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and
Potential
Metabolites
EPA/
OW/
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VI­
1
Final
draft
Chapter
VI.
Health
Effects
in
Humans
A.
Case
Reports
and
Clinical
Studies
Cyanogen
Chloride.
Human
toxicity
data
on
cyanogen
chloride
are
summarized
in
Table
VIII­
1.
No
studies
of
short­
term
oral
exposure
of
humans
to
cyanogen
chloride
were
located.

Data
are
available
on
short­
term
exposure
in
air,
which
results
in
both
inhalation
exposure
and
dermal/
ocular
exposure
to
the
cyanogen
chloride
vapor.
Cyanogen
chloride
was
used
as
a
poison
gas
by
the
military
in
World
War
I.
Its
effects
were
noted
to
be
quick­
acting,
but
reversible
if
exposure
was
below
a
critical
concentration
(
Prentiss,
1937).
Death
was
reported
as
occurring
via
rapid
paralysis
of
nerve
centers,
similarly
to
hydrogen
cyanide;
however
eye,
throat,
and
lung
irritation
and
coughing
were
noted
following
short
exposures
to
low
concentrations
(
Prentiss,

1937;
Flury
and
Zernik,
1931).
The
lethal
concentration
was
reported
as
400
mg
CNCl/
m3
for
10
minutes
(
Prentiss,
1937).
Exposure
to
50
mg
CNCl/
m3
for
1
minute
was
considered
"
unendurable"
(
Flury
and
Zernick,
1931).
By
contrast,
Aldridge
and
Evans
(
1946)
reported
that
a
concentration
of
60
mg
CNCl/
m3
was
not
"
unduly
irritating."
"
Copious
lacrimation"
was
reported
within
a
few
minutes
at
2.5
mg
CNCl/
m3
(
Prentiss,
1937).
These
concentration
estimates
are
subject
to
the
limitations
of
the
technology
of
that
period
in
measuring
and
maintaining
consistent
exposure
levels.
Longer
exposure
to
lower
concentrations
that
did
not
cause
immediate
nervous
system
effects
were
reported
to
result
in
hoarseness
and
slight
inflammation
of
the
conjunctiva
(
Flury
and
Zernick,
1931).
These
early
data
are
supported
by
a
more
recent
report
that
exposure
to
approximately
1.8
mg
CNCl/
m3
for
an
unspecified
duration
Drinking
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Cyanogen
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EPA/
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VI­
2
Final
draft
(
on
the
order
of
minutes)
resulted
in
severe
eye
and
nose
irritation
(
Michigan
Department
of
Public
Health,
1977,
as
cited
by
ACGIH,
1991).

Cyanide.
Several
studies
of
the
short­
terms
effects
of
cyanide
in
humans
following
suicide
attempts
or
accidental
poisoning
by
the
oral
and
inhalation
routes
were
located.
However,

many
of
these
studies
are
limited
by
inadequate
characterization
of
exposure.
Oral
toxicity
studies
for
cyanide
are
summarized
in
Table
VIII­
2,
and
inhalation
studies
are
summarized
in
Table
VIII­

3.

Liebowitz
and
Schwartz
(
1948)
report
a
case
of
cyanide
poisoning
following
ingestion
of
potassium
cyanide.
A
60­
year­
old
white
male
was
admitted
to
the
hospital
one
hour
after
ingesting
an
estimated
38­
63
mg/
kg
of
potassium
cyanide
(
15­
25
mg
CN/
kg).
On
admission,
the
patient
was
comatose
with
muscular
rigidity.
The
pulse
was
thready
with
a
rate
of
140
per
minute;
heart
sounds
were
inaudible.
Respirations
were
40
per
minute
and
stertorous.
The
skin
was
pink,
cold,
and
clammy,
and
the
pupils
were
dilated.
By
eight
hours
after
admission,
the
patient
was
alert,
and
the
symptoms
had
begun
to
subside
(
with
the
exception
of
weakness,

nausea,
and
an
enlarged
heart).
Blood
thiocyanate
was
measured
on
the
first,
second,
fourth,
and
fifth
days
of
hospitalization
and
found
to
be
negative.
Urinary
thiocyanate
peaked
on
the
second
day
of
hospitalization
and
total
thiocyanate
excretion
was
237
mg
over
a
72­
hour
period.
(
By
comparison,
a
total
of
1050­
1750
mg
CN
was
ingested,
assuming
a
70­
kg
body
weight.)
The
authors
were
unable
to
explain
why
this
patient
recovered
from
exposure
to
a
dose
that
was
about
30
times
the
estimated
lethal
dose.
However,
the
authors
noted
that
the
patient
was
a
chemist
Drinking
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who
used
thiosulfate
daily
in
his
work,
"
immersing
his
hands
in
it
frequently."
Therefore,

exposure
to
thiosulfate
may
have
had
an
antidote
effect.

Lasch
and
El
Shawa
(
1981)
report
the
effects
of
accidental
poisoning
in
children
who
ate
apricot
kernels
or
a
sweet
made
from
apricot
kernels.
In
two
episodes
of
poisoning,
24
children
developed
symptoms
of
cyanide
poisoning
within
two
hours
after
ingesting
apricot
kernels.
The
authors
noted
that
apricot
kernels
contain
the
cyanogenic
compound
amygdalin,
and
that
this
compound
can
be
hydrolyzed
to
cyanide
enzymatically
or
in
an
alkaline
environment.
The
authors
did
not
estimate
the
amount
of
amygdalin
consumed
or
the
amount
of
cyanide
produced,
although
the
severity
of
symptoms
appeared
to
correlate
with
amount
of
apricot
kernels
ingested.
Four
children
died.
The
remaining
children
recovered
after
developing
symptoms
of
vomiting,
nausea,

weakness,
confusion,
lethargy,
cyanosis,
and
coma
with
respiratory
depression.

Saincher
et
al.
(
1994)
report
the
acute
effects
of
cyanide
ingestion
in
a
23­
year­
old
man
who
had
ingested
1.4
mg/
kg
potassium
cyanide
(
0.56
mg
CN/
kg)
in
a
suicide
attempt.
The
patient
was
found
unconscious.
Following
administration
of
oxygen,
the
patient
recovered
consciousness
and
reported
numbness
in
thighs,
shortness
of
breath,
and
weakness
in
hip
flexors
and
hamstrings.
The
patient's
blood
cyanide
concentration
was
4.65
mg/
L
at
3
hours
following
ingestion.
Blood
concentrations
greater
than
2.5­
3.0
mg/
L
are
considered
fatal,
but
the
patient
recovered
without
antidote
therapy.

