Hydrogen cyanide chronic

Howard, J.W., and R.F.Hanzal. 1955. Chronic toxicity to rats of food treated with hydrogen cyanide. Agric. Food Chem. 3 325-329. 

Dyspnea was observed in workers chronically exposed (5-15 years) to 6.4-10.4 ppm of an unspecified cyanide form evolved from sodium cyanide and copper cyanide during electroplating (El Ghawabi et al. 1975) and in workers exposed to 15 ppm hydrogen cyanide (14 ppm cyanide) in a silver-reclaiming... 

Cyanide has not been shown to accumulate in the blood and tissues following chronic oral exposure to inorganic cyanides. Following the treatment of groups of 10 male and 10 female rats with hydrogen cyanide in the diet at < 10.4 mg CN /kg/day for 2 years, virtually no cyanide was found in plasma or kidneys (Howard and Hanzal 1955). Low levels were found in erythrocytes (mean of 1.9 pg/100 g). 

Following chronic occupational exposure to 0.19-0.75 ppm hydrogen cyanide, 24-hour urinary levels of thiocyanate were 6.23 (smokers) and 5.4 pg/mL (nonsmokers) in exposed workers as compared with 3.2 (smokers) and 2.15 pg/mL (nonsmokers) in the controls (Chandra et al. 1980). This study demonstrates that tobacco smoking contributes to higher thiocyanate levels excreted in the urine. No studies were located regarding excretion of cyanide in animals after inhalation exposure to cyanide. 

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. 

Chronic-Duration Exposure and Cancer. Some reports of occupationally exposed workers indicated that low concentrations of hydrogen cyanide may have caused neurological, respiratory, and cardiovascular effects (Blanc et al. 1985 Chandra et al. 1980, 1988 El Ghawabi et al. 1975 Kumar et al. 1992). The route of exposure was predominantly inhalation, although dermal exposure can also occur in the work place. The studies, however, lacked either information about exposure levels or used small cohorts of workers. Studies in populations that used cassava roots as a main source of their diet described the neurological effects of cyanide consumption (Osuntokun 1972, 1980). However, these effects may be due to a recently identified substance, scopeletin, rather than due to cyanide (Obidoa and Obasi 1991). 

For chronic exposure in animals, only one oral study in rats (hydrogen cyanide) was located (Howard and Hanzal 1955). However, the reliability of this study is low because of the unstable cyanide levels in their feed throughout the experiment due to evaporation of cyanide. Furthermore, no effects were found in the study besides nondose-related changes in weight gain in female rats, but not in male rats. No chronic studies in animals were located for the inhalation and dermal routes. Therefore, data are not sufficient to derive MRL values for chronic exposure. Additional chronic-duration studies in animals would be helpful to determine thresholds for target organs. 

Chronic toxicity refers to a chemical s ability to inflict systemic damage as a result of repeated exposures over a prolonged time period, to relatively low levels of the chemical. Some chemicals are extremely toxic and are known primarily as acute toxins (e.g., hydrogen cyanide) some are known primarily as chronic toxins (e.g., lead). Other chemicals, such as some chlorinated solvents, can cause either acute or chronic effects. 

Chandra, H., B.N.Gupta, S.K.Bhargava, S.H.Clerk, and P.N.Mahendra. 1980. Chronic cyanide exposure A biochemical and industrial hygiene study. J. Anal. Toxicol. 4(4) 161—165. Chaturvedi, A.K., D.C.Sanders, B.R.Endecott, and R.M.Ritter. 1995. Exposures to carbon monoxide, hydrogen cyanide and their mixtures Interrelationship between gas exposure concentration, time to incapacitation, carboxyhemoglobin and blood cyanide in rats. J. Appl. Toxicol. 15(5) 357—363. 

The acute toxicity of hydrazoic acid through inhalation and other routes of exposure has been found to be high to very high. The symptoms and the intensity of poisoning are similar to sodium azide. It is, however, less toxic than hydrogen cyanide. In humans, inhalation of its vapors can produce irritation of eyes and respiratory tract, bronchitis, headache, dizziness, weakness, and decreased blood pressure (Matheson 1983). Prolonged exposure to high concentrations can result in collapse, convulsion, and death. An exposure to 1100 ppm for 1 hour was lethal to rats. Chronic exposure to a low level of this compound in air may produce hypotension. 

Poisons can be acute (with immediate effect, e.g., hydrogen cyanide (HCN)) or chronic (referring to the systemic damage done after repeated exposure to low concentrations over long periods of time, e.g., heavy metals like mercury, lead, cadmium and also vinyl chloride). The chemicals most often associated with chronic toxicity are also carcinogens (e.g., benzene, cadmium compounds), which are problematic because when, if at all, the... 

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. 

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