EPA
Registration
Division
contact:
Mr.
Sidney
Jackson,
703­
305­
7610
Interregional
Research
Project
Number
4
(
IR­
4)

PP#
3E6762
and
5E6992
Summary
of
Petitions
EPA
has
received
pesticide
petitions
(
PP#
3E6762
and
5E6992)
from
IR­
4,
Center
for
Minor
Crop
Pest
Management,
681
U.
S.
Hgwy.
#
1
South,
North
Brunswick,
NJ
08902­
3390
proposing,
pursuant
to
section
408(
d)
of
the
Federal
Food,
Drug,
and
Cosmetic
Act
(
FFDCA),
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
part
180.572
by
establishing
a
tolerance
for
residues
of
bifenazate
(
1­
methylethyl
2­(
4­
methoxy[
1,1'­
biphenyl]­
3­
yl)
hydrazinecarboxylate)
and
diazinecarboxylic
acid,
2­(
4­
methoxy­[
1,1'­
biphenyl]­
3­
yl),
1­
methylethyl
ester
(
expressed
as
bifenazate)
in
or
on
the
raw
agricultural
commodities
pea,
garden
at
0.2
ppm
(
PP#
5E6992),
pea,
edible
podded
at
4.0
ppm
(
PP#
5E6992),
Vegetable,
tuberous
and
corm,
subgroup
1C
at
0.01
ppm
(
PP#
5E6992),
and
Fruit,
stone,
group
12
at
2.0
ppm
(
PP#
3E6762).
Additionally,
IR­
4
requests
that
the
existing
tolerances
for
peach
and
nectarine,
both
set
at
1.7
ppm
be
deleted
since
they
are
included
in
the
fruit,
stone,
group
12
tolerance
of
2.0
ppm.

EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408(
d)(
2)
of
the
FFDCA;
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
supports
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

A.
Residue
Chemistry
1.
Plant
metabolism.
The
nature
of
the
residues
of
bifenazate
in
plants
is
adequately
understood.
The
major
residue
in
all
plant
metabolism
studies
is
bifenazate.
A
minor,
but
significant
metabolite
is
the
diazene
D3598,
which
was
found
to
interconvert
readily
to/
from
bifenazate
in
the
plant
matrix
during
the
analytical
procedure.

2.
Analytical
method.
Crompton
has
developed
practical
analytical
methodology
for
detecting
and
measuring
residues
of
bifenazate
in
or
on
raw
agricultural
commodities.
As
D3598,
a
significant
metabolite,
was
found
to
interconvert
readily
to/
from
bifenazate,
the
analytical
method
was
designed
to
convert
all
residues
of
D3598
to
the
parent
compound
(
bifenazate)
for
analysis.
The
method
utilizes
reversed
phase
HPLC
to
separate
the
bifenazate
from
matrix
derived
interferences,
and
oxidative
coulometric
electrochemical
detection
for
the
identification
and
quantification
of
this
analyte.
Using
this
method
the
limit
of
quantitation
(
LOQ)
for
bifenazate
in
stone
fruit,
pome
fruit,
grapes,
strawberries,
and
cotton
was
0.01
ppm.
For
hops
the
LOQ
was
0.05
ppm.
The
limit
of
detection
for
this
method,
which
varies
with
matrix,
is
0.005
ppm.
The
analytical
method
for
bifenazate
and
its
major
metabolite
D3598
in
animal
samples
was
2
designed
using
the
same
principles
invoked
in
the
plant
method,
with
minor
modifications.
However,
in
animal
samples,
a
separate
aliquot
of
the
extract
was
used
to
determine
residues
of
A1530
and
its
sulfate
(
combined)
in
milk
and
meat
samples
(
these
metabolites
appeared
to
be
significant
in
goat
metabolism
studies).
The
extract
was
subjected
to
acid
hydrolysis
to
convert
the
sulfate
conjugate
to
A1530
before
it
was
quantified
by
HPLC
using
fluorescence
or
OCED
detectors.

