83
Ammonia
(
CAS
No.
7664­
41­
7)
Draft,
Unpublished
Version.
Government
of
Canada,
Environment
Canada.:

Arillo,
A.,
Margiocco,
C.,
Melodia,
F.,
Mensi,
P.,
and
Schenone,
G.
1981.
Ammonia
toxicity
mechanism
in
fish:
studies
on
rainbow
trout
(
Salmo
gairdneri
Rich.).
Ecotoxicol.
Environ.
Safety
5:
316­
328.
Kloppic,
E.,
Jasobasch,
G.,
and
Rapoprt,
S.
1967.
Enhancement
of
the
glycolytic
rate
by
action
of
ammonium
ion
on
phosphofructokinase
activity.
Original
in
German.
Acta.
Biol.
Med.
18:
37­
42.
Fromm,
P.
O.,
and
Gillette,
J.
R.
1968.
Effect
of
ambient
ammonia
on
blood
ammonia
and
nitrogen
excretion
of
rainbow
trout
(
Salmo
gaidneri).
Comp.
Biochem.
Physiol.
26:
887­
896.
Person­
LeRuyet,
J.,
Boeuf,
G.
Zambonin­
Infant,
J.,
Helgason,
S.,
and
Le
Roux,
A.
1998.
Short­
term
physiological
changes
in
turbot
and
seabream
juveniles
exposed
to
exogenous
ammonia.
Comp.
Biochem.
Physiol.
119A:
511­
518.
Randall,
D.
J.,
and
Wicks,
B.
J.
1999.
Fish:
ammonia
production,
excretion,
and
toxicity.
In
press.
Paper
presented
in
the
Fifth
International
Symposium
on
Fish
Physiology,
Toxicology,
and
Water
Quality.
University
of
Hong
Kong.

4.9
ADDITIONAL
REMARKS
(
a)
Remarks:
The
toxicity
of
ammonia
to
aquatic
organisms
is
highly
dependent
on
physicochemical
factors,
most
notably
pH
because
of
its
importance
in
chemical
speciation.
The
acute
toxicity
of
ammonia
is
also
influenced
to
a
lesser
degree
by
temperature,
carbon
dioxide,
dissolved
oxygen,
and
salinity.
In
aqueous
solution,
ammonia
exists
primarily
in
two
forms,
un­
ionized
ammonia
(
NH3)
and
ammonium
ion
(
NH4
+),
which
are
in
equilibrium
with
each
other
according
to
the
following
established
relationship:

NH3(
aq)
+
H2O
 
NH4
+
+
OH­

In
general,
as
pH
increases,
the
fraction
of
the
total
ammonia
which
is
un­
ionized
increases.
It
is
this
un­
ionized
ammonia
(
NH3)
which
is
generally
considered
to
be
the
primary
cause
of
toxicity
in
aquatic
systems.
Un­
ionized
ammonia
(
NH3)
is
more
toxic
to
aquatic
organisms
than
the
ammonium
ion
(
NH4
+)
because
the
un­
ionized
form
is
readily
soluble
in
the
lipid
of
the
cell
membrane
and
is
rapidly
absorbed
by
the
gill.
In
contrast,
the
charged
ion
is
not
readily
passed
through
the
charged­
line
hydrophobic
space
in
the
membrane.
EPA
studies
indicate
that
un­
ionized
ammonia
is
190
times
more
toxic
to
guppies
than
ammonium.
84
Ammonia
(
CAS
No.
7664­
41­
7)
Multiple
EPA
studies
have
shown
that
over
the
pH
range
of
6.5­
9.0,
the
toxicity
of
un­
ionized
ammonia
(
NH3)
increases
as
the
pH
decreases.
This
is
either
because
the
additional
hydrogen
ion
(
H+)
concentration
at
lower
pHs
increases
the
toxicity
of
unionized
ammonia
or
because
the
ammonium
ion
(
NH4
+)
exerts
some
level
of
toxicity
at
lower
pH.
However,
it
would
be
an
oversimplification
to
attribute
the
toxic
action
to
only
the
ammonium
ion
at
low
pH
and
to
only
unionized
ammonium
at
high
pH
because
most
likely
both
forms
participate
when
total
ammonia
concentration
is
high
enough
to
cause
toxicity
symptoms.
A
joint
toxicity
model
has
been
proposed,
with
ammonium
causing
most
toxicity
at
high
pH
values
and
ammonium
ion
also
contributing
to
toxicity
at
lower
pH
values.
This
is
supported
through
studies
demonstrating
that
at
a
low
pH
a
new
inward
flux
of
ammonium
ion
can
occur
across
the
gills
of
aquatic
species.
Reference:
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.
Erickson,
R.
J.
1985.
An
evaluation
of
mathematical
models
for
the
effects
of
pH
and
temperature
on
ammonia
toxicity
to
aquatic
organisms.
Water
Res.
19:
1047­
1058.
Evans,
D.
E.
and
Cameron,
J.
N.
1986.
Gill
ammonia
transport.
J.
Exp.
Zool.
239:
17­
23.
Thurston,
R.
V.,
Russo,
R.
C.,
Phillips,
G.
R.
1983.
Acute
toxicity
of
ammonia
to
fathead
minnows.
Trans.
Am.
Fish.
Soc.
112:
705­
711.
U.
S.
Environmental
Protection
Agency
(
USEPA).
1998c.
1998
Update
of
Ambient
Water
Quality
Criteria
for
Ammonia.
Office
of
Water,
Washington,
D.
C.
EPA
822­
R­
98­
008.
U.
S.
Environmental
Protection
Agency
(
USEPA).
1985.
Ambient
Water
Quality
Criteria
for
Ammonia
 
1984.
Washington,
D.
C.:
Office
of
Water
Regulations
and
Standards,
Criteria
and
Standards
Division.
EPA­
504/
5­
85­
006.

(
b)
Remarks:
The
amount
of
un­
ionized
ammonia
as
a
percent
of
total
ammonia
in
aqueous
solution
is
dependent
on
pH
and
temperature.
The
authors
derive
this
relationship
and
provide
a
table
showing
the
percent
of
un­
ionized
ammonia
at
various
pH
values
and
temperatures.
Reference:
Emerson,
K.,
Russo,
R.
C.,
Lund,
R.
E.,
and
Thurston,
R.
V.
1975.
Aqueous
ammonia
equilibrium
calculations:
effect
of
pH
and
temperature.
J.
Fish.
Res.
Board
Can.
32:
2379­
2383.
85
Ammonia
(
CAS
No.
7664­
41­
7)
5.
TOXICITY
*
5.1
ACUTE
TOXICITY
5.1.1
ACUTE
ORAL
TOXICITY
Not
an
applicable
route
of
exposure.

5.1.2
ACUTE
INHALATION
TOXICITY
(
a)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
]
Species/
strain:
Rat
(
Wistar)
Exposure
Time:
60
minutes
Value:
LC50
(
male)
=
9,850
mg/
m3
air
(
14,111
ppm)
LC50
(
female)
=
13,770
mg/
m3
air
(
19,727
ppm)
Method:
Male
and
female
SPF­
bred
rats
were
exposed
to
an
ammonia
atmosphere.
Each
dose
group
consisted
of
5
males
and
5
females
and
they
were
exposed
to
an
ammonia/
air
mixture
at
a
rate
of
25
L/
min.
Animals
were
exposed
for
10,
20,
40,
or
60
minutes.
After
exposure,
they
were
housed
5
per
cage
for
an
observation
period
of
14
days.
Food
and
water
were
available
during
the
observation
period,
but
were
withheld
during
exposure.
Body
weight
was
recorded
at
days
1,
2,
4,
7,
and
14.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Liquid
ammonia
(
NH3)
in
a
pressurized
cylinder
(
UKF­
SBB,
The
Netherlands)
Remarks:
Clinical
symptoms
included
eye­
irritation,
especially
in
animals
exposed
for
60
minutes,
wet
noses,
and
nasal
discharge.
Autopsy
revealed
haemorrhagic
lungs.
Reference:
Appelman,
L.
M.,
ten
Berge,
W.
F.,
and
Reuzel,
P.
G.
J.
1982.
Acute
inhalation
toxicity
study
of
ammonia
in
variable
exposure
periods.
Am.
Ind.
Hyg.
Assoc.
J.
43(
9):
662­
665.

