Cyanide compounds exposure

Numerous biological and abiotic factors are known to modify the biocidal properties of free cyanide, including water pH, temperature, and oxygen content life stage, condition, and species assayed previous exposure to cyanide compounds presence of other chemicals and initial dose tested. There is general agreement that ... 

Hydrogen cyanide (HCN) is a colorless, rapidly acting, highly poisonous gas or liquid that has an odor of bitter almonds. Most HCN is used as an intermediate at the site of production. Major uses include the manufacture of nylons, plastics, and fumigants. Exposures to HCN may occur in industrial situations as well as from cigarette smoke, combustion products, and naturally occurring cyanide compounds in foods. Sodium nitroprusside (Na2[Fe(CN)5 N0]-2H20), which has been used as an antihypertensive in humans, breaks down into nonionized HCN. 

Oral exposure to cyanide usually results from accidental, homicidal, or suicidal ingestion of cyanide salts. Sodium cyanide and potassium cyanide are the most frequently studied cyanide compounds. Copper cyanide, potassium silver cyanide, silver cyanide, and calcium cyanide are other compounds that humans could encounter through oral or dermal exposure. Cassava roots and certain fruit pits contain compounds that can be broken down to form cyanide. Cassava roots form the staple diet of some populations in Africa, Central and South America, and Asia. However, it must be noted that cassava roots are notoriously deficient in protein and other nutrients and contain many other compounds, in addition to cyanide, that could be responsible for some of the observed toxic effects. Thiocyanate is a metabolite of cyanide that is formed in the body after exposure to cyanide compounds. When possible, all oral exposures are expressed as mg CN/kg/day. 

When comparing the available acute lethal toxicity information for cyanide compounds, it was concluded that, for oral exposure, the molar lethal toxicities of hydrogen cyanide, sodium cyanide, and potassium cyanide are similar. Rabbits appeared to be more susceptible to the lethal toxicity of these three compounds than rats (Ballantyne 1988). 

Hydrogen cyanide is a fire hazard and may be explosive when an excess of a strong acid is added to confined hydrogen cyanide. Solutions of some cyanide compounds are not stable and may decompose upon exposure to air or light. 

Caution. Because of the toxicity of metal cyanide compounds, all reactions must be carried out in a well-ventilated fume hood, in particular avoiding exposure to acid. 

The effects from cyanide poisoning are those of progressive histotoxic tissue hypoxia (Figure 10-2). The symptoms, signs, and physical findings are directly related to the dose of cyanide, the route of exposure, and the type of cyanide compound. In addition to the effects described below, cyanogen chloride also produces irritation of the eyes and... 

Response to a toxic dose varies from acute to chronic. An acute effect is generally characterized by a single, rather high exposure with a rapid onset of symptoms and a quick resolution to the crises (e.g., ingesting some cyanide compounds will lead rapidly to death). Chronic responses are those associated with low-level, repeated exposures over long periods with a gradual onset of symptoms. Some chronic effects are caused by the bioaccumulation of toxics (i.e., accumulation in the body tissues), like PCBs or by latency periods in which symptoms are not realized until long after exposure, as is the case with asbestosis. There is a wide spectrum of responses between acute and chronic affects. 

The purpose of the distillation method is to release the total cyanide from the water sample under controlled conditions and to convert it into a form in which it can be measured using one of the methods described. This means the total cyanide which occurs in organic and inorganic cyanide compounds or complexes and which can be split up under the same conditions as those prevailing in the environment (temperature up to 30 C, exposure to light, aeration, shift in pH, breakdown by microbes). The differentiation between total cyanide and easily released cyanide ( easily decomposed cyanide ) results from the choice of decomposition conditions in the distillation flask. 

Exposure to cyanides can be especially hazardous and requires an urgent response if gaseous hydrogen cyanide is inhaled or soluble cyanide compounds are ingested. Inhalation of dusts of cyanide compounds or skin absorption of these compounds is less hazard-... 

Unlike other closely related cyanide compounds, CK is not used extensively in industrial manufacturing or synthesis processes, although it may be detected as a trace pollutant in water sources as a consequence of chlorination. However, the National Institute for Occupational Safety and Health (NIOSH) has estimated that 1391 workers were potentially exposed in the workplace to CK in the USA through IH and dermal eontactwith CK where it was produced or used [National Oeeupational Exposure Survey (NOES) Survey 1981-1983]. ... 

As a class of compounds, the two main toxicity concerns for nitriles are acute lethality and osteolathyrsm. A comprehensive review of the toxicity of nitriles, including detailed discussion of biochemical mechanisms of toxicity and stmcture-activity relationships, is available (12). Nitriles vary broadly in their abiUty to cause acute lethaUty and subde differences in stmcture can greatly affect toxic potency. The biochemical basis of their acute toxicity is related to their metaboHsm in the body. Following exposure and absorption, nitriles are metabolized by cytochrome p450 enzymes in the Hver. The metaboHsm involves initial hydrogen abstraction resulting in the formation of a carbon radical, followed by hydroxylation of the carbon radical. MetaboHsm at the carbon atom adjacent (alpha) to the cyano group would yield a cyanohydrin metaboHte, which decomposes readily in the body to produce cyanide. Hydroxylation at other carbon positions in the nitrile does not result in cyanide release. 

---