Cyanide industrial exposure

Cyanide can enter your body if you breathe air, eat food, or drink water that contains cyanide. Cyanide can enter your body through the skin, but this is common only for people who work in cyanide-related industries. Exposure to contaminated water, air, or soil can occur at hazardous waste sites. Once it is in your body, cyanide can quickly enter the bloodstream. Some of the cyanide is changed to thiocyanate, which is less harmful, and leaves the body in the urine. Some... 

Peden NR, Taha A, McSorley PD, et al. 1986. Industrial exposure to hydrogen cyanide Implications for treatment. Br Med J 293 538. 

Most cases of intoxication from industrial exposure have been mild, with rapid onset of eye irritation, headache, sneezing, and nausea weakness, light-headedness, and vomiting may also occur. Acute exposure to high concentrations may produce profound weakness, asphyxia, and death. Acrylonitrile is metabolized to cyanide by hepatic microsomal reactions. Deaths from acute poisoning result from inhibition of mitochondrial cytochrome oxidase activity by metabolically liberated cyanide. Inhalation of more moderate concentrations for a longer period of time leads to damage to the liver tissues in addition to central nervous system (CNS) effects. ... 

The symptoms of cyanide poisoning are well known from industrial exposure or exposure to cyanide in smoke from residential or industrial fires. Early signs and symptoms of acute cyanide poisoning include attempts of the... 

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). 

Hydrogen cyanide (HCN) is a colorless, rapidly acting, highly poisonous gas or liquid that has an odor of bitter almonds. Most HCN is used as an intermediate at the site of production. Major uses include the manufacture of nylons, plastics, and fumigants. Exposures to HCN may occur in industrial situations as well as from cigarette smoke, combustion products, and naturally occurring cyanide compounds in foods. Sodium nitroprusside (Na2[Fe(CN)5 N0]-2H20), which has been used as an antihypertensive in humans, breaks down into nonionized HCN. 

ACGIH (American Conference of Governmental Industrial Hygienists). 1996. Documentation of the Threshold Limit Values and Biological Exposure Indices Hydrogen cyanide. Seventh ed., ACGIH, Cincinnati, OH. 

Chandra, H., B.N.Gupta, S.K.Bhargava, S.H.Clerk and P.N.Mahendra. 1980. Chronic cyanide exposure—A biochemical and industrial hygiene study. J. Anal. Toxicol. 4 161-165. 

Hardy, H.L., W.M.Jeffries, M.M.Wasserman, and W.R.Waddell. 1950. Thiocyanate effect following industrial cyanide exposure—report of two cases. New Engl. J. Med. 242 968— 972. 

No acute-, intermediate-, or chronic-duration inhalation MRLs were derived for cyanide because of the limitations associated with the available studies. Many of the animal and human studies used lethality, or serious effects, such as coma, as the end point. Two epidemiological studies are available however, one study lacked good exposure data, and the other study involved occupational exposure in the electroplating industry where exposure to other chemicals may have occurred. 

Vesey et al. 1976) and a series of commercially important, simple, aliphatic nitriles (e.g., acetonitrile, propionitrile, acrylonitrile, n-butyronitrile, maleonitrile, succinonitrile) (Willhite and Smith 1981) release cyanide upon metabolism. These drugs and industrial chemicals have been associated with human exposure to cyanide and have caused serious poisoning and, in some cases, death. 

Cyanide in the body is biotransformed to thiocyanate quickly. People may also be exposed to thiocyanate from dietary, industrial, and medical sources. The plasma concentration of thiocyanate has also been used as an index of long-term exposure to cigarette smoke (Liu and Yun 1993). Some authors have determined thiocyanate in body fluids as a measure of cyanide exposure, while others measure cyanide concentrations in body fluids as a measure of cyanide exposure. 

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