United States Office of Water December 1981
Environmental Protection Regulations and Standards (WH-553) EPA-440/4-85-008
Agency Washington DC 20460
Water ' ' " ' ' '
vEPA An Exposure
and Risk Assessment
for Cyanide
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DISCLAIMER
This is a contractor's final report, which has been reviewed by the Monitoring and Data Support
Division, U.S. EPA. The contents do not necessarily reflect the views and policies of the U.S.
Environmental Protection Agency, nor does mention of trade names or commercial products
constitute endorsement or recommendation for use.
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REPORT DOCUMENTATION »• «E«>«T NO. 2.
PAGE EPA-440/4-85-008
. Title and Subtitle
An Exposure and Risk Assessment for Cyanide
. Authors) Fiksel, J.; Cooper, C.; Eschenroeder, A.; Goyer, M. :
Perwak, J.; Scow, K. ; Thomas, R.; Tucker, W. and Wood. M.
. Performing Organization Namo and Addre*a
Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
2. Sponsoring Organization Nam* and Address
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. Recipient's Accession No.
s. Report Date Final Revision
December 1981
c.
ft. Performing Organization Rapt. No.
10. Proiaet/Taik/Work Unit No.
II. Contracted or Grant(Q) No.
(0 C-68-01-3857
(G) C-68-01-5949
13. Type of Report & Period Covered
Final
14.
5. Supplementary Notes
Extensive Bibliographies
C. Abstract (Unite 200 word*)
I
This report assesses the risk of exposure to cyanide. This study is part of a program
to identify the sources of and evaluate exposure to 129 priority pollutants. The
analysis is based on available information from government, industry, and technical
publications assembled in March of 1981.
The assessment includes an identification of releases to the environment during
production, use, or disposal of the substance. In addition, the fate of cyanide in
the environment is considered; ambient levels to which various populations of humans
and aquatic life are exposed are reported. Exposure levels are estimated and
available data on toxicity are presented and interpreted. Information concerning all
of these topics is combined in an assessment of the risks of exposure to cyanide for
I various subpopulations.
. Document Analyst* a. Descriptors
Exposure
Risk
Water Pollution
Air Pollution
b. Identlfler»/Open-Ended Terms
Pollutant Pathways
Risk Assessment
c. COSATI neld/6roup
Effluents
Waste Disposal
Food Contamination
Toxic Diseases
Cyanide
. Availability Statement
Release to Public
19. Security Class (This Report)
Unclassified
20. Security Class (This Page)
21. No. of Pages
129
22. Price
$14.50
See instruction* on Reverse
OPTIONAL FORM 272 (4-77)
(Formerly NTIS-35)
Department of Commerce
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EPA-440/4-85-008
March 1981
(Revised December 1981)
AN EXPOSURE AND RISK ASSESSMENT
FOR CYANIDE
by
Joseph Fiksel
Charles Cooper, Alan Eschenroeder, Muriel Cover,
Joanne Perwak, Kate Scow, Richard Thomas,
William Tucker, and Melba Wood
Arthur D. Little, Inc.
Michael W. Slimak
U.S. Environmental Protection Agency
EPA Contract 68-01-3857
68-01-5949
Monitoring and Data Support Division (WH-553)
Office of Water Regulations and Standards
Washington, D.C. 20460
OFFICE OF WATER REGULATIONS AND STANDARDS
OFFICE OF WATER AND WASTE MANAGEMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
U.S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, IL 60604-3590
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FOREWORD
Effective regulatory action for toxic chemicals requires an
understanding of the human and environmental risks associated with the
manufacture, use, and disposal of the chemical. Assessment of risk
requires a scientific judgment about the probability of harm to the
environment resulting from known or potential environmental concentra-
tions. The risk assessment process integrates health effects data
(e.g., carcinogenicity, teratogenicity) with information on exposure.
The components of exposure include an evaluation of the sources of the
chemical, exposure pathways, ambient levels, and an identification of
exposed populations including humans and aquatic life.
This assessment was performed as part of a program to determine
the environmental risks associated with current use and disposal
patterns for 65 chemicals and classes of chemicals (expanded to 129
"priority pollutants") named in the 1977 Clean Water Act. It includes
an assessment of risk for humans and aquatic life and is intended to
serve as a technical basis for developing the most appropriate and
effective strategy for mitigating these risks.
This document is a contractors' final report. T.t has been
extensively reviewed by the individual contractors end by the EPA at
several stages of completion. Each chapter of the draft was reviewed
by members of the authoring contractor's senior technical staff (e.g.,
toxicologists, environmental scientists) who had not previously been
directly involved in the work. These individuals were selected by
management to be the technical peers of the chapter authors. The
chapters were comprehensively checked for uniformity in quality and
content by the contractor's editorial team, which also was responsible
for the production of the final report. The contractor's senior
project management subsequently reviewed the final report in its
entirety.
At EPA a senior staff member was responsible for guiding the
contractors, reviewing the manuscripts, and soliciting comments, where
appropriate, from related programs within EPA (e.g., Office of Toxic
Substances, Research and Development, Air Programs, Solid and
Hazardous Waste, etc.). A complete draft was summarized by the
assigned EPA staff member and reviewed for technical and policy
implications with the Office Director (formerly the Deputy Assistant
Administrator) of Water Regulations and Standards. Subsequent revi-
sions were included in the final report.
Michael W. Slimak,.Chief
Exposure Assessment Section
Monitoring & Data Support Division (WH-553)
Office of Water Regulations and Standards
IX
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TABLE OF CONTENTS
Page
LIST OF FIGURES vi
LIST OF TABLES vii
ACKNOWLEDGMENTS ix
1.0 RISK ASSESSMENT SUMMARY 1-1
2.0 INTRODUCTION 2-1
References 2-3
3.0 MATERIALS BALANCE 3-1
3.1 Introduction 3-1
3.2 Summary 3-1
3.3 Production 3-6
3.3.1 Hydrogen Cyanide 3-6
3.3.2 Sodium and Potassium Cyanide 3-6
3.3.3 Iron Blue ' 3-9
3.4 Air Emissions 3-9
3.4.1 Automobile Exhaust 3-9
3.4.2 Chemical Processing . 3-9
3.4.3 Other Sources 3-11
3.5 Discharges to Water 3-11
3.5.1 Organic Chemical Manufacturing 3-11
3.5.2 Metal Finishing 3-12
3.5.3 Iron and Steel Making 3-12
3.5.4 Ore Mining and Processing 3-13
3.5.4.1 Cyanidation of Gold-Silver Ores 3-13
3.5.4.2 Flotation of Copper-Moly and Lead-Zinc Ores 3-13
3.5.4.3 Releases from Ore Processing 3-13
3.5.5 Steam-Electric Power Plants 3-14
3.5.6 Road Salt 3-15
3.5.7 POTWs 3-15
References 3-16
4.0 ENVIRONMENTAL DISTRIBUTION 4-1
4.1 Introduction 4-1
4.2 Environmental Fate 4-1
4.2.1 Aquatic Fate 4-1
4.2.1.1 Volatilization 4-1
4.2.1.2 Hydrolysis 4-3
4.2.1.3 Biodegradation 4-4
4.2.1.4 Cyanide-Iron Complexing 4-6
4.2.1.5 Fate in the Vicinity of Sources 4-6
iii
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TABLE OF CONTENTS (Continued)
4.2.2 Atmospheric Fate 4-10
4.2.2.1 Background Concentrations 4-10
4.2.2.2 Urban Concentrations 4-12
4.2.3 Fate in Soil 4_13
4.3 Monitoring Data b-15
4.3.1 Introduction b-15
4.3.2 National Monitoring Results 4_16
4.3.3 Local Monitoring Results 4-18
References b-25
5.0 EFFECTS AND EXPOSURE— BIOTA 5_1
5.1 Effects on Biota • 5_^
5.1.1 Introduction 5_j_
5.1.2 Toxicity to Aquatic Organisms 5-1
5.1.2.1 Interpretation of Experimental Results 5-1
5.1.2.2 Toxicity of Free Cyanide 5-2
5.1.2.3 Toxicity of Other Cyanide Compounds 5-11
5.1.2.4 Bioaccumulation 5-14
5.1.2.5 Influence of Environmental Factors 5-14
5.1.3 Toxicity to Wildlife S-U
5.2 Biotic Exposure to Cyanide 5-15
5.2.1 Introduction 5-15
5.2.2 Effects Levels 5_17
5.2.3 Exposure Levels 5-18
5.2.4 Summary of Exposure to Freshwater Organisms 5-19
5.2.5 Summary of Potential Exposure to Marine Organisms 5-19
References 5-20
6.0 EFFECTS AND EXPOSURE— HUMANS 6-1
6.1 Human Toxicity 6-1
6.1.1 Introduction 6-1
6.1.2 Metabolism and Bioaccumulation 6-1
6.1.3 Animal Studies 6-5
6.1.3.1 Mechanism of Action 6-5
6.1.3.2 Carcinogenicity, Mutagenicity, and Adverse 6-5
Reproductive Effects
6.1.3.3 Chronic Effects 6-5
6.1.3.4 Subchronic Effects 6-6
6.1.3.5 Acute Effects 6-11
6.1.4 Human Studies 6-16
6.1.4.1 Overview 6-16
6.1.4.2 Controlled Human Studies 6-16
6.1.4.3 Epidemiologic Studies 6-18
6.1.5 Summary 6-20
iv
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TABLE OF CONTENTS (Continued)
6.2 Human Exposure 6_2,
6.2.1 Introduction 6-21
6.2.2 Ingestion 6-21
6.2.2.1 Food 6~2i
6.2.2.2 Drinking Water 5_22
6.2.3 Absorption 6-22
6.2.4 Inhalation 6-22
6.2.4.1 Occupational Exposure g_22
6.2.4.2 Exposure of the General Population 6-22
6.2.4.3 Exposure to Identified Subpopulations 6-25
6.2.5 Summary 6-27
References 6_2g
7.0 RISK CONSIDERATIONS 7-1
7.1 Risk Considerations for Humans 7-1
7.2 Risk Considerations for Non-Human Biota 7_2
7.2.1 Risk Considerations for Aquatic Organisms 7-3
7.2.2 Risk Considerations for Terrestrial Organisms 7-4
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LIST OF FIGURES
Figure
No. Page
4-1 Cyanide Hydrolysis at Temperatures from 08C to 30°C
for 7 < pH > 8 over 0-20 Days 4-5
4-2 Rate of Cyanide Complex Formation with Iron as a
Function of Cyanide Concentration in Water (CN/Fe - 1) 4-7
4-3 Example of Results of Fate Model: Cyanide Concentrations
Downstreams of a Small and Large Point Source on a Small 4-9
River
4-4 Estimated and Measured HCN Concentrations in Ambient
Air, New York City 4-14
4-5 Total Cyanide—85th Percentile Map 4-17
4-6 Locations of Steel Plants and Water Quality Monitoring
Stations Along the Beaver (Ohio) and Monongahela
(Pennsylvania) Rivers in the Vicinity of Pittsburgh 4-22
6-1 Metabolism of Cyanide in Mammalian Species 6-2
7-1 Comparison of Ranges of Uncertainty for Acute Effects
of and Exposure to Cyanide in Humans 7-2
vi
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LIST OF TABLES
Table
No. Page
3-1 Estimated Annual Environmental Releases of
Total Cyanide, 1976 3-3
3-2 Emissions from Hydrogen Cyanide Production 3-7
3-3 Estimated Environmental Releases from Production 3-8
3-4 Estimated Air Emissions of HCN from Chemical
Processing Operations 3-10
4-1 Locations of Water Quality Monitoring Stations in
the Pittsburgh Metropolitan Area 4-19
4-2 Sampling Distribution for Mean Levels of Total Cyanide
for 89 Water Quality Monitoring Stations in the
Pittsburgh Metropolitan Area, 1965 to 1979 4-20
4-3 Sampling Distribution of Mean Levels of Total Cyanide
in Industrial Effluent for 46 Water Quality Monitoring
Stations in the Pittsburgh Metropolitan Area, 1965 to
1979 4-21
4-4 Upstream-Downstream Comparison of Monitored Levels of
Total Cyanide in Sequential Order of Location Along
the Lower Monongahela River 4-24
5-1 Reported Acute Effects of Free Cyanide on Fish —
Flow through Experiments 5-3
5-2 Reported Acute Effects of Free Cyanide on Fish —
Static Experiments 5-5
5-3 Reported Effects of Free Cyanide on Aquatic Invertebrates 5-9
5-4 Reported Sublethal Effects of Free Cyanide on Fish 5-10
5-5 Reported Effects of Organic and Other Cyanide Compounds
on Fish 5-12
5-6 Reported Effects of Metal Cyanide Compounds on Fish 5-13
5-7 Reported Effects of Inhaled Cyanide and Cyanide
Compounds on Laboratory Animals 5-16
6-1 Effect of Prolonged Ingestion of KCN on Thyroid Weight
and Plasma Levels of Thyroid-Stimulating Hormone in
Protein-Deficient Rats 6-7
vii
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Table
No.
LIST OF TABLES - Cont'd
Page
6-2 Action of Long-Term Intake of SCN~ on the Thyroid
Size and the Organic Iodine Metabolism in Rats 6-8
6-3 Effect of Maternal SCN Ingestion on Thyroid Weight
in Rats 5 Days Post Partum 6-10
6-4 Lethality of HCN Inhaled by Experimental Animals 6-13
6-5 Tolerances Established for HCN and Ca(CN>2 in Food 6-23
6-6 Occupations with Potential Exposure to Cyanides 6-24
6~7 Estimated Human Exposure to Cyanide 6-28
viii
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ACKNOWLEDGMENTS
The Arthur D. Little, Inc., task manager for this study was Joseph
Fiksel. Other major contributors were Charles Cooper (biotic exposure),
Muriel Goyer (human effects), Joanne Perwak (human exposure), Richard
Thomas and Alan Eschenroeder (environmental fate), Kate Scow (biotic
effects), William Tucker (materials balance), and Melba Wood (monitoring
data).
ix
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1.0 RISK ASSESSMENT SUMMARY
The overall acute risks to humans as a result of the presence of
cyanide in the environment appear to be negligible. This is because of
the ability of the human to detoxify cyanide rapidly at low exposure
levels typically found in the environment. The chronic risks of human
exposure are not yet known. On the other hand, there may be significant
risks to aquatic biota exposed to cyanide in the vicinity of major point
source discharges. The important findings that lead to these conclusions
are summarized below.
The major point sources of cyanide releases to water are discharges
from Publicly Owned Treatment Works (POTWs), iron and steel production,
and the organic chemicals industries. These account for approximately
89% of the estimated 14,000 kkg discharged annually to surface water.
The metal finishing and organic chemicals industries account for 90% of
the influent to POTWs, so that the metals and organic chemicals industries
are the dominant sources of both direct and indirect aqueous discharges.
POTW effluents account for about 61 to 71% of direct discharges to water.
Another source of direct releases to surface water is non-point runoff
from the use of cyanide as an anti-caking agent road salt. The chemical
production process for cyanide does not appear to be a significant source
of cyanide releases to water.
Emissions of cyanide to air are conservatively estimated to be
approximately 20,000 kkg/yr., with over 90% due to automobile exhaust.
The resulting background concentrations of hydrogen cycnaide in air
would roughly be <65 ng/m^, assuming that rainout and degradation are
relatively slow removal processes. However, based on comparison with
carbon monoxide levels from automobile emissions, cyanide concentrations
in urban air could frequently be >20 ug/m3. Rainwater concentrations of
cyanide under these conditions would be on the order of 5 uS/1-
Hazards to aquatic organisims occur primarily in the immediate
vicinity of a major point source of cyanide. The long-term impact of
non-point runoff on cyanide levels in any particular water body is
expected to be negligible because the use of road salt is so widely
dispersed. However, pulses of non-point runoff due to storm events may
result in temporary elevated concentrations. The major fate mechanisms
affecting cyanide in water were found to be volatilization and biodegrad-
ation. Photolysis may also be an important process in transforming
complexed cyanide into free cyanide; however, the rate could not be
determined. Therefore, a conservative assumption is that all cyanide
discharged was in the free form. Rate constants were estimated for
volatilization and biodegradation, and these were applied to cyanide
effluents under a variety of assumptions concerning weather, discharge
rates, and recieving media. The resulting ambient concentration estimates
decreased rapidly as the distance increased from the source. These
results implied that cyanide exposure for aquatic life would be highly
localized in the vicinity of point source dischargers.
1-1
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Analysis of STORE! surface water monitoring data revealed that only
about 40% of observations across the U.S. exceed the EPA criterion
of 3.5 ug/1 for protection of freshwater life. However, it is probable
that waters near cyanide dischargers will show elevated cyanide concen-
trations. The Pittsburgh area was selected for detailed study of ambient
and effluent stations along one river, and increased cyanide levels were
noted at locations downstream of several steel plant effluents.
Cyanide is toxic to certain freshwater fish at concentrations of
approximately 10 ug/1, with chronic effects being reported at concen-
trations as low as 5 ug/1. Cold-water fish species appear to be more
snesitive than warm-water species, although laboratory results show some
exceptions. Aquatic invertebrates were found to be considerably less
sensitive than finfish in freshwater. For marine species, existing data
are insufficient to estimate absolute toxic levels. In freshwater fish,
chronic or sublethal effects generally occur at levels only slightly
below the acute LC$Q levels. This suggests that the chance of adverse
effects rises rapidly once the concentration has surpassed a certain
species-dependent threshold level.
Because cyanide degrades rapidly in the aquatic environment (half-
life on the order of tens of hours), the risks to aquatic life are
restricted to within a few river miles of major point sources.
However, because of the great variability in experimental conditons and
in species sensitivity to environmental stress, the percentage of fish
that could die at a certain environmental concentration cannot be accu-
rately predicted. Moreover, because of the sparse nature of ambient
monitoring data, it is presently not possible to estimate the percentage
of fish that are exposed to potentially toxic levels. Cyanides in
sewage do not presently occur at high enough levels to inhibit waste
treatment in POTWs. Risks to terrestrial wildlife are expected to be
small.
Cyanide's potency as an acute human toxicant is due to its inhibi-
tion of respiratory enzymes, resulting in anoxia. However, moderate
continuous doses of cyanide can be sustained without ill effects, since
detoxification mechanisms are relatively rapid. The human lethal
dose of hydrogen cyanide taken orally is believed to be between 50 and
90 milligrams or approximately 1 mg/kg for a 70-kilogram man. The lethal
dose of cyanide salts ranges between 200-250 milligrams or approxi-
mately 3 mg/kg for a 70-kilogram man. Inhalation of concentrations of
hydrogen cyanide >300 ug/1 are fatal within minutes; and inhalation of
concentrations of about 90-135 ug/1 may be fatal within 30-60 minutes.
Toxicological studies involving the effects of chronic cyanide
exposure have been inconclusive. No definitive studies of the carcino-
genic, mutagenic or teratogenic/reproductive effects of cyanide have
been reported. The only chronic feeding study showed no signs of
toxicity during a two-year study period. Although a number of reports
have implicated cyanide with several neuropathies, the evidence is not
conclusive.
1-2
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The maximum exposure of the general population from drinking water
sources is estimated to be 0.5 ng/day and the exposure of the general
population via inhalation is estimated to be about 1.25 ug/day. For
those exposed to industrial and automotive emissions, the exposure to
cyanide through inhalation may increase to 0.25-1.0 mg/day. All these
exposures are insignificant compared with the potential exposure from
naturally occurring sources, such as certain foods, and do not appear to
represent a significant risk to the general populations.
There are several subpopulations that may be exposed voluntarily to
elevated cyanide levels, primarily through the inhalation route. Exposure
to cyanide is estimated to range from 0.25 to 18.0 mg/day for subpopula-
tions of 14 million smokers. Exposure for 1,000-20,000 industrial workers
could range as high as 70 mg/day, assuming a concentration at the maximum
industry standards of 5 mg/m^. The total exposures for these subpopulations
are of the same magnitude as the lethal acute exposure level of 50-90
milligrams. However, the risk of acute effects is not significant
because of the long time period of exposure and the rapid detoxification
rate. Although these selected subpopulations may experience some risk
from chronic exposure, these risks are not quantifiable because of
insufficient data on the effects of chronic exposure.
1-3
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2.0 INTRODUCTION
The Office of Water Regulations and Standards, Monitoring and Data
Support Division, the U.S. Environmental Protection Agency, is conducting
a program to evaluate the exposure to and risk of 129 priority pollutants
in the nation s environment. The risks to be evaluated included poten-
tial harm to human beings and deleterious effects on fish and other
biota. The goal of the task under which this report has been prepared
is to integrate information on cultural and environmental flows of
speciric priority pollutants and to estimate the risk based on receptor
exposure to these substances. The results are intended to serve as a
rasulatory
This report provides a brief, but comprehensive, summary of the
production, use, distribution, fate, effects, exposure, and potential
risks of cyanide. Cyanides are known to be potentially harmful to most
living organisms, and are frequently found in the environment in low
concentrations due to both commercial use and natural occurrence The
purpose of this risk assessment was to quantify the exposure of humans
and non-human biota in the U.S. to cyanides, with primary emphasis on
water-related exposure routes, and to evaluate the possible health risks
associated with such exposure. The technical work described in this
^HSflT*; °rif*nally Perf°™ed ^ early 1979; the report was revised in
mid-1981 to reflect more recent materials balance and monitoring data.
The overall approach followed in this report integrates data on
sources, environmental fate, and toxic effects in order to identify
signincant pathways of exposure and risk (Arthur D. Little, Inc. 1980)
Since an assessment must be performed for the nation as a whole, it is
necessary to develop observations about the general distribution and
impact of a pollutant in the environment. Based upon rates of discharge
and of downstream degradation and volatilization, the fate of cyanide
discharged into surface water was described. Due to the short half-life
of cyanide in water the geographical distribution of this pollutant is
tar from uniform. Monitoring data, primarily from STORET, were used to
determine its environmental distribution and to investigate its presence
discharsers by comparison to
The known toxic effects of cyanide are mostly of an acute nature
although possible chronic effects were also investigated for both humans
and aquatic life. Therefore, the analysis of potential risks dealt
mainly with the likelihood of short-term exposure to concentrations of
cyanide in the lethal range. The element cyanide is found in the
environment in numerous chemical species. Cyanide occurs most commonly
2-1
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as hydrogen cyanide (HCN), potassium cyanide (KCN), or sodium cyanide
(NaCN). Aqueous solutions of cyanide salts will tend to form HCN at a
pH of 8 or less, whereas at higher pH cyanide appears mainly in the form
of the free ion (CN ). Cyanide also appears in organic complexes, but
this risk assessment has focused upon the presence of free cyanide,
either as HCN or CN~, since this is by far the most toxic form of the
substance.
The term "free cyanide" is used to denote cyanide in the form of
the simple CN~ anion, which can be destroyed (or measured) by alkaline
chlorination. Hence the term "cyanide amenable to chlorination" or
"cyanide A." The term "total cyanide" is used herein to describe all
forms of cyanide including cyanide complexes that are not readily
destroyed by alkaline chlorination. Wherever data permit, the concentra-
tion of HCN or CN" is distinguished from the concentrations of other
chemical species.
The report is organized as follows:
Chapter 3.0 presents a materials balance for cyanide
that considers quantities of the chemical consumed in
various applications, the form and amount of pollutant
released to the environment, particularly releases to
water, the environmental compartment initially re-
ceiving it, and, to the degree possible, the locations
and timing of releases.
Chapter 4.0 describes the ultimate distribution of
cyanide by considering the physicochemical and bio-
logical fate processes that transform or transport
cyanide, and by presenting monitoring data for the
nation as a whole, as well as for areas in the
vicinity of major cyanide dischargers.
Chapter 5.0 considers toxicological effects on and
exposure to biota, predominantly aquatic biota.
Chapter 6.0 describes the available data concerning
the toxicity of cyanide for humans and laboratory
animals and quantifies the likely level of human
exposure via major known exposure routes.
Chapter 7.0 presents a range of exposure conditions
for humans and other biota and compares these with
the available data on effects levels from Chapters 5.0
and 6.0, in order to assess the risk presented by
various exposures to cyanide.
2-2
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REFERENCE
Arthur D. Little, Inc. Integrated exposure risk assessment methodology.
Contract 68-01-3857. Washington, DC: Monitoring and Data Support
Division, Office of Water Regulations and Standards, U.S. Environmental
Protection Agency; 1980.
2-3
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3.0 MATERIALS BALANCE
3.1 INTRODUCTION
Cyanide discharges to the environment may result during the produc-
tion of various cyanide compounds or during transportation and use of
cyanide compounds, or they may be inadvertently formed, particularly
during combustion. In this chapter, the annual releases of cyanide to
the environment in the U.S. are estimated. The releases considered in-
clude HCN gas to the air, and total cyanides to water and solid waste
from major human sources. This risk assessment addresses direct dis-
charges of cyanide to water in greater detail, even though these appear
to be much smaller than atmospheric emissions of HCN gas.
The most recent available data were used in deriving emission esti-
mates. Many were based on data specifically for 1976, while others re-
flect conditions and practices during the mid-1970*s. There is no reason
to believe that cyanide discharges to the environment fluctuated sharply
during that period. Therefore, the estimated environmental releases are
believed to be reasonably representative.
3.2 SUMMARY
The production of 177,000 kkg of cyanide compounds and their subse-
quent (typically inplant) use in the organic chemical industry results
in a direct discharge to water of about 1300-1400 kkg/year, 10-14% of the
national total of direct discharges and 75% (about 10,000 kkg) of discharges
to POTWs. Production of cyanide or cyanide compounds is also estimated
to result in 182 kkg/year of acrylonitrile wastes injected into deep
wells and approximately 50 kkg/year of solid wastes of complex iron
cyanides from the manufacture of iron blue. If properly managed, these
wastes should contribute negligibly to cyanide in surface waters.
The production of iron and coke at iron- and steel-making facilities
results in the direct discharge of 1407 kkg cyanide per year, or 10-14% of
the estimated national total. There are relatively few (less than 100) major
coke and blast furnace facilities, and more than 50% of the production
capacity is located in 10 major steel-producing urban areas. Therefore,
iron and steel production plants are significant local sources. Effluents
from blast furnaces also account for about 2% of the cyanide in influ-
ent to POTWs.
The magnitude of aquatic discharges from metal finishing operations
with cyanide baths is uncertain, but recent data indicate that these
discharges comprise about 0.5% (about 65 kkg) of the direct aquatic
discharge to the nation's waters and 16% of the cyanide in influents to
POTWs. Most (90%) of the cyanides in POTWs are estimated to come from
the metal finishing and organic chemicals industry.
3-1
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The ore mining and dressing industry is estimated to release 2-20
kkg/year or only 0.01 to 0.2% of the national total of cyanide releases,
as a result of recent changes in wastewater management practices. How-
ever, the relatively large volumes of wastewater handled at only a few
mining operations using the froth flotation and cyanidation process may
still lead to locally significant discharges.
Cyanide is used as an anti-caking agent in road salt in the form of
iron blue, which may be degraded to simple cyanides. Releases from this
source to surface water are estimated to total 940 kkg. These are dis-
tributed widely yet have been reported to result in high concentrations
in surface waters. The collection and disposal of large-volume snow/salt
mixtures during street clearing may result in significant contamination
of small urban watersheds though there is no evidence that this has re-
sulted in high concentrations of cyanide.
Estimates of discharges from ash ponds at coal-fired power plants
are highly uncertain, but available data indicate that ash ponds may be
a significant source, both of direct discharge and input to POTWs.
Approximately 61-71% of the national load of cyanide to surface waters
is discharged from POTWs, making them the largest source type.
Although the chemical form of the cyanide ion, particularly whether
it is free or complexed, is significant to its toxicity and chemical be-
havior, relatively little information is available regarding the ratio
of free to total cyanide in major cyanide-containing waste streams.
Available analyses for iron and steel effluents indicate that the ratio
varies widely (38-90%, Huff & Huff, 1977); 23-36% of the total cyanide
at three Chicago POTWs was present as free cyanide.
Table 3-1 presents the most important known man-made sources of
cyanide to the environment. The sources of many of the estimates are
two reports by Versar, Inc. (1978 a,b), which contain details regarding
the rationale behind these estimates. The rationale for items estimated
independently, which include production losses, atmospheric emissions,
mining effluents, and iron and steel effluents, is discussed below.
The accuracy of most of the numbers in Table 3-1 is ±50% at best,
since they are based on national production of capacity figures multi-
plied by emission factors derived from sources of variable quality and
representativeness, rather than on widespread sampling of actual sources.
However, the estimates presented for organic chemicals, metal finishing,
the iron and steel industry, and POTWs are based on recent sampling and
analysis data, and may be used with greater confidence. Estimates of
atmospheric emissions by Eimutis jet al. (1978) are probably conserva-
tively high.
3-2
-------
TABLE 3-1. ESTIMATED ANNUAL ENVIRONMENTAL RELEASES OF TOTAL CYANiDF,, 1976
Source
OJ
I
"'A'lyiLlJ.onji' 1
-------
TABU; 3-1. ESTIMATED ANNUAL ENVIRONMENTAL RELEASES OF TOTAL CYANIDE, 1976 (Continued)
Source
Production and Processes
Inorganic Chemicals
Mining Operations
Photographic Chemicals
Metal Heat Treatment
Pigments
Metal Finishing
Anti-Caking Agents
Agricultural Pest Control
~
Air
A
A
A
A
A
A
62b
Wan»r
Dlrect POTW Ot!
2b, 208 NA
2.3a NA
A NA
NA
65h 20411'
^ NA
63b NA
llPl" ^PM £»S1I1 \ \l!* 1 Alr\
'"-* v1--" c
-------
TABLE 3-1. ESTIMATED ANNUAL ENVIRONMENTAL RELEASES 0V TOTAL CYANIDE, 1976 (Continued)
Source
and Processes
Automobile Exhaust
Incineration
Cigarette Smoke
I'OTW's
Air
18000b
8-80b
6-3AOe
Annual Re lease_(k kg/year)
Water
Direct POTW
*
*
6300-9800
Production or Use
Other (CN~ equivalent)
NA
U)
Oi
National releases from
quantifiable sources
19287-20892
10273-13853
Notes: *Not expected to be a significant source.
