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Hydrogen cyanide (CASRN 74-90-8
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0060
Hydrogen cyanide;
CASRN 74-90-8
Health assessment information on a chemical substance is included in IRIS
only after a comprehensive review of chronic toxicity data by U.S. EPA
health scientists from several Program Offices and the Office of Research
and Development. The summaries presented in Sections I and II represent
a consensus reached in the review process. Background information and
explanations of the methods used to derive the values given in IRIS are
provided in the Background Documents.
STATUS OF DATA FOR Hydrogen cyanide
File First On-Line 01/31/1987
Category (section) |
Status |
Last Revised |
|---|---|---|
| Oral RfD Assessment (I.A.) | on-line | 02/01/1993 |
| Inhalation RfC Assessment (I.B.) | on-line | 09/01/1994 |
| Carcinogenicity Assessment (II.) | no data |
_I. Chronic Health Hazard Assessments for Noncarcinogenic Effects
_I.A. Reference Dose for Chronic Oral Exposure (RfD)
Substance Name — Hydrogen cyanide
CASRN — 74-90-8
Last Revised — 02/01/1993
The oral Reference Dose (RfD) is based on the assumption that thresholds
exist for certain toxic effects such as cellular necrosis. It is expressed
in units of mg/kg-day. In general, the RfD is an estimate (with uncertainty
spanning perhaps an order of magnitude) of a daily exposure to the human
population (including sensitive subgroups) that is likely to be without
an appreciable risk of deleterious effects during a lifetime. Please refer
to the Background Document for an elaboration of these concepts. RfDs
can also be derived for the noncarcinogenic health effects of substances
that are also carcinogens. Therefore, it is essential to refer to other
sources of information concerning the carcinogenicity of this substance.
If the U.S. EPA has evaluated this substance for potential human carcinogenicity,
a summary of that evaluation will be contained in Section II of this file.
__I.A.1. Oral RfD Summary
Critical Effect |
Experimental Doses* |
UF |
MF |
RfD |
|---|---|---|---|---|
Rat Chronic Oral Howard and Hanzal,
|
NOAEL: 10.8 mg/kg/day cyanide converted to 11.2 mg/kg/day of hydrogen cyanide |
100 |
5 |
2E-2 mg/kg/day |
Weight loss, thyroid Rat Subchronic to Philbrick et al., 1979 |
LOAEL: 30 mg/kg/day CN cyanide (31 mg/kg/day hydrogen cyanide) |
*Conversion Factor: molecular weight conversion factor = 27/26 [MW HCN = 27; MW CN = 26]
__I.A.2. Principal and Supporting Studies (Oral RfD)
Howard, J.W. and R.F Hanzal. 1955. Chronic toxicity to rats of food treated with hydrogen cyanide. Agric. Food Chem. 3: 325-329.
An RfD of 1.6 mg/day is recommended based on cyanide (CN) content.
In this 2-year dietary study, rats (10/sex/group) were administered food fumigated with hydrogen cyanide (HCN). The average daily concentrations were 73 and 183 mg CN/kg diet. From the data reported on food consumption and body weight, daily estimated doses were 4.3 mg and 10.8 mg CN/kg bw. The average food CN concentrations were estimated based on the authors' data for concentrations at the beginning and end of each food preparation period and by assuming a first-order rate of loss for the intervening period. There were no treatment-related effects on growth rate, no gross signs of toxicity, and no histopathologic lesions.
Studies by Philbrick et al. (1979) showed decreased weight gain and thyroxin levels and myelin degeneration in rats at 30 mg/kg/day CN. Other chronic studies either gave higher effect levels or used the subcutaneous route (Crampton et al., 1979; Lessell, 1971; Herthing et al., 1960). Human data do not provide adequate information from which to derive an RfD because effective dose levels of chronically ingested CN are not documented. Therefore, the study of Howard and Hanzal (1955) provides the highest NOAEL, 10.8 mg/kg/day, for CN and is chosen for the derivation of an RfD for CN of 1.5 mg/day or 0.02 mg/kg/day.
