Teratogenicity cyanide

Developmental Effects. No studies were located regarding developmental effects in humans after any route of exposure and in animals after inhalation and dermal exposure. However, studies in rats (Singh 1981) and hamsters (Frakes et al. 1986a) fed a cassava diet suggested that cyanide may have teratogenic and fetotoxic effects at maternally toxic doses, but Singh (1981) indicated that the results... 

Nitriles are cyanogenic substances — substances that produce cyanide when metabolized. It is likely that nitriles are teratogens because of maternal production of cyanide in pregnant females. A study of the teratogenic effects on rats of saturated nitriles, including acetonitrile, propionitrile, and n-butyronitrile, and of unsaturated nitriles, including acrylonitrile, methacrylonitrile, allylnitrile, m-2-pcntenenitrile, and 2-chloroacrylonitrile, has shown a pattern of abnormal embryos similar to those observed from administration of inorganic cyanide.6... 

SAFETY PROFILE Moderately toxic by intraperitoneal route. An experimental teratogen. Other experimental reproductive effects. Mutation data reported. NitrUes usually have cyanide-Uke effects. See also CYANIDE. Easily oxidized and unstable. A storage hazard it polymerizes to an explosive yellow solid. When heated to decomposition it emits toxic fumes of CN and NOx. For fire and explosion hazards see CYANIDE. 

SAFETY PROFILE A poison by ingestion, intraperitoneal, and subcutaneous routes. An experimental teratogen. Mutation data reported. When heated to decomposition, or on contact with acid or acid fumes, it emits highly toxic homes of cyanides and SOx. See also THIOCYANATES. 

Carcinogenesis Bioassay (feed) Clear Evidence mouse, rat NCITR NCI-CG-TR-6,77. Cyanide and its compounds are on the Community Right-To-Know List. SAFETY PROFILE Suspected carcinogen with experimental carcinogenic, tumorigenic, and teratogenic data. Moderately toxic by intraperitoneal route. Human mutation data reported. When heated to decomposition it emits toxic fumes of NOx, CN, and Na20. 

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. 

SAFETY PROFILE Poison by ingestion and intravenous routes. Moderately toxic by inhalation and skin contact. Human mutation data reported. A skin and severe eye irritant. An experimental teratogen. Other experimental reproductive effects. When heated to decomposition or in reaction with water, steam, acid, or acid fumes it produces toxic fumes of CN, CT, and NOx. Used as an insecticide. See also NITRILES and CYANIDE. 

Acute and subchronic toxicity, teratogenicity, and biochemical mechanism studies of a series of structurally similar aliphatic nitriles indicated that although the toxicological profiles were generally the same for most of the compounds, there were unique differences, too (Johannsen and Levinska, 1986). In this respect, acetonitrile was different from the other nitriles within the homologous series. Nitriles liberated cyanide both in vivo and in vitro. Tanii and Hashimoto (1984a,b, 1985) observed a dose-cyanide liberation relationship in liver and hepatic microsomal enzyme system in mice pretreated with carbon tetrachloride. For most nitriles, the toxicity was greatly reduced by carbon tetrachloride pretreatment. By contrast, certain nitriles, exhibited an increase of toxicity as a result of such pretreatment. 

Sodium cyanide is a teratogen, causing fetus damage and developmental abnormalities in the cardiovascular system in hamsters (NIOSH 1986). 

Research is needed on low-level, long-term cyanide intoxication in mammals by oral and inhalation routes in the vicinities of high cyanide concentrations, especially on the incidence of skin dermatitis, nasal lesions, and thyroid dysfunction, and on urinary thiocyanate concentrations. These types of studies may provide a more valid rationale in establishing standards and threshold limit values for HCN and inorganic cyanide. Data are scarce on the carcinogenic, teratogenic, and mutagenic properties of cyanide, and on the distribution and transformation of cyanides in air, land, or water. Additional analysis of available information and more research in these areas is recommended. Finally, more research is needed... 

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