3.
Magnitude
of
residues.
A
complete
crop
residue
program
has
been
completed
for
bifenezate
in
the
major
growing
areas
of
the
US
for:

Peas:
°
Crompton
is
proposing
crop­
specific
tolerances
of
4
ppm
on
edible
podded
peas
and
0.2
ppm
on
succulent
shelled
peas
(
pigeon
pea,
pea).
Note:
These
are
crop­
specific
tolerances
for
peas
only
and
not
crop
group
tolerances,
which
would
include
bean
crops.

Tuberous
and
corm
vegetables:
°
Crompton
is
proposing
a
tolerance
of
0.01
ppm
on
tuberous
and
corm
vegetables,
based
on
field
trial
studies
in
which
no
quantifiable
residues
were
found
at
a
limit
of
quantitation
of
0.01
ppm.

Stone
fruit:
°
Crompton
is
proposing
a
crop
group
tolerance
for
stone
fruit
of
2
ppm.
Plums
and
prune
(
fresh)
will
not
be
included
in
this
crop
group
tolerance
because
a
tolerance
of
0.3
ppm
already
exists.
In
addition,
current
crop­
specific
tolerances
for
nectarines
and
peaches
are
1.7
ppm.
The
proposed
crop
group
tolerance
means
that
the
tolerances
for
nectarines
and
peaches
will
increase
to
2
ppm.

B.
Toxicological
Profile
1.
Acute
toxicity.
Bifenazate
Technical,
Acramite­
50WS
have
low
acute
oral,
dermal,
and
inhalation
toxicity
in
laboratory
animals.
The
oral
LD
50
in
rats
and
mice
is
greater
than
5
g/
kg
for
Acramite
50WS
and
the
technical
material.
The
dermal
LD
50
in
rats
of
Bifenazate
Technical
and
both
formulations
is
greater
than
5
g/
kg.
The
inhalation
LC
50
in
the
rats
of
Bifenazate
Technical
and
Acramite
50WS
was
found
to
be
greater
than
4.4,
5.2
and
1.8
mg/
l,
respectively.
In
eye
irritation
studies,
Acramite­
50WS
was
a
slight
irritant,
and
Bifenazate
Technical
was
nonirritating
The
product
was
found
to
be
non­
irritating
to
the
skin
of
rabbits
and
non­
sensitizing
on
the
skin
of
guinea
pigs.

2.
Genotoxicity.
Bifenazate
was
evaluated
and
found
to
be
negative
in
the
Ames
Reverse
Mutation,
Mouse
Lymphoma,
CHO
Chromosome
Aberration
and
Mouse
Micronucleus
assays.
3
3.
Reproductive
and
developmental
toxicity.
Rabbit
Teratology
Study:
A
range­
finding
study
conducted
in
pregnant
New
Zealand
White
rabbits
at
dosage
levels
of
125,
250,
500,
750
and
1,000
mg/
kg/
day
demonstrated
maternal
toxicity
at
dosage
levels
of
500
mg/
kg/
day
and
greater
and
abortions
at
dosage
levels
of
250
mg/
kg/
day
and
greater.
Bifenazate
was
then
administered
by
oral
gavage
to
pregnant
New
Zealand
White
rabbits
at
dosage
levels
of
10,
50
and
200
mg/
kg/
day.
No
test
article
related
effets
were
seen
at
any
dose
level.
The
NOAEL
for
maternal
and
developmental
toxicity
was
greater
than
200
mg/
kg/
day.

Rat
Teratology
Study:
Bifenazate
did
not
produce
developmental
toxicity
when
administered
by
oral
gavage
to
pregnant
Sprague­
Dawley
CD
rats
at
dosage
levels
of
10,
100
and
500
mg/
kg/
day.
A
reduction
in
maternal
body
weight
gain
was
seen
at
dosage
levels
of
100
and
500
mg/
kg/
day.
Clinical
observations
at
500
mg/
kg/
day
included
red
material/
staining
on
body
surfaces,
pale
extremities
and
brown
discharge.
No
developmental
or
teratogenic
effects
were
observed
at
any
dosage
level.
The
NOAEL
for
maternal
toxicity
was
10
mg/
kg/
day
and
the
NOAEL
for
developmental
toxicity
was
greater
than
500
mg/
kg/
day.

