Cyanide exposure

The most important rule when working with hydrogen cyanide is never to work alone. This appHes especially to sampling and opening lines and equipment. A second person must be in view at all times about 9 to 10 m away, must be equipped to make a rescue, and must be trained in first aid for hydrogen cyanide exposure. 

Barron, M.G. and I.R. Adelman. 1985. Temporal characterization of growth of fathead minnow (Pimephales promelas) larvae during sublethal hydrogen cyanide exposure. Comp. Biochem. Physiol. 81C 341-344. 

Homan, E.R. 1987. Reactions, processes and materials with potential for cyanide exposure. Pages 1-21 in B. 

Lennon, R.E., J.B. Hunn, R.A. Schnick, and R.M. Buress. 1970. Reclamation of ponds, lakes, and streams with fish toxicants a review. Food Agricul. Organ. United Nations, FAO Fish. Technol. Paper 100 57-61. Lesniak, J.A. and S.M. Ruby. 1982. Histological and quantitative effects of sublethal cyanide exposure on oocyte development in rainbow trout. Arch. Environ. Contam. Toxicol. 11 343-352. 

Ruby, S.M., D.R. Idler, and Y.P. So. 1986. The effect of sublethal cyanide exposure on plasma vitellogenin levels in rainbow trout (Salmo gairdneri) during early vitellogenesis. Arch. Environ. Contam. Toxicol. 15 603-607. 

Blank, T.L. 1983. Inhalation Pilot Study of Hydrogen Cyanide Exposure in Sprague-Dawley Rats. 

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. 

Yamanaka, S., Y.Takaku, and Y.Takaesu. 1991. Validity of salivary thiocyanate as an indicator of cyanide exposure from smoking. Bull. Tokyo Dental Coll. 32 157-163. 

Vitamin B12 is a chemical substance containing cyanide that is beneficial to your body because it prevents anemia (iron-poor blood). The cyanide is bound in Vitamin B12 so that it does not serve as a source of cyanide exposure and cannot harm you. You can find more information on the harmful effects of cyanide in Chapter 2. 

Blood and urine levels of cyanide and thiocyanate can be measured, and small amounts of these compounds are always detectable in blood and urine. We do not know the exact cyanide exposure levels linked with high levels of cyanide or thiocyanate in body fluids. Harmful effects can occur when blood levels of cyanide are higher than 0.2 parts per billion (ppb), but some... 

This section provides information regarding known health effects of cyanide exposure. Exposure to hydrogen cyanide (HCN) gas is most common by inhalation. In the discussion below, inhalation exposures are expressed as ppm hydrogen cyanide. Exposure to cyanide can also occur by inhalation of cyanogen gas, a dimer of cyanide. However, cyanogen breaks down in aqueous solution into cyanide ion (CN1) and OCN" ions (Cotton and Wilkinson 1980). The rate of the breakdown depends on pH and is... 

Respiratory Effects. Initially, respiration is stimulated, but later dyspnea occurs in patients admitted to a hospital after acute hydrogen cyanide exposure (Chen and Rose 1952 Peden et al. 1986 Potter 1950). The levels of exposure in these accidental poisonings were not provided. Nasal irritation was reported in volunteers exposed to 16 ppm cyanogen (8 ppm cyanide) for 6-8 minutes (McNemey and Schrenk 1960). No effects were reported at 8 ppm cyanogen (4 ppm cyanide). 

Carcinogenesis. No studies were located regarding carcinogenic effects of cyanide exposure in humans or animals following any route of exposure. Therefore, no mechanism of carcinogenesis can be discussed. 

Immunological and Lymphoreticular Effects. No studies were located regarding immunological/lumphoreticular effects in humans or animals after cyanide exposure by any route. Therefore, the potential for cyanide to cause immunological/lymphorcticular effects in humans cannot be assessed. 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

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