Document ID: EPA-HQ-OPP-2004-0301-0006
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2004-09-10T04:00Z

inc.

Phenol
RED
Document
Prepared
for:
Office
of
Pesticide
Programs
Antimicrobials
Division
U.
S.
Environmental
Protection
Agency
1801
South
Bell
Street
Arlington,
VA
22202
TABLE
OF
CONTENTS
1.0
EXECUTIVE
SUMMARY
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1
2.0
PHYSICAL/
CHEMICAL
PROPERTIES
CHARACTERIZATION
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8
2.1
Chemical
Identification
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8
2.2
Physical/
Chemical
Properties
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8
3.0
HAZARD
CHARACTERIZATION
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10
3.1
Hazard
Profile
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10
3.2
FQPA
Considerations
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25
3.3
Dose­
Response
Assessment
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27
3.4
Endocrine
Disruption
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28
4.0
EXPOSURE
ASSESSMENT
AND
CHARACTERIZATION
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29
4.1
Summary
of
Registered
Uses
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29
4.2
Dietary
Exposure/
Risk
Pathway
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29
4.2.1
Methodology
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30
4.2.2
Acute
Dietary
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30
4.2.3
Chronic
Dietary
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30
4.3
Water
Exposure/
Risk
Pathway
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31
4.4
Residential
Exposure/
Risk
Pathway
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33
4.4.1
Residential
Handler
Scenarios
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33
4.4.1.1
Paint
Exposures
and
Risks
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33
4.4.1.2
Disinfectant/
Deodorizing
Spray
and
Towlette
Exposures
and
Risks
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34
4.4.2
Residential
Postapplication
Exposure
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37
5.0
AGGREGATE
RISK
ASSESSMENTS
AND
RISK
CHARACTERIZATIONS
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38
5.1
Acute
and
Chronic
Oral
Risk
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38
5.2
Short­,
Intermediate­,
and
Long­
Term
Dermal
Risk
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38
5.2
Short­,
Intermediate­,
and
Long­
Term
Inhalation
Risk
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39
6.0
OCCUPATIONAL
EXPOSURE
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44
6.1Occupational
Handlers..................................................................................................
44
6.2
Occupational
Postapplication.................................................................................
48
7.0
ENVIRONMENTAL
FATE
ASSESSMENT
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48
8.0
ECOTOXICOLOGY
ASSESSMENTS
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49
8.1
Terrestrial
Animals
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49
8.2
Freshwater
Fish
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49
8.3
Freshwater
Invertebrates
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51
8.4
Estuarine
and
Marine
Organisms
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53
8.5
Plants
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53
9.0
REFERENCES
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54
LIST
OF
TABLES
Table
2.1.
Chemical
Identification
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Table
2.2.
Physical/
Chemical
Properties
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Table
2.2
Physical/
Chemical
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Table
3.1.
Acute
Toxicity
of
Phenol
and
Phenol
salts
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Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
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Table
3.3
Summary
of
Toxicological
Doses
and
Endpoints
for
Phenol/
Sodium
phenate
for
Use
in
Human
Risk
Assessment
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Table
4.1.
EPA
Registration
Numbers
for
Phenol
Products
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Table
4.2.
Summary
of
Dietary
Exposure
and
Risk
for
Phenol
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Table
4.3.
Calculation
of
Dermal
and
Inhalation
MOE
for
Residential
Handlers
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Table
4.4.
Short­
and
Intermediate­
term
Risks
Associated
with
Postapplication
Exposure
to
Disinfectant
on
Carpets
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Table
5.1
Short
and/
or
intermediate
term
aggregate
oral/
dermal
risk.
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Table
5.2
Short­
and/
or
intermediate
term
aggregate
inhalation
risk.
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Table
6.1.
Calculation
of
Dermal
and
Inhalation
MOE
for
Commercial/
Institutional
Scenarios
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Table
8.1.
Acute
Toxicity
of
Phenol
to
Freshwater
Fish
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Table
8.2.
Acute
Toxicity
of
Phenol
to
Freshwater
Invertebrates
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Table
8.3.
Acute
Toxicity
of
Phenol
to
Marine/
Estuarine
Invertebrates
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Table
8.4.
Chronic
Toxicity
of
Phenol
to
Marine/
Estuarine
Invertebrates
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Page
1
of
57
1.0
EXECUTIVE
SUMMARY
Phenol
(
hydroxybenzene,
carbolic
acid,
phenyl
hydroxide)
and
sodium
phenate,
is
registered
with
the
Office
of
Pesticides
Programs
(
OPP)
as
an
active
ingredient
and
used
as
an
intermediate
in
the
production
of
epoxy
resins
and
various
other
products,
as
a
general
disinfectant,
and
in
medicinal
preparations.
It
is
used
to
control
Animal
Pathogenic
Bacteria
(
Gand
G+
Vegetative),
Pseudomonas
SPP.,
Mycobacterium
SPP.
(
Tubercle
Bacilli),
Animal
Pathogenic
Fungi,
Hydrophilic
Viruses,
Poliovirus
Type
1,
Parvovirus,
Lipophilic
Viruses,
Vaccinia
Virus,
Influenza
A2
(
Hong
Kong,
Japan,
Japan
305/
57
Asian
Strain),
HIV­
I
(
Human
Immunodeficiency
Virus),
and
mold/
mildew.

Formulated
as
a
pressurized
and
ready­
to­
use
liquid,
phenol
is
registered
for
use
as
a
sanitizer,
bacteriostat,
fungicide/
fungistat,
tuberculocide,
disinfectant,
and
virucide
(
EPA
Reg.
No.
707­
159).
Phenol
has
a
number
of
use
sites
including
indoor
food
uses
in
eating
establishments
on
equipment
and
utensils,
non­
food
indoor
uses
in
commercial­
transportation
facilities,
institutional/
industrial
floors,
industrial
premises/
equipment,
laundry
equipment,
paints,
latex,
and
specialty
industrial
products.
Indoor
residential
uses
of
phenol
encompass
the
bathroom
premises,
hard
surfaces,
diaper
pails,
dogs/
canines,
household/
domestic
dwellings,
and
solid
waste
containers
(
garbage
cans).
Phenol
also
has
indoor,
medical
uses
on
surgical
instruments
and
pacemakers
(
critical
items),
catheters
and
inhalation
equipment
(
semi­
critical
items),
bedpans
and
furniture
(
noncritical
items),
non­
conductive
floors,
critical
premises
(
burn
wards),
noncritical
premises,
patient
premises,
and
institution
premises
(
human/
veterinary).
Phenol
is
also
found
in
over­
the­
counter
drugs
for
the
treatment
of
various
conditions,
including
insect
bites,
poison
ivy,
diaper
rash,
antiseptics,
and
acne
(
21
CFR
§
310.531
and
§
310.545).
Concentrations
in
these
formulations
range
from
1.6­
8.2%.

Phenol
is
produced
through
both
natural
and
anthropogenic
processes.
It
is
naturally
occurring
in
some
foods,
in
human
and
animal
wastes,
and
in
decomposing
organic
material,
and
it
is
produced
endogenously
in
the
gut
from
the
metabolism
of
aromatic
amino
acids.
Phenol
has
been
isolated
from
coal
tar,
but
is
now
synthetically
manufactured.
Currently,
the
largest
use
of
phenol
is
as
an
intermediate
in
the
production
of
phenolic
resins,
which
are
used
in
the
plywood,
adhesive,
construction,
automotive,
and
appliance
industries.
Production
and
use
of
phenol
and
its
products,
especially
phenolic
resins
and
caprolactam,
exhaust
gases,
residential
wood
burning
and
cigarette
smoke
are
potential
sources.

Hazard:
Phenol
has
a
moderate
order
of
acute
toxicity
via
the
oral
and
dermal
routes
of
exposure
(
Toxicity
Category
II
or
III)
and
produces
severe
and
marked
irritation
to
the
eyes
and
skin
(
Toxicity
Category
I
or
II).
Phenol
concentrations
used
in
acute
inhalation
studies
failed
to
induce
mortality
in
the
study
animals;
therefore,
toxicity
endpoints
and
a
toxicity
category
could
not
be
established.

In
the
subchronic
database,
oral
range­
finding
studies
in
both
the
rat
and
the
mouse
were
completed.
Although
the
studies
were
non­
guideline
(
due
to
the
lack
of
subchronic
parameters),
Page
2
of
57
systemic
toxicities
were
noted
at
10,000
ppm
in
the
rat
and
mouse,
based
on
a
decrease
in
mean
body
weight
gain.
In
a
two­
week
inhalation
study,
rats
had
elevated
plasma
Mg2+
levels
(
Hypermagnesaemia)
and
exhibited
toxic
effects
in
the
central
nervous
system
(
CNS).

Phenol
was
administered
in
two
developmental
guideline
studies
in
the
rat
and
mouse
at
concentrations
of
30,
60,
or
120
mg/
kg/
day
and
70,
140,
or
280
mg/
kg/
day,
respectively.
There
was
no
evidence
of
toxicity
in
these
animals
at
concentrations
below
the
high­
dose.
Fetal
body
weight
was
significantly
reduced
at
120
(
rat)
and
280
(
mouse)
mg/
kg/
day.
Additionally,
female
mice
experienced
increased
mortality
and
clinical
signs
of
CNS
toxicity
(
tremors,
ataxia,
lethargy)
at
the
high­
dose
(
280
mg/
kg/
day).
The
NOAEL
was
determined
to
be
60
mg/
kg/
day.

In
a
two­
generation
reproductive
study
in
rats
exposed
to
200,
1,000,
or
5,000
ppm
phenol
in
drinking
water
for
10
weeks/
generation,
there
were
decreases
in
water
and
food
consumption,
body
weight
and
body
weight
gain
at
the
high­
dose
(
potential
reduced
palatability).
Offspring
toxic
effects
including
decreases
in
body
weight
and
litter
survival
were
observed
at
5,000
ppm.
This
occurred
concurrently
with
maternal
toxicity
(
decreased
maternal
body
weight);
believed
to
be
secondary
to
the
animals'
aversion
to
the
flavor
of
the
phenol­
treated
water
and
resulted
in
decreased
maternal
as
well
as
offspring
body
weight.
In
a
non­
guideline
reproductive
study
(
Bishop,
et
al.
1997),
phenol
was
administered
to
mice
at
a
concentration
of
350
mg/
kg.
There
were
no
treatment­
related
clinical
signs
or
mortality
observed
in
maternal,
reproductive,
and
developmental
parameters
and
the
lowest­
observable
adverse
effects
level
(
LOAEL)
was
not
established
(
highest
dose
tested,
350
mg/
kg).

Two
carcinogenicity
studies
performed
by
the
National
Cancer
Institute
did
not
report
an
increased
incidence
of
neoplasms
in
male
and
female
mice
or
rats
following
administration
of
phenol,
with
the
exception
of
a
statistically
significant
increase
in
the
occurrence
of
leukemia,
lymphoma,
or
interstitial­
cell
tumors
in
low­
dose
male
rats.
Due
to
the
lack
of
significant
tumors
in
high­
dose
males
and
the
absence
of
significant
neoplasms
in
mice
and
female
rats,
phenol
was
found
to
be
non­
carcinogenic
in
the
2­
year
drinking
water
studies.
Although
phenol­
treated
rats
and
mice
experienced
a
decrease
in
mean
body
weight
and
body
weight
gain,
the
reduction
was
not
significantly
different
from
the
respective
controls
and
chronic
toxicity
was
not
observed
at
phenol
concentrations
up
to
5,000
ppm.
A
20­
week
dermal
study
exhibited
effects
of
chronic
irritation
and
hair
growth
inhibition
with
administration
of
3
mg
phenol
(
in
200
uL
acetone).
A
single
papilloma
was
found
7
weeks
into
the
study,
but
there
was
no
evidence
that
it
was
significantly
increased
or
treatment­
related.
In
a
special,
mechanistic
study,
there
was
no
evidence
of
tumor
initiation
or
hepatocyte
GSH
depletion
following
administration
of
100
mg/
kg/
day
phenol.
Phenol
is
classified
as
a
Group
D
carcinogen;
there
is
inadequate
or
no
human
or
animal
evidence
of
carcinogenicity.

The
results
of
the
mutagenicity
studies
indicated
that
phenol
was
not
mutagenic
in
Salmonella
typhimurium
or
Drosophila
melanogaster
and
did
not
induce
micronuclei
or
bone
marrow
chromosomal
aberrations
in
mice.
However,
mutagenic
effects
were
observed
in
Chinese
Hamster
Ovary
cells
and
spermatocytes
in
mice
and
HL60
cells.
The
genotoxic
potential
of
Page
3
of
57
phenol
appears
to
depend
on
the
competing
processes
of
activation
to
a
genotoxic
form
and
metabolic
inactivation
(
e.
g.,
via
conjugation).
Phenol
tended
to
be
negative
in
bacterial
gene
mutation
assays,
but
was
positive
or
equivocal
in
mammalian
cell
gene
mutation
assays.
Phenol
tended
to
induce
micronuclei
in
mice
when
administered
intraperitoneally,
but
was
negative
(
or
positive
only
at
very
high
doses)
when
administered
orally.
This
difference
is
likely
due
to
the
first­
pass
conjugation
and
inactivation
of
orally
administered
phenol.
Phenol
was
also
positive
in
in
vitro
micronucleus
tests
with
human
lymphocytes
and
Chinese
Hamster
Ovary
cells.
Results
from
DNA
damage
assays
are
inconsistent,
but
they
tend
to
show
that
phenol
can
cause
sister
chromatid
exchanges
or
cell
transformation
if
it
is
not
metabolically
inactivated.
Overall,
phenol
did
not
exhibit
strong
mutagenic
effects.

The
Antimicrobial
Division
Toxicolgy
Endpoint
Selection
Committee
(
ADTC)
committee
noted
neurotoxic
signs
from
acute
dermal
toxicity
studies
(
Brown,
et
al.,
1975
­
convulsions;
OTS
0515567­
tremors;
Conning,
et
al.,
1970
­
stimulation
of
motor
nerve
endings
or
spinal
motor
centers)
and
from
a
15­
day
inhalation
study
(
tilting
plane
results
showed
an
effect
in
treated
rats).
As
noted
in
the
Intergrated
Risk
Information
System
(
IRIS)
Toxicological
profile,
numerous
CNS
effects
have
been
observed
following
phenol
dosing.
Tremors
were
observed
in
one
animal
that
later
died
(
apparently
of
dehydration)
following
dosing
in
drinking
water
(
ClinTrials
BioResearch,
1998).
Tremors
have
also
been
observed
in
several
gavage
studies
in
rats
and
mice
(
43735402;
Dow
Chemical
Co.,
1994;
Moser
et
al.,
1995).
However,
in
a
specialized
13­
week
neurotoxicity
study
in
male
and
female
rats
that
included
a
Functional
Observational
Battery
Study
(
FOB)
and
a
detailed
neurohistopathology
evaluation
(
ClinTrials
BioResearch,
1998),
the
only
observed
nervous
system
effects
were
tremors
in
one
animal
and
decreased
motor
activity
in
females.
A
short­
term
gavage
screening
study
(
Moser,
et
al.,
1995)
found
that
the
only
effect
in
an
FOB
was
a
marginal
decrease
in
motor
activity
and
increased
rearing
post­
exposure.
Part
of
this
could
be
attributed
to
the
dehydration
observed
in
the
study.

Toxicity
Endpoints:
The
toxicity
endpoints
used
in
this
document
to
assess
potential
risks
include
the
chronic
dietary
reference
dose
(
RfD),
and
short­,
intermediate­
and/
or
long­
term
incidental
oral,
dermal,
and
inhalation
doses.
The
endpoints
selected
were
reviewed
by
the
ADTC
in
2004.

Dietary
Endpoints:
On
March
9,
2004,
the
ADTC
reviewed
the
available
toxicology
data
for
phenol
and
discussed
endpoint
selection
for
use
as
appropriate
in
occupational/
residential
exposure
risk
assessments.
The
ATDC
determined
that
for
acute
dietary
risk,
there
was
no
appropriate
endpoint
for
assessment.
The
conclusion
was
based
upon
examination
of
the
hazard
data
which
might
be
used
in
support
of
such
an
endpoint.
Body
weight
effects
observed
are
not
believed
to
be
the
result
of
a
single
exposure,
and
there
were
no
other
effects
from
the
data
that
were
considered
reflective
of
an
adverse
effect
from
a
single
exposure.
An
acute
RfD
value
was
not
selected.

For
chronic
dietary
risk,
the
ATDC
cited
the
published
chronic
RfD
value
in
EPA's
Integrated
Risk
Information
System
(
IRIS)
database.
This
RFD
value
is
based
upon
an
Page
4
of
57
unpublished
developmental
toxicity
study
conducted
according
to
GLP
guidelines
(
Argus
Research
Laboratories,
1977).
The
chronic
RfD
value
was
determined
to
be
0.6
mg/
kg/
day.
The
ATDC
determined
that
a
special
hazard­
based
safety
factor
was
not
required
for
phenol
and
could
be
reduced
to
1x.

Based
on
Agency
policy,
a
RfD
modified
by
a
FQPA
safety
factor
is
a
population
adjusted
dose
(
PAD).
The
chronic
RfD
value
was
calculated
to
be
0.6
mg/
kg/
day,
based
on
a
maternal
No
Obsevable
Adverse
Effects
Level
(
NOAEL)
value
of
60
mg/
kg/
day
and
an
uncertainty
factor
of
100
(
10x
interspecies
extrapolation,
10x
intraspecies
variation).
The
Agency
calculated
a
chronic
PAD
to
be
0.6
mg/
kg/
day.

Dermal
Endpoints:
The
maternal
toxicity
NOAEL
of
60
mg/
kg/
day
was
selected
for
shortand
intermediate­
term
dermal
risk
assessments
from
a
developmental
toxicity
study
in
rats
(
Argus,
1997)
based
on
decreased
body
weight
gain
at
the
LOAEL
of
120
mg/
kg/
day.
A
dermal
absorption
factor
of
50%
is
used
since
an
oral
endpoint
was
selected.
A
target
margin
of
exposure
(
MOE)
of
100
was
selected
for
the
dermal
risk
assessment,
based
on
10x
for
differences
among
humans
(
intra
species
variability)
and
10x
for
differences
between
the
test
animals
and
humans
(
inter
species
extrapolation).

Inhalation
Endpoints:
The
endpoint
used
for
inhalation
risk
assessment
is
a
LOAEL
of
0.1
mg/
L
(
26
mg/
kg/
day)
from
a
published
inhalation
toxicity
study
(
Dalin
and
Kristoffersson
(
1974)
)
based
on
alterations
in
sliding
angle
from
tilting
plane
test,
and
significant
increases
in
liver
enzymes.
An
uncertainty
factor
of
300
is
applied
to
this
risk
assessment
for
short­
and
intermediate­
term
risk
assessments
(
10x
interspecies
extrapolation,
10x
intraspecies
variation,
3x
for
use
of
a
LOAEL).
For
long­
term
risk
assessments,
an
uncertainty
factor
of
1,000
is
applied
to
the
risk
assessment
(
10x
interspecies
extrapolation,
10x
intraspecies
variation,
3x
for
use
of
a
LOAEL,
3x
for
lack
of
a
long­
term
study).