(
b)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
]
Species/
strain:
Albino
ICR
mice
Exposure
Time:
1
hour
Value:
LC50
=
4230
ppm
un­
ionized
NH3
Method:
Groups
of
12
mice
each
were
exposed
simultaneously
to
three
concentrations
of
NH3
gas
(
1,190­
4,860
ppm
depending
on
which
of
the
three
experiments)
in
air
using
a
dynamic
inhalation
exposure
system.
The
control
group
was
exposed
to
air
only.
The
mice
were
allowed
free
access
to
food
and
water
during
the
experiment,
except
while
in
chamber
tubes.
The
mice
were
acclimated
for
at
least
1week
prior
to
the
experiment.
Sampling
86
Ammonia
(
CAS
No.
7664­
41­
7)
and
analyses
were
conducted
every
3­
5
minutes.
Animals
were
observed
for
14
days
following
exposure.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Ammonia
(
NH3)
gas
(
Matheson,
East
Rutherford,
NJ)
Remarks:
At
high
NH3
concentrations,
mortality
usually
occurred
within
30
minutes
of
initiation
of
exposure.
Twenty­
five
percent
of
animals
exposed
to
3950
ppm
and
greater
did
not
survive.
Percent
mortality
in
higher
concentrations
(
4220­
4860
ppm)
ranged
from
41.6
to
100%.
The
lungs
of
animals
that
died
during
exposure
were
congested
with
evidence
of
hemorrhage.
The
lungs
of
animals
from
every
treatment
group
sacrificed
displayed
a
mild
to
moderate
degree
of
chronic
focal
pneumonitis
histologically.
The
liver
and
heart
weights
were
increased
in
animals
that
died
during
exposure
to
4860
ppm.
Reference:
Kapeghian,
J.
C.,
Mincer,
H.
H.,
Jones,
A.
B.,
Verlangieri,
A.
J,
and
Waters,
I.
W.
1982.
Acute
inhalation
toxicity
of
ammonia
in
mice.
Bull.
Environ.
Contam.
Toxicol.
29:
371­
378.

(
c)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
]
Species/
strain:
Rat
Exposure
time:
1
hour
Value:
LC50
=
5137
mg/
m3
(
7338
ppm)
Method:
Rats
were
exposed
for
one
hour
to
several
concentrations
of
ammonia.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
Remarks:
Inhalation
produced
immediate
nasal
and
eye
irritation
followed
by
labored
breathing
in
all
test
groups.
Surviving
rats
necropsied
after
14
days
showed
moderate
mottling
of
the
liver
at
the
5474
and
6888
mg/
m3
(
7820
and
9840
ppm)
test
levels.
Reference:
MacEwen,
J.
D.
and
Vernot,
E.
H.
1972.
Toxic
hazards
research
unit
annual
technical
report.
NTIS
AD
755­
358.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
d)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
X]
Species/
strain:
Rat
Exposure
time:
5,
15,
30
or
60
minutes
Value:
LC50
(
5­
m)
=
18,693
mg/
m3
(
26,704
ppm)
LC50
(
15­
m)
=
11,342
mg/
m3
(
17,372
ppm)
LC50
(
30­
m)
=
7035
mg/
m3
(
10,050
ppm)
LC50
(
60­
m)
=
7939
mg/
m3
(
11,342
ppm)
NOEL
(
5,
15,
30,
&
60­
m)
=
100
mg/
m3
(
144
ppm)
Method:
White
rats
were
exposed
to
high
concentrations
of
ammonia
(
6000,
3000,
and
1000
mg/
m3,
equivalent
to
6814,
4307
and
1436
ppm)
via
inhalation.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
87
Ammonia
(
CAS
No.
7664­
41­
7)
Remarks:
Other
effects
included
dyspnoea,
irritation
of
the
respiratory
tract
and
eyes,
cyanosis
of
the
extremities,
and
increased
excitability.
In
associated
studies,
rats
exposed
to
3000,
1000
or
300
mg/
m3
(
4307,
1436,
431
ppm)
exhibited
a
drop
in
static
muscular
tension
and
other
sublethal
effects.
No
effects
were
observed
in
rats
exposed
to
100
mg/
m3
(
144
ppm)
for
5,
15,
30
or
60
minutes.
Reference:
Propkopieva,
A.
S.
et
al.
1973.
Materials
for
a
toxicological
characteristic
of
the
long­
term
effect
of
ammonia
on
the
organisms
of
animals
after
brief
exposure.
Gig.
Tr.
Prof.
Zabol.
(
Russian)
6:
56­
57.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
e)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
]
Species/
strain:
Mouse
Exposure
time:
1
hour
Value:
LC50
=
3386
mg/
m3
(
4837
ppm)
Method:
Mice
were
exposed
for
one
hour
to
several
concentrations
of
ammonia.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
Remarks:
Inhalation
produced
immediate
nasal
and
eye
irritation
followed
by
labored
breathing
in
all
test
groups.
Mild
congestion
of
the
liver
was
also
observed
in
surviving
mice
in
the
two
highest
dose
levels
of
3185
and
4004
mg/
m3
(
4550
and
5720
ppm).
Reference:
MacEwen,
J.
D.
and
Vernot,
E.
H.
1972.
Toxic
hazards
research
unit
annual
technical
report.
NITS
AD
755­
358.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
f)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
]
Species/
strain:
Mouse
Exposure
time:
10
minutes
Value:
LC50
=
7060
mg/
m3
(
10,152
ppm)
Method:
Groups
of
20
mice
were
exposed
to
9
concentrations.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
Remarks:
The
LC50
was
calculated
from
the
mortality
observed
at
10
days.
Most
deaths
occurred
rapidly,
with
equally
rapid
recovery
of
survivors.
Reference:
Silver,
S.
D.
and
McGrath,
F.
P.
1948.
J.
Ind.
Hyg.
Toxicol.
30:
7­
9.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
g)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
88
Ammonia
(
CAS
No.
7664­
41­
7)
Species/
strain:
Rabbit,
cat
Exposure
time:
1
hour
Value:
See
remarks
Method:
Animals
were
placed
in
a
static
gassing
chamber
of
400
L
capacity
and
exposed
to
from
3.5
to
8.7
mg
un­
ionized
NH3/
L.
Experiments
were
performed
upon
54
rabbits
and
18
cats
subdivided
into
6
groups.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
Remarks:
Exposure
to
ammonia
increased
the
respiratory
tract
fluid
output
two­
to
three­
fold
in
cats
and
rabbits.
Inhalation
of
ammonia
had
no
appreciable
effect
upon
the
water
content
of
respiratory
tract
tissues
of
rabbits
and
cats.
Following
gassing
with
ammonia,
the
iron
content
of
the
tracheal,
bronchial,
and
alveolar
portions
increased
in
rabbits.
There
was
an
initial
slight
drop
in
blood
hemoglobin
in
the
first
4
or
5
hours
of
exposure,
followed
by
a
return
to
normal
levels
by
8
hours
in
both
cats
and
rabbits.
Definite
lipemia
was
observed
in
rabbits.
Reference:
Boyd,
E.
M.,
MacLachlan,
M.
L.,
and
Perry,
W.
F.
1944.
Experimental
ammonia
gas
poisoning
in
rabbits
and
cats.
J.
Ind.
Hyg.
Toxicol.
26:
29­
34.

(
h)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
(
RD50)
Species/
strain:
Male
Swiss­
Webster
mice
Exposure
time:
30
minutes
Value:
A
concentration
of
212
mg/
m3
(
303
ppm)
decreases
the
respiratory
frequency
by
50%
(
RD50)
in
mice.
Method:
Mice
were
exposed
to
atmospheric
concentrations
ranging
from
70­
560
mg/
m3
(
100­
1000
ppm).
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
Remarks:
Ammonia
is
a
sensory
irritant
to
rodents.
Reference:
Barrow,
C.
S.,
Alarie,
Y.
and
Stock,
M.
F.
1978.
Sensory
irritation
and
incapacitation
evoked
by
thermal
decomposition
products
of
polymers
and
comparisons
with
known
sensory
irritants.
Arch.
Environm.
Health
33:
79­
88.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
i)
Type:
LC0
[
];
LC100
[
];
LC50
[
X];
LCL0
[
];
Other
[
]
Species/
strain:
Wistar
rats
(
male
and
female)
Exposure
time:
10,
20,
40,
or
60
minutes
Value:
LC50
(
10­
m)
=
28,130
mg/
m3
(
40,300
ppm)
LC50
(
20­
m)
=
19,960
mg/
m3
(
28,595
ppm)
LC50
(
40­
m)
=
14,170
mg/
m3
(
20,300
ppm)
LC50
(
60­
m)
=
11,590
mg/
m3
(
16,600
ppm)
Method:
Ten
animals
(
5
males,
5
females)
were
exposed
to
each
of
a
series
of
ammonia
concentrations
in
an
inhalation
cylinder
for
89
Ammonia
(
CAS
No.
7664­
41­
7)
10,
20,
40
or
60
minutes.
After
exposure,
rats
were
housed
in
wire
mesh
cages
for
an
observation
period
of
14
days.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
evolved
from
a
pressurized
cylinder
of
liquid
ammonia.
Remarks:
Clinical
signs
of
restlessness,
eye
irritation,
nasal
discharge,
mouth
breathing,
and
labored
respiration
were
seen
during
exposure.
Reference:
Appelman,
L.
M.,
ten
Berg,
W.
F.,
and
Reuzel,
P.
G.
J.
1982.
Acute
inhalation
toxicity
study
of
ammonia
in
rats
with
variable
exposure
periods.
Am.
Ind.
Hyg.
Assoc.
J.
43(
9):
662­
665.

