Document ID: EPA-HQ-OPP-2004-0301-0011
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2004-09-10T04:00Z

Page
1
of
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Phenol/
Sodium
Phenate
Summary
September
15,
2004
USES
Phenol
is
registered
for
use
as
a
sanitizer,
bacteriostat,
fungicide/
fungistat,
Tuberculocide,
disinfectant,
and
Virucide.
Further,
phenol
has
a
number
of
use
sites
including
indoor
food
uses
in
eating
establishments
on
equipment
and
utensils,
non­
food
indoor
uses
in
commercialtransportation
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
(
semicritical
items),
bedpans
and
furniture
(
noncritical
items),
non­
conductive
floors,
critical
premises
(
burn
wards),
noncritical
premises,
and
institutional
premises
(
human,
veterinary).

FORMULATIONS
Phenol/
Sodium
Phenate
is
formulated
as
a
pressurized
liquid
(
aerosol
spray),
as
a
liquid
concentrate,
as
a
ready­
to­
use
liquid,
and
as
an
impregnated
towelette.

HEALTH
EFFECTS
Phenol/
Sodium
Phenate
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.

Phenol/
Sodium
Phenate
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
and
280
mg/
kg/
day
in
both
rat
and
mouse
studies.
Additionally,
female
mice
experienced
increased
mortality
and
clinical
signs
of
central
nervous
system
toxicity
(
tremors,
ataxia,
lethargy)
at
the
high­
dose
(
280
mg/
kg/
day).
In
a
non­
guideline
developmental
study
(
Kavlock,
1990),
there
were
decreases
in
rat
maternal
body
weight
gain
in
maternal
and
offspring.
Page
2
of
5
In
a
2­
generational
reproductive
study
in
rats
exposed
to
200,
1000,
or
5000
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
5000.
This
occurred
concurrently
with
maternal
toxicity
(
decreased
maternal
body
weight);
believed
to
be
secondary
to
the
animals'
aversion
to
the
flavor
of
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
sand
the
LOAEL
was
not
established
(
highest
dose
tested,
350
mg/
kg).

Two
carcinogenicity
studies
performed
by
the
National
Cancer
Institute
did
not
exhibit
an
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
5000
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.

RISKS
Food
Risk
­
the
Antimicrobials
Division
Toxicity
Endpoint
(
ADTC)
committee
determined
that
for
acute
dietary
risk,
there
was
no
appropriate
endpoint
for
assessment
of
acute
dietary
exposure.
AS
a
result
acute
dietary
estimates
were
not
calculated.

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
product
may
come
in
contact
with
food,
which
in
turn
may
be
digested.
An
acute
RfD/
PAD
value
was
not
selected,
thus
acute
dietary
risk
was
not
evaluated.
For
chronic
dietary
exposure,
children
have
highest
percent
of
chronic
PAD,
at
36%.
For
adult
males
and
females,
te
dietary
exposure
is
9%,
and
7.5%
respectively,
which
is
below
the
Agency's
level
of
concern
(
100%
of
the
PAD).

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
3
of
5
biodegradation
of
phenol
is
sufficiently
rapid
so
that
the
probability
of
ground
water
contamination
will
be
low.
Because
phenol
absorbs
light
in
the
region
of
290­
330
nm,
phenol
might
photo­
degradate
directly
in
surface
water.
Phenol
is
not
expected
to
absorb
to
sediment
in
the
water
column.

Acute/
Chronic
Risk:
The
acute
and
chronic
aggregate
risk
assessments
generally
include
both
dietary
and
drinking
water
exposure.
Drinking
water
exposure
is
not
expected
from
the
use
of
phenol
and
phenol
salt.

Dietary
exposure
was
aggregated
with
dermal
and
incidental
exposures
from
use
of
phenol
cleaning
products
on
carpet.
The
aggregate
margin
of
Exposure
(
MOE)
was
found
to
be
acceptable
(
aggregate
MOE
of
273,
acceptable
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
only;
exposures
are
not
felt
to
be
long­
term.
Based
on
the
above,
for
adults,
chronic
dietary
exposure
is
aggregated
with
the
dermal
exposure
from
cleaning
scenario.
(
The
painting
scenario
was
not
chosen
to
aggregate
since
dermal
MOEs
for
both
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
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
preservative
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
paint
brush/
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
therefore
are
of
concern:
1)
painting
using
airless
sprayer
(
MOE
=
21),
and
2)
wiping
hard
surfaces
using
a
towelette
(
MOE
=
70)

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

Environmental
Risk:
Based
on
the
low
likelihood
of
environmental
exposure
from
registered
indoor
uses,
coupled
with
phenol's
rapid
degradation
in
air,
water
and
soil,
as
well
as
low
toxicity
of
phenol
to
fish,
aquatic
invertebrates,
phenol
and
salt
are
not
of
environmental
Page
4
of
5
concern
at
this
time.

Ecological
Risk:
No
submitted
ecological
hazard
data
were
available
to
perform
a
risk
assessment
for
phenol
or
sodium
phenate;
instead,
data
from
published
literature
were
sued
where
available.

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
and
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
sodium
phenate
are
not
required
for
the
indoor
uses
of
phenol/
sodium
phenate.

Freshwater
Fish
­
Freshwater
fish
toxicity
studies
using
the
TGAI
to
establish
the
toxicity
of
phenol
to
fish.
Data
generally
are
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
OPPTS
Guideline
(
i.
e.,
850.1075
(
e)(
4)(
i)(
A))
also
may
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.

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
the
phenol
is
moderately
toxic
to
coldwater
species,
such
as
the
rainbow
trout,
and
slightly
toxic
to
warmwater
species,
such
as
the
bluegill.

Incidence
Report
Assessment:
A
total
of
10
individual
incidence
cases
submitted
to
the
EPA
Office
of
Pesticide
Programs
are
associated
with
exposure
to
phenol
and
/
or
sodium
phenate
containing
products.
Dermal
and
inhalation
ate
the
two
primary
route
of
exposure.

The
most
common
symptoms
reported
for
cases
of
dermal
exposure
were
skin
irritation/
burning,
rash,
itching,
skin
discoloration/
redness.

The
most
common
symptoms
reported
for
cases
of
inhalation
exposure
were
respiratory
irritation/
burning,
asthma/
difficult
breathing,
throat/
chest
congestion
and
sore
throat.
Headache
drowsiness,
night
sweats
and
heart
palpitation
have
also
been
reported
when
exposed
to
the
chemical
through
both
dermal
and
inhalation
exposure
routes.
Page
5
of
5
HOW
THE
RISK
PICTURE
MAY
CHANGE
Changes
and
refinements
to
the
risk
assessment
may
occur
after
consideration
of
the
public
comments.