Rat
Reproduction
Study:
Bifenazate
showed
no
effects
on
reproduction
when
fed
to
two
generations
of
male
and
female
Sprague­
Dawley
CD
rats
at
dietary
concentrations
of
20,
80
and
200
ppm.
At
a
dosage
level
of
200
ppm
there
was
a
reduction
in
body
weight
gain
in
F0
males
and
females.
Food
consumption
was
unaffected.
There
was
a
reduction
in
body
weight
gain
in
F1
females
at
all
dosage
levels
and
in
F1
males
at
80
and
200
ppm
in
the
absence
of
effects
on
food
consumption.
Since
the
20
ppm
F1
males
did
not
have
a
significant
reduction
in
body
weight
gain,
this
dosage
level
can
be
considered
a
NOEL
for
systemic
adult
toxicity.
The
reduction
in
body
weight
gain
in
the
F1
females
at
20
ppm
would
not
be
considered
biologically
significant
because
no
effects
were
observed
on
reproductive
parameters
or
in
the
F2
litter.
The
reproductive
and
developmental
NOEL
was
greater
than
200
ppm
(
10
mg/
kg/
day).

4.
Subchronic
toxicity.
Thirteen
Week
Rat
Feeding
Study:
Bifenazate
was
fed
to
male
and
female
Sprague
Dawley
CD
rats
for
thirteen
weeks
at
dietary
concentrations
of
40,
200
and
400
ppm.
At
dosage
levels
of
200
and
400
ppm
there
was
a
reduction
in
red
blood
cell
count
and
hemoglobin.
Food
intake
was
reduced
for
200
ppm
females
and
200
and
400
ppm
males.
Histopathological
effects
were
seen
in
the
liver,
spleen
and
adrenal
cortex
in
males
and
females
at
200
and/
or
400
pm.
The
maximum
tolerated
dose
(
MTD)
was
exceeded
in
females
at
200
ppm
and
in
males
and
females
at
400
ppm.
The
NOAEL
for
subchronic
toxicity
in
rats
was
40
ppm
(
2
mg/
kg/
day).

Neurotoxicity
assessment:
No
treatment
related
effects
were
seen
on
neurobehavior
in
a
standard
Functional
Observation
Battery
conducted
at
weeks
8
and
13
of
the
thirteen­
week
rat
feeding
study.
No
overt
signs
of
anti­
cholinergic
activity,
and
no
statistically
significant
effects
on
cholinesterase
activity
were
seen
in
rats
in
a
two
week
feeding
study
at
dose
levels
up
to
400
ppm.
Plasma,
erythrocyte
and
brain
cholinesterase
activity
were
evaluated
in
male
and
female
rats
fed
bifenazate­
treated
diet
at
0,
20,
200,
or
400
ppm
for
two
weeks.
All
animals
survived
until
study
4
termination
and
effects
were
only
seen
on
body
weight
gain
and
food
consumption.
The
NOAEL
for
cholinergic
inhibition
was
greater
than
400
ppm
(
20
mg/
kg/
day).

Thirteen
Week
Dog
Feeding
Study:
Bifenazate
was
fed
to
male
and
female
Beagle
dogs
for
thirteen
weeks
at
dietary
concentrations
of
40,
400
and
1,000
ppm.
At
dosage
levels
of
400
and
1,000
ppm
there
was
a
reduction
in
red
blood
cell
count,
hemoglobin
and
hematocrit.
Liver
weights
were
increased
at
400
and
1,000
ppm
and
centrilobular
hepatocellular
hypertrophy
was
seen
in
females
at
400
ppm
and
males
and
females
at
1,000
ppm.
The
NOAEL
for
subchronic
toxicity
in
dogs
was
40
ppm
(
1
mg/
kg/
day).

