Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
1
Final
draft
Chapter
IV.
Human
Exposure
Since
cyanide
is
the
primary
metabolite
of
cyanogen
chloride
and
the
surrogate
used
for
the
dose­
response
assessment
(
see
Appendix
A),
this
section
addresses
both
cyanogen
chloride
and
cyanide
exposure.
Future
work
enhancing
this
assessment
could
include
thiocyanate,
since
cyanide
is
metabolized
to
thiocyanate,
and
thiocyanate
accounts
for
at
least
some
of
the
toxic
effects
of
cyanide
exposure.
Exposure
to
cyanate
and
cyanamide
is
not
addressed.
Exposure
to
these
chemicals
is
of
less
concern
for
the
cyanogen
chloride
assessment,
since
they
represent
a
small
portion
of
the
cyanogen
chloride
dose,
and
they
are
not
metabolized
through
the
cyanide/
thiocyanate
pathway.

A.
Drinking
Water
Exposure
Cyanogen
chloride
has
been
identified
as
a
drinking
water
disinfection
byproduct
under
the
Information
Collection
Rule
(
U.
S.
EPA,
1994a)
and
is
being
assessed
for
regulatory
consideration
in
the
Stage
2
Disinfectants/
Disinfection
Byproducts
Rule
to
be
promulgated.
HCN
has
been
identified
as
a
known
metabolite
of
cyanogen
chloride
and
is
a
known
contaminant
in
drinking
water.
Therefore,
this
section
will
examine
the
occurrence
of
these
compounds
in
drinking
water.

Cyanogen
chloride
is
formed
in
raw
water
during
chlorination
and
increases
when
ammonium
chloride
is
added
prior
to
chlorination
(
Ohya
and
Kanno,
1987)
or
if
ammonia
is
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
2
Final
draft
present
in
the
source
water
(
WHO,
2000).
Most
cyanide
in
waters
commonly
occurs
as
HCN
(
ATSDR,
1997).

A.
1
National
Occurrence
Data
for
Cyanogen
Chloride
This
section
presents
the
data
collected
from
the
Information
Collection
Rule
(
ICR)

databases,
which
provide
data
from
surface­
water
and
groundwater
systems
serving
at
least
100,000
persons.
This
data
base
includes
information
gathered
for
the
18
months
from
July
1997
to
December
1998.

The
ICR
generated
plant­
level
sets
of
data
that
link
water
quality
and
treatment
from
source
to
tap,
and
that
aid
in
understanding
the
seasonal
and
spatial
variability
in
these
relationships.
The
database
contains
information
from
18
monthly
or
6
quarterly
samples
from
7/
97
to
12/
98,
from
approximately
300
large
systems
covering
approximately
500
plants.

However,
because
cyanogen
chloride
is
formed
when
chlorine
reacts
with
organic
material
in
the
presence
of
ammonia,
only
plants
that
used
chloramine
as
a
primary
or
secondary
disinfectant
were
required
to
monitor
for
cyanogen
chloride.
Thirty­
five
percent
of
the
surface­
water
plants
and
23%
of
the
groundwater
plants
reported
cyanogen
chloride
observations.
In
addition,

analysis
for
cyanogen
was
required
only
for
two
sample
locations:
finished
water
(
at
the
end
of
the
treatment
plant,
before
water
enters
the
distribution
system)
and
distribution
system
(
DS)

maximum
(
at
a
point
in
the
distribution
system
that
has
the
longest
residence
time,
as
designated
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
3
Final
draft
by
the
water
system).
For
other
chemicals
monitored
in
the
ICR,
four
distribution
locations
were
sampled.
The
samples
were
tested
for
influent
and
finished
water­
quality
parameters
(
e.
g.,
TOC,

temperature,
pH,
alkalinity),
disinfection
byproduct
(
DBP)
levels,
and
disinfectant
residuals.
Over
the
18­
month
period,
738
finished­
water
samples
were
taken
from
140
plants
and
610
DS
maximum
samples
were
taken
from
117
plants
with
surface
water
as
their
source.
During
this
same
period,
146
finished­
water
samples
were
taken
from
28
plants
and
135
DS
maximum
samples
were
taken
from
26
plants
with
groundwater
as
their
source.
For
more
detailed
information,
such
as
sampling
frequencies,
refer
to
the
ICR
Data
Analysis
Plan
(
U.
S.
EPA,

2000a).

A.
1.1
Quarterly
Finished
Water
and
Distribution
Maximum
for
Cyanogen
Chloride
The
data
in
Table
IV­
1
were
taken
from
the
online
version
of
the
ICR
database
(
U.
S.

EPA,
2000b),
and
the
explanation
of
the
methods
used
was
taken
from
the
Draft
EPA
Document
on
Stage
2
Occurrence
and
Exposure
Assessment
for
Disinfectants
and
Disinfection
Byproducts
(
D/
DBPs)
in
Public
Drinking
Water
(
U.
S.
EPA,
2000c).
Data
presented
in
the
table
have
been
taken
from
the
ICR
database
as
provided
to
avoid
misrepresentation
or
misinterpretation.

Therefore,
although
all
data
in
the
table
are
presented
with
two
decimal
points
(
as
provided
in
the
ICR
database),
this
does
not
necessarily
represent
the
actual
precision
of
the
data.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
4
Final
draft
Table
IV­
1.
Cyanogen
Chloride
Quarterly
Distribution
System
Finish
and
Maximum
Source
Quarterly
Dist.
Sys.
Plants
N
Pct
ND
%
Mean
µ
g/
L
Median
µ
g/
L
STD
µ
g/
L
Min
µ
g/
L
Max
µ
g/
L
p10
µ
g/
L
p90
µ
g/
L
SW
Finished
140
738
16.26
3.25
2.30
3.34
0.00
20.60
0.00
7.40
DS
Max
117
610
22.46
3.02
2.10
3.23
0.00
18.30
0.00
8.00
GW
Finished
28
146
31.51
2.12
1.10
2.78
0.00
14.50
0.00
6.30
DS
Max
26
135
38.52
1.63
0.80
2.40
0.00
16.30
0.00
4.70
Source:
SW
­
Surface
Water,
GW
­
Groundwater
Quarterly
Dist.
Sys.:
Finished
Water:
Sample
point
at
the
end
of
the
treatment
plant,
before
water
enters
the
distribution
system
DS
Max
(
Distribution
System
Maximum):
Sample
point
in
the
distribution
system
that
has
the
longest
residence
time,
as
designated
by
the
water
system.
Plants:
Number
of
plants
sampled
N:
Number
of
samples
Pct
ND:
Percent
samples
nondetect
(
detection
limits
not
provided)
Mean:
Arithmetic
mean
of
all
samples
Median:
Median
value
of
all
samples
STD:
Standard
deviation
Min:
Minimum
Value
Max:
Maximum
Value
p10:
10th
percentile
p90:
90th
percentile
Examination
of
the
data
using
the
Student's
t­
test
indicates
that
the
mean
concentrations
of
cyanogen
chloride
in
the
finished
water
were
not
significantly
different
(
at
p
=
0.05)
from
the
mean
cyanogen
chloride
concentrations
at
the
distribution
maximum
in
either
the
surface­
water
or
groundwater
plants.
However,
the
finished
and
DS
maximum
mean
cyanogen
chloride
concentrations
in
surface
water
were
significantly
higher
(
at
p
=
0.05)
than
their
respective
concentrations
in
groundwater.
The
lowest
mean
concentrations
are
associated
with
the
highest
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
5
Final
draft
percentage
of
nondetects,
which
were
treated
as
0
in
the
calculation
of
the
mean,
median,

