Spacecraft Maximum Allowable Concentrations for Selected Airborne Contaminants Volume 4 (2000) / Chapter Skim
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B15 Hydrogen Cyanide
B15 Hydrogen Cyanide
Pages 330-365
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From page 330... ...
1 ppm = 1.10 mg/m3 1 mg/m3 = 0.91 ppm OCCURRENCE AND USE HCN is used mainly in the production of acrylonitrile, methyl methacrylate, sodium cyanide, and cyanuric chloride (Hartung 1982~. HCN can be generated when acid is added to cyanide salts (Gosselin et al.
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From page 331... ...
HCN concentrations reached 15 ppm in 10% ofthose f~res; the maximum HCN concentration detected was 40 ppm. Increased serum concentrations ofthiocyanate (a metabolite of HCN)
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From page 332... ...
Liver HCN concentrations in both dogs were half those in the brain; for the human, the liver HCN was two-thirds that in the brain. in contrast to those results from inhalation exposures, six rats given KCN or NaCN at 4 mg CN-/kg orally and an unspecified number of rabbits gavaged with 1 1 .9-20.3 mg CN /kg had five times the HCN in the liver as in the brain (Ahmed and Farooqui 1982; Ballantyne 1983~.
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(1984) found that exposing monkeys to HCN gas at 100-147 ppm for 30 min via face mask produced no appreciable decline in blood cyanide concentrations ~ h after the exposure.
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When rats were given potassium cyanide in drinking water at a daily dose of 40, 80, or 150 mg/kg for 13 w, both blood cyanide and urinary thiocyanate concentrations increased proportionally with the doses (Leuschner et al.
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The toxic effects of this direct-acting poison are similar in humans and in animals (NTP 1993~. Acute or Short-Term Exposures Neurological Effects Humans Being the most sensitive to tissue hypoxia, the brain is a primary target of cyanide toxicity.
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From page 336... ...
breathed the HCN atmosphere for 2 min without showing any symptoms, but a similar HCN atmosphere had "at other times caused dizziness." Also, no toxic effects were noted for human volunteers breathing HCN gas generated by dropping 0.75 oz of NaCN into acid per 1000 ft3 of space (estimated HCN concentration of 360 ppm)
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led to vomiting, convulsions, or death, but the dogs could tolerate HCN at 30 ppm. Guinea pigs could tolerate HCN at 200 ppm for 1.5 h without toxic signs.
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Prolonged hypoxia or anoxia, which can occur when HCN concentrations are high enough or the exposure duration is long enough, can result in permanent brain damage. Humans Long-term cerebellar spasmodic symptoms were documented in one man after he recovered from a coma after acute HCN intoxication (Fiessinger et al.,1938~.
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Another worker rushed to rescue the man and soon complained of headache, nausea, and throat irritation; when admitted to a hospital, the rescuer had crushing chest pain, profuse diaphoresis, vomiting, andtachycardia. Another worker who had been standing 3 m from the bath experienced throat irritation, nausea, vomiting, profuse diaphoresis, sinus bradycardia (36 beats per min)
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Effects on the Respiratory System Humans HCN poisoning in humans produces biphasic changes in respiration (i.e., initial rapid and deep respiration) , followed by slow and irregular respiration (Pannenter 1926; WOO]
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A 10-min exposure to HCN at 40 mg/m3 killed one of three dogs; the two survivors required 24 to 72 h to recover. None of four dogs exposed to HCN at 40 mg/m3 for ~ min died; however, one developed CNS sequelae manifested by weakness and "dementia" 48 h after the exposure.
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From page 342... ...
During the 2-mo study, breathing-zone air samples and urine samples were collected three times a week from each worker. Average HCN concentrations in the three facilities were 6.4 ~ 6.9, 8.1 it 8.2, and 10.4 ~ 10.9 ppm (mean ~ standard deviation)
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From page 343... ...
Lacking this information and other details, assessment of any correlation between symptoms and exposure concentrations is difficult. Nevertheless, the symptoms noted above are similar to those resulting from acute cyanide exposures; therefore, it cannot be ruled out that the clinical toxicity experienced by these workers might have resulted from periods of exposures to higher concentrations than those measured during the survey.
