Reproductive toxicity cyanide

Reproductive Toxicity. No data were located regarding reproductive effects of cyanide in humans. One animal study reported increased resorptions in rats following oral exposure to a cassava diet (Singh 1981). Because some human populations use cassava roots as the main source of their diet, further... 

Ballantyne and Salem discuss the experimental and human clinical toxicology of cyanides with particular reference to their potential for apphcation as chemical warfare weapons and use by terrorists. They consider repeated exposure toxicity as well as specific organ, tissue, and functional end-point toxicity. Among the functional end-point toxicities, they review neurotoxicity, cardio-toxicity, vascular toxicity, developmental and reproductive toxicity, and genotoxicity. They conclude this review of the toxicology of cyanide by describing emergency first aid and poison-control... 

Considering the epidemiological study (Ministry of Health, Mozambique 1984a,b) and the drinking water study with rats (NTP 1993) as co-critical studies, the RfDe for CK is 0.03 mg kg" d" . The critical effects identified in the two studies (nervous system and reproductive toxicity, respectively) are consistent with toxic effects of cyanides. 

The 12.5 mg/kg/day dose was identified as the LOAEL, based on all the reproductive effects observed in male rats, and the 4.5 mg/kg/day dose was identified as the NOAEL. This NOAEL was used with an uncertainty factor of 100 (10 for extrapolation of animals to humans and 10 for human variability) to derive an MRL. It is important to note that this MRL was based on a study using sodium cyanide, which is a soluble form of cyanide. In addition, a LOAEL of 1.04 mg/kg/day based on systemic and reproductive effects in dogs was identified (Kamalu 1993). However, this study was not used to derive the intermediate oral MRL because dogs are not a good model for human toxicity because dogs have very low levels of rhodenase, an enzyme which is used to detoxify cyanide. 

Administered in the diet for 13 weeks to rats at 12.5mg/kg/day, sodium cyanide caused a number of reproductive effects including decreases in testis weight and spermatid counts in males and alterations in estrous and proe-strous cycles in females. Adverse developmental effects have been observed in rodents at maternally toxic doses. ... 

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 Poison by ingestion, inhalation, and intraperitoneal routes. Moderately toxic by skin contact. Experimental reproductive effects. Combustible when exposed to heat or flame. To fight fire, use CO2, dry chemical. Thermally unstable. Contact with moisture (water), acids, or alkalies may cause a violent reaction above 40°. Concentrated aqueous solutions may undergo explosive polymerization. Mixture with 1,2-phenylenediamine salts may cause explosive polymerization. When heated to decomposition or on contact with acid or acid fumes, it emits toxic fumes of CN and NOx. See also CYANIDE and AMIDES. 

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. 

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. 

The systemic toxicity of CK results from its transformation to free cyanide thus, CK is expected to elicit the same toxic effects as cyanide. Therefore, in the absence of chemical-specific subchronic or chronic human or animal studies for CK, an oral RfDe can be derived based on results of experimental studies with HCN or other cyanides. The nervous system, reproductive system, and thyroid are considered target organs for chronic toxicity of cyanides. 

It should also be noted that cyanide toxicity to fish increases with any reduction in dissolved oxygen below 100%. The presence of zinc and ammonia results in a greater than additive increase in toxicity (Moran, 1998). Fish are about 1000 times more sensitive to cyanide than are humans. Even if the levels are less than lethal, there are still toxic effects, including physiological and pathological responses. For example, cyanide can reduce swimming ability, which will leave fish more vulnerable to predators, or interfere with reproductive capacity, which can lead to deformed offspring. It should be noted that cyanide toxicity in fish increases three- fold with a 12°C decrease in temperature. As well, 17 parts per thousand (ppt) of chloride ion or 8.8 ppt (Moran, 1998) is known to decrease the survival time (UNEP/ OCHA, 2000). 

---