standard
deviation,
and
p10
values
(
U.
S.
EPA,
2000b).
The
median
concentrations
in
groundwater
and
surface
water
for
cyanogen
chloride
were
lower
than
the
means.
The
median
concentrations
of
cyanogen
chloride
in
finished
and
DS
maximum
samples
in
surface
water
were
2.3
and
2.1

g/
L,
respectively.
The
median
concentrations
of
cyanogen
chloride
in
finished
and
DS
maximum
samples
in
groundwater
were
1.1
and
0.8

g/
L,
respectively.
The
mean
concentrations
of
cyanogen
chloride
in
finished
and
DS
maximum
samples
in
surface
water
were
3.25
and
3.02

g/
L,
respectively.
The
mean
concentrations
of
cyanogen
chloride
in
finished
and
DS
maximum
samples
in
groundwater
were
2.12
and
1.63

g/
L,
respectively.

A.
2
National
Occurrence
Data
for
Cyanide
This
section
summarizes
information
gathered
from
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide.

Cyanide
occurs
most
commonly
in
water
as
HCN.
Based
on
data
obtained
from
the
EPA
STORET
database
from
the
late
1970s
to
the
early
1980s,
the
mean
cyanide
concentration
in
most
surface
waters
was
no
greater
than
3.5

g/
L
(
Fiksel
et
al.,
1981).
However,
37
of
50
states
had
locations
where
cyanide
concentrations
exceeded
this
level.
Surface
water
in
areas
of
southern
California,
North
Dakota,
Iowa,
northwest
Georgia,
western
New
York,
and
western
Pennsylvania
exceeded
200

g/
L
cyanide
(
Fiksel
et
al.,
1981).
Cyanide
was
detected
in
water
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
6
Final
draft
from
the
Great
Lakes
at
concentrations
greater
than
1

g/
L
(
Great
Lakes
Water
Quality
Board,

1983).
Concentrations
of
cyanide
in
104
samples
collected
during
1980
and
1981
at
various
points
on
the
Ohio
River
and
its
tributaries
ranged
from
<
5
to
80

g/
L
(
Ohio
River
Valley
Sanitation
Commission,
1982).
Based
on
data
from
the
Nationwide
Urban
Runoff
Program
as
of
1982,
cyanide
was
detected
in
16%
of
the
samples
in
4
of
15
urban
areas
evaluated,
with
concentrations
ranging
from
2
to
33

g/
L.
Localesevaluated
included
Denver,
Colorado;
Long
Island,
New
York;
Austin,
Texas;
and
Bellevue,
Washington
(
Cole
et
al.,
1984).

Cyanide
has
been
detected
in
groundwater
below
landfills
and
disposal
sites
(
Anonymous,

1990;
Myers,
1983).
A
maximum
concentration
of
1200

g/
L
cyanide
was
found
in
shallow
groundwater
less
than
3
meters
below
an
inactive
drum
recycling
facility
in
Miami,
Florida
(
Myers
et
al.,
1983).

A.
2.1
National
Drinking
Water
Contaminant
Occurrence
Database
Data
on
Cyanide
The
National
Drinking
Water
Contaminant
Occurrence
Database
(
NCOD)
was
developed
to
satisfy
the
statutory
requirements
set
by
Congress
in
the
1996
Safe
Drinking
Water
Act
(
SDWA)
amendments
and
supports
the
U.
S.
EPA's
decisions
related
to
identifying
contaminants
for
regulation
and
subsequent
regulation
development
(
U.
S.
EPA,
2001c).
The
NCOD
contains
only
Public
Water
System
(
PWS)
data
reported
to
the
Safe
Drinking
Water
Information
Service
and
may
be
from
several
sampling
points
within
a
water
system.
The
data
were
collected
from
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
7
Final
draft
thousands
of
existing
drinking­
water
sources,
both
small
and
large,
for
surface
water,

groundwater
under
the
direct
influence
(
UDI)
of
surface
water,
and
groundwater.
The
data
contained
in
the
NCOD
are
updated
periodically
from
existing
sources
and
change
over
time.
The
data
presented
herein
are
from
the
most
recent
quarter
year
updated
on
April
28,
2000
(
Table
IV­

2)
(
U.
S.
EPA,
2001c).
Since
the
NCOD
is
updated
quarterly,
data
from
previous
quarters
were
not
available,
and
a
yearly
average
could
not
be
calculated.
However,
these
data
are
expected
to
represent
the
most
recent
average
concentrations
of
cyanide
across
the
United
States.
The
EPA
STORET
data,
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide,
is
over
11
years
old
and
presents
data
for
a
limited
number
of
locations.
Therefore,
it
is
believed
that
the
NCOD
data
is
the
most
representative
of
current
cyanide
concentrations
in
drinking
water
across
the
U.
S.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
8
Final
draft
Table
IV­
2.
National
Drinking
Water
Contaminant
Occurrence
Database
Public
Water
Supply
­
National
Drinking
Water
Data
for
Cyanide
PWS
Category
PWS
Size
(
population)
Total
Analyses
#
Analyses
w/
Detects
#
PWS
w/
Analyses
#
PWS
w/
Detects
Min
ug/
L
Max
ug/
L
Average
ug/
L
Standard
Deviation
ug/
L
Surface
Water
Very
Small
0
­
500
105
3
46
3
2
4300
1435
2481
Small
501
­
3,300
253
3
97
3
1
7
3.7
3.1
Medium
3,301
­
10,000
216
5
58
4
2
9000
1807
4020
Large
10,001
­
100,000
521
15
92
8
2
10,000
5340
5156
Very
Large
100,000
+
187
7
16
4
20
120
57.9
38.7
All
Systems
1282
33
309
22
1
10,000
2844
4446
Groundwater
UDI
Surface
Water
Very
Small
0
­
500
 