+No data available for quantification, but suspected to be a significant source
ANo data available for quantification; cyanide ion is likely to be present in the effluents
**Deep well Injection.
***Solid waste to landfill.
NA=not applicable.
aVersar, Inc. (I978a)
"Arthur D. Little, Inc. estimate
cEimutis et^ aJL. (1978)
dVersar, Inc. (1978b)
^-Surge-on General (1979)
Versar, Inc.
Versar, Inc.
(1981a)
(1981b)
1Versar, Inc. (1981c)
.Versar, Inc. (I98ld) (assuming all plants at Best Practicable Technology)
Communication from H. Healy (1981), EPA/MDSD, based on analysts of Versar, Inc. (1981d) and
U.S. '',PA (1980).
-------
3.3 PRODUCTION
3.3.1 Hydrogen Cyanide
Hydrogen cyanide is produced by two processes (U.S. EPA 1975a,
Lowenheim and Moran 1975). In the first process, HCN is produced by
reaction of natural gas and ammonia with air (Andrussow Process) :
2CH4 + 2NH3 + 302 - 2HCN -t- 6H 0
Eimutis et_ al. (1978) estimated significant air emissions from this pro-
cess, as shown in Table 3-1. However, in this analysis it was conserva-
tively assumed that all wastes from this process are waterborne (i.e.,
no air emissions), with raw waste loads of 0.7-2.1 kg/kkg of HCN. The
effluent may be treated by alkaline chlorination to give final effluent
containing 0.0002-0.005 kg/kkg of oxidizable cyanide (U.S. EPA 1975d)
and 0.5 kg/kgg of total cyanide.
In the second process, HCN is a byproduct from the reaction of
propylene, air, and ammonia to produce acrylonitrile (Sohio Process):
C3H6 + m3 * 1>5 °2 " CH2 * 2 HCN + 3H2° + byPr°ducts (aceto-
nitrile, hydrogen cyanide)
The off-gas from the purification section contains about 2 Ib of HCN
per ton of acrylonitrile (Monsanto 1973). This is incinerated to
destroy HCN before the .of f-gas is vented to the atmosphere. Assuming a
reasonable estimate of 95-99% efficiency, air emissions were estimated
at 0.02-0.1 Ib of HCN per ton of acrylonitrile (0.01-0.05 kg/kkg).
There are no wastewater effluents.
In 1976, about 75% of HCN was produced by the direct process (SRI
1976), leading to the estimated emission shown in Table 3-2.
3.3.2 Sodium and Potassium Cyanide
The alkali metal cyanides are produced by direct neutralization of
aqueous HCN with NaOH or KOH, respectively. This is a simple process,
which generates no wastes. Water is removed by drying, which provides
a potential for some losses during production. Though there are no
specific data with which to calculate emissions, the emissions can be
estimated by assuming that 10% is lost to effluent and that effluent
treatment by alkaline chlorination is 99% efficient (U.S. EPA 1975b).
The high efficiency of alkaline chlorination has been demonstrated in
metal finishing operations. On this basis the total discharge is esti-
mated to be 0.1% of the 26,420 kkg produced, or 26 kkg, as shown in
Table 3-3.
3-6
-------
TABLE 3-2. EMISSIONS FROM HYDROGEN CYANIDE PRODUCTION
Process/Source
Production of HCN
Untreated air emissions
Untreated wastewater effluent
kkg/year
Direct
Process
232,000
1 £.1 I.O1
Byproduct
Process
78,000
78
Total
310,000
240-565
Treated air emissions
Treated wastewater effluent
Total CN
Oxidizable CN
10-30
0.1-0.3
0.8-4.0
10.8-34
Source: Arthur D. Little, Inc.
3-7
-------
TABLE 3-3. ESTIMATED ENVIRONMENTAL RELEASES FROM
PRODUCTION OF CYANIDE COMPOUNDS, 1976
Production Aqueous Discharge
(kkg) (kkg)
Sodium Cyanide 26,420 26
Iron Blue 3,740 io
Zinc Cyanide 3 7-
Sodium and Potassium
Ferrocyanides 1,169
Potassium Cyanide 935
Other Heavy-metal i
Cyanides 701
In the form of complex cyanides.
Source: Arthur D. Little, Inc.
3-8
-------
The same assumptions may be used to estimate discharges of other
metal cyanides that are produced by similar processes, but in much smal-
ler quantities. Aqueous wastes from the manufacture of sodium and
potassium ferrocyanides may contain small amounts of complex cyanides,
but quantitative data are not available. About 1-2 kkg are estimated to
be released to the environment from these processes.
3.3.3 Iron Blue
The process for iron blue starts with sodium ferrocyanide (i.e., a
complex cyanide), ferrous sulfate, and ammonium sulfate. The end pro-
duct is also a complex and insoluble cyanide. Wastewater effluent is
treated to remove most of the cyanide as a solid product; therefore, the
small amounts of cyanide that are discharged will be solids that are
not removed by the solids separation systems. About 50-100 kkg of com-
plex iron cyanide is contained in the solid waste after treatment, and,
assuming good solid separation technology, (i.e., total suspended solids
in the waste effluent of 20-30 mg/1) from 1 kkg to 10 kkg of complex
cyanide would be discharged to the environment each year.
3.4 AIR EMISSIONS
The major air emissions of hydrogen cyanide and other volatile
cyanide-containing compounds occur either from incomplete combustion of
fuels in the presence of nitrogen compounds or from chemical processing
operations.
3.4.1 Automobile Exhaust
Cyanides have been detected in exhaust gases from automobiles; the
average rate of hydrogen cyanide emissions has been reported to be 12
mg/mile (General Motors 1975). The estimated fleet composite emission
factor for hydrocarbons in automobile exhaust was 8 g/mile in 1976 (U.S.
EPA 1975c). The resultant CN/HC emission ratio (1.5 x 10~3) multiplied
by the total annual hydrocarbon emissions of 12 x 106 kkg/year (U.S.
EPA 1978a) yields an estimate of HCN emissions of 18,000 kkg/year.
Applying the above-mentioned ratio to estimates of exhaust emissions
compiled by U.S. EPA (1978a), the largest cyanide emissions from automo-
bile exhausts would occur in areas of the highest traffic density, such
as California (210 kkg CN/year) or the combined states of New York and
New Jersey (1500 kkg tons CN/year). (The fate of such emissions is dis-
cussed in Section 4.2.).
Hydrocarbon emissions from vehicle exhaust have been steadily de-
creasing since 1976. U.S. EPA (1975c) estimated that vehicular emissions
or hydrocarbons would decrease to 2.7 gn/mile (667.) reduction by 1985.
Assuming that cyanide emissions will be reduced proportionately, sig-
nificant reductions in cyanide emissions from vehicular exhaust are ex-
pected.
3-9
-------
TABLE 3-4. ESTIMATED AIR EMISSIONS OF HCN FROM
CHEMICAL PROCESSING OPERATIONS
Manufacturing Source Emissions (kkg/year)
Methyl Methacrylate x 510
Acrylonitrile (HCN byproduct) 636
Hydrogen Cyanide 274
Total 2,420
Source: Eimutis _et al. (1978).
3-10
-------
3.4.2 Chemical Processing
Gaseous HCN emissions have been reported for three chemical process
industries (Eimutis et al. 1978) and are listed in Table 3-4. The emis-
sions in the table were estimated by considering the various process
streams and by carrying out materials balances of the constituents in
the streams rather than from actual air emissions measurements. Further-
more, Eimutis e_t al. (1978) adopted conservative assumptions in the cal-
culations, such as assuming that product losses were all released to the
air. In the estimates of waterborne emissions (Section 3.3), some of
these losses were attributed to water. Hence, the estimates should be
considered as approximations only.
3.4.3 Other Sources
Cyanides are also released into the atmosphere from a number of other
sources, such as petroleum refineries, steel mills, and solid waste in-
cinerators. However, very few emission measurements have been carried
out and their emission rates have not been estimated.
A potential source of gaseous HCN emissions is the solid waste in-
cineration of cyanide-containing plastics such as acrylonitrile. Approxi-
mately 80,000 kkg of cyanide in acrylonitrile are manufactured annually,
and eventually all of this becomes solid waste. If one assumes that 57,
of all solid waste is incinerated, 4,000 kkg of cyanides in acrylonitrile
are being burned annually, not all of which is released into the atmosphere.
Experiments conducted under ideal conditions indicate that the com-
bustion of acrylonitrile releases only 0.2% of the cyanide found in the
acrylonitrile. The remainder is apparently converted to carbon dioxide
(U.S. Bureau of Mines 1951).
Granted that combustion conditions in solid waste incinerators may be
less than ideal, a conservative upper bound estimate for HCN release from
acrylonitrile combustion is 27, of the CN contained in the acrylonitrile,
leading to an annual release of HCN to the atmosphere from acrylonitrile
combustion of 8-80 kkg/yr.
3.5 DISCHARGES TO WATER
3.5.1 Organic Chemical Manufacturing
The estimated release to water in Table 3-1, by Versar, Inc. (1981a),
is based on sampling and analysis of effluents from the organic chemical
industry. The rate of direct discharge reflects a treatment efficiency
of 97.6%, while the indirect discharge total results from an average treat-
ment efficiency of 16.7%. These treatment efficiencies are representative
of industry averages based upon a comparison of raw and final effluent
loading at the sampled facilities.
The organic chemical industry is difficult to characterize because
of the diversity of products and processes, and rapid changes in tech-
nology. Most of the facilities in this subcategory are part of complex
plants, which are integrated to produce, or use, products that are outside
of the conventional industry definition.
3-11
-------
There are approximately 2000 direct dischargers in this subcategory
and 1750 indirect dischargers. The industry is widely distributed in
the eastern half of the United States and on the West Coast, with
especially large numbers of facilities in the Delaware River Valley
northeastern New Jersey, and the Houston area.
3.5.2 Metal Finishing
The metal finishing industry, the largest consumer of inorganic CN
uses CN solutions at relatively high concentrations. The metal finishing
industry is comprised of numerous small "job" shops and larger volume
captive plating shops. Most of the small job shops are assumed to
discharge to POTWs.
Los Angeles, Detroit, Providence, and Grand Rapids are the leading
cities for metal plating employment with 12, 6, 4 and 3% of the nation-
wide employment, respectively (U.S. DOC 1976,1977).
Sources of cyanides from metal finishing processes include:
• cleaning solution;
• copper, zinc, brass, silver, and gold plating solutions; and
• metal stripping.
Cyanide concentrations in processing solution range from 0.1 g/1 to
1.073 g/1. Process rinse waters and batch dumping of cleaning solution
are the major effluent contamination pathways. The average cyanide
concentrations in the effluent of 55 shops sampled in the Providence
RI area was 8.4 mg/1, with values ranging from 0.01 mg/1 to 44 mg/l'
(Thibault et al. 1980). Cyanide is present in the effluent as a free
ion and/or complexed with metals such as iron, nickel, copper, and zinc.
The free ion is readily destroyed by conventional chlorine oxidation
treatment processes, while iron and nickel cyanide complexes are stable
and require more vigorous oxidizing conditions.
3.5.3 Iron and Steel Making
Three major subcategories of the iron and steel industry discharge
cyanide: by-product coke plants, iron making, and sintering. Of
these three, cyanide discharges from coking and iron making are much
greater than discharges from sintering. The cyanide loadings of Table
3-1 are based on the assumption that all facilities discharge at the
BPT (Best Practicable Technology) limitation. If the BAT (Best Available
Technology) limitation were achieved, the estimated total direct discharges
from the iron and steel industry would be reduced from 1407 kkg/year to
76 kkg/year.
3-12
-------
Iron and steel making is concentrated in a few areas of the country.
Iron and steel employment is greatest in the following cities: Pittsburgh
(16%), Gary (13%), Youngstown (6%), and Chicago (5%) (U.S. DOC 1976,
1977). In a survey of Illinois steelmakers, Huff and Huff (1977)
found that three plants discharging to the Calumet River contributed 516
Ib/day or about 90 kkg cyanide/year; the fraction of free cyanide present
in effluents ranged from 38% to 90%. The Pennsylvania Department of
Environmental Resources estimates a total point source loading of 3150
Ib/day (520 kkg/yr) in the lower 21 miles of the Monongahela River.
3.5.4 Ore Mining and Processing
In the mineral processing industry, cyanide is used as a solvent
in precious metal ore processing and as a reagent in the flotation of
copper-moly ores and lead-zinc ores.
3.5.4.1 Cyanidation of Gold-Silver Ores
Cyanidation is standard practice around the world. Cyanide solu-
tion is used to dissolve the precious metals, the solution is separated
from waste solids, and finally gold or silver is precipitated from the
clear solution with zinc dust.
United States companies using this practice in 1976 were: Homestake
Mining Co. - Lead, South Dakota; Carlin Gold Mining Co. (Division -
Newmont Corp.) - Near Elko, Nevada; Cortex Gold Mines - Near Elko,
Nevada (the major operations at this mine closed in 1978); Magma
Copper Co., San Manuel Division - Arizona.
3.5.4.2 Flotation ofCopper-Moly and Lead-Zinc Ores
In the processing of copper-molybdenite ores, the bulk sulfite
flotation concentrate containing iron, copper, and moly-sulfides is
processed in a second stage of flotation in which cyanide is used to
depress the iron and copper minerals so that the moly can be floated.
At least 12 major mines in the U.S. were using this practice in 1976.
Most of these mines were in Arizona, with others in Nevada, New Mexico,
and Utah.
In processing lead-zinc ores (and copper, lead, zinc ores), cyanide
is used to depress the zinc minerals while the lead minerals are floated.
Nine major mines in the U.S. were using this process in 1976, located in
Colorado, Missouri, Idaho, Utah, and Washington.
3.5.4.3 Releases from Ore Processing
In general, good process control and the retention of mill wastes
in tailings ponds to promote oxidation have been adequate for the reduc-
tion of cyanide to less than detectable concentrations in the final ef-
fluents. Many of the mining operations in which cyanide is used as a
solvent or as a reagent have zero discharge; that is, all solution is
3-13
-------
recycled and reused and nothing is discharged. Zero discharge is defined
as Best Practicable Technology (BPT) for the cyanidation process in arid
climates (40CFR440.22).
All of the gold-silver cyanidation plants (Homestake, Carline, Cortez,
Magma) are reported to have zero discharge. At the Homestake Mine, a
$15 million tailings disposal and solution recycle system was completed
in 1976 (Sisselman 1976). Operations that use cyanide as a reagent in
arid climates have zero discharge. These include essentially all of the
mines processing copper-moly ores in Arizona, Utah, Nevada, and New
Mexico.
At some of the lead-zinc ore mines and mills, effluent is discharged
from tailings ponds. However, when the effluents contain cyanide, they
are treated to remove it or reduce its concentration. Cyanide is added
as an ore depressant at concentrations ranging from 1-50.4 mg/1 (average -
11 mg/1). Below is a list of some lead/zinc mines, their mine capacity,
and CN discharges (U.S. EPA 1979):
Mine
Location
Missouri
Missouri
Utah
Missouri
New York
Idaho
Maine
Ore Processed
(kkg/year)
1,032,000
972,300
•>
1,482,000
1,009,100
709,000
209,000
_ Nature of Discharge
Treated mine effluent
Secondary pond effluent
Treated effluent
Final discharge
Lagoon overflow
Treated tailings water
Average
[CN] mg/1
(# of samples)
<0
<0
0
<0
<0
.02
.02
.06
.02
.1
(N
(N
(N
(N
(N
«
sat
49)
2)
5)
10)
9)
<0.03
(93% treatment efficiency)
Final treated effluent <0.02
These data reflect 5,413,000 (37%) of the 14,600,000 kkg of Pb/Zn ore
processed at mines that discharge to surface waters in the United States
and, therefore, can be regarded as representative of national conditions.
By incorporating the above information with data on water use by
mining industries (U.S. Bureau of Census 1972), it is estimated that
the annual discharge of CN associated with mining operations is less
than 2 kkg/year. Versar, Inc. (1981b) estimated the cyanide discharges
from the ore mining and dressing industry at 20 kkg/yr, based on flow-
weighted average concentration of 18 ug/1.
3.5.5 Steam-Electric Power Plants
The estimates for ash pond discharge in Table 3-1 are based on analy-
sis of a small number of waste streams, and, therefore, are approxima-
tions only. The high combustion temperatures and well controlled com-
bustion conditions in power plant boilers suggest that utility boilers
3-14
-------
are not a major source of cyanide. Nonetheless, ash ponds have been ob-
served to contain elevated levels of cyanide (U.S. EPA 1978b). There are
no analytical data to indicate the degree of complexation of cyanide in ash
ponds, but it may be roughly similar to that in iron and steel effluents.
Coal consumption, and corresponding discharge of cyanide from ash
ponds, is concentrated in the Appalachian and North Central states. In
1976, 60% of coal produced in the U.S. was burned in Ohio, Pennsylvania,
Illinois, Indiana, West Virginia, Kentucky, Michigan, Missouri, North
Carolina, and Tennessee (U.S. DOE 1977). Since very sparse data exist
on cyanide in power plant waste streams, there is a high degree of un-
certainty associated with the estimates in Table 3-1.
3.5.6 Road Salt
Ferrocyanides and iron blue are added to road salt to prevent
it from caking. The salt is spread on the road surface during the winter
months in the Northern U.S. Virtually all of this salt is probably washed
off the roads and into streams and storm sewers. Due to the fact that
much of the road salt used in the U.S. is distributed on highways in
sparsely populated areas, it is probable that cyanides in road salt are
distributed diffusely across the country. The metropolitan areas with
the greatest reported usage of road salt are Detroit (27 kkg CN/year);
New York (17 kkg CN/yr); Rochester (16 kkg CN/yr); Chicago (13 kkg CN/yr);
and Milwaukee (12 kkg CN/yr)(Salt Institute 1975). The CN released from
road salt is in the complexed form of ferrocyanide.
3.5.7 POTWs
The discharge of cyanide from POTWs has been estimated by three
different methods, all based on data reported by Feiler (1980), compiled
from sampling and analysis at 20 POTWs. One estimation approach was
to take the average effluent cyanide concentration (210 yg/1) times
the total effluent flow rate of all POTWs in the U.S. (34,000 MGD;
Marshall 1978) resulting in an estimated cyanide discharge of 9800 MT/
year. This approach is based on the assumption that the effluents con-
centrations at the 20 plants surveyed were representative of all plants
across the country. An alternate approach is to use the total cyanide
discharged from the 20 plants (169 MT/year) and the fact that the histori-
cal flow rates of these plants represent 2.7% of total U.S. POTW ef-
fluent flow to estimate a total discharge of 6300 MT/yr. This approach
is probably the most accurate if the 20 plants are representative of all
plants on a flow capacity basis. Finally, the percent removal of cyanide
in the 20 plants was approximately 15%. Then for the total influent
to POTWs given by Table 3-1 of 18405 kkg/yr., the resultant discharge of
cyanide would be 6400 kkg/yr. The similarity of the discharge estimates
is encouraging, but all are based on the assumption that the 20 plants
surveyed by Feiler (1980) are representative of all U.S. POTWs. Effluents
from three treatment plants in Chicago were analyzed in 1975, and 23-36%
of the total cyanide was present as free cyanide.
3-15
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REFERENCES
Arthur G. McKee & Co. Water pollution abatement technology: Capabili-
"''1 ^ ^^
Eimutis, E.G.; Quill, R.P.; Rinaldi, G.M. Source assessment: Non-criteria
pollutant emissions (1978 update). Report EPA-600/2-78-004t. Washington
DC: U.S. Environmental Protection Agency; 1978. '
Feiler, H. Fate of priority pollutants in publicly owned treatment works
Interim report. EPA-440/ 1-80-301. Washington, DC: Effluent Guideline?'
Division, U.S. Environmental Protection Agency; 1980.
General Motors, Inc. General Motors emissions control system develop-
ment. Report to the U.S. Environmental Protection Agency; 1975.
Huff L.L.; Huff, J.E. The economic impact of alternative CN standards
in Illinois. Report No. 77/03. State of Illinois Institute for
Environmental Quality; 1977.
Marshall, R.A. Statistical support for analytical survey of publiclv
oTlL^TT PlantS> °raft final rep°rt' Part l' Co^"« EPA 68-
01-3887. Washington, DC: U.S. Environmental Protection Agency; 1978.
Monsanto Research Corporation. Potential pollutants from petrochemical
processes. Report MRC-DA-406. Control Systems Laboratory! U.S. En^iro
nental enviro
.
nental Protection Agency; 1973.
handbook. Menlo
DC:
3-16
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U.S. Bureau of the Census. Water use in mineral industries. Census of
mineral industries. Washington, DC: U.S. Department of Commerce; 1972.
U.S. Department of Commerce (U.S. DOC). County business patterns, 1975
and 1976. Washington, DC: U.S. DOC; 1976 and" 1977.
U.S. Department of Energy (U.S. DOE). Bituminous coal and lignite
distribution. Energy data reports. Washington, DC: U.S. DOE; 1977.
U.S. Environmental Protection Agency (U.S. EPA). Development document
for effluent limitations guidelines. Significant inorganic products
segment of the inorganic chemicals manufacturing point source category.
Washington, DC: Effluent Guidelines Division, U.S. EPA; 1975a.
U.S. Environmental Protection Agency (U.S. EPA). Development document
for effluent limitations guidelines and proposed new source performance
standards for the electroplating point source category. Report EPA
440/1-75/040. Washington, DC: U.S. EPA; 1975b.
U.S. Environmental Protection Agency (U.S. EPA). Supplement No. 5 for
compilation of air pollutant emission factors. 2nd ed. AP-42.
Washington, DC: U.S. EPA; 1975c.
U.S. Environmental Protection Agency (U.S. EPA). Development document
for interim final effluent guidelines and new source performance
standards for the significant organic products segment of the organic
chemicals manufacturing point source category. Washington, DC:
Effluent Guidelines Division, U.S. EPA; 1975d.
U.S. Environmental Protection Agency (U.S. EPA). 1975 National emis-
sions report. Report EPA-450/2-78-020; 1978a.
U.S. Environmental Protection Agency (U.S. EPA). Technical report for
revision of steam electric effluent limitations guidelines. Washington,
DC: Effluent Guidelines Division, U.S. EPA: 1978b.
U.S. Environmental Protection Agency. Development document for BAT
effluent limitations guidelines and new source performance standards
for the ore mining and dressing industry. Preliminary draft report by
Calspan Advanced Technology Center. Contract EPA 68-01-4845. Washington,
DC: Effluent Guidelines Division, U.S. EPA; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Development document
for effluent limitation guidelines and standards for the iron and steel
point source category. EPA 440/1-80/024-6. Washington, DC: Effluent
Guidelines Division, U.S. EPA; 1980.
3-17
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Versar, Inc. Production and use of cyanide. Washington, DC: Monitoring
and Data Support Division, U.S. Environmental Protection Agency; 1978a.
Versar, Inc. Gross annual discharge to the waters in 1976: Cyanide
Washington, DC: Monitoring and Data Support Division, U.S. Environ-
mental Protection Agency; 1978b.
Versar, Inc. Environmental data summary and analysis for the organic
chemical industry. Preliminary draft report. Washington, DC: Monitoring
and Data Support Division, Office of Water Regulations and Standards
U.S. Environmental Protection Agency; 198la.
Versar, Inc. Environmental data summary and analysis for the ore mining
and dressing industry. Preliminary draft report. Washington, DC-
Monitoring and Data Support Division, Office of Water Regulations'and
standards, U.S. Environmental Protection Agency; 1981b.
Versar Inc. Environmental data summary and analysis for the metal
finishing industry. Preliminary draft report. Washington, DC: Monitoring
and Data^Support Division, Office of Water Regulations and Standards,
u.b. Environmental Protection Agency; 1981c.
Versar Inc. Environmental data summary and analysis for the iron and
andeDai ,UStry' *reUminar7 draft reP°rt' ^shington, DC Monitoring
and Data Support Division, Office of Water Regulations and Standards
U.S. Environmental Protection Agency; 1981d. "naaras,
3-18
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4.0 ENVIRONMENTAL DISTRIBUTION
4.1 INTRODUCTION
This chapter provides a link between the estimates of environmental
releases of cyanide developed in Chapter 3.0 and the assessment of expo-
sure to cyanide developed subsequently in Chapters 5.0 and 6.0 for
aquatic and human receptors, respectively. The discussion considers
first the physical and chemical processes that transform and transport
cyanide through various environmental media and determine its ultimate
distribution. Available data are then presented concerning concentra-
tions of cyanide measured in environmental media.
Because of the short half-life of cyanide in water and air, special
consideration is given to the distribution of cyanide in the vicinity
of the major sources of releases identified in Chapter 3.0. By use of
simple fate models, the behavior of cyanide is profiled for a variety
of source and receiving media conditions. Monitoring data are also
analyzed for the United States as a whole to determine the distribution
of cyanide in surface waters.
4.2 ENVIRONMENTAL FATE
4.2.1 Aquatic Fate
A total of six primary fate mechanisms could contribute to the
degradation or reduction of cyanides in water. These are: (1) adsorp-
tion onto sediment, (2) complexing with other materials in the water,
(3) hydrolysis, (4) photolysis, (5) volatilization, and (6) biodegrada-
tion. Four of these mechanisms are addressed below in terms of their
significance to cyanide degradation. Since adsorption onto sediment
does not occur at a detectable rate (Chester Engineers 1977). this
process was eliminated from further consideration. In sunlight, it is
likely that photolysis plays a role in breaking down cyanide complexes
to form HCN. Because this process has not been documented sufficiently,
it is assumed that all cyanide in the water was present as HCN. Thus,
an upper limit is placed on the amount of HCN possibly present. As a
result of these assessments, only four processes were considered in
greater detail: volatilization, hydrolysis, biodegradation, and
complexing.
4.2.1.1 Volatilization
The method presented by Southworth (1979) has been used to determine
the rate of volatilization of cyanide (HCN) from water. The approach is
based on a transfer process across the air-water liquid-film interface.
The rate of volatilization is assumed to be a simple first-order
exponential decay with rate constant 1L/depth. K. is the overall mass-
transfer coefficient:
4-1
-------
H k + k,
3 1
Here H is the dimensionless Henry's law constant, assumed to be
0.004 in the calculations, since it is relatively invariant over the
temperature range of interest. H represents an equilibrium distribution
of the substance between the gas and liquid phases, k is the gas phase
exchange constant and k the liquid phase exchange conltant, both in
cmhr--1-. The gas-phase Exchange constant k is a function of wind and
current velocity: s
I
k ' [1137-5 < + "' < 1
' ^ L*-fcW/«^V» . * r V I I " "
g wind current' ^Mol. Wt. HCN
The liquid phase exchange constant k. is also a function of current
and wind velocity. •"•
k - 23 51 (Vcurrent) n Q*Q 32 ..5 . -1
1 R 0.673 U>y69 (Mol. Wt. HCN} Cmhr
for Vwind I1'9 m '"c"1. ^
k. - 23.51 ( current) 0.969 , 32 ,.5 0.526 (V . . - 1.0)
R 0.673 CMol. Wt. HCN} e wind
cmhr
f°rVwind " 1-9 msec'1
where: Mol. Wt. HCN » 1 + 12 4- 14 = 27
Vwind = wind Velocit7» m sec'1
Vcurrent = current velocity, m sec"1
R » stream depth, m.
The volatilization rate constant K can be determined from:
K -*L
V 100R
and the equation describing volatilization becomes:
n - n e ~Kvt
o
with: nQ - initial concentraton in water (assuming complete and
uniform mixing at all times), mg/1
t » time, hr.
4-2
-------
Southworth (1979) points out that "in a given water body, bulk fluid
mixing and phenomena such as stratification may play a large role in
determining the overall impact of interface controlled processes in
removing toxicants. Thus, the approach used yields theoretical maximum
volatilization rates, which may be reduced by bulk fluid properties.
Other factors which may affect volatilization are the presence of surface
films, waves, and aerosol formation."
Dodge and Zabban (1952) conducted experiments in batch quantities
to determine volatilization rates of cyanides. Their results generally
agree with the method described above when the original experimental data
are reduced by the Southworth (1979) method. This supports the validity
of the method. In addition, information on H, Henry's constant, shows
that the variance of this quantity with temperature is small over the
0°-20°C range.
In the absence of a more precise description of the volatilization
process, the rate of volatilization of HCN from water is assumed to equal
the rate predicted by the equations above.
4.2.1.2 Hydrolvsis
Chester Engineers (1977) provides information on tests conducted to
determine the hydrolysis rates of cyanide in river water. River water
samples were sterilized to remove biological action. Initial tests were
run with sodium cyanide at a concentration of 150 ug/1 (2)~1 CN,
potassium ferri-cyanide at 185 Ug/1, and cuprous cyanide at 180 ug/1.
Experiments were run at temperatures of 10, 20, and 27°C with a pH of
5, 6, 7, or 8. Some samples were kept in the dark and some were exposed
to sunlight. As the pH increased, the rate of degradation of sodium
cyanide decreased. At a pH of 5, the rate was 100% greater than at a
pH of 8. Cuprous cyanide rates were ^40% less than those for sodium
cyanide and potassium ferricyanide. For all three cyanide compounds,
the average rate at 10°C was 46% less than at 20°C. The average quasi
first-order rate constant at 108C and at pH between 7 and 8 was 0.0002 hr
and at 23°C was 0.0033 hr"1.
The following rate model for pH between 7 and 8 was established as
a result of the tests for cyanide hydrolysis:
^ = -0.0029 (0.959)2°'Tn
at
where: n m concentration, mg/1
T • temperature, °C
t * time, hr.
Integrating the equation for n becomes:
20-T
-0.0029 (0.959) t
n * n e
o
4-3
-------
A plot of concentration versus time is shown in Figure 4-1 Half-
lives at 0, 10, 20, and 30«C are about 23, 15, 10 and 6.8 days, respec
tively. _At temperatures of interest, times to half concentration as a
result or nydrolysis only appear to be in the range of about lO-'O
days .
No other data were available to verify this model.
