Document ID: EPA-HQ-OPPT-2002-0027-0048
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2002-06-13T04:00Z

Phosphorus
trichloride
PROPOSED
1
:
05/
2002
United
States
Environmental
Protection
Agency
Office
of
Pollution
Prevention
and
Toxics
PHOSPHORUS
TRICHLORIDE
(CAS
Reg.
No.
007719­
12­
2)

PROPOSED
ACUTE
EXPOSURE
GUIDELINE
LEVELS
(AEGLs)

"PUBLIC
DRAFT"

Federal
Register
­
May
2002
PROPOSED
1:
05/
2082
PHOSPHORUS
TRICHLORIDE
(CAS
Reg.
No.
007719­
12­
2)

PROPOSED
ACUTE
EXPOSURE
GUIDELINE
LEVELS
(AEGLs)

Oak
Ridge
National
Laboratory,
managed
by
UT­
Battelle,
LLC,
for
the
U.
S.
Dept.
of
Energy
under
contract
DE­
AC05­
000R22725.

2
PHOSPHORUS
TRICHLORIDE
PREFACE
PROPOSED
1:
092002
Under
the
authority
of
the
Federal
Advisory
Committee
Act
(FACA)
P.
L.
92­
463
of
1972,
the
National
Advisory
Committee
for
Acute
Exposure
Guideline
Levels
for
Hazardous
Substances
(NAC/
AEGL
Committee)
has
been
established
to
identify,
review
and
interpret
relevant
toxicologic
and
other
scientific
data
and
develop
AEGLs
for
%ligh
priority,
acutely
toxic
chemicals.

AEGEs
represent
threshold
exposure
limits
for
the
general
public
and
are
applicable
to
emergency
exposure
periods
ranging
from
10
minutes
to
8
hours.
AEGL­
2
and
AEGL­
3
levels,
and
AEGL­
1
levels
as
appropriate,
will
be
developed
for
each
of
five
exposure
periods
(10
and
30
minutes,
1
hour,
4
hours,
and
8
hours)
and
will
be
distinguished
by
varying
degrees
of
severity
of
toxic
effects.
It
is
believed
that
the
recommended
exposure
levels
are
applicable
to
the
general
population
including
infants
and
children,
and
other
individuals
who
may
be
sensitive
and
susceptible.
The
three
AEGLs
have
been
defined
as
follows:

AEGL­
1
is
the
airborne
concentration
(expressed
as
ppm
or
mg/
m3)
of
a
substance
above
which
it
is
predicted
that
the
general
population,
including
susceptible
individuals,
could
experience
notable
discomfort,
irritation,
or
certain
asymptomatic,
non­
sensory
effects.
However,
the
effects
are
not
disabling
and
are
transient
and
reversible
upon
cessation
of
exposure.

AEGL­
2
is
the
airborne
concentration
(expressed
as
ppm
or
mg/
m3)
of
a
substance
above
which
it
is
predicted
that
the
general
population,
including
susceptible
individuals,
could
experience
irreversible
or
other
serious,
long­
lasting
adverse
health
effects,
or
an
impaired
ability
to
escape.

AEGL­
3
is
the
airborne
concentration
(expressed
as
ppm
or
mg/
m3)
of
a
substance
above
which
it
is
predicted
that
the
general
population,
including
susceptible
individuals,
could
experience
life­
threatening
health
effects
or
death.

Airborne
concentrations
below
the
AEGL­
1
represent
exposure
levels
that
can
produce
mild
and
progressively
increasing
but
transient
and
nondisabling
odor,
taste,
and
sensory
irritation
or
certain
asymptomatic,
nonsensory
effects.
With
increasing
airborne
concentrations
above
each
AEGL,
there
is
a
progressive
increase
in
the
likelihood
of
occurrence
and
the
severity
of
effects
described
for
each
corresponding
AEGL.
Although
the
AEGL
values
represent
threshold
levels
for
the
general
public,
including
sensitive
subpopulations,
such
as
infants,
children,
the
elderly,
persons
with
asthma,
and
those
with
other
illnesses,
it
is
recognized
that
certain
individuals,
subject
to
unique
or
idiosyncratic
responses,
could
experience
the
effects
described
at
concentrations
below
the
corresponding
AEGL.

...
111
3
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
092002
TABLE
OF
CONTENTS
...
PWlEFAGE
......................................................................
111
LISTOFAPPENDICES
............................................................
v
LISTOFTABLES
................................................................
v
EXECUTIVESUMMARY
.........................................................
vi
1
.
INTRODUCTION
.........................................................
1
2
.
HUMANTOXICITYDATA
.................................................
2
2.1
AcuteLethality
......................................................
2
2.2
NonlethalToxicity
...................................................
2
2.3
Epidemiologic
Studies
.................................................
4
2.4
DevelopmentaVReproductive
Toxicity
.....................................
4
2.4
Genotoxicity
........................................................
4
2.6
Carcinogenicity.
.....................................................
4
2.7
Summary
..........................................................
4
3
.
ANIMALTOXICITYDATA
.................................................
4
3.1
AcuteLethality
......................................................
4
3.1.1
Rats
........................................................
4
3.1.3
Cats
.........................................................
5
3.2.1
Rats
........................................................
5
6
3.2.3
Cats
........................................................
6
3.4
Genotoxicity
........................................................
6
3.6
Summary
..........................................................
7
3.1.2
Guinea
pigs
...................................................
5
3.2
Nonlethal
Toxicity
...................................................
5
3.2.2
Guineagigs
..................................................

3.3
DevelogmenWRegroductive
Toxicity
.....................................
6
3.5
Carcinogenicity
......................................................
6
...............................................
SPECIAL
CONSIDERATIONS
7
7
4.1
Metabolism
and
Disposition
............................................
4.2
Mechanism
of
Toxicity
................................................
7
4.3
Structure­
Activity
Relationships
..........................................
8
4.4
Other
Relevant
Information
.............................................
8
4.4.1
Species
Variability
..............................................
8
4.4.2
Concurrent
Exposure
Issues
......................................
8
iv
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
5
.
DATA
ANALYSIS
AND
PROPOSED
AEGL­
1
....................................
8
5.1
Summary
of
Human
Data
Relevant
to
AEGL­
1
...............................
8
5.2
SurnmaryofAnimalDataRelevanttoAEGL­
1
..............................
8
5.3
Derivation
of
AEGL­
1
................................................
8
6
.
DATA
ANALYSIS
AND
PROPOSED
AEGL­
2
...................................
9
6.1
Summary
of
Human
Data
Relevant
to
AEGL­
2
..............................
9
Summary
of
Animal
Data
Relevant
to
AEGL­
2
...............................
9
6.2
6.3
Derivation
of
AEGL­
2
...............................................
10
7
.
DATA
ANALYSIS
AND
PROPOSED
AEGL­
3
..................................
11
7.1
Summary
of
Human
Data
Relevant
to
AEGL­
3
..............................
11
7.2
Summary
of
Animal
Data
Relevant
to
AEGL­
3
.............................
11
7.3
Derivation
of
AEGL­
3
...............................................
1B
8
.
SUMMARY
OF
PROPOSED
AEGLS
.........................................
12
8.1
AEGL
Values
and
Toxicity
Endpoints
....................................
12
8.2
Comparison
with
Other
Standards
and
Criteria
.............................
13
8.3
Data
Adequacy
and
Research
Needs
.....................................
15
9
.
REFERENCESCITED
.....................................................
16
APPENDIX
A
(Derivation
of
AEGL
Values)
...........................................
APPENDIX
B
(Derivation
Summaries
for
Phosphorus
Trichloride
AEGL
Values)
...............
18
24
LIST
OF
TABLES
TABLE
1
.
Physical
and
Chemical
Data
for
Phosphorus
Trichloride
.......................
1
TABLE
2
.
Acute
Lethality
of
Phosphorus
Trichloride
in
Laboratory
Species
................
7
TABLE
3
.
AEGL­
1
for
Phosphorus
Trichloride
......................................
9
TABLE
4
.
AEGL­
2
for
Phosphorus
Trichloride
.....................................
10
TABLE
6
.
Extant
Standards
and
Guidelines
for
Phosphorus
Trichloride
..................
13
TABLE
5
.
AEGL­
3
for
Phosphorus
Trichloride
..............
:
......................
12
V
PHOSPHORUS
TRICHLORIDE
PROPOSED
I:
05!
2002
EXECUTIVE
S
W
R
Y
Phosphorus
trichloride
(CAS
no.
007719­
12­
2)
is
a
colorless,
clear
fuming
liquid
with
a
pungent,
irritating
odor.
In
the
presence
of
water,
the
chemical
decomposes
rapidly
in
a
highly
exothermic
reaction
to
phosphonic
acid,
hydrogen
chloride?
and
pyrophosphonic
acids.

No
acute
lethality
data
are
available
in
humans.
Qualitative
data
regarding
human
exposures
indicate
signs
and
symptoms
of
exposure
consistent
with
a
highly
irritating
chemical;
ocular
and
dermal
irritation,
respiratory
tract
irritation,
shortness
of
breath,
and
nausea.

Lethality
data
in
animals
are
available
for
rats,
cats,
and
guinea
pigs.
Cursory
studies
conducted
nearly
one
hundred
years
ago
in
Germany
provided
preliminary
data
on
lethal
and
nonlethal
effects
in
cats
and
guinea
pigs
following
various
treatment
regimens
with
inhaled
phosphorus
trichloride.
Although
results
of
the
studies
indicated
the
respiratory
tract
to
a
be
a
critical
target,
the
methods
and
results
of
these
studies
were
not
verifiable.
Weeks
et
al.
(1964)
reported
4­
hr
LC,,
values
of
104.5
ppm
and
50.1
ppm
for
rats
and
guinea
pigs,
respectively.
An
unpublished
study
by
Hazleton
Laboratories
(1
983)
identified
a
NOAEL
of
3.4
ppm
and
a
LOAEL
(histopathologic
changes
in
the
respiratory
tract)
of
1
1
pprn
following
repeated
exposure
(6
hrs/
day,
5
daydweek
for
four
weeks)
of
rats.
There
are
no
data
regarding
reproductive/
developmental
toxicity,
genotoxicity
,
or
carcinogenicity
of
phosphorus
trichloride.
Definitive
data
regarding
the
mechanism
of
action
of
phosphorus
trichloride
are
unavailable.
Decomposition
products
(hydrogen
chloride,
phosphonic
acid,
and
pyrophosphonic
acids)
are
responsible,
at
least
in
part,
for
the
contact
irritation
reported
by
humans,
and
the
irritation
and
tissue
damage
observed
in
animal
species.

The
concentration­
time
relationship
for
may
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
Cn
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5.
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
1
when
extrapolating
to
longer
time
points
using
the
c"
x
t
=
k
equation.
For
10­
minute
AEGL­
3
values
were
set
at
equivalence
to
the
30­
minute
values
due
to
uncertainties
in
extrapolating
from
the
experimental
exposure
durations
of
4
hours
and
greater.