FQPA
Safety
Factor:
The
ATDC
determined
that
a
special
hazard­
based
safety
factor
was
not
required
for
phenol
and
could
be
reduced
to
1x.

Dietary
Exposure:
The
Agency
has
conducted
a
dietary
exposure
and
risk
assessment
for
use
of
phenol
in
a
ready­
to­
use
disinfecting
solution.
A
counter
top
that
is
treated
with
this
product
may
come
into
contact
with
food,
which
in
turn
may
be
ingested.
An
acute
RfD/
PAD
value
was
not
selected,
thus
the
acute
dietary
risk
was
not
evaluated.
For
chronic
dietary
exposure,
children
had
the
highest
percentage
of
the
chronic
PAD,
at
36%.
For
adult
males
and
females,
the
dietary
exposure
is
9.0%
and
7.5%,
respectively,
which
is
below
the
Agency's
level
of
concern
(
100%
of
the
cPAD).

Water
Exposure
and
Risk:
Phenol's
use
in
the
production
of
resins
and
other
manufacturing
industries
and
as
a
general
disinfectant
allows
for
the
possibility
of
ground
and
surface
water
contamination.
Despite
phenol's
high
water
solubility
and
poor
sorption
to
soil,
Page
5
of
57
biodegradation
of
phenol
is
sufficiently
rapid
so
that
the
probability
of
groundwater
contamination
will
be
low.
Because
phenol
absorbs
light
in
the
region
of
290­
330
nm,
phenol
might
photodegrade
directly
in
surface
water.
Phenol
is
not
expected
to
absorb
to
sediment
in
the
water
column.

Residential
Exposure
and
Risk:
Phenols
and
salts
are
formulated
as
a
soluble
concentrate,
towelette,
ready­
to­
use
solution
an
aerosol
spray.
Based
on
product
labels,
all
formulations
are
liquid.
The
following
scenarios
were
considered
for
residential
handlers
of
phenol­
containing
products:
(
1)
application
of
paint
treated
with
a
material
preservative
using
paintbrush/
roller
and
airless
sprayer,
(
2)
use
of
disinfectant/
deodorizing
spray
on
hard
non­
porous
surfaces,
and
(
3)
use
of
disinfectant
towelette
on
hard
non­
porous
surfaces.
Inhalation
and
dermal
exposures
were
addressed
for
residential
populations
using
surrogate
data
from
the
Chemical
Manufacturers
Association
(
CMA,
1992),
and
several
studies
which
relate
to
the
use
patterns
of
phenol.
Using
surrogate
unit
exposure
data,
application
rates
from
labels,
and
EPA
estimates
of
daily
amount
handled,
exposure
and
risks
to
handlers
and
postapplication
scenarios
were
assessed.
At
this
time,
EPA
does
not
have
available
chemical­
specific
handler
or
postapplication
exposure
studies
that
meet
Agency
guidelines.

The
calculated
inhalation
MOEs
for
the
painting
scenarios
resulting
from
aerosol
inhalation
is
above
the
target
of
300
for
roller/
brush
(
6500)
and
slightly
below
(
290)
for
the
airless
sprayer.
However,
for
inhalation
exposure
to
vapors
resulting
from
painting,
the
MOE
exceeds
the
Agency's
level
of
concern
(
27).
This
is
considered
to
be
conservative
given
that
the
exposure
value
used
represents
the
highest
24­
hour
inhalation
dose.
Inhalation
MOEs
for
the
use
of
the
disinfectant
on
hard
surfaces
do
not
exceed
the
Agency's
level
of
concern.

The
calculated
dermal
MOEs
for
the
following
scenarios
were
below
the
target
MOE
of
100,
and
are
therefore
of
concern:
painting
using
a
paintbrush/
roller
(
MOE
=
31)
and
painting
using
an
airless
sprayer
(
MOE
=
12).
The
use
of
phenol
for
hard
surface
disinfection
did
not
exceed
the
Agency's
level
of
concern.

Residential
postapplication
exposures
(
adults
and
children)
are
expected
to
be
minimal
because
the
majority
of
exposure
is
expected
occur
through
contact
with
dry
surfaces
(
e.
g.
paints)
and
the
end
use
products
are
expected
to
be
diluted.
The
residential
post­
application
scenario
considered
in
this
assessment
is
exposure
to
residue
from
carpets
that
have
been
machine­
cleaned
with
a
product
containing
phenol
(
and
phenol
salts).
The
residential
post­
application
exposures
result
from
the
dermal
and
incidental
oral
routes
of
exposure
to
toddlers
from
residue
on
carpets
that
have
been
machine­
cleaned
with
a
product
containing
phenol
(
and
phenol
salts).
While
the
label
also
indicates
that
the
product
may
be
sprayed
directly
onto
carpets,
this
scenario
was
not
evaluated
due
to
lack
of
data
regarding
application
rates.
However,
it
is
believed
that
the
carpet
shampoo
represents
the
high
end
of
the
exposures
to
toddlers
on
carpets.
Calculated
dermal
and
incidental
oral
MOEs
for
toddlers
crawling
on
carpet
and
incidental
oral
ingestion
are
above
the
level
of
concern
(
MOEs
of
21,000
and
86,000
respectively).
Postapplication
inhalation
exposures
were
also
evaluated
for
the
paint
and
carpet
scenarios
and
found
not
to
exceed
the
Agency's
level
Page
6
of
57
of
concern.

Aggregate
Exposure
and
Risk:
In
order
for
a
pesticide
registration
to
continue,
it
must
be
shown
that
the
use
does
not
result
in
"
unreasonable
adverse
effects
on
the
environment".
Section
2
(
bb)
of
FIFRA
defines
this
term
to
include
"
a
human
dietary
risk
from
residues
that
result
from
a
use
of
a
pesticide
in
or
on
any
food
inconsistent
with
standard
under
section
408..."
of
FFDCA.
Consequently,
even
though
no
pesticide
tolerances
have
been
established
for
phenol,
the
standards
of
FQPA
must
still
be
met,
including
"
that
there
is
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
pesticide
chemical
residue,
including
all
anticipated
dietary
exposures
and
other
exposures
for
which
there
are
reliable
information."
Aggregate
exposure
is
the
total
exposure
to
a
single
chemical
(
or
its
residues)
that
may
occur
from
dietary
(
i.
e.,
food
and
drinking
water),
residential,
and
other
non­
occupational
sources,
and
from
all
known
or
plausible
exposure
routes
(
oral,
dermal,
and
inhalation).
Aggregate
risk
assessments
were
conducted
for
acute
(
1
day),
short­
term
(
1­
30
days),
intermediate­
term
(
1­
6
months)
and
chronic
(
several
months
to
lifetime)
exposures.

Acute/
Chronic
Aggregate
Risk:
The
acute
and
chronic
aggregate
risk
assessments
generally
include
both
dietary
and
drinking
water
exposures.
Drinking
water
exposure
is
not
expected
from
the
indoor
uses
of
phenol
and
phenol
salts;
thus,
drinking
water
exposure
is
not
assessed
in
this
document.

The
ADTC
determined
that
for
acute
dietary
risk,
there
was
no
appropriate
endpoint
for
assessment
of
acute
dietary
exposure.
As
a
result,
acute
dietary
risk
estimates
were
not
calculated.

Cumulative
chronic
dietary
risk
estimates
from
indirect
food
uses
(
i.
e.,
exposure
to
disinfectant
solutions
and
room
deodorizers)
were
calculated
to
be
36%
for
children,
9.0%
for
adult
females,
and
7.5%
for
adult
males,
indicating
no
risk
of
concern
from
dietary
exposure
For
children,
dietary
exposure
was
aggregated
with
dermal
exposure
and
incidental
exposure
from
use
of
phenol
cleaning
products
on
carpet.
The
aggregate
Margin
of
Exposure
was
found
to
be
acceptable
(
aggregate
MOE
of
273,
acceptable
MOE
of
100).

Short­
and
Intermediate­
Term
Aggregate
Risk:
In
accordance
with
the
policy
of
the
Office
of
Pesticide
Programs,
short­,
intermediate­,
and
long­
term
aggregate
risk
typically
includes
dietary
exposures
(
food
and
water)
and
residential
exposures
that
can
be
thought
of
as
occurring
together.
For
homeowner
residential
scenarios,
exposures
are
interpreted
as
only
short­
or
intermediate­
term;
exposures
are
not
felt
to
be
long­
term.

Based
on
the
above,
for
adults,
chronic
dietary
exposure
is
aggregated
with
the
dermal
exposure
from
one
cleaning
scenario.
(
The
painting
scenario
was
not
chosen
to
aggregate
since
the
dermal
MOEs
for
both
the
airless
sprayer
and
brush/
roller
already
exceed
the
Agency's
level
of
concern
for
handlers
(
i.
e.,
Page
7
of
57
an
individual
who
paints
his/
her
house).
For
toddlers,
aggregate
exposure
would
involve
dietary
exposure
and
dermal
plus
incidental
oral
exposures
to
treated
carpets.

Occupational
Exposure
and
Risk:
Six
commercial/
institutional
premises
scenarios
have
been
considered
in
this
assessment:
(
1)
use
as
a
material
perservative
as
a
liquid
pour,
(
2)
use
of
disinfectant
solutions
in
hemodialysis
machines,
(
3)
application
of
paint
treated
with
a
material
preservative
using
airless
sprayer,
(
4)
application
of
paint
treated
with
a
material
preservative
using
paintbrush/
roller,
(
5)
use
of
disinfectant/
deodorizing
spray
on
hard
non­
porous
surfaces,
and
(
6)
use
of
disinfectant
towelette
on
hard
non­
porous
surfaces.

The
calculated
dermal
MOEs
for
the
following
scenarios
are
below
the
target
MOE
of
100,
and
are
therefore
of
concern:
(
1)
painting
using
an
airless
sprayer
(
MOE=
21),
and
(
2)
wiping
hard
surfaces
using
a
towelette
(
MOE=
70).

The
calculated
inhalation
MOE
for
use
of
an
airless
sprayer
in
painting
(
MOE=
88)
was
below
the
target
MOE
for
short­
and
intermediate­
term
exposure
(
Target
MOE
=
300).
The
MOEs
for
inhalation
exposure
to
vapors
also
exceed
the
Agency's
level
of
concern.

Ecotoxicity:
Phenol
is
not
expected
to
bioaccumulate
in
plants,
even
though
plants
readily
absorb
phenol,
because
of
the
high
respiratory
decomposition
rate
of
phenol
to
CO
2.
Phenol
does
not
pose
concerns
to
aquatic
organisms
due
to
the
low
BCF
and
the
rapid
biodegradation
in
water.
Page
8
of
57
2.0
PHYSICAL/
CHEMICAL
PROPERTIES
CHARACTERIZATION
2.1
Chemical
Identification
Chemical
identification
parameters,
including
chemical
and
common/
trade
names,
chemical
family,
CAS
Number,
and
molecular
formula
are
provided
in
Table
2.1.

Table
2.1.
Chemical
Identification
Parameter
Phenol
Phenol
salt
(
Sodium
phenate)

Synonyms
Carbolic
Acid;
Hydroxybenzene
Sodium
Phenolate;
Phenol,
Sodium
Salt
Common/
Trade
Names
Phenol;
Cabolic
Acid
Sodium
Phenate;
Permicide;
Sporicidin
Chemical
Family
Phenols
Phenols
CAS
Number
108­
95­
2
139­
02­
6
Molecular
Formula
C6H6O
C6H6ONa
2.2
Physical/
Chemical
Properties
The
physical
and
chemical
properties
of
the
Technical
Grade
Active
Ingredient
(
TGAI)
of
phenol
and
phenol
salts
are
shown
in
Table
2.2.

Table
2.2.
Physical/
Chemical
Properties
Parameter
Phenol
Phenol
Salt
(
Sodium
phenate)

Molecular
Weight
94.11
116.10
Color
Colorless
to
light
pink
White
to
reddish
Physical
State
Crystalline
solid
Crystalline
needles
or
rods
Specific
gravity
1.07
at
20oC
Not
Found
Acid
Dissociation
Constant
(
pKa)
9.9
at
25

C
Not
Found
Dissociation
Constant
in
water
(
Ka)
1.28
x
10­
10
Not
Found
pH
Mildly
acidic
Alkaline
in
aqueous
solutions
Stability
Stable
at
normal
conditions
Stable
at
normal
conditions
Melting
point
43.0

C
40.9

C
(
ultra
pure
material)
Not
Found
Boiling
point
181.8

C
at
760
mm
Hg
Not
Found
Water
Solubility
67
g/
L
in
water
at
16

C
Highly
soluble
in
water
Log
KOW
1.46
at
25oC
Not
Found
Table
2.2.
Physical/
Chemical
Properties
Parameter
Phenol
Phenol
Salt
(
Sodium
phenate)

Page
9
of
57
Vapor
Pressure
°
0.341
mm
Hg
at
25

C
°
2.48
mm
Hg
at
50

C
°
41.3
mm
Hg
at
100

C
Not
Found
Relative
Vapor
Density
(
air
=
1)
3.24
Not
Found
Saturation
concentration
in
air
0.77
g/
m3
at
20

C
Not
Found
Page
10
of
57
3.0
HAZARD
CHARACTERIZATION
A
detailed
hazard
assessment
for
phenol
and
phenol
salts
is
included
in
the
appendix
of
this
report.
Generally,
phenol
and
phenol
salts
are
readily
absorbed
by
the
inhalation,
oral,
and
dermal
routes.
The
portal­
of­
entry
metabolism
for
the
inhalation
and
oral
routes
appears
to
be
extensive
and
involves
sulfate
and
glucuronide
conjugation
and,
to
a
lesser
extent,
oxidation.
Once
absorbed,
phenol
is
widely
distributed
in
the
body,
although
the
levels
in
the
lung,
liver,
and
kidney
are
often
reported
as
being
higher
than
in
other
tissues
(
on
a
per­
gram­
tissue
basis).
Elimination
from
the
body
is
rapid,
primarily
as
sulfate
and
glucuronide
conjugates
in
the
urine,
regardless
of
the
route
of
administration.
Phenol
does
not
appear
to
accumulate
significantly
in
the
body.

3.1
Hazard
Profile
Acute
Toxicity.
The
acute
toxicity
database
for
phenol
technical
is
considered
complete.
No
additional
studies
are
required
at
this
time.
Phenol
has
a
moderate
order
of
acute
toxicity
via
the
oral
and
dermal
routes
of
exposure
(
Toxicity
Category
II
or
III)
and
produces
severe
and
marked
irritation
to
the
eyes
and
skin
(
Toxicity
Category
I
or
II).
Phenol
concentrations
used
in
acute
inhalation
studies
failed
to
induce
mortality
in
the
study
animals;
therefore,
toxicity
endpoints
and
a
toxicity
category
could
not
be
established.
The
acute
toxicity
data
for
phenol
are
summarized
in
Table
3.1.

Subchronic
Toxicity.
In
the
subchronic
database,
oral
range­
finding
studies
in
both
the
rat
and
the
mouse
were
completed.
Although
the
studies
were
non­
guideline
(
due
to
the
lack
of
subchronic
parameters),
systemic
toxicities
were
noted
at
10,000
ppm
in
the
rat
and
mouse,
based
on
a
decrease
in
mean
body
weight
gain.
In
a
two­
week
inhalation
study,
rats
had
elevated
plasma
Mg2+
levels
(
Hypermagnesaemia)
and
exhibited
toxic
effects
in
the
central
nervous
system.

Developmental
Toxicity.
The
toxicity
profile
for
phenol
presented
several
developmental
and
reproductive
toxicity
studies
found
in
the
open
literature.
These
studies
are
also
referred
to
in
the
IRIS
update.
In
addition,
the
National
Toxicology
Program
conducted
developmental
toxicity
studies
in
both
rats
and
mice.
The
ADTC
considered
the
NTP
studies
to
be
acceptable
for
regulatory
purposes.
Published
reports
by
Kavlock
(
1990)
and
Bishop
(
1997)
were
considered
unacceptable
for
purposes
of
determining
the
developmental
toxicity
of
phenol,
based
on
study
design.

In
the
NTP
rat
developmental
toxicity
study
(
MRID
#
43735402),
phenol
(
in
distilled
water)
was
administered
to
groups
of
23
rats/
dose
via
gavage
at
dose
levels
of
0,
30,
60,
or
120
mg/
kg/
day
from
gestation
days
(
GD)
6
to
15.
No
significant
maternal
toxicity
was
observed
up
to
the
high­
dose
of
120
mg/
kg/
day
tested
in
this
study.
In
offspring,
the
only
effect
noted
was
a
significant
decrease
in
mean
fetal
body
weight,
but
no
teratogenic
effects
were
observed.
Therefore,
the
maternal
toxicity
LOAEL
is
greater
than
120
mg/
kg/
day
and
the
developmental
toxicity
LOAEL
is
120
mg/
kg/
day.
The
maternal
NOAEL
is
60
mg/
kg/
day.

In
the
NTP
mouse
developmental
toxicity
study
(
MRID
#
43735401),
phenol
was
administered
in
distilled
water
to
groups
of
31­
36
mice/
dose
by
gavage
at
dose
levels
of
0,
70,
140,
or
280
Page
11
of
57
mg/
kg/
day
from
gestation
days
(
GD)
6
to
15.
Clinical
signs
of
toxicity
were
observed
in
maternal
animals
at
a
dose
of
280
mg/
kg/
day,
which
included
signs
of
neurotoxicity
(
tremors,
ataxia,
lethargy).
In
addition,
maternal
body
weight
was
decreased
during
the
treatment
period
(
31%
decrease)
and
entire
gestation
period
(
28%
decrease).
Offspring
in
the
280
mg/
kg/
day
dose
group
experienced
an
increase
in
cleft
palate
in
8
of
214
fetuses
(
3
litters),
but
this
increase
was
not
statistically
significant.
The
fetuses,
male
and
female
combined,
exhibited
reduced
mean
fetal
weights.
The
high­
dose
(
280
mg/
kg/
day)
was
fetotoxic
due
to
significant
reductions
(
18%)
from
controls
in
mean
fetal
weight
in
treated
animals.
The
maternal
and
developmental
toxicity
NOAEL
was
140
mg/
kg/
day,
and
the
maternal
and
developmental
toxicity
LOAEL
was
280
mg/
kg/
day
in
this
study.

Reproductive.
In
a
two­
generation
reproductive
toxicity
study
conducted
by
Ryan
et
al
(
2001),
phenol
(
100%
purity)
was
administered
to
groups
of
30
Sprague­
Dawley
rats/
sex/
dose
in
drinking
water
at
concentrations
of
200,
1,000,
or
5,000
ppm
(
14,
70,
and
310
mg/
kg/
day
for
males
and
20,
93,
and
350
mg/
kg/
day
for
females,
respectively)
for
both
generations.
There
were
treatment­
related
decreases
from
control
in
body
weight
and
body
weight
gain
in
P1
generation
rats
treated
with
phenol.
These
reductions
were
concomitant
with
decreases
in
food
and
water
consumption
and
observed
in
the
high­
dose
rats.
There
were
also
treatment­
related
decreases
from
controls
in
F1
body
weight
in
the
5000
ppm
phenol­
treated
rats.
The
lower
maternal
body
weight
may
have
contributed
to
the
lower
birth
weight
of
F1
generation
as
a
result
of
the
decreased
food
and
water
consumption
during
lactation
and
decreased
palatability.
The
maternal
toxicity
NOAEL
is
1,000
ppm
in
the
P1
and
F1
generations.
The
maternal
toxicity
LOAEL
is
5,000
ppm
based
on
decreases
in
water
and
food
consumption,
body
weight
(
average
11%
decrease
during
pre­
mating
weeks
1
and
10,
gestation,
and
lactation)
and
body
weight
gain
(
average
18%
decrease
during
pre­
mating
weeks
1
through
10)
in
the
P1
and
F1
generations.
These
effects
are
associated
with
flavor
aversion
to
phenol
in
the
drinking
water.

