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

EPA
Registration
Division
contact:
Mr.
Dan
Rosenblatt,
Chief,
Minor
Use
Team,
(
703)
308­
9366
Interregional
Research
Project
No.
4,
Pesticide
Tolerance
Petition
AGENCY:
US
Environmental
Protection
Agency
("
EPA")

Petition
Number:
A­
27200­##­
05
EPA
has
received
a
pesticide
petition
(
A­
27200­##­
05)
from
Interregional
Research
Project
No.
4,
Rutgers,
The
State
University
of
New
Jersey,
681
U.
S.
Highway
No.
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
by
establishing
a
tolerance
for
residues
of
pirimiphos­
methyl
in
or
on
the
raw
agricultural
commodity
sunflower
seeds
at
10
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
Residue
in
Plants
(
860.1300):
EPA
stated
that
the
residue
in
stored
grain
is
adequately
understood
based
on
a
corn
grain
metabolism
study
(
MRID
42903501).
In
this
study,
the
parent
constituted
>
96%
of
the
total
radioactive
residue
(
TRR)
immediately
after
treatment,
but
declined
to
64­
67%
of
the
TRR
following
12
and
24
weeks
of
storage.
The
maximum
level
of
the
des
ethyl
metabolite
detected
was
10.3%
of
the
TRR.
The
IR­
4
Project
believes
that
these
data,
along
with
the
magnitude
of
residue
data
that
are
summarized
below,
can
be
used
to
estimate
the
levels
of
des
ethyl
pirimiphosmethyl
in
sunflowers.
The
ChemSAC
concluded
a
waiver
from
collecting
des­
ethyl
metabolite
field
trial
data
was
acceptable.
The
nature
of
the
residues
of
pirimiphos­
methyl
is
adequately
understood,
and
an
acceptable
analytical
method
is
available
for
enforcement
purposes.
Based
on
these
results,
the
establishment
of
the
tolerance
proposed
for
sunflower
in
Section
F
of
this
volume
and
the
registration
of
this
use
would
provide
an
effective
pesticide
for
the
control
of
stored
grain
insects,
including
Indian
meal
moth.

2.
Analytical
method.
The
samples
were
analyzed
using
the
working
method
titled
"
Pirimiphos­
Methyl:
Magnitude
of
the
Residue
on
Sunflower",
a
method
very
similar
to
the
reference
method,
"
Determination
of
Residues
of
Pirimiphos­
methyl
and
its
Phosphorus­
containing
metabolites
in
Crops,
Water
and
Animal
Tissues.
Residue
Analytical
Method
No.
11A,
ICI
Plant
Protection
Limited.".
No
analysis
of
metabolites
was
conducted.

Sunflower
seeds
are
blended
with
20%
acetone/
hexane,
filtered,
and
then
partitioned
with
hexane/
acetonitrile
to
remove
the
oil.
Sunflower
oil
samples
are
dissolved
in
hexane
and
partitioned
with
hexane/
acetonitrile
to
remove
the
oil.
The
combined
acetonitrile
layers
are
concentrated
prior
to
cleanup.
Processed
meal
samples
are
homogenized
with
20%
acetone/
hexane,
filtered,
and
then
concentrated.
Oil
is
removed
via
a
hexane/
acetonitrile
partition.
Samples
from
all
matrices
are
then
cleaned
up
by
a
Florisil
cleanup
procedure.
All
samples
are
analyzed
for
pirimiphos­
methyl
using
a
Hewlett­
Packard
5890
gas
chromatograph
with
a
flame
photometric
(
FPD)
operated
in
the
phosphorus
mode
(
526
nm
filter).

Method
suitability
was
evaluated
both
prior
to
sample
analysis
and
concurrently
with
sample
analysis.
The
method
was
validated
prior
to
sample
analysis
using
commercially
obtained
dried
sunflower
root.
The
method
validation
recoveries
ranged
from
81
to
92%
in
seeds,
85
to
106%
in
meal,
and
80
to
93%
in
oil.
Concurrent
recoveries
obtained
during
sample
analysis
ranged
from
85
to
106%
in
seeds,
78
to
92%
in
meal,
and
86
to
94%
in
oil.

3.
Magnitude
of
residues.
At
each
trial,
a
single,
post­
harvest
application
of
the
test
substance
was
made
to
the
treated
seeds.
The
application
rates
ranged
from
0.481
to
0.488
lb
ai
per
30
tons
grain
(
seed).
In
each
trial,
the
application
was
made
using
spray
equipment
that
simulated
the
manner
in
which
harvested
seeds
would
be
treated
in
a
commercial
setting,
and
the
spray
volume
was
sufficient
to
provide
adequate
dispersal
of
the
test
substance.

Untreated
seeds
were
sampled
prior
to
the
treated
seeds
on
the
same
day
as
the
application.
In
one
trial,
additional
samples
were
collected
for
processing
into
meal
and
oil.
These
samples
were
processed
at
the
GLP
facility
at
Texas
A&
M
University.

The
total
residues
of
pirimiphos­
methyl
ranged
from
4.73
to
9.67
ppm
in
seeds.
Meal
samples
and
oil
samples
had
lower
residues
than
treated,
unprocessed
seeds
collected
from
the
same
trial,
indicating
that
no
concentration
of
pirimiphos­
methyl
occurs
in
the
processed
commodities.

The
maximum
storage
intervals
for
field­
treated
samples
in
this
study
were
106
days
for
meal,
111
days
for
oil,
and
205
days
for
seeds.
Storage
stability
samples
were
fortified
with
pesticide
at
5.00
ppm
soon
after
the
receipt
of
the
samples
by
the
analytical
laboratory.
The
storage
stability
samples
were
held
in
frozen
storage
under
similar
conditions
to
the
field
generated
samples.
After
freezer
storage
periods
of
205
days
(
seeds),
106
days
(
meal)
and
111
days
(
oil),
the
storage
stability
samples
were
analyzed
for
pesticide.

The
recoveries
for
the
storage
stability
samples
were
in
the
ranges
59
to
71%
for
seeds,
83
to
86%
for
meal,
and
90
to
104%
for
oil.
Concurrent
recoveries
for
spikes
analyzed
along
with
the
storage
stability
samples
ranged
from
76
to
100%.
These
data
indicate
that
pirimiphos­
methyl
is
stable
under
the
conditions
in
which
the
samples
were
held
between
harvest
and
analysis.

In
response
to
EPA
data
call­
ins,
Agriliance
generated
and
submitted
the
following
studies
to
update
the
database
of
studies
supporting
pirimiphos­
methyl.
These
studies
have
not
to
date
been
evaluated
by
EPA.
It
is
not
anticipated
that
these
data
will
change
the
risk
assessment
or
terms
of
registration
of
pirimiphos­
methyl.