Quantitative
data
consistent
with
AEGL­
1
effects
were
unavailable.
Occupational
exposures
of
humans
to
1.8­
3.6
ppm
for
2­
6
hours
and
exposure
of
rats
to
3.4
ppm
for
6
hours/
day,
5
days/
week
for
4
weeks
were
without
notable
effect.
These
data
can
be
considered
a
NOAEL
for
AEGL­
1
effects.
Because
they
were
derived
from
controlled
experiments,
the
AEGL­
1
values
were
based
upon
the
Hazleton
Laboratories
(1983)
report.
These
data
as
well
as
the
AEGL­
1
values
are
supported
by
the
human
experience
data
reported
by
Sassi
(1952).
The
interspecies
uncertainty
factor
was
limited
to
3
because
of
the
concordance
of
the
animal
data
with
the
human
experience
and
because
the
most
sensitive
species
tested
(guinea
pig)
was
only
about
2­
fold
more
sensitive.
The
intraspecies
uncertainty
factor
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociation.
Additional
reduction
of
the
AEGL­
1
values
would
be
inconsistent
with
available
human
and
animal
data
.

Information
consistent
with
AEGL­
2
effects
were
limited
to
an
occupational
exposure
report
and
a
multiple
exposure
study
with
rats.
For
occupational
exposures,
there
was
notable
irritation
following
2­
6
vi
6
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
hours
of
exposure
to
approximately
14­
27
ppm
phosphorus
trichloride
and
more
severe
but
reversible
irritation
following
exposures
of
1­
8
weeks.
Reports
providing
qualitative
information
but
no
exposure
terms
affirmed
the
potential
for
respiratory
tract
irritation
following
acute
exposures
to
phosphorus
trichloride.
Data
for
rats
showed
upper
respiratory
tract
involvement
following
multiple
exposures
over
4
weeks
to
1
1
ppm
but
not
to
3.4
ppm
(Hazleton
Laboratories,
1983).
For
development
of
AEGL­
2
values,
the
1
1
ppm
exposure
in
rats
was
considered
a
NOAEL
for
AEGL­
2
effects.
Uncertainty
factor
application
was
the
same
as
for
the
AEGL­
1
tier.

AEGE­
3
values
were
developed
based
upon
a
3­
foPd
reduction
of
the
4­
hr
LCs0
(Weeks
et
al.,
1964)
as
an
estimate
of
the
lethality
threshold
(50.1
ppd3
=
16.7
ppm).
A
total
uncertainty
factor
adjustment
of
10
was
used
to
develop
the
AEGL­
3
values.
Animal
data
indicated
some
variability
in
the
toxic
response
to
phosphorus
trichloride
with
guinea
pigs
being
the
more
sensitive
among
the
species
tested.
Therefore,
uncertainty
adjustment
regarding
interspecies
variability
was
limited
to
3.
To
account
for
intraspecies
variability,
a
factor
of
3
was
applied.
The
uncertainty
of
intraspecies
variability
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociation.
The
total
uncertainty
factor
of
10
may
be
justified
by
human
exposure
data
showing
that
repeated
2
to
6­
hour
exposures
of
up
to
27
ppm
were
without
life­
threatening
consequences.
Furthermore,
the
results
ofthe
Hazleton
Laboratories
(1
983)
study
showed
no
fatalities
in
rats
following
multiple
6­
hour
exposures
to
1
1
ppm.
The
AEGL
values
for
phosphorus
trichloride
are
presented
in
the
table
below.

effects;
based
upon
respiratory
a
Based
upon
animal
data,
lethality
may
be
delayed.

References
Hazleton
Laboratories.
1
983.
Subacute
inhalation
toxicity
study
in
rats
­
phosphorus
trichloride.
Final
Report.
Project
No.
241­
141.
Hazleton
Laboratories
America,
Inc.
Unpublished.

Weeks,
M.
H.,
Mussleman,
N.
P.,
Yevich,
P.
P.,
Jacobson,
K.
H.,
Oberst,
F.
W.
1964.
Acute
vapor
toxicity
of
phosphorus
oxychloride,
phosphorus
trichloride
and
methyl
phosphonic
dichloride.
Amer.
Ind.
Hyg.
J.
25:
470­
475.

vii
7
PMBSPHQRUS
TIRICHLQRIDE
PROPOSED
1:
05/
2802
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
26
25
27
28
29
30
31
32
33
34
35
36
37
38
1.
INTRODUCTION
Phosphorus
trichloride
(CAS
No.
007719­
12­
2)
is
a
colorless,
clear,
finning
liquid
with
a
pungent,
irritating
odor
(Fee
et
al.,
1996).
Odor
threshold
information
is
unavailable
for
this
chemical.
The
primary
use
of
phosphorus
trichloride
is
for
the
production
of
phosphonic
acid
which,
in
turn,
is
used
in
the
production
of
the
herbicide,
glyophosphate.
Phosphorus
trichloride
decomposes
rapidly
in
water
in
highly
exothermic
reactions.
It
may
also
decompose
in
moist
air
to
hydrochloric
acid
and
hydrated
phosphoric
acid.
The
reaction
products
include
phosphonic
acid,
hydrogen
chloride,
pyrophosphonic
acids,
depending
on
the
mole
ratio
of
water
and
phosphorus
trichloride
(Fee
et
al.,
1996).
If
the
mole
ratio
of
water
and
phosphorus
trichloride
is
greater
than
three,
the
following
reaction
will
occur.

PCl,
+
3H20
­­+
H3PO3
+3HC1
If
the
mole
ratio
is
2.5
to
3,
reaction
products
will
be
a
mixture
of
phosphonic
acid
and
p
yrophosphonic
acids.

0
0
0
II
II
II
I
I
I
3PC13
+
8H20
+
9HCl
+HPOPH
+HPOH
HO
OH
OH
TABLE
1.
PHYSICAL
AND
CHEMICAL
DATA
FOR
PHOSPHORUS
TRICMLORIDE
Conversion
factors
in
Beliles
and
Beliles,
1993
1
PHOSPHORUS
TRICHLORIDE
PROPOSED
I:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
2.
HUMAN
TOXICITY
DATA
2.1
Acute
Lethality
No
acute
lethality
exposure­
response
data
or
case
reports
are
currently
available.

2.2
Nonlethal
Toxicity
Sassi
(1952)
summarized
twenty
cases
of
acute
(2­
6
hours)
or
"subacute"
(1­
8
weeks
of
work)
exposures
of
workers
to
phosphorus
trichloride.
The
concentration
of
phosphorus
trichloride
in
the
workrooms
ranged
from
10­
20
mdm3
(­
1.8­
3.6
ppm)
under
normal
conditions
to
80­
150
mg/
m3
(­
14­
27
ppm)
during
periods
when
the
plant
was
"out
of
order".
The
method
by
which
the
concentrations
were
determined
was
not
stated
in
the
translated
abstract.
For
the
acute
exposures,
workers
experienced
a
burning
sensation
in
the
eyes
and
throat,
photophobia,
chest
tightness,
dry
cough,
and
slight
bronchitis
which
occurred
within
2­
6
hours
of
exposure.
For
the
"subacute"
exposures,
pharyngeal
irritation,
coughing,
catarrh,
dyspnea,
and
asthmatic
bronchitis
occur
at
1­
8
weeks
of
exposure.
Slight
increases
in
body
temperature
and
moderate
leucocytosis
with
neutrophilia
were
also
reported
for
both
exposures.
Signs
and
symptoms
reportedly
resolved
in
three
to
six
days
for
the
acute
exposures
and
10­
15
days
for
the
subacute
exposures.
An
abstract
by
Wason
et
al.
(1982)
provided
information
on
an
assessment
of
27
individuals
exposed
to
phosphorus
trichloride
released
in
a
railroad
accident
in
1980.
The
report
indicated
that
the
phosphorus
trichloride
reacted
with
water
used
to
disperse
the
spillage
and
with
air
moisture
that
resulted
in
the
release
of
phosphoric
and
hydrochloric
acids
and
phosphorus
oxides.
No
information
was
provided
regarding
weather
conditions
(e.
g.,
wind,
temperature,
humidity)
at
the
time
of
the
accident.
Signs
and
symptoms
were
characteristic
of
exposure
to
irritants
and
included
burning
eyes
(86%),
shortness
of
breath
(59%),
throat
irritation
(59%),
lacrimation
(59%),
headache
(48%),
nausea
(48%),
burning
sensation
on
the
skin
(44%),
and
sputum
production
(41%).
Additional
effects
occurring
in
33%
or
less
of
the
patients
included
chest
pains,
wheezing,
skin
rash,
blurred
vision,
vomiting,
and
abdominal
pain.
Lactate
dehydrogenase
was
mildly
elevated
and
serum
bilirubin
andor
serum
transaminases
were
elevated
in
three
individuals.
Results
of
pulmonary
hction
tests
showed
greater
severity
of
effect
with
decreasing
distance
from
the
release
site.
At
two
months,
86%
of
the
individuals
who
were
within
1/
16
mile
were
hypoxemic
while
only
50%
of
those
1/
16
to
1/
8
mile
distance
were
hypoxemic.
There
were
no
exposure
durations
provided
(probably
>
1.5
hours
as
described
below)
and
no
exposure
concentrations
were
measured
or
estimated.
Wason
et
al.
(1984)
reported
in
more
detail
on
the
railroad
accident
involving
spillage
of
phosphorus
trichloride.
The
report
focused
on
seventeen
individuals
(16
men
and
one
woman,
ages
2
1­
59
years),
seven
of
whom
were
requested
to
return
for
follow­
up
study
after
the
initial
medical
examination.
Signs
and
symptoms
of
exposure
included
eye,
skin
and
throat
irritation,
nausea,
vomiting,
blurred
vision,
headache,
and
various
effects
associated
with
respiration
and
ventilation
(e.
g.,
wheezing,
cough,
chest
pain,
dyspnea,
sputum
production).
Chest
X­
rays
of
all
subjects
were
normal
and
there
was
no
evidence
of
hepatic
toxicity.
Spirometry
tests
revealed
that
the
subjects
(10
of
17)
who
were
closest
(within
1
10
yards)
to
the
accident
site
had
a
significant
decrease
in
vital
capacity,
maximal
breathing
capacity,
FEV,,
and
maximal
ventilatory
flow
rate
at
25%
of
vital
capacity.
An
improvement
in
the
ventilatory
changes
was
seen
one
month
later.
Subjects
closer
to
the
release
site
appeared
to
exhibit
signs
and
symptoms
of
greater
severity.
It
was
also
found
that
patients
that
were
exposed
for
less
than
one
and
a
half
hours
had
2
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
significantly
(p=
0.02)
greater
maximal
expiratory
flow
rates
at
25%
of
vital
capacity
than
did
those
individuals
exposed
for
longer
periods.
Water
was
used
to
disperse
the
spilled
phosphorus
trichloride
and,
as
noted
in
the
report,
the
actual
exposure
most
likely
involved
phosphonic
acid
and
hydrochloric
acid
more
so
than
phosphorus
trichloride.
Eight
subjects
were
exposed
for
less
than
one
and
a
half
hours
and
nine
were
exposed
longer
(duration
no1
specified).
Pulmonary
function
tests
in
the
seven
follow­
up
patients
one
month
after
the
accident
revealed
significant
improvements
in
vital
capacity,
FEV,,
peak
expiratory
flow
rate,
and
maximal
expiratory
flow
rate
at
50%
vital
capacity.
Although
this
report
provides
information
regarding
the
nonlethal
effects
in
humans
following
exposure
to
phosphorus
trichloride,
there
were
no
data
on
the
exposure
concentrations
and
it
is
uncertain
as
to
the
precise
chemicals
(i.
e.,
phosphorus
trichloride
and/
or
its
degradation
products)
to
which
the
people
were
exposed.
A
NIOSH
health
hazard
evaluation
of
workers
at
the
FMC
plant
in
Nitro,
West
Virginia
revealed
that
those
with
known
repeated
exposures
to
phosphorus
oxychloride
and/
or
phosphorus
trichloride
experienced
a
significantly
higher
(p<
O.
OO
1)
prevalence
(65%)
of
occasional
respiratory
symptoms
(chest
tightness,
wheezing,
difficulty
breathing)
compared
to
unexposed
workers
(5%)
(Tharr
and
Singal,
1980).
However,
no
correlation
was
found
between
results
of
pulmonary
function
tests
on
the
workers
and
exposure
to
these
chemicals.
The
study
utilized
37
exposed
workers
and
22
unexposed
workers.
Most
air
samples
were
below
detection
limits
although
one
employee
(with
respiratory
protection
of
a
chlorine
gas
mask)
was
exposed
to
6
mg
phosphorus
trichloride/
m3
(1
ppm)
for
one
hour
during
a
truck­
loading
operation
(no
effects
were
reported
for
this
individual).