There
were
no
treatment­
related
effects
on
reproductive
performance
in
either
the
P1
or
F1
generation.
The
estrus
cycle,
epididymal
sperm
count,
motility,
sperm
morphology,
testicular
sperm
count,
and
production
rate
were
unaffected
by
phenol
treatment
in
the
P1
and
F1
generations.
However,
the
percent
of
offspring
alive
after
PND
0
was
significantly
decreased
in
the
5,000
ppm
groups
with
a
10%
decrease
on
PND
4
for
the
P1
generation
and
decreases
of
28
and
24%
on
PND
4
and
7­
21,
respectively,
for
the
F1
generation.
The
reproductive
toxicity
NOAEL
is
greater
than
or
equal
to
5,000
ppm
in
the
P1
and
F1
generations
(
highest
dose
tested).
The
Reproductive
Toxicity
LOAEL
is
greater
than
5,000
ppm
in
the
P1
and
F1
generations
(
not
established).

There
were
treatment­
related
effects
for
both
F1
and
F2
generations
with
increases
in
litter
mortality
(
more
so
in
the
F2
generation)
and
reduced
offspring
body
weights
in
the
high­
dose
group.
This
occurred
concurrently
with
maternal
toxicity
(
decreased
maternal
body
weight);
believed
to
be
secondary
to
the
animals'
aversion
to
the
flavor
of
the
phenol­
treated
water
and
resulted
in
decreased
maternal
as
well
as
offspring
body
weight.
There
were
delays
in
vaginal
patency
of
F1
females
(
38.3
days
for
treated
females
vs.
34.6
days
for
control
females)
and
preputial
separation
of
F1
males
(
47.8
days
for
treated
males
vs.
44
days
for
control
males)
observed
with
decreases
in
pre­
and
post­
weaning
body
weights
in
the
high­
dose
group.
Therefore,
the
onset
of
puberty
was
delayed
and
attributed
to
decreased
food
and
water
consumption
and
reduced
body
weight.
The
offspring
toxicity
NOAEL
is
Page
12
of
57
1000
ppm.
The
offspring
toxicity
LOAEL
is
5,000
ppm
based
on
decreases
in
body
weight
of
F1
and
F2
offspring
(
5­
7%
on
PND
0;
15­
30%
on
PND
4­
21),
decreases
in
litter
survival
of
P1
and
F1
offspring
(
P1
generation:
90%
treated
vs.
99%
control
on
PND
4;
96%
treated
vs.
100%
control
animals
on
PND
7­
21
and
F1
generation:
67%
treated
vs.
93%
control
on
PND
4;
74%
treated
vs.
98%
control
on
PND
7­
21),
delays
in
preputial
separation
in
F1
males
(
47.8
days
for
treated
males
vs.
44
days
for
control
males),
and
delays
in
vaginal
patency
in
F1
females
(
38.3
days
for
treated
females
vs.
34.6
days
for
control
females).

Carcinogenicity.
Phenol
is
characterized
as
a
Group
D,
not
classifiable
as
to
human
carcinogenicity
(
This
group
is
used
for
agents
with
inadequate
human
and
animal
evidence
of
carcinogenicity
or
for
which
no
data
are
available).
The
updated
toxicological
review
in
the
EPA
IRIS
database
(
USEPA,
2002a)
provides
a
summary
of
the
weight
of
the
evidence
with
respect
to
the
carcinogenic
potential
of
phenol,
and
this
is
reproduced
in
part
below.

Dermally
administered
phenol
has
been
consistently
observed
to
be
a
promoter.
Several
authors
(
Salaman
and
Glendenning,
1957;
Boutwell
and
Bosch,
1959;
Wynder
and
Hoffmann,
1961)
observed
that
dermally
applied
phenol
promoted
DMBA­
initiated
skin
tumors.
These
studies
have
generally
reported
significant
skin
ulceration
at
all
phenol
doses
tested.
The
exception
is
Wynder
and
Hoffman
(
1961),
who
reported
that
5%
phenol
promoted
DMBA­
initiated
tumors
in
mice
in
the
absence
of
any
toxic
reactions.
When
the
same
phenol
dose
was
administered
in
different
volumes,
higher
promotion
activity
was
exhibited
by
the
more
concentrated
solution,
which
also
produced
severe
skin
ulceration,
suggesting
that
some
of
the
promotion
activity
may
have
been
related
to
the
rapid
cell
division
of
repair
of
skin
damage
(
Salaman
and
Glendenning,
1957).

A
mechanistic
study
conducted
by
Stenius
et
al.
(
1989)
was
designed
to
assess
the
toxicity
and
carcinogenicity
of
phenol
when
administered
to
partially
hepatectomized
male
SD­
rats.
Phenol
was
administered
by
gavage
5
days/
week
for
7
weeks
at
a
concentration
of
100
mg/
kg/
day.
Animals
were
sacrificed,
by
decapitation,
1
week
after
last
treatment.
Sections
of
the
rat
liver
were
prepared
and
stained
to
measure
for
induction
of
 ­
glutamyltranspeptidase
(
GGT)
positive
enzyme­
altered
foci
as
an
indicator
of
tumor
initiation.
Additional
studies
involved
single
oral
administrations
of
phenol
to
measure
inductions
of
hepatic
ornithine
decarboxylase
(
ODC),
glutathione
(
GSH)
depletion,
and
in
vivo
lipid
peroxidation.

Phenol
did
not
increase
the
number
or
volume
of
foci
and
was
found
to
have
no
tumor­
initiating
properties
within
the
confines
of
this
study.
Lipid
peroxidation
was
not
induced
following
administration
of
phenol
as
measured
by
malondialdehyde
(
MDA)
in
the
urine.
There
were
small
and
inconsistent
effects
observed
in
hepatic
ornithine
decarboxylase
(
ODC)
in
which
there
was
an
increase
at
the
mid­
dose,
but
a
decrease
at
the
high­
dose.
Observed
measurements
of
hepatic
ODC
were
18.8,
32.3,
and
11.4
pmol/
mg/
h
for
the
phenol
doses
of
0,
50,
and
100
mg/
kg/
day,
respectively.
Phenol
did
not
induce
GSH
depletion
in
hepatocytes.

Mutagenicity.
The
results
of
the
mutagenicity
studies
indicated
that
phenol
was
not
mutagenic
in
Salmonella
typhimurium
or
Drosophila
melanogaster
and
did
not
induce
micronuclei
or
bone
marrow
chromosomal
aberrations
in
mice.
However,
mutagenic
effects
were
observed
in
Chinese
Page
13
of
57
Hamster
ovary
cells
and
spermatocytes
in
mice
and
HL60
cells.
The
genotoxic
potential
of
phenol
appears
to
depend
on
the
competing
processes
of
activation
to
a
genotoxic
form
and
metabolic
inactivation
(
e.
g.,
via
conjugation).
Phenol
tended
to
be
negative
in
bacterial
gene
mutation
assays
but
was
positive
or
equivocal
in
mammalian
cell
gene
mutation
assays.
Phenol
tended
to
induce
micronuclei
in
mice
when
administered
intraperitoneally
but
was
negative
(
or
positive
only
at
very
high
doses)
when
administered
orally.
This
difference
is
likely
due
to
the
first­
pass
conjugation
and
inactivation
of
orally
administered
phenol.
Phenol
was
also
positive
in
in
vitro
micronucleus
tests
with
human
lymphocytes
and
Chinese
Hamster
ovary
cells.
Results
from
DNA
damage
assays
are
inconsistent,
but
they
tend
to
show
that
phenol
can
cause
sister
chromatid
exchanges
or
cell
transformation
if
it
is
not
metabolically
inactivated.
Overall,
phenol
did
not
exhibit
strong
mutagenic
effects.

Metabolism.
Phenol
is
essentially
completely
metabolized
in
24
hours.
Phenol
was
predominantly
conjugated
with
sulfate
and
lower
amounts
of
glucuronic
acid
and
the
metabolites
were
rapidly
excreted
in
the
urine.
The
major
metabolites
found
were
phenyl
sulfate,
quinol
sulfate,
phenyl
glucuronide,
and
quinol
glucuronide.

Neurotoxicity.
The
ADTC
committee
noted
neurotoxic
signs
from
acute
dermal
toxicity
studies
(
Brown
et
al.,
1975
­
convulsions;
OTS
0515567­
tremors;
Conning
et
al.,
1970­
stimulation
of
motor
nerve
endings
or
spinal
motor
centers)
and
a
15­
day
inhalation
study
(
tilting
plane
results
showed
an
effect
in
treated
rats).
There
were
no
neurotoxic
signs
of
phenol
noted
from
the
oral
studies
using
gavage
or
drinking
water
as
the
method
of
administration.
As
noted
in
the
IRIS
toxicological
profile,
numerous
CNS
effects
have
been
observed
following
phenol
dosing.
Tremors
were
observed
in
one
animal
that
later
died
(
apparently
of
dehydration)
following
dosing
in
drinking
water
(
ClinTrials
BioResearch,
1998).
Tremors
have
also
been
observed
in
several
gavage
studies
in
rats
and
mice
(
43735402;
Dow
Chemical
Co.,
1994;
Moser
et
al.,
1995).
However,
in
a
specialized
13­
week
neurotoxicity
study
in
male
and
female
rats
that
included
an
FOB
and
a
detailed
neurohistopathology
evaluation
(
ClinTrials
BioResearch,
1998),
the
only
observed
nervous
system
effects
were
tremors
in
one
animal
and
decreased
motor
activity
in
females.
A
short­
term
gavage
screening
study
(
Moser
et
al.,
1995)
found
that
the
only
effect
in
an
FOB
was
a
marginal
decrease
in
motor
activity
and
increased
rearing
post­
exposure.
Part
of
this
could
be
attributed
to
the
dehydration
observed
in
the
study.

Table
3.1.
Acute
Toxicity
of
Phenol
and
Phenol
salts
Guideline
Number
Study
Type/
Test
substance
(%
a.
i.)
MRID
Number/
Citation
Results
Toxicity
Category
870.1100
(
§
81­
1)
Acute
Oral­
Rat
Phenol
purity
>
99%
Berman,
et
al.,
1994
LD50
=
400
(
297­
539)
mg/
kg/
day
II
870.110
(
§
81­
1)
Acute
Oral
­
Rat
Phenol
purity
100%
OTS
#
­
0515567
86­
870001405
LD50
=
1,030
(
940­
1120)
mg/
kg/
day
III
870.1100
(
§
81­
1)
Acute
Oral­
Rat
Phenol
purity
not
reported
Flickinger,
1976
LD50
=
650
(
490­
860)
mg/
kg/
day
III
Table
3.1.
Acute
Toxicity
of
Phenol
and
Phenol
salts
Guideline
Number
Study
Type/
Test
substance
(%
a.
i.)
MRID
Number/
Citation
Results
Toxicity
Category
Page
14
of
57
870.1200
(
§
81­
2)
Acute
Dermal­
Rat
Phenol
purity
not
reported
Brown,
et
al.,
1975
LD50
(
Non­
occluded)
=
0.68
(
0.57­
0.78)
mL/
kg
LD50
(
Occluded)
=
0.50
mL/
kg
II
870.1200
(
§
81­
2)
Acute
Dermal­
Rabbit
Sodium
Phenate
purity
57%
OTS
#
­
0515564
86­
870001402
LD50
=
2,350
(
1,880­
2,940)
mg/
kg/
day
III
870.1200
(
§
81­
2)
Acute
Dermal­
Rabbit
Phenol
purity
100%
OTS
#
­
0515567
86­
870001405
LD50
=
0.63
(
0.56­
0.70)
mL/
kg
II
870.1200
(
§
81­
2)
Acute
Dermal­
Rat
Phenol
purity
laboratory
reagent
grade
Conning
et
al.,
1970
LD50
=
669.4
mg/
kg/
day
II
870.1200
(
§
81­
2)
Acute
Dermal­
Rabbit
Phenol
purity
not
reported
Flickinger,
1976
LD50
=
850
(
600­
1,200)
mg/
kg/
day
II
870.1300
(
§
81­
3)
Acute
Inhalation­
Rat
Phenol
purity
100%
OTS
#
­
0515567
86­
870001405
No
deaths
occurred
at
2.5
L/
min
for
8
hours
Not
established
870.1300
(
§
81­
3)
Acute
Inhalation­
Rat
Phenol
purity
not
reported
Flickinger,
1976
No
deaths
occurred
at
900
mg/
m3
for
8
hours
Irritation
and
timerelated
CNS
effects
Not
established
870.2400
(
§
81­
4)
Acute
Eye
Irritation­
Rabbit
Sodium
Phenate
purity
57%
OTS
#
­
0515564
86­
870001402
15%
solution
caused
corneal
necrosis
and
conjunctiva
lesions
II
870.2400
(
§
81­
4)
Acute
Eye
Irritation­
Rabbit
Phenol
purity
100%
OTS
#
­
0515567
86­
870001405
Severe
damage
to
the
cornea
at
15%
and
lesser
damage
in
5%
Not
established
870.2400
(
§
81­
4)
Acute
Eye
Irritation­
Rabbit
Phenol
purity
not
reported
Flickinger,
1976
Dose
not
provided.
Severe
conjunctiva,
iritis,
corneal
opacities
and
ulcerations
with
no
improvement
after
14
day
observation
period.
I
870.2500
(
§
81­
5)
Acute
Dermal
Irritation­
Rabbit
Sodium
Phenate
purity
57%
OTS
#
­
0515564
86­
870001402
Mild
to
marked
erythema
and
marked
capillary
injection
were
observed
in
50%
of
animals
tested
II
Table
3.1.
Acute
Toxicity
of
Phenol
and
Phenol
salts
Guideline
Number
Study
Type/
Test
substance
(%
a.
i.)
MRID
Number/
Citation
Results
Toxicity
Category
Page
15
of
57
870.2500
(
§
81­
5)
Acute
Dermal
Irritation­
Rabbit
Phenol
purity
100%
OTS
#
­
0515567
86­
870001405
10%
solution
caused
moderate
to
marked
erythema
Not
established
870.2500
(
§
81­
5)
Acute
Dermal
Irritation­
Rabbit
Phenol
purity
not
reported
Flickinger,
1976
Corrosive
I
Page
16
of
57
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Non­
guideline
­
Subchronic
(
Oral)
Range
Finding
Study
(
Rat)
Phenol
purity
not
reported
NIH
PB#
­
80­
1759
Acceptable
­
Non­
guideline
0,
100,
300,
,1000,
3,000,
and
10,000
ppm
NOAEL
=
3,000
ppm
LOAEL
=
10,000
ppm,
based
on
significant
decreases
in
mean
body
weight
gain.

Considering
the
test
article
was
administered
in
the
drinking
water,
palatability
at
the
high
dose
may
have
affected
water
consumption.

Non­
guideline
­
Subchronic
(
Oral)
Range
Finding
Study
(
Mouse)
Phenol
purity
not
reported
NIH
PB#
­
80­
1759
Acceptable
­
Non­
guideline
0,
100,
300,
1,000,
3,000,
and
10,000
ppm
NOAEL
=
3,000
ppm
LOAEL
=
10,000
ppm,
based
on
significant
decreases
in
mean
body
weight
gain.

Considering
the
test
article
was
administered
in
the
drinking
water,
palatability
at
the
high
dose
may
have
affected
water
consumption.

Special
Study
­
Nonguideline
Two
Week
Inhalation
Study
(
Rat)
Phenol
purity
not
reported
Dalin
and
Kristoffersson,
1984
Acceptable
­
Non­
guideline
600
+/­
10
L/
hr
in
an
inhalation
chamber
with
a
phenol
concentration
of
100
mg/
m3
CNS
effects
measured
by
the
"
tilting­
plane"
method
showed
significant
decreases
in
the
value
of
the
sliding
angle
after
exposure
to
phenol.
The
mean
sliding
angle
was
71.2
±
2.4
degrees
prior
to
phenol
administration
and
following
treatment
there
was
a
significant
decrease
(
6%)
to
66.8
±
1.7
degrees.
Rats
had
elevated
plasma
Mg2+
levels
(
Hypermagnesaemia)
and
exhibited
toxic
effects
in
the
central
nervous
system
(
CNS).