5.
Chronic
toxicity.
Dog
Chronic
Feeding
Study:
Bifenazate
was
fed
to
male
and
female
Beagle
dogs
for
one
year
at
dietary
concentrations
of
40,
400
and
1,000
ppm.
At
dose
levels
of
400
and
1,000
ppm,
there
was
a
reduction
in
food
consumption
in
males
and
reduced
body
weight
gain
in
males
and
females.
There
was
a
reduction
in
red
blood
cell
count,
hemoglobin
and
hematocrit
and
an
increase
in
bilirubin
at
400
and
1,000
ppm.
Histopathological
effects
on
bone
marrow,
kidney
and
liver
were
also
seen
at
these
dose
levels.
The
NOAEL
for
chronic
toxicity
in
dogs
was
40
ppm
(
1
mg/
kg/
day).

Rat
Chronic
Feeding/
Oncogenicity
Study:
Bifenazate
was
not
oncogenic
in
rats
when
fed
to
male
and
female
Sprague­
Dawley
CD
rats
for
two
years
at
dietary
concentrations
of
20,
80
and
160
in
females
or
20,
80
and
200
ppm
in
males.
Body
weight
gain
was
reduced
in
males
and
females
at
the
high
dosage
levels.
A
reduction
in
red
blood
cell
count
and
an
increase
in
splenic
pigment
were
seen
in
females
at
160
ppm,
while
high
dose
males
exhibited
a
reduction
in
total
cholesterol
and
an
increase
in
splenic
pigment.
At
a
dose
level
of
80
ppm
there
was
a
reduction
in
body
weight
gain,
a
decrease
in
red
blood
cell
count
and
an
increase
in
splenic
pigment
in
females.
There
was
no
increase
in
tumor
incidence
in
males
or
females
as
a
result
of
bifenazate
administration.
The
NOAEL
for
chronic
toxicity
in
rats
was
20
ppm
(
1
mg/
kg/
day).

Mouse
Oncogenicity
Study:
Bifenazate
was
not
oncogenic
when
fed
to
male
and
female
CD­
1
mice
for
eighteen
months
at
dietary
concentrations
of
10,
100
and
175
ppm
in
females
and
10,
100
and
225
ppm
in
males.
Body
weight
gain
was
reduced
in
males
and
females
at
the
high
dose
level.
A
reduction
in
red
blood
cell,
total
leukocyte
and
lymphocyte
counts
was
seen
in
males
at
225
ppm.
There
was
no
increase
in
tumor
incidence
in
males
or
females
as
a
result
of
bifenazate
administration.

6.
Animal
metabolism.
In
rat,
[
14C]­
bifenazate,
[
14C­
Phenyl]
Hydrazine
carboxylic
acid,
2­(
4­
methoxy­[
1,1?­
biphenyl]­
3­
yl)­
1­
methylethyl
ester
was
extensively
metabolized
when
it
was
given
orally
in
two
dose
levels
low
(
10
mg/
kg),
and
high
(
1000
mg/
kg).
Although
2/
3
of
the
dosed
radioactivity
was
excreted
in
the
feces,
bifenazate
depicted
a
good
degree
of
absorption
as
indicated
from
the
level
of
radioactivity
in
the
bile.
In
the
bile
radioactivity
study,
about
70%
of
the
C­
14
was
collected
from
the
cannulated
bile
ducts
of
low
dosed
rats
indicating
an
active
level
5
of
absorption
and
enterohepatic
circulation.

In
general,
the
major
metabolites
present
in
feces,
urine
and
bile
resulted
from
several
well
known
metabolic
reactions,
including
hydrazine
oxidation
to
diazene
(
D3598),
molecular
scission
with
loss
of
the
hydrazine
carboxylic
acid
portion
of
the
molecule
to
yield
4­
methoxybiphenyl
(
D1989)
followed
by
demethylation
to
form
4­
hydroxybiphenyl
(
A1530).
Metabolites
resulted
from
aromatic
hydroxylation,
and
conjugation
with
glucuronic
acid
or
sulfate
were
also
identified.