workers
from
the
aforementioned
FMC
Corp.
group
revealed
that
half
of
the
exposed
workers
reported
significantly
(p<
O
,002)
more
episodes
of
respiratory
effects
(wheezing,
breathlessness,
and
chest
tightness)
compared
to
the
unexposed
workers
who
reported
no
such
effects
(Moody,
1981).
Results
of
pulmonary
function
tests
did
not
reveal
significant
findings
regarding
effects
of
phosphorus
trichloride
(or
phosphorus
oxychloride)
exposure.
No
significant
difference
in
pulmonary
function
(FEV,)
was
found
in
the
exposed
workers
vs
the
unexposed
workers
over
a
two­
year
period.
The
small
sample
size,
however,
reduces
the
power
of
the
study
to
detect
such
changes
and,
therefore,
compromises
the
apparent
negative
finding.
Although
lacking
exposure
terms,
there
is
information
regarding
accidental
releases
of
phosphorus
trichloride
in
Illinois
(pers.
comm.).
Two
significant
releases
of
phosphorus
trichloride
occurred
in
1988
fi­
om
a
chemical
plant
in
Sauget,
Illinois.
The
first,
on
April
17,
resulted
from
overfilling
a
railroad
tanker,
with
an
estimated
6,000­
12,000
pounds
released
in
the
railroad
yard.
The
plume
caused
the
evacuation
of
approximately
22
square
blocks,
and
417
citizens
of
neighboring
Rush
City
and
East
St.
Louis,
Illinois
reported
to
area
hospitals
for
treatment.
Two
of
these
citizens
were
admitted
overnight
and
subsequently
released.
Eye
and
respiratory
irritation
were
the
main
symptoms
reported.
The
second
incident
resulted
from
failure
of
a
rupture
disk
during
start­
up
procedures
at
the
plant
on
July
3
1.
It
was
calculated
that
no
more
than
50
pounds
of
phosphorus
trichloride
were
released
from
the
plant,
and
the
plant's
security
and
industrial
hygiene
personnel
were
able
to
visually
track
and
bound
the
plume
that
moved
into
Rush
City.
Their
reports
indicated
that
the
plume
traveled
approximately
two
miles
before
dissipating.
This
plume
caused
244
citizens
to
report
to
area
hospitals
for
treatment.
Eight
of
these
citizens
were
admitted;
seven
were
kept
overnight
and
released,
while
the
eighth
was
kept
for
three
days
before
release.
This
patient's
history
of
asthma
contributed
to
the
severity
of
effects,
and
the
asthma
was
also
aggravated
by
the
exposure
to
the
phosphorus
trichloride.
The
main
complaints
of
the
citizens
were
eye,
nose,
and
throat
irritation.
No
measurements
of
airborne
concentrations
were
made
during
either
incident.
A
follow­
up
study
conducted
by
NIOSH
on
26
of
the
exposed
workers
and
1
1
of
the
unexposed
2.3
Epidemiologic
Studies
3
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
a
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
No
epidemiologic
studies
of
phosphorus
trichloride
toxicity
are
currently
available.

2.4
DevelopmentaYReproductive
Toxicity
Data
regarding
the
reproductive/
developrnental
toxicity
of
phosphorus
trichloride
in
humans
are
not
available.

2.5
Genotoxicity
No
human
genotoxicity
data
for
phosphorus
trichloride
are
currently
available.

2.6
Carcinogenicity
Information
regarding
the
potential
carcinogenicity
of
phosphorus
trichloride
in
humans
is
not
available.

2.7
Summary
There
are
no
data
regarding
lethal
exposures
of
humans
to
phosphorus
trichloride
but
some
information
on
nonlethal
exposures
is
available.
Workers
exposed
to
phosphorus
trichloride
following
a
railroad
car
spill
exhibited
signs
and
symptoms
consistent
with
exposure
to
a
highly
irritating
chemical.
Although
the
reports
of
this
accident
describe
qualitatively
the
effects
of
exposure,
there
are
no
quantitative
exposure­
response
terms.
Pulmonary
function
deficits
(e.
g.,
vital
capacity,
FEVI,
peak
expiratory
flow
rate,
maximal
expiratory
flow
rate
at
50%
vital
capacity)
that
correlated
with
distance
from
the
release
showed
improvement
at
one
month
following
the
exposure.
The
effects
reported
could
be
attributed
to
phosphorus
trichloride
decomposition
products
(phosphonic
acid
and
hydrogen
chloride)
as
well
as
the
parent
compound.
In
an
occupational
exposure
setting,
workers
experienced
a
burning
sensation
in
the
eyes
and
throat,
photophobia,
chest
tightness,
dry
cough,
and
slight
bronchitis
following
2­
6
hours
of
exposure
to
approximately
14­
27
ppm
phosphorus
trichloride.
Exposure
of
workers
to
these
levels
for
1­
8
weeks
resulted
in
pharyngeal
irritation,
coughing,
catarrh,
dyspnea,
and
asthmatic
bronchitis.
Increases
in
body
temperature
and
moderate
leucocytosis
with
neutrophilia
were
also
reported
for
both
exposure
durations,
but
all
signs
and
symptoms
resolved
upon
removal
from
the
exposure.

3.
ANIMAL
TOXICITY
DATA
3.1
Acute
Lethality
3.1.1
Rats
Weeks
et
al.
(1
964)
reported
on
the
acute
lethality
of
phosphorus
trichloride
in
female
rats
exposed
for
four
hours
to
an
atmosphere
of
phosphorus
trichloride
generated
by
passing
nitrogen
gas
through
the
liquid
test
material.
Chemical
analysis
was
used
to
determine
the
amount
of
the
test
material
in
the
exposure
chamber.
The
rats
were
observed
for
14
days
after
removal
from
exposure.
The
rats
were
restless
and
exhibited
labored
breathing
during
the
exposure.
During
the
exposure,
the
eyes
were
closed
and
there
was
considerable
porphyrin
secretion
around
the
eyes.
Deaths
occurred
over
a
period
of
ten
days
indicating,
under
the
conditions
of
this
experiment,
a
notable
latency
period
in
the
lethal
response.
The
4
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
4
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
nostrils
and
paws
of
the
exposed
rats
exhibited
swelling,
edema,
discoloration
and
subsequent
sloughing
of
tissues
that
was
consistent
with
the
activity
of
a
corrosive
agent.
Microscopic
examination
revealed
necrosis
of
epithelium
and
supporting
structures
in
the
nostrils
but
pulmonary
damage
was
considered
to
be
negligible.
The
investigators
noted
that
the
primary
site
of
damage
appeared
to
be
the
kidneys
and
was
characterized
by
nephrosis
of
tubules
in
the
cortico­
medullary
region.
A
4­
hr
LC5,,
of
104.3
pprn
was
calculated
and
reported
by
the
investigators.
The
exposure
concentrations
tested
to
obtain
this
value
were
not
reported
and,
therefore,
there
was
no
infoxmation
regarding
the
exposure­
response
relationship.

3.1.2
Guinea
pigs
Weeks
et
al.
(1964)
also
examined
the
lethal
response
of
guinea
pigs
exposed
for
four
hours
to
phosphorus
trichloride.
The
experimental
protocol
was
as
described
for
the
experiments
with
rats
(Section
3.1.1).
Based
upon
the
published
report,
the
response
of
guinea
pigs
was
similar
to
that
of
rats;
restlessness,
signs
of
ocular
and
nasopharyngeal
irritation,
and
renal
damage.
With
the
exception
of
the
4­
hr
LCso
of
50.1
ppm,
no
additional
exposure­
response
data
were
provided.

pigs
exposed
to
623
ppm
phosphorus
trichloride
died
shortly
after
3
hours
of
exposure.
Results
of
early
inhalation
exposure
experiments
reported
by
Butjagin
(1904)
showed
that
guinea
3.1.3
Cats
Butjagin
(1904)
reported
that
test
animals
(guinea
pigs
and
cats)
died
shortly
after
3­
hour
exposure
to
623
ppm.
In
another
experiment,
one
cat
exposed
to
694
ppm
died
after
306
minutes.

3.2
Nonlethal
Toxicity
3.2.1
Rats
Although
the
Weeks
et
al.
(1964)
study
reported
on
lethality
in
rats
exposed
to
phosphorus
trichloride,
no
information
was
provided
regarding
nonlethal
effects.

In
an
unpublished
study
conducted
for
the
Monsanto
Company
(Hazleton
Laboratories,
1983),
groups
of
15
Sprague­
Dawley
rats
(1
S/
sex/
group)
were
exposed
to
phosphorus
trichloride
vapor/
aerosol
for
6
hours/
day,
5
daydweek
for
four
weeks.
Over
the
four­
week
period,
nominal
exposure
concentrations
were
0.5,
3.0,
or
10.0
ppm
and
analytical
concentrations
were
0.49,
3.37,
and
10.96
ppm.
The
test
atmosphere
was
generated
by
passing
air
(200­
990
cc/
minute
.depending
upon
the
test
concentration
group)
over
the
headspace
above
a
non­
specified
volume
of
phosphorus
trichloride
in
a
flask.
The
vapor
was
then
carried
to
the
test
chambers
via
Teflon@
tubing.
Sample
concentrations
were
determined
three
times
per
day
by
collecting
chamber
samples
in
impingers
containing
20
mL
of
sodium
hydroxide.
The
samples
were
subsequently
analyzed
in
a
chloride
meter
and
expressed
as
ppm
phosphorus
trichloride.
Over
the
4­
week
exposure
period,
concentration
excursions
deviated
from
target
values
by
­2.0,.
+12.3,
and
+9.6%
for
the
low,
medium,
and
high­
dose
groups,
respectively.
A
control
group
was
exposed
to
filtered
air
under
the
same
conditions.
No
rat
died
during
the
exposure
period
and
no
treatment­
related
adverse
effects
were
observed.
All
rats
were
sacrificed
and
necropsied
on
day
29.
Histological
alterations
in
the
maxillo­
and
nasoturbinates
and
in
the
lateral
wall
of
the
nasal
cavity
were
observed
in
seven
male
and
four
females
of
the
high­
dose
group;
the
remaining
high­
dose
rats
exhibited
no
remarkable
findings
in
the
nasal
cavities
and
turbinates.
Squamous
metaplasia
of
the
respiratory
epithelium
was
also
present
in
six
males
and
four
5
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
females
of
the
high­
dose
group.
There
were
no
treatment­
related
effects
on
hematologic
or
biochemical
parameters,
and
no
ophthalmologic
effects
or
body
weighuorgan
weight
changes
were
observed.
Under
the
conditions
of
this
study,
3.4
ppm
was
considered
a
No­
Observed­
Adverse
Effect
Level
(NOAEL)
in
rats.