870.3700a
(
§
83­
3)
Developmental­
Rat
Phenol
purity
99.9%
MRID#
43735402
Acceptable
­
Non­
guideline
0,
30,
60
or
120
mg/
kg/
day
Maternal
Toxicity
NOAEL

120
mg/
kg/
day
(
highest
dose
tested)
LOAEL
>
120
mg/
kg/
day
(
not
established)
Reproductive
Toxicity
NOAEL

120
mg/
kg/
day
(
highest
dose
tested)
LOAEL
>
120
mg/
kg/
day
(
not
established)
Developmental
Toxicity
NOAEL
=
60
mg/
kg/
day
LOAEL
=
120
mg/
kg/
day,
based
on
reduced
fetal
weight
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
17
of
57
870.3700a
(
§
83­
3)
Developmental­
Rat
Phenol
purity
90%
Argus,
1997
(
U.
S.
EPA
IRIS
database)
Acceptable
­
Guideline
3
time
daily
with
0,
20,
40,
or
120
mg/
kg/
dose
(
0,
60,
120,
or
360
mg/
kg/
day)
Maternal
Toxicity
NOAEL
=
60
mg/
kg/
day
LOAEL
=
120
mg/
kg/
day,
based
on
small
decreases
in
maternal
body
weight
Developmental
Toxicity
NOAEL
=
120
mg/
kg/
day
LOAEL
=
360
mg/
kg/
day,
based
on
decreased
fetal
body
weight
and
delayed
ossification
870.3700a
(
§
83­
3)
Developmental­
Mouse
Phenol
purity
99.9%
MRID
#
34735401
Unacceptable
(
Upgradable)
0,
70,
140,
or
280
mg/
kg/
day
Maternal
Toxicity
NOAEL
=
140
mg/
kg/
day
LOAEL
=
280
mg/
kg/
day,
based
on
increased
mortality,
significant
reductions
in
body
weight,
and
clinical
signs
of
CNS
toxicity
(
tremors,
lethargy,
and
ataxia)
Reproductive
Toxicity
NOAEL

280
mg/
kg/
day
(
highest
dose
tested)
LOAEL
>
280
mg/
kg/
day
(
not
established)
Developmental
Toxicity
NOAEL
=
140
mg/
kg/
day
LOAEL
=
280
mg/
kg/
day,
based
on
reduced
fetal
weight
and
an
apparent
increase
in
the
incidence
of
cleft
palate
Non­
guideline
­
Developmental
Toxicity
­
Rat
Phenol
purity
>
99%
Narotsky
and
Kavlock,
1995
(
J.
Toxicol.
Env.
Health
45(
2))
Acceptable
­
Non­
guideline
40,
and
53.3
mg/
kg/
day
Maternal
Toxicity
NOAEL
<
40
mg/
kg/
day
(
lowest
dose
tested)
LOAEL
=
40
mg/
kg/
day,
based
on
reduced
body
weight
gains
and
severe
respiratory
signs
Reproductive
Toxicity
NOAEL
=
40
mg/
kg/
day
LOAEL
=
53.3
mg/
kg/
day,
based
on
significantly
reduced
litter
sizes,
full
resorption,
and
prenatal
loss
Developmental
Toxicity
NOAEL

53.3
mg/
kg/
day
(
highest
dose
tested)
LOAEL
>
53.3
mg/
kg/
day
(
not
established)
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
18
of
57
870.3800
(
§
83­
4)
Reproduction
­
Rat
Phenol
purity
100%
Ryan
et
al.,
2001
(
Intl.
J.
of
Tox.
Vol.
20)
Acceptable­
Guideline
0,
200,
1,000,
and
5,000
ppm
Males:
0,
14,
70,
and
310
mg/
kg/
day
Females:
0,
20,
93,
and
350
mg/
kg/
day
Maternal
Toxicity
NOAEL
=
1,000
ppm
in
the
P1
and
F1
generations
LOAEL
=
5,000
ppm
based
on
decreases
in
water
and
food
consumption,
body
weight
(
average
11%
decrease
during
premating
weeks
1
and
10,
gestation
and
lactation)
and
body
weight
gain
(
average
18%
decrease
during
pre­
mating
weeks
1
through
10)
in
the
P1
and
F1
generations.
These
effects
are
associated
with
flavor
aversion
to
phenol
in
the
drinking
water
Reproductive
Toxicity
NOAEL

5,000
ppm
in
the
P1
and
F1
generations
(
highest
dose
tested)
LOAEL
>
5,000
ppm
in
the
P1
and
F1
generations
(
not
established)
Offspring
Toxicity
NOAEL
=
1,000
ppm
LOAEL
=
5,000
ppm
based
on
decreases
in
body
weight
of
F1
and
F2
offspring
(
5­
7%
on
PND
0;
15­
30%
on
PND
4­
21),
decreases
in
litter
survival
of
P1
and
F1
offspring
(
P1
generation:
90%
in
treated
animals
vs.
99%
in
control
animals
on
PND
4;
96%
in
treated
animals
vs.
100%
in
control
animals
on
PND
7­
21.
F1
generation:
67%
in
treated
animals
vs.
93%
in
control
animals
on
PND
4;
74%
in
treated
animals
vs.
98%
in
control
animals
on
PND
7­
21)
and
delays
in
preputial
separation
in
F1
males
(
47.8
days
for
treated
males
vs.
44
days
for
control
males)
and
vaginal
patency
in
F1
females
(
38.3
days
for
treated
females
vs.
34.6
days
for
control
females)
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
19
of
57
870.4200a
(
§
83­
2)
Carcinogenicity
­
Rat
Phenol
purity
98.47%
NIH
PB#
80­
1759
Acceptable
­
Non­
guideline
0,
2,500,
or
5,000
ppm
Male:
0,
322,
or
645
mg/
kg/
day
Female:
0,
360,
or
721
mg/
kg/
day
NOAEL

5,000
ppm
(
highest
dose
tested)
for
both
male
and
female
rats
LOAEL
>
5,000
ppm
(
not
established)

Various
neoplasms
were
observed
in
both
control
and
treated
rats.
The
low
dose
male
rats
exhibited
increased
tumor
occurrence
over
controls.
Pheochromocytomas
of
the
adrenal
medulla
were
found
in
44%
of
low
dose
males;
significantly
higher
(
p=
0.046)
than
the
26%
in
controls
and
18%
in
high
dose
males.
The
incidence
of
either
leukemia
or
lymphomas
in
high
dose
and
low
dose
males
were
higher
than
controls,
but
were
only
significantly
higher
(
p=
0.008)
in
low
dose
treated.
The
incidence
of
interstitial­
cell
tumors
in
the
testis
of
males
is
also
significantly
higher
(
p=
0.05)
in
low
dose
males
than
control;
found
in
49
of
the
50
animals.
Results
of
histopathologic
examinations
suggest
phenol
may
have
increased
the
incidence
of
pheochromocytoma,
leukemia
or
lymphoma
in
low
dose
male
rats.
Females
did
not
exhibit
increased
incidences
of
tumors
at
any
time
in
this
study.
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
20
of
57
870.4200b
(
§
83­
2)
Carcinogenicity
­
Mouse
Phenol
purity
98.47%
NIH
PB#
80­
1759
Acceptable
­
Non­
guideline
0,
2,500,
or
5,000
ppm
Male:
0,
590,
or
1,180
mg/
kg/
day
Female:
0,
602,
or
1,204
mg/
kg/
day
NOAEL

5,000
ppm
(
highest
dose
tested)
for
male
and
female
mice
LOAEL
>
5,000
ppm
(
not
established)

Neoplasms
observed
in
treated
animals
were
of
the
usual
number
and
type
found
in
mice.
Uterine
endometrial
stromal
polyps
were
increased
in
5
of
48
high­
dose
female
mice,
although
this
was
not
significantly
different
from
similar
historical
control
mice.
Any
other
neoplasms
noted
were
occurrences
normally
associated
with
aged
B6C3F1
mice
and
were
not
treatment
related.

Results
of
the
histopathologic
examinations
suggest
phenol
was
not
toxic
or
carcinogenic
to
B6C3F1
mice
under
the
conditions
of
this
2
year
drinking
water
carcinogenic
bioassay;
no
tumor
at
any
site
in
the
mice
could
be
clearly
associated
with
the
administration
of
phenol
in
this
study.

Non­
guideline
­
Mechanistic
Study
Phenol
purity
99.5%
Stenius
et
al.,
1989
(
Carcinogenesis
Vol.
10)
Acceptable
­
Non­
guideline
0
or
100
mg/
kg/
day
5
days/
week
for
7
weeks
NOAEL

100
mg/
kg
(
highest
dose
tested)
LOAEL
>
100
mg/
kg
(
not
established)

Phenol
is
not
a
potent
stimulator
of
foci
development
and
can
be
regarded
at
a
negative
control
in
this
study
because
it
should
not
be
susceptible
to
oxidation­
reduction
reactions.

870.5100
(
§
84­
2)
Bacterial
reverse
mutation
test
Phenol
purity
not
reported
Florin,
et
al.
1980
(
Toxicology
Vol.
15)
Acceptable
­
Non­
guideline
2.3
­
2343

g/
plate
3

mol/
plate
Negative
There
was
no
evidence
of
induced
mutant
colonies
over
background.
Positive
controls
produced
the
appropriate
responses
in
the
corresponding
strains
of
the
bacterial
reverse
mutagenesis
test.
S.
typhimurium
did
not
show
mutagenic
activity
in
the
presence
or
absence
of
metabolic
activation
when
phenol
was
administered
at
3

mol/
plate.
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
21
of
57
870.5100
(
§
84­
2)
Bacterial
reverse
mutation
test
Phenol
purity
99.9%
Haworth
et
al.,
1983
(
Env.
Mutagenesis
Suppl.
Vol.
1)
Acceptable
­
Non­
guideline
0,
33,
100,
333,
1,000,
2,500,
and
3,333

g/
plate
Negative
There
was
no
evidence
of
induced
mutant
colonies
over
background.
Positive
controls
produced
appropriate
responses
in
corresponding
strains
of
the
bacterial
reverse
mutagenesis
test.
S.
typhimurium
did
not
show
mutagenic
activity
in
the
presence
or
absence
of
metabolic
activation
following
administration
of
phenol.

870.5100
(
§
84­
2)
Bacterial
reverse
mutation
test
Phenol
purity
98%
Pool
and
Lin,
1982
(
Food
Chem.
Tox.
Vol.
20)
Acceptable
­
Non­
guideline
0.5,
5,
50,
500,
and
5,000

g/
plate
Negative
The
most
abundant
phenolic
compounds
found
in
smokehouse
smoke
condensates
were
not
mutagenic
in
the
Salmonella
Typhimurium
assay.
There
was
no
evidence
of
mutagenic
activity
following
administration
of
phenol
to
5
bacterial
strains
of
S.
typhimurium
in
the
presence
or
absence
of
metabolic
activation.

870.5100
(
§
84­
2)
Bacterial
reverse
mutation
test
Phenol
purity
not
reported
Gocke
et
al.,
1981
(
Mutat.
Res.
Vol.
90)
Acceptable
­
Non­
guideline
0
­
3,000

g/
plate
Negative
Phenol
was
not
mutagenic
in
the
bacterial
strains
in
the
absence
of
metabolic
activation.
Phenol
showed
mutagenic
effects,
in
the
presence
of
metabolic
activation,
predominantly
in
the
Ames
tester
strains
of
S.
typhimurium
that
are
sensitive
for
frameshift
mutagens
(
ie.,
TA
98).
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
22
of
57
870.5275
(
§
82­
4)
Sex­
linked
recessive
lethal
test
in
Drosophila
melanogaster
Phenol
purity
not
reported
Gocke
et
al.,
1981
(
Mutat.
Res.
Vol.
90)
Acceptable
­
Non­
guideline
50
mM
Negative
Phenol
was
administered
to
D.
melanogaster
and
3543,
3458,
and
2139
chromosomes
were
tested
for
sex­
linked
recessive
lethals
in
Broods
1,
2,
and
3,
respectively.
There
were
no
significant
increases
in
recessive
lethals
observed
following
administration
of
phenol
to
Broods
1,
2,
and
3
and
only
17
(
0.48%),
6
(
0.17%),
and
7
(
0.33%)
sex­
linked
recessive
lethals,
respectively,
were
measured
in
the
chromosomes
tested.

After
feeding
phenol
to
adult
flies,
the
frequency
of
recessive
lethals
was
increased,
but
not
to
significant
levels.
Phenol
was
not
mutagenic
within
the
confines
of
this
study.

870.5275
(
§
82­
4)
Sex­
linked
recessive
lethal
test
in
Drosophila
melanogaster
Phenol
purity
99.9%
Woodruff
et
al.,
1985
(
Env.
Mutagenesis
Vol.
7)
Acceptable
­
Non­
guideline
Feeding:
0
and
2,000
ppm
Injection:
0
and
5,250
ppm
Negative
Phenol
was
tested
up
to
cytotoxic
concentrations
2,000
and
5,250
ppm
in
feeding
and
injection
studies,
respectively.
The
number
of
sex­
linked
recessive
lethal
mutations
in
the
feeding
study
were
7
and
11
at
the
0
and
2,000
ppm
doses,
respectively.
The
injection
assay
resulted
in
5
(
0
ppm)
and
6
(
5,250
ppm)
sex­
linked
recessive
lethal
mutations,
while
the
feeding
study
exhibited
0.12
(
0
ppm)
and
0.17
(
2,000
ppm)
lethals.
These
sex­
linked
recessive
lethal
mutations
were
not
significantly
different
from
those
found
in
controls.
One
cluster
of
32
lethals
and
one
cluster
of
86
lethals
were
observed
in
the
treated
feeding
experiment.
Phenol
was
negative
in
inducing
sex­
linked
recessive
lethal
mutation
in
D.
melanogaster.
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
23
of
57
870.5300
(
§
84­
2)
In
Vitro
mammalian
call
gene
mutation
test
Phenol
purity
not
reported
Pashin
and
Bahitova,.
1982
(
Mutation
Res.
Vol.
104)
Acceptable
­
Non­
guideline
Phenol:
0,
25,
50,
100,
250,
and
500

g/
mL
Benzo[
a]
pyrene
and
Phenol
mix:
100,
250,
500

g/
mL.
The
mixture
includes
the
addition
of
sodium
Phenobarbital
metabolic
activation.
Positive
At
doses
of
25,
50,
100,
250,
and
500

g/
mL
phenol,
there
was
a
dose­
dependent
increase
in
the
number
of
revertant
colonies
(
1.2­,
1.2­,
1.7­,
2.5­,
and
4.3­
fold
increases,
respectively).
Statistically
significant
increases
were
observed
in
the
frequency
of
AGr
(
selective
agent,
8­
azaguanine
added
to
determine
resistant
mutants)
mutants
over
spontaneous
levels
with
52
and
72%
increases
at
250
and
500

g/
mL,
respectively.
The
combination
of
phenol
with
benzo[
a]
pyrene
at
a
concentration
of
12

g/
mL,
exhibited
an
increase
in
frequency
of
8­
azaguanine
resistant
colonies
with
increasing
concentrations
of
phenol.
The
results
were
the
same
as
the
sum
of
the
separate
effects
of
phenol
and
benzo[
a]
pyrene
and
the
researchers
concluded
that
phenol
did
not
block
or
activate
the
mutagenicity
of
benzo[
a]
pyrene.

870.5375
(
§
84­
2)
In
Vitro
mammalian
chromosome
aberration
test
Phenol
purity
not
reported
(
high
commercial
grade)
Kolachana
et
al.,
1993
(
Cancer
Res.
Vol.
53)
Acceptable
­
Non­
guideline
HL60
cells
exposed
for
30
minutes
to
100

M
phenol
Positive
Phenol
increased
the
steady
state
level
of
8­
hydroxy­
2'­
deoxyguanosine
in
DNA
of
human
leukemia
HL60
cells.
The
increase
in
this
oxidative
damage
product
was
3.5­
fold
and
indicates
genotoxic
effects
resulting
from
active
oxygen
following
exposure
to
phenol.

870.5380
(
§
84­
2)
Mammalian
spermatogonial
chromosomal
aberration
test
­
Rat
Phenol
purity
not
reported
Bulsiewicz,
1977
(
Folia
Morphology
Vol.
36)
Acceptable
­
Non­
guideline
0.08,
0.8,
or
8.0
mg/
L/
day
for
30
days
for
5
generations
Positive
There
was
evidence
of
a
concentration­
related
(
0.08­
8.0
mg/
L)
positive
response
of
spermatogonial
chromosome
aberrations
in
Porton
strain
male
mice
following
30
days
of
exposure
to
phenol
in
water.
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
24
of
57
870.5385
(
§
84­
2)
Mammalian
bone
marrow
chromosome
aberration
test
­
Mouse
Phenol
purity
not
reported
(
high
commercial
grade)
Kolachana
et
al.,
1993
(
Cancer
Res.
Vol.
53)
Acceptable
­
Non­
guideline
75
mg/
kg/
day
Negative
Individual
treatment
with
phenol,
hydroquinone,
or
catechol
did
not
significantly
increase
8­
hydroxy­
2'­
deoxyguanosine
levels
in
mouse
bone
marrow
cells
compared
to
the
control
with
only
11,
7,
and
26%
increases,
respectively,
in
treated
cells
over
control)

870.5395
(
§
84­
2)
Mammalian
erythrocyte
­
Mouse
Phenol
purity
not
reported
Barale
et
al.,
1990
Acceptable
­
Non­
guideline
40,
80,
and
160
mg/
kg/
day
Negative
There
was
no
significant
increase
in
the
frequency
of
micronucleated
polychromatic
erythrocytes
in
bone
marrow
of
Swiss
CD­
1
male
mice
after
treatment
with
phenol
(
40­
160
mg/
kg).
However,
when
phenol
is
combined
with
hydroquinone
(
40­
80
mg/
kg)
a
significant
dose­
related
increase
was
observed.

870.5395
(
§
84­
2)
Mammalian
erythrocyte
­
Mouse
Phenol
purity
99%
Chen
and
Eastmond,
1995
(
Carcinogenesis
Vol.
16)
Acceptable
­
Non­
guideline
50,
75,
100,
or
160
mg/
kg/
day
Negative
There
was
no
significant
increase
in
the
frequency
of
micronucleated
polychromatic
erythrocytes
in
bone
marrow
of
CD­
1
male
mice
following
treatment
with
phenol
(
50­
160
mg/
kg)
alone.
However,
when
phenol
is
combined
with
hydroquinone
(
60
mg/
kg),
a
significant
increase
in
MNPCEs
was
observed.
The
data
suggest
that
phenol
genotoxic
when
combined
with
hydroquinone.

870.5395
(
§
84­
2)
Mammalian
erythrocyte
­
Mouse
Phenol
purity
not
reported
Gocke
et
al.,
1981
(
Mutation
Res.
Vol.
90)
Acceptable
­
Non­
guideline
47,
98,
and
188
mg/
kg/
day
Negative
There
were
no
significant
increases
in
the
frequency
of
micronucleated
polychromatic
erythrocytes
in
mouse
bone
marrow
cells
at
the
concentrations
of
phenol
used
in
this
study.
Phenol
was
not
mutagenic
in
NMRI
mouse
bone
marrow
cells.
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
25
of
57
870.7485
(
§
85­
1)
Metabolism
and
pharmacokinetics
­
Rat
Phenol
purity
not
reported
Capel
et
al.,
1972
(
Xenobiotica
Vol.
2)
Acceptable
­
Non­
guideline
25
mg/
kg/
day
An
average
of
95%
of
14C
dose
of
phenol
(
25
mg/
kg)
was
excreted
in
the
urine
in
24
hours.
Four
metabolites,
the
sulfates
and
glucuronides
of
phenol
and
quinol,
were
found
in
the
urine
of
rats
after
an
oral
dose
of
phenol.
The
phenyl
sulfate
and
quinol
sulfate
metabolites
represented
54
and
1%,
respectively
of
the
metabolites
recovered
in
the
urine.
The
remaining
phenol
metabolites
recovered
from
the
urine
were
phenyl
glucuronide
(
42%)
and
quinol
glucuronide
(
2%).

870.7485
(
§
85­
1)
Metabolism
and
pharmacokinetics
­
Rat
Phenol
purity
not
reported
Hughes
and
Hall,
1995
Acceptable
­
Non­
guideline
350
nmol/
kg
Absorption
of
phenol
was
extensive
following
iv,
oral,
and
it
administration
while
dermal
absorption
was
slightly
lower
by
comparison.
Phenol
was
predominantly
conjugated
with
sulfate
and
lower
amounts
of
glucuronic
acid.
These
metabolites
were
rapidly
excreted
in
the
urine.
Phenol
was
distributed
throughout
the
body
in
low
amounts
and
appeared
to
concentrate
in
liver,
lung,
and
kidney.
The
data
suggest
that
the
exposure
of
phenol
to
rats
by
oral,
dermal,
intratracheal,
and
intravenous
routes
resulted
in
rapid
absorption,
conjugation,
and
elimination
in
urine.

