Document ID: EPA-HQ-OPP-2006-0678-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-08-11T04:00Z

FILE
NAME:
company.
wpt
(
1/
1/
2006)
(
xml)
Template
Number
P25
ATTENTION:

All
commodity
terms
must
comply
with
the
Food
and
Feed
Commodity
Vocabulary
database
(
http://
www.
epa.
gov/
pesticides/
foodfeed/).

All
text
in
blue
font
(
instructions
for
preparing
the
document),
should
be
removed
prior
to
sending
the
document
to
the
Federal
Register
Staff.
Instructional
text
and
prompts
in
green
font
should
also
be
removed.

COMPANY
FEDERAL
REGISTER
DOCUMENT
SUBMISSION
TEMPLATE
(
1/
1/
2006)

EPA
Registration
Division
contact:
[
Marilyn
Mautz,
703­
305­
6785]

TEMPLATE:

[
Arysta
LifeScience
North
America
Corporation]

[
Insert
petition
number]

EPA
has
received
a
pesticide
petition
([
insert
petition
number])
from
[
Arysta
LifeScience
North
America
Corporation],
[
15401
Weston
Parkway,
Suite
150,
Cary,
NC
27513]
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.

1.
by
establishing
a
tolerance
for
residues
of
[
3­
dodecyl
­
1,4­
dihydro­
1,4­
dioxo­
2­
naphthyl
acetate
and
its
metabolite
2­
dodecyl­
3­
hydroxy­
1,4­
naphthoquinone
expressed
as
acequinocyl
equivalents
]
in
or
on
the
raw
agricultural
commodity
[
Tree
Nuts
(
Crop
Group
14)]
at
[
0.02]
parts
per
million
(
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
acequinocyl
in
plants
is
adequately
2
understood
based
on
three
crops;
apples,
oranges
and
eggplant.
The
major
residue
in
all
plant
metabolism
studies
is
acequinocyl.
A
minor
but
significant
metabolite
is
acequinocyl­
OH
(
2­
dodecyl­
3­
hydroxy­
1,4­
naphthoquinone).
The
proposed
tolerance
expression
is
the
parent,
acequinocyl
and
its
hydroxy
metabolite,
acequinocyl­
OH.]

2.
Analytical
method.
[
The
analytical
method
to
quantitate
residues
of
acequinocyl
and
acequinocyl­
OH
in/
on
nut
crops
utilizes
high
pressure
liquid
chromatography
(
HPLC)
using
mass
spectrometric
(
MS/
MS)
detection.
The
target
limit
of
quantitation
(
LOQ)
is
0.01
ppm.]

3.
Magnitude
of
residues.
[
The
proposed
use
of
acequinocyl
calls
for
a
maximum
application
rate
of
2
applications
at
0.3
lb
ai
per
acre
per
application,
with
a
21­
day
interval
between
applications.
The
pre­
harvest
interval
is
7
days.
The
maximum
residues
expressed
as
acequinocyl
equivalents
in/
on
pecan
nutmeats
were
0.0153
ppm.
The
crop
field
trial
data
are
adequate
to
support
the
proposed
tolerance
of
0.02
ppm
for
the
crop
group
tree
nuts.]

B.
Toxicological
Profile
1.
Acute
toxicity.
[
Acequinocyl
technical
has
low
acute,
dermal
and
inhalation
toxicity
in
laboratory
animals.
The
oral
LD50
(
M/
F)
in
the
rat
and
mouse
was
>
5000
mg/
kg.
The
dermal
LD50
(
M/
F)
was
>
2000
mg/
kg.
The
inhalation
LC50
was
reported
as
>
0.84
mg/
l.
In
the
eye
and
dermal
irritation
studies,
acequinocyl
technical
was
not
an
eye
or
skin
irritant
to
rabbits
and
was
not
a
skin
sensitizer
in
guinea
pigs.]

2.
Genotoxicty.
[
Acequinocyl
was
found
to
be
negative
in
the
Ames
reverse
mutation,
mouse
lymphoma,
Chinese
hamster
lung
(
CHL)
chromosome
aberration
and
mouse
micronucleus
assays.]