32.2
Guinea
Pigs
In
experiments
reported
by
Butjagin
(1904),
guinea
pigs
were
exposed
to
phosphorus
trichloride
at
various
concentrations
for
different
durations
(1
­
6
hours).
Only
minor
effects
(restlessness,
salivary
and
nasal
secretions,
coughing,
irregular
respiration)
were
observed
following
6­
hour
exposure
to
0.7
1
ppm
or
1­
hour
exposure
to
1.78
to
5.36
ppm.
In
the
report
summary,
it
was
also
noted
that
exposures
of
50­
90
ppm
for
one
hour
produced
severe
signs
of
toxicity.
The
phosphorus
trichloride
concentrations
were
determined
by
measurement
of
chlorine.
It
appears
that
only
1
to
3
animals
were
used
for
any
given
exposure
and,
for
some
experiments,
the
same
animals
were
used.

3.2.3
Cats
Butjagin
(1904)
also
conducted
experiments
with
adult
cats
(2.1­
4.0
kg)
exposed
to
phosphorus
trichloride
as
previously
described
for
guinea
pigs.
The
results
were
similar
to
those
reported
for
the
guinea
pigs;
6­
hour
exposure
to
0.71
ppm
or
1­
hour
exposure
to
1.78
to
5.36
ppm
produced
signs
of
restlessness
and
nasopharyngeal
irritation.
Six­
hour
exposures
to
concentrations
of
135
to
303
ppm
rapidly
produced
signs
of
severe
irritation
(salivary,
nasal,
and
ocular
secretions,
breathing
through
the
mouth,
irregular
and
severely
labored
respiration).
Histological
examination
at
six
to
seven
days
after
exposure
revealed
severely
damaged
nasal
septum
and
bronchioles,
and
pulmonary
edema.
Inasmuch
as
these
animals
were
terminated
for
necropsy,
it
is
likely
(based
upon
the
findings)
that
they
may
not
have
survived.
In
summary,
the
study
author
reported
that
one­
hour
exposure
to
50­
90
ppm
resulted
in
severe
signs
of
toxicity.
It
appears
that
for
at
least
some
of
the
experiments,
the
same
cats
were
used.

3.3
DevelopmentaVReproductive
Toxicity
No
data
are
available
regarding
the
developmental/
reproductive
toxicity
of
phosphorus
trichloride
in
animals.

3.4
3.5
3.6
Genotoxicity
No
data
are
currently
available
regarding
the
genotoxicity
of
phosphorus
trichloride.

Carcinogenicity
No
data
are
available
regarding
the
carcinogenic
potential
of
phosphorus
trichloride
in
animals.

Summary
of
Toxicity
Data
In
Animals
Definitive
quantitative
exposure­
response
toxicity
data
in
animals
were
limited.
Median
lethal
exposure
concentrations
for
rats
&d
guinea
pigs
are
available
and
shown
in
Table
2.
A
report
by
Weeks
et
6
13
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
Species
Rat
Cat
1
2
3
4
5
6
7
8
9
10
11
12
Lethality
Value
Reference
4­
hrLCx,
:
104.3
ppm
lethality
at
306
min,
694
ppm
Weeks
et
al.,
1964
Butjagin,
1904
13
~
~~

Cat
Guinea
pig
Guinea
pig
14
lethality
at
3
hours,
623
ppm
4­
hr
LCso
:
50.1
ppm
lethality
at
3
hours,
623
ppm
ButjaginJ
904
Weeks
et
a1.,
1964
ButjaginJ904
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
al.
(1964)
provided
an
adequate
description
of
experimental
protocol
and
4­
hr
EC,,
value
for
rats
(4­
hr
Lcs0=
104.3
gpm)
and
guinea
pigs
(4­
hr
ECs0=
50.
1
ppm).
Additional
data
obtained
from
limited
numbers
of
cats
and
guinea
pigs
exposed
to
various
concentrations
of
phosphorus
trichloride
for
varying
durations
described
both
lethal
and
nonlethal
responses
(Butjagin,
1904).
An
unpublished
study
by
Hazleton
Laboratories
(1983)
showed
that
multiple
6­
hour/
day
exposures
of
male
and
female
rats
to
phosphorus
trichloride
at
11
ppm
over
four
weeks
produced
only
histologic
changes
in
the
nasal
turbinates
while
exposure
to
3.4
ppm
failed
to
produce
any
notable
effects.
The
available
information
affirms
that
exposure
to
vapors
of
phosphorus
trichloride
may
produce
dermal,
ocular,
and
nasopharyngeal
irritation
as
well
as
pulmonary
and
renal
damage.
Additionally,
based
upon
limited
data
in
rats,
cats
and
guinea
pigs,
there
appears
to
be
latency
period
in
the
lethal
response
to
phosphorus
trichloride.

~~

rTABLE
2.
ACUTE
LETHALITY
OF
PHOSPHORUS
TRICHLORIDE
IN
LABORATORY
SPECIES1
4.
SPECIAL
CONSIDERATIONS
4.1
Metabolism
and
Disposition
Data
on
the
metabolism
and
disposition
of
phosphorus
trichloride
are
not
currently
available.

4.2
Mechanism
of
Toxicity
The
mechanism
of
toxicity
of
phosphorus
trichloride
is
currently
unknown.
The
lethal
toxicity
of
phosphorus
trichloride
does
not,
however,
appear
to
be
explained
solely
by
the
activity
of
the
irritant
degradation
products
(hydrogen
chloride
and
phosphonic
acid).
The
rapid
exothermic
reaction
in
the
presence
of
water
may
contribute
to
localized
tissue
damage
and
also
explain,
in
part,
the
greater
toxicity
of
phosphorus
trichloride
relative
to
hydrogen
chloride
and
phosphonic
acid.

4.3
Structure­
Activity
Relationships
7
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
0512002
]I
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
Barbee
et
al.
(1995)
conducted
an
acute
toxicity
study
of
oxalyl
chloride
(COCl),
in
which
groups
of
10
rats
were
exposed
for
one
hour
to
0,462,866,
1232,
1694,
or
2233
pprn.
The
1­
hr
LC,,
was
found
be
1840
ppm.
Phosphorus
trichloride
produces
many
of
the
same
signs
and
symptoms
as
does
phosphorus
oxychloride
following
acute
inhalation
exposures
(Weeks
et
al.,
1964;
ACGIH,
1991)
and
also
undergoes
rapid
hydrolysis
to
phosphonic
acid
and
hydrogen
chloride.

4.4
Other
Relevant
Information
4.4.1
Species
Variability
Data
are
insufficient
to
reliably
describe
species
variability
in
the
toxic
response
to
inhaled
phosphorus
trichloride.

4.4.2
Concurrent
Exposure
Issues
No
concurrent
exposure
issues
of
special
concern
have
been
identified
that
could
be
directly
incorporated
in
the
development
of
AEGL
values
for
phosphorus
trichloride.

5.
DATA
ANALYSIS
AND
PROPOSED
AEGL­
1
5.1
Summary
of
Human
Data
Relevant
to
AEGL­
1
Quantitative
human
data
consistent
with
AEGL­
1
effects
were
not
available.
Information
regarding
human
exposures
to
phosphorus
trichloride
indicate
acute
exposures
result
in
dermal
and
ocular
irritation,
irritation
of
the
respiratory
tract,
headache,
nausea,
and
shortness
of
breath.

5.2
Summary
of
Animal
Data
Relevant
to
AEGL­
1
The
only
animal
data
available
that
were
consistent
with
AEGL­
1
severity
effects
were
those
provided
in
the
report
by
Butjagin
(1904).
In
this
study,
cats
and
guinea
pigs
exposed
to
phosphorus
trichloride
concentrations
of
0.71
to
1.78
ppm
for
up
to
six
hours
exhibited
restlessness,
salivary
and
nasal
secretions,
coughing,
and
irregular
respiration.
Hazleton
Laboratories
(1983)
reported
a
NOAEL
of
3.4
ppm
for
rats
following
multiple
6­
hr/
day
exposures.
This
was
bounded
by
a
NOEL
of
0.5
ppm
and
LOAEL
(1
1
ppm).

5.3
Derivation
of
AEGL­
1
Data
consistent
with
AEGL­
1
effects
come
from
an
older
study
in
cats
and
guinea
pigs
(Butjagin,
1904).
There
are
no
odor
threshold
data
and
no
quantitative
data
in
humans.
Because
of
the
uncertainties
regarding
exposure
atmosphere
measurements
from
a
study
conducted
almost
100
years
ago
and
the
fact
that
individual
test
animals
may
have
been
exposed
to
multiple
exposure
regimens,
the
data
from
Butjagin
(1904)
were
not
used
in
the
development
of
AEGL­
1
values.
Data
from
the
Hazleton
Laboratories
study
suggested
that
an
exposure
above
0.5
ppm
may
be
consistent
with
AEGL­
1
effects
as
multiple
6­
hour
exposures
to
this
concentration
over
a
four­
week
period
were
without
effect.
The
Hazleton
Laboratories
study
identified
3.4
ppm
as
a
NOAEL
for
rats
receiving
multiple
6­
hour
exposures
over
a
period
of
4
8
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
8§/
2002
TABLE
3.
AEGL­
1
VALUES
FOR
PHOSPHORUS
TRICHLORIDE
AEGL
Level
1
0­
min
3
O­
min
1
­hr
4­
hr
8­
hr
AEGL­
1
0.78
ppm
0.78
ppm
0.62
ppm
0.39
ppm
0.26
ppm
?
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
1%
19
20
21
22
23
24
25
26
27
2%
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
weeks.
Sassi
(1952)
reported
that
occupational
exposures
of
1.8
to
3.6
ppm
for
2
to
6
hours
were
without
notable
effect.
Hn
lieu
of
additional
data.
the
experimentally
determined
NOAEL
3.4
ppm
was
considered
a
NOAEL
for
development
of
AEGE­
1
values.
Data
for
humans
and
animals
indicate
some
variability
in
the
toxic
response
to
phosphorus
trichloride.
However,
upon
comparison
to
human
data
(albeit
limited),
rodents
appear
to
be
somewhat
more
sensitive
to
the
respiratory
effects
of
phosphorus
trichloride.
Therefore,
uncertainty
adjustment
regarding
interspecies
variability
was
limited
to
3.
To
account
for
intraspecies
variability,
a
factor
of
3
was
applied.
The
uncertainty
of
intraspecies
variability
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociation.
The
attenuated
uncertainty
factors
may
be
justified
by
the
limited
human
exposure
data
(Sassi,
1952)
suggesting
that
humans
could
experience
2
to
6­
hour
exposures
of
up
to
3.6
ppm
with
no
apparent
effect
and
the
fact
that
AEGL­
1
development
is
based
upon
an
exposure
that
was
without
a
discernible
effect.
The
AEGL­
1
values
for
phosphorus
trichloride
are
shown
in
Table
3
and
their
derivations
shown
in
Appendix
A.