Several
authors
(
Uitti
et
al.,
1985;
Carella
et
al.,
1988;
Rosenberg
et
al.,
1989;
and
Grandas
et
al.,
1989)
report
the
development
of
symptoms
of
parkinsonism
in
patients
who
Drinking
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4
Final
draft
recovered
from
ingestion
of
a
single
dose
of
cyanide.
The
four
cases
included
an
18­
year­
old
male
who
ingested
5.6­
7.6
mg/
kg
cyanide
in
a
suicide
attempt
(
Uitti
et
al.,
1985),
a
46­
year­
old
woman
who
ingested
an
unreported
amount
of
cyanide
by
accidental
poisoning
(
Carella
et
al.,

1988),
a
46­
year­
old
man
who
ingested
8.6
mg/
kg
cyanide
in
a
suicide
attempt
(
Rosenberg
et
al.,

1989),
and
a
39­
year­
old
man
who
ingested
an
unknown
amount
of
cyanide
in
a
suicide
attempt
(
Grandas
et
al.,
1989).
In
all
cases,
the
patients
recovered
from
the
acute
symptoms
of
cyanide
poisoning
with
treatment,
and
a
neurologic
examination
immediately
following
the
poisoning
was
normal.
Follow­
up
neurologic
examination
at
times
of
3
weeks
(
Rosenberg
et
al.,
1989),
4
months
(
Uitti
et
al.,
1985),
or
1
year
(
Grandas
et
al.,
1989;
Carella
et
al.,
1988),
revealed
that
the
patients
had
developed
symptoms
of
parkinsonism,
including
generalized
rigidity,
bradykinesia,

tremors
of
tongue
and
eyelids,
slow­
shuffling
gait,
and
a
weak
dysphonic
voice.
A
computerized
tomography
(
CT)
scan
or
magnetic
resonance
imaging
(
MRI)
showed
lesions
in
the
putamen
and
globus
pallidus
regions
of
the
brain
in
three
of
the
cases
(
Uitti
et
al.,
1985;
Rosenberg
et
al.,

1989;
and
Grandas
et
al.,
1989).

Potter
(
1950)
reported
a
case
study
of
a
worker
accidentally
exposed
via
inhalation
to
an
undetermined
concentration
of
hydrogen
cyanide.
Early
symptoms
were
dizziness,
dyspnea,
and
weakness
of
legs.
This
was
followed
by
deep
unconsciousness,
accompanied
by
absent
reflexes,

stertorous
respiration,
rapid
pulse,
fixed
and
unreactive
pupils,
and
convulsions.
The
subject
recovered
with
treatment,
and
no
after­
effects
were
reported.
In
another
case
report,
a
worker
was
found
unconscious
lying
in
tank
sludge
after
working
without
protective
gear
in
a
plating
tank
containing
silver­
cyanide
sludge
(
Singh
et
al.,
1989).
The
duration
of
exposure
was
unknown,
but
the
tank
air
was
later
measured
to
contain
200
ppm
hydrogen
cyanide
(
213
mg
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CN/
m3).
He
had
dermal
evidence
of
chemical
burns,
and
was
apnoeic,
with
a
rapid
pulse,
fixed
and
dilated
pupils,
and
no
recorded
blood
pressure
or
response
to
pain.
Blood
cyanide
was
804

mol/
L
within
½
hour
of
arrival,
and
decreased
to
15

mol/
L
at
18
hours
after
arrival
and
following
detoxification
efforts.
The
patient
died
within
3
days
despite
extensive
treatment.

A
case
report
of
a
worker
accidentally
exposed
to
a
brief
stream
of
liquid
hydrogen
cyanide
on
his
hand
(
amount
not
specified)
reported
that
the
worker
became
deeply
unconscious
within
5
minutes
of
exposure
(
Potter,
1950).
Breathing
was
stertorous,
and
his
face
was
flushed
and
reflexes
were
absent.
The
subject
recovered
with
treatment.
Dizziness,
weakness,
and
a
throbbing
pulse
were
reported
when
three
workers
wearing
gas
masks
providing
"
excellent
respiratory
protection"
entered
an
atmosphere
containing
2%
hydrogen­
cyanide
gas
(
Drinker,

1932).
These
toxic
effects
were
attributed
to
the
dermal
absorption
of
the
gas.

One
early
case
study
reports
acute
effects
of
hydrogen
cyanide
following
dermal
exposure
(
Drinker,
1932).
Three
men
using
hydrocyanic
acid
gas
as
a
fumigant
were
working
in
an
atmosphere
containing
2%
HCN.
The
men
were
wearing
gas
masks
that
appeared
to
be
giving
adequate
respiratory
protection.
After
about
10
minutes,
the
men
developed
symptoms
of
dizziness,
weakness
and
throbbing
pulse
before
they
lost
consciousness.
The
symptoms
persisted
several
hours
following
exposure.
The
authors
concluded
that
the
symptoms
were
due
to
dermal
absorption
of
the
HCN.

Thiocyanate.
No
relevant
inhalation
or
dermal
toxicity
studies
were
identified.
There
is
a
large
amount
of
data
on
the
toxicity
of
thiocyanate
in
humans,
as
summarized
in
Table
VIII­
4.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
1This
text
expands
on
the
summary
of
thiocyanate
toxicity
found
in
an
Issue
Paper
prepared
by
U.
S.
EPA's
Superfund
Health
Risk
Technical
Support
Center
in
June
1996.

EPA/
OW/
OST/
HECD
VI­
6
Final
draft
However,
most
of
these
data
involve
the
short­
term
use
of
thiocyanates
to
decrease
blood
pressure
in
hypertensive
patients.
Data
on
the
toxicity
of
thiocyanate
in
normotensive
humans
are
limited
to
an
acute­
exposure
study
conducted
by
Smith
and
Rudolf
(
1928),
a
12­
week
study
conducted
by
Dalhberg
et
al.
(
1984),
and
a
study
on
women
in
India
who
ingested
thiocyanate
in
milk
for
5
years
(
Banerjee
et
al.,
1997).
The
latter
two
studies
are
addressed
in
the
section
on
epidemiology
studies
of
thiocyanate.