870.7485
(
§
85­
1)
Metabolism
and
pharmacokinetics
­
Mouse
Phenol
purity
not
reported
Capel
et
al.,
1972
(
Xenobiotica
Vol.
2)
Acceptable
­
Non­
guideline
25
mg/
kg/
day
Intestinal
conjugation
of
phenol
prior
to
absorption
was
significant
only
at
low
dose,
the
first­
pass
intestinal
conjugation
alone
does
not
explain
lack
of
carcinogenicity
of
phenol
at
much
higher
doses.
The
data
suggest
that
a
combination
of
first
pass
conjugation
and
zonal
segregation
of
hepatic
enzymes
may
contribute
to
the
greater
production
of
hydroquinone
after
oral
administration
of
benzene
than
phenol.
Hydroquinone
and
other
metabolites
may
be
the
metabolic
basis
for
carcinogenic
and
genotoxic
effects
observed
with
benzene
but
not
phenol.
Table
3.2.
Toxicity
Profile
of
Phenol/
Sodium
Phenate
Guideline
Number/
Study
Type/
Test
Substance
(%
a.
i.)
MRID
Number
(
Year)/
Citation/
Classification/
Doses
Results
Page
26
of
57
870.7600
(
§
85­
3)
Dermal
Penetration
Phenol
purity
not
reported
Behl
and
Linn,
1983
(
J
Pharm.
Sci.
Vol.
72)
Acceptable
­
Non­
guideline
0.5,
1.0,
2.0,
4.0,
and
6.0%
(
w/
v)
in
saline
solution
Age
and
hydration
have
little
effect
on
the
permeability
of
phenol
through
human
and
mouse
skin
and
the
effects
on
the
skin
were
a
result
of
destroyed
barrier
integrity.
Permeation
of
and
chemical
denaturation
by
phenol
were
found
to
be
similar
between
mouse
and
human
skin
tissue;
indicating
that
the
hairless
mouse
is
an
adequate
model
for
chemical
permeability
in
humans.
The
results
suggest
that
the
stratum
corneum
is
proportionally
impaired
as
the
phenol
concentration
is
increased.

3.2
FPQA
Considerations
Under
the
Food
Quality
Protection
Act
(
FQPA),
P.
L.
104­
170,
promulgated
in
1996
as
an
amendment
to
the
Federal
Insecticide,
Fungicide,
and
Rodenticide
Act
(
FIFRA)
and
the
Federal
Food,
Drug
and
Cosmetic
Act
(
FFDCA),
the
Agency
was
directed
to
"
ensure
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
infants
and
children"
from
aggregate
exposure
to
a
pesticide
chemical
residue.
The
law
further
states
that
in
the
case
of
threshold
effects,
for
purposes
of
providing
this
reasonable
certainty
of
no
harm,
"
an
additional
tenfold
margin
of
safety
for
the
pesticide
chemical
residue
and
other
sources
of
exposure
shall
be
applied
for
infants
and
children
to
take
into
account
potential
pre­
and
post­
natal
toxicity
and
completeness
of
the
data
with
respect
to
exposure
and
toxicity
to
infants
and
children.
Notwithstanding
such
requirement
for
an
additional
margin
of
safety,
the
Administrator
may
use
a
different
margin
of
safety
for
the
pesticide
residue
only
if,
on
the
basis
of
reliable
data,
such
margin
will
be
safe
for
infants
and
children."

On
March
9,
2004,
the
Antimicrobials
Division's
Toxicity
Endpoint
Selection
Committee
(
ADTC)
reviewed
the
available
toxicology
data
for
phenol.
The
ATDC
concluded
that
there
are
low
concerns
and
no
residual
uncertainties
for
pre
and/
or
postnatal
toxicity
with
phenol
for
any
of
the
available
studies.
Conservative
NOAELs
were
established
for
all
developmental
and
offspring
effects.
The
developmental
and
reproductive
toxicity
studies
conducted
with
phenol
provide
adequate
information
on
the
dose­
response
relationships
for
developmental
and
reproductive
toxicity
and
are
considered
adequate
studies
for
regulatory
purposes.
The
ATDC
concluded
that
there
is
no
evidence
for
susceptibility
of
phenol
from
the
available
data
on
developmental
and
reproductive
toxicity.
The
hazard
based
default
special
FQPA
safety
factor
(
1x)
can
be
reduced
when
assessing
dietary
and
nonoccupational
risks
from
the
uses
of
phenol.
Page
27
of
57
3.3
Dose­
Response
Assessment
The
doses
and
toxicologic
endpoints
selected
by
ADTC
for
various
exposure
scenarios
are
summarized
in
Table
3.3
below.

Table
3.3
Summary
of
Toxicological
Doses
and
Endpoints
for
Phenol/
Sodium
phenate
for
Use
in
Human
Risk
Assessment
Exposure
Scenario
Dose
(
mg/
kg/
day)
used
in
risk
assessment
UF
Special
FQPA
SF(
1x)
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Acute
Dietary
(
gen
population)
This
risk
assessment
is
not
required.

Acute
Dietary
(
females
13­
49)
This
risk
assessment
is
not
required.

Chronic
Dietary
(
all
populations)
NOAEL=
60
UF
=
100
Chronic
RfD
=
0.6
mg/
kg/
day
Chronic
PAD
=
0,6
mg/
kg/
day
FQPA
SF
=
1x
Developmental
toxicity
study
in
rats
(
Argus,
1997)
NOAEL
based
on
decreases
in
maternal
body
weight
gain
at
120
mg/
kg/
day
(
LOAEL).

Incidental
Oral
Short­
Term
(
1
­
30
Days)

Residential
Only
NOAEL=
60
mg/
kg/
day
MOE
=
100
Developmental
toxicity
study
in
rats
(
Argus,
1997)
NOAEL
based
on
decreases
in
maternal
body
weight
gain
at
120
mg/
kg/
day
(
LOAEL).

Incidental
Oral
Intermediate­
Term
(
1
­
6
Months)

Residential
Only
NOAEL=
60
mg/
kg/
day
MOE
=
100
Developmental
toxicity
study
in
rats
(
Argus,
1997)
NOAEL
based
on
decreases
in
maternal
body
weight
gain
at
120
mg/
kg/
day
(
LOAEL).

Dermal1
Short
and
intermediateterm
NOAEL
=
60
mg/
kg/
day
MOE
=
100
Developmental
toxicity
study
in
rats
(
Argus,
1997)
NOAEL
based
on
decreases
in
maternal
body
weight
gain
at
120
mg/
kg/
day
(
LOAEL).
Table
3.3
Summary
of
Toxicological
Doses
and
Endpoints
for
Phenol/
Sodium
phenate
for
Use
in
Human
Risk
Assessment
Exposure
Scenario
Dose
(
mg/
kg/
day)
used
in
risk
assessment
UF
Special
FQPA
SF(
1x)
and
Level
of
Concern
for
Risk
Assessment
Study
and
Toxicological
Effects
Page
28
of
57
Inhalation
(
All
durations)
LOAEL
=
0.1
mg/
L
(
26
mg/
kg/
day)
MOE
=
300
(
ST,
IT)

MOE
=
1,000
(
LT)
Dalin
and
Kristofferson:
Physiological
Effects
of
a
Sub­
lethal
Concentration
of
Inhaled
Phenol
on
the
Rat.
Ann.
Zool.
Fennici
11:
193­
199,
1974
LOAEL
of
0.1
mg/
L,
based
on
alterations
in
sliding
angle
from
tilting
plane
test,
and
significant
increases
in
liver
enzymes
Cancer
Data
inadequate
for
assessment
of
human
carcinogenic
potential
(
USEPA,
2002a)

1a
dermal
absorption
factor
of
50%
should
be
used
since
an
oral
endpoint
was
selected.
Dermal
absorption
data
were
available
from
the
IRIS
Toxicological
profile
for
phenol.
From
the
available
data,
dermal
absorption
percentages
of
20­
50%
have
been
observed
from
in
vivo
and
in
vitro
studies.
The
ADTC
selected
the
50%
dermal
absorption
value
for
phenol
for
use
in
risk
assessments
as
a
conservative
value.
This
value
also
takes
into
account
the
irritant
properties
of
phenol
which
may
increase
its
dermal
absorption.

3.4
Endocrine
Disruption
The
Food
Quality
Protection
Act
(
FQPA;
1996)
requires
that
EPA
develop
a
screening
program
to
determine
whether
certain
substances
(
including
all
pesticides
and
inerts)
"
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen,
or
such
other
endocrine
effect...."
Following
the
recommendations
of
its
Endocrine
Disruptor
Screening
and
Testing
Advisory
Committee
(
EDSTAC),
EPA
determined
that
there
was
a
scientific
basis
for
including,
as
part
of
the
program,
the
androgen
and
thyroid
hormone
systems,
in
addition
to
the
estrogen
hormone
system.
EPA
also
adopted
EDSTAC's
recommendation
that
the
Program
include
evaluations
of
potential
effects
in
wildlife.
For
pesticide
chemicals,
EPA
will
use
FIFRA
and,
to
the
extent
that
effects
in
wildlife
may
help
determine
whether
a
substance
may
have
an
effect
in
humans,
FFDCA
authority
to
require
the
wildlife
evaluations.
As
the
science
develops
and
resources
allow,
screening
of
additional
hormone
systems
may
be
added
to
the
Endocrine
Disruptor
Screening
Program
(
EDSP).
When
the
appropriate
screening
and/
or
testing
protocols
being
considered
under
the
Agency's
EDSP
have
been
developed,
phenol
and
sodium
phenate
may
be
subjected
to
additional
screening
and/
or
testing
to
better
characterize
effects
related
to
endocrine
disruption.
Page
29
of
57
4.0
EXPOSURE
ASSESSMENT
AND
CHARACTERIZATION
Phenol
and
phenol
salts
are
active
ingredients
in
disinfectant,
deodorizer
and
cleaner
formulations.
Exposure
to
phenol
and
phenol
salts
can
occur
on
commercial,
institutional
and
industrial
premises
and
equipment,
medical
premises
and
equipment,
residential
and
public
access
premises,
and
at
food
handling
establishments.

4.1
Summary
of
Registered
Uses
Concentrations
of
phenol
and
phenol
salts
in
products
range
from
1.6
%
to
8.2%
(
1.6%
being
the
most
common
concentration).
These
formulations
have
bactericidal,
virucidal,
fungicidal
and
tuberculocidal
properties,
kill
mold
and
mildew
and
eliminate
odors.
All
formulations
are
in
liquid
form
and
include
ready­
to­
use
solutions,
pressurized
liquids
and
impregnated
materials
(
towelettes).
At
least
one
product
reviewed
is
an
industrial
additive
used
as
a
preservative
for
polishes,
cleansers,
paints,
and
protectants.

Use
site
categories
for
these
formulations
include
commercial,
institutional
and
industrial
premises
and
equipment,
medical
premises
and
equipment,
food
handling
establishments
and
residential
and
public
access
premises.

Table
4.1
lists
the
active
EPA
registration
numbers
of
the
products
containing
phenol
and
phenol
salts
evaluated
in
this
document.

Table
4.1.
EPA
Registration
Numbers
for
Phenol
Products
Use
Category
Formulation
EPA
Registration
Numbers
Disinfectant/
Deodorizer
Aerosol
Spray
8383­
4,
69658­
3,
75480­
1,
8383­
3
Concentrate
8383­
6
Towelette
8383­
7
Material
Preservative
Ready­
to­
Use
8383­
1
4.2
Dietary
Exposure/
Risk
Pathway
The
Agency
has
carried
out
the
dietary
exposure
and
risk
assessment
for
use
of
phenol
and
phenol
salts
as
an
active
ingredient
in
that
may
result
in
dietary
exposure.
A
detailed
dietary
exposure
assessment
is
presented
in
the
appendix.

Two
products
currently
registered
can
be
used
to
disinfect
counter
tops
in
kitchens,
among
other
areas.
One
product
is
a
ready­
to­
use
solution,
while
the
other
is
a
wettable
disposable
cloth
that
is
impregnated
with
phenol
and
sodium
phenate.
A
counter
top
that
has
been
treated
with
either
of
Page
30
of
57
these
products
may
come
into
contact
with
food
prepared
on
the
counter
top,
which
in
turn
may
be
ingested.
Although
neither
product
label
states
that
it
should
be
used
on
food
preparation
equipment,
it
is
possible
that
food
could
be
prepared
or
placed
on
treated
kitchen
counter
tops
before
being
eaten.

No
residue
chemistry
data
were
submitted
by
registrants,
nor
were
any
data
requested
by
the
Agency,
as
these
uses
do
not
fall
under
the
guidelines
associated
with
residue
chemistry
(
OPPTS
GLN
860.1300,
OPPTS
GLN
860.1340,
OPPTS
GLN
860.1500).
The
Agency
has
used
available
methods
to
estimate
phenol
residues
on
food
due
to
migration
of
these
products.

4.2.1Methodology
As
noted
in
the
dietary
exposure
chapter
of
the
phenol
RED,
the
Agency
used
the
following
approach
to
calculation
of
dietary
exposure
for
phenol
as
a
disinfectant
solution
(
end
use).

EDI
=
(
wash
solution,
mg/
cm2)
x
(
AR)
(
wt.
fraction
of
wash
solution
)
x
MF(
fraction
of
pesticide
migrating
to
food)
x
SA(
surface
area
of
exposure)/
BW­­­­­­­­­­­­­­­­­­­­­­­­(
1)

Where
EDI
=
Estimated
Daily
Intake,
mg/
kg/
day)
AR
=
Application
Rate
SA
=
Surface
area
to
containing
the
pesticide
to
which
food
is
exposed
MF
=
Fraction
of
pesticide
migrating
to
food,
assuming
10%
BW
=
Body
weight,
adult
male
=
70
kg,
adult
female
=
60
kg
and
a
child
=
15
kg
A
value
of
10%
was
used
for
the
migration
of
residues
to
food
due
to
the
high
vapor
pressure
of
phenol.
Confirmatory
data
will
be
needed
to
support
this
value.

4.2.2Acute
Dietary
Exposure
and
Risk
The
ADTC
determined
that
for
acute
dietary
risk,
there
was
no
appropriate
endpoint
for
assessment
of
acute
dietary
exposure.
This
conclusion
was
based
on
examination
of
the
hazard
data
which
might
be
used
in
support
of
such
an
endpoint.
Body
weight
effects
observed
were
not
felt
to
be
the
result
of
a
single
exposure,
and
there
were
no
other
adverse
effects
from
the
data
that
were
considered
reflective
of
a
single
exposure.
An
Acute
RfD/
PAD
value
was
not
selected.
As
a
result,
evaluation
of
acute
dietary
risk
was
not
necessary.

4.2.3Chronic
Dietary
Exposure
and
Risk
For
chronic
dietary
risk,
the
ADTC
cited
the
published
chronic
RfD
value
in
EPA's
Integrated
Risk
Information
System
(
IRIS)
database.
This
Reference
Dose
value
is
based
upon
an
unpublished
developmental
toxicity
study
conducted
according
to
GLP
guidelines
(
Argus
Research
Laboratories,
1997).
In
this
study,
pregnant
Crl:
CDRBR
VAF/
Plus
Sprague­
Dawley
rats
(
25
per
group)
received
Page
31
of
57
phenol
by
oral
gavage
on
GDs
6
through
15.
Dosing
was
three
times
daily
with
0,
20,
40,
or
120
mg
phenol/
kg/
dosage
using
a
dosing
volume
of
10
mL/
kg.
The
authors
noted
that
the
test
material
was
90%
phenol
United
States
Pharmacopeia
(
USP);
the
authors
adjusted
the
dosage
calculations
for
test
material
purity.

The
chronic
PAD
value
was
calculated
to
be
0.6
mg/
kg/
day,
using
the
maternal
NOAEL
value
of
60
mg/
kg/
day
and
an
uncertainty
factor
of
100
(
10x
interspecies
extraploation,
10x
intraspecies
variation).
The
ADTC
determined
that
a
special
FQPA
hazard­
based
safety
factor
was
not
required
for
phenol,
and
could
be
reduced
to
1x.

Chronic
dietary
risks
for
adult
male,
adult
female,
and
children
exposure
to
disinfectant
solutions
use
is
shown
in
Table
4.2.
The
disinfectant
use
assumed
a
transfer
efficiency
to
food
of
10%.
On
the
basis
of
this
and
other
assumptions
used,
cumulative
chronic
dietary
risk
estimates
from
the
indirect
food
uses
were
calculated
to
be
36%
for
children,
9.0%
for
adult
females,
and
7.5%
for
adult
males.
Thus,
from
the
indirect
food
uses
of
phenol,
no
risk
of
concern
was
identified
for
chronic
dietary
exposure.

Table
4.2.
Summary
of
Dietary
Exposure
and
Risk
for
Phenola
Population
Subgroup
EDI
(
mg/
person/
day)
Chronic
Dietary
Dietary
Exposure
%
cPAD
b
Disinfectant
Solutions
Adult
male
3.2400
4.50e­
02
7.50
Adult
female
3.2400
5.40e­
02
9.0
Child
3.2400
2.16e­
01
36.0
a­­
For
adults
males,
chronic
exposure
analysis
is
based
on
a
body
weight
of
70
kg.
For
adults
females,
chronic
exposure
analysis
is
based
on
a
body
weight
of
60
kg.
For
children,
exposure
is
based
on
a
body
weight
of
15
kg.

b­­%
cPAD
=
dietary
exposure
(
mg/
kg/
day)
*
100
/
cPAD,
where
cPAD
for
adults
and
children
=
0.6
mg/
kg/
day.

4.3
Water
Exposure/
Risk
Pathway
Phenol
appears
to
have
degradation
pathways
in
air
(
calculated
half
life
less
than
a
day)
water
(
measured
half
life
less
than
a
day),
aerobic
and
anaerobic
soils
(
degradation
half
lives
less
than
5
days).
It
is
not
likely
to
bioaccumalate
in
aquatic
organisms.
(
Measured
BCF
in
goldfish
is
0.28
and
1.3
in
golden
orfe).
Data
on
plants
show
that
due
to
a
high
respiratory
decomposition
of
phenol
into
carbon
dioxide
(
mineralization);
it
is
also
not
likely
to
accumulate
in
plants.
Due
to
multimedia
degradation
pathways,
phenol
is
not
likely
to
be
an
environmental
concern.
Page
32
of
57
Phenol's
use
in
the
production
of
resins
and
other
manufacturing
industries
and
as
a
general
disinfectant
allows
for
the
possibility
of
ground
and
surface
water
contamination.
Despite
phenol's
high
water
solubility
and
poor
sorption
to
soil,
biodegradation
of
phenol
is
sufficiently
rapid
so
that
the
probability
of
groundwater
contamination
will
be
low.
Because
phenol
absorbs
light
in
the
region
290­
330
nm,
phenol
might
photodegrade
directly
in
surface
water.
Phenol
is
not
expected
to
absorb
to
sediment
in
the
water
column.
Page
33
of
57
4.4
Residential
Exposure/
Risk
Pathway
A
detailed
human
exposure
risk
assessment
for
phenol
and
phenol
salts
is
provided
in
the
attached
Appendix.
The
summary
of
the
exposures
and
risks
to
the
residential
population
are
presented
below.

4.4.1
Residential
Handler
Scenarios
The
following
scenarios
were
considered
for
residential
handlers
of
phenol­
containing
products:

°
Application
of
paint
treated
with
a
material
preservative
using
an
airless
sprayer
and
a
paintbrush/
roller,
°
Use
of
disinfectant/
deodorizing
spray
on
hard
non­
porous
surfaces,
and
°
Use
of
disinfectant
towelette
on
hard
non­
porous
surfaces.

Using
surrogate
unit
exposure
data,
application
rates
from
labels,
EPA
estimates
of
daily
amount
handled,
and
two
exposure
models,
exposure
and
risks
to
handlers
were
assessed.