Pharmacokinetic
parameters:
The
maximum
plasma
concentration
(
C
max
,
calculated
as
ppm
D2341
equivalents)
was
reached
much
earlier
following
the
low
dose
(
5­
6
h)
than
the
high
dose
(
18­
24
h).
Elimination
half­
lives
(
t
1/
2
)
were
marginally
longer
at
the
high
dose
(
12­
16
h)
than
at
the
low
dose
(
12­
13
h).
There
were
no
obvious
and
consistent
sex
differences
in
the
pharmacokinetic
parameters.

7.
Metabolite
toxicology.
In
a
single
dose
oral
toxicity
limit
test
in
rats,
the
oral
LD
50
of
the
diazene
product
of
bifenazate
was
estimated
to
be
approximately
5,000
mg/
kg.
At
two
hours
and
at
seven
days
post­
dosing,
no
effects
were
seen
on
erythrocyte
cholinesterase
inhibition
in
male
or
female
rats.
In
addition,
no
effect
on
plasma
cholinesterase
inhibition
was
seen
in
male
rats
at
seven
days
only.
Since
this
effect
was
seen
only
in
plasma
of
females
at
one
time
point,
it
is
most
likely
a
pseudocholinesterase
effect
without
biological
significance.
In
a
dermal
toxicity
screen,
the
LD
50
of
the
diazene
was
estimated
to
be
>
2,000
mg/
kg.

Mutagenicity
screens
with
the
diazene
showed
it
to
be
weakly
positive
in
the
Salmonella
plate
incorporation
(
Ames)
assay
in
TA98
with
activation
and
negative
in
the
L5178Y
mouse
lymphoma
and
mouse
micronucleus
assays.

8.
Endocrine
disruption.
There
are
no
known
reported
adverse
reproductive
or
developmental
effects
in
domestic
animals
or
wildlife
as
a
result
of
exposure
to
this
chemical.

A
standard
battery
of
required
toxicity
tests
have
been
conducted
on
bifenazate.
No
effects
were
seen
in
the
reproduction
or
teratology
studies
to
indicate
that
bifenazate
has
an
effect
on
the
endocrine
system.
Bifenazate
administration
to
rats
for
90
days
at
dose
levels
of
200
and
400
ppm
resulted
in
an
increased
incidence
of
vacuolation
in
the
zona
fasciculate
of
the
adrenal
cortex
in
male
rats.
No
effect
was
seen
at
a
dose
level
of
40
ppm
(
2
mg/
kg/
day).
However,
in
the
chronic
rat
feeding
study,
no
effect
was
seen
on
the
adrenal
cortex
in
male
rats
fed
200
ppm
for
one
year.
Furthermore,
fasting
glucose
levels
were
not
reduced
at
any
dose
level
in
males
or
females
in
either
study.
The
zona
fasciculate
is
the
site
of
cortisol
production
and
cortisol
is
required
for
gluconogenesis
during
fasting.
The
finding
that
fasting
glucose
levels
are
not
affected
would
suggest
that
adrenal
cortex
functionality
is
not
impaired
at
any
dose
level
by
bifenazate.

9.
Toxicology
Endpoints
(
special
sensitivities).
The
following
are
the
toxicology
endpoints
for
6
the
exposure
assessments:

a)
Acute
Endpoint.
An
acute
reference
dose
for
dietary
exposure
was
not
established,
as
there
were
no
effects
observed
in
any
oral
toxicity
studies
that
were
attributable
to
a
single
dose.

b)
Short­
Term
Endpoint.
The
endpoint
for
acute
dermal
exposure
is
based
on
the
NOEL
of
80
mg/
kg/
day
from
the
21­
day
dermal
toxicity
study
in
rats.
Use
of
a
100­
fold
safety
factor,
a
margin
of
exposure
(
MOE)
of
100,
is
appropriate
and
acceptable.

c)
Intermediate
Endpoint.
An
intermediate
exposure
endpoint
is
not
required.
Residential
exposure
from
the
landscape
use
is
expected
to
be
very
limited,
and
bifenazate
is
not
used
on
turf.

d)
Chronic
Endpoint.
The
endpoint
for
chronic
exposure
is
based
upon
the
NOEL
of
1
mg/
kg/
day
which
was
obtained
in
the
chronic
rat
and
dog
feeding
studies.
The
RfD
for
chronic
effects
is
0.01
mg/
kg/
day
using
a
100­
fold
safety
factor.