Cyanide is metabolized extensively in the liver, indicating that the only relevant route of administration for quantitative risk assessment in the derivation of an oral RfD is the oral route of administration.
__I.A.3. Uncertainty and Modifying Factors (Oral RfD)
UF — According to the U.S. EPA (1985), an uncertainty factor of 100 is used to derive the RfD (10 for species extrapolation, 10 for sensitive population).
MF — A modifying factor of 5 is used to account for the apparent tolerance to cyanide when it is ingested with food rather than when it is administered by gavage or by drinking water.
__I.A.4. Additional Studies/Comments (Oral RfD)
Decreased protein efficiency ratio was produced by dietary cyanide treatment of rats during gestation, lactation, and postweaning growth phase in the Tewe and Maner (1981a) experiment; the dose level of cyanide (10.6 mg/kg/day) producing that effect is slightly lower than the currently accepted NOAEL of 10.8 mg/kg/day (U.S. EPA, 1985). Furthermore, Tewe and Maner (1981b) tested sows. Possible effects observed at about 9.45 mg/kg/day were proliferation of glomerular cells of the kidneys and reduced activity of the thyroid glands in the young sows. However, the number of animals in this experiment was very small. A Japanese study (Amo, 1973) indicated that 0.05 mg/kg/day of cyanide obtained from drinking water decreased the fertility rate and survival rate in the F1 generation and produced 100% mortality in the F2 generation in mice. However, these data are not consistent with the body of available literature.
__I.A.5. Confidence in the Oral RfD
Study — Medium
Database — Medium
RfD — Medium
The confidence in the study is medium because adequate records of food consumption and body weight were maintained, and animals of both sexes were tested at two doses for 2 years. The database is rated medium because a small but sufficient number of studies support the chosen study. Medium confidence in the RfD follows. Additional chronic/reproductive studies are needed to support a higher level of confidence in the RfD.
__I.A.6. EPA Documentation and Review of the Oral RfD
Source Document — U.S. EPA, 1984
Other EPA Documentation — U.S. EPA, 1985
Agency Work Group Review — 08/05/1985
Verification Date — 08/05/1985
__I.A.7. EPA Contacts (Oral RfD)
Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).
_I.B. Reference Concentration for Chronic Inhalation Exposure (RfC)
Substance Name — Hydrogen cyanide
CASRN — 74-90-8
Last Revised — 09/01/1994
The inhalation Reference Concentration (RfC) is analogous to the oral RfD and is likewise based on the assumption that thresholds exist for certain toxic effects such as cellular necrosis. The inhalation RfC considers toxic effects for both the respiratory system (portal-of-entry) and for effects peripheral to the respiratory system (extrarespiratory effects). It is expressed in units of mg/cu.m. In general, the RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily inhalation exposure of the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Inhalation RfCs were derived according to the Interim Methods for Development of Inhalation Reference Doses (EPA/600/8-88/066F August 1989) and subsequently, according to Methods for Derivation of Inhalation Reference Concentrations and Application of Inhalation Dosimetry (EPA/600/8-90/066F October 1994). RfCs can also be derived for the noncarcinogenic health effects of substances that are carcinogens. Therefore, it is essential to refer to other sources of information concerning the carcinogenicity of this substance. If the U.S. EPA has evaluated this substance for potential human carcinogenicity, a summary of that evaluation will be contained in Section II of this file.
__I.B.1. Inhalation RfC Summary
Critical Effect |
Exposures* |
UF |
MF |
RfC |
|---|---|---|---|---|
CNS symptoms and Occupational Study El Ghawabi et al., |
NOAEL: None LOAEL: 7.07 mg/cu.m (6.4 ppm) |
1000 |
1 |
3E-3 mg/cu.m |
*Conversion Factors and Assumptions — MW = 27. Assuming 25 C and 760 mmHg, LOAEL (mg/cu.m) = LOAEL (ppm) x 27/24.45 = 7.07 mg/cu.m. This is an extrarespiratory effect of a gas exposure. The LOAEL is based on an 8-hour TWA occupational exposure. MVho = 10 cu.m/day, MVh = 20 cu.m/day. LOAEL(HEC) = 7.07 mg/cu.m x (MVho/MVh) x 5 days/7 days = 2.5 mg/cu.m.