Smith
and
Rudolf
(
1928)
administered
oral
doses
of
325
mg
sodium
thiocyanate
(
233
mg
SCN;
10
mg
SCN/
kg­
day,
assuming
a
reference
body
weight
of
70
kg)
to
6
healthy
adults
(
sex
not
specified)
for
1
week.
A
15­
30
mm
Hg
decrease
in
systolic
blood
pressure
was
observed.

Blood
pressure
was
the
only
endpoint
measured;
the
authors
noted
that
the
subjects
did
not
complain
of
any
symptoms.

In
the
first
half
of
the
1900s,
thiocyanate
(
in
particular,
sodium
thiocyanate
and
potassium
thiocyanate)
was
used
to
treat
hypertension.
1
A
number
of
papers
have
been
published
that
report
the
effectiveness
of
thiocyanate
in
reducing
blood
pressure;
some
also
discuss
the
adverse
effects
associated
with
this
treatment.
However,
in
general,
these
studies
mainly
focused
on
blood
pressure
and
did
not
examine
other
endpoints.
The
reported
effectiveness
of
thiocyanate
in
reducing
blood
pressure
varies
greatly
from
study
to
study.
Andersen
and
Chen
(
1940)
reviewed
a
number
of
human
studies,
and
found
that
decreases
in
blood
pressure
have
been
observed
in
12­

100%
of
patients
treated
with
thiocyanate.
This
large
inter­
study
variation
in
the
effectiveness
of
Drinking
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Table
VI­
1.
Serum
Thiocyanate
and
Thyroid
Hormone
Levels
in
Women
Exposed
for
>
5
Years
to
Thiocyanate
in
Milk.

Endpoint
Thiocyanate­
exposed
women1
Mean
SE
Non­
exposed
controls
Mean
SE
SCN
(

mol/
l)
230.0**
10.0
90.8
9.0
T
4
(
nmol/
l)
87.8**
6.6
125.4
11.5
T
3
(
nmol/
l)
2.39
0.32
1.71
0.16
TSH
(

U/
ml)
2.49**
0.20
1.09
0.28
1Mean
values
with
their
standard
errors
for
thirty­
five
nonsmoking
subjects.
**
Mean
values
were
significantly
different
from
those
for
the
control
group,
P
<
0.01.
Adapted
from
Banerjee
et
al.
(
1997)

thiocyanate
in
decreasing
blood
pressure
is
partly
due
to
differences
in
the
criteria
used
to
determine
a
significant
decrease
in
systolic
blood
pressure
and
in
the
underlying
cause
of
the
hypertension
(
i.
e.,
essential
hypertension
versus
hypertension
secondary
to
renal
failure).
The
magnitude
of
the
decrease
in
blood
pressure
typically
ranged
from
10
to
50
mm
Hg,
although
decreases
of
100
mm
Hg
have
been
reported.
The
decrease
in
blood
pressure
was
often
seen
within
several
weeks
of
treatment
initiation.
Typically,
blood
pressure
would
return
to
pretreatment
levels
shortly
after
termination
of
the
thiocyanate
treatment.
Ayman
(
1931)
noted
that
the
magnitude
of
the
decrease
in
blood
pressure,
as
well
as
the
onset
of
the
decrease
were
doserelated
The
large
individual
variations
in
blood
pressure,
however,
make
a
determination
of
the
dose­
dependency
of
the
magnitude
of
change
and
the
duration
of
onset
difficult
to
independently
evaluate.
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The
most
commonly
reported
adverse
effects
in
hypertensive
patients
treated
with
thiocyanate
were
weakness,
fatigue,
and
nausea/
vomiting.
Other
observed
effects
include
thyroid
toxicity
(
enlarged
thyroid,
myxedema,
decreased
basal
metabolic
rate),
dermatitis
(
pruritus,

exfoliative
dermatitis,
and
maculopapular
eruption),
neurotoxicity,
and
angina.
Some
of
these
effects
may
have
been
secondary
to
the
rapid
decrease
in
blood
pressure.
As
noted
earlier,
most
of
these
studies
were
not
designed
to
adequately
assess
toxicity.

When
thiocyanate
treatment
was
first
introduced
in
the
early
1900s,
high
doses
of
thiocyanates
were
used,
resulting
in
"
toxic
psychosis"
deaths
(
Domzalski
et
al.,
1953).
In
all
cases
but
one
(
which
involved
co­
administration
of
bromide),
blood
thiocyanate
levels
were
14
mg
SCN/
100
mL
or
higher.
When
thiocyanate
treatment
was
reintroduced
in
1925,
lower
doses
were
used,
and
many
physicians
followed
similar
treatment
regimes,
administering
97.2­
324
mg
potassium
thiocyanate
or
sodium
thiocyanate
one
to
five
times
per
day.
In
the
papers
reviewed
during
the
preparation
of
this
criteria
document,
the
lowest
dose
tested
was
97.2
mg
potassium
thiocyanate
(
58.1
mg
thiocyanate)
administered
three
times
per
day
for
the
first
week,
two
times
per
day
for
the
second
week,
and
one
time
per
day
for
1­
2
weeks
(
time­
weighted
average
[
TWA]

dose
of
1.5­
1.7
mg
SCN/
kg­
day,
assuming
a
reference
body
weight
of
70
kg)
(
Palmer
and
Sprague,
1929;
Palmer
et
al.,
1929).
In
this
study,
42.4%
of
the
59
hypertensive
subjects
had
a
decrease
in
systolic
blood
pressure
of
30
mm
Hg
or
more.
Adverse
effects
(
weakness,
angina,

and
precordial
distress)
were
observed
in
six
subjects.

