Hydrogen cyanide

Hydrogen cyanide (HCN, prussic acid) was isolated by the Swedish chemist Carl Wilhelm Scheele in 1782, and Justus von Liebig established its chemical structure in 1826. [1] Natural sources include the pits of apricots, cherries, and almonds (where amygdalin and other cyanogenic glycosides hydrolyze to release HCN), cassava roots (a major food staple in tropical regions that must be properly processed to detoxify), and combustion of nitrogen-containing materials like wool, silk, and polyurethane foam. Industrial production uses the Andrussow process (methane + ammonia + oxygen over platinum catalyst) or the Blausäure process (methane + ammonia without oxygen). [2] Annual global production exceeds 1 million tons. The primary industrial use (~80%) is in the production of adiponitrile (a nylon precursor), acrylic acid esters (for coatings), and sodium or potassium cyanide for gold and silver mining (cyanide heap leaching). During WWI, HCN was used as a chemical weapon (Vincennite by France) and during WWII, Zyklon B (hydrogen cyanide adsorbed on pellets) was used by Nazi Germany in extermination camps. Cyanide poisoning from fires (burning polyurethane and other nitrogen-containing materials) is a significant cause of death in building fires — fire smoke can contain lethal HCN concentrations, and smoke inhalation victims who respond poorly to oxygen may have concurrent cyanide poisoning. [3]

Industrial workers in chemical manufacturing (adiponitrile, acrylic esters, sodium cyanide), gold mining operations, electroplating, and fumigation are occupationally exposed to HCN gas or cyanide solutions. Fire victims inhale HCN from burning nitrogen-containing materials (furniture foam, carpets, wool, silk). Dietary exposure occurs from improperly processed cassava, bitter almonds, and fruit pits (amygdalin in apple seeds, cherry pits). Suicidal ingestion of cyanide salts is a rare but documented exposure in certain occupational settings.

HCN is one of the most rapidly acting systemic asphyxiants known — it inhibits cytochrome c oxidase (Complex IV of the mitochondrial electron transport chain), blocking cellular oxygen utilization. [2] At high concentrations, unconsciousness occurs within seconds and death within minutes. At lower concentrations: headache, dizziness, rapid heart rate, and metabolic acidosis from anaerobic metabolism. The LC50 in humans is approximately 150 ppm for 1 hour exposure. Fire victims who have inhaled smoke from burning plastics and nitrogen-containing materials may have life-threatening cyanide poisoning superimposed on carbon monoxide poisoning, and standard oxygen treatment for CO poisoning may be inadequate — cyanide antidote is increasingly included in fire victim treatment protocols.

Chemical manufacturing workers, gold mine extraction workers (cyanide heap leaching), electroplaters, pest control fumigators, and emergency responders at industrial HCN releases face the highest occupational risks. Fire victims in structure fires involving synthetic materials and furnishings face acute cyanide poisoning risk. People in countries where cassava is a dietary staple but processing methods are inadequate face dietary cyanide risk.

1. NEVER enter any space with potential HCN accumulation (fumigated spaces, cyanide plating baths, chemical plant areas with detected HCN) without supplied-air breathing apparatus. 2. Industrial facilities must have HCN detectors with audible alarms, ventilation, and cyanide antidote kits (hydroxocobalamin, Cyanokit) immediately accessible. 3. Fire rescue workers and paramedics responding to structure fires should have cyanide antidote available for smoke inhalation victims. 4. Do not consume bitter almonds, apricot kernels, or apple seeds in quantity — they contain sufficient amygdalin to cause HCN poisoning. 5. Properly process cassava using soaking, fermentation, and cooking methods before consumption.