__I.B.2. Principal and Supporting Studies (Inhalation RfC)
El Ghawabi, S.H., M.A. Gaafar, A.A. El-Saharti, S.H. Ahmed, K.K. Malash, and R. Fares. 1975. Chronic cyanide exposure: A clinical, radioisotope, and laboratory study. Br. J. Ind. Med. 32: 215-219.
El Ghawabi et al. (1975) studied 36 male workers employed in the electroplating sections of three factories in Egypt. Cyanide exposure was from a plating bath that contained 3% copper cyanide, 3% sodium cyanide, and 1% sodium carbonate. Breathing zone air samples were taken to determine the levels of airborne cyanide to which the men were exposed. Twenty normal male volunteers of the same age group and socioeconomic status who had no exposure to cyanide were chosen as controls. None of the exposed or control workers currently smoked cigarettes. Participants were prohibited cyanide-containing foods during the course of the investigation. Complete medical histories were taken, and medical exams were performed. Thyroid function (uptake of radiolabeled iodine) was assayed and urinary levels of thiocyanate were recorded. The men were exposed for a duration of 5-10 years, although one man was exposed for 15 years. The breathing zone cyanide concentrations ranged from 4.2-12.4 ppm (4.63-13.69 mg/cu.m), with a mean of 6.4-10.4 ppm (7.07- 11.45 mg/cu.m), in the three factories. Symptoms reported more frequently in the exposed workers included (in decreasing order of frequency) headache, weakness, and changes in the senses of taste and smell. Lacrimation, abdominal colic, and precordial (lower stomach) pain, salivation, and nervous instability occurred less frequently. No attempt was made by the authors to analyze the incidence of these symptoms for concentration response. Twenty of the exposed workers had thyroid enlargement to a mild or moderate degree, although there was no correlation between the duration of exposure and either incidence or degree of enlargement. The thyroid function test did indicate significant differences in uptake (p < 0.001) between controls and exposed individuals after 4 and 24 hours. It is known that thiocyanate, which is elaborated from cyanide by the enzyme rhodanese, may block uptake of iodine by the thyroid and cause iodine-deficiency goiters (Hartung, 1983). A correlation was found to exist between urinary excretion of thiocyanates and breathing zone concentrations of cyanides. Although this study is limited by small sample size, it used well-matched controls and a biological index of exposure (urinary thiocyanate). These results document that chronic, low- level exposure to cyanide can be associated with CNS symptoms and thyroid effects. The lowest mean concentration recorded in the three factories, 6.4 ppm (7.07 mg/cu.m), is designated as a LOAEL.
__I.B.3. Uncertainty and Modifying Factors (Inhalation RfC)
UF — A factor of 10 is used for sensitive human subpopulations. A factor of 10 is also used for the lack of a NOAEL. Partial factors of 3 each are used for deficiencies in the database (lack of chronic and multigenerational reproduction studies) and for less than chronic duration. The total uncertainty factor is 1000.
MF — None
__I.B.4. Additional Studies/Comments (Inhalation RfC)
Several reports on occupationally exposed workers indicate that chronic exposure to low concentrations of cyanide can cause neurological, respiratory, cardiovascular, and thyroid effects (Blanc et al., 1985, and Chandra et al., 1980). Occupational exposure to cyanide occurs primarily via inhalation, although dermal exposure also can occur in the workplace. Although all these studies have limitations, they corroborate that long-term exposure to low levels of inhaled cyanide produces CNS and thyroid effects, thereby supporting the principal study of El Ghawabi et al. (1975). Hydrogen cyanide (HCN) is noted for its acute systemic toxicity, which would be expected to occur at concentrations well below those at which any portal-of-entry (respiratory tract) effects would be anticipated.
