Environmental & Health Effects

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Description

Environmental and Health Effects of Cyanide
 This document is a general summary of cyanide's effects on human health and the environment, and is not intended to be a complete reference on all the environmental and health effects of cyanide.
Human Health Effects
Cyanide is produced in the human body and exhaled in extremely low concentrations with each breath. It is also produced by over 1,000 plant species including sorghum, bamboo and cassava. Relatively low concentrations of cyanide can be highly toxic to people and wildlife.
Cyanide is acutely toxic to humans. Liquid or gaseous hydrogen cyanide and alkali salts of cyanide can enter the body through inhalation, ingestion or absorption through the eyes and skin. The rate of skin absorption is enhanced when the skin is cut, abraded or moist; inhaled salts of cyanide are readily dissolved and absorbed upon contact with moist mucous membranes.
The toxicity of hydrogen cyanide to humans is dependent on the nature of the exposure. Due to the variability of dose-response effects between individuals, the toxicity of a substance is typically expressed as the concentration or dose that is lethal to 50% of the exposed population (LC50 or LD50). The LC50 for gaseous hydrogen cyanide is 100-300 parts per million. Inhalation of cyanide in this range results in death within 10-60 minutes, with death coming more quickly as the concentration increases. Inhalation of 2,000 parts per million hydrogen cyanide causes death within one minute. The LD50 for ingestion is 50-200 milligrams, or 1-3 milligrams per kilogram of body weight, calculated as hydrogen cyanide. For contact with unabraded skin, the LD50 is 100 milligrams (as hydrogen cyanide) per kilogram of body weight.
Although the time, dose and manner of exposure may differ, the biochemical action of cyanide is the same upon entering the body. Once in the bloodstream, cyanide forms a stable complex with a form of cytochrome oxidase, an enzyme that promotes the transfer of electrons in the mitochondria of cells during the synthesis of ATP. Without proper cytochrome oxidase function, cells cannot utilize the oxygen present in the bloodstream, resulting in cytotoxic hypoxia or cellular asphyxiation. The lack of available oxygen causes a shift from aerobic to anaerobic metabolism, leading to the accumulation of lactate in the blood. The combined effect of the hypoxia and lactate acidosis is depression of the central nervous system that can result in respiratory arrest and death. At higher lethal concentrations, cyanide poisoning also affects other organs and systems in the body, including the heart.
Initial symptoms of cyanide poisoning can occur from exposure to 20 to 40 ppm of gaseous hydrogen cyanide, and may include headache, drowsiness, vertigo, weak and rapid pulse, deep and rapid breathing, a bright-red color in the face, nausea and vomiting. Convulsions, dilated pupils, clammy skin, a weaker and more rapid pulse and slower, shallower breathing can follow these symptoms. Finally, the heartbeat becomes slow and irregular, body temperature falls, the lips, face and extremities take on a blue color, the individual falls into a coma, and death occurs. These symptoms can occur from sublethal exposure to cyanide, but will diminish as the body detoxifies the poison and excretes it primarily as thiocyanate and 2 amino thiazoline 4 carboxilic acid, with other minor metabolites.
The body has several mechanisms to effectively detoxify cyanide. The majority of cyanide reacts with thiosulfate to produce thiocyanate in reactions catalyzed by sulfur tranferase enzymes such as rhodanese. The thiocyanate is then excreted in the urine over a period of days. Although thiocyanate is approximately seven times less toxic than cyanide, increased thiocyanate concentrations in the body resulting from chronic cyanide exposure can adversely affect the thyroid. Cyanide has a greater affinity for methemoglobin than for cytochrome oxidase, and will preferentially form cyanomethemoglobin. If these and other detoxification mechanisms are not overwhelmed by the concentration and duration of cyanide exposure, they can prevent an acute cyanide-poisoning incident from being fatal.
Some of the available antidotes to cyanide poisoning take advantage of these natural detoxifying mechanisms. Sodium thiosulfate, administered intravenously, provides sulfur to enhance the sulfur transferase-mediated transformation of cyanide to thiocyanate. Amyl nitrite, sodium nitrite and dimethyl aminophenol (DMAP) are used to increase the amount of methemoglobin in the blood, which then binds with cyanide to form non-toxic cyanomethemoglobin. Cobalt compounds are also used to form stable, non-toxic cyanide complexes, but as with nitrite and DMAP, cobalt itself is toxic.
Cyanide does not accumulate or biomagnify, so chronic exposure to sublethal concentrations of cyanide does not appear to result in acute toxicity. However, chronic cyanide poisoning has been observed in individuals whose diet includes significant amounts of cyanogenic plants such as cassava. Chronic cyanide exposure is linked to demyelination, lesions of the optic nerve, ataxia, hypertonia, Leber's optic atrophy, goiters and depressed thyroid function.
There is no evidence that chronic cyanide exposure has teratogenic, mutagenic or carcinogenic effects