Convulsions cyanide toxicity

Effects produced by exposure to acrylonitrile, particularly after acute exposures, are characteristic of cyanide toxicity. These effects can be detected in people exposed by evaluating signs and symptoms such as limb weakness, labored and irregular breathing, dizziness and impaired judgement, cyanosis and convulsions. While tests are not specific for acrylonitrile-induced toxicity, they do identify potential health impairment. Studies to develop more specific biomarkers of acrylonitrile-induced effects would be useful in assessing the potential health risk of acrylonitrile near hazardous waste sites. 

In addition to binding to cytochrome c oxidase, cyanide inhibits catalase, peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, and succinic dehydrogenase activities. These reactions may make contributions to the signs of cyanide toxicity (Ardelt et al. 1989 Rieders 1971). Signs of cyanide intoxication include an initial hyperpnea followed by dyspnea and then convulsions (Rieders 1971 Way 1984). These effects are due to initial stimulation of carotid and aortic bodies and effects on the central nervous system. Death is caused by respiratory collapse resulting from central nervous system toxicity. 

Mnemonic for Recognition of Cyanide Toxicity F-A-T R-E-D C-A-T-S Dizziness, Death, recent Depression history Confusion, Coma, Convulsions... 

Cyanide binds to the in the heme of the cytochrome aaj component of cytochrome c oxidase and prevents electron transport to Oj. Mitochondrial respiration and energy production cease, and cell death rapidly occurs. The central nervous system is the primary target for cyanide toxicity. Acute inhalation of high concentrations of cyanide (e.g., smoke inhalation during a fire) provokes a brief central nervous system stimulation rapidly followed by convulsion, coma, and death. Acute exposure to lower amounts can cause lightheadedness, breathlessness, dizziness, numbness, and headaches. 

Manufacture, Shipment, and Analysis. In the United States, sodium and potassium thiocyanates are made by adding caustic soda or potash to ammonium thiocyanate, followed by evaporation of the ammonia and water. The products are sold either as 50—55 wt % aqueous solutions, in the case of sodium thiocyanate, or as the crystalline soHds with one grade containing 5 wt % water and a higher assay grade containing a maximum of 2 wt % water. In Europe, the thiocyanates may be made by direct sulfurization of the corresponding cyanide. The acute LD q (rat, oral) of sodium thiocyanate is 764 mg/kg, accompanied by convulsions and respiratory failure LD q (mouse, oral) is 362 mg/kg. The lowest pubhshed toxic dose for potassium thiocyanate is 80—428 mg/kg, with hallucinations, convulsions, or muscular weakness. The acute LD q (rat, oral) for potassium thiocyanate is 854 mg/kg, with convulsions and respiratory failure. 

In humans, acute exposure to acrylonitrile results in characteristics of cyanide-type toxicity. Symptoms in humans associated with acrylonitrile poisoning include limb weakness, labored and irregular breathing, dizziness and impaired judgment, cyanosis, nausea, collapse, and convulsions (Baxter 1979). However, the doses that produce these effects were not clearly defined. Workers exposed to 16 to 100 ppm for 20 to 45 minutes complained of headaches and nausea, apprehension and nervous irritation (Wilson et al. 1948). The workers exposed to acrylonitrile vapors fully recovered. In a study with human volunteers exposed to acrylonitrile at doses of 2.3 and 4.6 ppm, no symptoms attributable to effects on the nervous system were observed (Jakubowski et al. 1987). 

SAFETY PROFILE Human poison by inhalation, skin contact, and intravenous routes. Experimental poison by ingestion, inhalation, skin contact, subcutaneous, intravenous, intraperitoneal, and intramuscular routes. A nerve gas. Vapor does not penetrate skin liquid does so rapidly. The primary physiological action is on the sympathetic nervous system, causing a vasoparesis (partial paralysis of the vasomotor nerves, which control the diameter of the blood vessels). Vapors when inhaled can cause nausea, vomiting, and diarrhea, which can be followed by muscular twitching and convulsions. Flammable when exposed to heat or flame can react with oxidizing materials. When heated to decomposition it emits very toxic fumes of POx, CN, and NOx. See also PARATHION and CYANIDE. 

DOT CLASSIFICATION 6.1 Label Poison SAFETY PROFILE A deadly human poison by ingestion. A experimental poison by ocular, subcutaneous, intravenous, intramuscular, and intraperitoneal routes. Experimental teratogenic and reproductive effects. Human systemic effects by ingestion convulsions, pulse rate increase. Mutation data reported. Reacts with acids or acid fumes to liberate deadly HCN. When heated to decomposition it emits very toxic fumes of K2O, CN", and NOx. See also CYANIDE. 

NIOSH REL (Nitriles) CL 6 mg/mVl5M SAFETY PROFILE Poison by ingestion, intraperitoneal, and intravenous routes. An experimental teratogen. A human skin irritant and allergen. In the preparation of sponge rubber, an azo compound is used that decomposes to form tetramethylsuccinonitrile or TMSN. Rats exposed to a concentration of 90 ppm exhibit their first convulsion after 1.5-2 hours or less. Rats exposed to concentration of 5.5 ppm exhibited their first convulsions in 27-31 hours and were dead in 31-46 hours. Absorbed by skin. The fatal dose in humans is thought to be about 25 mg/kg of body weight. TSN is slowly detoxified by the body. This nitrile is different from other nitriles in that thiosulfate is a poor antidote for intoxication. When heated to decomposition it emits toxic fumes of CN and NOx. See also NITRILES and CYANIDE. 

The acute toxicity of butyronitriles is thought to be due to release of cyanide through metabolism of the parent compound. Signs of acute butyronitrile intoxication including dyspnea, ataxia, and convulsions are similar to those noted with acute cyanide intoxication. The onset and duration suggests that these nitriles require metabolism to elicit toxicity. Cyanide and thiocyanate have both been found in urine and... 

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