A group of 36 former workers with known long-term exposure to HCN fumes in a silver-reclaiming facility were studied by Blanc et al. (1985). In this retrospective study, the former workers were subjected to physical examinations, laboratory studies, and a questionnaire designed to determine levels of exposure, symptoms during employment, and current symptoms. Workers were categorized into low-, moderate-, or high-exposure groups depending on their work histories, but no exposure levels were quantified. The possibility existed for dermal exposure to cyanide. The median time elapsed since last employment at the facility was 10.5 months; the mean duration of employment was only 11 months. Statistically significant trends were found between the incidence of symptoms that occurred during active employment (headache, dizziness, nausea, and bitter almond taste) and those reported currently (after adjustment for time elapsed since exposure) and the qualitative index of exposure, suggesting a concentration-response relationship. Some of these symptoms persisted for 7 or more months after exposure. Even though none of the workers were found to have palpable thyroid gland abnormalities, mucosal erosion, or focal neurological deficits, clinical tests revealed decreases in vitamin B12 absorption and folate levels, and statistically significant increases in thyroid-stimulating hormone levels that, in combination with the central effects, suggest the occurrence of long-term toxic effects associated with exposure to cyanide.
Chandra et al. (1980) also reported that 23 workers chronically exposed to cyanide fumes in an electroplating and case-hardening factory experienced subjective signs of cyanide toxicity. Venous blood samples were taken at the end of the work shift, and urine samples were collected at the start of the work shift and every 2 hours throughout the shift. Breathing zone and atmospheric air samples were taken during the work shift. Smoking and nonsmoking workers were considered separately for both the exposed workers and the 20 nonexposed control workers that were matched for age, sex, and socioeconomic status. The atmospheric cyanide concentrations ranged from 0.2- 0.9 mg/cu.m with a mean of 0.45 mg/cu.m, and breathing zone cyanide concentrations ranged from 0.1-0.2 mg/cu.m with a mean of 0.15 mg/cu.m. Blood and urine cyanide and thiocyanate concentrations were elevated in the exposed workers as compared with the controls. The authors reported that the exposed workers complained of "typical symptoms" of cyanide toxicity, but these data were not presented. No effect levels were designated in this study.
Neurological and thyroid effects such as noted by El Ghawabi et al. (1975) also have been reported among populations consuming natural sources of cyanide, especially cassava. A major outbreak of over 1000 cases of paraparesis (partial paralysis affecting the lower limbs) was reported in Mozambique where the daily cyanide intake via cassava ingestion was estimated at 15-31.5 mg (approximately 0.2-0.45 mg/kg) (Casadei et al.,1984; Cliff et al., 1984). The clinical findings ranged from headache, vomiting, and slight weakness to blindness and paralysis of all four limbs. These symptoms, however, could not be definitely attributed to chronic cyanide intoxication because both patients and controls had similarly high blood levels of thiocyanate. Clear decreases in radioiodine uptake after cassava consumption was observed by DeLange and Ermans (1971) in a study of 131 inhabitants of Idjwi Island. Neuropathy and chronic cyanide intoxication from cassava ingestion has been reviewed (Osuntokun, 1981).
No statistically significant increases in the incidence of histopathological changes in the lungs or cardiovascular tissue were noted in rabbits continuously exposed to a single concentration of 0.5 ppm HCN for 1 or 4 weeks (Hugod, 1979).
Extensive involvement of the CNS in cyanide toxicity was demonstrated by Valade (1952) who exposed groups of four dogs to 50 mg/cu.m hydrogen cyanide in a varying number of 30-minute inhalation periods conducted at 2-day intervals. In the longest term exposure (19 inhalation periods), two of the four dogs died. Autopsies of the dead and surviving dogs all showed lesions in the brain consisting of vasodilation, hemorrhages, and various other cellular lesions.
The study of Lewis et al. (1984), in which rats were exposed to cyanogen, a cyanide dimer, was not considered appropriate for derivation of this RfC.