The
need
for
an
additional
safety
factor
for
infants
and
children
was
evaluated.
Bifenazate
was
not
carcinogenic
in
rodents
and
did
not
produce
reproductive
effects
in
rats
or
developmental
toxicity
in
rats
and
rabbits.
These
data
indicate
that
children
would
not
be
more
sensitive
to
dietary
bifenazate
than
the
general
population,
therefore,
a
chronic
RfD
of
0.01
mg/
kg/
day,
which
is
sufficient
to
protect
the
general
population,
would
provide
adequate
protection
to
infants
and
children.
Therefore,
the
application
of
an
additional
10X
safety
factor
is
not
necessary.

Due
to
the
general
inaccessibility
of
agricultural
use
sites
to
children
and
given
the
low
mammalian
dermal
and
inhalation
toxicity
of
Acramite­
50WS,
both
exposure
and
risk
to
children
will
be
insignificant.

C.
Aggregate
Exposure
1.
Dietary
exposure.
Based
on
dietary,
drinking
water,
and
non­
occupational
exposure
assessments,
there
is
reasonable
certainty
of
no
harm
to
the
US
population,
any
population
subgroup,
or
infants
and
children
from
chronic
exposure
to
bifenazate.

i.
Food.
Chronic
dietary
exposures
were
estimated
utilizing
the
Dietary
Exposure
Evaluation
Model
software
with
Food
Commodity
Intake
Database
(
DEEM­
FCID),
version
2.00.
Default
processing
factors
from
DEEM
7.73
were
used
for
all
crops
to
estimate
residues
in
foods
consumed
by
humans
in
accordance
with
standard
EPA
practice
when
processing
studies
are
not
7
available.
One
hundred
percent
crop
treated
is
assumed
for
all
crops,
with
the
exception
of
soybeans,
for
which
1.5%
crop
treated
was
used.

Using
existing
%
cPAD
for
existing
tolerances
from
68
FR
55494­
5503
(
9/
26/
03)
for
the
chronic
dietary
exposure
to
the
US
Population
(
total)
was
estimated
was
25.7%
of
the
cPAD
(
0.00257
mg/
kg/
day).
The
most
highly
exposed
subpopulation,
children
aged
1­
2,
has
an
estimated
total
bifenazate
exposure
equal
to
91.2%
of
the
cPAD.
The
total
chronic
dietary
exposure
associated
with
current
and
proposed
uses
of
bifenazate
has
been
demonstrated
to
be
less
than
the
cPAD
(
0.01
mg/
kg/
d)
and
are
therefore
not
of
concern.
It
is
important
to
remember
that
this
assessment
is
quite
conservative
because
it
includes
tolerance
level
residues
in
all
current
and
proposed
crops
(
with
the
exception
of
tomatoes,
for
which
EPA
used
average
residues
from
field
trials)
and
the
assumption
of
100%
crop
treated
for
all
crops
except
soybeans.
Actual
exposures
are
likely
to
be
considerably
less
than
those
estimated
here.