Several
studies
used
moderate
dose
levels
(
1.7­
2.8
mg
SCN/
kg­
day).
Ayman
(
1931)

reported
on
the
toxicity
and
therapeutic
effect
of
thiocyanate
in
26
patients
administered
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
9
Final
draft
potassium
thiocyanate
using
a
variety
of
treatment
protocols.
The
individual
doses
ranged
from
100
to
400
mg
potassium
thiocyanate,
one
to
four
times
per
day.
The
total
daily
dose
of
potassium
thiocyanate
ranged
from
200
to
1200
mg
potassium
thiocyanate,
corresponding
to
1.7
to
10
mg
SCN/
kg­
day,
with
the
most
common
low
dose
being
3
x
100
mg
potassium
thiocyanate
(
2.6
mg
SCN/
kg­
day).
The
duration
of
dosing
at
the
lower
doses
was
for
42­
109
days,
and
resulted
in
decreases
in
blood
pressure
in
only
3/
13
subjects.
These
decreases
were
considered
slight
to
moderate,
and
occurred
only
after
prolonged
treatment.
By
contrast,
mild
toxic
effects
(
weakness,
fatigue,
and
diarrhea)
were
reported
in
5/
14
of
these
subjects.
Treatment
at
the
higher
doses
was
for
4­
89
days.
Decreases
of
30­
40
mm
Hg
systolic
and
10­
30
mm
Hg
diastolic
were
observed
in
12/
14
patients.
The
author
noted
that
the
marked
toxic
symptoms
precluded
continuation
of
the
treatment.
Adverse
effects
(
weakness,
fatigue,
"
laziness",
drowsiness,

diarrhea,
abdominal
cramps,
tremors,
numbness
in
upper
body)
were
observed
in
12/
14
patients.

Barker
et
al.
(
1941)
administered
300
mg/
day
potassium
thiocyanate
(
180
mg
SCN/
day;

2.6
mg
SCN/
kg­
day)
for
2­
10
years.
(
Although
it
is
not
clearly
reported,
there
may
have
been
interruptions
in
the
dosing
schedule.)
Goldring
and
Chasis
(
1931)
used
326
mg/
day
potassium
thiocyanate
or
sodium
thiocyanate
(
190
mg
SCN/
day,
assuming
all
was
in
the
form
of
potassium
thiocyanate;
2.8
mg
SCN/
kg­
day)
for
14­
78
days.
In
the
Barker
et
al.
(
1941)
study,
the
dose
was
increased
or
decreased
as
needed,
based
on
comparison
to
the
target
blood
concentration
and
signs
of
toxicity,
respectively.
The
doses
at
which
symptoms
were
observed
were
not
reported,

but
the
most
severe
effects
were
seen
at
blood
concentrations
of
20
mg
SCN/
100
mL
blood
and
higher.
Decreases
in
systolic
blood
pressure
(
magnitude
of
response
not
reported)
were
observed
in
67%
of
the
subjects
in
the
Barker
et
al.
(
1941)
study,
and
32.4%
of
the
subjects
in
the
Goldring
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
2The
study
author
reported
the
concentrations
as
amounts
of
"
cyanates,"
but
discussed
using
thiocyanate
standards.
Therefore,
it
appears
that
the
concentrations
in
blood
are
actually
of
thiocyanate.
Therefore,
discussion
of
the
results
of
this
study
uses
the
term
(
thio)
cyanate
where
the
authors
referred
to
"
cyanate"
levels.

EPA/
OW/
OST/
HECD
VI­
10
Final
draft
and
Chasis
(
1931)
study
had
a
decrease
in
blood
pressure
of
at
least
45
mm
Hg
systolic
and
31
mm
Hg
diastolic.
In
the
Barker
et
al.
(
1941)
and
Goldring
and
Chasis
(
1931)
studies,

neurological
effects
(
depression,
aphasia,
slurring
speech,
mental
confusion,
disorientation,

hallucinations
of
sight
and
hearing,
and
unsteady
gait)
were
observed.
Signs
of
thyroid
toxicity
(
enlarged
thyroid
and
myxedematous
facies
with
decreased
basal
metabolic
rate)
were
also
observed
in
some
of
subjects
in
the
Barker
et
al.
(
1941)
study.
Barker
et
al.
(
1941)
noted
that
"
it
is
not
unusual
to
see
fatigue,
secondary
anemia,
and
a
dry
scaling
skin
appear
after
many
months
of
continuous
ingestion
of
cyanates."
It
is
not
known
if
this
statement
is
referring
to
results
of
the
study
or
general
observations
in
patients
being
treated
with
thiocyanate.
The
incidence
of
adverse
effects
was
18/
246
in
Barker
et
al.
(
1941)
and
13/
50
in
Goldring
and
Chasis
(
1931).
Two
subjects
in
the
Goldring
and
Chasis
(
1931)
study
died.
Russell
and
Stahl
(
1942)
reported
deaths
in
several
patients
receiving
potassium
thiocyanate,
one
receiving
only
400
mg/
day
(
3.4
mg
SCN/
kg­
day)
for
approximately
one
week.
Markedly
decreased
renal
clearance
may,
however,

have
led
to
increased
blood
thiocyanate
levels,
and
contributed
to
the
death.

Barker
(
1936)
treated
45
patients
(
with
systolic
blood
pressure
well
over
200
mm)
with
sodium
or
potassium
thiocyanate.
After
a
basal
level
of
thiocyanate
in
blood
was
attained,

increasing
doses
were
administered,
until
sharp
falls
in
blood
pressure
or
toxicity
were
observed.

The
concentration
of
thiocyanate
in
the
blood
was
followed,
with
reduction
of
blood
pressure
seen
in
35
of
45
patients.
The
author
noted
that
the
optimum
therapeutic
level
was
in
the
range
of
8­
12
mg
thiocyanate/
100
mL
blood2,
with
significant
toxicity
beginning
to
appear
at
blood
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
11
Final
draft
(
thio)
cyanate
levels
of
15­
30
mg.
Dosages
were
adjusted
for
each
individual
to
maintain
a
blood
(
thio)
cyanate
level
of
10
mg,
because
clearance
increased
with
repeated
dosing.
Slight
toxicity
was
noted
in
many
patients
at
blood
(
thio)
cyanate
levels
above
5
or
10
mg/
100
mL,
and
included
weakness,
disease,
and
fatiguing
more
easily.
These
toxic
symptoms
were
not
considered
disturbing
until
above
blood
(
thio)
cyanate
levels
of
10­
15
mg/
100
mL.
Above
20
mg
(
thio)
cyanate/
100
mL
in
blood,
toxicity
increased
rapidly;
serious
manifestations
were
noted
at
levels
of
35­
50
mg
(
thio)
cyanate/
100
mL.
There
was
high
variability
among
individuals,
with
different
blood
(
thio)
cyanate
levels
obtained
with
widely
varying
doses.