Crop
Residue
Data
MRID
Subject
45311801
Magnitude
residues
in
stored
corn
45311802
Magnitude
residues
in
processed
corn
fractions
45311803
Magnitude
residues
in
stored
sorghum
grain
45311804
Magnitude
residues
in
processed
sorghum
fractions
46315501
14C
nature
and
magnitude
residues
in
corn
grown
from
treated
seed.

B.
Toxicological
Profile
1.
Acute
toxicity.
The
Agency
granted
a
waiver
from
the
requirement
of
conducting
acute
toxicity
studies
on
technical
pirimiphos­
methyl
and
has
acceptable
acute
toxicity
studies
on
75%
formulation
(
EPA,
1992)
In
rats,
pirimiphos­
methyl
is
acutely
toxic
via
the
dermal
route
of
exposure
but
has
low
toxicity
via
the
oral
and
inhalation
routes
of
exposure.
It
causes
eye
and
skin
irritation
in
rabbits.
The
estimated
acute
oral
LD50
for
pirimiphos­
methyl
(
75%
a.
i.)
in
rats
is
2.4
g/
kg
(
2.1
to
2.8
g/
kg)
(
Toxicity
Category
II;
Guideline
81­
1;
MRID
#
00126257).
The
acute
dermal
LD50
value
for
pirimiphosmethyl
(
75%
a.
i.)
in
rabbits
was
>
3.2
ml/
kg
(
3.5
g/
kg)
for
females
and
between
2.0­
3.2
ml/
kg
for
males
(
2.2­
3.5
g/
kg)
(
Toxicity
Category
III;
Guideline
81­
2;
MRID
#
00126257).
The
acute
inhalation
LC50
pirimiphos­
methyl
(
90.6%
a.
i.)
was
>
5.04
mg/
L
(
analyzed
concentration
4.7
mg/
L;
Toxicity
category
IV;
Guideline
81­
3;
MRID
#
41556304).
Pirimiphos­
methyl
is
irritating
following
ocular
exposure.
In
a
primary
eye
irritation
study,
pirimiphos­
methyl
(
75%
a.
i.)
produced
reversible
opacity
in
the
rabbit
eye
(
Toxicity
Category
II;
Guideline
81­
4;
MRID
00126527).
A
primary
dermal
irritation
study
with
the
75%
formulation
of
pirimiphos­
methyl
showed
that
it
causes
moderate
irritation
at
72
hours
in
rabbits
(
Toxicity
Category
III;
Guideline
81­
5;
MRID
00126257).
The
dermal
sensitization
studies
in
guinea
pigs
using
pirimiphos­
methyl
(
75%
formulation)
showed
3
that
the
compound
is
not
a
skin
sensitizer
(
Guideline
81­
6;
MRID
00126257;
00129341).

2.
Genotoxicty.
Sufficient
data
are
available
to
satisfy
the
data
requirements
for
mutagenicity
testing.
With
the
exception
of
the
dominant­
lethal
assay,
all
other
studies
are
acceptable.
The
available
studies
submitted
to
the
Agency
in
conjunction
with
the
published
data
indicate
that
pirimiphosmethyl
is
not
mutagenic
in
bacteria
or
cultured
mammalian
cells.
Pirimiphos­
methyl
did,
however,
induce
SCE
in
vitro
but
was
not
clastogenic
either
in
vitro
or
in
vivo
and
was
not
genotoxic
in
primary
rat
hepatocytes.
The
data
suggest,
therefore,
that
the
genotoxic
activity
demonstrated
in
the
SCE
assay
is
not
expressed
in
vivo.
Confidence
in
this
conclusion
is
high
since
the
suggestive
evidence
of
test
material
interaction
with
the
target
cells
noted
in
the
submitted
bone
marrow
cytogenetic
assay
was
supported
by
the
findings
of
Rajani
et
al
(
1986).
Based
on
these
considerations,
the
Hazard
ID
SARC
(
meeting
of
January
12,
1998)
concluded
that
there
is
no
concern
for
mutagenicity
at
this
time.

3.
Reproductive
and
developmental
toxicity.
Sufficient
data
are
available
to
assess
the
reproductive
and
developmental
toxicity
for
pirimiphos­
methyl.
In
the
prenatal
developmental
toxicity
and
reproduction
studies,
maternal/
parental
NOELs
were
less
than
or
equivalent
to
offspring
NOELS.
No
CNS
malformations
were
noted
in
fetuses
or
pups.
Based
on
the
comparison
of
the
NOELS
and
LOELS
for
maternal/
parental
and
developmental
toxicity,
no
increased
sensitivity
was
noted
among
fetuses
or
pups.
In
a
dominant
lethal
assay,
pirimiphos­
methyl
did
not
induce
pre­
and
post­
implantation
losses.
Furthermore,
no
differences
in
sensitivity
for
ChE
inhibition
were
noted
among
younger
rats
compared
to
older
rats.
Reproductive
Toxicity
Study
in
Rats
In
a
2­
generation
reproduction
study,
pirimiphos­
methyl
(
86.7%
a.
i.)
was
administered
to
male
and
female
Sprague­
Dawley
CD
rats
in
the
diet
at
concentrations
of
0,
10,
40,
or
160
ppm
(
corresponding
to
0.87,
3.43
or
13.72
mg/
kg/
day
in
males
and
0.98,
3.88
or
15.41
mg/
kg/
day
for
females
for
the
premating
periods).
There
were
no
effects
on
reproductive
parameters
of
either
generation
and
there
were
no
clinical
signs.
The
LOEL
for
systemic
and
reproductive
toxicity
is
>
160
ppm
(
13.72
mg/
kg/
day
for
males
and
15.41
mg/
kg/
day
for
females).
The
NOEL
for
systemic
and
reproductive
toxicity
is
$
160
ppm
(
13.72
mg/
kg/
day
for
males
and
15.41
mg/
kg/
day
for
females).