(
j)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
]
Species/
strain:
ICR
mice
(
male)
Exposure
time:
1
hour
Value:
LC50
=
2960
mg/
m3
(
4,230
ppm)
Method:
Four
groups
of
12
mice
were
exposed
to
each
of
three
concentrations
of
NH3
gas
in
air.
The
1
hour
exposure
was
followed
by
a
14
day
observation
period.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
(
NH3)
gas
Remarks:
Lungs
of
mice
that
died
during
exposure
were
diffusely
haemorrhagic.
A
mild
to
moderate
degree
of
chronic
focal
pneumonitis
was
also
observed.
Reference:
Kapeghian,
J.
C.,
Mincer,
H.
H.,
Jones,
A.
B.,
Verlangieri,
A.
J.,
and
Waters,
I.
W.
1982.
Acute
inhalation
toxicity
of
ammonia
in
mice.
Bull
Environ.
Contam.
Toxicol.
29:
371­
378.

(
k)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
Species/
strain:
Cat
Exposure
time:
10
minutes
Method:
Twenty
cats
were
randomly
placed
into
four
groups
of
five
cats
each.
Baseline
pulmonary
function
tests
were
performed.
All
the
animals
were
exposed
to
1,000
ppm
ammonia
gas
for
10
min.
One
group
was
euthanized
after
24
hours
and
the
other
three
groups
were
tested
on
days
7,
21,
and
35
post­
exposure.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Anhydrous
ammonia
(
NH3)
Remarks:
Twenty­
four
hours
after
exposure,
cats
had
severe
dyspnea,
anorexia,
and
dehydration.
Auscultation
revealed
bronchial
breath
sounds,
sonorous
and
sibulent
ronchi,
and
course
rales.
Lungs
showed
varying
degrees
of
congestion,
hemorrhage,
edema,
interstitial
emphysema,
and
collapse.
There
was
no
significant
change
in
Anatomical
Dead
Space
(
ADS).
The
only
significant
change
in
Functional
Residual
Capacity
(
RFC)
was
on
day
21,
at
which
time
this
value
almost
doubled.
Seven
days
after
exposure
to
ammonia
gas,
the
epithelial
damage
was
healed.
90
Ammonia
(
CAS
No.
7664­
41­
7)
Reference:
Dodd,
K.
T.
and
Gross.
D.
R.
1980.
Ammonia
inhalation
toxicity
in
cats:
a
study
of
acute
and
chronic
respiratory
dysfunction.
Arch.
Environ.
Health
35(
1):
6­
14.

(
l)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
Species/
strain:
New
Zealand
White
rabbit
Exposure
time:
2.5
to
3.0­
hours
Value:
BUN
(
pre­
exposure)
=
19.4
mg/
100
mL
BUN
(
post­
exposure)
=
24.6
mg/
100
mL
Blood
pH
(
pre­
exposure)
=
7.34
Blood
pH
(
post­
exposure)
=
7.36
Blood
CO2
(
pre­
exposure)
=
14.3
meq/
L
plasma
Blood
CO2
(
post­
exposure)
=
18.9
meq/
L
plasma
Method:
Sixteen
adult
female
rabbits
were
exposed
to
50
ppm
in
experiment
1
and
100
ppm
ammonia
in
experiment
2.
Each
experiment
ran
from
7.5
to
9
hours
duration
with
ammonia
exposure
occurring
only
during
the
second
2.5
to
3.0
hour
segment.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Anhydrous
ammonia
(
NH3)
Remarks:
The
decline
in
respiration
rate
was
essentially
linear
over
the
7.5
hour
period
for
both
groups
under
control
conditions.
The
decrease
in
respiration
rate
upon
exposure
to
ammonia
was
highly
significant
and
essentially
the
same
for
the
50
ppm
and
100
ppm
exposure
levels.
BUN
=
Blood
Urea
Nitrogen.
Reference:
Mayan,
M.
H.
and
Merilan,
C.
P.
1972.
Effects
of
ammonia
inhalation
on
respiration
rate
of
rabbits.
J.
Anim.
Sci.
34(
3):
447­
452.

(
m)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
Species/
strain:
Guinea
pigs
Exposure
time:
6
to
18­
weeks
Method:
Twelve
male
guinea
pigs
were
used
for
experimentation
and
6
for
controls.
Exposure
to
ammonia
was
for
6
hours
per
day,
5
days
per
week.
At
intervals
of
6
weeks,
4
experimental
and
2
control
animals
were
sacrificed.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Anhydrous
ammonia
(
NH3)
Remarks:
Animals
exposed
for
6
and
12
weeks
showed
no
abnormalities
which
could
be
attributed
to
ammonia.
After
18
weeks,
animals
showed
considerable
congestion
of
spleens,
livers
and
kidneys,
and
early
degenerative
changes
in
the
suprarenal
gland.
Upper
tubules
of
the
kidneys
showed
fairly
marked
cloudy
swelling
with
precipitated
albumen
in
the
lumens
and
some
casts.
Reference:
Weatherby,
J.
H.
1952.
Chronic
toxicity
of
ammonia
fumes
by
inhalation.
Proc.
Soc.
Exp.
Biol.
Med.
81:
300­
301.

(
n)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
91
Ammonia
(
CAS
No.
7664­
41­
7)
Method:
Summary
of
animal
inhalation
studies
for
ammonia.
Remarks:
The
acute
effects
of
ammonia
in
animals
was
reviewed
as
part
of
a
health
effects
assessment
prepared
in
1990
for
The
Fertilizer
Institute.
In
summary,
acute
exposure
to
high
concentrations
of
ammonia
in
air
to
animals
can
result
in
death
[
LC50
values
as
low
as
2961
mg/
m3
(
3796
ppm)
in
mice
and
5137
mg/
m3
(
6586
ppm)
in
rats
for
a
one­
hour
exposure.]
Acute
exposures
to
ammonia
in
the
range
of
200­
700
mg/
m3
(
256­
897
ppm)
resulted
in
excessive
irritation
and
nasal
and
mouth
secretions,
depressed
respiratory
rates,
and
lung
edema
and
hemorrhage
[
it
should
be
noted
that
some
experiments
showed
no
ill
effects
at
levels
as
high
as
700
mg/
m3
(
897
ppm)].
One
frequently
observed
result
of
acute
exposure
is
the
cessation
of
tracheal
ciliary
activity.
For
directly
exposed
tracheas,
ciliary
beating
stopped
after
exposure
to
as
low
as
2.1
mg/
m3
(
3
ppm).
However,
experiments
which
produced
cessation
without
recovery
utilized
concentrations
in
the
range
of
280­
1400
mg/
m3
(
359­
1795
ppm).
Reference:
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.

(
o)
Type:
LC0
[
];
LC100
[
];
LC50
[
];
LCL0
[
];
Other
[
X]
Species/
strain:
Duroc
pigs
Exposure
time:
5­
weeks
Values:
NOAEL
=
61
ppm.
Methods:
Duroc
pigs
were
exposed
for
5
weeks
to
the
following
ammonia
concentrations:
8,
43,
72
and
102
mg/
m3
(
12,
61,
103,
and
146
ppm).
Exposures
were
conducted
under
controlled
environmental
conditions
of
21.1oC
dry­
bulb
temperature
and
77%
relative
humidity.
Thirty
six
pigs
with
an
average
initial
weight
of
approximately
54
kg
were
allotted
into
four
2.7
x
4.9
m.
compartments.
Ammonia
was
introduced
into
three
of
the
four
compartments
in
the
supply
air
ducts.
To
control
introduction,
a
corrosion
resistant
pressure­
regulating
valve
was
mounted
on
the
bulk
tank.
The
ammonia
was
metered
from
this
valve
into
a
low­
pressure
chamber
that
was
maintained
at
0.14
to
0.21
kg
per
square
centimeter
gauge
pressure.
Three
stainless
steel
needle
valves
led
from
the
low­
pressure
chamber
through
rotameters
and
then
into
the
supply
air
ducts
of
the
three
compartments.
Ammonia
levels
were
measured
daily
by
bubbling
a
known
quantity
of
air
through
dilute
sulfuric
acid
and
back
titrating
with
dilute
sodium
hydroxide.
GLP:
Yes
[
]
No
[
X]
?
[
]
Results:
Coughing
and
nasal,
lacrimal,
and
oral
secretions
were
observed
in
pigs
exposed
for
5
weeks
to
103
and
146
ppm
ammonia.
No
significant
effects
were
seen
at
12
and
61
ppm
for
the
same
exposure
duration.
Test
Substance:
Atmospheric
ammonia
(
NH3)
92
Ammonia
(
CAS
No.
7664­
41­
7)
Remarks:
The
authors
reported
that
ammonia
exposures
(
12­
146
ppm)
caused
a
highly
significant
adverse
effect
upon
feed
consumption
and
average
daily
gain.
However,
no
statistical
evaluations
were
performed
and
furthermore,
the
data
presented
do
not
appear
to
support
these
conclusions.
Reference:
Stombaugh,
D.
P.,
Teague,
H.
S.,
and
Roller,
W.
L.
1969.
Effects
of
atmospheric
ammonia
on
the
pig.
J.
Anim.
Sci.
28(
6):
844­
847.