3.
Reproductive
and
developmental
toxicity.
[
i.
Rat
teratology.
Acequinocyl
technical
was
administered
by
oral
gavage
to
pregnant
Sprague
Dawley
rats
at
dose
levels
of
0,
50,
150,
500
or
750
mg/
kg/
day.
Common
signs
in
the
descendants
included
vaginal
discharge,
pallor,
pale
eyes,
hypoactivity,
piloerection,
slow
or
irregular
breathing,
intra­
uterine
hemorrhage
and
blood
stained
stomach
and/
or
intestinal
contents.
Maternal
NOEL=
150
mg/
kg/
day
based
on
3
these
signs.
Developmental
NOEL=
500
mg/
kg/
day
based
on
increase
in
certain
skeletal
variants
that
may
be
attributed
to
the
observed
maternal
toxicity.

ii.
Rabbit
teratology.
Groups
of
New
Zealand
white
rabbits
received
acequinocyl
technical
by
gavage
at
doses
of
0,
30,
60
or
120
mg/
kg/
day.
Maternal
NOEL=
60
mg/
kg/
day
based
on
reduction
in
maternal
body
weight
and
5
females
were
sacrificed
at
120
mg/
kg/
day.
Fetal
NOEL=
60
mg/
kg/
day
due
to
skeletal
variations
in
the
thoraco­
lumbar
ribs.

iii.
Rat
reproduction
study.
Acequinocyl
technical
was
fed
to
two
generations
of
male
and
female
Sprague
Dawley
rats
at
dietary
concentrations
of
0,
100,
800,
or
1500
ppm
(
0,
7.3,
59
or
111
mg/
kg/
day
for
males
and
0,
8.7,
69
or
134
mg/
kg/
day
for
females).
Systemic
and
pup
NOEL=
100
ppm
(
7.3
and
8.7
mg/
kg/
day).
Systemic:
Hemorrhage
and
swollen
body
parts
were
seen
at
800
and
1500
ppm
in
F1
males
.
At
800
and
1500
ppm,
treatment
related
clinical
signs,
hemorrhagic
effects,
subcutaneous
bleeding
on
body
parts
and/
or
cranium
and/
or
brain
were
seen
in
the
F1
pups.
At
800
and
1500
ppm
toxicity
seen
in
F2
pups
included
subcutaneous
bleeding
on
body
parts
and/
or
cranium
and/
or
brain
at
weaning.]

4.
Subchronic
toxicity.
[
i.
Rat
feeding
study.
Fischer
rats
received
acequinocyl
technical
at
dietary
concentrations
of
0,
100,
400,
1600
or
3200
ppm
(
0,
7.57,
30.4,
120,
253
mg/
kg/
day,
respectively
for
males
and
0,
8.27,
32.2,
129,
286
mg/
kg/
day,
respectively
for
females)
for
13
consecutive
weeks.
Treatment
related
yellow
brown
urine
in
all
animals
of
both
sexes
at
400
ppm
suggested
the
presence
of
the
metabolite
of
the
test
material.
Macroscopic
examination
on
the
surviving
animals
revealed
no
treatment
related
abnormalities.
At
3200
and
1600
ppm,
macroscopic
and
microscopic
examination
of
the
mortalities
revealed
hemorrhaging
of
muscle
and
other
organs.
NOEL=
400
ppm
(
30.4
mg/
kg/
day
for
males
and
32.2
mg/
kg/
day
for
females).

ii.
Mouse
feeding
study.
Groups
of
CD­
1
(
ICR)
BR
mice
received
acequinocyl
technical
by
oral
route
at
concentrations
of
0,
100,
500,
1000
or
1500
ppm
(
0,
16,
81,
151,
295
mg/
kg/
day
respectively
for
males
and
0,
21,
100,
231,
342
mg/
kg/
day
respectively
for
females)
for
13
weeks.
At
100
ppm,
there
were
hepatic
histopathological
lesions
and
an
increase
in
relative
liver
weight.
A
clear
NOEL
for
both
sexes
was
not
determined.
4
iii.
Dog
feeding
study.
Acequinocyl
technical
was
administered
via
gelatin
capsule
to
male
and
female
beagle
dogs
at
dose
levels
of
0,
40,
160,
640
or
1000
mg/
kg/
day
once
a
day
7
days
a
week
for
13
weeks.
At
40,
160
and
640
mg/
kg/
day
colored
feces
was
observed
in
both
sexes.
At
160
and
640
mg/
kg/
day,
treatment
related
decrease
in
body
weight
gain
in
males
and
an
increased
platelet
count
for
females
was
observed.
Macroscopic
and
microscopic
examinations
on
the
surviving
animals
revealed
no
treatment
related
abnormalities.
A
clear
NOEL
was
not
determined.

iv.
28­
day
dermal
toxicity.
Groups
of
Sprague
Dawley
rats
received
daily
dermal
applications
of
acequinocyl
technical
at
doses
of
0,
40,
200
or
1000
mg/
kg/
day
for
6
hours/
day
for
28
days
followed
by
a
14
day
treatment
free
period
only
in
the
high
dose
group.
There
were
no
macroscopic
findings.
Red
staining
occurred
on
the
back
of
the
animals
and
was
only
seen
in
the
morning
after
dosing.
There
was
no
evidence
of
systemic
toxicity.
NOEL=
1000
mg/
kg/
day.]