Developmental
Toxicity
Study
in
Rats
Four
groups
of
twenty­
four
mated
female
Alpk:
AP
(
Wistar­
derived)
rats
were
administered
pirimiphosmethyl
(
88.5%
a.
i.)
in
corn
oil
by
gavage
at
dose
levels
of
0,
1.5,
15,
or
150
mg/
kg/
day
from
gestational
days
7 
16,
inclusive.
A
single
treatment­
related
mortality
occurred
at
150
mg/
kg/
day.
Twenty
of
the
twenty­
three
surviving
rats
showed
some
signs
of
toxicity
including
abnormal
gait,
changes
in
behavior,
irregular
respiration,
urinary
incontinence
and
body
tremors.
During
dosing
and
post­
dosing
periods,
reduction
in
body
9
weight
gain
(
57
and
22%,
respectively)
accompanied
by
decrease
in
food
consumption
(
15
and
30%,
respectively)
were
noted
in
dams.
No
significant
toxicological
effects
were
observed
at
15
mg/
kg/
day.
However,
in
the
absence
of
individual
animal
data
the
maternal
findings
could
not
be
confirmed.
Consequently,
the
maternal
LOEL
and
NOEL
could
not
be
determined.
There
are
no
developmental
effects
noted
in
the
study
at
doses
up
to
150
mg/
kg/
day.
However,
in
the
absence
of
data
on
individual
fetuses
and
litters,
the
lack
of
developmental
findings
could
not
be
confirmed.
Consequently,
the
developmental
LOEL
and
NOEL
could
not
be
determined.
This
study
is
classified
as
Unacceptable
/
Guideline
and
does
not
satisfy
the
guideline
requirements
of
a
developmental
toxicity
study
(
83­
3a)
in
rats
(
MRID
00151623).
Developmental
Toxicity
Study
in
Rabbits
Four
groups
of
New
Zealand
White
rabbits
were
dosed
at
levels
of
0,
12,
24
or
48
mg/
kg/
day
of
pirimiphos
methyl
in
corn
oil
(
a.
i.)
on
days
6
through
18
of
gestation.
Their
pups
were
delivered
by
caesarian
section
on
day
29.
The
only
toxic
response
evident
was
inhibition
of
plasma
ChE
(
37%)
and
RBC
ChE
(
44%)
at
24
mg/
kg/
day.
Higher
levels
of
inhibition
were
noted
at
48
mg/
kg
and
brain
AChE
(
38%)
was
also
inhibited.
There
were
no
other
indications
of
maternal
toxicity
and
there
were
no
indications
of
effects
on
fetal
development.
The
LEL
is
24
mg/
kg­
bw/
day
based
on
ChE
inhibition
and
the
NOEL
is
12
mg/
kg­
bw/
day
for
maternal
toxicity.
The
LOEL
for
developmental
toxicity
is
>
48
mg/
kgbw/
day
and
the
NOEL
is
$
48
mg/
kg/
day.
This
study
is
classified
as
Acceptable/
Guideline
and
satisfies
the
guideline
requirements
of
a
developmental
toxicity
study
(
83­
3b)
in
rabbits
(
MRID
43206301)

4.
Subchronic
toxicity.
28­
Day
Rat
Feeding
Study
In
a
28­
day
feeding
study,
pirimiphos­
methyl
(
97.0%
a.
i.)
was
administered
to
three
groups
of
SPF­
Wistar
rats
(
12/
sex/
dose/
group)
at
dose
levels
of
0,
5,
8,
10
or
50
ppm
(
equivalent
to
0,
0.25,
0.4,
0.5
or
2.5
mg/
kg/
day,
respectively)
for
28
days.
The
purpose
of
the
study
was
to
determine
the
sensitivity
of
younger
rats
(
approx.
6
week
old)
for
ChE
inhibition
(
5/
sex/
group)
in
comparison
to
that
determined
in
older
rats
(>
12
week
old)
in
other
studies.
The
LOEL
was
50
ppm
(
2.5
mg/
kg/
day)
based
on
plasma
ChE
inhibition
in
both
sexes.
The
NOEL
was
10
ppm
indicating
no
differential
sensitivity
from
older
rats
(
NOEL
for
ChE
Inhibition=
8­
10
ppm
or
0.4­
0.5
mg/
kg/
day).
this
study
is
classified
as
Unacceptable/
Nonguideline
(
MRID
00129343)

13­
Week
Dog
Oral
Study
In
a
thirteen
week
study,
pirimiphos­
methyl
(%
a.
i.
not
reported)
was
administered
to
four
groups
of
beagle
dog
(
4/
sex/
dose)
at
dose
levels
of
0,
2,
10
or
25
mg/
kg/
day
in
a
corn
oil
capsule
once
daily,
seven
days/
week
for
thirteen
weeks.
The
doses
were
selected
based
on
the
results
of
a
preliminary
study
in
which
a
dose
of
50
mg/
kg/
day
was
severely
toxic
to
dogs.
A
reversible
and
non­
progressive
inhibition
of
plasma
ChE
and
dose­
related
inhibition
in
RBC
ChE
levels
were
noted
in
both
sexes
at
all
dose
levels
($
20%
beginning
Week
1).
No
significant
effect
on
brain
ChE
level
was
observed.
However,
the
data
are
questionable
because
the
post­
mortem
to
assay
time
was
not
reported.
The
systemic
toxicity
LOEL
was
2
mg/
kg/
day
based
on
plasma
and
RBC
ChE
inhibition
in
both
sexes.
The
NOEL
was
<
2
mg/
kg/
day.
This
study
is
classified
as
Unacceptable
/
Guideline
and
does
not
meet
the
requirement
of
a
subchronic
toxicity
study
in
dogs
(
82­
1)
(
MRID
00080743).

21­
Day
Rabbit
Dermal
Toxicity
In
a
21­
day
dermal
toxicity
study,
three
groups
of
10
New
Zealand
white
rabbits
(
5/
sex)
per
group
were
treated
with
intact
skin
and
three
groups
of
10
rabbits
(
5/
sex)
per
group
were
treated
with
abraded
skin
at
dosages
of
4,
40
or
400
mg/
kg/
day
of
pirimiphos­
methyl
(
90.6%)
in
propylene
glycol
six
hours
per
day,
five
days/
week
for
a
total
of
15
applications
over
a
three
week
period.
The
systemic
toxicity
LOEL
is
4
mg/
kg/
day
based
on
RBC
ChE
inhibition
in
females
with
intact
(
21%)
or
abraded
(
23%)
skin.
The
systemic
toxicity
NOEL
is
<
4
mg/
kg/
day.
The
dermal
toxicity
LOEL
is
400
mg/
kg/
day
for
males
and
females
based
on
the
findings
of
skin
reactions;
the
dermal
toxicity
NOEL
is
40
mg/
kg/
day
for
males
and
females.
This
study
is
classified
as
Unacceptable/
guideline
and
does
not
meet
the
requirements
of
a
21­
day
dermal
toxicity
study
in
rabbits
(
82­
2)
(
MRID
00129342)