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Tn fact, Grabois measured only airborne HCN concentrations in an apricot-kerne] processing plant and did not assess health effects.
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However, in addition to long-tern~ cyanide exposure, deficiency of hydroxocobalamin, which is involved in one of cyanide's metabolic pathways, also is thought to contribute to this condition. Animals The effects of cyanide and thiocyanate on the CNS was assessed in rats that were fed a diet containing potassium cyanide at 500 ppm or potassium thiocyanate at 2240 ppm for ~ 1.5 mot Both compounds produced demyelination in the white matter of the spinal cord (Philbrick et al.
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From page 346... ...
Thus, the intake of HCN can be calculated from the NaCN values (Table 15-3~. If the intake of NaCN from drinking water is assumed to be roughly continuous, then an equivalent continuous inhalation exposure concentration of HCN that would produce the same body burden can be estimated Tom the amount of water consumed.
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From page 347... ...
Minimal changes were present in hematological, clinical chemistry, and urinalysis values; however, these changes were considered neither biologically significant nor related to the effects of cyanide. Weights ofthe left caudal epididymis in all groups of exposed males were significantly lower than those of the controls (see section on developmental toxicity)
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From page 348... ...
The cyanide exposure also suppressedbody-weight gain. Calculations of equivalent airborne HCN exposure concentrations reveal that daily ingestion of food containing KCN at 1500 ppm would give the same body burden of HCN as inhaling air containing HCN at 86.S ppm.
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As shown in Table 15-4, the equivalent inhalation exposure concentrations of HCN for rats were ~ .9, 5.9, or ~ 5.6 ppm; those for mice were 3.8, 12.1, or 34.7 ppm. Mild but statistically significant decreases in the weight of the left caudal epididymis were seen in the exposed male rats and in some of the mate mice; marginal reduction of sperm motility was seen in the exposed rats but not in the mice (see Table 15-5~.
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(1991) reported a higher mortality in rats exposed to both CO (2000 to 3750 ppm)
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352 1 us)
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353 oo oo oo ~C~ _ __ _ _ _ _ _ _ _ _ _ _ _ _ .
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The major difficulty in setting exposure limits for HCN is the lack of good dose-response inhalation data from human and animal studies. Even with the data from a few epidemiological studies on HCN-exposed workers, the correlation between exposure concentrations and cyanide toxicity cannot be established with certainty.
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From page 356... ...
ACs Set Based on CNS Effects in Humans The most relevant data for setting exposure limits come from the reports of 36 workers in three electroplating factories where cyanide salts were used (E! Ghawabi et al.
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NTP concluded that those changes are probably not biologically significant and are insufficient to decrease fertility in rats; however, NTP cautioned that "humans are considered to be relatively more sensitive than rats to such changes." Thus, 300 ppm in drinking water or the equivalent of ~ 6 ppm continuous (24-h) inhalation exposure was treated as the no-observed-adverseeffect level (NOAEL)
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From page 358... ...
358 SMACs FOR SELECTED Al~ORNE CONTAMINANTS RECOMMENDATIONS The major difficulty in setting exposure limits for HCN is the lack of controlled human inhalation exposure data, or good dose-response inhalation data from animals. It is recommended that experiments be carried out to better elucidate the concentration response of HCN at exposure concentrations at 20 ppm and below.
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359 CL cn^ o ._ Ct =: V A)
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1970. A review of cyanide concentrations found in human organs.
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1980. Chronic cyanide exposure - A biochemical and industrial hygiene study.
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Toxicokinetic aspects of chronic cyanide exposure in the rat. Toxicol.
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Occupational Exposure to Hydrogen Cyanide and Cyanide Salts (NaCN, KCN, and Ca(CN)
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1992. The in vivo effects of cyanide and its antidotes on rat brain cytochrome oxidase activity.
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1991. Validity of salivary thiocynate as an indicator of cyanide exposure from smoking.
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