4.2.1.3 Biodegradation
waters. River water samples were taken and microorganisms (bacteril)
added to the samples II £ Ind'ttf i OcuU ^h
containing acclimated microorganisms . (There are 1 5
" ij
„ Hours for c an
Initially, the cells developed slowly until the microoganisms became
acclimated to the experimental environment. This involved changing the
microorganism population until the organisms capable of deriving energy
solely from cyanide became prevalent. Bacteria numbers increased at an
exponential rate until the cyanide was completely exhausted; and then
they rapidly declined. At this point, 50 mg/1 of sodium cyanide as CN
were again added to the test batches. Again, growth increased at an
exponential rate but with no acclimatization lag. Bacterial counts were
determined by the Standard Plate Count method.
As a result of these tests, the following equation was derived to
fit the observed data:
ff = -0.01 C(1.«-0.0333T) x
where: C = cyanide concentration, mg/1
X = microorganism concentration, mg/1
T » temperature, °C
Integrating, the equation for C at any time becomes:
C - [CQ 1-k - (O.OIXt) (1 - k)] ^
where: t » time, hr.
k = 1.49 - 0.0333T
CQ * initial cyanide concentration, mg/1
4-4
-------
1.0
.9
.8
.7
2 -6
i
<§ .5
re
Hydrolysis Half Life: 6.8
8 10 12
Time, Days
14 16 18 20
Source: Chester Engineers (1977).
FIGURE 4-1 CYANIDE HYDROLYSIS AT TEMPERATURES FROM 0°C TO 30°C FOR
pH BETWEEN 7 AND 8 OVER 0 TO 20 DAYS
4-5
-------
Depending upon the temperature, half-lives for cvanide
hours to as -ch as 60 *•«• *>* i->" 7
the range shown abovf was assu^eT C0ncentrati™ of
4-2.1.4 Cyanide-Iron Complexinq
behaviol'wiff IFon19^,^^0^' experiinents to Determine cyanide complexing
fS " foncentrations of CN near those in rivers are
foraati™ "tea were anywhere from 10-7 mg/1 ^^ t
mg/1 min ere rom - mg/1 ^^ to
4-2'1-5 Fate in the Vicinity of Sources
as th.
that depth and flow velocities of !^n rateS' Xt Was assumed
-Jor determinants oFthe raL. The hal'Sfe'l ^ ^T ^ WSre the
alone is on the order of less than ! d*v Z / V° volatil^ation
conditions mentioned above 7 C° 3 f€W dayS '
4-6
-------
-1
...
-3
jmL f
=> -6
I
4)
a
SC
3
o
-7
,.
-9
-10
-11
-12
-13
-14
-
-15
-6
Range of Laboratory
Data
Kijjjjl
-5-4-3-2 -10 1
Log10 (CN-Concentration mg 1"1)
FIGURE 4-2 RATE OF CYANIDE COMPLEX FORMATION WITH IRON AS A
FUNCTION OF CYANIDE CONCENTRATION IN WATER
(CN/Fe-1)
Source: Prober et^ al^ (1977)
4-7
-------
these processes. More data are available concerning biological waste
treatment. The results are similar to those of laboratory studies
intended to simulate naturally-occurring situations. Here, measurements
on river water and acclimated microorganisms were used to construct the
water model (Chester Engineers 1977). In the absence of typical concen-
tration data for these organisms in natural waters, a representative
value from the laboratory studies was used in the water model calcula-
tions. These give half-lives for biodegradation on the order of tens
of hours.
The volume of the discharge medium also had to be estimated. Since
the fate analysis intends to describe the range of possible situations
several values were assumed. Using data available for flow rates of
typical sizes of rivers, a distribution of flow rates for each river was
assumed. It was then possible to determine a range of expected condi-
tions. For a maximum concentration case, the receiving medium was
assumed to have twice the effluent flow rate, which diluted the concen-
tration in the effluent by a factor of two. The initial concentrations
for each of these conditions were determined. Using the stream flow
parameters and assumptions about water temperatures and wind speeds
the degradation rates were estimated for cyanide under the modeled '
conditions.
A further assumption in the fate calculations was that the dilution
TloTlll r±fan8ed ^ ^ m°VeS downstrea«" i^. river dimensions and
flow rate remain constant so that no water from other sources is added
and no evaporation reduces the initial volume. We assume no concentra-
tion gradients in the stream result from differential flow patterns or
dispersion^plumes downstream of an outfall. Once the effluent was
released, it was assumed to be completely and uniformly mixed in the
dilution volume. The only modifying mechanisms subsequently operating
on the water volume were volatilization and biodegradation. In practice
plume phenomena and topographic irregularities may result in higher cyanide
concentrations near a discharge site than those predicted in thf model
presented here. However, the relative magnitudes of the concentrations
estimated under various conditions provide a useful general comparison
of situations involving different industrial dischargers.
h.™ Detailed res^t3 of the fate modeling procedure are not presented
here since many different hypothetical cases were addressed. An
example of the results is shown in Figure 4-3. Because the concentra-
J; ? in^ndlyxdual cfses raay vary over several orders of magnitude,
it is difficult to make a general statement concerning the impact of
industry effluents. According to the calculations, cyanide sources did
not contribute significantly to high concentrations downstream. The
cyanides generally decayed to 50% levels within a few kilometers
although differences in environmental conditions have quite visible
efrects on the calculated degradation of cyanides. In most cases
the level of cyanide concentration is estimated to drop by an order
of magnitude or more within 30 km downstream. At higher initial con-
centrations and lower wind speeds and water temperatures, the distances
4-8
-------
en
o
13
i.
*j
c
OJ
u
o
o
-------
may be on the order of 50 km. At lower initial concentrations and higher
wind speeds and temperatures, this concentration may be reached 8-10 km
or less downstream. For the limiting cases, the characteristic distances
are at the higher end of the range.
Temperature is the controlling factor in biodegradation, whereas
current and wind speed are the controlling factors in volatilization.
Current speed does not have a larze variation; in most of the cases
codeled, it was about 0.2 m/sec. Wind speeds used in the calculations
are 1 m/sec and 10 m/sec. An increase in wind speed lowers the distance
tance needed to reach a .given concentration fay a factor of 4 or 5. An
increase in temperature from 10 to 20 8C has similar effect, reducing by
a factor of 2 to 4 the distance at which a given concentration is reached.
An increase in temperature at a low wind speed has more effect on degra-
dation rate than at a high wind speed (a factor of 4 vs. 2).
In summary, elevated concentrations of cyanide in rivers and streams
are expected to occur only within 10-30 km of discharge sources. Actual
calculation of these concentrations would require site-specific informa-
tion regarding the initial effluent concentrations and the relevant
environmental conditions.
4.2.2 Atmospheric
4.2.2.1 Background Concentrations
The background levels of HCN were estimated on an upper limit basis
by assuming that one-half of the entire air emissions (see Section
3.1) is emitted uniformly into the atmosphere over an area approximating
a four-sided region with Maine, Virginia, Missouri, and Wisconsin at its
corners. A box model (Lucas 1958) was used to obtain concentrations at
the downwind boundary of this region. The concentration in mass per
unit volume is approximated by:
X - QS/2HU for S » H
where: Q » Mass rate of emissions per unit area
S - Downwind length of the box
H » Mean mixing depth (height of the box)
U » Mean wind speed.
To obtain Q, it is assumed that one-half of the 3.7 x 104 kkg/yr
spreads over 1.5 x 106 km2. S is assumed to be 1500 km and H is 1 km
based on the average conditions of a summer morning along the Eastern
Seaboard (Holzworth 1972). For these climatic conditions, air trajec-
tories over the entire region average 4.5 m/sec for episode days.
(Bach 1975). Assuming no reactions or rainout, the downwind concentra-
tion obtained is 0.065 ug/m3.
4-10
-------
The assumption of negligible rainout is reasonable for upper bound
calculations because lifetimes of materials with very low vapor pressui
exceed a week if absorption on aerosol surfaces is a rate-limiting
process (Junge 1977). Residence time for the conditions of the box
model is S/U, which is less than 4 days. The concentration in rain drops
would be 1.6 x 10"^ yg/1 estimated above and the nondimensional Henry's
Law constant of 3.95 x 10~3 (mass per unit volume in liquid and gas
phases) derived from measured values in the literature at 25 °C (Dodge
and Zabban 1952).
Reactions of OH-radical with HCN were examined as the principal
pathway for potential atmospheric degradation. Because rate constants
could not be located in the literature, it was necessary to make esti-
mates based on reaction rates with other hydrogen-bearing compounds and
on the relative strengths of hydrogen atom bonding in these compounds.
Some of the rate constants (at 3008K) are as follows (Hampson and Garvin
1978):
Reactants Rate Constant (cm3/sec)
OH + C,H,. 2.6 x 10"13
/ o
OH + CH. 7.9 x 10"15
4
OH + NH3 1.6 x l(f 13
~-,e energies required to remove the first hydrogen atom from each of
these compounds are as follows (Schexnayder 1963):
Reaction Energy (eV)
CH •* CH + H 4.21
CH4 * CH3 + H 4.40
NH3 -* NH2 + H 4.42
The energy for HCN -»• CN + H ranges from 4.8 eV to 5.6 eV. Further
cleavage of the CN Bond to form C + N requires 7.5 to 8.2 eV. Therefore,
based on these progressions of bond energies and of reaction rate con-
stants, one would expect an extreme upper limit of, perhaps, 10~1- cm3/
sec for the OH + HCN reaction that leads to HCN destruction. An
additional reaction producing HOHCN as an intermediate does not involve
bond cleavage in the HCN and could proceed at a faster rate than that
given by 10~13 cm3/ sec. The HOHCN intermediate (if it exists) could
readily feed HCN back into the system.
4-11
-------
Using the observed range of OH-radical concentrations, the lifetimes
of pollutants can be estimated (Eschenroeder et. al. 1978). For the rate
constant of 10-13 Cm3/sec, the lifetime of HCN would vary between the order
of a month (in urban atmospheres) to a year in rural atmospheres. There-
fore, because both rainout and degradation occur on longer time scales than
the residence time in the box model, the conservative assumption for average
background concentration of HCN at 0.065 ug/m3 is justified.
4.2.2.2 U rb an Cone en t r at i on s
Combustion influences cyanide concentrations in the air of populated
areas. Measurements in flame zones indicate that HCN concentrations
exceed thermochemical equilibrium levels following the decay of hydro-
carbon species in rich hydrocarbon/air combustion (Haynes .et .al. 1974).
The buildup of HCN is postulated to be significant in the chain reactions
producing oxides of nitrogen. HCN is believed to be formed by the mech-
anism:
C + N2 * CN + N
C2 + N2 -»• 2CN
CH + N2 ->• HCN + N
M + CN + H -f HCN + M
and CN decays at about 2000°K via:
CN + C02 -»• OCN + CO
OCN + H •* CO + NH
OCN + H- -f CO + NH .
In steady-flow combustion, the latter three steps scavenge CN from
the system; however, internal combustion engines freeze high temperature
equilibrium concentrations into the exhaust gas because of the quenching
effect in the rapid cooling as a result of adiabatic expansion during
the power stroke. *
Consequently, motor vehicles constitute a source of HCN emissions
into air that is more significant than steady-flow combustion equipment.
Automobiles not equipped with catalytic converters emit 11-14 mg/mi of
HCN (U.S. EPA 1978), while catalytically equipped vehicle emissions are
on the order of 1 mg/mi under optimal operating conditions. Under
malfunction conditions, the catalytically equipped vehicles emit as much
(or sometimes several times as much) HCN as the noncatalytically equipped
4-12
-------
In central cities, the large majority of carbon monoxide in the
atmosphere comes from motor vehicles; thus, carbon monoxide is often
used as a surrogate for tracing vehicular pollutants. This is especially
valuable for tracing HCN, because neither HCN nor CO is significantly
affected by smog photochemistry in the scale of urban residence times.
One means of circumventing atmospheric modeling is to select a data base
of CO ambient measurements and to determine a typical CO/HCN emissions
ratio for use as a scaling factor.
The CO monitoring data base was selected from a national tabulation
of frequency distributions (U.S. EPA 1977a). Station number 023 in New
York City showed some of the highest levels in the nation and was chosen
as a prototype worst case. The range of CO/HCN ratios for the Federal
Test Schedule emission measurements is 2000-4000 for noncatalyst vehicles.
This is based on the 11-14 mg/mi HCN-range (U.S. EPA 1978) and on the
20-60 mg/mi CO range suggested by the standard emission factors tabula-
tions (U.S. EPA 1977b). Vehicles that have malfunctions or maladjustments
consistently exhibit ratios of 200-500 (U.S. EPA 1978). Based on these
ranges, a representative value of 1000 was assumed for the emissions
ratio of CO/HCN.
t
The application results of the emissions ratio to the New York
City Station 023 CO-concentration frequency distribution are shown in
Figure 4-4. For comparative purposes, some Bulgarian data on atmospheric
concentrations of HCN are indicated on the plot (Kalpasanov and
Kurchatova 1976).
The comparability of the measured data for the Sofia, Bulgaria
"industrial region" is striking. It is important to note that the New
York data are hourly averages and the Bulgarian data are daily averages.
Therefore, the factors of difference between the peaks, means, and median
reflect not only inaccuracies and emissions variations, but also an
expected bias because of the averaging times. For comparative purposes,
the "multimedia environmental goal" (MEG) ambient air level of 26 yg/m3
(U.S. EPA 1977c) is indicated by a horizontal broken line. (This MEG
value was arrived at by an heuristic process and has no averaging time
attached to it in the tabulations for ambient media.) Rainwater concen-
trations in an area of 20-40 yg/m3 ambient air concentration would be
in the 5-10 yg/1 range if equilibration occurred during the rainfall.
From these estimates, it may be concluded that significant HCN
concentrations in the ambient air occur only in urban areas and that
export or rainout are the principal removal mechanisms. Rainwater
concentrations are only in the ug/1 range, even during high atmospheric
loadings of HCN.
4.2.3 Fate in Soil
Because some cyanide may enter the soil such as plants, or
from applications and subsequent runoff of road salts, fate in soil
was investigated.
4-13
-------
so
20
I a
NY Max
Frequency Distribution of
One-Hr Concentrations «
New York City Monitoring
Sit* No. 023 Based on
Scaling Co-Ota by
Emissions Ratio of 10°
24-hr Maxima
(Kalpasanov
and
-------
Rangaswami and Balasubramanian (1963 a,b) found more micro-
organisms in the roots of cyanide producing plants than in the soil
surrounding the plants. When a cyanide solution was added to a suspen-
sion containing these microflora, the growth of bacterial microorganisms
increased; however, the growth of fungal organisms decreased. Some
microorganisms were inhibited 1 or 2 days but were not further inhibited.
Fungi added to soils containing cyanide producing plants were not
inhibited.
Strobel (1967) tested soil from several sites for their capability
to utilize cyanide. All nonsterilized soils were found to have cyanide
metabolizing ability, which was attributed to the microorganisms found
in the soil. Soil microorganisms were also found to immobilize cyanide
nitrogen. Carbon dioxide generation was detected and eventual ammonia
(NH3) fixation utilizing cyanide nitrogen was hypothesized. Strobel
(1967) concluded that cyanide carbon and nitrogen were converted to
carbonate and ammonia respectively by nonsterilized soils. The soils
most able to metabolize cyanide were from areas supporting plants that
synthesize cyanide compounds.
Allen and Strobel (1966) contend further that a cyanide cycle exists
in nature. Molecules of cyanide could be directly transferred from
plants to microorganisms. They could then be transferred by fungi and
bacteria back to plants as sources of nutrients without prior conversion
to C02 and NH3-
Although these studies indicate that these cyanide cycles occur only
in the soils and organisms found in the vicinity of cyanide producing
plants, it is reasonable to expect that cyanides will be degraded in
soils. Some time may be required to establish the populations capable
of degrading the compound. Time required to degrade the cyanides once
the population is established is not known, although in Strobel's (1967)
study, the ratio of carbon to nitrogen in the soil from degraded cyanide
leveled off after about 3 days incubation. Attempts to increase the rate
by pretreatment with 10"3 molar KCN to acclimate the population were
unsuccessful. Cyanide levels lethal to the microorganisms were not
stated in any of the references surveyed.
4.3 MONITORING DATA
A.3.1 Introduction
Cyanide proves to be a difficult substance to monitor since it does
not persist in the environment. Consequently, discharges into waterways
that may be undetected by periodic sampling methods currently used could
cause hazards to aquatic life.
The availability of water quality data concerning cyanide has
increased in recent years as more monitoring programs are implemented.
Of those states with sufficient monitoring data to provide adequate
4-15
-------
assessments, six states—Illinois, Indiana, Nevada, Ohio, Oklahoma, and
Tennessee--reported cyanide water quality problems in 1976 (U.S. EPA
iy/7d). The exact sources of discharges in these areas were not
mentioned in the condensed state reports.
The STORET water quality data system indicates the distribution of
ambient concentrations of cyanide; it serves here as the primary source
for monitoring data. Two levels of investigation were pursued in retriev-
ing water quality data for cyanide from STORET: national level for the
U.S. as a whole, and local level for a selected area. The monitoring
results from each are summarized below.
4.3.2 National Monitoring Results
Monitoring of cyanide in ambient waters around the nation aids in
pinpointing areas where cyanide concentrations exceed water quality
criteria for the protection of freshwater aquatic life and human
nealth.
The U.S. EPA has recommended the following water quality criteria
for cyanide (U..S. EPA 1980).
i
• Freshwater aquatic life - free cyanide criteria to protect
freshwater aquatic life: 3.5 ug/1 as a 24-hour average
and not to exceed 52 ug/1 at any time; and
• Human Health - ambient water quality criterion, 200 ug/1
(recommended to be identical with existing drinking
water standard).
With the mapping capabilities of the STORET Water Quality Control
Information System, locations at which the criteria levels are exceeded
can be examined. Figure 4-5 displays the 85th percentile of total
cyanide concentration as analyzed from 37702 observations recorded at
a/50 water quality stations, from 1975 through 1980 (U.S. EPA 1981)
Blank areas on the map indicate, for this data set, where monitoring
has not occurred. All remarked values were set equal to zero and only
stations with a minimum of four observations were included in the
analysis.
Data were aggregated by cell sized 30 minutes of latitude bv 30
minutes of longitude. Results for total of 682 cells were aggregated
in the following concentration ranges:
Concentration Range No Cells Percentage
less than or equal to 3.5 yg/1 413 si
greater than 3.5 yg/1 and less than 238 35
or equal to 52 ug/1
greater than 52 ug/1 and less than 13 2
or equal to 200 ug/1
greater than 200 ug/1 13 2
682 . 100%
Maximum value (for 85th percentile) is 1803 ug/1.
4-16
-------
IN:l1.r.nFNIM i",B'll •'.•"! AM NO
j I CHf. I 'J
',VAN;?[ IN
B! IH °LRCf NT ILFS
0 OOJ'>
« 0 003'. 10 0.0r,?0
• o.fii?o 'o o.^ooo
• • o.^ooo
OIAIF-. '0 12000000 OR 189. -»3 MIlfS/INCH
O- 00
MILES »IO'
56.63 T5
FIGURE 4-5 TOTAL CYANIDE - 85TH PERCENTILE MAP
-------
Overall, the majority of waters tested nationwide over time do
not exceed the lowest criterion of 3.5 ug/l recommended to protect
freshwater aquatic life, as a 24-hour average. Thirty-seven of the
tifty states (74%), do have some locales with cyanide concentrations
in ambient waters greater than 3.5 ug/l. In the latter two ranges,
areas in violation of the criteria are fewer in number and identified
easily with the map. Areas exceeding the criterion for freshwater
aquatic life include portions of southern California, northern Utah,
Missouri, Alabama, north central Texas, Kentucky, northwest Indiana,
Illinois, Ohio, and western Pennsylvania. Areas with levels exceeding
the human health criterion include portions of southern California
North Dakota, South Dakota, Iowa, northwest Georgia, western New York
and western Pennsylvania. j-«r«-,
4.3.3 Local Monitoring Results
Because of a heavy concentration of iron and steel operations the
Pittsburgn metropolitan area was selected for an examination of Si
eftect or cyanide discharges on concentrations in local surface water.
war / t0,tal °f 89 ^i^t stations and 46 effluent stations monitor
y ^ thePlttSbUrSh ^ Table 4-* shows ^e number of
on 1 e - sows e number o
monitoring stations located in each of the counties comprising the
metropolitan area. The majority of the stations are located Jn Che
Monongahela and Ohio Rivers near major steel operations?
The sampling distribution of mean levels of total CN from all
ambient monitoring stations between 1965 and 1979 is exhibited in
Table 4-2. Approximately 90% of the stations record mean concentrations
below the water quality criterion of 0.2 mg/1 for drinking water (NAS 1972)
Only 43* of the stations record mean concentrations at or below the recom-
f° ' ™- <^tribution corresponds
of CN levels
The sampling distribution of mean levels of total CN from all effluent
are" o^Ytati°nS *? ^ ln Table 4'3' G^ally, the effluent stations
RouehlvfiO-/ TV*"1 Plant outfall, leading to the Monongahela River.
Umft for Ll il J ta£ ^ recorded mean val"" ^ or below the mandatory
limit tor cyanide in the environment.
ment in thlTVl!" ^P*Ct °f ^"^ dischar§es °" the aquatic environ-
ment in the Pittsburgn area, relationships between ambient and effluent
both ^H-W6r T a^shed' Onl? Allegheny and Beaver Counties reported
both ambient and effluent data, which allowed an upstream-downstream
comparison. The ratio of ambient to effluent stations is 1.5 to 1 in
Allegheny Bounty and nearly 3 to 1 in Beaver County. Figure 4-6 shows
the locations of some ambient and effluent monitoring stations along
the Monongahela Ohio, and Beaver Rivers; and the location of mediu^
to large steel plant operations on the Monongahela River.
4-18
-------
TABLE 4-1. LOCATIONS OF WATER QUALITY MONITORING STATIONS
IN THE PITTSBURGH METROPOLITAN AREA
TYPE OF MONITORING/COUNTY
No
Ambient Stations
Allegheny County 61
Armstrong County 2
Beaver County 14
Washington County 1
Westmoreland County 11
89
Effluent
Allegheny County 41
Beaver County 5
46
Source: U.S. EPA (1979).
4-19
-------
TABLE 4-2. SAMPLING DISTRIBUTION OF AMBIENT MEAN LEVELS OF TOTAL
CYANIDE FOR 89 WATER MONITORING STATIONS IN THE
PITTSBURGH METROPOLITAN AREA, 1965 to 1979
CN
Concentration
Range
(rns/1)
0.00-0.01
0.02-0.03
0.04-0.05
0.06-0.07
0.08-0.09
0.10-0.22
0.23-0.35
0.36-0.51
0.52-0.67
0.68-0.83
0.84-0.99
1.00+
Number
38
27
6
3
1
4
3
0
0
2
1
4
S T A T I
Percent
43
30
7
3
1
5
3
—
—
2
1
5
0 N S
Cumulative
Percent
43
73
80
83
84
89
92
92
92
94
95
100
89 100.0
Source: U.S. EPA (1979).
4-20
-------
TABLE 4-3. SAMPLING DISTRIBUTION OF MEAN LEVELS OF TOTAL CYANIDE IN
INDUSTRIAL EFFLUENT FOR 46 WATER QUALITY STATIONS IN THE
PITTSBURGH METROPOLITAN AREA, 1965 to 1979
Concentration SI A T I 0 N S
Range
(mg/1)
0.00-0.01
0.02-0.03
0.04-0.05
0.06-0.07
0.08-0.09
0.10-0.22
0.23-0.35
0.36-0.51
0.52-0.67
0.68-0.83
0.84-0.99
1.00+
46 100.0
Number
7
6
5
2
2
5
4
3
3
1
0
8
Percent
15
13
11
4
4
11
9
7
7
2
—
17
Cumulative
Percent
15
28
39
43
47
58
67
74
81
83
83
100
Source: U.S. EPA (1979).
4-21
-------
"^Washington
County
County
Allegheny County
- Ambient Monitoring Stations
/\ - Effluent Monitoring Stations
Steel Plant
Yougnioqhenv River
FIGURE 4-6 LOCATIONS OF STEEL PLANTS AND WATER QUALITY MONITORING
STATIONS ALONG THE BEAVER (OHIO) AND MONONGAHELA (PENNSYLVANIA
RIVERS IN THE VICINITY OF PITTSBURGH
4-22
-------
Seven upstream-downstream pairs were established along an 18-mile
span of the lower Monongahela River for monitoring stations with common
sampling periods. Both ambient and effluent stations tend to be clus-
tered along the river, with outfalls usually about 2 miles apart.
Table 4-4 summarizes the data for the seven upstream-downstream pairs.
In the case of a cluster of monitoring stations, the range in mean values
is shown.
For two of the seven pairs, ambient mean values downstream were
higher than the upstream values. The highest effluent values occurred
in these two cases and also the downstream ambient stations are within
a quarter to one-half mile from the effluent stations at steel plant
outfall points. The two relationships represent adjacent steel plant
operations. This example suggests that high concentrations may occur
within one-half mile of an outfall, but that the cyanide levels down-
stream will diminish rapidly. The fate analysis in Section 4.2 also
supports this conclusion.
4-23
-------
TABLE 4-4.
ShQUhN
COMl>ARISONJi °P MONITORED LEVELS OF TOTAL CYANIDE
ORDER OF LOCATION ALONG THE LOWER MONONCAIIELA RIVER
UPSTREAM
Sampling
Years
1971-76
1971-75
1971-76
1971-74
1971-77
1971-76
f 1967-76
10
Range 1
Ambient
0.02
0.00
0.00
0.02
0.00
0.02
0.03
n
Mean Values
- 0.02
- 1.05
- 0.08
- 0.74
- 0.05
Miles From
Station to
Outfall
0.25
0.25
0.50
0.25 - 0.50
1
1
1.5
Range of Effluent
Mean Values
(ma/1)
0.01 - 0.03
0.13 - 0.14
0.60 - 1.99
0.00 - 1.18
0.01 - 2.69
0.24 - 0.81
0.09 - 0.11
u u w
Miles From
Outfall to
Stations
0.50
0.25 - 0.50
0.25
0.50 - 0.75
0.25 - 0.50
1.5
0.50 - 0.75
D_O..W N S T R E A M
Range In
Ajiibient Mean Values
["US/11
0.01
0.00
0.02 -
0.00 -
0.02 -
0.03 -
0.00 -
l.05a
0.08
0.74a
0.05
0.02
aCases in which downstream effect was observed.
Source: U.S. EPA (1979).
-------
REFERENCES
Bach, W.D., Jr. Investigation of ozone and ozone precursor concentra-
tions at non-urban locations in the eastern United States, phase two,
meteorological analyses. Report No. EPA-450/3-74-034-A. Washington,
DC: U.S. Environmental Protection Agency; February 1975.
Dodge, B.F.; Zabban, W. Disposal of plating room wastes, IV, batch
volatilization of hydrogen cyanide from aqueous solutions of cyanides.
Plating, 39:1133-9;'1952.
Eschenroeder, A.Q.; Irvine, E.; Lloyd, A.C.; Tashima, C.; Iran, K.
Investigation of profile models for toxic chemicals in the environment.
Prepared for the National Science Foundation. ERT P-50/1/2; February
1978.
Hampson, R.F., Jr.; Garvin, D. Reaction rate and photochemical data for
atmospheric chemistry - 1977. National Bureau of Standards; NBS SP 513;
May 1978.
Haynes, B.S.; Iverach, D.; Kirov, N.Y. The behavior of nitrogen species
in fuel rich hydrocarbon flames. Fifteenth symposium (international)
on combustion. Pittsburg, PA: Combustion Institute; 1974: 1103-111.
Holzworth, G.C. Mixing heights, wind speeds, and potential for urban
air pollution throughout the contiguous United States. U.S. Environ-
mental Protection Agency; AP-101; January 1972.
Junge, C.E. Basic considerations about trace constituents in the atmos-
phere as related to the fate of global pollutants. Fate of pollutants
in the air and water environments, Part One. Suffet, I.H. ed. Science
and technology, Vol. 8. New York, NY: John Wiley & Sons; 1977: 7-25.
Kalpasanov, Y.; Kurchatova, G. A study of the statistical distribution
of chemical pollutants in air. J. of the Air Pol. Cont. Assoc. 26(10):
981-985; 1976.
Knowles, C.J. Microorganisms and cyanide. Bacteriological Reviews
40(3):652-680; 1976.
Lucas, D.H. The atmospheric pollution of cities. Internat. J. of Air
Pol. 1:71-86; 1958.
National Academy of Sciences (NAS). Water Quality Criteria. Washington,
DC: National Academy of Sciences; 1972.
4-25
-------
Prober,^ R. et al. Treatment of coke oven and blast furnace effluents
to inhioit rormation of iron cyanide complexes. Proceedings of the
Jlst industrial wastes conference; Purdue Universitv, May 4-6 1976-
Ann Arbor Science Publishers, Inc.; Ann Arbor, MI- 1977
fSS^ri* V Balasu'°ramanian> A- Studies on the rhizosphere micro-
flora of sorghum in relation to hydrocyanic acid content of roots J
Mlcrobiol. 9:719-7
anc ac content
Mlcrobiol. 9:719-725; 1963a. (As cited by Knowles I976)
. Release of hydrocyan
the rhizosphere microflora and plant
Rangaswami, G. ; Balasubramanian, A. Release of hydrocyanic acid by
°3
Knowls
^ '* EXP* ^ 1:215-217>' 196*>- (As cited by
Schexnayder, C.J Jr. Tabulated values of bond dissociation energies
±n hi* T P°Centials' md electron affinities for some molecules fou^d
llinf^r MSratUre ?f ical "action.. National Aeronautics and Space
Administration. Technical Note D-1791; May 1963.
Southworth G.R. The role of volatilization in removing polycyclic
aromatic hydrocarbons from aquatic environments. Oak Ridge National
mens. a ge N
1979;1o7-514 ' BUUetln °f Environ»ent^ Contam. Toxicol.