5.
Chronic
toxicity.
Chronic
Toxicity
Study
in
Dogs
In
a
chronic
toxicity
study,
pirimiphos­
methyl
was
administered
to
four
beagle
dogs
in
gelatin
capsules
at
dose
levels
of
0,
0.5,
2,
or
10
mg/
kg/
day/
sex/
dose
for
two
years.
Numerous
study
deficiencies
were
identified
in
this
study.
While
previous
issues
have
been
raised
by
HED
about
the
significance
of
reported
findings
at
the
0.5
mg/
kg/
day
dose
level,
these
effects
may
in
reality
be
occurring
at
much
lower
dose
levels
than
the
reported
nominal
dosages
which
are
likely
varying
significantly
over
time
due
to
stability
problems,
batch
and
test
sample
changes.
Based
upon
the
findings,
the
LOEL
for
brain
and
plasma
ChE
inhibition
is
#
0.5
mg/
kg/
day
and
no
NOEL
was
determined;
the
LOEL
for
RBC
ChE
inhibition
is
2
mg/
kg/
day
and
the
NOEL
is
0.5
mg/
kg/
day.
The
systemic
NOEL
is
0.5
mg/
kg/
day
and
the
LOEL
is
2
mg/
kg/
day
based
on
clinical
sign
(
semi­
liquid
stool).
This
study
is
classified
as
Unacceptable/
Guideline
and
does
not
meet
the
requirements
of
a
chronic
toxicity
study
in
dogs
(
83­
1b)
(
MRID
92147036/
92147014).
Combined
Chronic
Toxicity
and
Carcinogenicity
Study
in
Rats
In
a
combined
chronic
toxicity/
carcinogenicity
study,
Wistar
(
SPF)
rats
(
72/
sex/
group)
were
administered
pirimiphos­
methyl
via
diet
at
dose
levels
of
0,
10,
50,
or
300
ppm
(
equivalent
to
0,
0.4,
2.1,
or
12.6
mg/
kg/
day)
for
two
years.
The
dosing
was
considered
to
be
adequate
to
evaluate
the
systemic
and
carcinogenic
potential
of
pirimiphos­
methyl.
Dose­
related
and
progressive
plasma
and
brain
ChE
inhibitions
were
seen
at
50
and
300
ppm.
RBC
ChE
inhibition
was
observed
at
300
ppm
at
various
time
points.
There
were
no
effects
on
body
weight,
food
consumption
and
hematology.
No
clinical
chemistry
data
were
available.
Of
the
42
high­
dose
male
rats,
there
were
pancreatic
islet
cell
adenomas
in
4
rats
and
a
carcinoma
in
one
rat
compared
to
0/
42
control
male
rats.
In
addition
to
several
study
deficiencies,
no
individual
animal
data
for
tumors
and
neoplastic
microscopic
findings
were
submitted.
Therefore,
the
carcinogenicity
of
pirimiphos­
methyl
can
not
be
assessed
due
to
insufficient
data
submitted.
Under
conditions
of
this
study,
the
NOEL
for
systemic
toxicity
was
300
ppm
(
12.6
mg/
kg/
day)
(
the
highest
dose
tested).
The
NOEL
for
plasma
and
brain
ChE
inhibition
was
10
ppm
(
0.4
mg/
kg/
day)
and
the
LOEL
was
50
ppm
(
2.1
mg/
kg/
day).
The
NOEL
for
RBC
ChE
inhibition
was
50
ppm
(
2.1
mg/
kg/
day)
and
the
LOEL
was
300
ppm
(
12.6
mg/
kg/
day).
this
study
is
classified
as
Unacceptable/
Guideline
and
does
not
meet
the
requirements
of
a
chronic
toxicity
study
in
rats
(
83­
5b)
(
MRID
92147035).

Carcinogenicity
Study
in
Mice
In
a
mouse
carcinogenicity
study,
pirimiphos­
methyl
(
86.7%
a.
i.,
Lot#
RS492/
B;
89.8%
a.
i.,
Lot#
20307­
00S)
was
administered
to
50
CD­
1
mice/
sex/
dose
at
dose
levels
of
0,
50,
200,
or
400/
300
ppm
(
0,
8.3,
33,
or
52
mg/
kg/
day
for
males
and
0,
9.7,
39,
or
61
mg/
kg/
day
for
females)
for
78
weeks.
A
satellite
study
was
concurrently
run
using
10
mice/
sex/
dose
but
for
52
weeks.
The
initial
400
ppm
dose
resulted
in
excessive
toxicity
and
moribundity
and
was
reduced
to
300
ppm
after
8
days.
At
200
ppm
mean
initial
body
weight
in
males
was
decreased
(.
9%),
p<
0.001)
and
clinical
signs
(
piloerection,
hunched
posture,
dark
eyes
and
hyperactivity)
were
noted
in
both
sexes.
At
300
ppm
male
body
weight
was
decreased
at
most
intervals
and
clinical
signs
were
more
frequent.
The
LOEL
for
systemic
effects
is
200
ppm
(
33%
and
39
mg
/
kg
/
day)
based
on
body
weight
effects
and
clinical
signs.
The
NOEL
is
50
ppm
(
8.3%
and
9.7&
mg/
kg/
day).
At
50
ppm,
inhibition
of
plasma
(
88%%
and
93%
&)
and
RBC
ChE
(
57%%
and
48%&)
and
brain
AChE
(
21%%,
p
<
0.05)
was
evident
at
week
52
and
a
similar
pattern
was
evident
at
week
78.
Higher
dose
levels
had
progressively
more
inhibition.
The
LOEL
for
ChE
inhibition
is
50
ppm
(
8.3%
and
9.7&
mg/
kg/
day)
based
on
depressed
plasma,
RBC
and
brain
ChE.
The
NOEL
for
ChE
is
<
50
ppm.
Dosing
was
considered
adequate
based
on
the
need
to
reduce
the
high
dosage
from
400
ppm
to
300
ppm
after
8
days
in
order
to
avoid
extreme
toxicity
and
excessive
mortality
and
the
consistent
inhibition
of
ChE/
AChE
at
all
dose
levels.
Under
the
conditions
of
this
study,
there
was
no
evidence
of
a
carcinogenic
effect
of
pirimiphos­
methyl
in
mice.
This
study
is
classified
as
Acceptable/
Guideline
and
satisfies
the
guideline
requirements
of
a
chronic
toxicity
study
in
mice
(
83­
2b)
(
MRID
43968401).
In
another
mouse
carcinogenicity
study,
pirimiphos­
methyl
(
97.8%
a.
i.)
was
administered
in
corn
oil
to
52
CFLP
mice/
sex/
group
at
dietary
levels
of
0,
5,
250
or
500
ppm
(
equivalent
to
0,
0.5,
25.9
or
45.0
mg/
kg/
day
for
males
and
0,
0.6,
27.6
or
50.6
mg/
kg/
day
for
females,
respectively)
for
80
weeks.
With
the
exception
of
250
ppm
dose
group,
each
group
consisted
of
12
additional
animals
for
cholinesterase
determination.
The
test
diet
for
the
highest
dose
groups
initially
contained
300
ppm
of
the
test
compound
(
the
duration
of
treatment
was
not
specified).
The
dose
was
then
increased
weekly
by
50
ppm
to
500
ppm.
No
brain
ChE
levels
were
measured.
At
500
ppm,
non­
progressive
but
marked
and
consistent
dose­
related
inhibition
of
activity
was
noted
in
RBC
ChE
(
84%
in
males
and
86%
in
females)
and
plasma
ChE
(
83%
in
males
and
85%
in
females).
At
5
ppm,
there
was
non­
significant
inhibition
in
RBC
ChE
(
30%
in
males
only)
while
only
borderline
but
statistically
significant
inhibition
of
plasma
ChE
activity
(
10%
in
males
and
22
%
in
females)
was
noted
compared
to
controls.
Gross
and
histopathological
examination
provided
no
evidence
indicating
altered
spontaneous
tumor
profile
of
the
CFLP
mouse.
The
systemic
LOEL
was
5
ppm
based
on
RBC
ChE
inhibition
in
males
(
0.5
mg/
kg/
day)
and
plasma
ChE
inhibition
in
females
(
0.6
mg/
kg/
day).
No
NOEL
was
established.
This
study
is
classified
as
Unacceptable
/
guideline
and
does
not
satisfy
the
guideline
requirements
of
a
carcinogenicity
study
in
mice
(
83­
2b)
(
MRID92147032).
However,
this
requirement
is
already
satisfied
by
the
recent
mouse
study
with
MRID
43968401.