As
reviewed
by
Gorman
et
al.
(
1949),
the
large
within­
study
variability
in
the
effectiveness
of
thiocyanate
in
decreasing
blood
pressure
and
the
incidence
of
adverse
effects
may
be
due
to
individual
differences
in
the
excretion
of
thiocyanate.
The
differences
in
individual
average
daily
excretion
rates
of
thiocyanate
can
vary
as
much
as
500%
(
Goldring
and
Chasis,
1931,
as
cited
by
Gorman
et
al.,
1949).
Because
of
the
large
potential
differences
in
thiocyanate
excretion,
a
number
of
physicians
advocated
monitoring
blood
thiocyanate
levels,
and
adjusting
dosages
to
maintain
therapeutic
blood
levels.
Blood
levels
between
5
and
14
mg/
100
mL
were
considered
optimal
for
reduction
of
blood
pressure
(
Barker,
1936;
Domzalski
et
al.,
1953;
Gorman
et
al.,

1949),
with
toxicity
(
muscular
fatigue,
nausea
and
vomiting,
dermatitis,
disorientation,
mental
confusion,
motor
aphasia,
hallucinations,
delirium,
convulsions,
and
death)
believed
to
occur
at
blood
levels
above
14­
20
mg/
100
mL.
Although
maintenance
of
a
blood
level
of
5­
14
mg/
100
mL
is
advocated
as
a
"
safe"
blood
level,
Beamish
et
al.
(
1954)
observed
thyroid
toxicity
(
decreases
in
protein­
bound
plasma­
iodine
concentration
and
thyroid
uptake
of
iodine)
in
subjects
with
blood
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
12
Final
draft
thiocyanate
levels
(
1.3­
5
mg/
100
mL)
below
the
therapeutic
range.
Normal
blood
thiocyanate
levels
are
0.2­
0.7
mg/
100
mL
(
Wood,
1975).

There
are
many
limitations
to
the
human
database
on
the
effects
of
thiocyanate
on
blood
pressure.
With
the
exception
of
the
Smith
and
Rudolf
(
1928)
study,
hypertensive
subjects
were
used,
and
no
control
group
was
used.
All
of
these
studies
(
Palmer
et
al.,
1929;
Goldring
and
Chasis,
1931;
Barker
et
al.,
1941;
Ayman,
1931)
showed
decreases
in
blood
pressure,
and
the
magnitude
of
the
change
(
where
reported)
was
10­
50
mm
Hg.
The
decrease
in
blood
pressure
observed
in
the
human
studies
was
considered
a
beneficial
effect
of
oral
exposure
to
thiocyanate
because
the
subjects
were
hypertensive.
If
oral
exposure
to
thiocyanate
resulted
in
a
30
mm
Hg
or
greater
decrease
in
systolic
blood
pressure
in
normotensive
as
well
as
hypertensive
individuals,

the
effect
would
be
considered
adverse.
In
the
Palmer
et
al.
(
1929)
study,
over
40%
of
the
subjects
had
a
decrease
in
systolic
blood
pressure
of
30
mm
Hg
or
greater;
the
subjects
were
orally
exposed
to
a
TWA
dose
of
1.5­
1.8
mg/
kg­
day
for
3­
4
weeks.
It
is
not
known
whether
the
magnitude
of
the
decrease
in
systolic
blood
pressure
would
be
the
same
if
normotensive
subjects
were
exposed
to
similar
doses.
Smith
and
Rudolf
(
1928)
demonstrated
a
15­
30
mm
Hg
drop
in
systolic
blood
pressure
in
normotensive
subjects
treated
with
3.3
mg
SCN/
kg­
day
for
1
week.
If
the
assumption
is
made
that
a
similar
magnitude
decrease
in
blood
pressure
would
be
observed
in
normotensive
as
was
observed
in
hypertensive
individuals,
then
the
TWA
dose
of
1.5­
1.7
mg/

kgday
used
in
the
Palmer
et
al.
(
1929)
study
is
a
LOAEL.

Only
one
study
evaluated
thyroid
function
in
patients
administered
thiocyanate
for
treatment
of
hypertension.
Blackburn
et
al.
(
1951)
reported
on
15
patients
(
4
men
and
11
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
13
Final
draft
women)
who
had
received
KSCN
for
hypertension
for
an
unspecified
duration,
and
developed
myxedematous
symptoms.
Blackburn
et
al.
(
1951)
also
reported
that
two
additional
patients
who
developed
thyroid
enlargement
without
clinical
symptoms.
Thiocyanate
treatment
was
terminated,
and
the
extrarenal
disposal
rate
(
a
measure
of
thyroidal
accumulation
of
radioiodine)

was
measured.
In
all
but
one
case,
the
extrarenal
disposal
rate
increased
as
blood
thiocyanate
levels
dropped.

Two
studies
reported
on
the
effects
of
thiocyanate
on
thyroid
function
in
normotensive
subjects;
one
of
these
is
addressed
in
the
section
on
epidemiological
studies.
Dahlberg
et
al.

(
1984)
tested
the
effects
of
sodium
thiocyanate­
supplemented
milk
on
thyroid
function
in
37
volunteers
in
Sweden
(
9
men
and
28
women)
aged
16
to
54
years.
The
subjects
were
given
the
milk,
which
provided
8
mg/
day
thiocyanate
(
0.11
mg
SCN/
kg­
day,
assuming
a
70­
kg
body
weight),
for
12
weeks.
No
significant
differences
from
pretest
levels
were
observed
for
serum
T3,

T4,
or
thyrotropic
hormone,
or
the
T3:
T4
ratio.
Average
serum
thiocyanate
levels
increased
from
0.4
mg/
100
mL
to
0.78
mg/
100
mL
in
non­
smokers
at
4
weeks,
and
from
0.84
mg/
100
mL
to
1.07
mg/
100
mL
in
smokers
after
12
weeks
of
exposure;
thiocyanate
levels
at
12
weeks
in
the
nonsmokers
were
somewhat
lower
than
at
4
weeks.
This
study
only
assessed
the
effect
of
thiocyanate
on
thyroid
toxicity
and
did
not
measure
blood
pressure.