5.
Chronic
toxicity.
[
i.
Dog
feeding
study.
Beagle
dogs
were
dosed
by
capsule
at
0,
5,
20,
80
or
320
mg/
kg/
day
for
1
year
with
acequinocyl
technical.
Minor
disturbances
in
platelet
counts
were
observed
in
both
sexes
at
80
and
320
mg/
kg/
day.
There
were
no
treatment
related
macroscopic
histopathological
findings.
Colored
feces
and/
or
abnormally
stained
sawdust
were
observed
for
all
treatment
groups.
Varying
degrees
of
discoloration
of
the
urine
were
observed
for
animals
receiving
20
mg/
kg/
day
or
more.
The
discoloration
was
considered
to
be
attributable
to
a
colored
metabolite
of
the
test
substance.
NOEL=
20
mg/
kg/
day.

ii.
Rat
feeding/
oncogenicity
study.
Groups
of
F344
rats
received
acequinocyl
technical
at
dietary
levels
of
0,
50,
200,
800
or
1600
ppm
(
0,
2.25,
9.02,
36.4,
74.0
mg/
kg/
day
for
males
and
0,
2.92,
11.6,
46.3,
93.6
mg/
kg/
day
for
females)
for
2
years.
NOEL=
200
ppm
(
9.02
and
11.6
mg/
kg/
day
for
males
and
females
respectively).
Corneal
abnormalities
and
hypertrophy
of
the
eye
were
observed
in
800
ppm
and
1600
ppm
males
and
1600
ppm
females.
At
800
ppm
and
1600
ppm,
PT
was
observed
to
be
longer
in
males
and
shorter
in
females
and
APTT
longer
in
females.
Reddish
brown
urine
was
observed
in
both
males
and
females.
There
was
no
incidence
of
tumors.

iii.
Mouse
oncogenicity
study.
Acequinocyl
technical
was
administered
in
the
diet
of
Crl:
CD­
1(
ICR)
BR
mice
at
0,
20,
50,
150
or
500
ppm
for
80
weeks.
NOEL=
20
ppm
(
lowest
dose
tested
equal
to
2.7
and
3.5
mg/
kg/
day
in
males
and
females
respectively),
based
on
brown
pigmented
cells.
At
50
and
500
ppm
in
both
sexes,
there
was
an
increase
incidence
of
fatty
hepatocytes.
Other
associated
findings
were
increased
liver
weight,
slight
increase
in
pale
livers
or
pale
areas
within
livers.
Glomerular
amyloidosis
was
statistically
increased
in
the
150
and
500
ppm
males.
Yellow
brown
urine
was
consistently
found
in
both
sexes
at
high
dose.
There
was
no
increase
in
the
incidence
of
tumors.]
5
6.
Animal
metabolism.
[
Sprague
Dawley
rats
were
dosed
orally
with
acequinocyl
labeled
14C­
phenyl
or
14C­
dodecyl.
Both
labels
were
used
in
the
single
low
dose
(
10
mg/
kg)
study.
The
high
dose
(
500
mg/
kg)
and
14­
day
repeat
dose
studies
(
10
mg/
kg/
day)
were
conducted
with
14C­
phenyl
acequinocyl
only.
Excretion
was
rapid,
with
most
of
the
dose
in
the
feces.
Less
than
15%
of
the
radioactivity
was
found
in
the
urine.
Absorption
was
about
25­
42%
based
on
the
bile
duct
cannulation
studies,
which
found
20­
33%
of
the
administered
dose
in
bile,
plus
5­
9%
in
urine
plus
cage
wash.
Acequinocyl
was
not
detected
in
urine
and
was
only
a
minor
component
(
1­
2%)
in
the
feces.
The
major
fecal
metabolite
(
12­
36%)
was
the
2­
hydroxy­
3­
dodecyl­
1,4­
naphthalenedione
(
acequinocyl­
OH
or
designated
R1).
Subsequent
oxidation
of
the
dodecyl
chain
yielded
butanoic
and
hexanoic
acids,
the
only
measurable
identified
urinary
metabolites.
2­(
1,2­
dioxotetradecyl)­
benzoic
acid
comprised
19­
40%
of
the
radioactivity
in
the
feces.
There
were
no
remarkable
differences
in
metabolite
disposition
due
to
gender
and
no
effect
of
pre­
dosing
for
2
weeks.
The
large
dose
slowed
transit
time
and
reduced
absorption.]