6.
DATA
ANALYSIS
AND'
PROPOSED
AEGL­
2
6.1
Summary
of
Human
Data
Relevant
to
AEGL­
2
Quantitative
exposure­
response
data
in
humans
are
not
available
for
development
of
AEGL­
2
values
for
phosphorus
trichloride.
Information
regarding
the
human
experience
is
limited
to
qualitative
notations
regarding
signs
and
symptoms
(ocular,
dermal,
and
respiratory
tract
irritation,
and
ventilatory
effects).
The
information
in
these
reports
suggest
that
acute
exposure
to
phosphorus
trichloride
could
cause
irritation
severe
enough
to
impair
egress
from
a
contaminated
area.
Sassi
(1953)
reported
that
workers
experienced
a
burning
sensation
in
the
eyes
and
throat,
photophobia,
chest
tightness,
dry
cough,
and
slight
bronchitis
following
2­
6
hours
of
exposure
to
approximately
14­
27
ppm
phosphorus
trichloride.
Although
these
effects
could
possibly
impair
escape,
thereby
by
qualifylng
as
being
consistent
with
AEGL­
2
tier
effects,
the
method@)
by
which
the
exposure
concentrations
were
determined
was
not
reported.
Exposure
concentrations
were
not
provided
in
other
reports
(with
the
exception
of
the
anecdotal
data
by
Tharr
and
Singa1,1980)
and
information
on
exposure
duration
was
limited.

6.2
Summary
of
Animal
Data
Relevant
to
AEGL­
2
Quantitative
data
in
animals
regarding
effect
severity
consistent
with
AEGL­
2
were
limited
to
data
on
guinea
pigs
and
cats
reported
by
Butjagin
(1904).
The
robustness
of
these
data
are,
however,
limited
due
to
the
small
numbers
of
animals
in
each
experiment
(Le.,
1
­
3)
and
the
fact
that
some
of
the
animals
were
apparently
used
in
more
than
one
experiment.
This
becomes
a
significant
concern
considering
the
additive
nature
of
irritatiodtissue
damage
and
the
possible
latency
in
activity
for
some
adverse
effects
of
phosphorus
trichloride
(e.
g.,
pulmonary
damage
and
renal
toxicity).
Consistent
with
human
acute
exposure
9
PMQSPHQRBIS
TRICHLORIDE
PRQPOSED
1:
85/
26)
02
AEGL
Level
AEGL­
2
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
1
0­
min
30­
min
1
­hr
4­
hr
8
­hr
2.5
ppm
2.5
ppm
2.0
ppm
1.3
ppm
0.83
pprn
reports,
the
predominant
response
by
animals
is
characterized
by
ocular,
nasopharyngeal,
and
pulmonary
irritation
and
subsequent
tissue
damage.
Animal
data
are
not
sufficient
to
provide
a
meaningful
exposure­
response
relationship.
The
responses
of
cats
and
guinea
pigs
in
the
Butjagin
study
were
reportedly
more
severe
at
higher
concentrations
and
occurred
more
quickly.
In
the
Butjagin
(1904)
report,
cats
and
guinea
pigs
exposed
to
5.36
ppm
for
one
hour
exhibited
restlessness,
signs
of
nasopharyngeal
irritation,
and
irregular
respiration.
A
6­
hour
exposure
of
cats
to
concentrations
of
135
to
303
ppm
resulted
in
s
i
p
s
of
severe
irritation
and
respiratory
distress.
Histological
examination
of
the
cats
exposed
to
135
to
303
pprn
revealed
perforated
nasal
septa,
bronchial
damage,
and
pulmonary
edema.
Additionally,
Weeks
et
al.
(
1964)
noted
renal
damage
in
rats
exposed
to
lethal
concentrations
of
phosphorus
trichloride.
However,
exposure­
response
data
were
not
provided
regarding
this
effect.
The
Hazleton
Laboratories
study
(1983)
in
rats
showed
that
multiple
6­
hour
exposures
to
11
ppm.
over
a
four­
week
period
produced
histologic
alterations
in
the
nasal
turbinates
but
no
effects
on
ophthalmologic
hematologic
or
biochemical
parameters,
and
no
overt
signs
of
toxicity.
Because
the
nasal
lesions
were
the
result
of
multiple
exposures
(5
daydweek)
over
four
weeks
and
not
of
a
severity
consistent
with
the
AEGL­
2
tier,
a
threshold
for
AEGL­
2
effects
in
rats
is
likely
at
an
undetermined
concentration
above
11
ppm
for
a
single
six­
hour
exposure.

6.3
Derivation
of
AEGL­
2
Data
upon
which
to
base
AEGL­
2
development
are
limited.
Sassi
(1953)
reported
on
occupational
exposures
of
2­
6
hour
durations
to
concentrations
of
14­
27
ppm
that
produced
effects
that
could
be
considered
only
marginally
consistent
with
AEGL­
2.
As
previously
noted,
the
animal
data
reported
by
Butjagin
(1904)
are
deficient
for
the
purpose
of
AEGL
development.
Although
the
results
from
the
Hazleton
Laboratories
(1983)
study
in
rats
exposed
to
for
6
hours/
day,
5
daydweek
for
four
weeks
did
not
define
a
response
consistent
with
AEGL­
2
severity,
the
11
ppm
exposure
that
resulted
in
histopathologic
alterations
in
the
respiratory
tract
may
be
considered
a
NOAEL
for
AEGL­
2
severity
effects.
Uncertainty
factor
application
and
time
scaling
were
as
described
for
AEGL­
1.
Data
from
available
reports
suggest
that
humans
are
not
especially
sensitive
to
the
effects
of
phosphorus
trichloride
when
compared
to
laboratory
animals.
As
such
fbrther
reduction
of
AEGL
values
by
the
application
of
greater
uncertainty
factors
dose
not
appear
warranted.
The
AEGL­
2
values
for
phosphorus
trichloride
are
shown
in
Table
4
and
their
derivation
outlined
in
Appendix
A.

31
32
33
34
35
10
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05L2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
7.
DATA
ANALYSIS
AND
PROPOSED
AEGL­
3
7.1
Summary
of
Human
Data
Relevant
to
AEGL­
3
Quantitative
data
are
not
available
regarding
lethality
in
humans
exposed
to
phosphorus
trichloride,

4
2
Summary
of
Animal
Data
Relevant
to
AEGL­
3
Weeks
et
al.
(1964)
provided
4­
hr
LC50
values
of
104.3
ppm
and
50.1
ppm,
respectively,
for
rats
and
guinea
pigs.
In
early
experiments
by
Butjagin
(1904),
guinea
pigs
and
cats
exposed
to
623
ppm
phosphorus
trichloride
died
within
three
hours,
and
a
cat
exposed
to
694
ppm
died
after
306
minutes
of
exposure.
In
the
absence
of
any
additional
quantitative
data,
the
median
lethality
values
derived
by
Weeks
et
al.
may
be
considered
as
a
basis
for
AEGL­
3
development
and
also
serve
to
a
limited
extent
as
an
index
of
species
variability.
Because
the
exposure­
response
data
used
to
derive
the
median
lethality
values
were
not
provided,
it
is
not
possible
to
determine
the
exposure­
response
relationship.

7.3
Derivation
of
AEGL­
3
Because
the
median
lethality
values
provided
by
Weeks
et
al.
(1964)
represent
the
only
quantitatively
determined
estimates
regarding
the
lethal
response
to
acute
inhalation
of
phosphorus
trichloride,
they
may
be
considered
as
the
basis
for
AEGL­
3
development.
The
4­
hr
LC50
values
for
rats
(104.3
ppm)
and
guinea
pigs
(50.1
ppm)
suggest
a
species
variability.
In
the
absence
of
exposure­
response
data,
the
lethality
threshold
was
estimated
as
a
3­
fold
reduction
of
the
rat
4­
hr
LCso
(104.3
p
p
d
3
=
34.8
PPm).
The
concentration­
time
relationship
for
many
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
C"
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5.
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
1
when
extrapolating
to
longer
time
points
using
the
c"
x
t
=
k
equation.
Because
of
the
uncertainty
in
extrapolating
from
a
4­
hour
exposure
to
a
10­
minute
exposure,
the
latter
was
set
equal
to
the
30­
minute
AEGL­
3.
A
total
uncertainty
factor
adjustment
of
10
was
used
to
develop
the
AEGL­
3
values.
Data
for
humans
and
animals
indicate
some
variability
in
the
toxic
response
to
phosphorus
trichloride
with
guinea
pigs
being
the
more
sensitive
(­
2­
fold)
among
the
laboratory
animals.
Limited
data
regarding
human
exposures
showed
that
2
to
6­
hour
exposures
to
14­
27
ppm
were
not
life­
threatening
(Sassi,
1952).
Therefore,
uncertainty
adjustment
regarding
interspecies
variability
was
limited
to
3.
To
account
for
intraspecies
variability,
a
factor
of
3
was
applied.
The
uncertainty
of
intraspecies
variability
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociation.
The
attenuated
uncertainty
factors
may
be
further
justified
by
limited
human
exposure
data
(Sassi,
1952)
suggesting
that
humans
could
experience
repeated
exposures
of
up
to
27
ppm
without
life­
threatening
consequences.
The
resulting
AEGL­
3
values
are
presented
in
Table
5
and
their
derivation
is
shown
in
Appendix
A.
Because
the
lethal
response
in
guinea
pigs
and
rats
was
delayed
up
to
10
days,
note
of
possible
delayed
response
has
been
made
regarding
AEGL­
3
values.

11
(8
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
a
Based
upon
animal
data,
lethality
may
be
delayed
8.
SUMMARY
OF
PROPOSED
AEGLS
8.1
AEGL
Values
and
Toxicity
Endpoints
The
AEGL­
1
values
are
based
upon
a
NOAEL
an
laboratory
study
in
which
rats
received
multiple
exposures
over
a
period
of
four
weeks.
Although
a
conservative
assumption,
the
use
of
a
NOAEL
in
the
development
of
the
AEGL­
1
values
may
be
justified
by
the
relative
paucity
of
definitive
exposure­
response
data.
and
the
fact
that
limited
information
regarding
the
human
experience
indicates
that
2
to
6­
hour
exposures
to
1.8­
3.6
ppm
was
without
effect.
The
AEGL­
2
values
were
based
on
histopathologic
alterations
detected
in
the
respiratory
tract
of
rats
following
multiple
exposures
over
four
weeks.
The
effects
on
the
respiratory
tract
were
consistent
with
mode
of
action
of
phosphorus
trichloride
and,
therefore,
were
considered
a
NOAEL
for
the
AEGL­
2
tier
effect
level
(i.
e.,
the
effects
were
neither
disabling
nor
irreversible).
Information
regarding
the
human
experience
suggests
that
2
to
6­
hour
exposures
to
1.8­
3.6
ppm
were
without
effect
and
that
exposure
to
14­
27
ppm
resulted
in
irritation
of
the
eyes
and
upper
respiratory
tract,
photophobia,
chest
tightness,
and
bronchitis.
Therefore,
further
reduction
of
the
AEGL­
2
values
does
not
appear
to
be
warranted.
The
AEGL­
3
values
were
developed
based
upon
lethality
data
in
laboratory
species.
The
AEGL­
3
values
were
developed
based
upon
a
4­
hr
LCso
value
for
rats
provided
in
a
study
by
Weeks
et
al.,
1964.
Data
pertaining
to
the
human
experience
also
indicate
respiratory
involvement
as
a
critical
effect.