*
­­
­­
­­
­­
­­
­­
­­

Small
501
­
3,300
­­
­­
­­
­­
­­
­­
­­
­­

Medium
3,301
­
10,000
3
0
1
0
­­
­­
­­
­­

Large
10,001
­
100,000
­­
­­
­­
­­
­­
­­
­­
­­

Very
Large
100,000
+
­­
­­
­­
­­
­­
­­
­­
­­

All
Systems
3
0
1
0
­­
­­
­­
­­

Groundwater
Very
Small
0
­
500
1353
23
818
18
3
32,700
4498
8539
Small
501
­
3,300
931
18
424
14
3
10,000
2254
4261
Medium
3,301
­
10,000
699
10
189
6
6
380
63.6
114
Large
10,001
­
100,000
1030
29
128
15
2
10,000
1065
3089
Very
Large
100,000
+
96
0
2
0
­­
­­
­­
­­

All
Systems
4109
80
1561
53
2
32,700
2194
5494
*
All
cells
with
"­­"
indicate
values
were
not
reported
in
the
NCOD
database.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
9
Final
draft
Average
cyanide
concentrations
in
surface
water
and
groundwater
were
calculated
only
for
those
samples
where
cyanide
was
detected.
Non­
detects
were
not
included
in
the
calculation
of
average
concentrations.
Examination
of
the
data
using
the
Student's
t­
test
indicates
that
there
were
no
statistically
significant
differences
(
at
p
=
0.05)
between
the
average
cyanide
concentrations
in
surface
water
and
groundwater.
The
overall
average
concentration
in
treated
surface
water
(
averaged
across
all
size
systems
that
detected
cyanide)
was
2844

g/
L
and
ranged
from
3.7

g/
L
to
5340

g/
L
in
different­
size
systems
(
Table
IV­
2).
The
minimum
concentration
was
non­
detect
and
the
maximum
was
10,000

g/
L.
Of
a
total
of
1282
samples
in
309
plants,

cyanide
was
detected
in
approximately
3%
(
33/
1282)
of
the
samples
in
7%
(
22/
309)
of
the
plants
treating
surface
water
(
Table
IV­
2).
In
groundwater
the
overall
average
concentration
of
cyanide
(
averaged
across
all
size
systems
that
detected
cyanide)
was
2194

g/
L
and
ranged
from
nondetect
to
4498

g/
L
in
different­
size
systems
(
Table
IV­
2).
The
minimum
concentration
was
nondetect
and
the
maximum
was
32,700

g/
L.
Of
a
total
of
4109
samples
in
1561
plants,
cyanide
was
detected
in
approximately
2%
(
80/
4109)
of
the
samples
in
approximately
3%
(
53/
1561)
of
the
plants
treating
groundwater
(
Table
IV­
2).
There
is
considerable
uncertainty
in
the
reported
average
concentrations,
since
there
were
several
orders
of
magnitude
separating
the
minimum
and
maximum
detected
levels,
and
only
a
few
analyses
with
detects.
This
means
that
the
calculated
averages
for
these
populations
may
be
highly
influenced
by
one
or
two
systems
with
high
cyanide
levels,
and
that
the
calculated
averages
do
not
accurately
reflect
the
cyanide
concentrations
to
which
these
populations
are
exposed.
Medians
were
not
available
from
the
NCOD
survey.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
10
Final
draft
In
a
total
of
three
samples
in
one
plant,
cyanide
was
not
detected
in
groundwater
under
the
direct
influence
of
surface
water.

A.
3
Factors
Affecting
the
Relative
Concentrations
of
Cyanogen
Chloride
and
Hydrogen
Cyanide
in
Drinking
Water
Cyanogen
chloride.
Cyanogen
chloride
is
formed
in
raw
water
during
chlorination.

Ohya
and
Kanno
(
1987)
found
that
the
formation
of
cyanogen
chloride
increased
when
ammonium
chloride
is
added
prior
to
chlorination.
This
was
presumed
to
be
due
to
the
reaction
of
humic
substance
with
chloramine.
According
to
the
WHO
Environmental
Health
Criteria
Monograph
on
Disinfectants
and
Disinfectant
Byproducts
(
WHO,
2000),
the
presence
of
ammonia
in
source
waters
during
disinfection
can
cause
chlorine
and
ozone
demand
and
participate
in
the
formation
of
cyanogen
chloride
and
other
nitrogenous
compounds.
Although
data
on
the
occurrence
of
ammonia
in
source
water
would
greatly
aid
the
understanding
of
the
potential
for
exposure
to
cyanogen
chloride
when
disinfectants
other
than
chloramine
are
used,

this
information
was
not
available
in
the
ICR
nor
the
NCOD
database.

Only
those
plants
that
used
chloramine
as
a
primary
or
secondary
disinfectant
were
required
to
monitor
for
cyanogen
chloride
for
inclusion
in
the
ICR
database.
Because
ammonia
in
the
source
waters
may
also
result
in
the
formation
of
cyanogen
chloride
during
disinfection
with
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
11
Final
draft
other
disinfectants,
the
number
of
plants
where
cyanogen
chloride
may
be
present
may
be
underrepresented
in
the
ICR
database.

Richardson
(
1998)
compared
the
relative
concentrations
of
DBPs
in
drinking
water
using
different
treatment
methods
and
found
that
cyanogen
chloride
is
a
byproduct
of
both
chlorination
and
chloramination.
However,
in
contrast
to
Ohya
and
Kanno
(
1987),
Richardson
(
1998)
believes
that
the
formation
of
the
halonitriles,
including
cyanogen
chloride,
may
be
caused
by
the
low
level
of
residual
chlorine
in
the
chloramination
process
and
not
by
chloramine
itself.
Cyanogen
chloride
was
not
produced
by
chlorine
dioxide
or
ozone
in
measurable
quantities.
The
levels
of
DBPs,
including
cyanogen
chloride,
were
lower
when
ozone
was
followed
by
chlorine.

Interestingly,
although
cyanogen
chloride
concentrations
in
water
treated
with
ozone
followed
by
chloramine
were
half
the
concentrations
observed
with
chlorination
alone,
they
were
twice
the
level
found
in
water
treated
with
chloramine
as
the
sole
disinfectant.

Krasner
et
al.
(
1989)
found
that
cyanogen
chloride
concentrations
in
water
pretreated
with
chlorination
and
post­
treated
with
ammonia
were
significantly
higher
than
in
water
treated
with
chlorine
alone.