I
n
response
to
EPA
data
call­
ins,
Agriliance
generated
and
submitted
the
following
studies
to
update
the
database
of
studies
supporting
pirimiphos­
methyl.
These
studies
have
not
to
date
been
evaluated
by
EPA.
It
is
not
anticipated
that
these
data
will
change
the
risk
assessment
or
terms
of
registration
of
pirimiphos­
methyl.
MRID
Subject
45717501
chronic
dog
(
capsule)
46193801
2
year
chronic/
carcinogenicity
rats
6.
Animal
metabolism.
Pirimiphos­
methyl
is
rapidly
absorbed,
metabolized
and
excreted
in
rats
and
dogs.
In
both
species,
2­
ethylamino­
4­
hydroxy­
6­
methylpyrimidine
is
the
major
metabolite.
The
metabolism
of
pirimiphos­
methyl
involves
extensive
cleavage
of
P­
O
bond
followed
by
N­
dealkylation
and
/
or
conjugation
resulting
in
a
loss
of
pyrimidine
group.
In
rats
given
a
single
oral
dose
of
(
2­
14Cpyrimidine
labelled
pirimiphos­
methyl
at
7.5
mg/
kg,
there
was
rapid
uptake
of
radioactivity
into
the
blood
and
was
followed
by
its
subsequent
disappearance
from
the
blood
(
MRID
00080739).
Greater
than
50%
of
the
radioactivity
present
in
the
blood,
30
minutes
after
the
dosing,
had
disappeared
1­
hr
post­
dosing.
Further
daily
dosing
of
the
labelled
compound
for
a
subsequent
3
days
did
not
increase
the
total
radioactive
residues
in
the
blood.
When
administered
for
4
days,
total
radioactive
residues
in
the
liver,
kidney
and
fat
did
not
exceed
2
mg/
kg
pirimiphos­
methyl
equivalents.
Only
small
amounts
of
unchanged
parent
compound
were
detected
in
the
fat
(
0.15
mg/
kg)
and
in
the
liver
and
kidneys
(
0.1
mg/
kg).
These
studies
provide
no
evidence
of
accumulation
of
parent
or
metabolites
in
the
liver,
kidney
or
adipose
tissue
of
rats
following
daily
dosing
with
pirimiphos­
methyl
over
4
days.
When
rats
were
administered
0.6
mg/
kg
of
14C­
ring
(
2­
C14­
pyrimidine)
labelled
pirimiphos­
methyl
orally
or
intraperitoneally,
73­
81%
of
the
dose
was
excreted
in
the
urine
within
the
first
24
hours,
indicating
rapid
absorption,
metabolism
and
excretion.
At
120
hr.
following
administration
of
a
single
oral
dose,
86%
and
15.2%
of
the
administered
dose
was
recovered
in
the
urine
and
feces,
respectively.
Following
intraperitoneal
administration,
the
excretion
was
similar
but
slower.
Dogs
administered
larger
doses
(
17­
18
mg/
g)
orally
also
excreted
most
of
the
material
in
the
urine
during
the
first
24­
48
hours
(
Bratt
and
Dudley,
1970
cited
in
1974
Evaluations
of
some
pesticide
residues
in
food).
Using
thin
layer
chromatography,
a
total
of
twelve
metabolites
were
identified
in
the
urine
of
the
two
species
following
single
p.
o.
doses
(
rats
100
mg/
kg;
dog
20
mg/
kg).
No
unchanged
parent
compound
was
detected
in
the
urine
and
none
of
the
metabolites
had
anticholinesterase
activity.
Five
of
the
twelve
metabolites
were
identified
using
authentic
standards.
In
both
species,
2­
ethylamino­
4­
hydroxy­
6­
methylpyrimidine
was
the
major
urinary
metabolite
(
30%
of
the
dose).
Another
most
predominant
metabolite
in
dog
was
4­
O­(
2­
diethylamine­
6­
methylpyrimidinyl)­
beta­
D­
glucosiduronic
acid
(
11%
of
dose),
and
in
the
rat
an
unidentified
phosphorus­
containing
product,
a
possible
dealkylated
derivative
of
either
pirimiphos­
methyl
or
its
oxygen
analogue
(
12%
of
dose).
Other
identified
urinary
metabolites
included
2­
amino­
4­
hydroxy­
6­
methylpyrimidine,
2[­
N­
ethyl­
N­(
2­
hydroxyethyl)
amino]­
4­
hydroxy­
6­
methylpyrimidine,
and
2­
diethylamino­
4­
hydroxy­
6­
methylpyrimidine
(
MRID
00080738,
00080739,
4365801).