4.4.1.1
Paint
Exposures
and
Risks
One
phenol
product
is
listed
for
use
as
an
industrial
additive,
and
lists
paint
as
a
possible
use.
The
label
recommends
that
between
2%­
5%
by
weight
of
active
ingredients
be
added.
As
a
conservative
measure,
it
is
assumed
that
the
treated
paint
is
comprised
of
5%
active
ingredient,
by
weight.
Assuming
that
paint
has
a
density
of
10
lbs
per
gallon,
the
concentration
of
phenols
in
paint
is
0.5
lbs
a.
i./
gallon.
Two
painting
scenarios
were
considered
in
this
assessment
for
homeowners:
use
of
an
airless
sprayer
and
use
of
a
paintbrush/
roller
to
paint
the
exterior
of
a
house.
It
is
assumed
(
Residential
SOPs)
that
a
homeowner
will
paint
up
to
15
gallons
per
day
with
an
airless
sprayer
and
up
to
2
gallons
per
day
with
a
brush/
roller,
that
the
exposures
will
be
short­
term
in
duration,
and
that
a
painter
will
be
exposed
through
both
the
dermal
and
inhalation
routes.
Due
to
the
fact
that
the
shortterm
toxicological
endpoints
for
the
dermal
and
inhalation
routes
of
exposure
are
derived
from
different
studies
and
produce
different
effects,
it
is
not
appropriate
to
combine
these
routes
of
exposure.
Consequently,
separate
MOEs
are
presented
in
the
risk
assessment.
The
results
of
the
assessment
are
presented
in
Table
4.3.
Based
on
these
assumptions
and
unit
exposure
data
from
the
Pesticide
Handlers
Exposure
Database
(
PHED),
the
dermal
MOEs
for
both
the
airless
sprayer
and
brush/
roller
are
of
concern
(
MOEs
=
12
and
31,
respectively,
target
MOE
=
100).
The
aerosol
portion
of
the
inhalation
route
slightly
exceeds
the
level
of
concern
(
MOE
=
290,
target
MOE
of
300)
for
the
airless
sprayer
use
only.

In
addition
to
the
aerosol
inhalation
risks
presented
in
Table
4.3
for
painters,
phenol
has
a
relatively
high
vapor
pressure
(
0.341
mmHg
@
25
C),
and
therefore,
EPA
is
also
the
concern
for
potential
vapor
inhalation
exposure.
To
determine
the
potential
inhalation
exposure
resulting
from
the
vapor
of
phenol,
the
WPEM
(
Wall
Paint
Exposure
Assessment
Model)
was
used
to
estimate
the
air
concentration.
Page
34
of
57
OPPT/
EETD
has
developed
the
model,
WPEM,
to
estimate
air
concentrations
from
painting.
More
information
and
access
to
WPEM
is
available
at
http://
epa.
gov/
opptintr/
exposure/
docs/
wpem.
htm.
In
summary,
WPEM
bases
its
air
concentration
estimates
on
models
developed
from
small
chamber
data
on
paints.

WPEM
is
a
user­
friendly,
flexible
software
product
that
uses
mathematical
models
developed
from
small
chamber
data
to
estimate
the
emissions
of
chemicals
from
oil­
based
(
alkyd)
and
latex
wall
paint.
This
is
then
combined
with
detailed
use,
workload
and
occupancy
data
(
e.
g.,
amount
of
time
spent
in
the
painted
room,
etc,)
to
estimate
exposure.
The
output
of
WPEM
was
evaluated
in
a
home
used
by
EPA
for
testing
purposes
and,
in
general,
the
results
were
within
a
factor
of
2.
The
WPEM
provides
exposure
estimates
such
as
Lifetime
and
Average
Daily
Doses,
Lifetime
and
Average
Daily
Concentrations,
and
peak
concentrations.
Specific
input
parameters
include:
the
type
of
paint
(
latex
or
alkyd)
being
assessed,
density
of
the
paint
(
default
values
available),
and
the
chemical
weight
fraction,
molecular
weight,
and
vapor
pressure.
(
WPEM
website).

Phenol
was
assessed
using
WPEM
for
latex
paints
indoors.
The
following
were
used
in
estimating
the
short­
term
vapor
inhalation
exposure
from
phenol
in
paints
using
the
WPEM:
a
vapor
pressure
of
0.341
mmHg
@
25C,
a
mw
of
94.11,
a
paint
weight
fraction
of
0.05,
and
default
model
parameters.
WPEM
estimated
a
peak
instantaneous
concentration
of
22.2
mg/
m3
and
a
acute
potential
dose
rate
(
representing
the
highest
24
hour
exposure)
of
0.98
mg/
kg/
day.
Although
the
peak
instantaneous
concentration
is
available,
it
is
not
representative
of
the
short­
term
inhalation
toxicological
endpoint.
The
highest
24­
hour
inhalation
dose
estimate
of
0.98
mg/
kg/
day
corresponds
to
a
short­
term
inhalation
MOE
of
27
(
i.
e.,
LOAEL
26
mg/
kg/
day
/
0.98
mg/
kg/
day).

4.4.1.2
Disinfectant/
Deodorizing
Spray
and
Towlette
Exposures
and
Risks
The
ready­
to­
use
sprays
and
the
solution
used
to
treat
the
towelette
contain
1.62%
phenol/
sodium
phenate
(
i.
e.,
no
further
dilution).
It
was
assumed
that
the
density
of
this
solution
is
the
same
as
the
density
of
water.
The
label
for
the
towelette
product
did
not
describe
the
quantity
of
product
to
be
used;
rather,
the
directions
state
that
the
towelette
is
to
be
used
to
wipe
the
surface,
and
then
the
surface
should
be
wiped
dry.
In
the
absence
of
more
specific
use
information,
it
was
assumed
that
a
homeowner
uses
up
to
0.5
liter
of
the
solution
in
wet
towelettes
in
a
single
day.
This
is
a
screeninglevel
assumption
that
does
not
trigger
a
risk
of
concern.
However,
refinements
to
this
input
may
be
necessary
for
the
aggregate
risks.
Similarly,
the
aerosol
spray
directions
state
that
the
product
can
be
sprayed
2­
4
seconds
to
deodorize
a
room,
but
no
data
were
available
describing
the
quantity
of
product
that
is
emitted
by
spraying
for
this
time.
Therefore,
0.5
liter
of
solution
was
also
assumed
for
use
of
the
aerosol
spray
(
i.
e.,
1­
can).
Both
the
wipe
and
sprays
are
assumed
to
be
represented
by
the
short­
term
exposure
duration
and
both
dermal
and
aerosol
inhalation
exposures
are
estimated
from
the
CMA
data
and
PHED.

In
addition
to
the
aerosol
inhalation
exposures,
there
is
the
concern
for
potential
vapor
inhalation
exposure
because
phenol
has
a
relatively
high
vapor
pressure
(
0.341
mmHg
@
25
C).
To
determine
the
potential
inhalation
exposure
resulting
from
the
vapor
of
phenol,
the
model
EFAST
(
Exposure
and
Fate
Page
35
of
57
Assessment
Screening
Tool)
was
used
to
estimate
the
air
concentration.
OPPT/
EETD
has
developed
the
model,
EFAST,
to
estimate
air
concentrations.
More
information
and
access
to
the
EFAST
model
is
available
at
http://
www.
epa.
gov/
opptintr/
exposure/.
In
summary,
EFAST
Version
1.0
bases
its
air
concentration
estimates
on
physical/
chemical
properties.
The
air
concentration
estimates
for
the
phenols
are
based
on
the
model's
standard
input
parameters.
The
following
information
is
presented
in
the
EFAST
model:

"....
it
is
assumed
to
contact
the
target
surface,
and
to
subsequently
volatilize
at
a
rate
that
depends
upon
the
chemical's
molecular
weight
and
vapor
pressure."

EFAST
presents
a
peak
air
concentration
as
well
as
a
daily
air
concentration.
The
peak
air
concentration
estimate
"...
is
the
highest
instantaneous
air
concentration
that
is
modeled
during
the
exposure
event."
This
peak
air
concentration
is
not
expected
for
any
appreciable
length
of
time.

EFAST
was
used
to
model
the
air
concentration
from
general
purpose
cleaners
using
a
weight
fraction
of
0.0162.
EFAST
indicates
a
peak
instantaneous
concentration
of
7.29
mg/
m3
from
this
activity.
Because
the
peak
concentration
does
not
represent
a
daily
inhalation
exposure,
the
daily
dose
rather
than
the
peak
estimate
from
EFAST
is
used
to
compare
to
the
short­
term
inhalation
toxicological
endpoint.
If
a
short­
term
toxicological
endpoint
of
less
than
one
day
were
to
be
generated
it
should
be
compared
to
the
peak
air
concentration
estimate.
However,
because
the
toxicological
endpoint
of
concern
is
based
on
greater
than
one
day
of
exposure,
the
daily
dose
rate
of
0.065
mg/
kg/
day
from
EFAST
is
used
in
this
assessment.
The
daily
dose
rate
is
based
on
the
average
daily
concentration
of
0.35
mg/
m3.

The
results
of
the
MOE
analysis
using
the
CMA
data
for
these
scenarios
are
presented
in
Table
4.3.
The
calculated
short­
term
dermal
MOEs
are
not
of
concern
for
any
of
the
scenarios
(
MOE
=
140
and
1,800,
for
wiping
and
mopping,
respectively).
The
calculated
short­
term
(
aerosol)
inhalation
MOEs
from
the
CMA
data
for
the
wiping
and
mopping
are
not
of
concern
(
MOE
=
1,500
and
79,000,
for
wiping
and
mopping,
respectively).
The
results
of
the
EFAST
model
indicate
a
short­
term
inhalation
MOE
from
the
vapor
of
phenol
to
be
400.
Therefore,
the
short­
term
vapor
inhalation
portion
of
phenol
is
also
not
of
concern
(
i.
e.,
above
the
target
MOE
of
300).
Page
36
of
57
Table
4.3.
Calculation
of
Dermal
and
Inhalation
MOE
for
Residential
Handlers
a
Exposure
Scenario
Method
of
Applicatio
n
Dermal
Unit
Exposure
(
mg/
lb
ai)
b
Inhalation
Unit
Exposure
(
mg/
lb
ai)
c
Appl.
Rate
d
(
lb
a.
i./
gal)
Amount
Treated
Absorbed
Dermal
Dose
(
mg/
kg/
day)
f
Dermal
MOE
g
Inhalation
Dose
(
mg/
kg/
day)
h
Inhalatio
n
MOE
i
Painting
Airless
Sprayer
79
(
Res
SOP
PHED)
0.83
(
Res
SOP
PHED)
0.5
15
gal/
day
4.94
12
0.089
290
Paintbrus
h/
Roller
230
(
Res
SOP
PHED)
0.28
(
Res
SOP
PHED)
0.5
2
gal/
day
1.92
31
0.0040
6500
Hard
Surface
Disinfection
Towelette
2870
(
CMA
no
glove)
67.3
(
CMA)
0.0357
lbs
a.
i./
liter
used
0.5
liter
of
product
0.427
140
0.017
1500
Aerosol
Spray
220
(
Res
SOP
PHED)
1.3
(
PHED)
0.0357
lbs
a.
i./
liter
used
0.5
liter
of
product
0.033
1800
0.00033
79,000
a
MOEs
rounded
to
2
significant
figures.
b
Dermal
unit
exposures
are
from
CMA
and
PHED
(
short­
pants
and
short­
sleeves
for
residential
uses
 
Residential
SOPs).
c
Inhalation
unit
exposures
are
from
CMA
and
PHED
study.
d
Application
rates
are
based
on
the
phenol
labels.
It
is
assumed
that
both
the
phenol
and
sodium
phenate
present
in
products
are
active
ingredients.
f
Abs.
dermal
dose
(
mg/
kg/
day)
=
[
unit
exposure
(
mg/
lb
ai)
*
Dermal
Absorption
Factor
(
0.5)
*
Appl.
rate
(
lb
ai/
gallon)
*
gallons
handled
/
Body
weight
(
60
kg).
g
Dermal
MOE
=
NOAEL
(
mg/
kg/
day)
/
Daily
Dose
[
Where
short­
term
dermal
NOAEL
=
60
mg/
kg/
day].
Target
MOE
is
100.
h
Inhalation
dose
(
mg/
kg/
day)
=
[
unit
exposure
(

g/
lb
ai)
*
0.001
mg/

g
unit
conversion
*
max
appl
rate
(
lb
ai/
gal)
*
gallons
handled
*
1
inhalation
absorption]
/
Body
weight
(
70
kg).
i
Inhalation
MOE
=
LOAEL
(
mg/
kg/
day)
/
Daily
Dose
[
LOAEL
for
all
durations
=
0.1
mg/
L
(
which
equals
0.1
mg/
L
*
10.26
L/
hr/
kg
*
6
hrs/
day
/
0.236
kg
=
26.08
mg/
kg/
day].
Target
MOE
is
300
for
short­
term.
Page
37
of
57
4.4.2Residential
Postapplication
Exposure
(
Dermal
and
Incidental
Ingestion)

Post­
application
exposures
can
occur
to
toddlers
from
the
dermal,
oral
(
incidental),
and
inhalation
(
high
vapor
pressure)
routes
from
carpets
that
have
been
machine­
cleaned
with
a
product
containing
phenol
(
and
phenol
salts).
Additionally,
adults
may
be
exposed
to
inhalation
exposures
after
this
use.
It
is
believed
that
the
carpet
shampoo
use
represents
the
high
end
of
the
exposures
to
toddlers
from
the
use
of
phenol
products.
The
carpets
have
been
assessed
rather
than
hard
surface
floors
because
the
products
appear
not
to
be
used
to
mop
floors.
Residential
carpets
are
believed
to
be
machine­
washed
on
an
intermittent
basis
(
perhaps
a
few
times
per
year),
facilities
such
as
day
care
centers
may
clean
the
carpets
more
often
but
are
still
believed
to
be
of
a
short­
term
duration
(
i.
e.,
carpets
machine­
washed
no
more
than
weekly).
Therefore,
only
the
short­
term
risks
have
been
presented.
There
is
also
the
potential
of
inhalation
exposure
from
vapors
resulting
from
painting
indoors
with
a
paint
containing
phenol.
Exposure
estimates
and
the
resulting
MOEs
are
also
presented
for
that
scenario.
Due
to
the
fact
that
the
short­
term
toxicological
endpoints
for
the
dermal
and
oral
routes
of
exposure
are
derived
from
the
same
study
and
produce
the
same
effect,
it
is
appropriate
to
combine
these
exposure
estimates.
These
estimates
are
combined
in
the
aggregate
exposure
section.

Dermal
Exposure
There
is
the
potential
dermal
exposure
to
toddlers
crawling
on
treated
carpets.
To
determine
toddler
exposure
to
residues
in
treated
carpet,
the
following
equation
was
used:

PDD
FR
x
SA
BW
=

where:

PDD=
Potential
daily
dose
FR
=
Flux
rate
of
chemical
from
material
(
mg/
m2/
day)
SA
=
Surface
area
of
the
body
which
is
in
contact
with
carpet
(
m2)
BW
=
Body
weight
(
kg)

The
following
conservative
assumptions
were
made
in
calculating
the
exposures/
risks
due
to
limited
data:

°
Toddlers
(
3
years
old)
are
used
to
represent
the
1
to
6
year
old
age
group
and
are
assumed
to
weigh
15
kg,
the
median
for
male
and
female
toddlers
(
USEPA,
2000).
A
body
surface
area
of
0.657
m2
has
been
assumed,
which
is
the
median
value.
°
The
label
did
not
provide
information
on
the
volume
of
disinfectant
to
be
used
for
carpet
cleaning.
Based
on
information
about
other
carpet
sanitizing
solutions,
it
was
assumed
that
2
ounces
of
disinfectant
are
mixed
with
a
gallon
of
water
(
for
rotary
floor
machines),
and
that
the
resulting
solution
is
applied
at
a
rate
of
1,000
sq.
ft.
per
gallon.
°
No
data
could
be
found
regarding
the
quantity
of
solution
residue
left
in
the
carpet
after
treatment.
As
a
conservative
measure,
it
has
been
assumed
that
25%
of
the
shampoo
remains
after
the
final
vacuuming
process.
°
No
leaching
data
were
available
that
could
be
used
to
estimate
a
flux
rate
of
the
chemical
from
the
Page
38
of
57
carpet.
Therefore,
Residential
SOPs
estimate
of
5%
of
the
amount
on
the
carpet
is
available
for
dermal
transfer.

The
estimated
dermal
dose
and
the
dermal
MOE
is
presented
in
Table
4.4.
The
calculated
dermal
MOE
is
greater
than
the
target
MOE
of
100
and
therefore
does
not
present
a
risk
of
concern
for
dermal
exposure
from
treated
carpets.
Page
39
of
57
Table
4.4.
Short­
term
Risks
Associated
with
Postapplication
Exposure
to
Disinfectant
on
Carpets.

Parameter
Value
Rationale
Application
Rate
1000
ft2/
gallon
of
solution
USEPA
Assumption
%
a.
i.
in
Formulated
Product
1.62%
Maximum
rate
listed
on
label
(#
8383­
3)

Formulated
Product
in
solution
2
oz/
gallon
Assumption
Density
of
cleaning
solution
1.0
g/
mL
Assumed
to
be
similar
to
density
of
water
Flux
Rate
of
Chemical
from
Carpet
0.13
mg/
m2/
day
(
Density)
*
(%
a.
i.)
*
(
Formulated
Product
in
Sol.)
*
(
25%
remaining)*
(
5%
transfer)
/
(
App.
Rate)
*
(
Conversion
Factors)

Surface
Area
of
Body
in
Contact
with
Carpet
0.657
m2
Median
surface
area
of
toddler
Dermal
Absorption
50%

Body
Weight
15
kg
Median
body
weight
of
toddler
Potential
Dermal
Exposure
0.0028
mg/
kg/
day
FR
*
SA
*
DA/
BW
Dermal
NOAEL
60
mg/
kg/
day
Dermal
MOE
21,000
(
Derm.
NOAEL)
/
(
Daily
Derm.
Dose).
Target
MOE
=
100.