5.1.3
ACUTE
DERMAL
TOXICITY
Remarks:
No
data
are
available
regarding
systemic
effects
of
dermal
exposure
to
ammonia
or
ammonium
compounds.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
93
Ammonia
(
CAS
No.
7664­
41­
7)
5.1.4
ACUTE
TOXICITY
BY
OTHER
ROUTES
OF
ADMINISTRATION
(
a)
Type:
LD0
[
];
LD100
[
];
LD50
[
X];
LDL0
[
];
Other
[
]
Species/
strain:
Mus
musculus
(
Albino
mice)
and
Gallus
domesticus
(
White
Leghorn
chicks)
Exposure
Time:
1­
hour
Value:
LD50
(
intravenous;
chicks)
=
2.72
mmol
CH3COONH4/
kg
LD50
(
intravenous;
mice)
=
5.64
mmol
CH3COONH4/
kg
LD50
(
intraperitoneal;
chicks)
=
10.44
mmol
CH3COONH4/
kg
LD50
(
intraperitoneal;
mice)
=
10.84
mmol
CH3COONH4/
kg
Method:
A
total
of
200
chicks
and
180
mice
were
used.
One­
half
to
1.5
mL
isotonic
saline
containing
ammonium
acetate
was
injected
rapidly
into
the
wing
vein
of
the
chicks
and
into
a
tail
vein
of
the
mice
for
intravenous
studies,
and
into
the
peritoneal
cavity
for
the
intraperitoneal
studies.
Ten
animals
were
exposed
to
each
of
eight
to
eleven
concentration
groups.
Animals
were
observed
continually
until
all
signs
of
acute
toxicity
disappeared
and
the
survivors
counted
after
1
hour.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Ammonium
acetate
(
CH3COONH4)
Remarks:
In
the
intravenous
studies,
reaction
began
immediately
in
both
species,
characterized
by
hyperventilation
and
clonic
convulsions.
In
individuals
who
died,
clonic
convulsions
were
followed
by
a
fatal
tonic
extensor
convulsion.
Mice
which
survived
showed
signs
of
hyperventilation
and
hyperirritability,
but
did
not
go
into
a
coma.
Chicks
exhibited
clonic
convulsions
followed
by
a
gradual
onset
of
coma
and
completely
recovered
in
50­
60
minutes.
The
reaction
to
the
intraperitoneal
dose
was
similar
between
the
two
species.
Clonic
convulsions
accompanied
by
a
gradual
onset
of
coma
began
10­
15
minutes
after
injection.
Animals
either
died
of
a
fatal
tonic
extensor
convulsion
or
recovered
in
50­
60
minutes.
Reference:
Wilson,
R.
P.,
Muhrer,
M.
E.,
and
Bloomfield,
R.
A.
1968.
Comparative
ammonia
toxicity.
Comp.
Biochem.
Physiol.
25:
295­
301.

(
b)
Type:
LD0
[
];
LD100
[
];
LD50
[
X];
LDL0
[
];
Other
[
]
Species/
strain:
Rat
Value:
LD50
(
intraperitoneal
dose)
=
8.2
mmol
NH4OCOCH3/
kg
Method:
Intraperitoneal
injection
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
acetate
Remarks:
Signs
included
hyperventilation,
clonic
convulsions,
coma
and
death.
These
signs
did
not
appear
until
15­
30
minutes
after
administration.
Reference:
Greenstein,
J.
P.,
Winitz,
M.,
Gullino,
P.,
Birnbaum,
S.
M.,
and
Otey,
M.
C.
1956.
Studies
on
the
metabolism
of
amino
acids
and
related
compounds
in
vivo.
III.
Prevention
of
ammonia
toxicity
by
arginine
and
related
compounds.
Arch.
Biochem.
94
Ammonia
(
CAS
No.
7664­
41­
7)
Biophys.
64:
342­
354.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
(
c)
Type:
LD0
[
];
LD100
[
];
LD50
[
X];
LDL0
[
];
Other
[
]
Species/
strain:
Mouse
Value:
LD50
(
intravenous
dose)
=
6.23
mmol
NH4OCOCH3/
kg
LD50
(
intravenous
dose)
=
5.05
mmol
NH4HCO3/
kg
LD50
(
intravenous
dose)
=
4.47
mmol
NH4CO3/
kg
LD50
(
intravenous
dose)
=
6.75
mmol
NH4Cl/
kg
LD50
(
intravenous
dose)
=
2.53
mmol
NH4OH/
kg
Method:
Intravenous
injection
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonium
acetate
(
NH4OCOCH3),
ammonium
bicarbonate
(
NH4HCO3),
ammonium
carbonate
(
NH4CO3),
ammonium
chloride
(
NH4Cl)
and
ammonium
hydroxide
(
NH4OH)
Remarks:
Toxic
signs
included
immediate
hyperventilation
and
clonic
convulsions
followed
by
coma,
tonic
convulsions
and
death.
Surviving
animals
recover
rapidly
and
completely.
Reference:
Warren,
K.
S.
1958.
The
differential
toxicity
of
ammonium
salts.
J.
Clin.
Invest.
37:
497­
501.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
d)
Type:
LD0
[
];
LD100
[
];
LD50
[
];
LDL0
[
];
Other
[
X]
Species/
strain:
White
rat
Exposure
Time:
3­
hours
Value:
Minimum
lethal
dose
=
6.80
mL
(
NH4)
2CrO4;
(
0.072
mg
(
NH4)
2CrO4­
N)
Minimum
lethal
dose
=
6.74
mL
NH4Cl;
(
0.072
mg
NH4Cl­
N)
Minimum
lethal
dose
=
6.21
mL
(
NH4)
2HPO4;
(
0.061
mg
(
NH4)
2HPO4­
N)
Minimum
lethal
dose
=
7.87
mL
No.
1
NH4HCO3;
(
0.073
mg
No.
1
NH4HCO3­
N)
Minimum
lethal
dose
=
5.60
mL
No.
2
NH4(
H)
CO3;
(
0.055
mg
No.
2
NH4(
H)
CO3­
N)
Minimum
lethal
dose
=
6.75
mL
NH4NO3;
(
0.065
mg
NH4NO3­
N)
Minimum
lethal
dose
=
10.00
mL
(
NH4)
2SO4;
(
0.094
mg
(
NH4)
2SO4­
N)
Minimum
lethal
dose
=
6.20
mL
NH4Br;
(
0.055
mg
NH4Br­
N)
Minimum
lethal
dose
=
6.30
mL
(
NH4)
2CO3
+
carbamide;
(
0.055
mg
(
NH4)
2CO3
+
carbamide­
N)
Minimum
lethal
dose
=
4.80
mL
(
NH4)
3PO4
neutral;
(
0.0384
mg
(
NH4)
3PO4
neutral­
N)
Minimum
lethal
dose
=
7.56
mL
(
H2)
NH4PO4;
(
0.05708
mg
(
H2)
NH4PO4­
N)
Minimum
lethal
dose
=
6.00
mL
NH4I
Minimum
lethal
dose
=
7.40
mL
NH4CrSO4
Method:
All
salts
(
ammonium
oxalate,
carbonate,
chromate,
chloride,
nitrate,
citrate,
sulfate,
tartrate,
hydrogen
phosphate,
acetate,
95
Ammonia
(
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No.
7664­
41­
7)
sarcolactate,
and
lactate)
were
made
to
approximate
5
percent
solution
and
injected
into
white
rats.
The
nitrogen
in
the
form
of
NH3
was
determined
in
three
5
percent
solutions.
Six
animals
were
used
for
each
series.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Various
ammonium
salts
(
ammonium
oxalate,
carbonate,
chromate,
chloride,
nitrate,
citrate,
sulfate,
tartrate,
hydrogen
phosphate,
acetate,
sarcolactate,
and
lactate)
Remarks:
Contrary
to
previous
reports
by
Rachford
and
Crane
(
1902),
the
current
study
demonstrated
that
the
toxicity
of
ammonium
salts
to
white
rats
is
directly
proportional
to
the
amount
of
un­
ionized
ammonia
present
(
i.
e.
rather
than
on
the
form
of
salt
used).
Note
that
while
this
study
is
old
(
1922),
it
does
provide
evidence
that
the
anion
of
the
salt
is
less
important
with
respect
to
toxicity
than
un­
ionized
ammonia.
Reference:
Underhill,
F.
P.
and
Kapsinow,
R.
1922.
The
comparative
toxicity
of
ammonium
salts.
J.
Biol.
Chem.
54:
451­
457.

5.2
CORROSIVENESS/
IRRITATION
5.2.1
SKIN
IRRITATION/
CORROSION
Remarks:
Ammonia
in
the
form
of
a
gas
or
an
aqueous
solution
is
a
recognized
skin
irritant.
Most
of
the
information
is
human
clinical
data
and
is
described
in
Section
5.11.
Reference:
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

5.2.2
EYE
IRRITATION/
CORROSION
(
a)
Remarks:
Subacute
and
chronic
exposure
of
animals
to
ammonia
in
the
range
of
200­
1000
ppm
has
been
found
to
produce
eye
damage.
At
100­
200
ppm,
moderate
to
severe
eye
irritation
occurred.
Reference:
BIBRA.
1995.
Toxicology
Profile:
Ammonia.
BIBRA
International.