7.
Metabolite
toxicology.
[
NA­
Remove]

8.
Endocrine
disruption.
[
A
standard
battery
of
toxicity
tests
have
been
conducted
on
acequinocyl.
No
effects
were
seen
to
indicate
that
acequinocyl
has
an
effect
on
the
endocrine
system.]

C.
Aggregate
Exposure
1.
Dietary
exposure.
[
The
tolerance
of
0.02
ppm
for
tree
nuts
(
Crop
Group
14)
along
with
the
currently
established
tolerances
for
acequinocyl
were
incorporated
into
the
aggregate
exposure
results
presented
below.
An
aggregate
risk
assessment
was
conducted
to
include
the
potential
chronic
dietary
exposure
from
applications
of
acequinocyl
on
tree
nuts.
Please
note
that
tolerances
on
almonds
and
pistachios
are
already
established.
Therefore,
this
assessment
only
additionally
incorporated
the
other
tree
nuts
for
which
tolerances
are
not
already
established.
This
chronic
risk
assessment
was
conducted
to
assess
dietary
exposures
from
acequinocyl
in
food
using
DEEM
(
Dietary
Exposure
Evaluation
Model
and
the
following
input
parameters:
tolerance
level
residues;
consumption
data
from
the
USDA
1994­
1998
Continuing
Survey
of
Food
Intakes
by
Individuals
(
CSFII);
100
percent
crop
treated
for
all
commodities;
default
processing
factors
for
all
commodities;
and
a
chronic
toxicological
endpoint
of
2.7
mg/
kg
bw
(
NOAEL);
0.027
mg/
kg
bw
(
chronic
RfD)
from
the
chronic
mouse
study.
Please
note
that
EPA
has
determined
that
there
is
no
endpoint
of
concern
attributable
to
a
single
dose
6
and,
therefore,
an
acute
reference
dose
(
aRfD)
was
not
established.
Therefore,
no
acute
exposure
assessment
is
necessary
(
FR,
Vol.
69,
No.
139,
7/
21/
04,
page
43528).]

i.
Food.
[
The
previous
chronic
dietary
food
exposure
estimates
to
acequinocyl
were
all
less
than
100%
of
chronic
RfD.
When
the
previous
risk
assessment
is
revised
to
include
all
tree
nuts,
the
chronic
dietary
food
exposure
estimates
to
acequinocyl
are
still
less
than
100%
of
chronic
RfD.
To
be
specific,
exposure
from
all
tree
nuts
has
very
little
effect
on
the
estimated
chronic
dietary
food
exposure
as
can
be
seen
from
the
following:
US
population
at
4.2%,
females
13­
49
at
2.4%,
and
all
infants
(<
1
year)
at
13.8%.
The
most
highly
exposed
population
was
children
1­
2
years
at
23.3%.]

ii.
Drinking
water.
[
The
available
environmental
fate
data
indicate
that
acequinocyl
does
not
persist
in
the
environment
nor
does
it
have
the
ability
to
leach
into
groundwater
resources.
Acequinocyl
degrades
rapidly
in
the
environment.
Aqueous
photolyis
T1/
2:
14
minutes,
soil
photolyis
T1/
2:
2
days,
aerobic
soil
metabolism
(
4
soils)
T1/
2:
<
3
days,
aerobic
aquatic
metabolism
T1/
2:
0.39
day
in
water
and
sediment,
hydrolysis
T1/
2:
pH4=
74
days,
pH7=
2.2
days,
pH9=
1.3
hours.
Acequinocyl
shows
low
soil
mobility.
The
DWEC
(
Drinking
Water
Estimated
Concentration)
for
chronic
exposures
is
estimated
to
be
0.24
ppb
for
surface
water
and
0.003
ppb
for
ground
water.
These
values
represent
results
of
the
PRZM/
EXAMS
(
surface
water)
and
SCI­
GROW
models
(
ground
water)
models
(
FR,
Vol.
69,
No.
139,
7/
21/
04,
page
43529),
respectively
since
the
proposed
use
on
all
tree
nuts
is
not
expected
to
result
in
higher
environmental
concentrations
than
those
from
the
currently
proposed
uses.
To
determine
drinking
water
exposure,
DWLOCs
(
drinking
water
levels
of
comparison)
were
calculated
and
used
as
a
point
of
comparison
against
the
model
estimates
of
the
pesticide
concentration
in
drinking
water.
For
acequinocyl,
the
chronic
DWLOC
values
were
greater
than
the
estimated
concentrations
(
DWECs)
in
surface
and
ground
water
for
each
population
group.
Therefore,
exposures
to
acequinocyl
in
drinking
water
do
not
pose
a
significant
human
health
risk.]