Incidental
Ingestion
In
addition
to
dermal
exposure,
infants
crawling
on
treated
carpets
will
also
be
exposed
to
phenol
via
incidental
oral
exposure
during
hand­
to­
mouth
activities.
To
calculate
incidental
ingestion
exposure
to
phenols
due
to
hand­
to­
mouth
transfer,
the
scenarios
established
in
the
Standard
Operating
Procedures
(
SOPs)
for
Residential
Exposure
Assessments
were
used.
These
scenarios
use
assumptions
that
are
similar
to
those
used
in
calculating
exposures
due
to
dermal
contact
of
phenols
from
toddlers
crawling
on
treated
carpets.
The
assumptions
above
in
the
dermal
assessment
(
Table
4.4)
estimates
the
transferable
residues
as
0.013
µ
g/
cm2
.
The
estimated
potential
ingestion
dose
rate
immediately
after
application
would
be
calculated
as
follows:

PDR
norm=
ISR
t
x
SA
x
FQ
x
SE
x
ET
x
0.001
mg/
µ
g
BW
where:

PDR
norm
=
Potential
dose
rate
(
mg/
kg/
day);
ISR
t
=
Indoor
Surface
Residue
(
µ
g/
cm2)
at
time
0;
SA
=
Surface
area
of
the
hands
that
contact
both
the
treated
area,
and
the
individuals
mouth
(
cm2/
event);
FQ
=
Frequency
of
hand­
to­
mouth
events
(
events/
hr);
Page
40
of
57
SE
=
Saliva
extraction
efficiency;
and,
ET
=
Exposure
Time
(
4
hrs/
day)
BW
=
Body
weight
(
15
kg)

The
surface
area
used
for
each
hand­
to­
mouth
event
is
20
cm2
.
It
is
assumed
that
there
are
20
handto
mouth
exposure
events
per
hour
(
90th
percentile).
The
short­
term
incidental
oral
NOAEL
of
60
mg/
kg/
day
should
be
used
as
the
toxicity
endpoint
for
this
scenario
because
of
the
intermittent
nature
of
carpet
shampoos
at
both
residents
and
day
care
centers.
The
potential
dose
rate
(
PDR)
using
this
equation
is
0.0007
mg/
kg/
day
resulting
in
a
hand­
to­
mouth
short­
term
MOE
for
toddlers
of
86,000.
Inhalation
Exposure
Carpet
Treatments:
Post­
application
inhalation
exposure
to
adults
and
toddlers
after
phenol
use
(
as
a
carpet
cleaner)
is
concern
because
of
the
relatively
high
vapor
pressure
of
phenol
(
i.
e.,
0.341
mm
Hg
@
25C).
No
postapplication
air
concentration
data
have
been
submitted
to
determine
potential
inhalation
risk
to
the
vapor
phase.
Therefore,
EFAST
was
used
to
present
a
screening­
level
estimate
of
the
potential
shortterm
inhalation
risk.
The
post­
application
estimates
are
based
on
the
EFAST
results
for
the
air
concentration
and
inhalation
dose
from
the
adult
handlers.
The
toddler
risk
estimates
are
corrected
for
the
lower
body
weight
(
i.
e.,
15
kg).

EFAST
was
used
to
model
the
air
concentration
from
carpet
cleaning
using
the
general
purpose
cleaner
portion
of
the
model
(
i.
e.,
specific
assessment
of
carpet
cleaners
are
not
available).
The
weight
fraction
is
0.002
(
1.62%
ai
x
2
fl
oz/
128
oz
per
gallon
conc
x
8
lb
per
gallon
density
of
carpet
wash/
water
=
weight
fraction
of
0.002
or
0.2
percent).
EFAST
indicates
a
peak
concentration
of
0.90
mg/
m3.
Because
the
peak
instantaneous
concentration
does
not
represent
a
daily
inhalation
exposure,
the
daily
dose
rather
than
the
peak
estimate
from
EFAST
is
used
to
compare
to
the
short­
term
inhalation
toxicological
endpoint.
If
a
short­
term
toxicological
endpoint
of
less
than
one
day
were
to
be
generated
it
should
be
compared
to
the
peak
air
concentration
estimate.
However,
because
the
toxicological
endpoint
of
concern
is
based
on
greater
than
one
day
of
exposure,
the
daily
dose
rate
of
0.008
mg/
kg/
day
from
EFAST
is
used
in
this
assessment
for
adults
based
on
an
average
daily
air
concentration
of
0.044
mg/
m3.
The
toddler's
dose
is
extrapolated
from
the
adult
value
presented
in
EFAST
and
is
estimated
as
0.038
mg/
kg/
day
for
toddlers
(
i.
e.,
0.008
mg/
kg/
day
x
71.8
kg
adult
BW
x
(
1/
15
kg
toddler
BW)).
The
inhalation
MOE
for
adults
is
not
of
concern
(
i.
e.,
MOE
=
LOAEL
of
26
mg/
kg/
day
/
0.008
mg/
kg/
day
=
3,300,
target
MOE
of
300).
Based
on
the
same
scenario,
the
toddler
inhalation
risk,
scaled
to
the
weight
of
the
toddler
is
not
of
concern
(
i.
e.,
MOE
=
LOAEL
of
26
mg/
kg/
day
/
0.038
mg/
kg/
day
=
680,
target
MOE
of
300).
The
risks
for
the
toddlers
were
scaled
by
body
weight
but
not
breathing
rate.
The
breathing
rate
of
a
toddler
is
lower
than
that
of
an
adult
and
therefore
the
MOEs
would
be
slightly
higher.
Page
41
of
57
Painting:

In
addition
to
the
estimates
provided
above
for
post­
application
inhalation
exposure,
estimates
are
provided
for
post­
application
inhalation
exposure
to
paints
because
of
the
high
vapor
pressure
of
phenol.
The
WPEM
used
in
the
painting
scenario
above
was
also
used
for
the
post­
application
assessment.
The
toddler
post­
application
assessment
from
WPEM
uses
a
body
weight
of
20.3
kg,
a
slight
deviation
from
EPA's
estimate
of
15
kg.
WPEM
estimated
a
peak
instantaneous
concentration
of
5.28
mg/
m3
after
painting
and
a
acute
potential
dose
rate
(
representing
the
highest
24
hour
exposure)
of
1.3
mg/
kg/
day.
Although
the
peak
instantaneous
concentration
is
available,
it
is
not
representative
of
the
short­
term
inhalation
toxicological
endpoint.
WPEM
also
estimates
an
average
daily
dose
with
a
daily
air
concentration
of
0.022
mg/
m3
and
a
dose
of
0.011
mg/
kg/
day
which
corresponds
to
a
MOE
of
2,400
(
i.
e.,
LOAEL
26
mg/
kg/
day
/
0.011
mg/
kg/
day).
The
short­
term
target
MOE
is
300,
and
therefore,
the
risk
is
not
of
concern.
Page
42
of
57
5.0
AGGREGATE
RISK
ASSESSMENTS
AND
RISK
CHARACTERIZATION
In
order
for
a
pesticide
registration
to
continue,
it
must
be
shown
that
the
use
does
not
result
in
"
unreasonable
adverse
effects
on
the
environment".
Section
2
(
bb)
of
FIFRA
defines
this
term
to
include
"
a
human
dietary
risk
from
residues
that
result
from
a
use
of
a
pesticide
in
or
on
any
food
inconsistent
with
standard
under
section
408..."
of
FFDCA.
Consequently,
even
though
no
pesticide
tolerances
have
been
established
for
phenol
and
phenol
salts,
the
standards
of
FQPA
must
still
be
met,
including
"
that
there
is
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
pesticide
chemical
residue,
including
all
anticipated
dietary
exposures
and
other
exposures
for
which
there
are
reliable
information."
Aggregate
exposure
is
the
total
exposure
to
a
single
chemical
(
or
its
residues)
that
may
occur
from
dietary
(
i.
e.,
food
and
drinking
water),
residential,
and
other
nonoccupational
sources,
for
all
known
or
plausible
exposure
routes
(
oral,
dermal,
and
inhalation).

5.1
Acute
and
Chronic
Dietary
Aggregate
Risk
The
acute
and
chronic
aggregate
risk
assessments
generally
include
both
dietary
and
drinking
water
exposures.
Drinking
water
exposure
is
not
expected
from
the
indoor
uses
of
phenol
and
phenol
salts;
thus,
drinking
water
exposure
is
not
assessed
in
this
document.

The
ADTC
determined
that
for
acute
dietary
risk,
there
was
no
appropriate
endpoint
for
assessment
of
acute
dietary
exposure.
As
a
result,
acute
dietary
risk
estimates
were
not
calculated.

Cumulative
chronic
dietary
risk
estimates
from
indirect
food
uses
(
i.
e.,
exposure
to
disinfectant
solutions
and
room
deodorizers)
were
calculated
to
be
36%
for
children,
9.0%
for
adult
females,
and
7.5%
for
adult
males,
indicating
no
risk
of
concern
from
dietary
exposure.

5.2
Short­,
Intermediate­,
and
Long­
Term
Aggregate
Risk
In
accordance
with
the
policy
of
the
Office
of
Pesticide
Programs,
short­,
intermediate­,
and
long­
term
aggregate
risk
typically
includes
dietary
exposures
(
food
and
water)
and
residential
exposures
that
can
be
thought
of
as
occurring
together.
For
homeowner
residential
scenarios,
exposures
are
interpreted
as
only
short­
or
intermediate­
term;
exposures
are
not
felt
to
be
long­
term.

The
study
and
endpoint
defining
toxicity
by
the
oral
and
dermal
routes
was
the
same
as
determined
by
the
ADTC
committee.
Therefore,
dietary,
incidental
oral,
and
dermal
exposure
scenarios
are
aggregated
as
appropriate.
Inhalation
exposures
are
considered
separately
as
there
was
a
route­
specific
study
and
different
toxic
effects
by
this
route
of
exposure.

Based
on
the
above,
for
adults,
chronic
dietary
exposure
is
aggregated
with
the
dermal
exposure
from
one
cleaning
scenario.
(
The
painting
scenario
was
not
chosen
to
aggregate
since
the
dermal
MOEs
for
both
the
airless
sprayer
and
brush/
roller
already
exceed
the
Agency's
level
of
concern
for
handlers
(
i.
e.,
an
individual
who
paints
his/
her
house.)
For
toddlers,
aggregate
exposure
would
involve
dietary
exposure
and
dermal
plus
incidental
oral
exposures
to
treated
carpets.

Inhalation
aggregate
exposures
were
not
considered
necessary,
as
the
exposures
arising
from
adult
activities
(
vapor
from
painting,
cleaning
products,
and
application
of
phenol
products
to
carpet)
and
toddlers
(
exposure
to
vapor
from
paint
and
from
carpet
cleaning
products)
were
felt
not
to
co­
occur.
Page
43
of
57
Thus
individual
Margins
of
Exposure
define
any
risks
of
concern
from
these
exposures.
Individual
Margins
of
Exposure
for
inhalation
exposure
scenarios
for
phenol
which
included
painting
(
roller
or
airless
sprayer)
and
hard
surface
disinfection
(
towelette
and
spray)
were
found
to
be
acceptable
for
these
scenarios
(
6500/
290
for
roller
and
airless
spraying
paint
scenarios;
1500
and
79,000
for
disinfection
towelette
and
spray
respectively).

As
the
study
and
endpoint
selected
for
phenol
describing
effects
from
dermal
and
oral
exposure
was
the
same
for
all
durations
of
exposure,
exposure
scenarios
can
be
aggregated
according
to
the
guidance
set
forth
in
HED
SOP
2000.2,
Risk
Assessment
Guidance.
This
approach
is
similar
to
that
using
the
Total
MOE
method
as
described
in
the
Office
of
Pesticide
Programs'
guidance
"
General
Principles
for
Performing
Aggregate
Exposure
and
Risk
Assessments"
(
USEPA,
2001).

The
results
of
this
approach
are
summarized
in
the
following
table:

Table
5.1
Short­
Term
and/
or
Intermediate­
Term
Aggregate
Oral/
Dermal
Risk
Calculations
(
Oral
and
Dermal
Endpoints
and
NOAELs
are
the
Same)

Population
Short
or
Intermediate­
Term
Scenario
NOAEL
mg/
kg/
day
Target
MOE1
Max
Exposure2
mg/
kg/
day
Average
Food
Exposure
mg/
kg/
day
Residential
Exposure3
mg/
kg/
day
Aggregate
MOE
(
food
and
residential)
4
Adult
Male
60
100
0.6
0.045
0.46
119
Adult
Female
60
100
0.6
0.054
0.46
117
Toddlers
60
100
0.6
0.216
0.0035
273
110x
intraspecies,
10x
interspecies
uncertainty
factors
applied.
2
Maximum
Exposure
(
mg/
kg/
day)
=
NOAEL/
Target
MOE
3
Residential
Exposure
=
Dermal
exposure
from
cleaning
(
adults);
dermal
+
incidental
oral
exposure
from
carpets
(
toddlers)

4
Aggregate
MOE
=
[
NOAEL
÷
(
Avg
Food
Exposure
+
Residential
Exposure)]
Target
MOE
of
100.

As
noted
in
the
above
table,
aggregate
MOEs
are
not
of
concern
for
adults
or
children
based
on
the
scenarios
aggregated.
Page
44
of
57
6.0
Occupational
Exposure
A
detailed
human
exposure
risk
assessment
for
phenol
and
phenol
salts
is
provided
in
the
Appendix.
The
summary
of
the
occupational
exposures
and
risks
are
presented
below.

6.1
Occupational
Handlers
Inhalation
and
dermal
handler
exposures
were
addressed
for
occupational
populations
using
surrogate
data
from
the
Chemical
Manufacturers
Association
(
CMA,
1992)
and
PHED.
Using
surrogate
unit
exposure
data,
application
rates
from
labels,
and
EPA
estimates
of
daily
amount
handled,
exposure
and
risks
to
handlers
and
postapplication
workers
were
assessed.
At
this
time,
EPA
has
not
identified
postapplication
scnearios
for
commercial
uses
that
are
not
addressed
by
the
residential
postapplication
exposure
assessment
(
e.
g.,
the
contacting
treated
surfaces
are
represented
by
children's
incidental
oral
and
dermal
exposures
while
crawling
on
treated
surfaces
such
as
carpets).

The
following
commercial/
institutional
scenarios
have
been
considered
in
this
assessment:

11.
Liquid
pour
of
the
formulated
product
as
a
material
preservative
(
paint),
12.
Use
of
disinfectant
solutions
in
hemodialysis
machines,
13.
Application
of
paint
treated
with
a
material
preservative
using
airless
sprayer,
14.
Application
of
paint
treated
with
a
material
preservative
using
paintbrush/
roller,
15.
Use
of
disinfectant/
deodorizing
spray
on
hard
non­
porous
surfaces,
and
16.
Use
of
disinfectant
towelette
on
hard
non­
porous
surfaces
For
hemodialysis
machines,
the
label
indicates
that
the
product
can
be
used
in
single­
patient
and
multiple­
patient
delivery
systems.
The
use
of
this
product
in
multi­
patient
delivery
systems
was
chosen
for
evaluation
since
it
involves
a
greater
volume
of
product
(
1.0
L
vs.
0.150
mL)
than
the
single­
patient
delivery
system.
It
was
assumed
that
the
machines
are
disinfected
daily
and
on
average,
a
worker
handles
3
machines
per
day.
Page
45
of
57
One
phenol
product
is
listed
for
use
as
an
industrial
additive,
and
lists
paint
as
a
possible
use.
The
label
recommends
that
between
2%­
5%
by
active
ingredients
be
added.
As
a
conservative
measure,
it
is
assumed
that
the
treated
paint
is
comprised
of
5%
active
ingredient,
by
weight.
Assuming
that
paint
has
a
density
of
10
lbs
per
gallon,
the
concentration
of
phenols
in
paint
is
0.5
lbs
a.
i./
gallon.
For
the
material
preservative
use
of
phenol,
primary
handlers
adding
the
product
during
the
manufacturing
of
paint
has
been
selected
to
represent
the
high
end
of
exposure
for
the
primary
handlers.
It
is
assumed
that
paint
is
produced
in
1,000
gallon
batches
(
i.
e.,
10,000
lbs).
In
addition,
painting
has
also
been
selected
to
represent
the
high
end
of
the
exposures
for
the
painters
using
the
preserved
paint.
Two
painting
scenarios
were
considered
in
this
assessment:
use
of
an
airless
sprayer
(
50
gallons
per
day)
and
use
of
a
paintbrush/
roller
(
5
gallons
per
day)
to
paint
the
exterior
and/
or
interior
of
houses.

The
sprays
and
the
solution
used
to
treat
the
towelette
contain
1.62%
phenol/
sodium
phenate.
It
was
assumed
that
the
density
of
this
solution
is
the
same
as
the
density
of
water.
The
label
for
the
towelette
product
did
not
describe
the
quantity
of
product
to
be
used;
rather,
the
directions
state
that
the
towelette
is
to
be
used
to
wipe
the
surface,
and
then
the
surface
should
be
wiped
dry.
In
the
absence
of
more
specific
use
information,
it
was
assumed
that
1
liter
of
the
solution
used
to
wet
the
towelette
is
used
by
the
exposed
individual
per
day.
Similarly,
the
aerosol
spray
directions
state
that
the
product
can
be
sprayed
2­
4
seconds
to
deodorize
a
room,
but
no
data
were
available
describing
the
quantity
of
product
that
is
emitted
by
spraying
for
this
time.
Therefore,
1
liter
of
solution
was
also
assumed
for
use
of
the
aerosol
spray.

The
results
of
the
MOE
analysis
for
these
scenarios
are
presented
in
Table
6.1.
The
estimated
short­
and
intermediate­
term
dermal
MOEs
for
the
following
scenarios
were
below
the
target
MOE
of
100,
and
are
therefore
of
concern:

°
Painting
using
an
airless
sprayer,
with
chemical
resistant
gloves
(
MOE
=
21);
and
°
Wiping
hard
surfaces
using
a
towelette
(
MOE
=
70).

The
estimated
short­
and
intermediate­
term
inhalation
MOEs
for
the
following
scenarios
were
below
the
target
MOE
of
300,
and
are
therefore
of
concern:

°
Painting
using
an
airless
sprayer
(
MOE
=
88).