No chronic, developmental, or reproductive inhalation toxicity studies are available for HCN. Developmental studies employing parenteral administration have provided evidence that cyanide-containing compounds can produce developmental effects. Doherty et al. (1983) showed exencephaly and encephalocele in the litters of pregnant hamsters that had been injected with succinonitrile at 4.56 mmole/kg (365 mg/kg). Tewe and Maner (1981) conducted a developmental study in which 20 female rats were fed a potassium cyanide- supplemented diet through a 19-day prepregnancy period and gestation. After parturition, two female rats from each litter were fed the same diet during a 28-day postweaning period. Cyanide intake was estimated at 37 mg/kg/day in the adults, and serum thiocyanate levels were significantly increased over controls. The only effect noted was in the postweaning female rats in which a decreased protein efficiency ratio was claimed. These results suggest that adult rats may be less sensitive than weanling rats to subtle metabolic effects of cyanide.
HCN is readily absorbed following inhalation, oral, and dermal exposures in both humans and animals. Landahl and Herrmann (1950) demonstrated in humans that 58-77% of inhaled HCN is retained in the lungs and 13-22% is retained in the nose.
The major route of metabolism for HCN is detoxification by the mitochondrial enzyme, rhodanese, to the less toxic compound, thiocyanate, although chronic excessive blood levels of this metabolite may interfere with thyroid function (Hartung, 1983). Rhodanese is present in mitochondria of all tissues, particularly the liver (Dahl, 1989). Rhodanese is present in rat nasal mucosal tissues, particularly in the olfactory region, at a seven-fold higher concentration (on a per mg mitochondrial protein basis) than in the liver, the kinetic constants being higher here than in the liver (Dahl, 1989; Lewis et al., 1991). The localization of rhodanese activity in the respiratory system has been shown to vary considerably between species. Aminlari et al. (1994) demonstrated that dogs had greater rhodanese activity in the nasal cavity than in the lower respiratory tract, but sheep had the reverse for this distribution.
__I.B.5. Confidence in the Inhalation RfC
Study — Low
Database — Low
RfC -- Low
The principal study gives evidence for toxic chronic effects of inhaled cyanide in humans, the critical effects occurring in the CNS and thyroid. Although the symptomatology was mostly subjective and self-reported among a small population of workers, the data in this report was consistent with that reported in other occupational studies. Only a LOAEL is assigned from this study. The dose-response relationship of thyroid effects in humans caused by thiocyanate is characterized by this study or the database. It has been established that chronic exposure to cyanides may interfere with thyroid function, apparently through excessive blood levels of thiocyanate (Hartung, 1983). Therefore, the confidence in this study is low/medium. The database was assigned low confidence as there were no chronic inhalation studies and no multigenerational reproductive studies available even in the oral database. Although portal-of-entry tissues were not examined in any available long-term inhalation study with HCN, it is reasonably anticipated that the systemic effects would still occur at concentrations well below those at which any portal-of-entry (respiratory tract) effects would be anticipated. Even though a low confidence in the RfC follows from these deficiencies, it should be noted that the detoxifying capacity for cyanide of the human nasal cavity has been demonstrated but not quantified. The kinetic parameters of this capacity indicate that the human nasal cavity may be able to detoxify appreciable amounts of cyanide when inhaled at low concentrations (Lewis et al., 1991). Low confidence is assigned to the RfC.
__I.B.6. EPA Documentation and Review of the Inhalation RfC
Source Document — This assessment is not presented in any existing U.S. EPA document.
Other EPA Documentation — U.S. EPA, 1984, 1992
Agency Work Group Review — 02/10/1993
Verification Date — 02/10/1993
__I.B.7. EPA Contacts (Inhalation RfC)
Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).
_II. Carcinogenicity Assessment for Lifetime Exposure
Substance Name — Hydrogen cyanide
CASRN — 74-90-8
This substance/agent has not undergone a complete evaluation and determination under US EPA's IRIS program for evidence of human carcinogenic potential.
_III.