Young
(
1994)
found
that
numerous
organic
byproducts
are
produced,
including
cyanogen
chloride,
when
aqueous
chlorine
reacts
with
the
amino
acids,
purines
and
pyrimidines.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
12
Final
draft
Hydrogen
Cyanide.
This
section
is
adapted
from
information
gathered
from
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide.

The
major
releases
of
cyanide
to
water
are
a
result
of
discharges
from
metal­
finishing
industries,
iron
and
steel
mills,
and
organic
chemical
industries
(
Fiksel,
et
al.,
1981).

Although
HCN
and
soluble
metal
cyanides
may
be
removed
from
water
by
aerobic
or
anaerobic
biodegradation,
the
primary
mechanism
is
expected
to
be
volatilization
(
Callahan
et
al.,
1979).

B.
Exposure
to
Sources
Other
Than
Drinking
Water
Cyanogen
chloride.
The
National
Occupational
Exposure
Survey
(
NOES)
conducted
by
the
National
Institute
for
Occupational
Safety
and
Health
(
NIOSH)
from
1980
to
1983
estimated
that
1393
workers
are
exposed
to
cyanogen
chloride
(
NIOSH,
1990).
Cyanogen
chloride
is
used
as
a
warning
agent
in
fumigant
gases
and
is
also
used
for
organic
synthesis.

Hydrogen
cyanide.
This
section
summarizes
information
gathered
from
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide.

Although
cyanide
occurs
naturally
in
the
fruits,
seeds,
roots,
and
leaves
of
numerous
plants,
and
is
released
to
the
environment
from
natural
fires
and
natural
biogenic
processes
from
higher
plants,
bacteria,
and
fungi
(
Cicerone
and
Zellner,
1983;
Crutzen
and
Carmichael
1993;
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
13
Final
draft
Fiksel
et
al.,
1981;
Knowles,
1988),
anthropogenic
sources
are
responsible
for
much
of
the
HCN
in
the
environment.

The
primary
sources
of
cyanide
releases
to
soil
appear
to
be
the
disposal
of
cyanide
wastes
in
landfills
and
the
use
of
cyanide­
containing
road
salts
(
Fiksel
et
al.,
1981).
However,
no
information
could
be
found
on
the
concentration
of
HCN
in
soil
or
sediments.
Because
of
its
highly
volatile
nature,
HCN
is
not
expected
to
be
present
at
the
surface
of
soils
in
any
appreciable
amount.
In
subsurface
soil,
low
concentrations
of
cyanide
would
probably
biodegrade
under
both
aerobic
and
anaerobic
conditions.

A
number
of
drugs
and
industrial
chemicals
have
been
associated
with
human
exposure
to
cyanide
and
have
caused
serious
poisoning
and,
in
some
cases,
death.
Drugs
that
release
cyanide
upon
metabolism
include
Laetrile
(
amygdalin),
formerly
used
in
clinical
trials
for
the
treatment
of
cancer
(
Khandekar
and
Edelman,
1979)
and
a
drug
used
to
reduce
high
blood
pressure
(
Aitken
et
al.,
1977;
Vesey
et
al.,
1976).
Industrial
chemicals
such
as
acetonitrile,
propionitrile,
acrylonitrile,

n­
butyronitrile,
maleonitrile,
and
succinonitrile
(
Willhite
and
Smith,
1981)
are
also
metabolized
to
cyanide.

Occupational
exposure
to
HCN
occurs
primarily
through
inhalation
and,
less
frequently,

through
dermal
exposure.
The
National
Occupational
Exposure
Survey
(
NOES)
conducted
by
the
NIOSH
from
1980
to
1983
estimated
that
over
250,000
workers
are
exposed
to
cyanide
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
14
Final
draft
compounds
with
4005
workers
exposed
to
HCN
(
NIOSH,
1990).
These
estimates
did
not
include
workers
potentially
exposed
to
trade­
name
compounds
that
contain
cyanide.
Occupations
where
workers
may
be
exposed
to
HCN
include
electroplating,
metallurgy,
cyanotype
printing,

pesticide
application,
firefighting,
steel
manufacturing,
gas­
works
operations,
and
metal
cleaning;

and
workers
involved
in
the
manufacture
of
cyanides
and
other
simple
aliphatic
nitriles,
methyl
methacrylate,
cyanuric
acid,
dyes,
pharmaceutical,
or
chelating
agents;
and
people
who
work
in
tanneries,
metal
cleaning,
photoengraving
or
photography,
and
as
blacksmiths
(
Fiksel
et
al.,
1981;

Lucas,
1992,
Willhite
and
Smith,
1981).
Workers
in
the
oil­
shale
retorting
industries
may
also
be
exposed
to
HCN
present
in
the
offgas
from
the
retorting
process.
Emergency
personnel,
police
and
firefighters,
and
medical
personnel
may
be
exposed
to
HCN
when
exposed
to
house
or
other
building
fires
(
Andrews,
et
al.,
1989),
or
during
resuscitation
efforts
or
the
removal
of
the
gastric
contents
of
postmortem
victims
of
cyanide
poisoning
(
Andrews,
et
al.,
1989).

In
a
survey
of
various
plating
facilities,
NIOSH
found
HCN
in
the
workplace
air
at
concentrations
ranging
from
0.001
to
4.3
mg/
m3
(
NIOSH,
1982;
NIOSH,
1976).
In
a
recent
NIOSH
survey
of
a
university
art
department
foundry,
4.3
mg/
m3
HCN
was
detected
in
the
smoke
produced
during
the
pouring
of
castings.
Although
the
ATSDR
document
provided
no
information
on
the
amount
of
time
and
frequency
that
these
workers
were
exposed
to
these
concentrations
of
HCN,
these
levels
were
below
the
NIOSH
recommended
15­
minute
short­
term
exposure
limit
(
STEL)
of
5
mg/
m3
for
HCN
(
reported
in
the
ASTDR
document
as
the
NIOSH
ceiling
limit).
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
15
Final
draft
B.
1
Dietary
Intake
Cyanogen
chloride.
There
are
no
quantitative
data
on
the
occurrence
of
cyanogen
chloride
in
food.
Cyanogen
chloride
was
not
included
among
the
analytes
measured
in
the
current
Total
Diet
Study
(
TDS),
sometimes
called
the
Market
Basket
Study,
an
ongoing
FDA
program
that
determines
levels
of
various
pesticide
residues,
contaminants,
and
nutrients
in
foods
(
U.
S.

FDA,
2002).