2.
Non­
dietary
exposure.
[
The
proposed
expansion
of
the
registration
for
applications
to
all
tree
nut
crops
not
already
registered
requires
evaluation
of
occupational
handler
and
postapplication
exposures
and
dietary
exposures
for
consumers.
The
proposed
registration
for
applications
by
commercial
applicators
and
residents
to
ornamentals
in
residential
settings
requires
evaluation
of
occupational
and
residential
handler
exposures
as
well
as
residential
postapplication
exposures.

Occupational
Handler
Exposure:
Short­
term
MOEs
for
occupational
handler
exposures
are
estimated
to
range
from
3,900
to
530,000,
depending
on
the
site
and
type
of
equipment
7
used.
MOEs
greater
than
100
indicate
a
reasonable
certainty
of
no
harm
is
anticipated
for
occupational
handlers
making
applications
of
Kanemite
 
15SC.
Based
on
the
anticipated
occupational
use
patterns
for
acequinocyl
products,
intermediate­
term
(
1
month
to
6
months)
and
long­
term
(
several
months
to
lifetime)
exposures
are
not
expected
for
occupational
handlers
of
acequinocyl.

Occupational
Postapplication
Exposure:
Estimated
MOEs
for
re­
entry
as
soon
as
the
spray
has
dried
range
from
960
to
13,000,
demonstrating
a
reasonable
certainty
of
no
harm
for
workers
who
re­
enter
treated
crops
on
the
day
of
application
as
soon
as
the
sprays
have
dried.

Residential
Handler
exposure:
MOEs
for
residential
handler
exposures
associated
with
all
types
of
handheld
equipment
are
estimated
to
range
from
2,900
to
430,000,
depending
on
the
type
of
equipment
used.

Residential
Postapplication
exposures:
Estimated
MOEs
are
2,900
for
youth
and
2,600
for
adults,
demonstrating
a
reasonable
certainty
of
no
harm
for
adults
and
youth
engaging
in
postapplication
activities
in
treated
ornamentals
on
the
day
of
application
after
sprays
have
dried.

In
summary,
all
residential
and
occupational
exposure
scenarios
are
associated
with
a
reasonable
certainty
of
no
harm
for
the
US
population
and
all
subpopulations.]

D.
Cumulative
Effects
[
There
is
no
information
available
to
indicate
that
toxic
effects
produced
by
acequinocyl
are
cumulative
with
those
of
any
other
compound.]

E.
Safety
Determination
1.
U.
S.
population.
[
The
chronic
dietary
food
exposure
(
including
all
current
and
proposed
uses)
to
acequinocyl
was
estimated
at
4.2%
of
the
cRfD
for
the
total
US
population.
The
calculated
DWLOCs
ranged
from
5,900
to
20,000
ppb
(
short­
term
residential
aggregate)
and
210
to
910
ppb
(
long­
term
residential
aggregate).
The
surface
and
groundwater
DWECs
for
acequinocyl
were
estimated
to
be
0.24
ppb
and
0.003
ppb,
respectively.
Since
the
chronic
DWECs
are
less
than
the
DWLOCs
for
all
population
subgroups,
the
chronic
aggregate
risk
estimates
are
below
the
level
of
concern.]
8
2.
Infants
and
children.
[
The
chronic
dietary
food
exposure
to
acequinocyl
was
estimated
at
13.8%
of
cRfD
for
all
infants
(<
1
year),
and
23.3%
of
cRfD
for
children
1­
2
(
most
highly
exposed).
The
calculated
DWLOCs
for
children
1­
2
were
5,900
ppb
(
short­
term
residential
aggregate)
and
210
ppb
(
long­
term
residential
aggregate).
The
surface
and
ground
water
DWECs
for
acequinocyl
were
estimated
to
be
0.24
ppb
and
0.003
ppb,
respectively.
Since
the
chronic
DWECs
are
less
than
the
DWLOCs
for
children
1­
2,
the
most
highly
exposed
subpopulation,
the
chronic
aggregate
risk
estimates
are
below
the
level
of
concern.]

F.
International
Tolerances
[
To
date,
no
Codex,
Canadian
or
Mexican
tolerances
exists
for
acequinocyl.]