12
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
8.2
Comparison
with
Other
Standards
and
Criteria
Existing
standards
and
criteria
for
phosphorus
trichloride
are
presented
in
Table
6
.

TABLE
6.
Extant
Standards
and
Guidelines
for
Phosphorus
Trichloride
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
­
­
­
Einsaztolerannvert
­
(Germany)
'

MAC
­
­
­
(The
Netherlandsy
NR:
Not
recommended.
Numeric
values
for
AEGL­
1
and
AEGL­
2
are
not
recommended
due
to
8
hour
0.26
ppm
0.83
ppm
1.8
ppm
­

0.5
ppm
0.2
ppm
­

0.2
ppm
0.5
ppm
0.5
ppm
0.2
ppm
e
lack
of
availab
data.
Absence
of
these
values
does
not
imply
that
exposure
below
the
AEGL­
3
is
without
adverse
effects.

13
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
P
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
'ERPG
(Emergency
Response
Planning
Guidelines,
American
Industrial
Hygiene
Association)
(AIHA,
1994)
The
ERPG­
1
is
the
maximum
airborne
concentration
below
which
it
is
believed
nearly
all
individuals
could
be
exposed
for
up
to
one
hour
without
experiencing
other
than
mild,
transient
adverse
health
effects
or
without
perceiving
a
clearly
defined
objectionable
odor.
The
EWG­
2
is
the
maximum
airborne
concentration
below
which
it
is
believed
nearly
dl
individuals
could
be
exposed
for
up
to
one
hour
without
experiencing
or
developing
irreversible
or
other
serious
health
effects
or
symptoms
that
could
impair
an
individual's
ability
to
take
protective
action.
The
EWG­
3
is
the
maximum
airborne
concentration
below
which
it
is
believed
nearly
all
individuals
could
be
exposed
for
up
to
one
hour
without
experiencing
or
developing
life­
threatening
health
effects.
As
of
2001,
phosphorus
trichloride
values
are
categorized
as
under
Ballot,
Review,
and
Consideration.

EEGL
(Emergency
Exposure
Guidance
Levels,
National
Research
Council)
(NRC,
1985)
is
the
concentration
of
contaminants
that
can
cause
discomfort
or
other
evidence
of
irritation
or
intoxication
in
or
around
the
workplace,
but
avoids
death,
other
severe
acute
effects
and
long­
term
or
chronic
injury.

OSHA
PEL­
TWA
(Occupational
Health
and
Safety
Administration,
Permissible
Exposure
Limits
­
Time
Weighted
Average)
(OSHA,
1993)
is
defined
analogous
to
the
ACGIH­
TLV­
TWA,
but
is
for
exposures
of
no
more
than
10
hourdday,
40
hourdweek.

*
OSHA
PEL­
STEL
(Permissible
E
osure
Limits
­
Short
Term
Exposure
Limit)
(OSHA,
1993)
is
defined
analogous
to
the
ACGIH­
2~­
STEL.

e
IDLH
(Immediately
Dangerous
to
Life
and
Health,
National
Institute
of
Occupational
Safety
and
Health)
(NIOSH,
1996)
represents
the
maximum
concentration
from
which
one
could
escape
within
30
minutes
without
any
escape­
impairing
symptoms,
or
any
irreversible
health
effects.

NIOSH
REL­
TWA
(National
Institute
of
Occupational
Safety
and
Health,
Recommended
Exposure
Limits
­
Time
Weighted
Average)
(NIOSH,
1999)
is
defined
analogous
to
the
ACGIH­
TLV­
TWA.

g
NIOSH
REL­
STEL
(Recommended
Exposure
Limits
­
Short
Term
Exposure
Limit)
(NIOSH,
1999)
is
defined
analogous
to
the
ACGIH­
TLV­
STEL.

ACGIH
TLV­
TWA
(American
Conference
of
Governmental
Industrial
Hygienists,
Threshold
Limit
Value
­
Time
Weighted
Average)
(ACGIH,
1997)
is
the
time­
weighted
average
concentration
for
a
normal
S­
hour
workday
and
a
40­
hour
work
week,
to
which
nearly
all
workers
may
be
repeatedly
exposed,
day
after
day,
without
adverse
effect.

ACGIH
TLV­
STEL
(Threshold
Limit
Value
­
Short
Term
Exposure
Limit
(ACGIH,
1997
is
defined
as
a
15­
minute
TWA
exposure
which
should
not
be
exceeded
at
any
time
d
wing
the
work
h
y
even
if
the
S­
hour
TWA
is
within
the
TLV­
TWA.
Exposures
above
the
TLV­
TWA
up
to
the
STEL
should
not
be
longer
than
15
minutes
and
should
not
occur
more
than
4
times
per
day.
There
should
be
at
least
60
minutes
between
successive
exposures
in
this
range.

J
MAK
(Maximale
Arbeitsplatzkonzentration
[Maximum
Workplace
Concentration
Deutsche
Forschungs­
gemeinschaft
[German
Research
Association],
Germany)
(DF
24
,
1999)
is
defined
analogous
to
the
ACGIH­
TLV­
TWA.
1
2
3
4
5
4
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
MAK
Spitzenbegrenzung
(Kategorie
II,
2)
Peak
Limit
Catego
II,
2]
(DFG,
1999
constitutes
the
maximum
average
concentrahon
to
which
wor
5iz
ers
can
be
exposel?
rfor
a
period
up
to
3
0
minutes,
with
no
more
than
2
exposure
periods
per
work
shift,
total
exposure
may
not
exceed
8­
hour
MAK.

Einsatztoleranzwert
Action
Tolerance
Levels]
(Vereiqigung
zur
Forderung
des
deutschen
BrandschutzGs
e.
V.
[IFederabon
I
or
the
Advancement
of
German
Fire
Prevenuon])
conwtutes
a
concentrahon
to
which
unprotected
firemen
and
the
general
population
can
be
exposed
to
for
up
to
4
hours
without
any
health
risks.

J
MAC
(Maxlmaal
Aanvaarde
Concentratie
[Maximum
Accepted
Concentration])
SDU
Uitgevers
under
the
auspices
of
the
Ministry
of
Social
Affairs
and
Employment],
The
Hague,
4
he
Netherlands
[2
000)
is
defined
analgous
to
the
ACGIH­
TLV­
TWA
8.3
creates
substantial
uncertainty
regarding
the
exposure­
response
relationship
for
the
toxic
response
to
this
chemical.
Although
qualitative
data
are
available
regarding
the
acute
inhalation
toxicity
of
phosphorus
trichloride
in
humans,
quantitative
exposure­
response
data
are
lacking.
Quantitative
exposure­
response
data
are
severely
limited
for
nonlethal
responses
in
animals.
These
deficiencies
result
in
an
incomplete
picture
of
the
exposure
concentration­
response
curve
and
exposure
duration­
response
for
phosphorus
trichloride.
Additional
data
are
also
needed
regarding
the
mechanism
of
action,
possible
systemic
effects
(e.
g.,
renal
toxicity),
and
latency
in
the
toxic
responses
(e.
g.,
pulmonary
damage)
following
acute
inhalation
exposure
to
phosphorus
trichloride.
Data
Adequacy
and
Research
Needs
The
overall
robustness
of
the
data
base
for
phosphorus
trichloride
toxicity
is
poor.
The
lack
of
data
15
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
PHOSPHORUS
TRICHLORIDE
9,
REFERENCES
CITED
PROPOSED
1:
05/
2002
ACGIH
(American
Conference
of
Governmental
Hygienists).
11991.
Documentation
ofthe
Threshold
Limit
Values
and
Biological
Exposure
Indices.
6th
ed.
ACGH,
Cinc.,
OH.
pp.
1261­
1262.

ACGM.
(American
Conference
of
Governmental
Hygienists).
1997.
Threshold
Limit
Values
for
Chemical
Substances
and
Physical
Agents
and
Biological
Exposure
Indices.
ACGIH.

AIHA
(American
Industrial
Hygiene
Association).
1999.
The
ATHA
1999
Emergency
Response
Planning
Guideline
an
d
W
or
k
PI
e
E
n
vi
ro
n
m
en
ta
1
E
P
2IC
X
os
UT
e
L
ev
el
G
ui
de
H
d
b
S
an
0
0
'
k.
A
m
er
In
d
16
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
US
tri
a1
H
gig
ie
ne
A
ss
oc
F
ai
rf
ax
V
A
Barbee,
S.
J.,
Stone,
J.
J.,
Hilaski,
R.
J.
1995.
Acute
inhalation
toxicology
of
oxalyl
chloride.
Am.
Ind.
Hyg.
J.
56:
74­
76.

Beliles,
R.
P.,
Beliles,
E.
M.
Phosphorus,
selenium,
tellurium,
and
sulfur.
In:
Clayton,
G.
D.,
Clayton,
F.
E.,
Eds.
Patty's
Industrial
Hygiene
and
Toxicology.
Vol.
II.
4th
ed.,
John
Wiley
&
Sons,
Inc.,
New
York.
pp.
790­
791.

Budavari,
S.,
O'Neil,
M.
J.,
Smith,
A.,
Heckelman,
P.
E.,
Kennedy,
J.
F.,
Eds.
1996.
Phosphorus
trichloride.
The
Merck
Index.
Merck
and
Co.,
Whitehouse,
NJ.

Butjagin,
P.
W.
1904.
Experimentelle
Studien
uber
den
Einflufs
technisch
und
hygienisch
wichtiger
Gase
und
Diimpfe
auf
den
Organismus.
Teil
XII.
Studien
uber
phosphortrichlorid.
Archiv
f.
Hyg.
49:
307­
335.

Fee,
D.
C.,
Gard,
D.
R.,
Yang,
C­
H.
1996.
Phosphorus
compounds.
In:
Kirk­
Othmer
Encyclopedia
of
Chemical
Technology.
Pp.
761­
765.
Vol.
18.
John
Wiley
&
Sons,
New
York.

German
Research
Association
peutsche
Forschungsgemeinschaft).
1
999.
List
of
MAK
and
BAT
Values
1999.
Commission
for
the
Investigation
of
Health
Hazards
of
Chemical
Compounds
in
the
Work
Area.
Report
No.
35.

Hazleton
Laboratories.
1983.
Subacute
inhalation
toxicity
study
in
rats
­
phosphorus
trichloride.
Final
Report.
Project
No.
24
1­
1
4
1,
Hazleton
Laboratories
America,
Inc.
Unpublished.

HSDB
(Hazardous
Substances
Data
Bank).
1998.
On­
line
Moody,
P.
1981.
Health
hazard
evaluation
Report
HETA
81­
089­
965
FMC
Corporation,
Nitro,
West
Virginia.
US.
Dept.
Health
and
Human
Services,
Center
for
Disease
Control,
National
Institute
for
Occupational
Safety
and
Health,
Cincinnati,
OH.

NOSH
(National
Institute
for
Occupational
Safety
and
Health).
1994.
Documentation
for
Immediately
Dangerous
to
Life
or
Health
Concentrations
(IDLHS).
National
Institute
for
Occupational
Safety
and
Health,
Cincinnati,
OH;
PB94195047,
National
Technical
Information
Service,
Springfield,
VA.

17
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
NIOSH
(National
Institute
for
Occupational
Safety
and
Health).
1999.
NOSH
Pocket
Guide
to
Chemical
Hazards.