ii.
Drinking
water.
Exposure
to
bifenazate
and
potential
residues
in
drinking
water
is
expected
to
be
neglible.
Bifenazate
(
half­
life
of
30
minutes)
degrades
rapidly
under
aerobic
conditions
to
D3598
(
half­
life
of
7
hours),
which
degrades
rapidly
to
D1989
(
half­
life
of
96
days).
Photodegradation
and
other
routes
of
dissipation
of
bifenazate
do
not
appear
to
be
significant.
Based
on
these
data,
the
residue
of
concern
was
considered
to
be
D1989.
Parent
and
D3598
were
not
included
as
residues
of
concern
in
drinking
later
due
to
the
short
half­
lives
of
these
compounds
and
the
lack
of
an
acute
dietary
endpoint.
Chronic
estimated
environmental
concentrations
(
EECs)
of
D1989
in
surface
and
ground
water
were
generated
using
FIRST
and
SCI­
GROW
(
1
application
at
0.75
lbs
ai/
acre).
The
FIRST
model
generated
an
EEC
of
6.4
ppb
and
SCI­
GROW
model
generated
an
EEC
of
<
0.001
ppb.
These
EEC
values
are
lower
than
the
drinking
water
levels
of
concern
(
DWLOC)
for
adults
(
260
ppb)
and
infants
1­
2
years
of
age
(
8.8
ppb).
The
EEC
values
discussed
were
those
reported
in
the
9­
26­
2003
Federal
Register.
Uses
on
proposed
crops
were
assumed
not
to
impact
the
EEC
estimates.

2.
Non­
dietary
exposure.
Food
uses
described
in
this
petition
are
strictly
agricultural,
and
will
not
add
to
any
residential
non­
dietary
exposure
that
may
exist.

D.
Cumulative
Effects
The
mechanism/
mode
of
action
of
bifenazate
on
the
mammalian
red
blood
cell,
which
is
target
organ
in
the
species
tested,
remains
to
be
elucidated.
The
lack
of
information
on
bifenazate
mode
of
action
precludes
an
assessment
of
cumulative
effects.
EPA
has
not
made
a
common
mechanism
of
toxicity
finding
as
to
bifenazate
and
any
other
substances
and
bifenazate
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.

E.
Safety
Determination
8
1.
U.
S.
population.
Based
on
the
toxicology
database
and
available
information
on
anticipated
residues,
chronic
dietary
exposure
to
the
U.
S.
population
(
total)
was
25.7%
of
the
cPAD.
The
FIRST
model
generated
an
EEC
of
6.4
ppb
and
SCI­
GROW
model
generated
an
EEC
of
<
0.001
ppb.
These
EEC
values
are
lower
than
the
drinking
water
levels
of
concern
(
DWLOC)
for
adults
(
260
ppb).
The
combined
MOE
from
the
limited
potential
for
short­
term
exposure
from
residential
uses
is
>
1000.
Based
on
these
assessments,
it
can
be
concluded
that
there
is
reasonable
certainty
of
no
harm
to
the
U.
S.
Population
or
any
population
subgroup
from
exposure
to
bifenazate.

2.
Infants
and
children.
Based
on
the
toxicology
database
and
available
information
on
anticipated
residues,
chronic
dietary
exposure
to
infants
(
under
1
year
of
age
was
67.3%
of
the
cPAD
and
to
children
(
1­
2
years
of
age)
was
91.2%
of
the
cPAD.
The
FIRST
model
generated
an
EEC
of
6.4
ppb
and
SCI­
GROW
model
generated
an
EEC
of
<
0.001
ppb.
These
EEC
values
are
lower
than
the
drinking
water
levels
of
concern
(
DWLOC)
for
infants
1­
2
years
of
age
(
8.8
ppb).
The
combined
MOE
from
the
limited
potential
for
short­
term
exposure
from
residential
uses
is
>
1000.
Based
on
these
assessments,
it
can
be
concluded
that
there
is
reasonable
certainty
of
no
harm
to
the
U.
S.
Population
or
any
population
subgroup
from
exposure
to
bifenazate.

F.
International
Tolerances
There
are
no
CODEX
or
other
international
MRLs
on
tolerances
for
the
requested
uses
with
the
exception
of
cherries
in
Japan.
In
Japan,
the
following
MRLs
have
been
established:
citrus
0.2
and
1.0,
apple
2.0,
pear
2.0,
peach
0.2,
cherry
3.0,
strawberry
3.0,
watermelon
0.2,
tea
2.0.
Canada
has
established
a
tolerance
on
apple
(
0.58
ppm)
and
grapes
(
1.0
ppm).
There
are
no
other
current
MRLs
or
tolerances
for
bifenazate.