(
b)
Remarks:
Ammonia,
partly
because
of
its
lipid
solubility,
penetrates
the
corneal
membrane
rapidly.
In
rabbits,
conjunctival
oedema
with
ischaemia
and
segmentation
of
the
limbal
vessels
were
noted
within
30
minutes.
In
rabbits
with
corneal
burns,
neovascularization
occurred
after
1
week,
but
it
was
delayed
in
animals
with
both
corneal
and
limbal
burns.
Reference:
National
Research
Council
(
NRC).
1979.
Ammonia.
Subcommittee
on
Ammonia.
Committee
on
Medical
and
Biologic
Effects
of
Environmental
Pollutants.
Division
of
96
Ammonia
(
CAS
No.
7664­
41­
7)
Medical
Sciences,
Assembly
of
Life
Sciences.
National
Research
Council.
Baltimore:
University
Park
Press.
NTIS
No.
PB
278­
027.

5.3
SKIN
SENSITISATION
Remarks:
No
specific
skin
sensitization
studies
were
identified.

*
5.4
REPEATED
DOSE
TOXICITY
(
a)
Species/
strain:
Male
and
female
Sprague­
Dawley
and
Long­
Evans
rats,
male
and
female
Princeton­
derived
Guinea
pigs,
male
New
Zealand
albino
rabbits,
male
squirrel
monkeys
and
purebred
male
beagle
dogs
Route
of
administration:
Inhalation
Exposure
period:
54,
90
or
114­
days
Frequency
of
treatment:
Repeated
dose
or
continuous
exposures
Dose:
155
(
221
ppm)
or
770
(
1100
ppm)
mg/
m3
(
repeated
dose)
127
(
181
ppm),
262
(
374
ppm),
455
(
650
ppm),
470
(
671
ppm)
mg/
m3
(
continuous
dose)
40
mg/
m3
(
continuous
dose)
Control
group:
Yes
[
X];
No
[
];
No
data
[
]
NOEL:
See
results
LOEL:
See
results
Results:
No
mortality
occurred
in
any
species
exposed
to
either
155
or
770
mg/
m3
in
the
repeated
dose
studies.
In
the
770
mg/
m3
exposure,
mild
to
moderate
lacrimation
and
dyspnea
were
evident
in
the
rabbits
and
dogs
in
the
first
week,
but
symptoms
disappeared
by
the
second
week.
In
rats
and
guinea
pigs,
the
lungs
showed
nonspecific
inflammatory
changes.
In
the
continuous
exposure
studies
with
rats,
no
mortality
or
other
treatment
related
effects
were
observed
at
127
mg/
m3.
No
mortality
was
observed
at
262
mg/
m3,
although
about
25%
of
the
rats
had
mild
nasal
discharge.
Continuous
exposure
of
rats
to
455
mg/
m3
resulted
in
the
death
of
50
of
51
rats
by
day
65.
All
showed
mild
signs
of
dyspnea
and
nasal
irritation.
Continuous
exposure
of
rats
to
470
mg/
m3
resulted
in
the
mortality
of
13
of
515
rats
and
4
of
15
guinea
pigs.
Marked
eye
irritation
was
noted
in
dogs
and
rabbits.
In
a
separate
experiment,
all
species
were
exposed
to
a
continuous
concentration
at
40
mg/
m3
for
114
days.
No
mortality
or
signs
of
toxicity
were
noted
in
any
of
the
animals.
Observations
at
necropsy
were
normal,
and
no
treatment
related
histopathological
findings
were
observed.
Method:
In
repeated
exposure
studies,
there
were
30
8­
hr/
day,
5­
day/
week
exposures.
In
the
continuous
exposure
studies,
rats
were
exposed
24
hours/
day
for
90
days.
In
separate
97
Ammonia
(
CAS
No.
7664­
41­
7)
experiments,
all
species
were
exposed
continuously
for
114
days.
The
rate
of
air
flow
to
the
inhalation
chambers
was
maintained
at
1.2
m3/
min
at
a
temperature
of
77
°
F.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonium
hydroxide
(
NH4OH)
Reference:
Coon,
R.
A.,
Jones,
R.
A.,
Jenkins,
Jr.,
L.
J.,
and
Siegel,
J.
1970.
Animal
inhalation
studies
on
ammonia,
ethylene,
glycol,
formaldehyde,
dimethylamine,
and
ethanol.
Toxicol.
Appl.
Pharmacol.
16:
646­
655.

(
b)
Species/
strain:
White
rats
Sex:
Female
[
];
Male
[
];
Male/
Female
[
];
No
data
[
X]
Route
of
administration:
Inhalation
Exposure
period:
3
months
Frequency
of
treatment:
25
or
60­
minutes
every
48­
hours
Dose:
30
and
100
mg/
m3
(
43
and
143
ppm)
Control
group:
Yes
[
X];
No
[
];
No
data
[
]
NOEL:
30
mg/
m3
LOEL:
100
mg/
m3
Results:
At
100
mg/
m3
there
was
mild
leucocytosis.
However,
there
were
no
differences
from
control
with
regard
to
oxygen
consumption,
neuromuscular
excitation
threshold,
heart
rate,
blood
sugar,
blood
residual
nitrogen
and
total
serum
protein.
No
effects
were
reported
at
the
low
dose
level.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Unspecified
ammonia
gas
Reference:
Propkopieva,
A.
S.
and
Yushkov,
G.
G.
1975.
Toxicology
of
ammonia
in
animals
repeatedly
exposed
for
short
lengths
of
time.
Gig.
Tr.
Prof.
Zabol.
(
Russian)
9:
54­
55.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
In
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.

(
c)
Species/
strain:
Sherman
and
Fisher
rats
Sex:
Female
[
];
Male
[
];
Male/
Female
[
];
No
data
[
X]
Route
of
administration:
Inhalation
Exposure
period:
75­
days
Frequency
of
treatment:
Not
specified
Dose:
average
concentration
of
105
mg/
m3
(
150
ppm)
Control
group:
Yes
[
X];
No
[
];
No
data
[
]
NOEL:
See
results
LOEL:
See
results
Results:
Histological
changes
in
the
olfactory
and
respiratory
epithelia
of
the
nasal
cavity
were
similar
for
all
exposed
rats,
showing
increased
thickness,
pyknotic
nuclei,
and
hyperplasia.
The
submucosa
was
oedematous
with
marked
dilation
of
the
small
vessels.
Lesions
decreased
posteriorly.
98
Ammonia
(
CAS
No.
7664­
41­
7)
Method:
Rats
were
exposed
via
inhalation
for
75
days
to
ammonia
from
natural
sources.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
gas
(
NH3)
Reference:
Broderson,
J.
R.,
Lindsey,
J.
R.
and
Cranford,
J.
E.
1976.
The
role
of
environmental
ammonia
in
respiratory
mycoplasmosis
of
rats.
Am.
J.
Pathol.
85:
115­
130.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
d)
Species/
strain:
Rat
Sex:
Female
[
];
Male
[
X];
Male/
Female
[
];
No
data
[
]
Route
of
administration:
Inhalation
Exposure
period:
Up
to
8­
weeks
Frequency
of
treatment:
Continuous
Dose:
350
mg/
m3
(
500
ppm)
Control
group:
Yes
[
X];
No
[
];
No
data
[
]
NOEL:
See
results
LOEL:
See
results
Results:
The
animals
were
sacrificed
after
different
times
of
exposure
to
establish
a
time
dependency
of
the
effects.
Nasal
irritation
began
on
the
4th
day
of
exposure.
After
3
weeks,
the
exposed
rats
showed
nasal
irritation
and
inflammation
of
the
upper
respiratory
tract
but
no
effects
were
observed
in
the
bronchioles
and
alveoli.
After
8
weeks,
none
of
these
inflammatory
lesions
were
present.
Method:
Twenty
seven
young
male
rats
were
exposed
to
a
continuous
atmospheric
concentration
of
ammonia.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
gas
(
NH3)
Reference:
Richard,
D.,
Bouley,
G.
and
Boudene,
C.
1978.
Effets
de
l'inhalation
continue
d'ammoniac
chez
the
rat
et
la
souris.
Bull.
Eur.
Physiopathol.
Resp.
14:
573­
582.
(
Original
in
French.)
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
e)
Species/
strain:
Sherman
and
Fisher
rats
Sex:
Female
[
];
Male
[
];
Male/
Female
[
];
No
data
[
X]
Route
of
administration:
Inhalation
Exposure
period:
35­
days
Frequency
of
treatment:
Not
specified
Dose:
175
mg/
m3
(
250
ppm)
Control
group:
Yes
[
X];
No
[
];
No
data
[
]
NOEL:
See
results
LOEL:
See
results
Results:
Histological
changes
in
the
olfactory
and
respiratory
epithelia
of
the
nasal
cavity
were
similar
in
all
exposed
rats,
showing
99
Ammonia
(
CAS
No.
7664­
41­
7)
increased
thickness,
pyknotic
nuclei
and
hyperplasia.
The
submucosa
was
oedematous
with
marked
dilation
of
small
vessels.
Lesions
decreased
posteriorly.
Method:
Rats
were
exposed
via
inhalation
for
35
days
to
purified
ammonia.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
gas
(
NH3)
Reference:
Broderson,
J.
R.
et
al.
1976.
Am.
J.
Pathol.
85:
115­
130.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
f)
Species/
strain:
Guinea
pig
Sex:
Female
[
];
Male
[
X];
Male/
Female
[
];
No
data
[
]
Route
of
administration:
Inhalation
Exposure
period:
18­
weeks
Frequency
of
treatment:
6
hours/
day;
5
days/
week
Post
exposure
observation
period:
Dose:
About
119
mg/
m3
(
170
ppm)
[
range
98­
140
mg/
m3
(
140­
200)
ppm]
Control
group:
Yes
[
X];
No
[
];
No
data
[
]
NOEL:
See
results
LOEL:
See
results
Results:
There
were
no
significant
findings
after
6
and
12
weeks.
In
animals
sacrificed
after
18
weeks,
there
was
relatively
mild
but
definite
congestion
of
the
liver,
spleen,
and
kidneys
with
degenerative
changes
in
the
adrenal
glands,
and
hemosiderosis
in
the
spleen
indicating
hematotoxicity.
There
was
cloudy
swelling
in
the
epithelium
of
the
proximale
tubules
of
the
kidney
as
well
as
albumin
precipitation
in
the
lumen
with
some
casts.
Method:
Twelve
male
guinea
pigs
(
plus
6
controls)
were
exposed
to
anhydrous
ammonia
gas
released
into
the
air
of
an
exposure
chamber.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Anhydrous
ammonia
gas
(
NH3)
Reference:
Weatherby,
J.
H.
1952.
Chronic
toxicity
of
ammonia
fumes
by
inhalation.
Proc.
Soc.
Exp.
Biol.
Med.
81:
300­
301.

