Hydrogen cyanide, toxic effects

Because of the small margin of safety, few controlled experimental studies of hydrogen cyanide toxicity have been conducted with human subjects. Barcroft (1931) exposed a man at a nominal concentration of 625 ppm for 1.5 min in an airtight chamber. Five minutes after the start of the experiment, the man developed a momentary feeling of nausea at 10 min, he had difficulty concentrating in a conversation. No toxic effects were observed in several human volunteers (number not reported) exposed at 240 or 360 ppm for 1.5-2 min (Grubbs 1917). 

Acetonitrile is slowly metabolized by cytochrome P450 in the liver to produce hydrogen cyanide. Toxicity is produced by the combined effect of circulating acetonitrile and cyanide. Cyanide exerts its toxicological effects by disrupting oxygen utilization at the cellular level. The disruption results in decreased oxygen utilization by body tissues and lactic acidosis. 

Toxicity The acute toxicity of cyanogen bromide is high. Toxic effects are similar to but not as severe as those of hydrogen cyanide. Toxic symptoms may include cyanosis, nausea, dizziness, headache, lung irritation, chest pain, and pulmonary edema, which may be fatal. Cyanogen bromide may cause chronic pulmonary edema. 

Hydrogen cyanide (prussic acid) is a liquid with a boiling point of 26°C. Its vapour is flammable and extremely toxic. The effects of acute exposure are given in Table 5.34. This material is a basic building block for the manufacture of a range of chemical products such as sodium, iron or potassium cyanide, methyl methacrylate, adiponitrile, triazines, chelates. 

The mechanism of hydrogen sulfide toxicity is in part similar to that of cyanide. Like cyanide, hydrogen sulfide can inhibit the enzyme cytochrome oxidase resulting in tissue hypoxia. Specific health effects are discussed in greater detail below. 

In spite of the complexity of dealing with atmospheres containing multiple toxicants, considerable progress has been made in understanding some of the effects from studies using rodents. For example, it is fairly well agreed that carbon monoxide and hydrogen cyanide appear to be additive when expressed as fractional doses required to cause an effect (21,22). Thus, as a reasonable approximation, the fraction of an effective dose of CO can be added to that of HCN and the time at which the sum becomes unity (100%) can be used to estimate the presence of a hazardous condition. 

Respiratory Effects. Breathing irregularities including Cheyne-Stokes respiration developed in two persons who fell into cisterns containing copper cyanide or potassium cyanide (Dodds and McKnight 1985 Trapp 1970) or whose hands were exposed to hydrogen cyanide (Potter 1950). The effects reflect the central nervous system toxicity of cyanide. 

An almond-like smell in the breath of a poisoned patient can warn a physician that the individual may be suffering from cyanide poisoning. Approximately 60-70% of the population can detect the bitter almond odor of hydrogen cyanide. The odor threshold for those sensitive to the odor is estimated to be 1-5 ppm in the air. However, even at high toxic concentrations up to 20% of all individuals are genetically unable to smell hydrogen cyanide (Snodgrass 1996). Some effects of cyanide that can also be used to monitor exposure are discussed in Section 2.5.2. 

A number of compounds act in synergy with cyanide to produce toxic effects. In smoke, hydrogen cyanide may interact with other toxicants (Birky and Clarke 1981). High blood cyanide levels were found in fire victims however, the carboxyhemoglobin levels were also high. Thus, it is difficult to assess the... 

In the section that follows, data needs are identified for cyanide forms for which toxicity data were available and were, therefore, summarized in Section 2.2. These forms include primarily sodium cyanide, potassium cyanide, and hydrogen cyanide. As seen from Figure 2-6, information is available regarding death, systemic effects of acute exposure, and neurological effects in humans after inhalation, oral, and dermal exposure to cyanide. In addition, information is available regarding chronic systemic effects in humans after inhalation and oral exposure. 

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