7.
Metabolite
toxicology.
EPA
has
waived
the
requirement
for
data
on
toxcicity
of
metabolites
(
see
above).
8.
Endocrine
disruption.
Pirimiphos
­
methyl
is
not
anticipated
to
have
endocrine
effects,

C.
Aggregate
Exposure
1.
Dietary
exposure
i.
Food.
Acute
Dietary
(
Food)
Risk
Acute
dietary
risk
is
calculated
considering
what
is
eaten
in
one
day
(
in
this
instance,
the
individual
who
consumed
the
most)
and
maximum,
or
high­
end
residue
values
in
the
food.
A
risk
estimate
that
is
less
than
100%
of
the
acute
Reference
Dose
(
aRfD)
(
the
dose
at
which
an
individual
could
be
exposed
on
any
given
day
and
no
adverse
health
effects
would
be
expected)
does
not
exceed
the
Agency's
risk
concerns.
The
PAD
(
Population
Adjusted
Dose)
is
a
modification
of
the
acute
RfD
or
chronic
RfD
to
accommodate
the
FQPA
Safety
Factor.
The
PAD
is
equal
to
the
acute
or
chronic
RfD
divided
by
the
FQPA
Safety
Factor
or:
PAD
=
RfD
(
acute
or
chronic)
FQPA
Safety
Factor
Endpoint
was
based
on
an
acute
neurotoxicity
study
in
rats
(
17/
sex/
dose).
Test
groups
received
a
single
oral
administration
of
pirimiphos
methyl
in
corn
oil.
After
24
hours,
plasma
cholinesterase
inhibition
was
observed
in
both
sexes
in
rats
dosed
at
15
mg/
kg/
day,
the
lowest
dose
tested.
The
LOAEL
is
15
mg/
kg/
day.
Acute
RfD
=
0.015
mg/
kg/
day.

°
The
3X
safety
factor
has
been
retained
in
accordance
with
the
Food
Quality
Protection
Act
(
FQPA)
of
1996
due
to
the
lack
of
a
complete
toxicity
database
for
assessing
the
potential
for
increased
sensitivity
of
infants
and
children
to
pirimiphos­
methyl.
The
data
are
not
adequate
to
evaluate
neurotoxicity
following
acute
and
long­
term
exposure,
or
to
assess
the
functional
development
of
young
animals
and
in
turn
the
susceptibility
to
infants
and
children.
The
Uncertainty
Factor
(
UF)
includes
the
10x
for
intra­
species
variation,
10x
for
inter­
species
extrapolation,
and
10x
for
the
use
of
the
Lowest
Observed
Adverse
Effects
Level
(
LOAEL)
as
well
as
the
severity
of
effects
(
marked
plasma
as
well
as
RBC
and
brain
ChEI)
seen
at
the
lowest
dose
tested.

°
FQPA
Acute
Population
Adjusted
Dose
(
aPAD)
=
0.005
mg/
kg/
day.

°
Acute
dietary
exposure
is
based
on
the
distribution
of
consumption
found
in
the
Dietary
Exposure
Evaluation
Model
(
DEEM).
The
DEEM
software
estimates
chronic
dietary
exposure
to
pesticides
in
foods
based
on
the
3­
day
average
of
consumption
data
collected
in
USDA's
Continuing
Surveys
of
Food
Intake
by
Individuals,
1989­
1992.
Probabilistic
acute
analyses
were
also
conducted
using
distributions
of
consumption
and
distribution
of
residue
levels
from
residue
monitoring
data.

°
Three
different
acute
analyses
were
conducted.
The
Tier
1
dietary
risk
analyses
were
conducted
two
ways,
one
assuming
tolerance
level
residues
for
all
commodities
(
and
½
the
limit
of
detection
for
High
Fructose
Corn
Syrup
(
HFCS)),
and
one
assuming
HFCS
residues
equal
to
zero.
These
two
Tier
1
assessments
were
conducted
as
worst
case
scenarios.
HFCS
was
the
driver
in
the
preliminary
risk
assessment
and
therefore
its
contribution
had
to
be
thoroughly
assessed.

°
A
refined
Tier
3
analyses
was
conducted
four
ways
due
to
inconsistencies
in
usage
data
regarding
popcorn.
Anticipated
residue
values
were
calculated
for
all
commodities
using
PDP
and
FDA
monitoring
data,
(
ii)
Anticipated
Residues
from
residue
trials
conducted
on
grain;
and
(
iii)
Anticipated
residues
in
livestock
commodities.
The
anticipated
residue
values
were
held
constant
among
the
four
probabilistic
assessments
for
all
commodities
with
the
exception
of
popcorn.

°
Assessment
two
of
the
four
analyses
conducted
in
Tier
3
was
considered
to
be
the
most
realistic
and
uses
conservative
%
CT
values,
and
is
what
is
represented
in
table
1
as
the
probabilistic
analysis.
Children
1­
6
years
are
the
most
highly
exposed
population
subgroup
at
the
99.9th
percentile.

°
Use
of
revised
anticipated
residues
result
in
significant
reduction
of
the
dietary
exposure
and
risk
estimates
compared
to
those
in
the
preliminary
analysis.

Highly
refined
acute
dietary
risk
assessments
for
pirimiphos
methyl
result
in
risks
that
are
below
the
Agency
level
of
concern.

Chronic
Dietary
(
Food)
Risk
Chronic
dietary
risk
is
calculated
by
using
the
average
consumption
value
for
food
and
average
residue
values
on
those
foods
over
a
70­
year
lifetime.
A
risk
estimate
that
is
less
than
100%
if
the
chronic
RfD
(
the
dose
at
which
an
individual
could
be
exposed
over
the
course
of
a
lifetime
and
no
adverse
health
effects
would
be
expected)
does
not
exceed
the
Agency's
risk
concern.
°
Endpoint
was
based
on
a
subchronic
neurotoxicity
study
conducted
in
rats.
Test
groups
were
fed
diets
containing
pirimiphos­
methyl
at
dose
levels
of
0,
0.2,
2.1
or
21.1mg/
kg/
day
for
males
and
0,
0.2,
2.4
or
24.7
mg/
kg/
day
for
females,
respectively
for
90
days.
Plasma
cholinesterase
inhibition
(
ChEI)
was
observed
in
all
test
groups.
The
Lowest
Observed
Adverse
Effect
Level
(
LOAEL)
for
brain
and
RBC
ChEI
was
0.2
mg/
kg/
day.
Chronic
Reference
Dose
(
RfD)
is
0.0002
mg/
kg/
day.

