JACC Report 53 – Cyanides of Hydrogen, Sodium and Potassium, and Acetone Cyanohydrin vol.II

Abstract

JACC 053 Vol II : Cyanides of Hydrogen, Sodium and Potassium, and Acetone Cyanohydrin (CAS No. 74-90-8, 143-33-9, 151-50-8 and 75-86-5), Volumes I and II | November 2007

This report has been produced as part of the ECETOC Joint Assessment of Commodity Chemicals (JACC) programme. It presents a critical evaluation of the toxicity and ecotoxicity data on hydrogen cyanide (HCN), sodium and potassium cyanides (NaCN and KCN) and acetone cyanohydrin (ACH). Most of these cyanides under physiological and environmental conditions will be present as HCN, which is the common toxic species (ACH dissociates into acetone and HCN). HCN (liquid or gas) and ACH (liquid) are used as chemical intermediates. NaCN and KCN (solids) are mainly used in silver and gold mining and in electroplating. All of these forms of cyanide are soluble in water. Local releases of cyanide into water will be removed by volatilisation within a few days. Cyanide in water can exist as free HCN, or as complexes and salts, which may dissociate again to free HCN or adsorb onto sediment. Elimination of complex cyanides may take longer than free cyanide. In the global environment, cyanide is distributed to air and water. The main source of HCN in the atmosphere is the combustion of biomass. Airborne HCN undergoes slow photolysis, but the major part is absorbed into the oceans, where cyanide is removed by chemical and/or biological degradation. The overall atmospheric lifetime of HCN is 5 to 6 months. Aquatic organisms (fish, invertebrates and algae) are very sensitive to cyanides. In the laboratory, concentrations as low as a few µg/l were found to be toxic. Water birds survived higher concentrations. In mammals, cyanides (HCN) are very toxic regardless of the route of entry. HCN is rapidly absorbed and distributed within the body, and blocks the function of organs with great oxygen demand such as brain, heart and testes. Cyanides can also be lethal upon skin contact (even if only a small area is exposed) or following eye contact. There is no concern on the reproductive toxicity, and mutagenic or genotoxic activity of cyanides. No reliable carcinogenicity studies in animals exist (the quick onset of toxicity renders such studies impractical). The dose rate is a critical factor in cyanide poisoning. The total amount of cyanide that can be tolerated is greater when the dose rate is below the detoxification rate. In long-term animal studies, where the dose is delivered over an extended period (such as in drinking water or in the diet) rather than in a bolus, no adverse effects were seen at levels markedly above the acute lethal dose. Cyanide is normally detoxified in the body and eliminated as thiocyanate (in urine). Though less toxic than cyanide, chronic exposure to thiocyanate can exacerbate the effects of low iodine content in the diet and result in goitre. This is endemic in peoples who consume cassava as a Cyanides of Hydrogen, Sodium and Potassium, and Acetone Cyanohydrin (CAS No. 74-90-8, 143-33-9, 151-50-8 and 75-86-5)ECETOC JACC No. 53 2 significant part of their diet, e.g. populations of Central Africa. Cassava is rich in cyanogenic glucosides. Worker health studies with cyanides are inadequate for determining a no-adverse effect level in humans. Other studies (nutritional, epidemiological and clinical) indicate the absence of thiocyanate-mediated toxicity to the thyroid gland from daily doses equivalent to an occupational exposure (8-hour) of 7.5 mg CN?/m3 (time-weighted average) for humans with sufficient dietary iodine and normal kidney function. The acutely toxic cyanide concentration that can be tolerated by humans may be of the same order of magnitude. Sensitive sub-populations would include individuals with insufficient dietary iodine, insufficient thiosulphate supply (e.g. in the case of malnutrition) and impaired renal function. Tolerable exposure levels for cyanide salt dust may be lower (maximum 2 times, assuming 100% absorption). Neurological disorders are known to occur in populations consuming food containing cyanogenic glucosides (e.g. cassava), particularly in combination with poor nutrition (when cyanide detoxification is impaired). There is no causal link between occupational exposure to cyanide and subjective symptoms of neurotoxicity. Parkinson-like symptoms have been reported in cases of acute cyanide poisoning (e.g. attempted suicide). Repeated low-dose exposure to cyanide has no such effects. During the preparation of this document, draft versions were made available to SCOEL a and IPCS CICAD b. A hazard/risk assessment will be required under current OECD and proposed EU schemes c,d