*
5.5
GENETIC
TOXICITY
IN
VITRO
A.
BACTERIAL
TEST
(
a)
Type:
Bacterial
gene
mutation
assay
System
of
testing:
Salmonella
typhimurium
and
E.
coli
Concentration:
Up
to
25,000
ppm
100
Ammonia
(
CAS
No.
7664­
41­
7)
Metabolic
activation:
With
[
];
Without
[
];
With
and
without
[
X];
No
data
[
]
Results:
Cytotoxicity
conc:
With
metabolic
activation:
25,000
ppm
Without
metabolic
activation:
25,000
ppm
Genotoxic
effects:
+
?
­
With
metabolic
activation:
[
]
[
]
[
X]
Without
metabolic
activation:
[
]
[
]
[
X]
Method:
The
cells
were
exposed
to
concentrations
of
the
ammonia
gas
up
to
25,000
ppm.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
gas
(
NH3)
Remarks:
With
and
without
liver
metabolic
activation
system.
Reference:
Shimizu
H.
et
al.
1985.
Jap.
J.
Ind.
Health.
27:
400.
(
cited
in
BIBRA
1995).

(
b)
Type:
Bacterial
gene
mutation
assay
System
of
testing:
Salmonella
and
Saccharomyces
Remarks:
WHO
and
Clement
report
that
ammonium
sulfate
was
found
to
be
non­
mutagenic
in
studies
performed
by
Litton
Bionetics,
Inc.
Reference:
Litton
Bionetics,
Inc.
1975.
Mutagenic
Evaluation
of
Compound
FDA
73­
42
Ammonium
Sulfate,
Granular,
Food
Grade,
Washington,
D.
C.
Litton
Bionetics.
(
NTIS
PB­
245506).
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.

B.
NON­
BACTERIAL
IN
VITRO
TEST
Type:
Cytogenetic
assay
System
of
testing:
Chick
fibroblasts
Concentration:
Unspecified
Metabolic
activation:
With
[
];
Without
[
];
With
and
without
[
];
No
data
[
X]
Method:
Not
specified
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonia
gas
(
NH3)
Remarks:
The
original
reference
reported
that
ammonia
induced
clumping
of
chromosomes,
arrested
spindle
formation,
and
induced
polyploidy
in
chick
fibroblasts.
The
original
study
was
reported
in
1932.
Reference:
Rosenfeld,
M.
1932.
Experimental
modification
of
mitosis
by
ammonia.
Arch.
Exp.
Zellforsch.
Gewebezuecht.
14:
1.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
101
Ammonia
(
CAS
No.
7664­
41­
7)
*
5.6
GENETIC
TOXICITY
IN
VIVO
Type:
Drosophila
mutagenicity
test
Species/
strain:
Drosophila
melanogaster
Remarks:
WHO,
BIBRA,
and
Clement
all
report
early
studies
suggesting
mutagenic
activity
occurred
upon
exposure
to
ammonia.
However,
this
activity
was
only
evident
at
doses
that
killed
98%
of
the
flies,
which
casts
significant
doubt
on
the
validity
of
the
results.
The
Clement
report
concludes
that
there
are
no
data
to
show
that
ammonia
is
mutagenic
in
mammals.
Reference:
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.
BIBRA.
1995.
Toxicology
Profile:
Ammonia.
BIBRA
International.

5.7
CARCINOGENICITY
(
a)
Species/
strain:
Swiss
and
C3H
mice
Sex:
Female
[
];
Male
[
];
Male/
female
[
X];
No
data
[
]
Route
of
administration:
Drinking
water
Exposure
period:
Life­
time
Frequency
of
treatment:
Ad
libitum
Control
group:
Yes
[
];
No
[
];
No
data
[
X];
Concurrent
no
treatment
[
];
Concurrent
vehicle
[
];
Historical
[
]
Results:
Life­
long
ingestion
in
drinking
water
did
not
produce
any
carcinogenic
effects,
and
had
no
effect
on
the
spontaneous
development
of
aderiocarcinoma
of
the
breast
in
C3H
females,
a
characteristic
of
this
strain.
GLP:
Yes
[
]
No
[
X]
?
[
]
Test
substance:
Ammonium
hydroxide
(
NH4OH)
Doses:
Unspecified
Remarks:
The
compound
tested
was
NH4OH,
which
forms
an
equilibrium
with
NH3
when
ammonia
is
dissolved
in
water.
No
further
information
is
given
in
source.
Reference:
Toth,
B.
1972.
Hydrazine,
methylhydrazine
and
methylhydrazine
sulfate
carcinogenesis
in
Swiss
mice.
Int.
J.
Cancer.
9:
109.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
b)
Species/
Strain:
All
102
Ammonia
(
CAS
No.
7664­
41­
7)
Remarks:
WHO
and
Clement
note
that
there
is
no
reliable
evidence
indicating
that
ammonia
is
carcinogenic.
BIBRA
notes
a
poorly
reported
study
(
Gaafar
et
al
1992)
in
which
one
of
50
adult
mice
exposed
15
minutes/
day,
6
days/
week
for
8
weeks
to
"
ammonia
vapour"
(
derived
from
a
12%
ammonia
solution,
but
not
further
specified)
developed
nasal
cancer.
However,
there
was
a
low
incidence
of
other
microscopic
changes
in
the
nasal
tissues
suggestive
of
a
tumorigenic
response.
Reference:
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.
BIBRA.
1995.
Toxicology
Profile:
Ammonia.
BIBRA
International.

(
c)
Species/
Strain:
Humans
Remarks:
Epidemiological
studies
by
Bittershol
that
have
been
widely
cited,
have
shown
excess
incidence
of
cancers
in
manufacturing
plants.
However,
the
study
has
methodological
flaws
and
confounding
influences
from
carcinogens
in
the
ambient
environment.
Reference:
Bittershol,
G.
(
1971)
Epidemiologic
study
on
cancer
of
workers
in
a
chemical
plant.
Arch.
Gesh.
38:
198­
209
(
Original
in
German).
Clement
Associates,
Inc.
1990.
Health
Effects
Assessment
for
Ammonia.
Prepared
for
The
Fertilizer
Institute,
Washington,
D.
C.