G•A; ^yanide utilization in soil. Soil Sci. 103:299-302-
S cited by Knowles 1976)
U.S. Environmental Protection Agency (U.S. EPA). Air quality data -
1975 annual statistics. Report No. EPA-450/2-77-002. Washington, DC:
Monitoring and Data Analysis Division; May 1977a. », ^-
^rotection A8ency ^.S. EPA). Compilation of air
Edltion-
U.S. Environmental Protection Agency (U.S. EPA). Multimedia environ-
mental goals for environmental assessment. Volume Two. MET charts and
Washington, DC:
U.S. Environmental Protection Agency (U.S. EPA). National water quality
inventory: 1976 report to Congress. Report No. EPA-440/9-76-024.
Washington, DC: U.S. Environmental Protection Agency; 1977d.
U.S. Environmental Protection Agency (U.S. EPA). Third annual catalyst
research program report. Report No. EPA-600/3-78-012. Washington, DC:
Office of Research and Development; January 1978.
U.S. Environmental Protection Agency (U.S. EPA). STORET. Washington
Standards?^ Sl;^?""0" DiViSi°n' ^^ °f
4-26
-------
U.S. Environmental Protection Agency (U.S. EPA). Water quality
criteria documents; availability. Federal Register 45(231)-.79331;
November 28, 1980.
U.S. Environmental Protection Agency (U.S. EPA). STORET. Washington,
DC: Monitoring and Data Support Division, Office of Water Planning and
Standards, U.S. EPA; 1981.
4-27
-------
5.0 EFFECTS AND EXPOSURE—BIOTA
5.1 EFFECTS ON BIOTA
5.1.1 Introduction
Cyanide is a rapidly acting, highly toxic substance. Most reported
research has focused on the acute toxicity of cyanide to freshwater fish.
Information regarding long-term effects and bioaccumulation is limited.
This chapter summarizes and discusses the data on the acute effects
of cyanide with regard to freshwater and saltwater fish and invertebrate
species, sublethal effects data for freshwater fish, and the potential
for bioaccumulation. In addition, the relationship between certain
environmental conditions and cyanide toxicity is considered. Finally,
the minimum concentrations of cyanide in water reported to have adverse
effects on various groups of aquatic organisms are presented.
5.1.2 Toxicity to Aquatic Organisms
5.1.2.1 Interpretation of Experimental Results
The toxic effects of cyanide on aquatic organisms that are most
commonly described in the literature include the following:
• LC50 - concentration lethal to 50% of the population in a
stated period of time.
• Reproductive effects - reduction in success of egg hatching,
decrease in viability of offspring at various life stages,
early or delayed hatching, etc.
• Sublethal effects - alteration of rate of respiration.
biochemical changes, organ or tissue damage, (e.g., cell
death), inhibition of locomotor activity, etc.
• Bioconcentration factor - concentration in the tissue of
an organism divided by the concentration in surrounding
water.
Usually cyanides are found in the form of simple alkali cyanides,
metal cyanides, or other complex cyanides (U.S. EPA 1977a). The cyanide
radical from alkali cyanides, commonly found in industrial wastes,
hydrolyzes in an aqueous solution to form free cyanide, which is defined
as any combination of HCN (hydrocyanic acid) and CN~ (cyanide ion)
(Lind et al., 1977). The predominant fraction between HCN and CN~
depends on the solution pH; when it is <9.0, as is common in natural
waters, HCN is considerably more prevalent, and the cyanide ion will
be present at lower concentrations.
5-1
-------
The toxicity to fish of solutions containing simple cyanides has
been primarily attributed to HCN, with CN as a minor contributing factor
(Wurhmann and Woker 1943, Bridges 1958, Doudoroff et. al. 1966). Even
the toxicity of metallocyanide complexes has been attributed to HCN
(Doudoroff e_t al_. 1966) , although certain metals may contribute additively
or synergistically to the overall toxicity. Since fish commonly live in
and thus are tested in water with a pH <9, HCN is more prevalent and con-
sequently highly significant in measured cyanide toxicity. HCN's greater
toxicity, however, is also attributed to its relatively lipid-soluble,
un-ionized form, which is readily absorbed by aquatic organisms. Charged
ions, such as CN~, are less toxic because of their difficulty in permeating
the charged protein surfaces of membranes in exposed areas of the body
(Broderius, et. al_. 1977).
During static aquatic toxicity experiments, cyanide levels will decline
because of the hydrolysis of CN to HCN and the consequent loss of HCN
through volatilization. This loss can have a considerable effect on the
results. A significantly greater percentage (100% killed) of minnows
died after 14 hours in a freshly prepared cyanide solution than in one
that stood for 24 hours (60% killed) before the fish were introduced
(Doudoroff 1956). Fish introduced into the solution at 96 hours were
not affected at all.
Cyanide will dissipate rapidly from a solution, and thus cyanide
toxicity measured by LCsn values is usually lower in static water
experiments than in flowthrough experiments, in which the cyanide is main-
tained at a constant concentration. However, reported results from the
two kinds of tests differ (only by =8% [Herbert and Merkens 1952; Dou-
doroff et al. 1966]), probably because cyanide acts rapidly and may have
toxic effects on organisms before it is dissipated. Another contribut-
ing factor may be that static conditions lead to low levels of dissolved
oxygen in water, which would increase the toxicity of the solution
(Doudoroff 1976).
For this risk assessment, the effects of simple cyanides on aquatic
organisms are emphasized. Organic cyanides (nitriles) and metallocyanide
complexes vary widely in their behavior in water and their toxicity. It
is also difficult to determine how significant the cyanide component is
in the overall toxic effect observed. The effects data reported here are
focused on selected compounds that are dissociated readily to form free
cyanide. Unless otherwise noted, the concentrations for simple cyanides
reported in Tables 5-1 through 5-3 are concentrations of free cyanide
(referring to both the CN~ ion and molecular HCN present).
5.1.2.2 Toxicity of Free Cyanide
Cold freshwater fish were the most sensitive species to cyanide
(see Tables 5-1 and 5-2). LC$Q values ranged from 0.04 mg/1 to 0.126 mg/1
under flowthrough conditions. The lowest lethal threshold concentration
was 0.02 mg/1 for the rainbow trout. The majority of the studies indicate
that cyanide concentrations > 0.01 mg/1 are deleterious to cold water
fish.
5-2
-------
TABLE 5-1. REPORTED ACUTE EFFECTS OF FREE CYANIDE ON
FISH ~ FLOWTHROUGH EXPERIMENTS
Concentration
fppmj
0.006-.011
0.32
0.02
0.04-0.05
0.05
0.05
0.057
0.07
0.07
0.03
0.08
0.1
0.1
0.126
0.14
0.16
0.5
> 0.056
0.071
0.086
0.104
0.104
0.11
0.11-0.14
0.11-0.14
Soecies
CQIDHATER PISH
Brook Trout
(Salvelinus fontlnalis)
•
Rainbow Trout
(Salmo gairdneri)
Brown Trout
(Salmo truttal
Brook Trout
(Salvelinus fontlnalis)
»
»
Rainbow Trout
(Salmo gairdneril
Brown Trout
(Salmo truttal
Brook Trout
(Salve'inus fontinalis)
Rainbow Trout
(Salmo qairdnerl)
Rainbow Trout
(Salmo jairdneril
Brown Trout
(Salmo truttal
Brook Trout
(Salvelinus fontlnalisl
Rainbow Trout
(Salmo aairdnerl)
M
Brown Trout
(Salmo truttal
WARM yATER FISH
White Crappie
(Pomoxis anflulansl
Harlequin Fish
(Rasbora heteromorpha)
Smallmouth Bass
(Hicroptenjs dolemieui)
•
Bluegill
(Lepomis iBacrochirus)
Clchtld
(Cichlasoma bimaeulatuml
Bluegill
(Lepomis macrochirus'.
Redbreast Sunfish
(Lepomis auritus)
formulation
HCN
KCN
CN
KCN
KCN
CN
KCN
KCN
KCN
CN
NaCN
NaCN
NaCN
NaCN
NaCN
NaCN
KCN
CN
KCN
KCN
CN
NaCN
KCN
KCN
cf*e:t Conditions
MATCa(based on spawning 9'.15*C (varied
data) seasonally).
PH8, H « 236-
239 ppm
27 days - all survived
Lethal threshold con- 3°C
cent rat ion
24 hrs. - LCM 3°C
136 hrs. - LC100
40 days - all survived -9.5*C
Minimum lethal threshold 10°C
concentration
74 hrs. - average 17.5°C
survival time
10 days - 40S mortality 15.5*C
87 hrs. - LC5Q
Lethal threshold 12°-13*C
concentration
<2 h|r " l.C50 17'-]8'C,
ph 7.4-8.0
Threshold dose - 15.6*C
300 min.
288 hrs. - LC5Q 15.4*C
Total kill in 27 T/2 hrs.
39.0 min. mean survival
tine for small fish;
16.0 mm. for large fish
Mean death time * 1S.6°C
16 mm.
10 nrs.- 100S survival
uncertain - (Difficult jj'j
to compare this study
with others!
Lethal threshold con-
centration
Lethal threshold con- 2TC
centration at low oxygen
Lethal threshold con- 21*C
centration at high oxygen
Minimum lethal threshold 25°C
concentration
60 days - no mortality
150-300 min. - 50* • 25°C
aortalitv -(Difficult
to compare this study
with others)
150-350 mm. - 501 25°C
mortality
Saur-e
Koenst, et. al.
(1977)
Karsten (1934)
S. B. Ministry of
Technology (1963)
G. B. Dept. of
Environment (1972)
Karsten (1934)
Neil (1957)
Broderius (1977)
Herbert and
Hemens (1952)
Burdlck, Dean 4
Harris (1958)
Neil (1957)
G. B. Ministry of
Technology (196S)
ORNL/EPA (1978)
ORNL/EPA (1978)
Cardwell, et. al.
(1976)
ORNL/EPA (1978)
ORNL/EPA (1978)
ORHL/EPA (1978)
Renn (1955)
Abram (1964)
Burdick, Dean
i Harris (1955)
,.
ORNL/EPA (1973)
Brockway (1963!
Renn (1955)
„
5-3
-------
TABLE 5-1. REPORTED ACUTE EFFECTS OF FREE CYANIDE ON
FISH — FLOWTHROUGH EXPERIMENTS (Concinued)
Concentratio
(pomi
0.114
0.116
0.120
0.135
0.147
0.154
0.16
0.18
0.20
0.22
0.236
0.26
0.261
0.4S
0.49
0.49
n
Soecies
Fatnead Minnow
(Plmeohales promeUsl
Bluegill
(Lepomis macrochirus)
Fatnead Minnow
('inephaies aranelajil
Cicnlid
(CicSlasoma bi macula turn)
Guppy
{PoeciHa retlculatal
Bluegill
'Lepomis macrocnirus)
Channel Catfish
Cichlid
(Ocnlasona blmaculatum)
Guppy
(Potellla rttleulata)
Blacknose Dace
(E.linacntnvs atratuius)
Guppy
(Poecilla retleulatal
Guppy
(lebistes retlculatus)
Goldfish
(Carasslm auratm)
Bluegill
(Leponns nacroehlrus)
Thre«sp1n« Stickleback
(Gasterosteus aculeatus)
Eel
(Anquilla anquillal
Formulat
NaCN
NaCN
CN
NaCN
KCN
HCN
NaCN
Nacn
CN
KCN
KCN
CN
NaCN
-------
TABLE 5-2. REPORTED ACUTE EFFECTS OF FREE CYANIDE ON
FISH — STATIC EXPERIMENTS
Concentration
(pom;
0.05-0.08
0.07
0.09
0.11
a. 2
0.34-0.12
3.36
0.074
< 0.1
0.1
0.1-0.3
0.1-0.3
0.1-0.3
0.1-0.3
0.1-0.3
0.13-0.14
0.14
0.15
0.15
0.15
0.15
0.15
0.17
0.17
0.17
0.17
Species
COLDWATEB FISH
Srook Trout
{Salvelinus fontinalis)
(Uinbow Trout
iSalmp gairanerl)
Srook Trout
(Salvelinus fontlnalls)
Rainbow Trout
(Saline aairaneri)
UARMWATER FISH
3o)afish
(Carassms iuratus)
Cyprima Species
(Leucaso'us delineatus)
Harlequin Fish
(fiasbora heteromorpha)
Percid Fish
(Acerina cernua)
Carp
(Cyprtnus carpio)
Fathead Minnow
(Pimephales promelas)
European Minnow
(Phoxinus phoxinus)
Mn ga 1
(Cirrnina mrigala)
Green Sunfish
(Lesomls cy ant 11 us)
Threespine Stickleback
(Gastenasteus aculeatus)
Bluegill
(Lepomis macrochlrus)
Roach
(Rutilus rutilutl
Blueqill
(Lepomis macrochirus)
Largemouth Bass
(Micropterus salmoidesl
Rainbow Darter
(Etheostsma caeruleun)
Pickerel
(Esox Amerlcanus
venniculatusi
Rock aass
(AmolooMtes ruoestris)
Bluegill
(Leaomis Taerachirmi
Fomulation Effect Conditions
KCN Minimum lethal 8*-10'C
concentration
HCN 48 hrs. - LC5Q
KCN 48 hrs. - LCjg 8°-10°C
Lethal threshold
concentration
< 3 hrs. - average 18°C
survival time
f.C'1 72-96 hrs. - caused
mortality
KCN 2.5 nrs. - lethal 19.5CC
threshold concentration
168 hrs. - 20* mortality
KCN 100'- lortality - LC50 12eC
CN 24 hrs. - 401 mortality
CN 24 hrs or more - LC5Q
CN 24 hrs. or more - LC,.
CN 24 hrs. or more - LCjQ
CN 24 hrs. or more • LC,.
CN 24 hrs. or more - LC,-
KCN 96 hrs. - LC50 30*C
KCN LC5Q 1?«C
NaCN 11 hrs. - median 20*C
survival time
NaCN 96 hrs. - LC5Q 25'C
CN 96 hrs. - LC5Q
NaCN 96 hrs. - LCjQ Hara water
NaCN Lethal threshold
concentration
NaCN Letnal threshold
concentration
NaCN Lethal threshold
concentration
NaCN Lethal threshold
concentration
NaCN Lethal threshold
concentration
Source
ORNL/EPA (1978)
Brown (1963)
ORNL/EPA (1978)
Michigan Oept.
of Conservation
(1933)
G. 8. (1956)
Ellis (1937)
Malacca (1966)
Abram (1964)
Gillar (1962)
Silalchuk (1969)
Ooudoroff (1956)
Costa (1965)
Setn et. al.,
(1967)
Lewis and
Tarrant (1960)
Costa (1965)
Calms »
Scheier (1963)
GIMar (1962)
Broderius (1973)
Henderson, Pick-
ering 4 Lemke
(1961)
Suiter (1965)
ORNL/trA (1976)
Michigan Oept.
of Conservation
(1933)
-
"
"
•
5-5
-------
TABLE 5-2. REPORTED ACUTE EFFECTS OF FREE CYANIDE ON
FISH -- STATIC EXPERIMENTS (Continued)
Con cent ration
(pom) Sp»gi»<
0.17 Sluegill
(Lapomis iTaereehirus)
0.17-0.18
0.17-0.23
Formulation £f*K-t
NaCN «1Q nrs. - LC
KCN 96 hrs. - LC5Q
vriK f^f i- *
KC™ 96 hrs. - LC..
uonoi ti ons
18*C
18*-20°C
observes raoid
Source
Ooudoroff, et.
al., (1966)
Cairns i
Scheier (1963)
Cairns 1 Scheier
(1953. ISS9.
decline in some 1963, 1963)
0.2 European Minnow
[Phoxinus snoxInuiO
0.2
a-2 Harlequin Fish
(Rasfaora hetgromorpha)
0-2 Zebra Danio
(Sracnydamo rerial
0.2 Suppy
0.23 0.3S Fathead Minnow
(P_1mephales nromelas)
0.23 0.35
0 24 "
0-25 Black Bullhead
(Ictalurus me las)
°-25 Golden Shiner
(Notemloonm ervsoleuca^l
°-2« Tel lot. Bullhead
(Ictalurus natalit)
°-26- Pumpkin Seed
(Leponis nlbbosusl
0.28 BluMlll
(Leponis rcacrochlrm)
°-3 Cyprinid Species
(Leucasolus delineatus)
°-31 Goldfish
(Carassius iuratus)
0.33-0.45 81ueg111
(Lepomjs macroehirusl
°-39 Mottled Sculpin
(Cottus bairdil
0 40 MI
(Unidentified)
°-49 Zebra Oanlo
(Brachvdanlo rerto)
°-s Soldffsh
(Carassius auratus)
i °-53 Carp
(Cyprlnus earaiol
(Carassius auntus)
8 hrs. • average
survival time
KCN 5 hrs. - caused mortality
4 hrs - average survival
time
12 hrs. - averao*
80 hrs. - average
survival time
NaCN 96 hr. - LC-SO's- "ore
toxic In soft water
"*c't 96 hrs. - LCso soft and
hard water respectively
NaCN 48 hrs. - LC
toC" Not lethal In 72 hrs.
"•C" Not lethal 1n 72 hrs.
lt*at Lethal threshold
concentration
N»CN Lethal threshold
concentration
K0» 24-48 hrs. - LCj-
KC" 72 hrs - 1001 mortality
I OT tHOff A 1 i tv a*
\ *•• "wrba I i ty 45
0.14 ppm)
ttN 48-120 hrs. - caused
anrta T 4 f «
•eurfc4 1 1 C/
NaCS 96 hrs. - LCM
"4CN Lethal threshold
concentration
01 24 bn. - LCM
"CN 48 hrs. - LCM
*CN n hrs. - caused no
nortality
Lethal threshold
concentration
experiments
18-C
18.3° -22«C
18*C - Method
emo loved
unknown
*
18'C
25-C - Hard
and soft water
24.4-C
24.4'C
20*C
12*C
21.5'C
18'. We. .ore
toxic at higher
temperature.
Toxlcity not
affected by
water hardness
24'C. soft
water
NaCN 48 hrs. - caused 24'-28*C
mortality
Patrick, Ciirns J
Scheier (1963)
5. 8. (1956)
Malacca (1966)
6. 8. (1956)
•
6. 8. (1956)
ORNL/EPA (1978)
Henderson ,
Pickering I
Lemce (1961)
Black, et. al..
(1957)
ORW./EPA (1978)
OWL/EPA (1978)
Michigan D«pt.
of Conservation
(1933)
*
Turnbull. OeMann
* Ueston (19S4)
Gillar (1962)
Powers (1917)
OWL/EPA. (1978J
Michigan Oept.
of Conservation
(1933)
Schaut (1939)
ORNL/EPA (1978)
Bridges (1958)
Michigan Oept.
of Conservation
(1933)
Bridges (1956)
5-6
-------
TABLE 5-2. REPORTED ACUTE EFFECTS OF FREE CYANIDE ON
FISH — STATIC EXPERIMENTS (Continued)
Concentration
(ppm)
0.53
0.6
0.64
1.04
1.16
Species
Mudmlnnows
(Umbra lima)
Carp
(Cyprlnus carpio)
Mosquito F1sh
(Gambusla affinis)
Black Bullhead
(Ictalurus melas)
B1tterl1ng
(Rhodeus serlceus amarus)
Formulation Effect
NaCN
Conditions
KCN
KCN
KCN
KCN
Lethal threshold
concentration
72 hrs. - caused
mortality
24-96 hrs. - LC
'50
2T-23'C
28 hrs. - caused
mortality
8 hrs. - caused mortality 18.5<>-220C
Source
Michigan Qept.
of Conservation
(1933)
Nehring (1964)
Hall en, Greer 4
Lasater (1957)
Wells (1916)
Malacca (1966)
0.07
0.1-0.3
0.1-0.3
MARINE FISH
Marine Pin Perch HCN
(Laqodon rhomboides)
Eel CN
(Angullla jaoonica)
Eel CN
(Angullla anquilla)
24 hrs. - LC
50
24 hrs. or more - LC
13.7'-20.4°C
50
24 hrs. or more - LC
'50
Oaughtery J
Garrett (1951)
Oshima (1931)
Costa (1965)
5-7
-------
For fresh, warm-water fish under flowthrough conditions LC •«
ranged fro. 0.11 mg/1 to 0.45 mg/1 (see Table !-l) . iS results^ rom
wer. < neriTCS/T hlSher (SeS TablS 5-2); h°Wever« a11 LC50'S
were < 1.5 mg/1 and the majority were < 0.50 mg/1. Lethal threshold
concentrations under flowthrough conditions ranged from 0.071 mg/1 to
C um?^ f°r SiX Sp6Cies °f fish" Under static conditions, the
threshold concentrations for eleven species of fish fell generally below
0.5 mg/1, ranging from a very low 0.06 mg/1 to 0.53 mg/1. These
concentrations should not be considered as true threshold levels and
therefore, should not be used to define safe levels of cyanide in water
In many cases, the experiments were not conducted under the controlled '
Srt !T neCe"ar7 C° 'fcterain. the »« sensitive concentration.
Rather, these studies should be used in conjunction with median lethal
rn ^^"i6 inforaation was Available concerning the toxicity of cyanide
to saltwater species (see Tables 5-1 and 5-2). Static LC5o values £r
two species of eel were 0.1-0.3 mg/1 (Oshima 1931, Costa l§65a) A sLn
re^ortL r6"^^50 ^^ (°-°7 mg/1)' alS° from a stati= test, was °
reported for the marine pin perch (Daugherty and Garrett 1951 . This
fZ3r 1^ '5? Sensitivi^ of ^e salmonid species to cyanide Sder
flowthrough conditions. The solution was aerated; thus, high tox^ity
cannot be attributed to low oxygen supply. The test temperfture however
3 > iS difficu^ to determine whether
oin
this P«H?< I3" 6 T 7 "M±t±ve sPecies 0^ Aether some condition in
this particular experiment (e.g., fluctuating temperature) caused an
«?*?"£ 5eSP°nSe' ,M2re StUdy 1S needed reSardinS ^is and other salt-
water fish species before the toxicity of cyanide to marine and estuarine
biota as a group can be assessed.
Aquatic invertebrates were generally far less sensitive to cyanide
than vertebrate species (see Table 5-3). LC50 values ranged from 0.4 to
more than 3.0 mg/1. All species reported are found in freshwater sy terns.
Studies of the sublethal effects of cyanide on fish (see Table 5-4)
have generally measured changes in swimming ability, in oxygen consumption,
in development of eggs and larvae, and in some biochemical activities
The significance of these changes, especially the nonreproductive
type, on fish populations is difficult to determine. A 50% reduction
in swimming ability or a decrease in the rate of oxygen consumption may
have little impact except during periods of stress, e.g., a period of
limited food supply. In a similar way, lower reproductive success may
not influence population size except during a year of high mortality
when it could have a severe impact. The results of sublethal experiments
should be used with acute toxicity results to determine a general (order
of magnitude) estimate of the cyanide toxicity to each group of fish.
The reported concentrations of cyanide that caused sublethal effects
in fish did not vary radically from lethal levels. Concentrations ranged
5-8
-------
TABLE 5-3. REPORTED EFFECTS OF FUEL UYANlUt UN AQU«TIl INVERTEBRATES
Species
Concentration
Formulation (nig/1) Effect
Midge Fly
(Cricotopus bicinctus)
Cnai 1
•JltQ 1 1
(Physa heteroclita)
Snail
( Physa_ heterostropha)
V Daphnia
^ (Daphnia tnagna)
Lymnacea sp. (egg)
Caddlsfly larv.
(Hydropsyche sj. )
Mayfly larv.
( Stenonemarubrum)
Daphnia
(Daphnia magna)
it
Amphipod
/ r* __ _ * t
CN
CN
KaCN
KaCN
KaCN
KaCN
KaCN
KaCN
NaCN
NaCN
— — _ k -*! - J
< 3.2
0.432
1.08
0.48
0.4
130.0
2.0
0.5
0.8
< 3.4
0.49
no effect on
survival and
maturation
96 hrs. LC5Q
96 hrs. LC5Q
ll
96 hrs. LC5Q
96 hrs. LC5Q
48 hrs. LC5Q
48 hrs. LC,n
bt)
Toxicity threshold
2 days
Concentration
nearly immobilizes
Survive 3 hr<;_
l*UIIIJ 1 L 1 Uffl
Field study
Static
normal dissolved
oxygen
Low dissolved oxygen
Static
Static
Static, soft water,
20-22. 2°C
II
Static 23°C.
Field study
n.l/i0r
source
Surber (1960)
Patrick et. al.
(1968)
Cairns (1965)
..
Dowdenand
Bennett (1965)
li
Roback (1962)
»
Brinqmann and
Kuhn (1959)
Anderson
(1946)
r«»- * , 1 1 nci:i \
larus^ pulex]
Constant flow
Costa I1965b)
-------
TABLE 5-4. REPORTED SUBLETHAL EFFECTS OF FREE CYANIDE ON FISH
'3Cr
3.:C6-.311
3.31
3.31
3.01
3. 31-3. 10
0.02
0.02-0.33
0.025
0.35
0.019
0.044
0.06
0.09
n na.n i
"J . U7—'J . 1
3.10
0.10
1.5
Species
FRESHWATER FISH
Caldwater Soeeies
Brook Trout
(Salve! inus fontinalisl
Rainbow Trout-juv
(Salmo gairdneri )
Brook Trout
(Salve! inus fontlnalls)
Cono Salmon
(Oneorhvnchus kisutchl
Atlantic Salmon
(Sal-io salar)
Chinook Salmon
(Oneorhynthus tshawvtschal
Rainbow Trout-juv
(Sal no sairdneri)
Brown Trout
(Salmo trutta)
Brook Trout
(Salvelinus fontinalisl
Warm Water Soecies
Fathead Minnow
(Pimephales promelas)
"
Clchlid
(Ciehlasoma bimaeulatum)
»
|(
"
Mumr.ichog
"omulation
HCN
HCN
CN
NaCN
HCN
CN
HCN
CN
CN
HCN
CN
NaCN
NaCN
Effect
MATC (based on spawning
data)
Induced some degree of
hepatic necrosis
Impaired swimming
ability by 75"-
Impaired swimming
ability by 56S
Caused damage to develop-
ing embryos: effects
included delayed natcning.
reduced conversion of yolk
into body tissue, higher
incidence of abnormalities
Reduction in rate of
oxygen consumption
Reduced mean weight gain
by 40*-95X. Also *at
gain lower and higner
water content
Reduction in rate of
oxygen consumption
Impaired swimming
ability by 65%
Egg production
significantly reduced
Egg hatchabiHty
significantly reduced
Impaired swimming
ability
Impaired swimming
ability
Fin damage
Affected enzyme
activity in liver
^ 1 i"iujA<4 riAual AnmAM* /+£
So f
Koenst. et. al. ,
(1977)
Oixon and Leduc
M077)
( ' yt ' I
Neil (1957)
Brodertus (1970)
Leduc (1978)
Negilski (1973)
Oixon and Leduc
Carter (1962)
NeTl (1957)
Lind, et. al.,
(1977)
„
Brockway (1963)
Leduc (1966)
Leduc (1966)
Brockway (1963)
„
0.33
0.55
(Fundulus heteroclitusl
FISH
Gunner
(Tautoqolabrus adspersus)
Threespine Stickleoack
(Gaste-'osteus aeuleatusl
Curner
(Tautoaolabrus
embryos in late
embryonic stages
Develoonent of later
stages delayed
Development delayed and
disintegration of embryos
after several hours
Reduction in rate of
oxygen consumption
Develoonent ceased
Philips (1940)
Philips (1940)
Jones (1947)
Ptiilios (194Q)
5-10
-------
from 0.01 mg/1 to 0.10 mg/1 for cold-water species and 0.019-1.6 mg/1 for
warm-water species. Again, certain effects, such as reproduction, varied
considerably among species. Swimming ability was affected in several
species, however, at approximately the same concentration.
5.1.2.3 Toxicity of Other Cyanide Compounds
The reported effects of selected non-metal cyanide complexes on
aquatic organisms are presented in Table 5-5. The most toxic of the
organic compounds (and other miscellaneous forms) were cyanogen chloride,
lactonitrile, and malononitrile. For these compounds, LCso's were <1 mg/1,
Their toxicity was similar to that of a simple cyanide solution with the
same concentration of free cyanide. For many of the other organic com-
pounds, effects were observed at much higher concentrations. This may
result from their greater recalcitrance to hydrolysis and any other
reactions that liberate and make available the free cyanide portion of
the compound to organisms. The other cyanide ions, thiocyanate and
cyanate, were also reported as being much less toxic than free cyanide
(Doudoroff 1976).
It is difficult to generalize about the toxicity of metal cyanide '
complexes. The effect of the free cyanide fraction and/or the metal
ion can determine toxicity. In turn, these effects are influenced by
solution pH and other environmental conditions, synergistic interactions
and the compound's stability (e.g., its solubility, photodegradabilitv,
etc.).
Concentrations of selected metal cyanide compounds that have been
reported to have toxic effects on aquatic organisms are presented in
Table 5-6. These results have been selected only to provide an indication
of the concentration ranges of cyanide compounds with lower toxic levels
that affect aquatic organisms.
The toxicity of some of the less toxic cyanide complexes of metal
ions (e.g., nickel and iron) appear to depend on molecular HCN content
(Doudoroff 1966). Other metal cyanide complexes—silver, zinc, and
copper—were more toxic than other complexes, apparently because of the
higher toxicity of the ion present. In all test cases, except one,
effective concentrations were higher than those of simple cyanides tested
under the same conditions (Lipshuetz and Cooper 1955, Doudoroff 1956).
The exception was an experiment reporting zinc-cyanide and cadmium-cyanide
complexes as more toxic than simple cyanide, suggesting slight synergistic
activity (Doudoroff 1956). Another study on zinc contradicted these
results (Cairns and Scheier 1968). In this case, the zinc-cyanide com-
plex was less toxic. Not enough information about this assessment is
available to make any conclusions about the relative toxicities of zinc-
and cadmium-cyanide complexes and free cyanide.
In general, free cyanide appears to be the most toxic form
of cyanide in water. Any conclusions or decisions based on effects con-
centrations of free cyanide, therefore, would also cover the effects of
most cyanide compounds.