[reserved]
_IV. [reserved]
_V. [reserved]
_VI. Bibliography
Substance Name — Hydrogen cyanide
CASRN — 74-90-8
Last Revised — 11/01/1994
_VI.A. Oral RfD References
Amo, H. 1973. Effects of oral administration of cyanide and heavy metals in long term on breeding and chromosomes analyses of mice. Nagoya Shiritsu Diagaku Igakkai Zasshi. 24(1): 48-66.
Crampton, R.F., I.F. Gaunt, R. Harris et al. 1979. Effects of low cobalamin diet and chronic cyanide toxicity in baboons. Toxicology. 12: 221-234.
Hertting, G., O. Kraupp, E. Schnetz and S. Wuketich. 1960. Investigations about the consequences of a chronic administration of acutely toxic doses of sodium cyanide to dogs. Octa Pharmacol. Toxicol. 17: 27-43. (Eng. trans.)
Howard, J.W. and R.F. Hanzal. 1955. Chronic toxicity for rats of food treated with hydrogen cyanide. Agric. Food Chem. 3(4): 325-329.
Lessell, S. 1971. Experimental cyanide optic neuropathy. Arch. Opthalmol. 86(2): 194-204.
Philbrick, D.J., J.B. Hopkins, D.C. Hill, J.C. Alexander and R.G. Thomson. 1979. Effects of prolonged cyanide and thiocyanate feeding in rats. J. Toxicol. Environ. Health. 5: 579-592.
Tewe, O.O. and J.H. Maner. 1981a. Long-term and carry-over effect of dietary inorganic cyanide (KNC) in the life cycle performance and metabolism of rats. Toxicol. Appl. Pharmacol. 58(1): 1-7.
Tewe, O.O. and J.H. Maner. 1981b. Performance and pathophysiological changes in pregnant pigs fed cassava diets containing different levels of cyanide. Res. Vet. Sci. 30(2): 147-151.
U.S. EPA. 1984. Health Effects Assessment for Cyanides. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial Response, Washington, DC.
U.S. EPA. 1985. Drinking Water Criteria Document for Cyanide. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria Assessment Office, Cincinnati, OH for the Office of Drinking Water, Washington, DC.
_VI.B. Inhalation RfC References
Aminlari, M., T. Vaseghi, and M.A. Kargar. 1994. The cyanide-metabolizing enzyme rhodanese in different parts of the respiratory systems of sheep and dog. Toxicol. Appl. Pharmacol. 124: 67-71.
Blanc, P., M. Hogan, K. Mallin et al. 1985. Cyanide intoxication among silver-reclaiming workers. J. Am. Med. Assoc. 253: 367-371.
Casadei, E., P. Jansen, A. Rodrigues, A. Molin, and H. Rosling. 1984. Mantakassa: An epidemic of spastic paraparesis associated with chronic cyanide intoxication in a cassava staple area of Mozambique. 2. Nutritional factors and hydrocyanic acid content of cassava products. Bull. World Health Org. 62(3): 485-492.
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: 161-165.
Cliff, J., A. Martelli, E. Mondlane, A. Molin, and H. Rosling. 1984. Mantakassa: An epidemic of spastic paraparesis associated with chronic cyanide intoxication in a cassava staple area of Mozambique. 1. Epidemiology and clinical and laboratory findings in patients. Bull. World Health Organization. 62 (3): 477-484.
Dahl, A.R. 1989. The cyanide-metabolizing enzyme rhodanese in rat nasal respiratory and olfactory mucosa. Toxicol. Lett. (Amst). 45(2-3): 199-205.
Delange, F. and A.M. Ermans. 1971. Role of a dietary goitrogen in the etiology of endemic goiter on Idjwi Island. Am. J. Clin. Nutr. 24: 1354-1360.
Doherty, P.A., R.P. Smith, and V.H. Ferm. 1983. Comparison of the teratogenic potential of two aliphatic nitriles in hamsters: Succinonitrile and tetramethylsuccinonitrile. Fund. Appl. Toxicol. 3(1): 41-48.