*
5.8
TOXICITY
TO
REPRODUCTION
Type:
Fertility
[
];
One
generation
study
[
X];
Two
generation
study
[
];
Other
[
]
Species/
strain:
Yorkshire
x
Hampshire
x
Chester
White
gilts
(
a
young
sow)
Sex:
Female
[
];
Male
[
];
Male/
Female
[
X];
No
data
[
]
Route
of
Administration:
Inhalation
of
ammonia
in
air
environment
Exposure
Period:
6­
weeks;
10­
weeks
Frequency
of
treatment:
Continuous
Postexposure
observation
period:
Premating
exposure
period:
male:
female:
6
weeks
Duration
of
the
test:
6
weeks
Doses:
mean
7
ppm
NH3,
mean
35
ppm
NH3
Control
group:
Yes
[
];
No
[
X];
No
data
[
];
Concurrent
no
treatment
[
];
Concurrent
vehicle
[
];
Historical
[
]
NOAEL
Prenatal:
See
results
NOAEL
F1
Offspring:
See
results
NOAEL
F2
Offspring:
See
results
103
Ammonia
(
CAS
No.
7664­
41­
7)
Results:
At
the
end
of
two
weeks,
gilts
in
the
moderate
exposure
group
weighed
less
than
those
in
the
low
exposure.
After
2
weeks
gilts
acclimated
and
the
Mean
Daily
Gain
(
MDG)
was
similar
for
the
rest
of
the
experiment.
The
gilts
sacrificed
at
6
weeks
showed
that
the
animals
in
the
low
exposure
were
heavier.
At
day
30
of
gestation,
number
of
fetuses,
fetal
length,
and
fetusto
corpus
luteum
ratio
were
all
similar
between
the
two
groups.
Method:
From
2­
4.5
months
of
age,
gilts
were
exposed
naturally
to
Mycoplasma
hyponeumoniae
and
Pasteurella
multocida,
which
cause
enzootic
pneumonia
and
atrophic
rhinitis,
respectively.
At
4.5
months
of
age,
the
gilts
were
moved
to
one
of
two
rooms
and
exposed
to
either
low
(
mean
7
ppm)
or
moderate
(
mean
36
ppm)
aerial
concentrations
of
ammonia.
Each
exposure
group
consisted
of
40
individuals.
In
the
room
with
low
ammonia
concentration,
manure
was
flushed
weekly
to
maintain
a
0.3
m
depth.
In
the
room
with
moderate
ammonia
concentration,
manure
accumulated
to
0.48
m
depth.
Moderate
aerial
ammonia
concentration
was
obtained
initially
and
maintained
by
adding
anhydrous
ammonia
from
a
steel
tank.
Mean
Daily
Gain
(
MDG)
was
determined
by
weighing
the
gilts
biweekly.
Half
the
gilts
from
each
exposure
concentration
were
sacrificed
after
6
weeks.
The
remaining
gilts
were
maintained
in
their
respective
environments,
exposed
daily
to
mature
boars,
bred
at
first
estrus,
and
sacrificed
at
day
30
of
gestation.
GLP:
Yes
[
]
No
[
]
?
[
X]
Test
substance:
Ammonia
(
NH3)
obtained
by
flushing
of
manure
pits
weekly.
Remarks:
These
data
indicate
that
exposure
of
gilts
to
mean
aerial
ammonia
concentrations
of
36
ppm
depressed
MDG
for
2
weeks
but
failed
to
alter
onset
of
puberty
or
litter
size
through
day
30
of
gestation.
(
relative
to
exposure
to
7ppm).
Reference:
Diekman,
M.
A.,
Scheidt,
A.
B.,
Sutton,
A.
L.,
Green,
M.
L.,
Clapper,
J.
A.,
Kelly,
D.
T.,
and
Van
Alstine,
W.
G.
1993.
Growth
and
reproductive
performance,
during
exposure
to
ammonia,
of
gilts
afflicted
with
pneumonia
and
atrophic
rhinitis.
Am.
J.
Vet.
Res.
54(
12):
2128­
2131.

*
5.9
DEVELOPMENTAL
TOXICITY/
TERATOGENICITY
Remarks:
No
specific
studies
on
developmental
or
teratorgenic
effects
were
identified.

5.10
OTHER
RELEVANT
INFORMATION
A.
SPECIFIC
TOXICITIES
(
NEUROTOXICITY,
IMMUNOTOXICITY
etc.)

B.
TOXICODYNAMICS,
TOXICOKINETICS
(
a)
Type:
Animal
[
X];
Aquatic
[
];
Plant
[
];
Terrestrial
[
];
104
Ammonia
(
CAS
No.
7664­
41­
7)
Other
[
]
Results:
At
the
2
lowest
concentrations,
there
was
no
increase
in
bloodammonia
However,
after
8
hours
at
220
and
826
mg/
m3
unionized
NH3,
significant
increases
of
3.26
and
4.18
mg
NH3/
L
were
noted
indicating
pulmonary
absorption
of
ammonia.
These
levels
declined
over
time
at
higher
concentrations,
suggesting
that
compensation
was
occurring.
Findings
suggest
that
environmental
ammonia
concentrations
found
in
animal
holding
rooms
would
have
minimal
adverse
effects
in
healthy
rats.
Remarks:
Four
groups
of
rats,
8
per
group,
were
exposed
to
average
ammonia
concentrations
of
11,
23,
220
or
826
mg/
m3
(
15,
32,
310,
or
1,157
ppm)
for
24
hours.
Reference:
Schaerdel,
A.
D.,
White,
W.
J.,
Lang,
C.
M.,
Dvorchik,
B.
H.,
and
Bohner,
K.
1983.
Localized
and
systemic
effects
of
environmental
ammonia
in
rats.
Lab.
Anim.
Sci.
33(
1):
40­
45.

(
b)
Type:
Results:
Remarks:
Mucosal
cell
migration
rate
appears
to
be
accelerated
by
longterm
administration
of
0.01%
ammonia,
especially
in
the
antrum.
The
effect
of
ammonia
on
cell
kinetics
differs
between
the
antral
and
body
mucosa.
The
toxicity
of
NH3­
NH4
+
solution
to
rat
gastric
mucosa
was
enhanced
with
an
increase
in
pH
of
the
solution.
The
amount
of
un­
ionized
NH3
increases
with
increasing
pH,
and
it
causes
cell
damage.
In
the
body
mucosa,
which
is
an
acid­
secreting
mucosa,
the
cytotoxicity
of
ammonia
is
lessened
by
secreted
hydrochloric
acid
to
form
NH4Cl.
The
pH
in
the
antral
mucosa
is
higher
than
that
on
the
body
mucosa,
which
may
explain
the
different
effects
of
ammonia
on
the
gastric
mucosal
cell
migration
rate.
References:
Tsujii,
M.,
Kawano,
S.,
Tsuji,
S.,
Ito,
T.,
Nagano,
K.,
Sasaki,
Y.,
Hayashi,
N.,
Fusamoto,
H.,
and
Kamada,
T.
1993.
Cell
kinetics
of
mucosal
atrophy
in
rat
stomach
induced
by
longterm
administration
of
ammonia.
Gastroenterol.
104:
796­
801.

*
5.11
EXPERIENCE
WITH
HUMAN
EXPOSURE
(
a)
Type:
Occupational
exposure
Results:
There
were
no
differences
in
symptoms,
sense
of
smell,
acute
changes
in
lung
function
during
exposure,
or
changes
in
baseline
lung
function
in
exposed
workers
compared
to
control
workers.
There
was
no
relationship
demonstrated
between
the
level
of
exposure
to
ammonia
(
average
of
9.2
ppm)
and
acute
changes
in
lung
function
over
the
work
shift.
No
chronic
effects
on
lung
function
that
could
be
related
to
the
length
of
exposure
were
demonstrated.
105
Ammonia
(
CAS
No.
7664­
41­
7)
Remarks:
The
chronic
effects
of
ammonia
on
industrial
workers
to
levels
less
than
50
ppm
were
assessed.
The
study
also
examined
the
acute
effects
of
ammonia
exposure
on
the
respiratory
system,
eyes,
and
skin.
A
total
of
52
soda
ash
plant
workers,
6
maintenance
workers,
and
35
control
workers
were
assessed.
All
participants
were
male,
mean
age
40.5
years,
and
plant
tenure
approximately
15
years.
Exposed
workers
were
assessed
on
2
workdays;
on
the
first
and
last
workdays
of
their
workweek.
The
study
was
carried
out
over
a
period
of
one
week.
Maintenance
workers
were
assessed
on
one
workday
in
the
middle
of
their
workweek.
The
control
group
was
assessed
twice
on
two
separate
days
during
the
same
week.
All
participants
completed
a
questionnaire
regarding
past
occupational
exposures,
working
conditions,
smoking
history,
and
respiratory
symptoms
and
eye
and
skin
complaints.
Each
participant's
sense
of
smell
was
assessed
at
the
beginning
and
end
of
the
workweek.
Spriometry
was
performed
at
the
beginning
and
end
of
each
work
shift
on
both
test
days
so
that
each
worker
had
four
tests
done.
The
average
concentration
of
ammonia
to
which
workers
were
exposed
during
their
work
shifts
was
determined
using
NIOSH­
recommended
procedures.
Exposed
and
control
workers
were
sampled
over
one
work
shift.
The
average
sample
collection
period
was
8.4
hours.
The
mean
time­
weighted
average
(
TWA)
ammonia
exposure
of
the
exposed
group
was
9.2
ppm,
0.3
ppm
for
the
control
group.
Three
workers
were
exposed
to
TWA
concentrations
in
excess
of
25
ppm.
Reference:
Holness,
D.
G.,
Purdham,
J.
T.,
and
Nethercott,
J.
R.
1989.
Acute
and
chronic
respiratory
effects
of
occupational
exposure
to
ammonia.
Am.
Ind.
Hyg.
Assoc.
J.
50(
12):
646­
650.

(
b)
Type:
Inhalation
exposure
by
human
volunteers
Results:
After
acclimation,
continuous
exposure
to
100
ppm,
with
occasional
excursions
to
200
ppm,
is
easily
tolerated
with
no
observed
effect
on
general
health.
Remarks:
Six
unacclimated
male
and
female
volunteers
were
exposed
six
hours
per
day
over
a
six
week
period
to
concentrations
of
25,
50,
and
100
ppm
ammonia
in
an
industrial
environment,
under
strict
medical
surveillance.
Inurement
to
eye,
nose,
and
throat
irritation
was
demonstrated
after
two
to
three
weeks
in
addition
to
short­
term
subjective
adaptation.
There
were
no
significant
differences
between
subjects
or
controls
on
common
biological
indicators,
in
physical
examinations,
or
in
performance
of
normal
job
duties.
References:
Ferguson,
W.
S.,
Koch,
W.
C.,
Webster,
B.
A.,
and
Gould,
J.
R.
1977.
Human
physiological
response
and
adaptation
to
ammonia.
J.
Occup.
Med.
19(
5):
319­
326.