However,
Wu
et
al.
(
1998)
investigated
DBP
formation
in
the
preparation
of
instant
tea
with
water
containing
chlorine
residual.
Tea
polyphenols
or
tea
tannins
are
somewhat
similar
to
humic
substances
in
both
color
and
structure
and
have
the
potential
to
react
with
the
chlorine
residual
present
in
tap
water
to
form
DBPs.
Aquatic
humic
substances
were
compared
to
the
instant
tea
samples
in
terms
of
DBP
formation
under
selected
laboratory
conditions.
Wu
et
al.

(
1998)
incubated
instant
tea
with
water
treated
with
sufficient
chlorine
to
result
in
a
minimal
chlorine
residual
concentration
of
at
least
0.6
mg/
L
at
the
end
of
the
24­
hour
reaction
period.

They
found
that
all
of
the
DBPs
evaluated
were
present
except
for
the
cyanogen
halides,
including
cyanogen
chloride,
which
are
unstable
in
the
presence
of
free
chlorine
(
Xie
and
Reckhow,
1992).

In
contrast,
when
Wu
et
al.
(
1998)
incubated
instant
tea
with
sufficient
chloramine
to
result
in
a
minimal
residual
chloramine
concentration
of
2.4
mg/
L
at
the
end
of
the
24­
hour
reaction
period,

cyanogen
chloride
was
detected,
yet
at
lower
concentrations
than
in
the
aquatic
humic
samples.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
16
Final
draft
Hydrogen
cyanide.
This
section
summarizes
information
gathered
from
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide.

There
are
little
quantitative
data
on
the
occurrence
of
hydrogen
cyanide
in
food.
Cyanide
was
not
included
among
the
analytes
measured
in
the
current
Total
Diet
Study
(
TDS),
sometimes
called
the
Market
Basket
Study,
an
ongoing
FDA
program
that
determines
levels
of
various
pesticide
residues,
contaminants,
and
nutrients
in
foods
(
U.
S.
FDA,
2002).

Although
some
plants
contain
HCN,
and
HCN
can
be
present
in
food
as
residues
from
HCN
fumigation
(
Fiksel
et
al.,
1981),
the
primary
HCN
source
in
food
is
cyanogenic
glycosides.

HCN
is
released
during
maceration
in
which
intracellular
 ­
glucosidase
is
activated,
or
in
the
stomach
by
acid
hydrolysis
(
U.
S.
EPA,
1980;
Fiksel
et
al.,
1981;
Seigler,
1991),
or
in
the
gut
by
the
action
of
 ­
glucosidase
produced
by
microflora
(
WHO,
1992).
The
potential
toxicity
of
cyanogenic
plants
depends
on
their
bioavailability
(
Seigler,
1991)
and
their
ability
to
release
HCN
during
preparation
or
digestion
(
WHO,
1992).
Cyanogenic
glycosides
absorbed
intact
from
the
gut
are
not
metabolized
by
mammalian
enzymes
(
Seigler,
1991).

The
cyanogenic
content
of
a
food
is
usually
expressed
as
the
amount
of
HCN
released
by
acid
hydrolysis;
glycoside
concentrations
are
rarely
reported
(
WHO,
1992).
Over
2650
plant
species
produce
HCN.
These
include
almonds;
pits
from
stone
fruits
such
as
apricots,
peaches,

plums,
cherries;
sorghum;
soybeans;
lima
beans;
sweet
potatoes;
maize;
millet;
sugarcane;
bamboo
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
17
Final
draft
shoots;
and
cassava
(
Fiksel
et
al.,
1981)
which
is
a
major
starchy
food
for
more
than
300
million
people
in
many
tropical
countries
of
the
world
(
Seigler,
1991).

HCN
has
been
detected
in
cereal
grains
and
their
products
at
concentrations
ranging
from
0.001
to
0.45

g/
g,
in
soy­
protein
products
at
concentrations
ranging
from
0.07
to
0.3

g/
g,
and
in
lima
beans
at
concentrations
ranging
from
0.1
to
3
mg/
g
(
Honig
et
al.,
1983;
Towill
et
al.,

1978).
The
HCN
content
of
U.
S.
lima
beans
generally
ranges
from
0.1
and
0.17
mg/
g
(
Towill
et
al.,
1978).
The
HCN
equivalent
of
total
cyanogenic
content
(
i.
e.,
cyanogenic
glycosides,

cyanohydrins,
and
HCN)
of
cassava
root
ranges
from
91
to
1,515
mg/
kg
HCN
dry
weight
(
O'Brien
et
al.,
1992).

Depending
on
the
type
of
cultivar,
season,
and
geographical
area,
the
HCN
concentration
in
apricot
pits
may
vary
from
8.9
to
217

g/
g
on
a
weight
per
weight
basis
(
w/
w)
(
Lasch
and
El
Shawa,
1981).
Swain
et
al.
(
1992)
reported
a
mean
HCN
concentration
in
black
cherry
(
Prunus
serotina
Ehrh.)
fruits
at
a
concentration
greater
than
3

mole/
seed
at
maturity.
This
is
equivalent
to
a
mean
HCN
content
of
78

g/
seed;
insufficient
information
was
available
to
allow
conversion
of
these
results
to
weight
per
weight
units.
In
a
laboratory
study,
Voldrich
and
Kyzlink
(
1992)

found
that,
depending
on
the
glycoside
content
of
the
raw
fruits
and
the
conditions
of
heat
processing,
HCN
concentrations
in
canned
unpitted
fruits
(
peaches,
apricots,
plums,
and
cherries)

ranged
from
0
to
4
mg/
kg
(
w/
w).
As
reported
in
the
ATSDR
(
1997),
these
authors
concluded
that
a
70
kg
adult
could
consume
approximately
1
kg
of
canned
fruit
a
day
at
the
highest
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
18
Final
draft
concentration
of
4
mg/
kg
HCN
without
exceeding
the
allowable
daily
intake
(
ADI)
of
0.05
mg/
kg­
day.
However,
consumption
of
1
kg
of
canned
fruit
at
4
mg/
kg
HCN
would
result
in
a
dose
of
0.06
mg/
kg­
day
([
4mg/
kg
*
1
kg]/
70­
kg
body
weight),
which
would
slightly
exceed
the
ADI
of
0.05
mg/
kg­
day.
Therefore,
in
order
not
to
exceed
the
ADI
of
0.05
mg/
kg­
day,
it
is
estimated
that
a
70­
kg
adult
could
consume
1
kg
of
canned
fruit
a
day
at
a
concentration
of
3.5
mg/
kg
HCN
([
3.5
mg/
kg
*
1kg]/
70­
kg
body
weight),
or
consume
880
g
of
canned
fruit
a
day
at
a
maximum
concentration
of
4
mg/
kg
HCN
([
4
mg/
kg
*
0.88
kg]/
70­
kg
body
weight).
The
authors
further
correctly
concluded
that
a
safe
portion
for
a
15­
kg
child
would
be
only
about
180
grams
of
canned
fruit
at
a
maximum
concentration
of
4
mg/
kg
HCN.
This
is
equivalent
to
the
ADI
of
0.05
mg/
kg­
day.