The
aerosol
inhalation
exposure
and
risk
estimates
from
CMA
and
PHED
discussed
above
do
not
account
for
the
potential
vapor
inhalation
exposure
to
phenol
(
phenol
has
a
relatively
high
vapor
pressure).
Therefore,
the
potential
vapor
inhalation
exposure
to
handlers
are
addressed
by
modeling
of
the
air
concentrations.
Because
the
occupational
handlers
for
the
cleaning
products
use
the
same
weight
fraction
of
phenol
as
the
residential
handlers,
the
same
type
of
application
techniques
(
i.
e.,
wipes,
sprays),
and
will
clean
in
various
rooms
to
accommodate
the
additional
amount
handled
(
e.
g.,
moving
room­
to­
room
in
a
hotel),
the
air
concentrations
and
vapor
inhalation
risk
estimates
will
be
similar
to
those
experienced
by
the
residents
from
the
EFAST
assessment
presented
above.
Based
on
these
assumptions,
the
short­
and
intermediate­
term
vapor­
derived
inhalation
risks
are
not
of
concern
(
i.
e.,
MOEs
greater
than
the
target
MOE
of
300
for
the
average
daily
dose).
For
commercial
painters,
the
WPEM
estimated
a
peak
instantaneous
concentration
of
23
mg/
m3
while
painting.
WPEM
also
estimates
an
average
daily
dose
for
professional
painters
of
0.36
mg/
kg/
day
which
corresponds
to
a
MOE
of
72
(
i.
e.,
LOAEL
26
mg/
0.36
mg/
kg/
day).
This
risk
estimate
is
of
concern
(
ST/
IT
target
MOE
is
300
and
long­
term
target
target
MOE
is
1,000).
Table
6.1.
Calculation
of
Dermal
and
Inhalation
MOE
for
Commercial/
Institutional
Scenariosa
Page
46
of
57
Exposure
Scenario
Method
of
Applicati
on
Dermal
Unit
Exposure
(
mg/
lb
ai)
b
Inhalatio
n
Unit
Exposur
e
(
mg/
lb
ai)
c
Appl.
Rate
d
(
lb
a.
i./
gal)
Amount
Treated
Absorbed
Dermal
Dose
(
mg/
kg/
day
)
f
Dermal
MOE
g
Inhalation
Dose
(
mg/
kg/
day)
h
Inhalatio
n
MOE
i
Material
Preservative
(
Paint)
Liquid
Pour
0.135
(
CMA
gloves)
0.00361
(
CMA)
5%
by
weight
10,000
lbs
of
paint
0.56
110
0.030
870
Hemodialysis
Liquid
Pour
36.5
(
CMA
gloves)
1.89
(
CMA)
0.187
lbs
a.
i./
delivery
system
3
delivery
systems/
d
ay
0.171
350
0.015
1700
Painting
Airless
Sprayer
14
(
PHED
gloves)
0.83
(
PHED)
0.5
50
gal/
day
2.9
21
0.296
88
Paintbrus
h/
Roller
24
(
PHED
gloves)
0.28
(
PHED)
0.5
5
gal/
day
0.50
120
0.010
2600
Hard
Surface
Disinfection
Towelette
2870
(
CMA
no
gloves)
67.3
(
CMA)
0.0357
lbs
a.
i./
liter
used
1
liter
of
product
0.854
70
0.0343
760
Aerosol
Spray
81
(
PHED
gloves)
1.3
(
PHED)
0.0357
lbs
a.
i./
liter
used
1
liter
of
product
0.024
290
0.00066
39,000
a
MOEs
rounded
to
2
significant
figures.
b
Dermal
unit
exposures
are
from
CMA
and
PHED,
gloves
worn
as
indicated.
c
Inhalation
unit
exposures
are
from
CMA
and
PHED.
d
Application
rates
are
based
on
the
phenol
labels.
It
is
assumed
that
both
the
phenol
and
sodium
phenate
present
in
products
are
active
ingredients.
f
Abs.
dermal
dose
(
mg/
kg/
day)
=
[
unit
exposure
(
mg/
lb
ai)
*
Dermal
Absorption
Factor
(
0.5)
*
Appl.
rate
(
lb
ai/
gallon)
*
gallons
handled
/
Body
weight
(
60
kg).
g
MOE
=
NOAEL
(
mg/
kg/
day)
/
Daily
Dose
[
Where
short­
and
intermediate­
term
dermal
NOAEL
=
60
mg/
kg/
day].
Target
MOE
is
100.
h
Inhalation
dose
(
mg/
kg/
day)
=
[
unit
exposure
(

g/
lb
ai)
*
0.001
mg/

g
unit
conversion
*
max
appl
rate
(
lb
ai/
gal)
*
gallons
handled
*
1
inhalation
absorption]
/
Body
weight
(
70
kg).
i
MOE
=
LOAEL
(
mg/
kg/
day)
/
Daily
Dose
[
LOAEL
for
all
durations
=
0.1
mg/
L
(
which
equals
0.1
mg/
L
*
10.26
L/
hr/
kg
*
6
hrs/
day
/
0.236
kg
=
26.08
mg/
kg/
day].
Target
MOE
is
300
for
short­
and
intermediate­
term.
Page
47
of
57
6.2
Occupational
Postapplication
The
potential
short­
and
intermediate­
term
occupational
postapplication
exposures
to
phenol
are
based
on
the
relatively
high
vapor
pressure.
Postapplication
inhalation
exposure
is
expected
for
workers
remaining
in
areas
of
treatment
(
e.
g.,
medical
personnel,
janitors,
etc).
At
this
time,
air
concentration
measurements
taken
after
phenol
treatments
are
not
available.
In
addition,
modeled
results
for
inhalation
exposure
are
not
specific
for
occupational
postapplication
uses.
Therefore,
the
air
concentration
for
the
1.62%
product
in
the
EFAST
model
estimate
listed
in
the
residential
handler
section
above
was
used.
The
average
daily
air
concentration
is
0.352
mg/
m3.
Using
an
8­
hour
workday,
the
dose
is
estimated
to
be
0.050
mg/
kg/
day
(
i.
e.,
0.352
mg/
m3
x
1.25
m3/
hr
breathing
rate
x
8
hr/
day
x
(
1/
70
kg
BW)).
The
short­
and
intermediate­
term
inhalation
MOE
is
520,
and
therefore,
not
of
concern
(
i.
e.,
LOAEL
of
26
mg/
kg/
day
/
0.05
mg/
kg/
day,
target
MOE
=
300).

7.0
ENVIRONMENTAL
FATE
ASSESSMENT
Phenol
is
registered
with
OPP
as
an
active
product
and
is
used
as
an
intermediate
in
the
production
of
epoxy
resins,
the
production
of
various
other
products,
as
a
general
disinfectant
and
in
medicinal
preparations.
For
the
reregistration
eligibility
decision
(
RED)
process
the
Agency
has
relied
on
open
literature
and
fate
properties
of
Phenol
obtained
from
open
literature.
The
following
fate
properties
were
obtained
from
an
open
literature
search.

1.
Vapor
Pressure:
0.341
mm
Hg
2.
Henry
law
Constant
(
air/
water
partition
coefficent):
4.0
x
10­
7
m3/
mole
3.
Log
K
OC
(
organic
carbon
ratio
in
soil):
1.21­
1.96
4.
Log
K
OW
(
octanol/
water
partition
coefficient):
1.46
5.
Absorbs
light
in
the
region
of
290­
330
nm,
may
photodegrade
directly
in
surface
water.
6.
Half­
life
in
freshwater
<
1
day.
7.
Biodegrades
completely
in
soil
within
5
days.
8.
Estimated
half­
life
for
gas­
phase
reaction
of
phenol
with
photochemically
produced
hydroxyl
radicals
is
0.61
days
(
Overall
half­
life
<
1
day).
9.
Log
bioconcentration
factor
(
BCF)
is
0.28
in
goldfish
and
1.3
for
golden
orfe.

Phenol
is
not
expected
to
bioaccumulate
in
plants,
even
though
plants
readily
absorb
phenol,
because
of
the
high
respiratory
decomposition
rate
of
phenol
to
CO
2.
Phenol
does
not
pose
concerns
to
aquatic
organisms
due
to
the
low
BCF
and
the
rapid
biodegradation
in
water.
Page
48
of
57
8.0
ECOTOXICOLOGY
ASSESSMENT
Phenol
and
sodium
phenate
are
used
as
sanitizers,
primarily
for
hard
surfaces
and
as
materials
preservatives.
Outdoor
uses,
such
as
swimming
pool
waters
and
intermittently
flooded
areas,
were
once
registered
uses
for
phenol
and
sodium
phenate,
but
are
apparently
no
longer
supported
by
any
registrants.
The
following
assessment
of
ecological
and
environmental
risk
is
therefore
based
only
on
indoor
uses
for
these
chemicals.

8.1
Terrestrial
Animals
For
indoor
uses,
an
acute
oral
toxicity
study
using
the
technical
grade
of
the
active
ingredient
(
TGAI)
is
required
to
establish
the
toxicity
of
phenol
to
birds.
The
preferred
test
species
is
either
mallard
duck
(
a
waterfowl)
or
northern
bobwhite
quail
(
an
upland
game
bird).
No
avian
acute
toxicity
studies
were
identified
in
the
reviewed
literature
for
phenol
or
its
salts.
Avian
acute
oral
toxicity
testing
(
850.2100/
71­
1)
is
required
to
support
the
currently
registered
uses
of
phenol/
sodium
phenate.

Avian
dietary
toxicity
studies
using
the
TGAI
of
phenol
and
its
salts
are
not
required
for
the
indoor
uses
of
phenol/
sodium
phenate.

8.2
Freshwater
Fish
Freshwater
fish
toxicity
studies
using
the
TGAI
are
required
to
establish
the
toxicity
of
phenol
to
fish.
Data
are
generally
required
for
only
one
species.
Testing
in
two
fish
species
is
required
for
stable
chemicals
with
high
volume
effluents
(
e.
g.,
including,
but
not
limited
to,
egg
washing,
fruit
and
vegetable
rinses,
swimming
pools
or
materials
preservatives)
and
if
the
LC
50
in
the
first
species
is
greater
than
(>)
1
ppm.
The
preferred
test
species
are
rainbow
trout
(
a
coldwater
fish)
and
bluegill
sunfish
(
a
warmwater
fish),
although
other
test
species
identified
in
the
OPPTS
Guideline
(
i.
e.,
OPPTS
850.1075
(
e)(
4)(
i)(
A))
may
also
be
used.
Many
freshwater
fish
acute
toxicity
studies
were
identified
from
peer­
reviewed
literature,
but
no
studies
have
been
submitted
to
support
registration
of
phenol/
sodium
phenate.
Freshwater
fish
acute
toxicity
testing
(
850.1075/
72­
1)
on
one
species
is
required
to
support
the
currently
registered
uses
of
phenol/
sodium
phenate.

The
results
from
freshwater
fish
acute
toxicity
studies
obtained
from
peer­
reviewed
literature
are
summarized
in
the
table
below
(
Table
8.1).

Table
8.1.
Acute
Toxicity
of
Phenol
to
Freshwater
Fish
Organism
Results
­
LC50
(
mg/
L)
(
95%
Confidence
Limit)
Toxicity
Category
Comments
Reference
Rainbow
trout
(
Oncorhynchus
mykiss)
5.02
(
4.23
­
7.49)
moderately
toxic
­
96h
test
duration;
­
juvenile
organisms;
­
renewal
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002b
Rainbow
trout
(
Oncorhynchus
mykiss)
11.6
slightly
toxic
­
96h
test
duration;
­
flow­
through
system
­
used
active
ingredient
concentration
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002b
Organism
Results
­
LC50
(
mg/
L)
(
95%
Confidence
Limit)
Toxicity
Category
Comments
Reference
Page
49
of
57
Rainbow
trout
(
Oncorhynchus
mykiss)
13.1
(
11.9­
14.1)
slightly
toxic
­
48h
test
duration;
­
system
type
not
reported;
­
used
active
ingredient
concentration
Tisler
and
Zagorc­
Koncan,
1995
Rainbow
trout
(
Oncorhynchus
mykiss)
6.1
(
5.5­
6.8)
moderately
toxic
­
96h
test
duration;
­
flow­
through
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Rainbow
trout
(
Oncorhynchus
mykiss)
8.9
moderately
toxic
­
96h
test
duration;
­
flow­
through
system
U.
S.
EPA,
2002b
Rainbow
trout
(
Oncorhynchus
mykiss)
9.7
moderately
toxic
­
96h
test
duration;
­
flow­
through
system;
­
used
active­
ingredient
concentration
Hodson
et
al.,
1984;
U.
S.
EPA,
2002b
Rainbow
trout
(
Oncorhynchus
mykiss)
10.5
(
9.1
­
12.2)
slightly
toxic
­
96h
test
duration;
­
flow­
through
system;
­
used
active­
ingredient
concentration
U.
S.
EPA,
2002b
Rainbow
trout
(
Oncorhynchus
mykiss)
7.7
moderately
toxic
­
96h
duration;
­
flow­
through
system
U.
S.
EPA,
2002b
Rainbow
trout
(
Oncorhynchus
mykiss)
8.9
moderately
toxic
­
96h
duration;
­
flow­
through
system
U.
S.
EPA,
2002b
Bluegill
(
Lepomis
macrochirus)
17.4
(
11.9
­
25.3)
slightly
toxic
­
96h
test
duration;
­
flow­
through
system
­
used
active
ingredient
concentration.
U.
S.
EPA,
2002b
Bluegill
(
Lepomis
macrochirus)
13.5
slightly
toxic
­
96h
test
duration;
­
static
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002
Bluegill
(
Lepomis
macrochirus)
19.3
slightly
toxic
­
96h
test
duration;
­
juvenile
organisms;
­
renewal
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002
Bluegill
(
Lepomis
macrochirus)
11.5
slightly
toxic
­
96h
test
duration;
­
renewal
system;
­
used
active
ingredient
concentration.
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002
Bluegill
(
Lepomis
macrochirus)
23.9
(
20.2
­
31.5)
slightly
toxic
­
96h
test
duration;
­
static
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002
As
shown
in
Table
8.1,
acute
toxicity
for
freshwater
fish
ranged
from
5
mg/
L
(
rainbow
trout)
to
23.9
mg/
L
(
bluegill),
with
average
values
of
9.1
mg/
L
for
rainbow
trout
and
17.1
mg/
L
for
bluegill.
These
data
indicate
that
phenol
is
moderately
toxic
to
coldwater
species,
such
as
the
rainbow
trout,
and
Page
50
of
57
slightly
toxic
to
warmwater
species,
such
as
the
bluegill.

Fish
early
life
stage
testing
is
not
required
for
the
currently
registered
indoor
uses
of
phenol/
sodium
phenate.

8.3
Freshwater
Invertebrates
A
freshwater
aquatic
invertebrate
toxicity
test
using
the
TGAI
is
required
to
establish
the
toxicity
of
a
pesticide
to
aquatic
invertebrates.
The
preferred
test
species
is
Daphnia
magna
or
Daphnia
pulex.
Many
acute
toxicity
studies
were
identified
for
these
species
in
peer­
reviewed
literature,
but
no
studies
have
been
submitted
by
registrants
to
support
the
registered
uses
of
phenol
or
sodium
phenate.
Freshwater
invertebrate
acute
toxicity
testing
(
850.1010/
72­
2)
is
required
for
the
currently
registered
uses
of
phenol/
sodium
phenate.
The
results
of
the
studies
obtained
from
peerreviewed
literature
are
summarized
in
Table
7.2.

Table
8.2.
Acute
Toxicity
of
Phenol
to
Freshwater
Invertebrates
Organism
Results
­
EC50
(
mg/
L)
(
95%
Confidence
Limit)
Toxicity
Category
Comments
Reference
Water
flea
(
Daphnia
magna)
9.6
moderately
toxic
­
48h
test
duration;
­
static
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
7
moderately
toxic
­
50h
test
duration;
­
juvenile
organisms;
­
static
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
88
slightly
toxic
­
48h
test
duration;
­
static
system
EPA
AWQC,
1980;
and
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna
St.)
0.102
(
mmol/
L)
(=
9.6
mg/
L)
moderately
toxic
­
48h
test
duration;
­
renewal
system
Arambasic
et
al.,
1995
Water
flea
(
Daphnia
magna
Strauss)
33.9
(
30
­
39.2)
slightly
toxic
­
24h
test
duration;
­
system
type
not
reported
­
used
active
ingredient
concentration
Tisler
and
Zagorc­
Koncan,
1995
Water
flea
(
Daphnia
magna)
23.5
(
21
­
26.3)
slightly
toxic
­
48h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
6.6
moderately
toxic
­
48h
test
duration;
­
static
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna
Strauss)
4.2
moderately
toxic
­
48h
test
duration;
­
static
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
30
slightly
toxic
­
48h
test
duration;
­
static
system;
U.
S.
EPA,
2002b
Organism
Results
­
EC50
(
mg/
L)
(
95%
Confidence
Limit)
Toxicity
Category
Comments
Reference
Page
51
of
57
Water
flea
(
Daphnia
magna)
12.6
(
10.2
­
15.5)
slightly
toxic
­
48h
test
duration;
­
flow­
through
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
10
(
8.8
­
12)
moderately
to
slightly
toxic
­
48h
test
duration;
­
static
system;
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
15
slightly
toxic
­
48h
test
duration;
­
static
system;
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
5.5
(
4.9
­
6.3)
moderately
toxic
­
48h
test
duration;
­
system
type
not
reported;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
12*
(
7.3
­
20)
slightly
toxic
­
48h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
30.1*
slightly
toxic
­
48h
test
duration;
­
system
type
not
reported
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
32*
(
24
­
43)
slightly
toxic
­
48h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
8.6*
(
7.2
­
10.2)
moderately
toxic
­
48h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
19.8*
(
18
­
22)
slightly
toxic
­
48h
test
duration;
­
static
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
23*
slightly
toxic
­
48h
test
duration;
­
static
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
13*
(
10­
17)
slightly
toxic
­
48h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
11.2*
(
9.8
­
12.6)
slightly
toxic
­
48h
test
duration;
­
static
system;
­
used
active
ingredient
concentration
U.
S.
EPA,
2002b
Water
flea
(
Daphnia
magna)
8.3*
(
5.8
­
12.5)
moderately
toxic
­
48h
test
duration;
­
system
type
not
reported
U.
S.
EPA,
2002b
*
Endpoint
in
study
is
identified
as
LC
50
Page
52
of
57
As
shown
in
Table
8.2,
acute
toxicity
for
aquatic
invertebrates
(
Daphnia
magna)
ranged
from
4.2
mg/
L
to
88
mg/
L.
The
endpoint
for
these
studies
is
the
EC
50
for
immobilization
or
the
LC
50.
The
average
value
for
the
endpoint
concentrations
shown
in
Table
8.2
is
18.8
mg/
L.
Notably,
when
considering
only
the
studies
where
the
endpoint
is
reported
to
be
based
on
the
active
ingredient
concentration
(
Table
8.2),
the
average
concentration
is
relatively
lower
at
14.6
mg/
L.
These
data
results
indicate
that
phenol
is
moderately
to
slightly
toxic
to
aquatic
invertebrates.

8.4
Estuarine
and
Marine
Organisms
Acute
toxicity
testing
with
estuarine
and
marine
organisms
using
the
TGAI
is
not
required
for
the
indoor
uses
of
phenol/
sodium
phenate.
Several
studies
on
marine/
estuarine
invertebrates
were
found
in
the
ECOTOX
database
(
EPA,
2002b).
The
endpoints
from
these
studies
are
summarized
in
the
table
below:

Table
8.3.
Acute
Toxicity
of
Phenol
to
Marine/
Estuarine
Invertebrates
Organism
Results
­
LC50
or
EC
(

g/
L)
(
95%
Confidence
Limit)
Toxicity
Category
Comments
Reference
Mysid
(
Archaeomysis
kokuboi)
96­
hr
LC50
=
260
­
4530
(
formulation)
highly
to
moderately
toxic
­
96h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Opossum
shrimp
(
Americamysis
bahia)
96­
h
LC50
=
12,500
(
10,700
­
15,600)
(
formulation)
slightly
toxic
­
96h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Daggerblade
grass
shrimp
(
Palaemonetes
pugio)
96­
hr
LC50
=
5,800
(
4330
­
7,770)
moderately
toxic
­
96h
test
duration;
­
static
system
U.
S.
EPA,
2002b
Table
8.4.
Chronic
Toxicity
of
Phenol
to
Marine/
Estuarine
Invertebrates
Organism
Results
­
LOEC,
NOEC,
MATC
(

g/
L)
Comments
Reference
Opossum
shrimp
(
Americamysis
bahia)
mortality
27­
d
NOEC=
2,410
LOEC
=
6,880
MATC
=
4,080
­
27
day
test
duration;
­
flow­
through
system
U.
S.
EPA,
2002b
8.5
Plants
Terrestrial
and
aquatic
plant
testing
is
not
required
for
the
registered
indoor
uses
of
phenol/
sodium
phenate.
There
were
aquatic
phytotoxicity
endpoints
reported
in
the
ECOTOX
database
Page
53
of
57
(
EPA,
2002).
While
these
data
were
reported
in
summary
form,
they
indicate
that
phenol
demonstrates
low
toxicity
to
various
aquatic
plant
species,
with
4­
day
EC
50
values
ranging
from
12,000
ppb
(
duckweed,
Lemna
minor)
to
370,000
ppb
(
green
alga,
Chlorella
vulgaris).
9.0
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