(
c)
Type:
Inhalation
exposure
by
human
volunteers.
106
Ammonia
(
CAS
No.
7664­
41­
7)
Results:
Concentrations
of
72
ppm
or
higher
caused
discomfort
and
probably
would
not
be
tolerated
by
some
human
subjects.
Concentrations
of
50
ppm
or
less
could
be
tolerated
for
at
least
five
minutes
and
probably
much
longer.
The
level
of
50
ppm
appeared
to
be
below
the
threshold
concentration
causing
discomfort.
Remarks:
Ten
human
subjects
were
exposed
for
five
minutes
to
concentrations
of
32,
50,
72,
or
134
ppm
in
a
dynamic
chamber.
The
results
indicated
irritation
at
72
or
134
ppm
with
more
irritation
at
the
higher
level.
There
was
some
dryness
of
the
nose
in
one
or
two
subjects
exposed
to
32
or
50
ppm,
but
there
was
not
a
definite
irritation
at
these
levels.
Reference:
Keplinger,
M.
L.
1973.
Report
to
International
Institute
of
Ammonia
Refrigeration:
Irritation
Threshold
Evaluation
Study
With
Ammonia.
Industrial
BIOTEST
Laboratories,
Inc.

(
d)
Type:
Inhalation
exposure
by
human
volunteers
Results:
Silverman
et
al.
(
1949)
reported
on
7
human
volunteers
exposed
to
a
concentration
of
300
mg/
m3
(
500
ppm)
ammonia
for
30
min
using
an
oral­
nasal
mask.
All
7
experienced
upper
respiratory
irritation,
which
lasted
up
to
24
hours
in
2
of
the
volunteers.
Two
subjects
experienced
marked
lachrymation,
in
spite
of
the
exposure
being
by
oro­
nasal
mask.
The
average
respiratory
minute
volume
increased
markedly
compared
with
control
values,
and
in
the
5
subjects
in
which
minute­
by­
minute
expired
volumes
were
measured,
there
was
a
marked
cyclical
variation
in
minute
volume
with
a
period
of
4­
7
min.
No
coughing
was
noted.
After
exposure,
respiratory
minute
volumes
fell
to
levels
below
the
pre­
exposure
rate,
but
returned
to
pre­
exposure
values
within
5
min
of
exposure.
Ammonia
retention
decreased
progressively
until
an
equilibrium
of
24%
retention
(
ranging
from
4
to
30%)
was
reached
at
approximately
19
min
(
range
10­
27
min).
The
indices
of
nitrogen
metabolism
(
BUN,
NPN,
urine­
urea,
and
urine­
ammonia)
remained
normal.
The
carbon
dioxide
combining
power
did
not
change.
Remarks:
Seven
male
volunteers
were
exposed
to
350
mg/
m3
(
500
ppm)
NH3
for
30
minutes.
Reference:
Silverman,
L.,
Whittenberger,
J.
L.,
and
Muller,
J.
1949.
Physiological
response
of
man
to
ammonia
in
low
concentrations.
J.
Ind.
Hyg.
Toxicol.
31:
74­
78.
In
World
Health
Organization
(
WHO).
1986.
Ammonia
 
Environmental
Health
Criteria
54.
Geneva:
International
Programme
on
Chemical
Safety.

(
e)
Type:
Inhalation
exposure
by
human
volunteers.
Results:
No
effect
on
vital
capacity
(
VC),
forced
expiratory
volume
[
1
sec]
(
FEV1),
or
forced
inspiratory
volume
[
1
sec]
(
FIV1).
107
Ammonia
(
CAS
No.
7664­
41­
7)
Remarks:
Sixteen
volunteers,
eight
experts
(
29.53
yr)
and
eight
nonexperts
(
students,
18­
30
yr),
were
exposed
for
two
hours
to
ammonia
in
concentrations
of
50,
80,
110
and
140
ppm.
None
of
the
test
subjects
were
considered
to
be
hypersusceptible
to
non­
specific
irritants
or
demonstrated
a
decrease
in
respiratory
function.
Before
leaving
the
test
chamber,
every
subject
described
at
least
one
symptom
as
"
unbearable";
three
times
this
was
irritation
of
throat,
two
times
urge
to
cough,
and
one
time
each
for
smell,
irritation
of
eyes,
nose
or
breast,
headache,
and
general
discomfort.
All
subjects
perceived
a
hypo­
esthesia
of
the
exposed
skin
and
two
noted
excessive
lacrimation.
Reference:
Verberk,
M.
M.
1977.
Effects
of
ammonia
in
volunteers.
Arch.
Occup.
Environ.
Hlth.
39:
73­
81.

(
f)
Remarks:
As
reported
in
NRC
(
1979),
gaseous
ammonia
can
elicit
the
following
effects
at
the
concentration
specified.
400
ppm
(
in
air)
=
Immediate
throat
irritation
700
ppm
(
in
air)
=
Eye
irritation
 
1700
ppm
(
in
air)
=
Coughing
2500
­
6500
ppm
(
in
air)
=
Life
threatening
after
0.5
hour
500
­
10000
ppm
(
in
air)
=
Mortality
Reference:
National
Research
Council
(
NRC).
1979.
Ammonia.
Subcommittee
on
Ammonia.
Committee
on
Medical
and
Biological
Effects
of
Pollutants.
Division
of
Medical
Sciences,
Assembly
of
Life
Sciences.
National
Research
Council.
Baltimore:
University
Park
Press.
NTIS
No.
PB
278­
027.
108
Ammonia
(
CAS
No.
7664­
41­
7)
6.
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1992.
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International
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In
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Ammonia­
Environmental
Health
Criteria
54.
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120
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Zischke,
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231.
APPENDIX
A
­
SIDS
DATA
AVAILABILITY
SUMMARY
Ammonia
(
CAS
No.
7664­
41­
7)
SIDS
DATA
AVAILABILITY
SUMMARY
DATE:
January
27,
2003
Ammonia
CAS
No:
7664­
41­
7
Information
OECD
Study
GLP
Other
Study
Estimated
Method
Acceptable
SIDS
Testing
Recommended
STUDY
Y/
N
Y/
N
Y/
N
Y/
N
Y/
N
Y/
N
Y/
N
PHYSICAL­
CHEMICAL
DATA
2.1
2.2
2.3
2.4
2.5
2.6
2.12
Melting
Point
Boiling
Point
Density
Vapour
Pressure
Partition
Coefficient
Water
Solubility
pH
and
pKa
Values
Oxidation:
Reduction
Potential
Y
Y
Y
Y
Y
Y
Y
Y
N
N
N
N
Y
N
N
N
N
N
N
N
Y
N
N
N
N
N
N
N
N
N
Y
N
N
N
N
N
N
N
N
N
Y
Y
Y
Y
Y
Y
Y
Y
N
N
N
N
N
N
N
N
OTHER
P/
C
STUDIES
RECEIVED
Y
N
N
Y
N
Y
N
ENVIRONMENTAL
FATE
and
PATHWAY
3.1.1
3.1.2
3.2
3.3
3.5
Photodegradation
Stability
in
Water
Monitoring
Data
Transport
and
Distribution
Biodegradation
Y
Y
Y
Y
Y
N
N
N
N
N
N
N
N
N
N
N
Y
N
Y
N
N
N
N
N
N
Y
Y
Y
Y
Y
N
N
N
N
N
OTHER
ENV
FATE
STUDIES
RECEIVED
Y
N
N
Y
N
Y
N
ECOTOXICITY
4.1
4.2
4.3
4.5.1
4.5.2
4.6.1
4.6.2
4.6.3
Acute
Toxicity
to
Fish
Acute
Toxicity
to
Daphnia
Toxicity
to
Algae
Chronic
Toxicity
to
Fish
Chronic
Toxicity
to
Daphnia
Toxicity
to
Soil
Dwelling
Organisms
Toxicity
to
Terrestrial
Plants
Toxicity
to
Birds
Y
Y
Y
Y
Y
N
Y
Y
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
Y
Y
Y
Y
Y
N
Y
Y
N
N
N
N
N
N
N
N
Y
Y
Y
Y
Y
­
Y
Y
N
N
N
N
N
N
N
N
OTHER
ECOTOXICITY
STUDIES
RECEIVED
Y
N
N
Y
N
Y
N
TOXICITY
5.1.1
5.1.2
5.1.3
5.4
5.5
5.6
5.8
5.9
5.11
Acute
Oral
Acute
Inhalation
Acute
Dermal
Repeated
Dose
Genetic
Toxicity
in
vitro
.
Gene
mutation
.
Chromosomal
aberration
Genetic
Toxicity
in
vivo
Reproduction
Toxicity
Development/
Teratogenicity
Human
Experience
N
Y
N
Y
Y
Y
Y
Y
N
Y
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
N
Y
N
Y
Y
Y
Y
Y
N
Y
N
N
N
N
N
N
N
N
N
N
­
Y
­
Y
Y
Y
Y
Y
­
Y
N
N
N
N
N
N
N
N
N
N
OTHER
TOXICITY
STUDIES
RECEIVED
Y
N
N
Y
N
Y
N
APPENDIX
B
­
COMPREHENSIVE
BIBLIOGRAPHY
COMPREHENSIVE
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