In
an
analysis
of
233
samples
of
commercially
available
and
homemade
stone­
fruit
juices,

Stadelmann
(
1976)
reported
that
pitted­
fruit
juices
had
lower
HCN
concentrations
than
unpitted
or
partially­
pitted
fruit
juices,
indicating
that
the
pits
are
the
primary
source
of
cyanides
in
these
juices.
The
HCN
content
of
a
home­
made
mixed
cherry
juice
from
pitted
fruits
was
5.3
mg/
L
compared
to
23.5
mg/
L
HCN
in
a
cherry
juice
containing
100%
crushed
pits.
Stadelmann
(
1976)

also
reported
median
HCN
concentrations
of
4.6
mg/
L
in
commercial
cherry
juice,
2.2
mg/
L
in
commercial
prune
juice,
and
1.9
mg/
L
in
commercial
peach
juice.
Stadelmann
(
1976)

recommended
that
the
maximum
HCN
content
allowed
in
fruit
juice
should
be
set
at
a
level
of
5
mg/
L.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
19
Final
draft
B.
2
Air
Intake
Cyanogen
chloride.
There
is
no
information
in
the
available
literature
on
the
concentration
of
cyanogen
chloride
in
the
air.

Hydrogen
cyanide.
This
section
summarizes
information
gathered
from
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide.

Cyanide
is
released
to
the
air
primarily
as
HCN
gas
and,
to
a
lesser
extent,
as
particulate
cyanides.
The
major
sources
of
HCN
release
are
vehicle
exhaust
(
Fiksel,
et
al,
1981)
and
biomass
burning
(
Crutzen
and
Carmichael,
1993;
Lobert
and
Warnatz,
1993).
HCN
has
an
estimated
2.5­

year
residence
time
in
the
atmosphere
and
can
be
transported
over
long
distances
before
reacting
with
photochemically­
generated
hydroxyl
radicals.
Neither
photolysis
nor
deposition
by
rainwater
are
expected
to
be
significant
removal
mechanisms.

Ambient
air
concentrations
of
HCN
in
the
northern
hemisphere's
non­
urban
troposphere
range
from
160
to
166
ppt
(
177
ng/
m3
to
184
ng/
m3).
Although
ambient
air
monitoring
data
of
HCN
near
source
areas
(
e.
g.,
HCN­
manufacturing
industries,
coke­
production
industries,

wastedisposal
sites)
could
not
be
located
in
the
available
literature,
HCN
concentrations
in
these
areas
were
expected
to
be
higher
than
the
non­
urban
tropospheric
concentrations.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
20
Final
draft
People
who
smoke
and
nonsmokers
exposed
to
secondary
tobacco
smoke
may
also
be
exposed
to
HCN
at
concentrations
greater
than
background
levels
(
Fiksel,
et
al,
1981).
HCN
levels
in
mainstream
(
inhaled)
smoke
from
U.
S.
commercial
cigarettes
have
been
reported
to
range
from
10
to
400

g
per
cigarette.
The
ratio
of
HCN
concentration
in
sidestream
smoke
to
mainstream
smoke
ranges
from
0.006
to
0.27
(
Fiksel,
et
al,
1981).
Therefore,
nonsmokers
exposed
to
secondary
tobacco
smoke
could
be
exposed
to
0.06
(
10

g/
cigarette
×
0.006)
to
108

g
HCN/
cigarette
(
400

g/
cigarette
×
0.27).

B.
3
Dermal
Exposure
Cyanogen
chloride.
There
is
no
information
in
the
available
literature
on
dermal
exposure
to
cyanogen
chloride.

Hydrogen
cyanide.
According
to
information
presented
in
the
ATSDR
(
1997)

Toxicological
Profile
for
Cyanide,
dermal
absorption
of
HCN
is
not
a
significant
route
of
exposure
for
the
general
population.

C.
Overall
Exposure
Cyanogen
chloride.
The
relative
source
contribution
(
RSC)
for
cyanogen
chloride
is
derived
by
application
of
the
Exposure
Decision
Tree
approach
published
in
EPA's
Methodology
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
21
Final
draft
for
Deriving
Ambient
Water
Quality
Criteria
for
the
Protection
of
Human
Health
(
U.
S.
EPA,

2000d).
The
RSC
is
the
fraction
of
an
individual's
total
exposure
allocated
to
drinking
water.
An
RSC
of
20%
accounts
for
the
likelihood
of
exposure
to
cyanogen
chloride
or
cyanide
from
sources
other
than
tap
water,
such
as
ambient
air
and
food,
in
the
absence
of
adequate
data.
This
value
also
takes
into
account
the
potential
for
exposure
to
cyanide
(
a
key
cyanogen
chloride
metabolite)
via
food,
air,
and
smoking,
as
described
in
the
next
paragraphs.
The
data
are
not
adequate
to
quantify
the
contributions
of
each
source
for
an
overall
assessment
of
exposure.

There
are
very
limited
quantitative
data
on
the
presence
of
cyanogen
chloride
in
the
environment
and
on
cyanogen
chloride
exposure.
There
is
no
information
in
the
available
literature
on
the
concentration
of
cyanogen
chloride
in
the
air
and
no
information
in
the
available
literature
on
dermal
exposure
to
cyanogen
chloride.
No
quantification
of
cyanogen
chloride
body
burden
was
located,
but
the
rapid
metabolism
of
cyanogen
chloride
(
see
Chapter
3)
indicates
that
any
body
burden
would
be
negligible.
There
is
no
quantitative
data
on
dietary
levels.
Although
one
investigator
found
that
cyanogen
chloride
may
be
produced
from
the
reaction
of
instant
tea
with
water
containing
chloramine
residual,
no
quantification
of
cyanogen
chloride
concentration
was
provided.
Cyanogen
chloride
was
not
included
among
the
analytes
measured
in
the
current
FDA
Market
Basket
Study
(
U.
S.
FDA,
2002).