°
The
3X
safety
factor
has
been
retained
in
accordance
with
the
Food
Quality
Protection
Act
(
FQPA)
of
1996
due
to
the
lack
of
a
complete
toxicity
database
for
assessing
the
potential
for
increased
sensitivity
of
infants
and
children
to
pirimiphos­
methyl.
The
data
are
not
adequate
to
evaluate
neurotoxicity
following
acute
and
long­
term
exposure,
or
to
assess
the
functional
development
of
young
animals
and
in
turn
the
susceptibility
to
infants
and
children.
The
Uncertainty
Factor
(
UF)
includes
the
10x
for
intra­
species
variation,
10x
for
inter­
species
extrapolation,
and
10x
for
the
use
of
the
Lowest
Observed
Adverse
Effects
Level
(
LOAEL)
as
well
as
the
severity
of
effects
(
marked
plasma
as
well
as
RBC
and
brain
ChEI)
seen
at
the
lowest
dose
tested.

°
FQPA
Chronic
Population
Adjusted
Dose
(
cPAD)
=
0.00007
mg/
kg/
day.

°
Chronic
dietary
exposure
is
based
on
the
distribution
of
consumption
found
in
the
Dietary
Exposure
Evaluation
Model
(
DEEM).
The
DEEM
software
estimates
chronic
dietary
exposure
to
pesticides
in
foods
based
on
the
3­
day
average
of
consumption
data
collected
in
USDA's
Continuing
Surveys
of
Food
Intake
by
Individuals,
1989­
1992.
Probabilistic
acute
analyses
were
also
conducted
using
distributions
of
consumption
and
distribution
of
residue
levels
from
residue
monitoring
data.

°
Three
different
chronic
analyses
were
conducted.
The
Tier
1
dietary
risk
analyses
were
conducted
two
ways,
one
assuming
tolerance
level
residues
for
all
commodities
(
and
½
the
limit
of
detection
for
High
Fructose
Corn
Syrup
(
HFCS),
and
one
assuming
HFCS
residues
equal
to
zero.
These
two
Tier
1
assessments
were
conducted
as
worst
case
scenarios.
HFCS
was
the
driver
in
the
preliminary
risk
assessment
and
therefore
its
contribution
had
to
be
thoroughly
assessed
(
See
Table
2
on
the
following
page).

°
A
refined
Tier
3
analyses
was
conducted
four
ways
due
to
inconsistencies
in
usage
data
regarding
popcorn.
Anticipated
residue
values
were
calculated
for
all
commodities
using
PDP
and
FDA
monitoring
data,
(
ii)
Anticipated
Residues
from
residue
trials
conducted
on
grain;
and
(
iii)
Anticipated
residues
in
livestock
commodities.
The
anticipated
residue
values
were
held
constant
among
the
four
probabilistic
assessments
for
all
commodities
with
the
exception
of
popcorn.

°
Assessment
two
of
the
four
analyses
conducted
in
Tier
3
was
considered
to
be
the
most
realistic
and
uses
conservative
%
CT
values,
and
is
what
is
represented
in
table
1
as
the
probabilistic
analysis.
Children
1­
6
years
are
the
most
highly
exposed
population
subgroup
at
99.9th
percentile.

°
Use
of
revised
anticipated
residues
result
in
significant
reduction
of
the
dietary
exposure
and
risk
estimates
compared
to
those
in
the
preliminary
analysis.

°
Highly
refined
chronic
dietary
risk
assessments
for
pirimiphos
methyl
generally
result
in
risks
that
are
below
the
Agency's
level
of
concern.

ii.
Drinking
water.
Drinking
water
exposure
to
pesticides
can
occur
through
groundwater
and
surface
water
contamination.
EPA
considers
both
acute
(
one
day)
and
chronic
(
lifetime)
drinking
water
risks
and
uses
either
modeling
or
actual
monitoring
data,
if
available,
to
estimate
those
risks.
Modeling
is
considered
to
be
an
unrefined
assessment
and
provides
a
high­
end
estimate.
To
determine
the
maximum
allowable
contribution
of
treated
water
allowed
in
the
diet,
EPA
first
looks
at
how
much
of
the
overall
allowable
risk
is
contributed
by
food,
then
determines
a
"
drinking
water
level
of
comparison."

Since
there
are
no
outdoor
uses
which
would
result
in
water
contamination
associated
with
pirimiphosmethyl
use,
a
drinking
water
risk
assessment
was
not
conducted
on
this
organophosphate.
Based
on
uses
supported
through
reregistration,
human
health
risk
is
associated
with
potential
exposure
to
pirimiphos­
methyl
only
through
consumption
of
treated
crops
and
livestock
commodities,
and
in
occupational
settings.

2.
Non­
dietary
exposure.
HED
has
not
identified
any
homeowner
handler
or
residential
postapplication
scenarios.
As
such,
exposure
assessments
have
been
completed
for
occupational
handler
and
post­
application
scenarios.

D.
Cumulative
Effects
Since
drinking
water
and
residential
exposure
are
consider
to
be
negligible,
no
risk
assessment
has
been
considered
necessary.

E.
Safety
Determination
1.
U.
S.
population.

Following
implementation
of
risk
mitigation
measures
directed
in
the
iRED,
(
June
2001),
EPA
considers
that
the
risk
associated
with
the
use
of
pirimiphos­
methyl
according
to
revised
requirements
will
not
be
in
excess
of
that
permitted
under
FQPA.,
i.
e.
"
there
is
a
reasonable
certainty
of
no
harm".
2.
Infants
and
children.
The
FQPA
Safety
Factor
of
3X
has
been
retained
in
accordance
with
the
Protection
Act
(
FQPA)
of
1996
due
to
the
lack
of
a
complete
toxicity
database
potential
for
increased
sensitivity
of
infants
and
children
to
pirimiphos­
methyl.
necessary
to
complete
the
toxicity
database
include:
a
chronic
toxicity
study
in
and
a
combined
chronic
toxicity/
carcinogenicity
study
in
rats
(
870.4300).
As
well,
indication
of
additional
sensitivity
to
young
rats
or
rabbits
following
pre
and/
or
pirimiphos­
methyl
in
the
developmental
and
reproductive
toxicity
studies.