18
N
1
0
5
R
P
bl
ic
at
io
n
9
4­
1
1
6,
U
.s
D
eP
t.
H
ea
It
h
d
H
m
5
er
vi
ce
s;
U
.s
G
er
n
m
en
t
Pr
in
ti
n
U
an
U
an
ov
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
26)
02
1
2
3
4
5
6
7
8
9
IO
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
g
0
f3­
i
ce
W
as
hi
f3t
n,
D
.c
,

n
0
OSHA
(Occupational
Safety
and
Health
Administration).
1999.
Limits
for
Air
Contaminants.
Table
2­
1.
Code
of
Federal
Regulations
29,
Part
1910.
Office
of
the
Federal
Register
National
Archives
and
Records
Administration.

RTECS
(Registry
of
Toxic
Effects
of
Chemical
Substances),
1998.
On­
line
retrieval.

Sassi,
C.
1952.
Occupational
poisoning
due
to
phosphorus
trichloride.
AMA
Arch.
Ind.
Hyg.
Occ.
Med.
7,
178.
(English
translation
of
abstract.)

ten
Berge,
W.
F.,
Zwart,
A.,
Appelman,
L.
M.
1986.
Concentration­
time
mortality
response
relationship
of
irritant
and
systemically
acting
vapours
and
gases.
J.
Hazard.
Materials
13:
301­
309.

Tharr,
D.
G.,
Singal,
M.
1980.
Health
hazard
evaluation
determination.
Report
No.
HHE­
78­
90­
739,
FMC
Corp.,
Specialty
Chemicals
Div.,
Nitro,
WV.
NTIS
Publ.
No.
PB­
83­
161­
190.

Wason,
S.,
Gomolin,
I.,
Gross,
P.,
Lovejoy,
F.
H.,
Jr.
1982.
Phosphorus
trichloride
exposure
­
a
follow­
up
study
of
27
exposed
patients.
Vet.
Human
Toxicol.
24:
275­
276.(
ubsfracf)

Wason,
S.,
Gomolin,
I.,
Gross,
P.,
Mariam,
S.,
Lovejoy,
F.
H.
1984.
Phosphorus
trichloride
toxicity­
preliminary
report.
Amer.
J.
Med.
77:
1039­
1042.

Weeks,
M.
H.,
Mussleman,
N.
P.,
Yevich,
P.
P.,
Jacobson,
K.
H.,
Oberst,
F.
W.
1964.
Acute
vapor
toxicity
of
phosphorus
oxychloride,
phosphorus
trichloride
and
methyl
phosphonic
dichloride.
Amer.
Ind.
Hyg.
J.
25:
470­
475.

19
PHOSPHORUS
TRI(@
IHLQRI[
DE
PROPOSED
1:
6)
5/
2002
APPENDIX
A
DERIVATION
OF
AEGL
VALUES
20
27
1
2
3
4
5
4
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
PHOSBHQRUS
TRICHLORIDE
DERlVATIQN
OF
AEGL­
B
VALUES
Key
study:
Hazleton
Laboratories,
1983
Toxicity
endpoint:
NOAEL
of
3.4
ppm
for
rats
following
multiple
exposure
at
6
hrs/
day,
5
days/
week
for
4
weeks.

Scaling:

Uncertainty
factors:

1
O­
min
AEGL­
1
30­
min
AEGL­
1
l­
hr
AEGL­
1
4­
hr
AEGL­
1
8­
hr
AEGL­
1
PROPOSED
1:
05//
2002
The
concentration­
time
relationship
for
may
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
C
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5
(ten
Berge
et
al.,
1986).
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
P
when
extrapolating
to
longer
time
points
using
the
eP,
x
t
=
k
equation.
(3.4
ppm)
'
x
6
hrs
=
20.4
ppm
*
hrs
(n
=
1)
(3.4
~p
m
)~
x
6
hrs
=
235.8
ppm3
*
hrs
(n
=
3)

Interspecies
UF
=
3;
the
attenuation
of
this
uncertainty
factor
is
justified
by
the
fact
that
the
guinea
pig
appears
to
be
the
most
sensitive
species
tested
and
because
limited
human
exposure
data
(Sassi,
1952)
indicate
that
humans
have
experienced
routine
occupational
exposures
of
up
to
3.6
ppm
without
effect.
Intraspecies
UF
=
3;
contact
irritation
and
subsequent
tissue
damage
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociaton
and
direct
corrosive
action
of
these
components
on
epithelial
surfaces.
Additional
application
of
uncertainty
factor
adjustment
would
provide
AEGL­
3
values
that
are
inconsistent
with
limited
data
on
human
exposures.

The
10­
minute
AEiGL­
1,
was
set
equivalent
to
the
30­
minute
value
due
to
uncertainties
in
extrapolating
from
the
6­
hour
experimental
exposure
duration.

C3
x
0.5
hr
=
235.8
ppm3
­hr
C
=7.78ppm
30­
min
AEGL­
1
=
7.78
ppm/
lO
=
0.78
ppm
(4.4
mg/
m3)

C3
x
1
hr
=
235.8
ppm3­
hr
C
=6.18ppm
l­
hr
AEGL­
1
=6,18ppm/
lO
=0.62ppm(
3.5mg/
m3)

C3
x
4
hrs
=
235.8
ppm3­
hr
C
=
3.89
ppm
4­
hr
AEGL­
1
=
3.89
ppm/
lO
=
0.39
ppm
(2.2
mg/
m3)

C'
x
8
hrs
=
20.4
ppm­
hr
C
=2.55ppm
8­
hr
AEGL­
1
=
2.55
ppm/
lO
=
0.26
pprn
(1.5
mg/
m3)

21
PHQSPMORUS
TRICHLORIDE
PROPOSED
I:
05f2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
DERIVATION
OF
AEGE­
2
Key
study:
Hazleton
Laboratories,
1983
Toxicity
endpoint:
LOAEL
of
11
ppm
for
respiratory
tract
histopathologic
changes
in
rats
following
multiple
exposure
at
6
Rrslday,
5
daystweek
for
4
weeks.

Scaling:
The
concentration­
time
relationship
for
may
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
c"
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5
(ten
Berge
et
al.,
1986).
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
1
when
extrapolating
to
longer
time
points
using
the
C"
x
t
=
k
equation.
(1
1
pprn)
'
x6hrs
=
66
ppm
­
hrs
(n
=
1)
(1
1
~p
m
)~
x
6
hrs
=
7986
ppm3
hrs
(n
=
3)

Uncertainty
factors:
Interspecies
W
=
3;
the
attenuation
of
this
uncertainty
factor
is
justified
by
the
fact
that
the
guinea
pig
appears
to
be
the
most
sensitive
species
tested
and
because
limited
human
exposure
data
(SassiJ952)
indicate
that
humans
have
experienced
routine
occupational
exposures
of
up
to
3.6
ppm
without
effect.
Intraspecies
UF
=
3;
contact
irritation
and
subsequent
tissue
damage
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
disswiaton
and
direct
corrosive
action
of
these
components
on
epithelial
surfaces.
Adjustments
using
a
greater
level
of
uncertainty
uncertainty
would
provide
AEGL­
2
values
that
are
inconsistent
with
limited
data
on
human
exposures.

1
0­
min
AEGL­
2
The
10­
minute
AEGL­
2,
was
set
equivalent
to
the
30­
minute
value
(2.5
ppm)
due
to
uncertainties
in
extrapolating
from
the
6­
hour
experimental
exposure
duration
to
a
1
0­
minute
duration.

30­
min
AEGL­
2
1
­hr
AEGL­
2
4­
hr
AEGL­
2
C3
x
0.5
hr
=
7986
ppm3
­hr
C
=25.2ppm
30­
min
AEGL­
2
=
25.2
ppm/
lO
=
2.5
ppm
(14
mg/
m3)

C3
x
1
hr
=
7986
ppm3*
hr
C
=
20.0
ppm
1­
hr
AEGL­
2
=
20.0
ppm/
lO
=
2.0
ppm
(1
1
mg/
m3)

C3
x
4
hrs
=
7986
ppm3­
hr
C
=
12.6ppm
4­
hr
AEGL2
=
12.6
ppm/
lO
=
1.3
ppm
(7.3
mg/
m3)

22
PHOSPHORUS
TRICHLORIDE
1
8­
hr
AEGL­
2
2
3
4
C'x8hrs
=66ppmhr
C
=8.25ppm
8­
hr
AEGL­
2
=
8.25
ppm/
lO
=
0.83
ppm
(4.6
mg/
m3)

23
PROPOSED
1:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
PHOSPHORUS
TRICHLORIDE
DERIVATION
OF
AEGL­
3
Key
study:

Toxicity
endpoint:
Lethality
threshold
estimated
as
3­
fold
reduction
in
the
4­
hr
LCso
for
rats
Weeks
et
al.
1964
(104.3
ppd3
=
34.8
pprn),
delayed
response
possible.
PROPOSED
1:
05/
2002
Scaling:

Uncertainty
factors:

1
0­
min
AEGL­
3
30­
min
AEGL­
3
1
­hr
AEGL­
3
4­
hr
AEGL­
3
8­
hr
AEGL­
3
The
concentration­
time
relationship
for
may
initant
and
systemically
acting
vapors
and
gases
may
be
described
by
C"
x
t
=
k
,
where
the
exponent
n
ranges
fiom
0.8
to
3.5
(ten
Berge
et
al.,
1986).
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
1
when
extrapolating
to
longer
time
points
using
the
c"
x
t
=
k
equation.
(34.8
pprn)
'
x
4
hrs
=
139.2
ppm
9
hrs
(n
=
1)
(34.8
~p
m
)~
x
4
hrs
=
168,576.8
ppm3
*
hrs
(n
=
3)

Interspecies
UF
=
3;
the
attenuation
of
this
uncertainty
factor
is
justified
by
the
fact
that
the
guinea
pig
appears
to
be
the
most
sensitive
species
tested
and
because
limited
human
exposure
data
(Sassi,
1952)
indicate
that
humans
have
experienced
exposures
of
up
to
27
ppm
without
life­
threatening
consequences
Intraspecies
UF
=
3;
contact
initation
and
subsequent
tissue
damage
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphoric
acid
resulting
from
chemical
dissociaton
and
direct
corrosive
action
of
these
components
on
epithelial
surfaces.
Additional
application
of
uncertainty
factor
adjustment
would
provide
AEGL­
3
values
that
are
not
consistent
with
limited
data
on
human
exposures
or
with
the
results
ofrepeated
exposures
in
rats
wherein
exposure
to
1
1
ppm
6
hrdday,
5
daydweek
for
4
weeks
showed
only
histologic
changes
in
the
upper
respiratory
tract
and
no
overt
signs
of
toxicity
Due
to
uncertainties
in
extrapolating
from
a
4­
hour
to
lo­
minute
exposure,
the
1
0­
minute
AEGL­
3
is
set
equivalent
to
the
3O­
minute
value
(7.0
ppm).

