Hydrogen cyanide lethal exposure

CK in liquid or gas form is highly irritating to the eyes and upper respiratory tract. Inside the body, it converts to hydrogen cyanide, which inactivates certain enzyme systems that prevent cells from utilizing oxygen. Impacted skin may appear flushed. Low levels of exposure often cause weakness, headache, disorientation, nausea, and vomiting. Higher levels of exposure will result in loss of consciousness, terminate respiration, and cause death within 15 minutes. An immediate lethal dose often causes violent contractions of blood vessels accompanied by severe shock. This reaction may cause death prior to asphyxiation.1 ... 

When comparing the available acute lethal toxicity information for cyanide compounds, it was concluded that, for oral exposure, the molar lethal toxicities of hydrogen cyanide, sodium cyanide, and potassium cyanide are similar. Rabbits appeared to be more susceptible to the lethal toxicity of these three compounds than rats (Ballantyne 1988). 

Respiratory Effects. Respiratory effects commonly occur after inorganic cyanide poisoning by any route of exposure. Following inhalation, the first breath of a lethal concentration of hydrogen cyanide causes hyperpnea (Rieders 1971). The victims experience shortness of breath that may be rapidly (>1 minute) followed by apnea. Dyspnea was reported in patients who survived acute inhalation exposure to cyanide... 

Hydrogen cyanide is extremely toxic hy ingestion, inhalation, skin absorption, and all routes of exposure. An oral dose of 50 mg could be lethal to humans (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substances, 2nd ed.. New York John Wiley). Symptoms from acute poisoning include labored breathing, shortness of breath, paralysis, unconsciousness, and respiratory failure. Lower doses can cause headache, nausea and vomiting. Oral LDsoin mice is 3.7 mg/kg. Amyl nitrite is an effective antidote. 

Hydrogen cyanide is a dangerous acute poison by all toxic routes. Acute inhalation may cause death in seconds. Lethal effects due to inhalation of its vapor depend on its concentration in air and time of exposure. Inhalation of 270 ppm HCN in air can be fatal to humans instantly, while 135 ppm can cause death after 30 minutes (Patty 1963 ACGIH... 

The acute toxicity of hydrazoic acid through inhalation and other routes of exposure has been found to be high to very high. The symptoms and the intensity of poisoning are similar to sodium azide. It is, however, less toxic than hydrogen cyanide. In humans, inhalation of its vapors can produce irritation of eyes and respiratory tract, bronchitis, headache, dizziness, weakness, and decreased blood pressure (Matheson 1983). Prolonged exposure to high concentrations can result in collapse, convulsion, and death. An exposure to 1100 ppm for 1 hour was lethal to rats. Chronic exposure to a low level of this compound in air may produce hypotension. 

Cyanide is readily diffusible through epithelium. This property contributes to its lethal toxicity after inhalation of hydrogen cyanide (HCN) gas (the usual route of military exposure), ingestion of cyanide salts or cyanogens, or percutaneous absorption of cyanide from high-concentration solutions. Because cyanides are present at low concentrations in several naturally occurring environmental sources, it is not surprising that most animals have intrinsic biochemical pathways for detoxification of the cyanide ion. 

Cyanogen bromide is a volatile solid, which dissolves readily in water, diethyl ether, and alcohol. It is a highly toxic substance through inhalation, ingestion and skin contact. It is usitally considered about 2-3 times less toxic than hydrogen cyanide, but the exact lethal dose is imknown. In the developed coirrttries, the permissible workplace exposure limits in the air are 5 mg/m (as cyanide, time-averaged concentration in an 8-h shift), and 20 mg/m (as cyanide, peak concentration). 

As a class of compounds, the two main toxicity concerns for nitriles are acute lethality and osteolathyrsm. A comprehensive review of the toxicity of nitriles, including detailed discussion of biochemical mechanisms of toxicity and stmcture-activity relationships, is available (12). Nitriles vary broadly in their abiUty to cause acute lethaUty and subde differences in stmcture can greatly affect toxic potency. The biochemical basis of their acute toxicity is related to their metaboHsm in the body. Following exposure and absorption, nitriles are metabolized by cytochrome p450 enzymes in the Hver. The metaboHsm involves initial hydrogen abstraction resulting in the formation of a carbon radical, followed by hydroxylation of the carbon radical. MetaboHsm at the carbon atom adjacent (alpha) to the cyano group would yield a cyanohydrin metaboHte, which decomposes readily in the body to produce cyanide. Hydroxylation at other carbon positions in the nitrile does not result in cyanide release. 

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