The
mean
concentrations
of
cyanogen
chloride
in
finished
and
DS
maximum
samples
in
surface
water
were
3.25
and
3.02

g/
L,
respectively.
The
mean
concentrations
of
cyanogen
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
22
Final
draft
chloride
in
finished
and
DS
maximum
samples
in
groundwater
were
2.12
and
1.63

g/
L,

respectively.
There
were
no
statistically
significant
differences
between
the
concentration
of
cyanogen
chloride
in
finished
water
and
the
DS
maximum
samples
in
either
surface
water
or
groundwater.
However,
the
finished
and
DS
maximum
mean
cyanogen
chloride
concentrations
in
surface
water
were
significantly
higher
(
at
p
=
0.05)
than
their
respective
concentrations
in
groundwater.
Because
cyanogen
chloride
is
formed
when
chlorine
reacts
with
organic
material
in
the
presence
of
ammonia,
only
plants
that
used
chloramine
as
a
primary
or
secondary
disinfectant
were
required
to
monitor
for
cyanogen
chloride.
Thirty­
five
percent
of
the
surface
water
plants
and
23
percent
of
the
groundwater
plants
reported
cyanogen
chloride
observations
(
U.
S.
EPA,

2000c).

Although
NIOSH
(
1990)
estimated
that
1393
workers
were
exposed
to
cyanogen
chloride,
no
information
on
exposure
levels
was
available.

Hydrogen
cyanide.
The
relative
source
contribution
(
RSC)
for
cyanide
is
derived
by
application
of
the
Exposure
Decision
Tree
approach
published
in
EPA's
Methodology
for
Deriving
Ambient
Water
Quality
Criteria
for
the
Protection
of
Human
Health
(
U.
S.
EPA,

2000d).
The
RSC
is
the
fraction
of
an
individual's
total
exposure
allocated
to
drinking
water.
An
RSC
of
20%
accounts
for
the
likelihood
of
exposure
to
cyanide
from
sources
other
than
tap
water,
such
as
ambient
air
and
food,
in
the
absence
of
adequate
data.
The
available
data
are
sufficient
to
demonstrate
that
food,
air,
and
smoking
are
relevant
sources
of
exposure
to
cyanide
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
23
Final
draft
in
addition
to
drinking
water.
However,
the
data
are
not
adequate
enough
to
quantify
the
contributions
of
each
source
for
an
overall
assessment
of
exposure.

There
are
limited
quantitative
data
on
the
presence
of
cyanide
in
the
environment
and
cyanide
exposure.

Cyanide
concentrations
averaged
2844

g/
L
in
3%
of
the
samples
in
7%
of
the
plants
treating
surface
water.
In
2%
of
the
samples
in
3%
of
the
plants
treating
groundwater,
cyanide
concentrations
averaged
2194

g/
L.
There
was
no
statistically
significant
difference
between
the
overall
cyanide
concentrations
in
surface
water
and
groundwater.
As
discussed
above,
this
average
is
not
very
representative
of
overall
population
exposure,
in
light
of
the
small
number
of
water
systems
with
detectable
cyanide
levels,
and
the
wide
variability
in
the
systems
with
detectable
levels.

There
was
no
information
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide
on
the
concentration
of
HCN
in
soil
or
sediments.
However,
because
of
its
highly
volatile
nature
and
its
expected
tendency
to
biodegrade
and
leach
out
of
the
soil,
HCN
is
not
expected
to
be
present
in
soil
in
any
appreciable
amount.

Based
on
information
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide,

a
number
of
drugs
(
e.
g.,
Laetrile
and
a
drug
used
to
reduce
high
blood
pressure),
as
well
as
a
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
24
Final
draft
number
of
industrial
chemicals
(
acetonitrile,
propionitrile,
acrylonitrile,
n­
butyronitrile,

maleonitrile,
and
succinonitrile),
release
cyanide
upon
metabolism.
However,
exposure
to
these
substances
would
be
limited
to
a
subset
of
the
population.

According
to
information
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide,
the
National
Occupational
Exposure
Survey
(
NOES)
conducted
by
NIOSH
from
1980
to
1983
estimated
that
4005
workers
were
exposed
to
HCN.
NIOSH
found
HCN
in
the
workplace
air
at
concentrations
ranging
from
0.001
to
4.3
mg/
m3.
Although
the
ATSDR
document
provided
no
information
on
the
amount
of
time
and
frequency
that
workers
were
exposed
to
these
concentrations
of
HCN,
the
reported
levels
were
below
the
NIOSH
recommended
15­
minute
short­
term
exposure
limit
(
STEL)
of
5
mg/
m3
for
HCN.

Although
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide
reported
that
over
2650
plant
species
produce
cyanogenic
compounds,
cyanide
was
not
included
among
the
analytes
measured
in
the
current
FDA
Market
Basket
Study
(
U.
S.
FDA,
2002).
In
addition,
the
potential
toxicity
of
cyanogenic
plants
depends
on
the
bioavailability
of
cyanide
in
food
prepared
from
the
plants,
and
on
the
potential
for
release
of
cyanide
during
preparation
or
digestion.
Although
estimates
of
the
HCN
concentration
in
the
total
diet
of
a
U.
S.
adult
were
not
located
in
the
available
literature,
and
human
exposure
to
HCN
from
foods
in
which
it
occurs
naturally
in
the
United
States
is
expected
to
be
low,
the
exposure
to
HCN
in
food
was
expected
to
exceed
HCN
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
25
Final
draft
intake
from
inhalation
of
air
and
ingestion
of
drinking
water
(
Fiksel
et
al.,
1981).
The
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide
provided
no
quantitative
data.

Ambient
air
concentrations
of
HCN
in
the
northern
hemisphere's
non­
urban
troposphere
range
from
160
to
166
ppt
(
177
ng/
m3
to
184
ng/
m3)
(
ATSDR,
1997).
Based
on
an
atmospheric
concentration
of
170
ppt
(
188
ng/
m3)
and
a
daily­
average
inhalation
rate
of
20
m3,
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide
estimated
an
inhalation
exposure
to
the
general
U.
S.

non­
urban,
nonsmoking
population
of
3.8

g
cyanide/
day.

Smokers
could
be
exposed
to
10
to
400

g
HCN
per
cigarette.
Nonsmokers
exposed
to
secondary
tobacco
smoke
could
be
exposed
to
0.06
to
108

g
HCN/
cigarette.

According
to
information
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide,
dermal
absorption
is
not
a
significant
route
of
exposure
for
the
general
population.

Thiocyanate,
cyanate,
and
cyanamide.
Exposure
to
these
chemicals
was
not
assessed
for
this
document.
In
the
absence
of
data,
the
default
of
20%
is
used
for
the
RSC
for
these
chemicals.