C3
x
0.5
hr
=
168,576.8
ppm3
­hr
C
=
69.6
ppm
30­
min
AEGL­
3
=
69.6
ppm/
lO
=
7.0
ppm
(39
mg/
m3)

C3
x
1
hr
=
168,576.8
ppm3*
hr
C
=55.2ppm
I­
hr
AEGL­
3
=
55.2
ppm/
lO
=
5.6
ppm
(31
mg/
m3)

C3
x
4
h
r
~
=
168,576.8
ppm3­
hr
C
=
34.8
ppm
4­
hr
AEGL­
3
=
34.8
ppm/
lO
=
3.5
ppm
(20
mg/
m3)
'

24
PHOSPHORUS
TRICHLORIDE
C'
x
8
hrs
=
139.2
ppmhr
C
=
117.4
pgm
8­
hrAJ5GL­
3
=
17.4
ppm/
lO
=
1.8
ppm
(10
mg/
m3>
1
2
3
25
PROPOSED
1:
05/
2002
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
APPENDIX
B
DERIVATION
SUMMARY
FOR
PHOSPHORUS
TRICHLORIDE
AEGL
VALUES
3
3
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
ACUTE
EXPOSURE
GUIDELINES
FOR
PHOSPHORUS
TRICHLORIDE
(GAS
NO.
7719­
12­
2)

mGL­
1
VALUES
10
minutes
30
minutes
1
hour
4
hours
8
hours
0.78
ppm
0.78
ppm
0.62
ppm
0.39
ppm
0.26
ppm
Reference:
Hazleton
Laboratories,
1983
Test
SpecieslStrainlNumber:
Sprague­
Dawley
rats;
1
S/
sex/
group
Exposure
RouteJConcentrationsDurations:
Inhalation
exposure
(whole­
body)
to
0,0.5,3.0,
or
10.0
ppm
(nominal)
for
6
hrslday,
5
dayslweek
for
4
weeks
Toxicity
Endpoint:
No
effects
noted
at
3.4
ppm
(analytical)
following
multiple
exposure
of
rats
over
4
weeks
Time
Scaling:
The
concentration­
time
relationship
for
may
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
Cn
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5.
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
1
when
extrapolating
to
longer
time
points
using
the
Cn
x
t
=
k
equation.
For
10­
minute
AEGL­
1,
values
were
set
at
equivalence
to
the
30­
minute
values
due
to
uncertainties
in
extrapolating
from
the
experimental
exposure
durations
of
4
hours
or
greater.

Concentratioflime
SelectionRationale:
In
the
absence
of
exposure­
response
data
specific
for
AEGL­
1
effects,
the
exposure
to
3.4
ppm
at
6
hrs/
day,
5
daydweek
for
4
weeks
was
selected
as
a
conservative
basis
for
AEGL
development.

Uncertainty
FactorsRationale:
Total
uncertainty
application
of
10.
The
interspecies
uncertainty
factor
was
limited
to
3
because
of
the
concordance
of
the
animal
data
with
the
human
experience
and
because
the
most
sensitive
species
tested
(guinea
pig)
was
only
about
2­
fold
more
sensitive.
The
intraspecies
uncertainty
factor
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociation.
Furthermore,
the
AEGL­
1
is
based
upon
a
conservative
assumption
and
additional
reduction
of
the
AEGL­
1
values
would
be
inconsistent
with
available
human
and
animal
data.

Modifying
Factor:
Not
applicable
Animal­
to­
Human
Dosimetric
Adjustments:
Not
applicable
Data
Quality
and
Support
of
the
AEGL
Values:
Neither
human
nor
animal
quantitative
exposure­
response
data
are
available
regarding
effects
consistent
with
AEGL­
1
definition..
The
3.4
ppm
exposure
of
rats
over
4
weeks
was
selected
as
a
NOAEL
for
AEGL­
1.
Although
likely
to
be
a
conservative
basis
for
developing
AEGL­
1
values,
it
may
be
justified
due
to
the
relative
paucity
of
data
on
the
toxic
response
to
this
chemical.

27
PHOSPHORUS
TRICHLORIDE
PROPOSED
1:
0512002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
ACUTE
EXPOSURE
GUIDELINES
FOR
PHOSPHORUS
TRICHLORIDE
(CAS
NQ@
7'719­
12­
2)

AEGL­
2
VALUES
10
minutes
30­
minutes
1
hour
4
hours
8
hours
2.5
ppm
2.5
ppm
2,
O
ppm
1.3
ppm
0.83
ppm
Reference:
Hazleton
Laboratories,
1983
Test
SpeciedStraidNumber:
Sprame­
Dawley
rats;
1
5/
sex/
grouu
Exposure
Route/
Concentrations/
Durations:
Inhalation
exposure
(whole­
body)
to
0,0.5,3.0,
or
10.0
ppm
(nominal)
for
6
hrs/
day,
5
daysfweek
for
4
weeks
Toxicity
Endpoint:
Histopathologic
alterations
in
respiratory
tract
in
rats
exposed
to
1
1
ppm
(analyt~
cal),
6
hrs/
day,
5
daydweek
for
4
weeks.
There
were
no
concurrent
hematologic
or
biochemical
alterations
indicative
of
a
toxic
response,
and
there
were
no
ophthalmologic
effects.

Time
Scaling:
The
concentration­
time
relationship
for
may
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
C"
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5.
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
n
=
1
when
extrapolating
to
longer
time
points
using
the
C"
x
t
=
k
equation.
For
10­
minute
AEGL­
2,
values
were
set
at
equivalence
to
the
30­
minute
values
due
to
uncertainties
in
extrapolating
fiom
the
experimental
exposure
durations
of
4
hours
or
greater.

~~
~
~~

Concentration/
Time
SelectiodRationale:
The
multiple
exposure
of
rats
to
1
1
ppm
over
4
weeks
was
considered
a
conservative
estimate
and
NOAEL
for
AEGL­
2
effects
@e.,
the
effects
were
neither
disabling
nor
irreversible).

Uncertainty
FactorsRationale:
Total
uncertainty
application
of
10.
The
interspecies
uncertainty
factor
was
limited
to
3
because
of
the
concordance
of
the
animal
data
with
the
human
experience
and
because
the
most
sensitive
species
tested
(guinea
pig)
was
only
about
2­
fold
more
sensitive.
The
intraspecies
uncertainty
factor
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
from
chemical
dissociation.
Furthermore,
the
AEGL­
2
is
based
upon
a
histopathologic
changes
in
the
respiratory
tract
which
were
not
necessarily
irreversible
or
disabling.
Additional
reduction
of
the
AEGL­
2
values
would
be
inconsistent
with
available
human
and
animal
data.

Modifjring
Factor:
Not
Applicable
Animal­
to­
Human
Dosimetric
Adjustments:
Not
applicable
Data
Quality
and
Support
of
the
AEGL
Values:
Limited
information
regarding
the
human
experience
indicated
that
2
to
6­
hour
exposures
to
1.8­
3.6
ppm
were
without
effect
and
that
exposure
to
14­
27
ppm
irritation
of
the
eyes
and
upper
respiratory
tract,
photophobia,
chest
tightness,
and
bronchitis.
Because
the
effects
were
neither
disabling
nor
irreversible,
the
endpoint
used
for
AEGL­
2
development
is
considered
a
NOAEL
for
AEGL­
2
effects.

28
PHOSPHORUS
TRICHLORIDE
PROPOSED
I:
05/
2002
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
ACUTE
EXPOSURE
GUIDELINES
FOR
PHOSPHORUS
TRICHLORIDE
(CAS
NO.
77119­
12­
2)

AEGL­
3
VALUES
10
minutes
30
minutes
1
hour
4
hours
8
hours
7.0
pprn
7.0
ppm
5.6
ppm
3.5
ppm
1
.8
ppm
Reference:
Weeks,
M.
H.,
Mussleman,
N.
P.,
Yevich,
P.
P.,
Jacobson,
K.
H.,
Oberst,
F.
W.
1964.
Acute
vapor
toxicity
of
phosphorus
oxychloride,
phosphorus
trichloride
and
methyl
phosphonic
dichloride.
h
e
r
.
Ind.
Hyg.
J.
25:
470­
475.

Test
SpecieslStraiidNumber:
female
rats
/strain
not
specifiW20
per
group
Exposure
Route/
Concentrations/
Durations:
inhalatiordmedian
lethal
concentrations
derived
but
exposure
concentrations
Toxicity
Endpoint:
estimated
lethality
threshold
by
3­
fold
reduction
of
rat
4­
hr
LC50
of
104.3
ppm
Time
Scaling:
The
concentration­
time
relationship
for
may
irritant
and
systemically
acting
vapors
and
gases
may
be
described
by
e
x
t
=
k
,
where
the
exponent
n
ranges
from
0.8
to
3.5.
Due
to
the
limited
toxicity
data
for
this
chemical,
an
empirical
derivation
of
n
was
not
possible.
In
the
absence
of
an
empirically
derived
exponent
(n),
and
to
obtain
conservative
and
protective
AEGL
values,
temporal
scaling
was
performed
using
n
=
3
when
extrapolating
to
shorter
time
points
and
N
=
1
when
extrapolating
to
longer
time
points
using
the
C"
x
t
=
k
equation.
not
specified14
hrs
(34.8
pprn)
'
x
4
hrs
=
139.2
ppm
+
hrs
(n
=
1)
(34.8
~p
m
)~
x
4
hrs
=
168,576.8
ppm3
hrs
(n
=
3)

Concentratioflime
Selectionmationale:
a
3­
fold
reduction
of
the
rat
4­
hr
LCso
(104.3
ppd3
=
34.8
ppm)
was
used
as
Uncertainty
FactorsMationale:
an
estimate
of
the
lethality
threshold.

Total
Uncertainty:
10
Interspecies
UF
=
3
Intraspecies
UF
=
3
Data
for
humans
and
animals
indicate
some
variability
in
the
toxic
response
to
phosphorus
trichloride
but
LCso
values
for
rodents
exhibited
approximately
a
2­
fold
difference.
The
uncertainty
for
intraspecies
variability
was
limited
to
3
because
primary
effects
of
phosphorus
trichloride
(irritation
and
subsequent
tissue
damage)
appear
to
be
due,
in
part,
to
hydrogen
chloride
and
phosphonic
acid
resulting
fiom
chemical
dissociation
and
the
direct
corrosive
action
of
these
on
epithelial
tissue.
The
overall
uncertainty
factor
adjustment
of
10
may
be
justified
by
limited
human
exposure
data
suggesting
that
humans
could
experience
exposures
of
up
to
27
ppm
without
life­
threatening
consequences.
Furthermore,
the
results
of
a
multiple
exposure
studies
in
rats
(1
1
ppm
6
brdday,
5
daydweek
for
4
weeks)
showed
only
histologic
changes
in
the
upper
respiratory
tract
and
no
overt
signs
of
toxicity.

Modifying
Factor:
none
applied
Animal­
to­
Human
Dosimetric
Adjustments:
insufficient
data
29
PHOSPHORUS
TRICHLORIDE
PROPOSED
I:
05/
2002
Data
Quality
and
Support
for
the
AEGL
Values:
Lethality
data
are
limited
to
two
species
and
quantitative
data
for
humans
are
limited.
However,
comparison
ofthe
AEGL­
3
values
with
available
data
do
not
support
application
of
uncertainty
adjustment
greater
than
that
currently
applied.
Data
suitable
for
determining
exposure­
time
relationsRips
are
also
lacking
and
impact
on
temporal
extrapolation
efforts.
A
delayed
response
is
possible
as
demonstrated
in
the
Weeks
et
al.
(1
964)
study
in
which
deaths
of
guinea
pigs
occurred
up
to
10
days
post
exposure.

30