5-11
-------
TABLE 5-5. REPORTED EFFECTS OF ORGANIC AND OTHER CYANIDE COMPOUNDS ON FISH
Concentration
< 0.1 (0.04 CN)
0.22 (0.08 CN)
0.5
0.51 (0.19 CN)
0.71 (-0.25 CS)
2.6 (1.3 CN)
10.1
11.8
23 (12 CN)
33.5
S6
75 (30 CN)
78
78, 135
114
400
720
775
320, 1250
Species
Rainbow Trout
(Sal mo qairdneri)
Marine P1n Perch
(Lagodon rhomboides)
Rainbow Trout
(Salmo qairdnerf)
Bluegill
(Leaomis maerocriirusl
White Crappie
(Pomoxis annularis)
Golden Shiner
(Notemisonus crysoleucasl
Fathead Minnow
(Pimephales promelas)
"
•
Blueglll
(Lapomis maereehirusl
Marine P1n Perch
(Lagodon rhomboides)
Guppy
(Lebistes retieulatusj
Mosquito Fish
(Gambusla affinis)
Creek Chub
(Semotllus atromaculatus)
Blueglll
(Lepomis macrochlrus)
Fathead Minnow
(Pjmephales promelas)
Mosquito Fish
(Gambusia affinis)
Guppy
(Lebistes retleulatus)
Blueglll
(Lepomis macrochirusl
Guppy
(Lebistes retlculatus)
Fathead Minnow
(Pimephales aromelas)
Compound
Cyanogen
chloride
Lactonitrile
Malononitrile
Lactonitrile
Lactonitrile
Acrylonitrile
Acrylonitrile
Acrylonitrile
Acrylonitrile
Acrylonitrile
Aononium
Thlocyanate
Sodium
Cyanate
Benzonitrile
Benzonitrfle
Annonlum
Thlocyanate
Benzonitrlle
Adlponltrlle
Ad1pon1tr1le
Adlponltrlle
Effect
Lethal threshold
concentration
24 hr. LC5Q
72 hr. LCSQ
Fatal in 10 hrs.
96 hr. LC5Q
30 day LC5Q
96 hr. LC5Q
96 hr. LC5Q
24 hr. LC50
96 hr. LC5Q
All fish died
In 144 hrs.
LC50
96 hr. LC5Q
96 hr. LCSQ
96 hr. LC5fl
96 hr. LC5Q
96 hr. LC5Q
96 hr. LC5Q
96 hr. LC5Q
Conditions
Static, 17°-20'C
Static. 13.7°-20.4»C
Flow through, 25'C
1000-1850 Fathead Minnow. Suppy
and Blueglll
3600-4450 Fathead Minnow,
Guppy and Bluegill
Acetonitrile 96 hr. LC50.
Oxydlpro- 96 hr. LC.n,
pionitrile
50's
How through, soft
water, 2S°C
Flow through, soft
water. 25°C
Flow through, soft
water. 25"C
Static, soft water.
25'C
Static, variable
temperatures
Static, soft water,
25'C
Static, 16'-23°C
Static, soft water,
2S'C
Static. 25°C, hard
ft soft water
respectively
Static. 16'-23'C
Static, soft water,
25'C
Static, soft water,
25'C
Static, soft water.
25'C
Static. 25'C, soft
and hard water
respectively
Static. 25'C, soft
water
Static, 25'C, soft
water
Source
Allen, et. al
(1948)
Daughterly i
Garrett (1951
G. B. (1973)
Renn (1955)
Henderson, et,
al., (1961)
Oaughtery &
Garrett (1951)
Henderson, et.
al.. (1961)
Wallen, et. al
(1957)
Uashburn (1948
Henderson, et.
al.. (1961)
Henderson, et.
al., (1961)
Uallen. et. al
(1957)
Henderson, et.
al., (1961)
5-12
-------
TABLE 5-6. REPORTED EFFECTS OF METAL CYANIDE COMPOUNDS ON FISH
Compound
Z1nc - and Cadmium -
Cyanide Conplei
Concentration
(opml as CN
0.23 (NaCN)
0.18 (NtCN »
Species
Fathead Hlnno.
prone las)
Source
98 hr. USD's- Indicated slight Ooudoroff
synergutic activity (1956)
0.17 (NaCN •
C4S04)
Nickel-Cyanide
Silver-Cyenioe
Cooper-Cyanide
Conplei
Iron-Cyanide
Coaplei
0.40-0.84 Bluegill
(Lepomis nacrochirus)
0.18 (KCN) Bluegill
(irfpomis tnacrochirus)
0.28 (KCN • ZnClj)
0.42 (OH 8.5-6.6) Fathead Mlmo»
730.0 (OH B.O) ' ' '
0.95 (HeCN - Sluegill
N S04) (lepomis nacrechirus)
10 at OH 7.5 Bluegtll
(0.02 pom MOt). (Leogmil macrochtrusl
OH 6 5 (0.12
oe> HCN) and
OH 6.0 (0.19
DP* -01)
6.0 (freshwater) Threesome Stickleback
3.0 (teexater) (Gasterosteus aculeatus)
10.0 Bluegill
(Lepomis maerochlrusi
< 7.0
0.22 (KCN) Western Blactnos* Dace
(Rhtnichthys atratulus)
0.38 (KCN » CuCN
•/cole ratio CN/Cu
of 4.0)
0.47 (ratio 3.75)
0.71 (ratio 3.0)
0.25 (NaCN) Fathead NlimoH
0.2S (CuS04)
2.2 (NaOl • CuS04)
0.28 (KCN) Eel
(Anouilla 'aoonical
3.9 (K4fielCNJs or
lC;g'i of wtal cyanide com-
pletes illgntly greater than
those predictable on basis of
determined nolecular HCN levels
98 hr. ICSO,S
96 hr. I.CJQ. Concluded that
acute toiicity dependent on
•olecular HCN content
98 hr. LC5fl
Median resistance tine at pH 6.5
and 7.5 very similar Much more
rapid tone effects at OH 6.0.
Concluded that silver ion itself
has high toiicity
24 hr. LCM
24 hr. Uio
»6 hr. LCjg
24 hr. LCj(j.,. Toildty
decreased mth increased cooper.
Test solutions v*re not aged
to point of equilibrium
24 hr. USD's- Indicated that
conpleiing decreased ini lability
of both conpounds
Both iron-cyanide complexes
•ere lethal in sane period
of tine as KCN.
Ooudoroff,
et. a!.. (1966!
Cairns I
Scneier (19M)
Ooudoroff
(1956)
Ooudoroff
U«6!
Ooudoroff, et.
al.. (1966)
Brooeriul
(1973)
Broaerius
(1973)
Upshueu
and Cooper
(1955)
Ooudoroff
(1956)
Oshina (1931)
O.S5
BUcknos* Oict
(9hintcntnys itntulus)
Creek Chub
itromculitm)
Fatal in l-l'/Z hrs «nen Burdiek and
solutions tloosed to tight. Lipscnuetz
When solutions kept in dark. (1950)
lethal concentration considerably
higher (-1700 ppm)
Silvery Hinnoe
(Hyboanathus re-
300
kept in dart)"
30 (
partially illuminated)
2 (
eipoied to full light)
RaInbox Trout
(Sal"a
24 hr IC
M.S
Bucksteeg
own
500 (K3fe[0l1s
kept in dark)
500 (K4FeCC!«]j
kept in dart)
Bluegill
i"*croe«iruj)
ffsh survived > 18 hrs. in
*3Fe[Cf«]£ solution but tiedtan
survival time *as 145 minutes
in K«Fe[CK]{ solution
Attributed nigher tojticity of
latter compound to greater
instability (dissociation to
HCN)
Sroderius
(1973)
5-13
-------
5.1.2.4 Bioac cumulation
Cyanide does not appear to bioaccumulate in aquatic organisms (ORNL/
U.S. EPA 1978). If the cyanide concentration in water is not high enough
to kill an organism, cyanide is metabolized and discharged. In aquatic
systems, biodegradation is thought to be a predominant fate, of equal
importance to hydrolysis (Doudoroff 1976). If this is the case, residues
of cyanide found in fish tissue would indicate that the substance had
only recently entered the aquatic system.
5.1.2.5 Influence of Environmental Factors
The relationship between cyanide toxicity and water temperature is
not clear. At relatively high concentrations (0.3-1.0 ag/1 as CN) ,
cyanide is lethal more rapidly at higher temperatures, with an inversely
proportional relationship between temperature and the logarithm of time
to death (Wuhrmann and Woker, 1953, 1955, Sumner and Doudoroff 1938).
In bluegill, 96-hour LCso's are lower (cyanide is more toxic) at 30°C
(0.13-0.14 mg/1 as CN) than at 18° (0.17-0.18 mg/1) in both soft and
hard water. On the other hand, some evidence indicates that lower
concentrations of cyanide (<0.3 mg/1 as CN) are lethal more rapidly at
lower temperatures (Great Britain 1953); and, for rainbow trout, LC$o' s
are lower at very low temperatures — between 2-4°C — (Great Britain
1968, 1972) than at temperatures of 12-20°C.
.These differences may be due to slower metabolism at lower
temperatures, which would slow down detoxification in the body so that
cyanide would be more toxic at moderate concentrations. High concen-
trations of cyanide, however, may prevent the detoxification process
from handling the cyanide load. In this case, toxicity would increase
with the rate of metabolism (e.g., respiration rate) (Doudoroff 1976).
More research is needed before cyanide's behavior in varying water
temperatures of natural environments can be understood.
Reports of the effect of water hardness on freshwater toxicity
have been contradictory. Cyanide has been found to be less toxic in
hard waters (Henderson at. al. 1961), more toxic in hard waters
(Leclerc and Devlaminck 1950), and unaffected by water hardness (Cairns
and Scheier 1963, Burdick et_ al. 1958). Among the studies, the ranges
and har
-------
Cyanide is more toxic to fish in water containing low concentra-
tions of dissolved oxygen (<4 mg/1). Both the time of survival
(Dooming 1954, Burdick et al. 1958) and LC 's (Burdick et al. 1958,
Cairns and Scheier 1958) are reduced at lower oxygen levels.
5.1.3 Toxicity to Wildlife
No data were available concerning the effects of cyanide on wild-
life species; therefore, laboratory animal data were examined to
provide an indication of the cyanide concentration ranges toxic to
small mammals. Table 5-7 presents the results of reported laboratory
studies on cyanide toxicity through inhalation and Table 5-8 presents
lethal concentrations through ingestion.
When inhaled, cyanide is rapidly lethal to rats and rabbits at
concentrations of 100->1000 mg/1. Of those compounds reported,
cyanide in the form of HCN is most toxic because of its rapid release
to the body.
Ingested cyanide is reported lethal to rats and rabbits at con-
centrations of 8.7-39 mg/kg body weight. No exposure time was
reported; however, cyanide at these concentrations was probably
toxic immediately. No studies of long-term exposure to low concentra-
tions of cyanide were available. However, some evidence indicates that
mammals rapidly metabolize cyanide, and are not affected by levels too
low to be acutely toxic (see Section 6.1).
No information was available regarding toxicity of cyanide to
birds, via any exposure route (ORNL/U.S. EPA 1978).
5.2 BIOTIC EXPOSURE TO CYANIDE
5.2.1 Introduction
This section describes the potential for exposure of selected
aquatic organisms to harmful levels of cyanide in the ambient environ-
ment. The approach used in developing this section was as follows:
The findings of the toxicity assessment for biota (see Section 5.1)
were reviewed in conjunction with the U.S. EPA data on reported fish
kills attributed to cyanide for the 1972-77 period. This review
provided a basis for identifying potentially sensitive and important
receptors, and for identifying cyanide levels known or suspected to be
potentially harmful in the environment. Certain data were
emphasized in reviewing the laboratory data discussed in Section 5.1,
i.e., cyanide levels associated with organism mortality under acute
or chronic conditions, and cyanide levels associated with reduced
mobility or reproductive efficiency. Then, the distribution of
selected sensitive/important organisms at the national scale was
characterized. This distribution of sensitive receptors was compared
5-15
-------
TABLE 5-7. REPORTED EFFECTS OF INHALED CYANIDE AND CYANIDE
COMPOUNDS ON LABORATORY ANIMALS3
Concentration
in air (pom)
HO (0.12 mg/1)
3.5 (0.35 mg/1)
400 (0.85 mg/1)
400 (0.84 mg/1)
1.4 mg/1 ,
Species
Rat
Rabbit
Rat
Rabbit
Rat
Compound
HCN
HCN
Cyanogen
Cyanogen
Cyanogen
Chloride
Response
Fatal in 1.5 hr
Fatal
Fatal in 1 hr
Fatal in 1.8 hr
Fatal in 0.17 hr
Source
Dudley et al.
(1942)
H
McNerney and
Schrenk (I960;
Fassett (1963]
Spector (1956)
1200 (3.0 mg/1) Rabbit
2.2 mg/1 Goat
Fatal in 2 min Fassett (1963)
Fatal in 7-10 min Spector (1956)
TABLE 5-8. ACUTE TOXICITY OF ORAL-ADMINISTERED CYANIDE
TO LABORATORY ANIMALS
Concentration
mg/kg of body wt Species
8.7-11.5
15 (11-21)
23.5
39 (30-51)
Rat (male)
Rat
Rabbit
Rat
Cyanogen Iodide
Calcium Cyanide
Response
.a
Compound^
Potassium Cyanide Lethal
Sodium Cyanide LD
'50
Lethal
LD50
Source
Gaines (1965
Smyth et al.
(1969) ~~
Hunt (1923)
Smyth et al.
(1969)
No exposure time reported
5-16
-------
with the available information concerning the levels of cyanide found
nationally (Chapters 3.0 and 4.0) in order to identify possible areas
where aquatic biota may be at risk.
5.2.2 Effects Levels
In assessing aquatic exposure, the initial step was to review the
aquatic effect,-, discussed in Section 5.1 in relation to the distribution
of cyanide in surface waters.
Effects data were reviewed to identify sensitive, important aquatic
organisms for exposure/risk considerations and to identify ambient
threshold cyanide concentrations at (or above) levels that would incur
adverse effects.
From the laboratory results cited in Section 5.1 and in Towhill
.et _al. (1978), the following principal observations can be made:
• The lowest reported levels of cyanide effects were
approximately 10 yg/1 for both acute and chronic
effects. Neill (1957), Broderius (1970), and Leduc
(1978) reported, respectively, a 75% reduction in
the swimming ability over a one-month period, greater
than a 50% reduction in swimming ability in a two-
hour period, and damage to developing embryos in
greater than a 100-day period for various salroonids
exposed to concentrations of cyanide as low as
10 yg/1. Conversations with the U.S. EPA Environ-
mental Research Laboratory staff at Duluth
(Personal Communications, Environmental Research
Laboratory, Duluth, MN, 1980) indicate that the
lowest reported effects level for freshwater fish
is a chronic value of 5 ug/1, reportedly associated
with an absence of spawning in bluegill sunfish.
• These cyanide levels (M.Qug/1) correspond with a
detection limit commonly employed in past analyses
of ambient water quality. This implies that much
of the available monitoring data (see Section 3.3)
may not be sufficiently precise to allow useful
projections of risk to the most sensitive
receptors.
• The laboratory data summarized in Section 5.1
suggest strongly that the effects of cyanide
depend highly on the form of cyanide present in
the environment. Since available monitoring data
sometimes report only total cyanides, aquatic expo-
sure estimates based on these data are difficult to
compare with the dissolved concentrations reported
in toxicitv studies.
5-17
-------
Little, if any, basis exists for distinguishing
unusually sensitive species for the assessment of
cyanide risks in the aquatic environment. Most
but not all, of the older laboratory-based data
suggest that salmonids were the most sensitive
species, exhibiting adverse effects at levels of
exposures as low as 10-50 ug/l. However, as
previously mentioned, recent work with warm-water
species, including bluegills and fathead minnows,
suggests that these species can also experience
adverse effects as a result of chronic exposure
to cyanide concentrations < 50 ug/l.
as1 ansi*ni?i°I JiStrib^ion' no geographic region can be distin-
as a significant area o£ exposure because these species are
widespread in cold and warm waters. species are
5-2.3 Exposure Levels
r*i« ThS informati°n Presented previously concerning sources of cyanide
d±™r C!u""^/See Chapter 3'0)' ma^r environmental pathways that
determine the environmental distribution of cyanide (see Section 42)
and cyanide levels actually detected in surface water (see ScSon^ 3)
have the following implications for aquatic exposure levels.
• The fate calculations (see Section 4.2) imply that
exposure to cyanide concentrations >50 ug/l are
possible in ambient waters receiving discharges
from any of the large point-source wastewater
dischargers, such as iron and steel facilities,
steam-electric power plants, and POTWs. These'
calculations also imply that such elevated concen-
trations would be restricted to relatively localized
extensions of the receiving waters associated with
the several types of discharges. However, considering
the limitations of the "uniform mixing" assumption used
in these calculations, it is possible that even smaller
volumes of receiving water may actually be affected;
but that concentrations of cyanide might be higher
than the calculated levels. *
• Maximum concentrations of cyanide in surface water
occasionally exceed the 10-100 ug/l acute effects
thresholds discussed earlier. The STORET 85th
percentile values (see Section 4.3) suggest that
these high concentrations occur infrequently.
Some of the available monitoring data report
corresponding measurements of the more toxic,
5-18
-------
free cyanide concentration at given locations. Thus
any conclusions regarding exposure based on data for
total cyanide alone must be qualified.
5.2.4 Summary of Exposure to Freshwater Organisms
The information presented in this section suggests that the inci-
dence of localized exposure of finfish to harmful concentrations of
cyanide may be widespread and may often be associated with one or more
types of point source discharges. Because the actual exposure in any
specific water body depends on factors such as discharge volume,
discharge control, and the nature of receiving water mixing opportuni-
ties, no national average relevant to exposure levels exist. Therefore,
information is required on individual discharges and compliance with
discharge controls for an accurate assessment of exposure levels in
areas with point source discharges of cyanide. Even though these data
are not available, certain qualitative conclusions concerning aquatic
exposure are possible. Where cyanide levels exceed 5-7 ug/1, these
concentrations will probably be in the vicinity of point discharge
sources, and they will rapidly diminish at increasing distances from
the source. Hence, fish populations in surface waters are probably
exposed to these levels only at distances of several kilometers rather
than within a broad geographic area, unless there are numerous discharge
sources clustered together.
5-2.5 Summary of Potential Exposure to Marine Organisms
The limited data available indicate that marine species, such as
the pinfish (Lagodon rhomoboj^ . and eels, can be adversely affected
by levels of free cyanide between 50 yg/1 and 300 ug/1 (Daugherty and
Garrett 1951, Costa 1965a). Though this range is comparable with the
effects ranges reported for many freshwater fish species (see Section 5.1),
these data do not provide information on a large enough number of species
to be considered fully representative of potentially important marine
exposure situations. Marine finfish, such as the Atlantic silverside
(Menidia menidia). juvenile striped bass (Morone sexatilis), and menhaden
(Brevoortia). have been reported to be sensitive to various other contami-
nants in laboratory situations; and it is considered reasonably likely that
one or more such species could be more sensitive to cyanide than Lagodon.
However, in the absence of monitoring data for marine/estuarine
waters, the exposure of marine organisms to potentially toxic levels of
cyanide cannot be quantified. Reported fish kills (see Chapter 7.0)
provide anecdotal evidence of a few instances of high concentrations.
5-19
-------
REFERENCES
Abram, F.S.H. An application of harmonics to fish toxicoloey
Inc. J. Air Water Pollut. 8:325-338 1964. (AS cited by Doudoroff 1976)
Allen, L.A.; Blezard, N.; Wheatland, A.B. Formation of cyanogen chloride
"
Anderson B.C. The toxicity thresholds of various sodium salts
(L c™tededby Vs? Ill 1133***
Anderson, P D. An approach to the study of multiple toxicity through
the derivation and use of quantal response curves. Corvallis OR-
Oregon State University; 1974. ^^ams, UK.
.1'0' T°XiCity °f P°wer Plant chemicals to
life. U.S. Atomic Energy Comm. WASH-1249; 1973.
Black, H.H.; McDermott, G.N.; Henderson, C. ; Morre; W.A. ; Pahren H P
Sdu« ? ^ W3SCe ^^e-by-product coke. Proceedings of the eleven^'
industrial waste conference; 41:494-527; Lafayette, IN: Purdue
University; 1957. (As cited by Becker and Thatcher 1973)
o cyanide as a fish Poison. U.S. Fish Wildl. Serv.
Sci. Rep. Fish. No. 253; 1958. Up. (AS cited by Doudoroff 1976)
Bringmann G. ; Kuhn, R. The toxic effects of water on aquatic bacteria
- Gesun dheits - icbteria*
l^T^7:^'1" f°me 6ffeCCS °f sub-lethal levels of pen tachlor phenol
and cyanide on the physiology and behavior of a cichlid fish Cichlasoma
bimaculatum Linnaeus). Corvallis, OR: Oregon State
36p. thesis. (As cited by Doudoroff 1976)
S'i' Detf™ination of molecular hydrocyanic acid in water
comoL r f^ Chemiscr^ and toxicity to fish of the nickelocyanide
complex Corvallis, OR: Oregon State University; 1970. 93p. thesis
As cited cnesis.
(As cited by Doudoroff 1976)
and ^rn^c ;,f',u ! Ot molecular hydrocyanic acid in water
and studies of the chemistry and toxicity to fish of metal-cyanide
complexes. Corvallis, OR: Oregon State University; 1973. 287o
dissertation. (As cited by Doudoroff 1976)
5-20
-------
Broderius, S.J.; Smith, L.L.; Lind, D.T. Relative toxicity of free
cyanide and dissolved sulfide forms to the fathead minnow (Pimephales
promelas). J. Fish. Res. Bd. Can. 34 (12): 2323-2332; 1977.
Brown, V.M. The calculation of the acute toxicity of mixtures of poisons
to rainbow trout. Water Res. (Great Britain) 2:723-733; 1968. (As cited
by Doudoroff 1976)
Bucksteeg, W. Teste zur Beurteilung von Abwassem. [Tests for the
examination of waste waters.] Staedtehygiene 12(9):180-184; 1961.
(As cited by Doudoroff 1976)
Burdick, G.E.; Dean, H.J.; Harris, E.J. Toxicity of cyanide to brown
trout and smallmouth bass. N.Y. Fish Game J. 5:133-163; 1958. (As cited
by Doudoroff 1976)
Burdick, G.E.; Lipschuetz. Toxicity of ferro- and ferricyanide solutions
to fish, and determination of the cause of mortality. Trans. Am. Fish.
Soc. 78 [for 1948]:192-202; 1950.
Cairns, J., Jr. Biological concepts and industrial waste disposal problems,
Proceedings of the twentieth industrial waste conference; 49(4):49-59;
Lafayette, IN: Purdue University; 1965.
Cairns, J., Jr.; Scheier, A. The effect of periodic low oxygen upon
toxicity of various chemicals to aquatic organisms. Proceedings of the
twelfth industrial waste conference. Ser. No. 94 Eng. Bull., 42(3):
165-176; Lafayette, IN: Purdue University; 1958. (As cited by Doudoroff
1976)
Cairns, J., Jr.; Scheier, A. The relationship of bluegill sunfish body
size to tolerance for some common chemicals. Proceedings of the
thirteenth industrial waste conference. Ext. Ser. No. 96 [Eng. Bull. 43(3)]:
243-252; Lafayette, IN: Purdue University; 1959. (As cited by Doudoroff
1976)
Cairns, J., Jr.; Scheier, A. Environmental effects upon cyanide toxicity
to fish. Not. Nat. Acad. Nat. Sci. Philadelphia, No."361; 1963; lip.
(As cited by Doudoroff 1976)
Cairns, J., Jr.; Scheier, A. A comparison of the toxicity of some
common industrial waste components tested individually and combined.
Prog. Fish-Cult. 30:3-8; 1968. (As cited by Doudoroff 1976)
Cardwell, R.D.; Foreman, D.G.; Payne, T.R.; Wilbur, D.J. Acute toxicity
of selected toxicants to six species of fish. Report No. EPA-600/3-76-
008. Duluth, MN: U.S. Environmental Protection Agency; 1976:22-26,
97-101. (As cited by Doudoroff 1976)
Carter, L. Bioassay of trade wastes. Nature (London) 196:1304; 1962.
(As cited by Doudoroff 1976)
5-21
-------
Chen, C.W.; Selleck, R.E. A kinetic model of fish toxicitv
threshold. J. Water Pollut. Control Fed. 41 (3, Pt. 2)- R294-R308-
1969. (As cited by Doudoroff 1976) '
Costa, H.H. Responses of freshwater animals to sodium cyanide
solutions. I. Fish. Ceylon J. Sci. Biol. Sci. 5(2):41-87; 1965a
(As cited by Douderof f 1976) * l **'
Thl °f freshwater animals to sodium cyanide solutions
I. rish. Ceylon J. Sci. Biol. Sci. 5(2):41-87; 1965b (As cited
by Becker and Thatcher 1973)
and^ff ! J-M.5 Barrett, T.J. Toxicity levels of hydrocyanic acid
and some industrial by-products. Tex. J. Sci. 3:391-396: 1951 Us
cited U
cited fay Douderoff 1976)
r
63 1 1977
' G< Exposure of rainbow trout to sublethal levels
P°llut'
Doudoroff. P. Some Experiments on the toxicity of complex cyanides
n ^ « ?!Sf* WaStSS 28;1020-1040; 1956. (As cited bv
tJouderorf 1976)
Doudoroff, P. Toxicity to fish of cyanides and related compounds
" -7- '
Doudoroff, P.; Leduc, G. ; Schneider, C.R. Acute toxicity to fish of
tiin^r C°nta1inin8 fmPlex metal cyanides, in relation to concentra-
tions of molecular hydrocyanic acid. Trans. Am. Fish. Soc. 95-6-22-
1966. As cit '
1966. (As cited by Douderoff 1975)
^!?§ ^T^rT36"116^,' H'J- Toxicity of selected chemicals to certain
animals. J. Water Poll. Cont. Fed. 37 (9) :1308-1316; 1965. (As
cited by Becker and Thatcher 1973)
Downing, K.M. The influence of dissolved oxygen on the toxicity of
potassium cyanide to rainbow trout. J. Exp. Biol. 31:161-164- 1954
(As cited by Douderoff 1976) ' '
Dudley, H.C.; Sweeney, T.R.; Miller, J.W. Toxicology of Acrylonitrile
(Vinyl Cyanide) : II. Studies of effects of daily Inhalation. J Jnd
Hyg. Toxicol. 24(9):255-258; 1942. (As cited by Douderoff 1976)
and measurei»ent of stream pollution. U.S. Bur.
Fassett D.W Cyanides and nitriles. Industrial Hygiene and Toxicology,
T h* TMI S^' Fassett and D.D. Irish, eds. New York, NY:
John foiley and Sons, Inc.; 1963: 1991-2036. (As cited by Douderoff
5-22
-------
Gaines, T.B. Acute tOKicity of pesticides. Toxicol. Appl. Pharmacol.
14:515-534; 1969. (As cited by Douderoff 1976)
Gillar, J. The effect of cyanide on some aquatic animals [in Czech,
with Russian and German summaries]. Sb. Vys. Sk. Chem.-Technol.
Praze, Techno1. Vody 6(pt. l):435-457; 1962. (As cited by Douderoff
1976)
Great Britain, Department of Scientific and Industrial Research.
Water pollution research 1952. London: H.M. Stationery Office; 1953:
42-45. (As cited by Douderoff 1976)
Great Britain, Department of Scientific and Industrial Research.
Water pollution research 1955. London: H.M. Stationery Office; 1956:
37-38. (As cited by Doudoroff 1976)
Great Britain, Department of the Environment. Water pollution research
1971. London: H.M. Stationery Office; 1972: 38-40. (As cited by
Douderoff 1976)
Great Britain, Department of the Environment. Water pollution research
1972. London: H.M. Stationery Office, 1973: 39-41. (As cited by
Douderoff 1976)
Great Britain, Ministry of Technology. Water pollution research 1967.
London: H.M. Stationery Office; 1968: 61 and 65. (As cited by
Douderoff 1976)
Henderson, C.; Pickering, Q.H.; Lemke, A.E. The effects of some organic
cyanides (nitriles) on fish. Proceedings of the fifteenth industrial
waste conference; Lafayette, IN: Purdue University; 1961. (As cited
by Douderoff 1976)
Herbert, D.W.M.; Merkens, J.C. The toxicity of potassium cyanide
to trout. J. Exp. Biol. 29:632; 1952. (As cited by U.S. EPA 1977a)
Hunt, R. Cyanwasserstoff, Nitrilglukoside, Nitrile, Rhodanwasserstoff,
Isocyanide. Handbuch der Experimentellen Pharmakologie, Vol. I,
Heffter, A. ed. Berlin: Verlag Von Julius Springer; 1923: 702-832.
(As cited by Douderoff 1976)
Jones, J.R.E. The oxygen consumption of Gasterosteus aculeatus L.
in toxic solutions. J. Exp. Biol. 23:298-311; 1947. (As cited by
Douderoff 1976)
Karsten, A. Investigation of the effect of cyanide on Black Hills
Trout. Black Hills Eng. 22:145-174; 1934. (As cited by Douderoff 1976)
Koenst, W.M.; Smith, Jr., L.L.; Broderius, S.J. Effect of chronic
exposure of brook trout to sublethal concentrations of hydrogen cyanide.
Environ. Sci and Tech. 11:883-87; 1977.
5-23
-------
Leclerc, E. ; Devlaminck, F. Etude toxicologique de quelques substances
Seneralement presents dans les effluents d'usines a gaz. [Toxicological
studies of some subtances usually present in effluents from gas voTs]
Jjnt. Beige Etude Doc. Eaux, Bull. Mens. No. 8 [1950/11] :486:493; 1950
(As cited by Douderoff 1976) '
°f Cyanide on earl? life "ages of
35:166;197l ( ^^ ' "' °f the Fisheries R»«- Bd. of Can.
Leduc, G. ^Sorne physiological and biochemical responses of fish to
1976)
Lind, D.T.; Smith, Jr., L.L.; Broderius, S.J. Chronic effects of
Fed'
Lipschuetz M.; Cooper, A.L. Comparative toxicities of potassium cyanide
and potassium cuprocyanide to the western black-nosed dace (Rhinichthys
'' S ' '194-20*' 1955« (A. cited
Malacea, I. Contributions to knowledge of the toxic effects of cyanides
ammonia, mercury, and arsenic on some species of fish and on Daphnia '
[in Roumanian, with English, German, and Russian summaries]. Stud.