D.
Summary
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
26
Final
draft
Cyanogen
chloride.
The
ICR
database
(
U.
S.
EPA,
2000b)
contains
some
information
on
concentrations
of
cyanogen
chloride
in
drinking­
water
systems,
and
on
how
those
concentrations
vary
with
input­
water
characteristics
and
treatment
methods.
The
database
contains
information
from
6
quarterly
samples
from
7/
97
to
12/
98,
from
approximately
300
large
systems
covering
approximately
500
plants.
The
mean
concentrations
of
cyanogen
chloride
at
the
distribution
system
maximum
for
drinking
water
derived
from
surface
water
and
groundwater
were
3.02
and
1.63

g/
L,
respectively.
The
mean
concentration
of
cyanogen
chloride
in
finished
water
and
the
mean
distribution
system
maximum
were
significantly
higher
in
treated
surface
water
(
at
p
=
0.05)

than
their
respective
concentrations
in
treated
groundwater.
Because
cyanogen
chloride
is
formed
when
chlorine
reacts
with
organic
material
in
the
presence
of
ammonia,
only
plants
that
used
chloramine
as
a
primary
or
secondary
disinfectant
were
required
to
monitor
for
cyanogen
chloride.
Therefore,
35%
of
the
surface­
water
plants
and
23%
of
the
groundwater
plants
reported
cyanogen
chloride
observations
(
U.
S.
EPA,
2000c).

The
National
Occupational
Exposure
Survey
(
NOES)
conducted
by
NIOSH
from
1980
to
1983
estimated
that
1393
workers
were
exposed
to
cyanogen
chloride.

There
is
no
information
in
the
available
literature
on
the
concentration
of
cyanogen
chloride
in
the
air
and
no
information
in
the
available
literature
on
dermal
exposure
to
cyanogen
chloride.
Cyanogen
chloride
body
burden
is
expected
to
be
negligible,
in
light
of
its
rapid
metabolism.
There
is
no
quantitative
data
on
dietary
levels.
Although
one
investigator
found
that
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
27
Final
draft
cyanogen
chloride
may
be
produced
from
the
reaction
of
instant
tea
with
water
containing
chloramine
residual,
no
quantification
of
cyanogen
chloride
concentration
was
provided.

Cyanogen
chloride
was
not
included
among
the
analytes
measured
in
the
current
FDA
Market
Basket
Study
(
U.
S.
FDA,
2002).

Due
to
the
lack
of
data,
no
estimate
can
be
made
on
average
daily
exposure
to
cyanogen
chloride.
An
RSC
of
20%
is
used
for
cyanogen
chloride
to
account
for
the
likelihood
of
exposure
to
cyanogen
chloride
or
cyanide
from
sources
other
than
tap
water,
such
as
ambient
air
and
food,

in
the
absence
of
adequate
data.

Hydrogen
cyanide.
The
latest
information
on
concentrations
of
cyanide
in
public
water
supplies
drinking
water
comes
from
the
latest
quarterly
reporting
(
updated
April
28,
2000)
of
the
NCOD,
which
contains
information
from
thousands
of
drinking­
water
systems.
Cyanide
was
detected
in
7%
of
the
plants
(
3%
of
the
samples)
using
surface
water
as
a
source,
and
in
3%
of
the
plants
(
2%
of
the
samples)
using
groundwater
as
a
source.
Although
the
average
cyanide
concentrations
in
treated
surface
water
were
reported
as
2844

g/
L,
and
the
average
concentrations
in
treated
groundwater
were
reported
as
2194

g/
L,
there
was
no
statistically
significant
difference
between
the
two
cyanide
concentrations.
Average
cyanide
concentrations
in
surface
water
and
groundwater
were
calculated
only
for
those
samples
where
cyanide
was
detected.
Non­
detects
were
not
included
in
the
calculation
of
average
concentrations.
Therefore,

the
calculated
averages
may
not
accurately
reflect
the
cyanide
concentrations
to
which
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
28
Final
draft
populations
served
by
these
water
systems
are
exposed.
Medians
were
not
available
from
the
NCOD
survey.

There
was
no
information
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide
on
the
concentration
of
HCN
in
soil
or
sediments.
However,
because
of
its
highly
volatile
nature
and
its
expected
tendency
to
biodegrade
and
leach
out
of
the
soil,
HCN
is
not
expected
to
be
present
in
soil
in
any
appreciable
amount.

Based
on
information
presented
in
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide,

between
1981
and
1983,
4005
workers
were
potentially
exposed
to
HCN.
In
addition
to
HCN
concentrations
in
drinking
water,
there
are
some
limited
data
on
HCN
concentrations
in
air
and
food.

Based
on
an
atmospheric
concentration
of
170
ppt
(
188
ng/
m3)
and
a
daily
average
inhalation
rate
of
20
m3,
the
ATSDR
(
1997)
Toxicological
Profile
for
Cyanide
estimated
an
inhalation
exposure
to
the
general
U.
S.
non­
urban,
nonsmoking
population
of
3.8

g
cyanide/
day.

Although
concentrations
of
HCN
in
foods
are
expected
to
be
low,
one
author
estimated
that
intake
from
food
would
exceed
HCN
intake
from
inhalation
of
air
and
ingestion
of
drinking
water
(
Fiksel
et
al,
1981).
However,
estimates
of
the
HCN
concentration
in
the
total
diet
were
not
located
in
the
available
literature.
Cyanide
was
not
included
among
the
analytes
measured
in
the
current
FDA
Market
Basket
Study
(
U.
S.
FDA,
2002).
Therefore,
no
independent
estimate
of
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
IV­
29
Final
draft
daily
HCN
intake
from
food
could
be
made.
An
RSC
of
20%
accounts
for
the
likelihood
of
exposure
to
cyanide
from
sources
other
than
tap
water,
such
as
ambient
air
and
food,
in
the
absence
of
adequate
data.

HCN
is
a
metabolite
of
a
number
of
industrial
chemicals
(
acetonitrile,
propionitrile,

acrylonitrile,
n­
butyronitrile,
maleonitrile,
and
succinonitrile).
As
a
result,
occupational
or
environmental
exposure
to
these
chemicals
could
contribute
to
the
background
levels
of
HCN
in
biological
fluids.
HCN
is
also
a
metabolite
of
pharmaceuticals
such
as
Laetrile
and
a
drug
used
to
reduce
high
blood
pressure,
and
clinical
use
of
these
compounds
could
induce
a
body
burden
of
HCN.

Exposure
to
thiocyanate,
cyanate,
and
cyanamide
was
not
assessed
for
this
document.
In
the
absence
of
data,
the
default
of
20%
is
used
for
the
RSC
for
these
chemicals.
