cyanide. Agency for Toxic Substances & Disease Registry. July 2006. Pg 42. Retrieved 08/25/2016.]</ref>. High exposure can cause light-headedness, nausea, vomiting, stomach cramps, diarrhea, convulsions, harm to the brain and heart, comas, and can cause comas or death. Exposure to 0.05 mg of cyanide per kilogram of body weight per day for 15-364 days is considered to be the minimum accumulative cyanide exposure by the US CDC. Accumulative exposure can cause accumulative health risks, such as reproductive, respiratory, neurological, thyroid, and gastrointestinal issues <ref>[http://www.atsdr.cdc.gov/toxprofiles/tp8.pdf Toxicology Profile for Cyanide. Agency for Toxic Substances & Disease Registry. July 2006. Pg 21. Retrieved 08/25/2016.]</ref>. Upon learning about cyanogenic glycosides, brewers often question the toxicity of cherry pits in beer. Cherry pits have traditionally been used in [[lambic]] kriek beers in Belgium. However, the dilution of HCN from cherry pits in beer results in benign levels. Assuming full breakdown of these glycosides, and that none of the HCN boils off (25.6°C boiling temperature), levels of HCN introduced from cherry pits are too low to cause harm to adult humans. The EU regulates that alcoholic beverages cannot exceed 1 mg of HCN per ABV percentage (v/v%) per liter <ref>[http://ec.europa.eu/food/fs/sfp/addit_flavor/flav09_en.pdf COUNCIL DIRECTIVE of 22 June 1988 on the approximation of the laws of the Member States relating to flavourings for use in foodstuffs and to source materials for their production (88/388/EEC). The European Food Commission, Food Safety. Retrieved 08/26/2016</ref>. Luk Daenen, a glyoside researcher, calculated that for a 4% ABV alcohol beer, 4 mg of HCN per liter is allowed. With 200 grams of cherries per liter, and the pits being 10-14 grams of that weight, there is 22 - 30.8 amygdalin per liter of beer. Assuming maximum extraction of HCN, which is unlikely because the pits are not ground up when used in beer, this equates to 1.3 - 1.82 mg of HCN per liter of beer, which is less than the 4 mg of HCN per liter that the EU regulation states. Considering that ~42 mg of HCN is required to kill a person that weighs 70 kilograms (154 pounds), that person would need to drink around 23 liters of beer <ref>[https://www.uclouvain.be/cps/ucl/doc/inbr/documents/presentation-luk-daenen.pdf "Use of beta-glucosidase activity for flavour enhancement in specialty beers," slideshow by Luk Daenen. 2012. Retrieved 08/26/2016.]</ref>. 350 mL of alcohol would kill a 70 kilogram adult <ref>[http://www.alcohol.org.nz/alcohol-its-effects/health-effects/alcohol-poisoning "Alcohol Poisoning". NZ Health Promotion Agency. Retrieved 08/26/2016.]</ref>. The amount of 4% ABV beer required to kill a 70 kg adult from alcohol poisoning is around 8.75 liters. Alcohol would kill such a person far before cyanide poisoning would become a concern. Because of the high boiling point of HCN, cooking or boiling foods that contain high levels of cyanide will greatly eliminate the HCN (90-100% in some cases) <ref name="Chaouali"></ref>.

| Apricot pits, wet weight || 89-2170 (depends on region/strain) <ref name="Chaouali"></ref><ref name="who"></ref>