Prot. Epurarea Epelor 7(2) -.751-792; 1966. (As cited by Douderoff
y' f'M'; Schrenk' H'H- The acute toxicity of cyanogen. Am.
Hyg. Assoc. J. 21(l)sl21-124; 1960. (As cited by Douderoff 1976)
Michigan Department of Conservation, Institute for Fisheries Research.
The toxicity to fish life of cyanide solutions, and of the products
derived from certain chemical treatments of cyanide solutions. Rep.
No 207; Ann Arbor, MI: Inst. Fish. Res., University of Michigan;
(ph°tOStaCic ^ — > ' 1933. Up. (As cited
anf zlnc'on"5' Indivi^al fnd combined effects of cyanide, pentachlorphenol
and zinc on juvenile chinook salmon and invertebrates in model stream
communities. M.S thesis; Corvallis, OR: Oregon State University;
1973. 80p. (As cited by Douderoff 1976)
5-24
-------
Nehring, D. Die Schadwirkung von Kupfersulfat, Zinksulfat,
Kaliumzyanid, Ammoniak und Phenol gegenuber Karpfen (Cyprinnus
carpio) vora Wasser her und nach peroraler Applikation. [The toxicity
to carp (Cyprinus carpio) of copper sulfate, zinc sulfate, potassium
cyanide, ammonia, and phenol from water and after oral administration.]
Z. Fisch. Deren Hilfswiss., N.S. 12:717-724; 1964.
Neil, J.H. Some effects of potassium cyanide on speckled trout
(Salvelinus fontinalis). Proceedings of the fourth Ontario industrial
waste conference; Toronto, Canada: Water and Pollution Advisory
Committee, Ontario Water Resources Commission; 1957: 74-96. (As cited
fay Douderoff 1976)
Oak Ridge National Laboratories and U.S. Environmental Protection
Agency (ORNL/U.S. EPA). Reviews of the environmental effects of
pollutants. V. Cyanide. Report No. EPA-600/1-78-027; 1978.
Oshima, S. On the toxic action of dissolved salts and electrolytes
upon young eels (Anguilla japonica) [in Japanese]. J. Imp. Fish. Exp.
Sta. (Tokyo) No. 2:139-193; 1931. (As cited by Douderoff 1976)
Patrick, R.; Cairns, Jr., J.; Scheier, A. The relative sensitivity
of diatoms, snails, and fish to twenty common constituents of
industrial wastes. Prog. Fish-Cult. 30:137-140; 1968. (As cited by
Douderoff 1976)
Philips, F.S. Oxygen consumption and its inhibition in the development
of Fundulus and various pelagic fish eggs. Biol. Bull. (Woods Hole,
MA) 78:256-274; 1940. (As cited by Doudoroff 1976)
Powers, E.B. The goldfish (Carassius carassius) as a test animal
in the study of toxicity. III. Biol. Monogr. 4(4):123-193 [or pp. 3-73
of No. 4 only]; 1917. (As cited by Douderoff 1976)
Renn, C.E. Biological properties and behaviors of cyanogenic wastes.
Sewage Ind. Wastes 27:297-308; 1955. (As cited by Douderoff 1976)
Roback, S.S. Environmental requirements of Trichoptera. Biological
problems in water pollution. 3rd seminar, pp. 118-126. Report
999-WP-25. Cincinnati, OH: R.A. Taft Sanit. Eng. Center; 1965.
(As cited by Becker and Thatcher 1973)
Schaut, G.G. Fish catastrophies during droughts. J. Am. Water Works
Assoc. 31:771-821; 1939. (As cited by Douderoff 1976)
Seth, A.K.; Shrivastava, S.K.; George, M.G.; Bewtra, J.K. Monitoring
of certain toxic constituents in water supplies. Environ. Health
9:34-38, 1967. (As cited by Douderoff 1976)
Silaichuk, E.V. Effect of waste waters containing cyanides and hexavalent
chromium on the survival of certain aquatic organisms [in Russian].
Gig. Sanit. 34(12):78-79, 1969. (As cited by Douderoff 1976)
5-25
-------
Smyth, H.F., Jr.; Weil, C.S.; West, J.S.; Carpenter, C.P. An
exploration of joint toxic action: twenty-seven industrial chemicals
intubated in rats in all possible pairs. Toxicol, Appl. Pharmacol.
14:340-347; 1969. (As cited by Douderoff 1976)
Spector, W.S., ed. Handbook of toxicology, Vol. I, Acute toxicities
of solids, liquids and gases to laboratory animals. Philadelphia,
PA: W.B. Saunders Co.; 1956. 408p. (As cited by Douderoff 1976)
Sumner, F.B.; Doudoroff, P. Some experiments on temperature acclima-
tization and respiratory metabolism in fishes. Biol. Bull. (Woods
Hole, MA) 74:403-429; 1938. (As cited by Doudoroff 1976)
Surber, E.W. Cricotopus bicinctus. a midge-fly resistance to
electroplating wastes. Trans Amer. Fish. Soc. 88 (2):111-116; 1960.
(As cited by Becker and Thatcher 1973)
Surber, E.W. Water quality criteria for freshwater fishes. (Abstract)
Proceedings of the sixteenth annual conference of the southeastern game
fish comm.; 1965:435-436. (As cited fay Becker and Thatcher 1973)
Towill, Leighe; Drury, J.S.; Whitfield, B.L.; Lewis, E.B.; Galyan,
E.L.; Hammons, A.S. Review of the environmental effects of pollutants-
V. Cyanide. ORNL/EIS-1, EPA-600/1-78-027, October 1978.
Turnbull, H.; DeMann, J.G.; Weston, R.F. Toxicity of various refinery
materials to fresh-water fish. Ind. Eng. Chem. 46:324-333: 1954.
(As cited by Douderoff 1976)
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria—cyanide. Interim draft. Washington, DC: U.S. EPA; 1977a.
U.S. Environmental Protection Agency (U.S. EPA). Federal Guidelines:
state and local pretreatment programs. Volume 1, EPA-430/9-76-017a;
Washington, DC. Municipal Construction Division; January 1977b.
Wallen, I.E.; Greer, W.C.; Lasater, R. Toxicity to Gambusia affinis
of certain pure chemicals in turbid waters. Sewage Ind. Wastes
29:695-711; 1957. (As cited by Douderoff. 1976)
Washburn, G.N. The toxicity to warm-water fishes of certain cyanide
plating and carburizing salts before and after treatment by the
alkali-chlorination method. Sewage Works J. 20:1074-1083; 1948.
(As cited by Douderoff 1976)
Wells, M.M. Starvation and the resistance of fishes to lack of oxygen
and to KCN. Biol. Bull. (Woods Hole, MA) 31:441-452; 1916. (As
cited by Douderoff 1976)
Wuhrmann, K.; Woker, H. Beitrage zur toxicologie der fische. II.
Experimentelle untersuchungen uber die Ammoniak - und Blausaurevergiftung,
[Contributions to fish toxicology. II. Experimental investigations
of ammonia and hydrocyanic acid poisoning.] Schweiz. Z. Hydrol.
11:210-244; 1948. (As cited by Douderoff 1976)
5-26
-------
Wuhrmann, K.; Woker, H. Beitrage zur toxicologie der fische. VIII.
Uber die Giftwirkungen von Ainmoniak - und Zyanidlosungen mit verschiedener
Sauerstoffspannung und Teinperatur auf Fische. [Contributions to fish
toxicology. VIII. Concerning the toxicity to fishes of ammonia and
cyanide solutions with varying oxygen tension and temperature.]
Schweiz. Z. Hydrol. 15:235-260; 1953. (As cited by Douderoff 1976)
Wuhrmann, K.; Woker, H. Influence of temperature and oxygen tension
on the toxicity of poisons to fish. Int. Ver. Theor. Angew. Limnol.,
Verh. 12:795-801; 1955. (As cited by Douderoff 1976)
5-27
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6.0 EFFECTS AND EXPOSURE — HUMANS
6.1 HUMAN TOXICITY
6.1.1 Introduction
Cyanide is among the most potent and rapidly acting of all known
poisons. The toxic effects of hydrocyanic acid (HCN), sodium cyanide
(NaCN), potassium cyanide (KCN), and other soluble inorganic salts are
primarily attributable to the cyanide ion (CN) and its tendency for
complexation with certain metal ions. Cyanide binding to metallic
cofactors has been shown to inhibit 42 enzyme systems (Dixon and Webb
1958). Cytochrome oxidase, a key respiratory enzyme, is especially
sensitive to cyanide. A concentration of 3.3 x 10~s moles/ml of cyanide
completely inhibits cytochrome oxidase, thus preventing tissue utiliza-
tion of available oxygen (Chen and Rose 1952) and causing cytotoxic
anoxia. If untreated, it can be fatal, probably as a result of cerebral
anoxia (DiPalma 1971).
Due to cyanide's acute lethality, few long-term mammalian studies are
available for an/$|aysis. In addition, human populations are generally not
exposed to acutely toxic levels of cyanide (see Section b.2), except as an
occupational hazard; therefore, determinations of acute toxicity in labor-
atory animals do not appear relevant to human risk. Also, studies of
changes in biochemical parameters or transient physiological responses
lack evidence of associated mammalian toxicity. Epidemiologic studies
that were found are of little use in risk assessment because they do not
relate dose to effect; and those values for cyanide bioaccumulation
found in the literature do not provide a clear basis for the determination
of human exposure. Thus, the available toxicologic data on cyanide
presented in this chapter are sufficient for a qualitative analysis of
human risk, but are insufficient for a quantitative assessment of the
human risk associated with pollutant sources.
6.1.2 Metabolism and Bioaccumulation
For humans, the exposure routes of cyanide are inhalation, ingestion,
or absorption through the skin. Regardless of the intake route, cell mem-
branes are highly permeable to free cyanide, resulting in its rapid absorption
through alveolar membrane (Poison and Tattersall 1969), intestinal mucosa
(Gettler and Baine 1938), or skin (Potter 1950). The percentage of a given
dose absorbed is a function of the size of the dose and the absorption rate.
Once absorbed, cyanide appears rapidly in the blood and is subsequently
distributed throughout the body.
The metabolism of cyanide as summarized by Williams (1959) is shown
in Figure 6-1. In most mammalian species, conversion of the cyanide
ion to the relatively non-toxic thiocyanate ion creates a major detoxifi-
cation pathway for hydrogen cyanide and cyanide salts. Organic cyanides
also form thiocyanates if they are converted in vivo to the cyanide ion
6-1
-------
CN~
Cyanide
Sulfur Transferase
Major Pathway
60-80%
SCN~
Tblocyanate
Thiocyanate
Oxldase
T
Minor
Pathway
Excreted
in
Urine
Hydroxocobalamin
Cystine
HCN
in expired air
Cyanocobalanin
(Vitamin & )
2-iminothazolidine-
4-carboxylic acid
Cyanate
(HCNO)
CO,
Formic
acid
(HC0011)
Partially
fxcreted
Formate:;
Metabolism of
one-carbon
compounds
Source: Williams (1959)
of
-------
(Williams 1959). Rhodanese, Che mitochondrial enzyme sulfur transferase
that is widely distributed in animal tissues and particularly the liver,
mediates this reaction. Rhodanese transfers sulfur from endogenous supplies
of thiosulfate, a sulfur donor, to the cyanide ion (CN~). This forms
thiocyanate (SCN~"), which is readily excreted, primarily in the urine.
The endogeneous supply of thiosulfate is the step in the detoxification
pathway that limits the absorption rate (Williams 1959). A limited
amount of thiocyanate can be reconverted to cyanide when thiocyanate is
present; however, it will occur at a rather slow rate (Goldstein and
Reiders 1953, Himwich and Saunders 1948). Also, the presence of glutathione
s-transferases will catalyze a minor conversion of organic thiocyanate to
cyanide (Habig et. al. 1975).
The conversion to thiocyanate accounts for the detoxification of 60-80%
of absorbed cyanide (Williams 1959). Other relatively minor pathways for
detoxification and excretion include:
• Combination of cyanide with cystine to form 2-imino-thiazolidine-
4-carboxylic acid,
• Oxidation of cyanide to formic acid and carbon dioxide,
• Formation of cyanocobalamin (vitamin BI_), and
• Excretion of HCN through the lungs (Williams 1959).
The binding of free CN by methemoglobin in blood also reduces free cyanide
levels (Chen and Rose 1952, Williams 1959). McNamara (1976) has estimated
the detoxification rate in humans of intravenously administered HCN as
approximately 0.017 mg/kg/minute.
Crawley and Goddard (1977) studied the metabolism of K CN in female
rats after intravenous injection, pulmonary and gastric incubation, and
skin absorption. After intravenous injection, 4% of the administered
radioactivity was excreted in breath, 4% in feces, and 45% in urine within
24 hours; corresponding values after 7 days were 8% for breath, 14% for
feces and 68% for urine. The pattern of excretion and levels of radio-
activity in tissue found after inhalation exposure were similar to the
post-intravenous injection pattern. Some differences in tissue distribu-
tion, however, were apparent after skin absorption. Although the evapora-
tion of K^CN from the skin was largely overcome by spraying the area
with an artificial skin, some loss (15-30%) by this route still occurred.
Approximately 65% of the applied radioactivity was absorbed. At 24 hours,
26% of the absorbed activity was excreted in urine and 7.5% in feces.
After 24 hours, residues in fat were higher following skin application
than after intravenous injection (7.1% vs. 1.3%, respectively).
After subcutaneous injection of NaCN to rats, 2-amino-4-thiozolidine
carboxylic acid could be isolated from urine (Baumeister e_t al. 1975, Wood
and Cooley 1965).
6-3
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uriJ- and.McGlnit? <1977> f°"nd no significant difference in the
urinary excretion pattern in rats administered 5 mg/kg KCN subcutaneouslv
£ri * %rek f°r 8 WeekS' D°ublin* the dos'ing raie of KCN re- "
M8 S t iX"1?,?1?1" l6VelS °f UriUary ^hioc'yanates; i.e.!
^^^^
of Kc"JntStUr%ti0n,PhTr°n iS n0t Operati^ between thLilev^ls
cvanaL Jn thl ? f* F°Ulk6S U966) f°und that ««etlon of thio-
f2Tw-,^^
studies may have resulted because Smith and Foulkes (1966) measured
highly variable thiocyanate concentrations.
Normal blood cyanide levels are around 0.05 ug/ml in the -zeneral
population (Feldstein and Klendshaj 1954, Symington et al. 1978)
-» ., . rf
the cyanide level in blood and tissues.
6-4
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6.1.3 Animal Studies
6.1.3.1 Mechanism of Action
Cyanide has a tendency to form complexes with several metal ions,
particularly iron in the ferric (Fe^") state. Thus, enzyme systems
requiring metallic cofactors are susceptible to inhibition via cyanide
complexation to these metallic cofactors. Cytochrome oxidase, a terminal
enzyme in the mitochondrial electron transport chain, is particularly
sensitive to the effects of cyanide; a cyanide concentration of 3.3 x 10
moles/ml completely inhibits this enzyme by forming a relatively stable,
inactive coordination complex with its ferric ion (Chen and Rose 1952).
This complexation blocks utilization of cellular oxygen, producing histo-
toxic hypoxia. Under ordinary circumstances, the body is capable of
handling a small but continuous amount of cyanide by converting to
thiocyanate and restoring cell respiration. With prolonged or high
exposure levels, however, normal metabolic processes are saturated and
cytotoxic anoxia results. Chemoreceptors in the carotid and aortic
bodies trigger an inspiratory gasp and hyperpnea (an increase in the
depth of respiration). This is followed by a transient depression in the
central nervous system and finally hypoxic convulsions and death resulting
from respiratory arrest (Fassett 1963, Gosselin et_ a_l. 1976).
6.1.3.2 Carcinogenicity, Mutagenicity, and Adverse Reproductive Effects
No definitive studies on the carcinogenic, mutagenic, or teratogenic/
reproductive effects of cyanide have been reported. Rats fed a diet
fumigated with 300 yg/1 HCN exhibited no indications of any carcinogenic
effect after 2 years (Howard and Hanzal 1955); however, data are insufficient
for definitive conclusions (see Section b.1.3.3).
Thiocyanate, the major metabolic product of cyanide detoxification,
has been shown to produce inhibitory effects at high concentrations (0.7
ml of 1 M NaSCN/egg) on mesodermal and endodermal development of the
chick embryo (Nowiniski and Pandra 1946). In view of the high dose and
the large number of false positives generated in this closed system,
little confidence can be placed on this finding. Furthermore, in a feeding
study conducted with pregnant rats, Kreutler £££1. (1978) reported no
indications of adverse effects in pups born to dams administered 160 yg
SCN/ml in their drinking water 0^6.4 mg SCN/rat/day) beginning on day 2 of
pregnancy. Although this study was not conducted according to normal
teratogenicity testing protocols, it does suggest that a high plasma
concentration of thiocyanate is not of itself detrimental to progeny, at
least in rats.
6.1.3.3 Chronic Effects
Only one chronic feeding study has been conducted with cyanides.
Howard and Hanzal (1955) fed groups of 10 male and 10 female weanling
Carworth Farms rats a diet containing an average of 0, 100, or 300 ug/1
HCN for 2 years. In order to maintain cyanide concentrations at these
•"O
-------
levels, fresh food was fumigated with HCN and analyzed every 2 days
throughout the study. An average of all food residue analyzed over the
2-year period, however, indicated that the 300 ug/1 HCN dropped to 80.1
yg/1, and the 100 ug/1 HCN dropped to 51.9 Ug/l after 2 days of feeding
Therefore, dietary concentrations are more appropriately expressed as
ranges rather than definitive values.
No signs of toxicity were noted during the 2-year study. Food
consumption, growth rates, and survival of treated rats were comparable
with control animals. At termination, hematologic parameters (unspecified)
and gross pathologic findings were within normal limits and compatible
with those typically found in aging animals. Histopatho logic examination
of a representative number of rats (number unspecified) suggested no
abnormalities in the heart, lung, liver, kidney, spleen, adrenals,
thyroid, testes or uterus and ovary, the cerebrum and cerebellum, and/nr
stomach. At termination of the study, elevated thiocyanate levels were
noted in plasma, red blood cells, liver and kidney of HCN-treated
In view of the limited data and the uncertainties concerning exact
dosage, the only conclusion that can be drawn is that 80-300 ug/1 HCN in
the diet apparently presents no hazard to rats.
6.1.3.4 Subchronic Effects
The available data on subchronic administration of cyanide to experi-
mental animals are also limited. Kreutler and coworkers (1978) examined
the effect of prolonged ingestion of potassium cyanide on thyroid weight
and thyroid-stimulating hormone (TSH) . Young male albino rats were fed
a low-iodine, semi-purified diet containing either 2 or 20% casein for
2 weeks. After 2 weeks, these diets were supplemented with 0.2% KCN for
an additional 2-week period. A third group of animals received a 2%
casein, 0.2% KCN diet that had been supplemented with potassium iodide
The addition of cyanide to a 2% casein, low-iodine diet resulted in
significant (p <0.05) increases in thyroid weight and in plasma TSH (see
Table 6-1). The effect of cyanide was eliminated, however, by the
addition of iodine to the low-protein diet. No effect was noted on
thyroid weight, and little or no effect on TSH in rats fed the 20% casein
diet supplemented with KCN.
Two additional experiments examined the effects of long-term over-
loading of thiocyanate, the major breakdown product of cyanide (Kreutler
at al. 1978, Ennans _et al. 1972). Ermans and coworkers (1972) fed groups
of Wistar rats either a low-iodine or iodine-supplemented diet for
4 weeks. Each of the basic diets was further supplemented with 0, 1, 2,
or 5 mg thiocyanate per day. In the iodine-supplemented rats, a daily
dose of 1 mg SCN/day or greater produced a progressive depletion of the
iodine content of the thyroid; the level of plasma PB127I (protein-bound
iodine) remained unchanged (see Table 6-2). In the iodine-deficient rats,
the iodine content of the thyroid was already reduced by a factor of 10,
because SCN was not administered. Chronic overloading with SCN caused
6-6
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TABLE 6-1. EFFECT OF PROLONGED INGESTJON OF KCN ON THYROID WEIGHT AND PLASMA
LEVELS OF THYROID.-STIMULATING HORMONE IN PROTEIN-DEFICIENT RATS
Diet
2% casein
2% casein + KCN
2% casein + KCN + KI
20% casein
20% casein -I- KCN
No. of
Rats
24
16
14
11
10
% Change in
Body Weight
i SEM
- 30 ± I
- 31 + 1
- 33 ± 1
+ 37 ± 3
+ 41 ± 3
Thyjrpid Wt.
Plasma TSH
(mg + SEM) (m Unit/100 ml ± SEM)
8.1 + 0.6 5.5 + 1.1
17.5 + 0.7°
5.4 + 0.3^
11.6 ± 0.8
10.3 + 0.5
147
6.3
12.5
11
+ 151
+ 2.0
± 0.7
+ 2
Different from 2% casein group, p < 0.05.
Different from 2% casein + KCN group, p < 0.05.
Source: Kreutier jet _al. (1978).
-------
TABLE 6-2. ACTION OF LONG-TERM INTAKE OF SCN~ ON THE THYROID
SIZE AND THE ORGANIC IODINE METABOLISM IN RATS
Effect
Thyroid Weight
(mg/lOOg)
Thyroid Iodine
content (yg)
1 27
Plasma PB I
(wg/100 ml)
Iodine
Supply
5 yg/d
None
5 ug/d
None
5 ug/d
None
Controls
10.7
13.4
11.9
1.0
2.6
1.8
SCN
1 mg/d
12. 7a
11.2
10.5
0.7
2.3
1.3a
SCN
2 mg/d
12.8
14.7
7.9b
0.6a
2.2
1.2b
SCN
5 me/d
•* H*^ / U
11.9
7 6b
/ • \J
2 3
** * J
statistically different from the control value: p <0.01.
'Value statistically different from the control value: p <0.001.
Source; Ennans et_ al. (1972).
6-8
-------
an even greater reduction of the iodine content. All of the deficient
animals showed marked hyperplasia of the thyroid, but chronic overloading
with thiocyanate did not increase the hvperplasia. On the other hand, it
reduced significantly the level of PB^'I in the serum. The authors
suggest that prolonged ingestion of SCN may cause a transitory inhibition
of the thyroidal iodide pump, and consequently lead to the depletion of
iodine reserves. Another suggestion was the possibility that the increase
in renal clearance of iodine resulted from the saturation of tubular reab-
sorption by thiocyanate.
In another experiment, Kreutler et_ al. (1978) examined the relation-
ship between ingested SCN, plasma SCN, and thyroid weights in gravid rats
and their progeny. Maternal rats were fed either standard laboratory
chow or a low-iodine diet. Sodium thiocyanate was added to their drinking
water to provide concentrations of 0, 40, 80, or 160 yg SCN~/ml. The rats
drank ^40 ml of water daily; i.e., 0, 1.6, 3.2, or 6.4 mg SCN/rat/day.
Plasma SCN levels in maternal rats were elevated relative to the
concentration in their drinking water but varied widely over a fivefold
range (251 vs. 1526 yg/100 ml for the 0 and 160 yg/ml groups, respectively,
5 days post partum). Their pups also had increasing plasma SCN levels,
but with less variation (146 vs. 279 yg/100 ml, respectively). The addition
of SCN to the drinking water of iodine-deficient gravid rats resulted in
goiters in both the mothers and their progeny, particularly at the highest
concentration level of SCN intake (see Table 6-3). The pups showed a
progressive increase in relative thyroid weight as the maternal SCN" intakes
increased.
In summary, thiocyanate resulting from the detoxification of CN,
rather than the CN ion directly appears to exert an anti-thyroid action
in rats. Thiocyanate is known to compete with iodide for uptake by the
thyroid gland (Barker ej^ ad. 1941, Ermans e_t al. 1972); this finding
was substantiated by the more pronounced effects observed in iodine-
deficient animals.
Three additional studies have examined the subchronic effects of
cyanide administered by injection (Gallagher et al. 1975 , Smith e_t al.
1963, Ibrahim 1963). Intraperitoneal administration of increasing
daily doses of NaCN (0.1 mg NaCN/kg every second day; dose range 2.5-4.0
mg/kg) to male Wistar rats for 5 weeks produced signs of acute poisoning
immediately post-injection but no indications of prolonged toxicity except
for decreased body weights at termination (192 vs. 218 g for controlled
rats). At necropsy, cyanide-treated rats exhibited no gross or micro-
scopic pathology in the liver, kidney, or central nervous system (the only
tissues examined). Copper levels in the liver tissue were significantly
lower in cyanide-treated rats (11.3 vs. 15.2 ug/g dry weight for controls)
but were not below the normal range of this species (Gallagher et_ al_. 1975).
In the second study, however, noticeable cellular changes in the
cortex, hippocampus, and cerebellum with neuronal degeneration and cell
loss were noted in three adult Wistar rats injected subcutaneously with
0.5 mg KCN/rat once per week for 22 weeks. No ill effects were noted
prior to sacrifice (Smith et al. 1963, Smith and Duckett 1965).
6-9
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TABLE 6-3. EFFECT OF MATERNAL SCN INGESTION ON THYROID WEIGHT
IN RATS 5 DAYS POST PARTUM
Mothers
SCN~ in Water
(Ug/ml)
0
40
80
160
Thyroid Weight
(mg/lOOg body vt ± SEM)
10.7 +0.7
13.3 + 0.2 (p < 0.05)
13.6 + 1.2 (p < 0.05)
16.7 +1.8 (p < 0.05)
Pups
0
40
80
160
23.7 + 1.6
30.0 + 2.2 (p < 0.05)
33.0 + 6.0
42.8 + 5.5 (p < 0.05)
Source: Kreutler e£ al. (1978)
6-10
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Necrotic lesions and demyelination were also observed in the brain
tissue of rats given five subcutaneous injections of NaCN/week for
3 weeks. The initial dose was 8 mg/kg, with successive increments of
0.5-1.0 mg up to a maximum of 6 mg/rat/day (Ibrahim 1963).
Similar lesions of the central nervous system have also been observed
in dogs following repeated exposures by inhalation to 50 mg/m^ HCN for
varying durations (12-30 minutes) at either 2-or 8-day intervals. Vaso-
dilation and hemorrhages were most pronounced in the central gray nuclei,
brain stem, bulb and medulla cervicalis. Cellular lesions were manifested
by cytologic changes in Purkinje cells of the cerebellum and in the bulbar
gray nuclei. The author concluded that the lesions resulted from anoxia
caused by the inhibition of cytochrome oxidase (Valade 1952).
It is not clear if these lesions in brain tissue are related directly
to cyanide, thiocyanate, or general cytotoxic anoxia. The lesions are
similar to those produced by hypoxia (Bass 1968).
6.1-3.5 Acute Effects
Lethality
The acute toxic effects of cyanide result from the cytotoxic hypoxia
that it produces, which in turn depends on the rate of absorption and
the duration of exposure. The more rapidly tissues absorb a critical
concentration of cyanide, the more severe the effects.
Inhalation of HCN leads to the most rapid absorption in tissues pro-
ducing reactions within seconds and death within minutes (Gosselin et al.
1976). Death from ingestion of HCN or any compound releasing CN via
digestive processes and/or intestinal microflora may be delayed as long
as an hour, depending on the stomach contents and the release rate of
cyanide from the ingested compound (Gosselin et_ al. 1976). Toxic amounts
of cyanide may also be absorbed through the skin (Goodman and Gilman 1975).
An acute oral LD5Q (lethal dose to 50% of test animals) value of
3.7 mg/kg in mice has been reported for HCN with toxicity slightly
reduced for cyanide salts; i.e., oral LDso values between 5 and 10 mg/kg
in rats, rabbits, and dogs (RTECS 1977). Similar values are noted via
intraperitoneal or subcutaneous injection (RTECS 1977).
Gettler and Baine (1938) administered oral doses of 20, 50, and
100 mg of KCN (expressed as HCN) to three dogs; they died in 155, 21,
and 8 minutes, respectively. An analysis of the stomach contents
indicated that the three dogs had absorbed 14.4, 12.0, and 16.6 mg of
KCN (expressed as HCN), respectively. The authors calculated the lethal
oral absorbed dose for dogs as 1.06-1.40 mg/kg HCN.
Walton and Witherspoon (1926) attempted to quantify the skin absorp-
tion of HCN in rabbits and dogs. These experiments minimized HCN by
permitting entry through percutaneous absorption only. In one experiment,
6-11
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the shaved abdomens of eight guinea pigs were exposed to the vapor of
a 97% aqueous solution of HCN. Within minutes, the animals exhibited
rapid respiration, followed by general twitching of muscles, convulsions,
and then death. In a second experiment, these authors exposed the
shaved abdomen of nine dogs to various concentrations of airborne HCN
Exposure to 15,200 ug/1 HCN for 47 minutes was lethal; however, no
effects were noted in dogs exposed to 5000 ug/1 HCN for 180 minutes.
Fairley and coworkers (193A) reported similar results for rabbits and
guinea pigs.
HcNamara (1976) compiled a table on inhalation data, which indicates
that goats, sheep, pigs, monkeys, and guinea pigs have high resistance
to the lethal effects of hydrogen cyanide, whereas dogs, mice, rats,
and rabbits are relatively more sensitive (see Table 6-4).
Sato (1955) discovered that approximately 20% of mice exposed to
20 ug/1 HCN gas died within 4.5 hours and that some mice died after
4 hours exposure to 15 ug/1 HCN. Impaired mobility and respiration
were noted in mice exposed to 10 yg/1 HCN for 2 hours.
Except for one animal that died after an 8-minute exposure of 50 ug/1
HCN, sixteen rats exposed to 24-50 ug/l HCN for up to 22 minutes survived
(Moss et. al. 1951).