F.
International
Tolerances
Numerous
international
tolerances
exist
for
pirimiphos
methyl
in
a
wide
variety
of
crops.
No
MRLs
are
listed
for
Canada
or
Mexico
in
the
NAFTA
MRL
database.
The
most
significant
listings
are
for
Codex
Alimentarius,
European
Union,
and
Japan.
These
are
summarized
below:

Commodity
MRL
(
mg/
kg
)

Codex
Alimentarius
Cereal
grains
7
Edible
offal
(
mammalian)
0.01
Eggs
0.01
Meat
(
from
mammals)
0.01
Milks
0.01
Poultry
meat
0.01
Poultry,
Edible
offal
of
0.01
Wheat
bran,
Unprocessed
15
European
Union
Citrus
Fruit
Others
1
Grapefruit
1
Lemons
1
Limes
1
Mandarins
2
Oranges
1
Pomelo
1
Almonds
0,05
Brazil
Nuts
0,05
Cashew
Nuts
0,05
Chestnuts
0,05
Coconuts
0,05
Hazelnuts
0,05
Macadamia
Nuts
0,05
Pecans
0,05
Pine
Nuts
0,05
Pistachios
0,05
Tree
Nuts
Others
0,05
Walnuts
0,05
Apples
0,05
Pears
0,05
Pome
Fruit
Others
0,05
Quinces
0,05
Apricots
0,05
Cherries
0,05
Peaches
0,05
Plums
0,05
Stone
Fruit
Others
0,05
Bilberries
0,05
Blackberries
0,05
Cane
Fruit
Others
0,05
Cranberries
0,05
Currants
(
Black,
Red
and
White)
0,05
Dewberries
0,05
Gooseberry
0,05
Loganberries
0,05
Small
Fruit
and
Berries­
Others
0,05
Raspberries
0,05
Strawberries
0,05
Table
Grapes
0,05
Wild
Berries
and
Wild
Fruit
0,05
Wine
Grapes
2
Avocados
0,05
Bananas
0,05
Dates
0,05
Figs
0,05
Kiwi
Fruit
2
Kumquats
0,05
Litchis
0,05
Mangoes
0,05
Miscellaneous
Fruit
Others
0,05
Olives
0,05
Passion
Fruit
0,05
Pineapples
0,05
Pomegranates
0,05
Beetroot
0,05
Carrots
1
Celeriac
0,05
Horseradish
0,05
Jerusalem
artichoke
0,05
Parsley
root
0,05
Parsnips
0,05
Radishes
0,05
Root
and
Tuber
Vegetables
others
0,05
Salsify
0,05
Swedes
0,05
Sweet
potato
0,05
Turnip
0,05
Yams
0,05
Bulb
Vegetables
others
0,05
Garlic
0,05
Onions
0,05
Shallots
0,05
Spring
onion
0,05
Aubergine
0,05
Courgettes
0,05
Cucumbers
0,1
Cucurbits
edible
peel
others
0,05
Cucurbits
inedible
peel
others
0,05
Gherkins
0,05
Melons
1
Peppers
1
Solanacea
others
0,05
Squashes
0,05
Sweet
corn
0,05
Tomatoes
1
Watermelons
0,05
Broccoli
1
Brussels
sprouts
2
Cauliflower
1
Chinese
cabbage
0,05
Flowering
brassicas
others
1
Head
brassicas
others
0,05
Head
cabbages
0,05
Kale
0,05
Kohlrabi
0,05
Leafy
brassicas
others
0,05
Beet
leaves
(
chard)
0,05
Celery
leaves
0,05
Chervil
0,05
Chives
0,05
Cress
0,05
Herbs
others
0,05
Lamb's
lettuce
0,05
Lettuce
0,05
Lettuce
and
similar
others
0,05
Parsley
0,05
Scarole
0,05
Spinach
0,05
Spinach
and
similar
(
others)
0,05
Watercress
0,05
Witloof
(
Belgian
endives)
0,05
Beans
(
with
pods)
0,05
Beans
(
without
pods)
0,05
Legume
vegetables
fresh
others
0,05
Peas
(
with
pods)
0,05
Peas
(
without
pods)
0,05
Asparagus
0,05
Cardoons
0,05
Celery
0,05
Fennel
0,05
Globe
artichoke
0,05
Leeks
0,05
Rhubarb
0,05
Stem
vegetables
fresh
others
0,05
Cultivated
mushrooms
2
Wild
mushrooms
0,05
Beans
0,05
Lentils
0,05
Peas
0,05
Pulses
others
0,05
Cotton
seed
0,05
Linseed
0,05
Mustard
seed
0,05
Oilseeds
others
0,05
Peanuts
0,05
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Poppy
seeds
0,05
Rapeseed
0,05
Sesame
seeds
0,05
Soya
bean
0,05
Sunflower
seeds
0,05
Early
potatoes
0,05
Ware
potatoes
0,05
Tea
0,05
Hops
(
dried)
0,05
Barley
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Buckwheat
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Cereals
others
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Maize
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Millet
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Oats
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Rice
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Rye
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Sorghum
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Triticale
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
Wheat
5
(
MRL
Codex
accommodates
postharvest
treatment
of
the
commodity.)
MEAT
0201
Bovine
0,05
MEAT
0202
Bovine,
frozen
0,05
MEAT
0203
Swine
0,05
MEAT
0204
Sheep
or
goats
0,05
MEAT
0205
00
00
Horses,
asses,
mules,...
0,05
EDIBLE
OFALL
0206
Bovines,
swine,
sheep,
goats,..
.
0,05
FAT
0209
00
Pig
&
poultry
0,05
MEAT,
OFFAL
&
BLOOD
1601
00
Sausage
&
similar
0,05
MEAT,
OFFAL
&
BLOOD
1602
Meat
offal
or
blood
(
others)
0,05
MEAT
&
EDIBLE
OFFAL
0207
Poultry
of
heading
N
°
0105
0,05
MEAT
&
EDIBLE
OFFAL
0210
Edible
flours
&
meals;...
0,05
MEAT
&
EDIBLE
OFFAL
ex0208
Oth.
meat
&
edible
meat
offal
0,05
DAIRY
0401Milk
&
cream
0,05
DAIRY
0402
Milk
&
cream
0,05
DAIRY
0405
00
Butter,
other
fats,
oils...
0,05
DAIRY
0406
Cheese
&
curd
0,05
EGG
0407
00
Eggs
in
shell
0,05
EGG
0408
Eggs
(
not
in
shell)
&
yolks
0,05
Japan:

VEGETABLES
1.00
Except
...
Cauliflowers
5.00
Cucumbers
2.00
Melons
(
not
Watermelons)
0.10
Eggplants
3.00
Tomatoes
2.00
Beans
1.00
Peas
1.00
Potatoes
0.05
CITRUS
5.00
Except...
Mandarins
0.10
POME
FRUIT
1.00
Apricots
1.00
Cherries
1.00
Nectarines
0.10
Peaches
0.10
Plums
1.00
Blueberries
0.10
Currants
1.00
Gooseberries
1.00
Blackberries
0.10
Raspberries
1.00
Grapes
1.00
Strawberries
1.00
Avocados
0.10
Feijoas
1.00
Kiwifruit
1.00
Passionfruit
0.10
Persimmons
1.00
Tamarillos
1.00
CEREAL
GRAINS
1.00