B.
Epidemiological
Studies
Cyanogen
chloride.
Only
one
report
on
the
effects
of
longer­
term
exposure
to
cyanogen
chloride
in
humans
is
available.
Fourteen
men
who
worked
at
a
plant
that
manufactured
cyanogen
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
14
Final
draft
chloride
were
evaluated
(
Reed,
1920).
The
men
were
exposed
daily
to
cyanogen
chloride
in
the
air
for
eight
months.
The
air
concentration
of
cyanogen
chloride
was
not
measured,
but
was
characterized
as
having
a
continuous
presence
of
small
amounts
of
gas
with
occasional
instances
of
severe
exposure.
During
the
periods
of
severe
exposure,
men
reported
symptoms
such
as
dizziness,
nausea,
tearing,
blurring
of
vision,
gasping,
coughing,
staggering,
and
prostration
that
lasted
several
hours.
Chronic
symptoms
included
muscular
weakness;
lassitude;
lung
congestion;

irritation
of
eyes,
skin,
and
throat;
decreased
appetite;
and
severe
weight
loss.
The
authors
noted
that
the
symptoms
observed
are
very
similar
to
the
symptoms
observed
in
cases
of
chronic
cyanide
poisoning,
except
that
with
cyanogen
chloride
the
weight
loss
is
greater
and
there
is
severe
congestion
of
the
lungs.
The
authors
attributed
these
latter
effects
to
the
presence
of
"
chlorine."

In
light
of
the
irritative
effects
reported
for
short­
term
exposures
to
cyanogen
chloride
(
Flury
and
Zernick,
1931;
Prentiss,
1937),
it
is
plausible
that
the
observed
irritation
was
due
to
the
chlorine
moiety
in
cyanogen
chloride.

Cyanide.
No
longer­
term
studies
of
exposure
in
humans
by
the
oral
or
dermal
routes
were
located.

El
Ghawabi
et
al.
(
1975)
evaluated
the
effects
of
long­
term
occupational
exposure
to
cyanide
in
workers
in
the
electroplating
industry.
Thirty­
six
male
workers
from
three
electroplating
factories
in
Egypt
were
evaluated
for
occupational
and
medical
history.

Iodineuptake
tests
were
performed
to
assess
thyroid
function.
Blood
was
drawn
for
hematological
analysis
and
urine
was
collected
for
thiocyanate
determination.
Twenty
males
who
had
never
been
exposed
to
chemicals
and
who
did
not
smoke
were
used
as
the
control
population.
Cyanide
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
15
Final
draft
concentration
in
the
workplace
air
was
also
measured.
The
mean
cyanide
air
concentrations
for
the
three
plants
were
10.4,
6.4,
and
8.3
ppm
(
11.7,
7.2,
and
9.3
mg/
m3,
respectively).
Of
the
36
workers,
14
were
exposed
for
5
years,
14
were
exposed
for
5­
10
years,
7
were
exposed
for
10­
15
years,
and
only
one
was
exposed
for
greater
than
15
years.
Approximately
80%
of
the
workers
reported
symptoms
of
headache,
weakness,
and
alterations
of
taste;
only
30%,
20%,
or
0%
of
the
controls,
respectively,
reported
these
symptoms.
Other
symptoms
reported
by
workers
included
giddiness,
throat
irritation,
vomiting,
and
tearing.
Finally,
a
small
percentage
of
workers,
who
worked
in
the
factory
with
the
highest
air
concentration,
reported
symptoms
of
neurological
disorders,
such
as
salivation,
disturbances
of
accommodation,
and
psychosis.
Twenty
workers
(
56%)
had
mild
to
moderate
thyroid
enlargement,
although
none
of
the
workers
showed
clinical
symptoms
of
either
hypo­
or
hyper­
thyroidism.
In
a
thyroid
iodine­
uptake
study,
the
workers
had
a
statistically
significant
increase
in
iodine
concentration
in
the
thyroid
gland
compared
with
the
controls.
This
finding
is
the
opposite
from
the
expected
result
for
workers
exposed
to
an
antithyroid
agent.
However,
the
authors
noted
that
the
test
was
conducted
immediately
after
the
workers
had
been
away
from
work
for
two
days,
and
they
concluded
that
the
sudden
cessation
of
cyanide
exposure
caused
the
iodine­
depleted
gland
to
rapidly
accumulate
iodine.
Workers
had
significantly
higher
hemoglobin
and
lymphocyte
counts
than
did
controls.
Finally,
the
authors
noted
that
the
urinary
concentration
of
thiocyanate
was
linearly
related
to
cyanide
concentration
in
air.
This
study
is
limited
by
the
small
sample
size
and
the
possibility
that
workers
were
also
exposed
to
other
chemicals
in
the
work
place.
However,
the
study
does
indicate
that
the
thyroid
is
a
target
organ
in
humans
following
chronic
exposure
to
cyanide.
An
air
concentration
of
7.2
mg
CN/
m3
can
be
considered
to
be
a
LOAEL.
After
adjusting
for
intermittent
exposure
and
the
occupational
minute
volume,
the
LOAEL(
HEC)
was
2.6
mg
CN/
m3.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
16
Final
draft
Blanc
et
al.
(
1985)
reported
on
health
effects
in
a
group
of
36
male
silver­
reclaiming
workers.
The
workers
had
been
employed
at
the
facility
for
an
average
of
11
±
10.4
months
when
the
facility
was
cited
for
safety
violations
and
shut
down.
Environmental
monitoring,
after
the
plant
was
shut
down,
found
that
the
24­
hour
time­
weighted
average
(
TWA)
exposure
was
15
ppm
HCN
(
16
mg
CN/
m3).
After
adjusting
for
intermittent
exposure
and
the
occupational
minute
volume,
the
human
equivalent
concentration
was
5.7
mg
CN/
m3.
Workers
were
classified
into
low­,
moderate­,
or
high­
exposure
categories
based
on
their
primary
job
activity.
However,
no
information
was
provided
on
the
actual
exposure
of
the
workers
in
each
exposure
category.
In
addition,
no
information
was
provided
on
how
the
TWA
concentration
related
to
personal
exposure
of
workers.
A
thorough
medical
examination
was
conducted,
including
analysis
for
serum
biochemistry,
thyroid
hormones,
and
neurological
effects.
A
number
of
subjective
symptoms,
including
nausea,
dizziness,
syncope,
and
vomiting,
exhibited
a
relationship
to
the
exposure
index.
There
were
no
workers
with
palpable
thyroid
gland
abnormalities,
mucosal
erosion,
or
neurological
deficits.
All
individual
values
for
T3,
T4,
and
TSH
were
normal,