Lehmann (1903) noted that inhalation of 30-40 mg/m3 of HCN (27-36
Ug/1) did not affect cats after 4-to 5-hour exposures. However, cats
exposed to airborne HCN concentrations of 50 mg/m3 (45 jjg/i HCN) for
1.5 hours exhibited respiratory distress, increased salivary flow,
vomiting, dilatation of pupils, and convulsions. Most cats died after
exposure to HCN at 50-60 mg/m3 (45-54 ug/1) for 2.5-5 hours.
Haymaker and coworkers (1952) exposed six dogs individually to
concentrations of 620, 590, 700, 700, 165, and 690 mg/m3 HCN for periods
of 2.0, 2.0, 1.75, 1.75, 10.0, and 2.0 minutes, respectively. Dogs
exposed to the first three concentrations died within 20 hours; the
three remaining dogs were killed at 24, 26, and 28 hours, respectively,
post-exposure. Necrosis of brain gray matter was noted in some of the
dogs; definite alternations of structure were not observed in dogs that
died within 21 minutes of exposure but were noted in dogs that died
2.5 or more hours after exposure. Similar lesions, however, have been
reported from anoxia alone.
Aside from lethality, four basic categories of effects result from
acute exposure to cyanide: hematological, cardiovascular, neurological,
and metabolic. Information regarding these effects is summarized in the
following sections.
6-12
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TABLE 6-4. LETHALITY OF HCN INHALED BY EXPERIMENTAL ANIMALS
LCt_. (mg min/m ) for Various Exposure Times
Species
Dog
Mouse
Rat
Rabbit
0.5 tain
800
800
450
566
800
769
904
1 min 2 min 3 min 10 min
700 1000
616
750 1348 2300
911 1268 1100 736
1550 ' 2200 1800
932 2190
850
980 3200
30 min
5425
4890
Sheep
Cat
Monkey
Pig
Guinea pig
Goat
1441
1474
1616
1740
2500
2112
1300
2354
850 1226
1700
2100
2200
2170
Source: McNamara (1976),
6-13
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Effects on Metabolism
Isom and Way (1976) reported that intraperitoneal administration of
10 mg/kg KCN (a lethal dose) greatly depressed the enzymatic activity of
cytochrome oxidase in liver and brain tissues (15 and 18% of controls,
respectively) of male Swiss Webster mice.
Schubert and Brill (1968) found that inhibition of liver cytochrome
oxidase in mice, rats, and gerbils reached a. maximum 5-10 minutes after
the intraperitoneal administration of KCN. Depending on the dose, the
enzyme activity returned to normal 5-20 minutes after maximal inhibition
in mice but required up to 1 hour or more in rats and gerbils.
Inactivation of cytochrome oxidase by cyanide results in a shift of
aerobic to anaerobic metabolism accompanied by a marked accumulation of
lactate. The concentration of adenosine triphosphate (ATP) and phospho-
creatine decreases and adenosine diphosphate (ADP) increases. This
modification of normal metabolism may cause the cell to increasingly
utilize alternate pathways and/or to induce minor pathways in order to
maintain a balanced redox state and energy pool (Isom jejt' ail. 1975).
One of the most important alternate pathways utilized during cyanide
exposure is the pentose phosphate pathway. Administration of 5 mg/kg of
KCN to mice increased catabolism of carbohydrates by the pentose phosphate
pathway with a decline in utilization of the Embden-Meyerhoff-Tricarboxylic
Acid cycle and glucuronate pathway (Isom e_t al. 1975).
Significant cyanide poisoning is also invariably associated with
lactic acidosis. As oxidative phosphorylation is prevented by cyanide,
the rate of glycolysis is markedly increased through the Pasteur effect.
This increases lactic acid generation and leads to lactic acidosis
(Graham et al. 1977).
Dechatelet and coworkers (1977) have shown that cyanide stimulates
both oxygen uptake and hexose monophosphate shunt activity in phagocytizing
human polymorphonuclear leukocytes.
Effects on Cardiovascular System
Electrocardiographic abnormalities observed in dogs given lethal
doses of cyanide (as the cyanogenic glycoside of laetrile) included a
notable decrease in the heart rate (bradycardia) accompanied by sinus
irregularity, and eventually, complete suppression of P waves, ventricu-
lar tachycardia, fibrillation, and cardiac arrest (Schmidt 1978).
Reflex bradycardia has been demonstrated in dogs anesthetized by 50
Ug of cyanide administered directly into the common carotid arteries.
Even after selective surgical denervation of the carotid sinus, the same
dose of cyanide produced a marked bradycardia. After surgical denerva-
tion of the carotid body alone, however, the same dose of cyanide had no
effect on the heart rate. Therefore, it was concluded that the bradycardia
originated in the carotid body chemoreceptors (Jacobs e_t al. 1971).
6-14
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Christel and coworkers (1977) have demonstrated a correlation of
heart rate and respiratory rate with plasma cyanide levels in dogs.
Within three minutes after the oral administration of 24 mg/kg KCN, the
cyanide concentration in the plasma rose to 40 uM, and respiration and
heart rate slowed down. Within a short time, respiration resumed and the
heart rate returned to normal.
In an abstract, Laube .et _al. (1966) reported that low doses of NaCN
administered to dogs by slow intravenous infusion produced increased car-
diac output; marked increased coronary flow and oxygen saturation of venous
sinusal blood; decreased myocardial oxygen, lactate, and pyruvate consump-
tion; increased cardiac respiratory quotient, which was demonstrated by
an increased carbon dioxide production; and excess myocardial lactate,
which suggests the occurrence of myocardial anaerobic metabolism.
Effects on Brain and Central Nervous System
In a series of experiments with rats and monkeys, Brierley and coworkers
(1975, 1976, 1977) demonstrated that histotoxic hypoxia resulting from intake
of cyanide can lead to damage in the gray and/or white matter of the brain ,
in the presence of secondary effects on respiration and circulation only.
The critical contribution of the secondary effects of cyanide on
respiration and circulation in the genesis of brain damage was confirmed
in the rat (Brierley et al. 1976). NaCN (0.014 mg/minute/lOOg) was
infused intravenously into rats while the major parameters of respiratory
and cardiac function were recorded. Neuropathological examination of the
brains from 19 rats indicated typical ischemic cell change in only one
animal in which major secondary effects had occurred, particularly on the
circulation (Brierley 1976).
Experiments with 11 adult monkeys (Macaca mulatta) demonstrated that
the cytotoxic hypoxia resulting from cyanide does not cause neuronal damage
until the secondary effects on respiration and particularly on circulation
are considerable. Intravenous infusion of NaCN did not produce typical
ischemia in the brain or any other type of cell change unless major effects
on the circulation were present. In most animals, the EEC, ECG, respira-
tory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCC^,
and body temperature were recorded. Blood gases, pH, lactate, and pyruvate
were estimated in arterial and venous sinus blood samples. An initial
hyperventilation occurred with tetany in all animals. A rapid rate of
cyanide infusion led to apnea. Bradycardia usually precipitated an
isoelectric or near-isoelectric EEC, with additional hypotension.
Neither epileptic seizures nor their EEC concommitants were observed at
any stage. Three animals died of heart failure. Brain damage of the
white matter was seen in four animals that survived up to 98 hours.
Ischemic neuronal alterations, restricted to the striatum of one animal,
were attributed to major circulatory problems (Brierley jat_ ail. 1977).
Lessel (1971) injected rats subcutaneously three times per week with
increasing doses of NaCN (0.4-1.75 mg/lOOg). These rats developed
demyelinative and necrotic lesions in the corpora callosa (70% of the
6-15
-------
.nirnals) and in the optic nerve (20% of the animals). The optic neuropathy
was bilateral focal and retrobulbar. All rats with optic neuropathies
had marked callosal lesions (Lessell 1971).
6.1.4 Human Studies
6.1.4.1 Overview
Few controlled studies have been conducted with cyanide in humans
and the data that are available deal primarily with acute exposure. If
death does not result from acute cyanide exposure, recovery is usually
complete and prompt. The literature reports of alleged sequelae in
animals to acute cyanide poisoning; most of these deal with lesions in
the central nervous system (Smith et al. 1963). These lesions, however
Iff *? fSrve^ C°,be dir6^ effe"S °f <***<»•• bu' "'her an indirect
effect of CN-induced anoxia (Smith et al. 1963). Insufficient data are
available on the effects of chronic exposure to low levels of cyanide
Epidemiologic studies, however, have linked chronic cyanide exposure to
various human neuropathies, such as tobacco amblyopia, Leber's optic
atrophy, and Nigerian nutritional neuropathy (Baumeister et al 1975
Smith and Duckett 1965, Ermans et al. 1972, Osuntokun et aT.~970) . '
6.1.4.2 Controlled Human Studies
Oral Toxic ity
The human lethal dose of ingested HCN is believed to be 50-90 mg-
this corresponds to approximately 1 mg/kg for a 70-kg man. The toxicity
of the cyanide salts is somewhat lower because of slower absorption
»'?*' 2??oN25° mg °r aPProximately 3 mg/kg for a 70-kg man (Gettler and
Baine
Recoveries, however, from the ingestion of 3-5 g KCN without therapy
(Liebowitz and Schwartz 1948) and from 4-6 g KCN with prompt treatment
(Ison et aL 1975) have been reported. Edwards and Thomas (1978) reported
the survival of a 48-year-old chemist who swallowed 413 mg of pure KCN
on an empty stomach. When admitted to a hospital, approximately 40 minutes
later, the subject was unconscious with unrecordable blood pressure- he
underwent cardiorespiratory arrest immediately. Spontaneous respiration
returned at three hours with supportive treatment; consciousness returned
after 8 hours. Approximately 60 minutes after ingestion, peak blood
cyanide reached 38 mg/1. Similar findings were observed in a 21-year-old
male who survived ingestion of 600 mg of KCN. In this case, lactic acidosis
and pulmonary edema were the major manifestations of cyanide poisonine
(Graham et al. 1977).
Results of oral CN intoxication, however, must be interpreted
carefully as the presence of food in the digestive tract may retard absorp-
tion. Gettler and Baine (1938) reported that absorption of 0.5-1.5 mg/kg
expressed as HCN is lethal to humans regardless of the amount of cyanide
ingested.
6-16
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Clinical manifestations of cyanide intoxication by ingestion can
appear within seconds to minutes of exposure. If the stomach is empty
and the free gastric acidity is high, absorption and poisoning are rapid.
Toxic symptoms include vertigo, hyperpnea, dyspnea, headache, palpitations,
cyanosis, and unconsciousness with asphyxial convulsions, preceding death
(DeBusk and Seidl 1969). After ingestion of cyanide salts, however, death
may be delayed as long as an hour (Gosselin _et al. 1976).
Dermal Toxicity
Diffusion cell measurements of absorption of NA CN solutions (1, 10,
or 40% w/v) across human epidermis (1.8 cm2) at 30°C indicate that
absorption rates are strongly dependent on pH. The permeability constant
for HCN was calculated to be 25 times greater than that of cyanide ion
(Dugard and Mawdsley 1978).
Skin contact with concentrated cyanide solutions can be lethal (Tovo
1955) or produce permanent disability (Collins and Martland 1908). Contact
with inorganic cyanide solutions as dilute as 0.5% KCN have produced head-
aches, dizziness, and skin irritation (Nolan 1908). The typical skin
lesion is manifested in eczematoid dermatitis, rash, or skin discoloration
(Tovo 1955, Collins and Martland 1908, Nolan 1908). Prolonged intimate
contact with solutions of cyanide salts has caused caustic burns and even
death (Tovo 1955).
Cohen and coworkers (1974) reported no nasal or skin irritation in
15 human volunteers who underwent dermal exposure to 0.006 mg/m^ of
airborne cyanide.
Inhalation Toxicity
Although the fatal human inhalation dose of HCN has not been firmly
established, it appears that concentrations above 90 yg/1 (^ 100 mg/m3)
are lethal (Flury and Zernik 1931, Lazareff 1956, Lazareff 1971).
Lethality, however, is a function of both concentration and duration
of exposure because exposure to concentrations of 90-135 ug/1 may be fatal
after 30-60 minutes, while exposure to 300 yg/1 is fatal within a few
minutes (NIOSH 1976).
Controlled experiments with human volunteers have not exceeded
500-625 mg/m^ for approximately 1-minute durations. Grubbs (1917)
reported no ill effects on several volunteers exposed to ^ 501 mg/m^
NaCN gas for 2 minutes or 750 mg/m^ for 1-1/2 minutes. Similarly, Katz
and Longfellow (1923) reported that in experiments during the war, men
were exposed to concentrations of 500 mg/m^ for approximately 1 minute
without injury.
Barcroft (1931) records how he submitted himself (70 kg) and
a dog (^ 12 kg) to an atmosphere of 550-688 mg/m^ HCN until the dog
became unconscious (91 seconds). The dog subsequently recovered and
6-17
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Barcroft reported no adverse effects except for a momentary feeling of
nausea; he experienced difficulty in concentrating on conversation
approximately 10 minutes after exposure terminated.
Wexler et al. (1957) observed the execution of four men by HCN in-
halation (concentrations were not reported). These men exhibited striking
electrocardiographic aberrations and had a marked decrease in heart rate
during the first three minutes, accompanied by sinus irregularity and
eventually, by the complete disappearance of P waves. A secondary in-
crease in heart rate, but not up to the pre-exposure rate, was observed
during the 3rd and 4th minutes along with the irregular reappearance of
P waves. All four subjects showed A-V dissociation with a secondary de-
crease in rates during the 5th minute. During the 6th and 7th minutes,
the heart rates again showed a slight increase and a return to normal
sinus rhythm. Thereafter, the heart rates decreased progressively.
Normal A-V conduction in one man and incomplete A-V block in another
were maintained throughout the 13-minute observation. A third subject
developed a 2:1 heart block, and, finally, a complete heart block. The
fourth subject's heart had normal A-V conduction until the 14th minute,
when it developed ventricular tachycardia and ventricular fibrillation.
Although these changes in cardiovascular activity may not reflect the
effects of lower concentrations of cyanide, they do indicate that cyanide
exerts no specific effect on the myocardium, but rather induces effects
typical of hypoxia. Another complication of the toxic effect of cyanides
on the myocardium is left ventricular failure and increased pulmonary
capillary pressure resulting in pulmonary edema (Graham et_ a^. 1977).
Intravenous Administration
Sixteen healthy soldiers were given 0.11-0.2 mg NaCN/kg intravenously
to stimulate respiration. Electrocardiograms of 15 of the 16 men revealed
a sinus pause, without evidence of auricular acticity, persisting for
0.88-4.2 seconds. This sinus pause immediately preceded or accompanied
the respiratory stimulation. Immediately after the pause, marked sinus
irregularity and a decreased heart rate occurred, which persisted for
periods ranging from a few seconds to 2 minutes. Heart rates then
accelerated to above pre-injection rates. Heart rate and rhythm were
generally restored within three minutes. The 16th subject failed to
show a sinus pause and exhibited only a slight acceleration in heart
rate. One of the subjects reported a momemtary "dim-out" during the
test (Graham et_ al. 1977).
6.1.4.3 Epidemiologic Studies
The literature contains many reports of accidental or intentional
fatal poisoning by cyanide; however, the dose is frequently unknown
(Gettler and Baine 1938, Bogusz 1976, Winek et_ al. 1978, Braico et al.
1979). Winek and coworkers (1978) reported that blood cyanide levels in
six cases of suicide by cyanide ingestion ranged from 0.4 mg% to 4.5 mg%.
In addition, NIOSH (1976) reports several cases of accidental occupational
exposure to HCN and cyanide salts. Since epidemiologic studies have not
generally related dose to effect, and have been reported in detail else-
where (NIOSH 1976), they will not be reviewed in detail here.
6-18
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Hardy and coworkers (1950) described 2 men exposed continuously to
low concentrations of HCN (4-6 ug/1) aerosols generated by case hardening.
Both men complained of headache and fatigue. They demonstrated a slight
lid lag, enlarged thyroids, and excessive perspiration. One of the two
men also experienced dizziness and mental confusion, slurring of speech,
occasional abdominal cramps, nausea, vomiting and a coarse tremor of the
extremities followed by a temporary (24-hour) paralysis. The enlarged
thyroids are probably attributable to the thiocyanate resulting from
continuous detoxification of minute quantities of cyanide.
Of 36 non-smoking male employees exposed to 4.2-12.4 ug/1 cyanide
in electroplating shops, 20 (56%) had slight to moderate thyroid
enlargement. No correlation was found between the period of exposure
and the size of the thyroid. Thyroid131! uptakes at 4 and 24 hours
were significantly higher (p <0.001) in workers than in 20 normal male
controls, (38.7 vs. 22.4% and 49.3 vs. 39.9%, respectively). The 72-hour
PB131i was within normal limits. Hematologic studies indicate CN-exposed
workers had significantly higher hemoglobin and lymphocytic counts than
controls. Workers also reported the following symptoms of exposure:
headache, weakness, changes in taste and smell, perception, irritation
of the throat, vomiting and effort-dyspnea; lachrymation, abdominal
colic, precordial pain, and nervous instability were reported less
frequently (El Ghawabi e_t al. 1975).
Chronic intake of cyanide from tobacco smoke and/or ingestion of
cyanogenic foods has been implicated as a contributing factor to several
human diseases, i.e., tobacco amblyopia, retrobulbar neuritis with
pernicious anemia, optic atrophy of Leber, and Nigerian nutritional ataxic
neuropathy (Osuntokun et al. 1970).
Nutritional ataxic neuropathy is prevalent in Nigeria and has been
linked with the intake of cassava, a staple root crop containing cyanogenic
glycosides. In Nigerian patients with this disease, elevated plasma and
urinary levels of thiocyanate are associated with lesions of the skin,
mucous membranes, optic and auditory nerve atrophy, and sensory spinal
ataxia (Baumeister et al. 1975, Osuntokun et al. 1970, trmans et al. 19/2).
Osuntokun and coworkers (1969) compared the prevalence of neurologic
disorders in two Nigerian villages that differed in the amount of cassava
eaten (64.3% cassava meals vs. 10.8% in the other village), but were
similar in populations (mean age, weight, height, etc.). Degenerative_
neuropathy occurred with a relatively high frequency in the village with
high cassava consumption. Factors other than cyanide intake, however,
may be involved, such as environmental or genetic differences.
Ermans and coworkers (1972) have also suggested that diets high in
cassava and low in iodine and protein may contribute to the development
of goiter and cretinism. These changes are attributable to SCN which
competes with iodide for uptake by the thyroid gland. Cyanide intake
is also associated with neuropathies, particularly tobacco amblyopia
and Leber's optic atrophy, which are characterized by visual field
defects (Baumeister et ail. 1975, Smith and Duckett 1965).
6-19
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Tobacco amblyopia occurs only in smokers; its etiology is believed
to be related to an inability to detoxify cyanide. The main symptom of
this disease is a central scotoma (an area of depressed vision within
the visual field). Vascular changes and degeneration of ganglion cells
in the retina and the nerve fibers of the nervus opticus are also seen
(Baumeister et al. 1975). Data substantiating 812, particularly hydro-
xocobalamin, as an effective treatment supports speculation that the
detoxification of cyanide is distributed in these patients (Chisholm
et al. 1967).
Leber's optic atrophy may be a congenital abnormality in cyanide
metabolism, which becomes apparent when the body is confronted with a
source of cyanide. Patients with this disease 'have a significantly
higher proportion of cyanocobalomine in the total B]_2 content of serum
than persons having normal vision (Baumeister jilt al. 1975).
Although several reports have connected cyanide with several neuro-
pathies, the evidence is primarily circumstantial. In addition, they
are not epidemiologic data and, therefore, cannot be incorporated into
a risk assessment.
6.1.5 Summary
6.1.5.1 Ambient Water Quality Criteria - Human Health
The U.S. EPA (1980) has established an ambient water quality criterion
for cyanides of 200 ug/1 for the protection of human health from the toxic
properties of cyanide ingested through water and contaminated aquatic
organisms. The criterion is based on the U.S. Public Health Service
Drinking Water Standards of 1962.
6.1.5.2 Other Risk Considerations
Cyanide is an acute poison, which is readily absorbed from the
alveolar membrane, intestinal mucosa and/or skin, and rapidly appears
in the blood. The more quickly a critical concentration of cyanide is
attained in the tissues, the more severe the effects. In sufficient
doses, cyanide produces rapid death by inhibiting key respiratory enzymes
and thereby preventing the body from utilizing available oxygen. At
nonlethal doses, cyanide is detoxified to the relatively nontoxic thio-
cyanate ion. Thus, exposure to small but continuous doses of cyanide
may produce no visible effects, while high doses of cyanide over a short
time interval saturate normal detoxification mechanisms, which results
in acute lethality. Minimum lethal doses of HCN for humans are approxi-
mately 50-90 mg by ingestion and approximately 100-150 mg/m^ by inhalation.
No indications of adverse effects were noted in the single long-term
study available for cyanide; however, limitations of the study do not
allow definitive conclusions. No data were available on the carcinogenic,
mutagenic, or teratogenic/reproductive effects of cyanide. Subchronic
studies suggest that thiocyanate, the major metabolite of cyanide, may
6-20
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exert an antithyroidal action in rats. The majority of available experi-
mental data deal with the acute effects of exposure to levels of cyanide
not normally encountered by humans from pollutant sources.
In humans, cyanide exposure occurs through ingestion, inhalation,
or skin absorption. Acute exposure to cyanide leads either to death or
complete recovery. Little is known about the effects of chronic exposure
to low levels of cyanide. Epidemiological studies have circumstantially
implicated cyanide exposure as a factor in several neurological disorders.
Dose/effect data were insufficient to permit quantification of risk;
however, the data do suggest that long-term overloading with thiocyanate_
resulting from cyanide exposure may be a factor in certain human debilities
or diseases.
6.2 HUMAN EXPOSURE TO CYANIDE
6.2.1 Introduction
The preceding sections have demonstrated that while cyanide is used
widely, its presence in the environment is generally localized. Thus,
significant exposure of the general population to cyanide would be
unlikely. However, certain exposure situations do exist that are higher
than normal safe levels. This section will attempt to identify those
subpopulations exposed to higher levels of cyanide through various
routes.
6.2.2 Ingestion
6.2.2.1 Food
The primary source of cyanide in food is cyanogenic glycosides.
Plants containing these natural compounds produce HCN upon hydrolysis.
As many as 1000 species of plants, including such edible items as al-
monds, stone fruits, sorghum, cassava, lima beans, sweet potatoes, maize,
millet, sugarcane, and bamboo shoots exhibit the capability to produce
HCN (Conn 1969, Ermans et al. 1972). Through the consumption of these
foods, cyanide has contributed to the mortality of both humans and livestock.
Maximum concentrations of cyanide released by bitter cassava, sorghum,
and lima beans may be as high as 100-300 mg/100 g (Ermans e_t al. 1972).
These high levels are primarily concentrated in areas of Africa where
cassava is the basic food for millions of people (Conn 1969). Breeding
or choosing low cyanide varieties of some species has decreased the
consumption of cyanide (Conn 1969). For example, different varieties
of cassava roots may contain from 27-378 mg/kg cyanide (Esquivel and
Maravalhas 1973). Depending on the variety, lima beans may contain
10-312 mg/100 g cyanide. Samples of the two U.S. varieties, Arizona
and America, were found to contain 17 and 10 mg/100 g, respectively
(Montgomery 1969).
6-21
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Thus, human exposure in the United States to naturally-occurring
cyanide in food would generally be low. No estimation of average
cyanide intake from this source was performed because of variations in
the cyanide content of food. However, a worst-case consumption could be
as much as 300 mg/day, assuming a concentration of 300 mg cyanide/100 g,
and a consumption of 100 g. Such a dose would probably be lethal, but
is not likely to occur in the U.S., where both cyanide concentrations
and consumption of such foods is lower.
Exposure to cyanide can result from residues in food. Both HCN and
Ca(CN)2 are registered as fumigants of several foods including citrus fruits
and grains (Ouelette and King 1977). Tolerances established for these
uses are shown in Table 6-5. Towill et al. (1978) report that these
residues can persist for an extensive time period. However, no basis
was given for this statement. If the tolerance for citrus is 50 mg/kg,
assuming 200 g/day consumption, the maximum expected exposure would be
10 mg/day cyanide.
6.2.2.2 Drinking Water
The current recommended limit of cyanide in drinking water is 0.01
mg/1, and a mandatory limit of 0.2 mg/1 (U.S. DREW 1962). In 1970, a survey
of 969 water supply systems in the United States was taken to assess the
quality of drinking water compared with the 1962 U.S. Public Health
Service Drinking Water Standards. The maximum concentration of cyanide
found in 2,595 distribution samples was 0.008 mg/1 (U.S. DREW 1970).
The U.S. EPA (1975) conducted a survey of water supply systems serving
interstate carriers. Of 297 analyses for cyanide, 21 or 7.1% failed to
meet the recommended limit. The maximum reported level of cyanide was
0.260 mg/1, although this level appeared somewhat questionable. Using
this value as a worst case and assuming a 2-I/day consumption, a
maximum expected exposure to cyanide from drinking water would be 0.5
mg/day. A more prevalent exposure level, at concentrations of less than
0.010 mg/1, would be 0.02 mg/day.
6.2.3 Absorption
Dermal exposure to cyanide can occur in an occupational setting
as discussed in the next section. Dermal exposure to the general
population through water has not been assessed; however, it is expected
to be very low, considering the low concentration of cyanide in drink-
ing water.
6.2.4 Inhalation
6.2.4.1 Occupational Exposure
A detailed discussion of occupational exposure to cyanide is beyond
the scope of this report. The U.S. DHEW (1976) reported that the number
of workers with potential exposure to HCN and NaCN has been estimated
at 1,000and 20,000, respectively. Table 6-6 lists occupations with
potential exposure to cyanides. The NIOSH recommended standard for
6-22
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TABLE 6-5. TOLERANCES ESTABLISHED FOR HCN AND Ca(CN) IN FOOD
Food
Spices
Tolerance (mg/kg)
HCN5
250
CaCCN)
N.A.
•2-
Barley, buckwheat, corn and
other grains
75
25
Citrus fruits
50
N.A.
Almonds, beans (dried),
cashews and other nuts
25
N.A.
Cucumbers, lettuce, radishes,
and tomatoes
N.A.
aPast harvest use
N.A. « not applicable
Source: 40:CFR 180
6-23
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TABLE 6-6. OCCUPATIONS WITH POTENTIAL EXPOSURE TO CYANIDES
Acid dippers
Acrylate makers
Acrylonitrile makers
Adipic acid makers
Adiponitrile makers
Aircraft workers
Almond flavor makers
Ammonium salt makers
Art printing workers
Blacksmiths
Blast furnace workers
Bone distillers
Bronzers
Browners, gun barrel
Cadmium platers
Case hardeners
Cellulose product treaters
Cement makers
Coal tar distillery workers
Coke oven operators
Cyanide workers
Cyanogen makers
Disinfectant makers
Dyemakers
Electroplaters
Executioners
Exterminators
Fertilizer makers
Firefighters
Fulminate mixers
Fumigant makers
Fumigators of fruit trees,
apiaries, soil, ships,
railway cars, warehouses,
stored foods
Galvanizers
Gas purifiers
Gas workers
Gilders
Gold extractors
Gold refiners
Heat treaters
Hexamethylenediamine makers
Hydrocyanic acid makers
Hydrogen cyanide workers
Insecticide and rodenticide makers
Jewelers
Laboratory technicians
Metal cleaners
Metal polishers
Methacrylate makers
Mirror silverers
Mordanters
Nylon makers
Organic chemical synthesizers
Oxalic acid makers
Phosphoric acid makers
Photoengravers
Photographers
Pigment makers
Plastic workers
Polish makers
Rayon makers
Rubber makers
Silver extractors
Silver refiners
Solderers
Steel carburizers
Steel hardeners
Steel galvinizers
Tannery workers
Temperers
Tree sprayers
White cyanide makers
Zinc platers
Zinkers
Source: U.S. DHEW (1976)
6-24
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employee exposure to HCN is 5 mg/m CN (4.7 mg/kg) for an 8-hour work
period. This level was determined as a ceiling concentration based on
a 10-minute sampling period. The recommended standard for exposure to
cyanide salts is also 5 mg/m3 CN, with HCN and cyanide salts not to ex-
ceed a combined value of 5 mg/m3 (U.S. DHEW 1976). The NIOSH criteria
document also contains recommendations on medical surveillance, labeling
of HCN, and salts, personal protective equipment and clothing, work
practices and control procedures, and monitoring and recordkeeping re-
quirements. Thus, it appears that this agency has considered cyanide
exposure in the workplace in some detail.
6.2.4.2 Exposure of the General Population
The materials balance in Chapter 3 suggests that automobile exhaust
is the largest distributed source of cyanide to the atmosphere. Fate
calculations estimated a concentration of 0.065 yg/m3 cyanide in the air
of the northeastern United States. For an average inhalation rate of
19.2 m3/day, an exposure of 1.25 ug/day would result.
6.2.4.3 Exposure of Identified Subpopulations
Certain subpopulations have been identified as having potentially
higher exposure to cyanide than the general population. These subpopula-
tions include smokers; residents near manufacturing facilities, smelters,
etc.; persons exposed to high levels of automobile exhaust; and persons
exposed to fires.
Exposure through Cigarette Smoke
The Surgeon General's Report (1979) has stated that HCN in mainstream
(inhaled) smoke varies from 10 to 400 ug/cigarette in U.S. commercial
cigarettes. Thus, exposure of smokers to cyanide could range from 10 to
40,000 yg/day HCN, depending on the type of cigarette smoked, the amount
inhaled, and the number of cigarettes smoked, assuming a range of 1-100
per day cigarettes smoked (Surgeon General 1979). Considering that an
estimated 33.2% of adults over 17, or 54.1 million persons smoke in the
United States (Surgeon General 1979), this exposure is widespread. Of
smokers, 25-30% smoke more than 25 cigarettes/day (Surgeon General 1979);
thus, a large segment of the population could be exposed to cyanide levels
in the 250 to 10,000 ug/day range, or greater.
In addition, non-smokers may be exposed to cyanide through inhalation
of sidestream smoke. The Surgeon General's Report (1979) states that side-
stream smoke contains 0.6-37% as much HCN as mainstream smoke, or a maximum
of 160 ug/cigarette in the sidestream smoke. Although no measurements of
HCN have been taken in smoke-filled rooms, concentrations may be estimated
from measurements of CO levels, which have been summarized by Burns (1975).