El Ghawabi, S.H., M.A. Gaafar, A.A. El-Saharti, S.H. Ahmed, K.K. Malash, and R. Fares. 1975. Chronic cyanide exposure: A clinical, radioisotope, and laboratory study. Br. J. Ind. Med. 32: 215-219.
Hartung, R. 1983. Cyanides and nitriles. In: Patty's Industrial Hygiene and Toxicology, Third Revised Ed. p. 4845-4900.
Hugod, C. 1979. Effect of exposure to 0.5 ppm HCN singly or combined with 200 ppm CO and/or 5 ppm nitric acid on coronary arteries, aorta pulmonary artery, and lungs in the rabbit. Int. Arch. Occup. Environ. Health. 44: 13-23.
Landahl, H.D. and R.G. Herrmann. 1950. Retention of vapors and gases in the human nose and lung. AMA Arch. Ind. Hyg. Occup. Med. 1: 36-45.
Lewis, T., W.K. Anger, and R.K. Te Vault. 1984. Toxicity evaluation of subchronic exposures to cyanogen in monkeys and rats. J. Environ. Pathol. Toxicol. Oncol. 5: 151-163.
Lewis, J.J., C.E. Rhoades, P.-G. Gervasi, W.C. Griffith, and A.R. Dahl. 1991. The cyanide-metabolizing enzyme rhodanese in human nasal respiratory mucosa. Toxicol. Appl. Pharmacol. 108: 114-120.
Osuntokun, B.O. 1981. Cassava diet, chronic cyanide intoxication and neuropathy in the Nigerian Africans. Wld Rev. Nutr. Diet. 36: 141-173.
Tewe, O.O. and J.H. Maner. 1981. Long-term and carry-over effect of dietary inorganic cyanide (KCN) in the life cycle performance and metabolism of rats. Toxicol. Appl. Pharmacol. 58: 1-7.
U.S. EPA. 1984. Health Effects Assessment for Cyanides. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, for the Office of Emergency and Remedial Response, Washington, DC.
U.S. EPA. 1992. Drinking Water Criteria Document for Cyanide. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH, for the Office of Drinking Water, Washington, DC.
Valade, P. 1952. Lesions du systeme nerveaux central dans les intoxications chroniques experimentales par l'acide cyanhydrique gazeux. Academie National de Medecine. 136: 280-285.
_VI.C. Carcinogenicity Assessment References
None
_VII. Revision History
Substance Name — Hydrogen cyanide
CASRN — 74-90-8
| Date |
Section |
Description |
|---|---|---|
| 03/31/1987 | I.A.6. | Documentation corrected |
| 03/01/1988 | I.A.2. | Text revised |
| 03/01/1988 | III.A. | Health Advisory added |
| 08/01/1990 | IV.F.1. | EPA contact changed |
| 06/01/1991 | VI. | Bibliography on-line |
| 01/01/1992 | I.A.7. | Primary contact changed |
| 01/01/1992 | IV. | Regulatory actions updated |
| 02/01/1993 | I.A.7. | Minor text change |
| 03/01/1993 | I.B. | Inhalation RfC now under review |
| 09/01/1994 | I.B. | Inhalation RfC on-line |
| 09/01/1994 | VI.B. | Inhalation RfC references on-line |
| 11/01/1994 | VI.B. | Osuntokun, 1981 reference clarified |
| 04/01/1997 | III., IV., V. | Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementary Data were removed from IRIS on or before April 1997. IRIS users were directed to the appropriate EPA Program Offices for this information. |
| 01/09/2002 | I., II. | This chemical is being reassessed under the IRIS Program. |
_VIII. Synonyms
Substance Name — Hydrogen cyanide
CASRN — 74-90-8
Last Revised — 01/31/1987
- 74-90-8
- Aero Liquid HCN
- Cyclon
- Cyclone B
- Evercyn
- Formic Anammonide
- Formonitrile
- Hydrogen Cyanide
- Prussic Acid
- Zaclondiscoids