although
the
average
TSH
value
was
higher
than
the
mean
laboratory
control
value.
The
difference
was
statistically
significant
for
the
high­
exposure
workers.
However,
since
it
is
not
possible
to
correlate
the
TWA
concentration
of
5.7
mg
CN/
m3
with
the
actual
exposure
of
highexposure
workers,
it
is
not
possible
to
designate
this
concentration
as
an
adverse
effect
level.

Thiocyanate.
Banerjee
et
al.
(
1997)
evaluated
thyroid
hormone
levels
in
35
women
in
India
who
ingested
thiocyanate
from
a
commercial
milk
product
supplemented
with
bacteriocide
known
as
the
LP
system
(
lactoperioxidase­
thiocyanate­
hydrogen
peroxide
system).
The
LP
system
produces
OSCN
(
the
actual
bacteriostat)
from
the
reaction
of
peroxide
with
thiocyanate.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
3EPA's
standard
body
weight
default
value
is
70
kg
for
adults,
including
both
men
and
women,
and
the
default
average
body
weight
for
women
in
the
U.
S.
is
65.4
kg
(
U.
S.
EPA,
1997b).
However,
since
women
in
India
are
smaller
than
American
women,
a
lower
average
body
weight
of
60
kg
was
used,
taking
into
account
the
uncertainty
in
the
overall
estimate;
no
information
was
located
on
average
body
weight
of
adult
Indian
women.

EPA/
OW/
OST/
HECD
VI­
17
Final
draft
In
these
systems,
thiocyanate
is
typically
present
in
the
milk
at
30­
50
mg/
L
(
45
mg/
L
average).

These
35
women
who
had
regularly
consumed
250
mL/
day
of
the
LP
milk
for
more
than
five
consecutive
years
were
matched
for
age,
dietary
habits,
and
socioeconomic
status
to
an
equal
number
of
women
who
consumed
a
similar
amount
of
untreated
raw
milk.
Assuming
a
body
weight
of
60
kg
for
these
women3,
and
that
all
of
the
thiocyanate
was
ingested
as
SCN,
rather
than
as
OSCN,
the
exposed
women
ingested
approximately
0.19
mg
SCN/
kg­
day.
All
subjects
had
no
prior
history
of
thyroid
disease.
Both
the
thiocyanate­
exposed
and
non­
exposed
control
groups
were
analyzed
for
urinary
and
serum
SCN
and
for
serum
T
3,
T
4
and
TSH.
The
average
serum
level
of
thiocyanate
was
230

mol/
L
(
1.3
mg/
100
mL)
in
the
exposed
group,
and
91

mol/
L
(
0.53
mg/
100
mL)
in
the
controls
(
Table
VI­
1).
The
thiocyanate­
exposed
group
had
significantly
lower
levels
of
serum
T
4
and
higher
levels
of
TSH
than
the
non­
exposed
group.
T
3
levels
were
slightly
elevated
in
the
thiocyanate­
exposed
group,
but
the
change
was
not
statistically
significant.
This
study
identifies
0.19
mg
SCN/
kg­
day
as
a
LOAEL
for
thyroid
effects
in
humans.

However,
it
is
unclear
if
the
presence
of
OSCN
(
rather
than
only
SCN)
exacerbated
the
effects
of
thiocyanate
on
the
thyroid.
In
addition,
the
study
authors
did
not
address
whether
the
study
population
might
constitute
a
sensitive
population.
For
example,
one
may
hypothesize
that
the
study
subjects
may
have
had
protein­
deficient
diets,
since
much
of
the
population
of
India
is
malnourished.
An
iodine
deficiency
appears
less
likely,
since
the
study
population
was
from
Calcutta,
a
coastal
city,
and
seafood
is
a
major
source
of
iodine.
People
who
are
protein
deficient
or
iodine
deficient
would
be
more
susceptible
to
effects
of
thiocyanate
on
T
4
levels.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
18
Final
draft
C.
Summary
of
Human
Studies
Cyanogen
Chloride.
Cyanogen
chloride
was
used
as
a
nerve
agent
during
World
War
I,

with
rapid
lethality
resulting
from
sufficiently
high
exposures.
Acute
exposure
to
lower
concentrations
resulted
in
irritation
of
the
eyes,
throat,
and
lungs
(
Flury
and
Zernick,
1931;

Prentiss,
1937;
Michigan
Department
of
Public
Health,
1977).
Only
one
epidemiology
study
of
the
human­
health
effects
of
cyanogen
chloride
exposure
was
located.
Reed
(
1920)
reported
on
symptoms
in
a
group
of
14
men
at
a
plant
that
manufactured
cyanogen
chloride.
No
exposure
levels
were
available,
but
the
symptoms
reported
during
periods
of
high
exposure
included
dizziness,
nausea,
and
prostration
that
lasted
several
hours.
Chronic
symptoms
included
weakness,
lassitude,
and
eye,
nose
and
throat
irritation.
The
observed
symptoms
are
consistent
with
those
seen
following
cyanide
exposure.
The
irritative
effects
and
lung
congestion
were
attributed
to
co­
exposure
to
chlorine.

Cyanide.
Case
reports
of
accidental
exposure
to
cyanide
and
hydrogen
cyanide
indicate
that
exposure
via
the
oral,
inhalation,
and
dermal
routes
are
of
concern.
The
reported
symptoms
include
dizziness,
weakness,
nausea,
and
a
rapid
pulse;
these
symptoms
can
progress
to
convulsions,
unconsciousness,
and
death
(
Saincher
et
al.,
1994;
Liebowitz
and
Schwartz,
1948;

Potter,
1950;
Drinker,
1932).
Similar
symptoms
were
reported
for
all
three
routes
of
exposure.