The results are not consistent but apparently depend on a number of vari-
ables, such as room size, number of smokers, and ventilation. They show
levels of 38-80 yg/1 CO in rooms (38-93 m3) where 30-80 cigarettes'had
been smoked with no ventilation. The Surgeon General's Report (1979)
reported levels of 10 to 20 mg CO in mainstream smoke/cigarette
6-25
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with a sidestream/mainstream CO ratio of 2.5, or a maximum of 50 m*
CO produced in sidestream smoke/cigarette. Using the ratio between CO and
HCN in sidestream smoke (50 mg CO/160 ug HCN) and an assumed room concen-
tration of 80 mg/kg CO, a level of 0.3 mg/m3 HCN is calculated. Alterna-
tively, using 160 ug HCN/cigarette and assuming a room size of 48 m3 with
no ventilation in which 40 cigarettes were smoked, a concentration of
0.13 mg/mj HCN is calculated. Problems do result from using CO levels
to estimate HCN levels because CO in a smoke-filled room would be due to
sidestream and exhaled mainstream smoke. In addition, the concentration
of CO and HCN would be influenced by the type and amount of tobacco
smoked, extent of inhalation, size of room, ventilation, and duration of
smoking (Surgeon General 1979). Though actual measurements of HCN in
such a situation might be enlightening, the maximum calculated values
for exposure are still lower than the occupational standard of 5 mg/m3
(U.S. DREW 1976).
Exposure of Residents near Manufacturing Facilities and Other Air
Dischargers " ~~ ~ '
The materials balance considerations have shown that cyanide dis-
charges to air do occur. The only monitoring data available come from
Sofia and an "industrial area" in Bulgaria (Kalpasanov and Kurchatova 1976)
where a maximum concentration of 0.013 mg/m3 HCN was reported. Using an in-
halation of 19.2 m3/day, an inhalation exposure of 0.25 mg/day was estimated.
Exposure from Automobile Emissions
Previous sections have shown that concentrations of cyanide in urban
air largely result from automobile emissions. The calculated 90th per-
centile, 1-hour average in New York City was 0.031 mg/m3, while the
maximum hourly reading calculated was 0.057 mg/m3. Using this maximum,
inhalation in New York City might be as high as 1.1 mg/day.
Exposure in Fires
Carbon monoxide is a significant toxic substance produced in fires.
Hydrogen cyanide and other organic cyanides, however, may be released
from burning urethanes, acrylonitriles or polyamides in plastics and may
result in some hazard to persons exposed. Symington et al. (1978) inves-
tigated cyanide exposure in fires through blood cyanide and thiocyanide
levels. Statistical analysis of the results by tnese authors showed
that non-fatal and fatal casualties (overcome by smoke) showed significantly
elevated cyanide levels. The authors suggested that some of the subjects
may have been exposed to lethal cyanide concentrations, but generally the
major effect of cyanide in fires is its contributions to the effects of
carbon monoxide.
Gold ejt al. (1978) examined the air immediately surrounding fire-
fighters for evidence of cyanide exposure. HCN was detected in about
one-half the samples taken. Of the 43 samples in which cyanide was
6-26
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detected, 11 were from fires involving specific materials, such as an
upholstered chair, mattresses, tires, vehicles, and rubber insulated
wire. The maximum reported level of HCN was 2.8 mg/m3 in air. Exposure
would depend on the time involved. Using the maximum concentration,
however, and a maximum three-hour exposure without breathing apparatus,
an exposure of 13.4 mg/three-hour period would result. (This time is
strictly an example. Firefighters are the only persons who purposely
expose themselves to smoke for such extended periods and perhaps longer.)
Levine and Radford (1978) calculated the absorbed cyanide from
levels of thiocyanate in firefighters. The maximum cyanide absorbed
from fires was calculated to be between 0.24-0.36 mg CN/kg body weight.
This estimate is higher than the estimate described above, but the
assumptions involved in both cases do not allow a preference. Therefore,
a firefighter may be exposed to 0.0003-0.4 mg CN/kg, or 0.02 to 28 mg
per exposure.
6.2.5 Summary
Table 6-7 summarizes various estimates of exposure for cyanide. This
table demonstrates that smokers are probably receiving the largest amounts
of cyanide. Firefighters, who are subject to occupational exposure, also
may receive high doses. With the exception of smokers, the general popu-
lation is not exposed to large amounts of cyanide. Levels in drinking
water and ambient air are low. Although levels in some food may be high,
they are probably low in the United States. Thus, other than naturally-
occurring cyanide, no evidence of significant exposure to cyanide in the
human diet exists.
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TABLE 6-7. ESTIMATED HUMAN EXPOSURE TO CYANIDE3
General
Large
Route of Exposure
Food- ingest ion
Estimated Exposure
._._. (rng/day)
Worst-case 10-300
General
Large
Small
Drinking water-lngestion
Drinking water-ingestion
Maximum 0.02
Worst-case 0.5
K)
co
General-Northeastern-U.S.
Smoke rs
Non-smokers exposed to
smoke-filled room,
time factor
Large
Inhalation-ambient air
Large-54.] million Inhalation
adults
Potentially large Inhalation
0.00125
0.01-40
2-6
Residents near industrial
areas
Small
Inhalation
0.25
Residents in urban areas
Large
Inhalation
1.1
Firefighters or other
persons exposed to fires
Small
Inhalation
0.02-28 ms exposure
See text for assumptions.
-------
REFERENCES
Ballantyne, B. Changes in blood cyanide as a function of storage time
and temperature. J. Forensic Sci. Soc. 16(4):305-210; 1975.
Barker, M.H.; Lindberg, H.A.; Wald, M.H. Further experiences with thio-
cyanates. J. Am. Med. Assoc. 117(19):1591-1594; 1941.
Barcroft, J. The toxicity of atmospheres containing hydrocyanic acid
gas. J. Hyg. 31:1-24; 1931. (As cited in McNamara 1976)
Bass, N.H. Pathogenesis of myelin lesions in experimental cyanide
encephalopathy. Neurology 18:167-167; 1968. (As cited in Gosselin
et.al. 1976)
Baumeister, R.G.H.; Schievelbein, H.; Zickergref-Rudel, G. Toxicological
and clinical aspects of cyanide metabolism. Arzneim Forsch. 25(7):1056-
1064; 1975.
Bogusz, M. Disappearance of cyanide in blood and tissues after fatal
poisoning. Forensic Sci. 7(2):173; 1976.
Braico, T.; Humbert, J.R.; Terplan, L.; Lehotoy, M. Laetrile intoxica-
tion. Report of a Fatal Case. New Eng. J. Med. 300:238-240; 1979.
Brierley, J.B. Comparison between effects of profound arterial hypo-
tension and cyanide on the brain of Macaca mulatta. Adv. Neurol. Hypoxia
10:213-221; 1975.
Brierley, J.B.; Brown, A.W.; Calverley, J. Cyanide intoxication in the
rat: Physiological and neuropathological asepcts. J. Neurol. Neurosurg.
Psychiatry 39(2):129-140; 1976.
Brierley, J.B.; Prior, P.F.; Calverley, J.; Brown, A.W. Cyanide intoxica-
tion in Macaca mulatta. Physiological and neuropathological aspects.
J. Neurol. Sci. 31(1):133-157; 1977.
Burns, D.M. Consequences of smoking—the involuntary smoker. Proc.
Third World Conf. on Smoking and Health. 11:51-58; 1975.
Burrows, G.E.; Liu, D.H.; Way, J.L. Physiologic disposition of Na^CN
in mice. Proc. West Pharmacol. Soc. 19:412-415; 1976.
Chen, K.K.; Rose, C.L. Nitrite and thiosulfate therapy in cyanide
poisoning. J. Am. Med. Assoc. 149(2):113-119; 1952.
Chisholm, I.A.; Bronte-Stewart, J.; Foulds, W.S. Hydroxocobalamin versus
cyanocobalamin in the treatment of tobacco amblyopia. Lancet 2:450-451;
1967.
6-29
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Christel D.; Eyer, P.; Hegemann, M. ; Kiese, M. ; Lorcher, W. ; Weger, N.
Pharmacokinetics of cyanide in poisoning of dogs, and the effect of
4-aimethylaminophenol or thiosulfate. Arch. Toxicol. 38(3) :177-189;
A./ 7 / •
Cohen, S.R.; Davis, D.M. ; Kramkowski, R.S. Clinical manifestations of
oC= toxicity~ nasal lesions in electroplate workers. Cutis
8—568; 1974.
Collins, J.; Martland, H.S. Disease of the primary motor neurones
causing the clinical picture of acute anterior poliomyelitis: the
result of poisoning by cyanide of potassium— a clinickl and experimen-
tal contribution to the toxic effects of cyanide of potassium upon the
peripheral motor neurones. J. Nerv. Ment. Dis. 35:417-426; 1908. (As
cited in NIOSH 1976)
Conn, E.E. Carcinogenic glycosides. J. Agric. Food Chem. 17(3) :519-526;
Crawley, F.E. ; Goddard, E.A. Internal dose from carbon-14 labelled
compounds. The metabolism of carbon-14 labelled potassium cyanide in
the rat. Health Phys. 32(3) : 135-142; 1977.
De Busk, R.F.; Seidl, L.G. Attempted suicide by cyanide: a report of
two cases. Calif. Med. 110(5) :394-396; 1969.
Dechatelet, L.R. ; McPhail, L.C.; Shirley, P.S. Effect of cyanide on
NADPH oxidation by granules from human polymorphonoclear leukocytes
Blood 49(3):445-454; 1977.
DiPalma, J.R. , ed. Noxious gases and vapors: I. carbon monoxide,
cyanides, methemoglobin, and sulf hemoglobin. Drill's pharmacology in
medicine. New York, NY: McGraw-Hill Book Co.; 1971: 1189-1205.
Dixon, M. ; Webb, E.C. Enzymes. New York, NY: Academic Press, Inc.-
1958: 373-376.
Dugard, P.H.; Mawdsley, S.J. Percutaneous absorption of cyanide from
aqueous sodium cyanide. Abstract from The seventeenth annual society
of toxicology meeting; Abstr. #104. San Francisco, CA.
Edwards, A.C.; Thomas, I.D. Cyanide poisoning. Lancet 8055:92-93;
January 14, 1978.
El Ghawabi, S.H.; Gaafar, M.A.; El-Saharti, A.A. ; Ahmed, S.H.; Malash,
K.K. ; Fares, R. Chronic cyanide exposure: a clinical, radioisotope, and
laboratory study. Br. J. Ind. Med. 32(3) :215-219; 1975.
Ermans, A.M.; Delange, F. ; Van der Velden, M. ; Kinthaert, J. Possible
role of cyanide and thiocyanate in the etiology of endemic cretinism.
Adv. Exp. Med. Biol. 30:455-486; 1972.
6-30
-------
Esquivel, T.F.; Maravalhas, N. Rapid field method for evaluating hydro-
cyanic toxicity of cassava root, tubers. J. Agr. Food Chemical 21(2):
321-322; 1973.
Fairley, A.; Linton, E.G.; Wild, F.E. The absorption of hydrocyanic acid
vapor through the skin with notes on other matters relating to acute
cyanide poisoning. J. Hyg. 34:382-294; 1934.
Fassett, D. Cyanides and nitriles. Patty, F.H., ed. Industrial hygiene
and toxicology, Vol. II, toxicology. 2nd Revised Edition. New York.
NY: Interscience Publ.; 1963: 1991-2001.
Flury, F.; Zernik, F. HCN (hydrocyanic acid, prussic acid). Noxious
gases—vapors, mist, smoke and dust particles. Berlin: Verlag von Julius
Springer; 1931: 400-415. (As cited in NIOSH 1976)
Gallagher, C.H.; Reeve, V.E.; Wright, R. Copper deficiency in the rat.
Relationship to chronic cyanide poisoning. Aust. J. Exp. Biol. Med. Sci.
53(5):343-348; 1975.
Gettler, A.O.; St. George, A.V. Cyanide poisoning. Am. J. Clin. Pathol.
4:429-437; 1934.
Gettler, A.O.; Baine, J. The toxicology of cyanide. Am. J. Med. Sci.
195:182-198; 1938.
Gold, A.W.; Burgess, A.; Clougherty, E.V. Exposure of firefighters to
toxic air contaminants. Am. Ind. Hyg. Assoc. J. 39:534-539; 1978.
Goldstein, F.; Reiders, F. Conversion of thiocyanate to cyanide by an
erythrocytic enzyme. Am. J. Physiol. 173:287-290; 1953. (As cited in
NIOSH 1976)
Goodman, L.S.; Gilman, A. The Pharmacological basis of therapeutics,
5th ed. New York, NY: Macmillan Publishing Co., Inc.; 1975: 904-905.
Gosselin, R.E.; Hodge, H.C.; Smith, R.P.; Gleason, M.N. Clinical toxi-
cology of commercial products, 4th ed. Baltimore, MD: The William and
Wilkins Co.; 1976: 105-112.
Graham, D.L.; Laman, D.; Theodore, J.; Rubin, E.D. Acute cyanide
poisoning complicated by lactic acidosis and pulmonary edema. Arch.
Intern. Med. 137(8) :1051-1055; 19,77.
Grubbs, S.B. Detection of hydrocyanic acid gas, use of small animals
for this purpose. U.S. Public Health Report 32(16):565-569; 1917. (As
cited in McNamara 1976)
Habig, W.H.; Keen, J.H.; Jakoby, W.B. Glutathion S-Transferase in the
formation of cyanide from organic thiocyanates and as an organic nitrate
reductase. Biochem. Biophys. Res. Conramn. 64(2):501-506; 1975.
6-31
-------
Hardy, H.L.; Jefferies, W. McK.; Wasserman, M.M.; Waddell, W.R. Thio-
cyanate effect following industrial cyanide exposure. Report of two
cases. N. Eng. J. Med. 242:968-972; 1950.
Haymaker, W.; Ginzler, A.M.; Ferguson, F.L. Residual neuropathological
effects of cyanide poisoning—a study of the central nervous system of
23 dogs exposed to cyanide compounds. Mil. Surg. 111:231-246; 1952.
Himwich, W.A.; Saunders, J.P. Enzymatic conversion of cyanide to thio-
cyanate. Am. J. Physiol. 153:348-354; 1948.
Howard, J.W.; Hanzal, R.F. Chronic toxicity for rats of food treated
with hydrogen cyanide. J. Agric. Food Chem. 3:325-329; 1955.
Ibrahim, M.Z.M.; Briscoe, P.B. Jr.; Bayliss, O.B.; Adams, C.W.M. The
relationship between enzyme activity and neuroglia in the prodromal and
demyelinating stages of cyanide encephalopathy in the rat. J. Neurol.
Neurosurg. and Psychiatry 26:479-486; 1963.
Isom, G.E.; Way, J.L. Lethality of cyanide in the absence of inhibition
of liver cytochrome oxidase. Biochem. Pharmacol. 25(5):605-608; 1976.
Isom, G.E.; Liu, D.H.; Way, J.L. Effect of sublethal doses of cyanide
on glucose catabolism. Biochem. Pharmacol. 24(8):871-875; 1975.
Jacobs, L.; Sampson, S.R.; Comroe, J.H. Jr. Carotid sinus versus carotid
body origin of nicotine and cyanide bradycardia in the dog. Am. J.
Physiol. 220(2):472-476; 1971.
Kalpasanov, Y.; Kurchatova, G. A study of the statistical distribution
of chemical pollutants in air. J. Air Pollut. Conti. Assoc. 26(10):981-
985; 1976.
Katz, S.H.; Longfellow, E.S. Test papers for estimating hydrocyanic
acid gas in air. U.S. Bureau of Mines Report, Invest. 2504; 1923.
(As cited in McNamara 1976)
Kreutler, P.A.; Varbanov, V.; Goodman, W.; Claya, G.; Stanbury, J.B.
Interactions of protein deficiency, cyanide, and thiocyanate on thyroid
function in neonatal and adult rats. Am. J. Clin. Nutr. 31(2):282-289;
1978.
Laube, M.; Schmitt, H.; Peltier, J.; Droillat, M. Abstract. Action of
sodium cyanide on cardiac metabolism and systemic, pulmonary and coronary
hemodynamics. Arch. Int. Pharmacodyn Ther. 159(1):206-218; 1966.
Lazareff, N.V. ed. Toxic substances in industry. Inorganic and elemen-
tary compound. A manual for chemists, engineers, and physicians, 6th
ed. Leningrad: Khimiya; 1971: 228-240. (As cited in NIOSH 1976)
6-32
-------
Lazareff, N.V. Harmful substances in industry, Part II—inorganic and
organometallic compounds. Warsaw: State Technical Publishings; 1956:
224-235. (As cited in NIOSH 1976)
Lehmann, K.B. About the toxicity of gaseous HCN and hydrogen phosphide
with a demonstration. Klin Wochenschr 40:918-919; 1903. (As cited in
NIOSH 1976)
Lessell, S. Experimental cyanide optic neuropathy. Arch. Ophthalmol.
86(2):194-204; 1971.
Levine, M.S.; Radford, E.P. Occupational exposures to cyanide in
Baltimore firefighters. J. Occup. Med. 20(l):53-56; 1978.
Liebowitz, D.; Schwartz, H. Cyanide poisoning. Report of a case with
recovery. Am. J. Clin. Pathol. 18:965-970; 1948. (As cited in
Gosselin et al. 1976)
Maliszweski, T.F.; Bass, D.E. 'True' and 'apparent' thiocyanate in
body fluids of smokers and nonsmokers. J. Appl. Physiol. 8:289-291-
1955.
McNamara, B.P. Estimates of the toxicity of hydrocyanide acid vapors
in man. Edgewood Arsenal Technical Report EB-TR-76023. U.S. Dept. of
the Army; August 1976.
Mehta, C.S.; McGinity, J.W. Chronic administration of cyanide: urinary
excretion of thiocyanate in male and female rats. Acta. Pharmacol.
Toxicol. (KBH) 41(l):49-52; 1977.
Montgomery, R.D. Cyanogens: in toxic constituents of plant foodstuffs.
Liener, I.E. ed. 1969: 143-157. (As cited in Towill e_t al. 1978)
Moss, R.H.; Jackson, C.F.; Seiberlich, J. Toxicity of carbon monoxide
and hydrogen cyanide gas mixtures—a preliminary report. Arch. Ind.
Hyg. Occup. Med. 4:53-64; 1951. (As cited in NIOSH 1976)
National Institute for Occupational Safety and Health (NIOSH). Criteria
for a recommended standard . . . occupational exposure to hydrogen
cyanide and cyanide salts [NaCN, KCN, and CA(CN)2]- Washington, DC:
U.S. Dept. of Health, Education and Welfare, Public Health Service,
Center for Disease Control; 1976.
Nolan, J.W. Potassium cyanide poisoning. J. Am. Med. 50:365; 1908.
(As cited in NIOSH 1976)
Nowiniski, W.W.; Pandra, J. Influence of sodium thiocyanate on the
development of the chick embryo. Nature 157:414; 1946.
Osuntokun, B.O.; Monekosso, G.L.; Wilson, J. Relationship of a degener-
ative tropical neuropathy to diet: report of a field study. Br. Med. J
1:547-550; 1969.
6-33
-------
~
°f ChemiCal S^stances, 1977 Edition, Vol. II
. B s
^
gen°;va;idUina!i; T'i Irf' M'D ThS allowable concentration of hydro-
gen cyanide in air. Bull. Inst. Public Health 4:3-5; 1955.
Schmidt, E.S.; Newton, G.W. ; Sanders, S.M. ; Lewis J P - Conn F F
Laetrile toxicity studies in dogs. J. ^.^^ 23910':
ues n ogs. J. . 239(0): 943-947;
Schubert J.; Brill, W.A. Antagonism of experimental cyanide
of cytochrome
^
209(26)
Sunshine, I.; Finkle, B. The necessity for tissue studies in fatal
cyanide poisonings. Int. Arch. Gewerbepathol. Gewerbehyg. 20:558-561;
Symington, IS; Anderson, R. A. ; Thomson, I.; Oliver, J.S. ; Harland, W.A. ;
K.err, j.w. Cyanide exposure in fires. Lancet 2(2080) : 91-92; 1978.
1 n§.dUe ^ f N abS°rbed throuSh skin. Minerva Med.
. (As cited in NIOSH 1976)
6-34
-------
Towill. L.E.; Drury, J.S.: Whitfield, B.L.; Lewis, E.B.; Galyan, E.L.;
Mammons, A.S. Reviews of the environmental effects of pollutants: V
Cyanide, ORNL/EIS-81; EPA-600/1-78-027; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Chemical analysis of
interstate carrier water supply systems. EPA-430/9-75-005; April 1975.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for cyanides. Washington, DC: Criteria and Standards Division,
Office of Water Regulations and Standards; IPA 440/5-80-037; 1980.
U.S. Department of Health, Education, and Welfare (U.S. DREW). Occupa-
tional exposure to hydrogen cyanide and cyanide salts. Public Health
Service, October 1976.
U.S. Department of Health, Education, and Welfare (U.S. DREW). Drinking
water standards. Washington, DC: Dept. of Health, Education, and
Welfare; 1962.
Valade, P. Injuries to the central nervous system in chronic experi-
mental poisoning by hydrocyanic acid gas. Bull. Acad. Natl. Med. Paris
136:280-285; 1952. (As cited in NIOSH 1976)
Walton, D.C.; Witherspoon, M.G. Skin absorption of certain gases. J.
Pharmacol. 26:315-324; 1926.
Wexler, J.; Whittenberger, J.L; Dumke, P.R. The effect of cyanide on
the electrocardiogram of man. Am. Heart J. 34:163-173; 1957.
Williams, R.T. Detoxication Mechanisms, 2nd ed. New York, NY: John
Wiley and Sons, Inc.; 1959: 390-409.
Winek, C.L.; Fusia, E.; Collom, W.D.; Shanor, S.P. Cyanide poisoning as
a mode of suicide. Forensic Sci. ll(l):51-55; 1978.
Wood, J.L.; Cooley, S.L. Detoxification of cyanide by cystine. J. Biol.
Chem. 218:449-457; 1965.
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7.0 RISK CONSIDERATIONS
7.1 RISK CONSIDERATIONS FOR HUMANS
Based upon the exposure and toxicity estimates in the preceding
chapters, the general population of the U.S. does not appear to be under
any substantial risk due to the discharge of cyanide into the environ-
ment. Levels of human exposure to cyanide are for the most part well
below the acute effect thresholds for humans. The inhalation effect
threshold is about 100 mg/m^, whereas through ingestion the threshold
is about 1 mg/kg body weight. Isolated instances can occur where the
oral threshold is exceeded by ingestion of food containing high concen-
trations of naturally-occurring cyanides. However, cyanide levels in
U.S. drinking water are less than 8 ug/1. Smoke inhalation, especially
for cigarette smokers, may result in high doses, but over the time period
involved the body's detoxification mechanisms provide adequate protection.
The only reasonable scenario under which acute poisoning is possible
would be accidental ingestion or inhalation of a large single dose over
a short time interval. This could conceivably occur in an occupational
setting, or as a result of contact with a major cyanide discharge site.
However, the probability of individual exposures of this type is negli-
gible. Risk quantification is not feasible without additional "investiga-
tion.
The potential exposures of humans to cyanide and the potential acute
effects of cyanide inhalation or ingestion are summarized in Figure 7-1.
The range of acute lethal doses for both exposure routes is well in ex-
cess of the typical environmental exposure levels. Intake through in-
halation over a short period (1 hour or less) may be above 10 mg for
heavy smokers or people exposed to fires, as shown previously in
Table 6-7, but these are the only instances in which inhalation may
possibly approach a lethal level. The fatal human inhalation dose of
HCN is not firmly established, but concentrations above 100 mg/m are
generally fatal to living organisms. In addition, ingestion of large
quantities of foods containing naturally occurring cyanide is the only
scenario that might conceivably result in a lethal ingested dose. Sub-
lethal doses can be tolerated with no permanent adverse effects, due to
the body's detoxification mechanism, so that the risk of acute effects
due to ingestion appears to be extremely low.
The chronic or subchronic effects of cyanide exposure are not com-
pletely understood, due to the limited availability of toxicologic data.
Cyanide has been implicated with thyroid disorders, and various neuro-
pathies, but appears to play only an indirect role in the incidence of
such disorders via long-term overloading with thiocyanate, cyanide's
major detoxification product. In the absence of suitable dose-response
data, no quantitative evaluation of chronic risk can be made. However,
it is certainly possible that subpopulations with high chronic exposure
levels, such as smokers or firefighters, may be susceptible to increased
incidence of these diseases.
7-1
-------
Potential for
Occurrence
i
N>
Completely
Possible
Strongly
Possible
Moderately
Possible
Weakly
Possible
Barely
Possible
Acute Lethal
Oral Dose
Lethal Dose
by Inhalation
« 1 hr)
0.01
100
1000
Cyanide
Intake
(rug)
FIGURE 7-1 COMPARISON OF RANGES OF UNCERTAINTY FOR ACUTE EFFECTS
OF AND EXPOSURE TO CYANIDE IN HUMANS
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7.2 RISK CONSIDERATIONS FOR NON-HUMAN BIOTA
The information presented in this report suggests that the in-
cidence of localized risks to finfish due to exposure to cyanide
may be widespread and may often be associated with one or more types of
point-source discharges, particularly those associated with iron and
steel manufacture, steam-electric power plants, and electroplaters. The
information available is, however, insufficient for determining whether
this is an exposure problem of national dimensions for the various source
types, or whether the problem is dependent upon such local factors as
discharge volume, degree of discharge control, and extent of receiving
water volume. The extent of information on individual discharge monitor-
ing and compliance status available for this assessment was insufficient
to provide a basis for a quantitative exposure assessment, either in the
nation as a whole or in local areas. In particular, the absence of these
data prevents understanding the extent to which recent point source con-
trols may have reduced or eliminated exposure risks.
Despite the above limitations, certain qualitative conclusions
are possible concerning the risks to non-human biota. Where cyanide levels
do exceed 5 to 7 ug/1, they will probably be in the vicinity of point
discharge sources, and will diminish rapidly at increasing distances
from the source. Hence, fish populations in surface waters are probably
affected only over distances of several kilometers rather than over
a broad geographic area. This type of exposure is exemplified by the
fishkill incidents that have been associated with cyanide in the past.
As far as terrestrial organisms are concerned, the risk from cyanide
is not quantifiable, but appears to be considerably less than the risk
to aquatic life.
7.2.1 Risk Considerations for Aquatic Organisms
Aquatic organisms may be exposed to scattered, highly localized risks
as a result of cyanide in surface waters. Both acute and chronic effects
on aquatic organisms may occur at cyanide concentrations in the range of
10 yg/1. Such concentrations have been observed infrequently at various
locations throughout the United States. The fate analysis in this report
indicates that the half-life of cyanides in surface water is relatively
short; consequently, elevated concentrations in water would be expected
only within a few kilometers of point-source dischargers. The potential
aquatic risks may be associated with local batch-type discharges, even
though the total annual discharges may not result in a sufficient loading
to create observable steady-state concentrations. Dispersive emissions
of cyanide, such as in road salt usage, are expected to contribute negli-
gibly to high localized, ambient concentrations of cyanide compared with
the cyanide contributions of point sources.
From an examination of reported fish kills attributed to cyanide,
it appears that both isolated and recurring incidents of risk in fresh
and estuarine waters can be associated with several types of man-made
sources of cyanide. Reports of chronic recurrences in given locations
7-3
-------
appear to be somewhat more common in the pre-1976 period; however
reports compiled through 1977 indicate that episodes of cyanide-related
fisn kills still occurred, and in some locales, occasionally more than
once a year. Twenty incidents were reported between 1972 and 1977.
In all, 16 reported fish kills were related to activities in the
metals industry: 11 due to general metals production and 5 due to
iron and steel production. Five other fish kills were reported to result
o resut
£°?nS tiVit*eS °Vhe chemi'al industry, three from industrial discharges
to POTWs, and one from mining activities. Three reported incidents were
the result of unknown (or unreported) causes.
This distribution of incidents is not mutually exclusive, since
several of the incidents were attributed to more than one of the activi-
ties cited. Though metal production, including iron and steel production
contributed to the majority of these incidents, it is evident that other
activities have been associated with reported fish kills, and that in
several instances, no suspected source of cyanide was found or reported.
Because of the paucity of data on cyanide exposure to saltwater
organisms, it is difficult to assess the risks. However, the U.S. EPA's
™S«™i records indicate a history of five reported kills of more than
30,000 fish, each attributed to cyanide in the estuarine headwaters of
Chesapeake Bay near Sparrows Point, MD during 1972-73.
The materials balance presented in Section 3.1 indicates that
industrial activities reportedly associated with cyanide-related fish
kills are known to have created point-source (water) discharge of the
pollutant. However, aquatic risks may be diminishing because the
release of cyanide from some of these activities (e.g., iron and steel
manufacture) is decreasing as a result of ongoing (NPDES) water pollu-
tion control initiatives. This may explain, for example, the absence
of recent reports of fish kills from areas such as Sparrows Point, MD,
where five large incidents were reported during 1972-73.
7-2.2 Risk Considerations for Terrestrial Organisms
The potential for exposure of terrestrial organisms to significant
levels of cyanide appears to be small, although it is difficult to
quantify. As indicated in Section 3.2.6, concentrations of cyanide in
air are negligible in relation to the effect levels for mammals discussed
in Section 4.1.5. Likewise, terrestrial mammals may be exposed to ambient
surface water concentrations generally <0.1 mg/1. Consequently, it is
extremely unlikely that these organisms will ingest lethal quantities of
cyanide. For example, in order to ingest 10 mg/kg (which approximates
the lethal oral dose given in Table 5-8, Section 4.1.5) an animal would
have to drink 100 I/kg body weight. However, there have been incidences of
cyanide poisoning in livestock that had consumed vegetative matter
enriched with natural cyanides. The possibility for man-made con-
tributions of cyanide to create similar situations remains unquantified.
U.S. Environmental Protection Agency
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