Symptoms
characteristic
of
parkinsonism
have
been
reported
among
subjects
who
recover
from
acute
cyanide
poisoning
(
Uitti
et
al.,
1985;
Carella
et
al.,
1988;
Rosenberg
et
al.,
1989;
and
Grandas
et
al.,
1989).
Studies
of
long­
term
exposure
to
cyanide
were
conducted
in
Egypt
with
36
workers
exposed
to
cyanide
in
the
electroplating
industry
(
El
Ghawabi
et
al.,
1975)
and
in
the
U.
S.
with
36
workers
in
the
silver­
reclaiming
industry
(
Blanc
et
al.,
1985).
In
El
Ghawabi
et
al.
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
19
Final
draft
(
1975),
air
concentrations
were
monitored.
Reported
symptoms
included
headache,
weakness,

throat
irritation,
and
vomiting.
A
small
percentage,
who
were
exposed
to
the
highest
concentrations,
reported
neurological
disorders.
Mild
to
moderate
thyroid
enlargement
was
reported
in
56%
of
the
workers,
although
none
of
the
workers
had
clinical
evidence
of
hypo­
or
hyper­
thyroidism.
This
study
identified
a
LOAEL
of
7.2
mg
CN/
m3,
corresponding
to
a
LOAEL(
HEC)
of
2.6
mg
CN/
m3.
In
Blanc
et
al.
(
1985),
a
single
24­
hour
TWA
measurement
found
a
concentration
of
16
mg
CN/
m3
(
corresponding
to
a
HEC
of
5.7
mg
CN/
m3),
but
this
TWA
was
not
correlated
with
the
actual
exposure
of
any
of
the
three
worker
exposure
categories
(
high,
medium,
or
low
exposure).
Several
subjective
symptoms
exhibited
a
relationship
to
the
exposure
index;
no
thyroid
effects
or
neurological
deficits
were
observed.
Both
studies
are
limited
by
small
sample
size
and
the
possibility
of
co­
exposure
to
other
chemicals.
In
addition,

Blanc
et
al.
(
1985)
is
limited
by
an
incomplete
characterization
of
exposure
for
each
of
the
exposure
categories.

Thiocyanate.
No
relevant
inhalation
or
dermal
toxicity
studies
of
thiocyanate
exposure
of
humans
were
identified.
There
is
a
significant
amount
of
data
on
thiocyanate
orally
administered
to
humans,
because
thiocyanate
was
used
for
many
years
to
treat
hypertension.
However,
data
on
the
effects
in
normotensive
humans
is
limited.
Adverse
effects
observed
included
weakness,

nervous­
system
effects
(
including
slurred
speech,
disorientation,
and
hallucinations),
and
enlarged
thyroid.
Some
of
the
observed
effects
may
have
been
due
to
a
rapid
decrease
in
blood
pressure.

While
the
decreased
blood
pressure
was
a
beneficial
effect
for
the
hypertensive
subjects,
the
same
change
could
be
adverse
in
normotensive
subjects,
although
it
is
unclear
if
the
drop
in
blood
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
4
OSCN
is
not
reported
as
one
of
the
ions
which
are
known
to
inhibit
iodine
transport
in
the
thyroid
(
Wolff,
1998).

EPA/
OW/
OST/
HECD
VI­
20
Final
draft
pressure
would
be
as
large
in
normotensive
subjects.
Doses
were
reported
inconsistently,
but
doses
of
1.7­
2.8
mg
SCN/
kg­
day
had
a
relatively
low
incidence
of
adverse
effects.

Two
studies
evaluated
thyroid
effects
of
thiocyanate
in
normotensive
populations.

Dahlberg
et
al.
(
1984)
found
no
effect
on
serum
T
3,
T
4,
or
thyrotropic
hormone,
or
the
T
3:
T
4
ratio
in
37
volunteers
administered
8
mg/
day
thiocyanate
in
milk
(
0.11
mg
SCN/
kg­
day)
for
12
weeks.

Maximum
serum
thiocyanate
levels
were
0.78
mg/
100
mL
in
non­
smokers
and
1.07
mg/
100
mL
in
smokers.
Banerjee
et
al.
(
1997)
evaluated
thyroid
hormone
levels
in
35
women
in
India
who
ingested
thiocyanate
and
hydrogen
peroxide
as
a
bacteriocide
in
milk
for
at
least
5
years,

compared
with
matched
women
ingesting
raw
milk.
The
exposed
women
ingested
approximately
0.19
mg
SCN/
kg­
day.
The
average
serum
level
of
thiocyanate
was
230

mol/
L
(
1.3
mg/
100
mL)

in
the
exposed
group,
and
91

mol/
L
(
0.53
mg/
100
mL)
for
matched
women.
The
thiocyanateexposed
group
had
significantly
lower
levels
of
serum
T
4
and
higher
levels
of
TSH
than
the
nonexposed
group.
Together,
these
two
studies
identify
an
apparent
NOAEL/
LOAEL
pair.
The
primary
uncertainty
in
that
identification
is
whether
the
Indian
population
was
more
susceptible
to
the
effects
of
thiocyanate,
due
to
such
potential
factors
as
low
protein
intake
or
low
iodide
intake.

Another
uncertainty
is
whether
OSCN
(
to
which
the
Indian
women
were
exposed)
is
more
toxic
than
the
equivalent
amount
of
SCN.
4
Since
the
thyroid
responds
rapidly
to
changes
in
iodine
or
related
ions,
progression
of
the
effect
with
increased
exposure
duration
from
12
weeks
to
5
years
would
not
be
expected.
Beamish
et
al.
(
1954)
observed
thyroid
toxicity
(
decreases
in
proteinbound
plasma­
iodine
concentration
and
thyroid
uptake
of
iodine)
in
subjects
with
blood
Drinking
Water
Criteria
Document
for
Cyanogen
Chloride
and
Potential
Metabolites
EPA/
OW/
OST/
HECD
VI­
21
Final
draft
thiocyanate
levels
(
1.3­
5
mg/
100
mL)
comparable
to
those
reported
by
Banerjee
et
al.
(
1997),
but
no
information
on
intake
(
in
mg/
kg­
day)
was
reported.
