Interregional
Research
Project
No.
4
(
IR­
4)

PP#
4E6848
Summary
of
Petitions
EPA
has
received
a
pesticide
petition
(
4E6848)
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
180.493
by
establishing
a
tolerance
for
residues
of
dimethomorph
[(
E,
Z)
4­[
3­(
4­
chlorophenyl)­
3­(
3,4­
dimethoxyphenyl)­
1­
oxo­
2­
propenyl]­
morpholine]
in
or
on
the
raw
agricultural
commodity
Brassica
head
and
stem
(
Subgroup
5A)
at
2.0
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.
[
Based
upon
the
results
of
metabolism
studies
conducted
on
potato,
grape,
and
lettuce,
the
nature
of
the
residues
in
brassica,
head
and
stem
(
Subgroup
5A)
is
considered
to
be
understood.
The
results
of
the
potato
metabolism
study
show
only
negligible
residues
in
tubers,
0.01­
0.02
parts
per
million
(
ppm)
total
radioactive
residues
(
TRR).
This
is
in
contrast
to
the
aerial
portions
of
the
plant,
which
were
found
to
have
up
to
23.5
ppm
TRR,
thus
demonstrating
that
translocation
of
dimethomorph
downward
within
the
plant
was
not
significant.
Almost
all
of
the
radioactive
residue
(
97.8%)
was
extractable
from
the
plant
at
harvest.
In
the
aerial
portion
of
the
plant,
approximately
70%
of
the
TRR
was
identified
as
dimethomorph.
No
metabolites
were
identified
that
require
regulation.
The
results
of
the
grape
metabolism
study
showed
that
the
TRR
in/
on
grapes
harvested
35
days
following
the
last
of
four
applications
[
0.8
lb
active
ingredient
per
acre
(
ai/
A)
per
application
for
four
consecutive
weeks]
for
a
total
rate
of
3.2
lb
ai/
A
was
14.6
ppm.
Unmetabolized
dimethomorph
accounted
for
87.3%
of
the
TRR
(
12.7
ppm).
No
metabolites
were
identified
that
require
regulation.
The
results
of
the
lettuce
metabolism
study
showed
that
the
TRR
in/
on
lettuce
leaves
harvested
4
days
following
the
last
of
4
applications
[
approximately
1.0
lb
ai/
A
per
application
with
a
9
to
11
day
spray
interval],
for
a
total
rate
of
4.1
lb
ai/
A,
was
102
ppm.
Of
this
total
residue,
98.5%
was
extractable
and
unmetabolized
dimethomorph
accounted
for
greater
than
93%
of
the
extractable
TRR.
No
metabolites
were
identified
that
require
regulation.]

2.
Analytical
method.
[
A
reliable
method
for
the
determination
of
dimethomorph
residues
in
brassica,
head
and
stem
(
Subgroup
5A
exists;
this
method
is
the
FDA
Multi­
Residue
Method,
Protocol
D,
as
published
in
the
Pesticide
Analytical
Manual
I.]
3.
Magnitude
of
residues.
[
The
residue
data
for
Brassica,
head
and
stem
(
Subgroup
5A)
submitted
to
support
this
tolerance
petition
were
collected
from
7
cabbage
(
head)
and
6
broccoli
(
stem)
studies
conducted
in
cabbage
and
broccoli
producing
regions
of
the
United
States.
Trials
were
conducted
using
multiple
applications
(
7)
of
dimethomorph
applied
at
0.2
lb
ai/
A
with
a
maximum
seasonal
rate
of
1.4
lb
ai/
A
(
1.4X
the
proposed
label
rate).
Dimethomorph
residues
observed
in
these
field
trials
for
cabbage
ranged
from
<
0.05
ppm
to
1.52
ppm
when
harvested
7
days
after
the
last
application
and
for
broccoli
ranged
from
0.12
ppm
to
0.52
ppm
when
harvested
7
days
after
the
last
application.

Therefore,
a
tolerance
of
2.0
ppm
in
or
on
brassica,
head
and
stem
(
Subgroup
5A)
is
proposed.]

B.
Toxicological
Profile
1.
Acute
toxicity.
[
i.
Oral
LD50
studies
were
conducted
on
dimethomorph
technical:
a.
An
acute
oral
toxicity
study
in
the
Sprague­
Dawley
rat
for
dimethomorph
technical
with
a
LD50
of
4,300
milligrams/
kilogram
body
weight
(
mg/
kg
b.
w.)
for
males
and
3,500
mg/
kg
b.
w.
for
females.
Based
upon
EPA
toxicity
criteria,
the
acute
oral
toxicity
category
for
dimethomorph
technical
is
Category
III
or
slightly
toxic.
b.
An
acute
toxicity
study
in
the
CD­
1
mouse
for
dimethomorph
technical
with
a
LD50
of
greater
than
5000
mg/
kg
b.
w.
for
males
and
3699
mg/
kg/
b.
w.
for
females.
Based
on
the
EPA
toxicity
category
criteria,
the
acute
oral
toxicity
category
for
dimethomorph
technical
is
Category
III
or
slightly
toxic.
ii.
Oral
LD50
studies
were
conducted
on
the
two
isomers
(
E
and
Z)
alone:
a.
An
acute
oral
toxicity
study
in
the
Wistar
rat
for
the
E­
isomer
with
a
LD50
greater
than
5,000
mg/
kg
b.
w.
for
males
and
approximately
5,000
mg/
kg
b.
w.
for
females.
b.
An
acute
oral
toxicity
study
in
the
Wistar
rat
for
the
Z­
isomer
with
a
LD50
greater
than
5,000
mg/
kg
b.
w.
for
both
males
and
females.
iii.
An
acute
dermal
toxicity
study
in
the
Wistar
rat
for
dimethomorph
technical
with
a
dermal
LD50
greater
than
5,000
mg/
kg
b.
w.
for
both
males
and
females.
Based
on
the
EPA
toxicity
category
criteria,
the
acute
dermal
toxicity
category
for
dimethomorph
is
Category
IV
or
relatively
non­
toxic.
iv.
A
4­
hour
inhalation
study
in
Wistar
rats
for
dimethomorph
technical
with
a
LC50
greater
than
4.2
mg/
L
for
both
males
and
females.
Based
on
the
EPA
toxicity
category
criteria,
the
acute
inhalation
toxicity
category
for
dimethomorph
technical
is
Category
IV
or
relatively
non­
toxic.
v.
A
skin
irritation
study
was
performed
using
New
Zealand
White
rabbits.
Based
on
the
EPA
toxicity
criteria,
the
skin
irritation
toxicity
category
for
dimethomorph
technical
in
this
study
is
Category
IV
or
non­
to­
slightly
irritating.
vi.
An
eye
irritation
study
using
New
Zealand
White
rabbits
demonstrated
dimethomorph
technical
produced
moderate
conjunctival
redness,
slight
to
moderate
chemosis
and
slight
discharge
three
hours
after
treatment.
Based
on
the
EPA
toxicity
criteria,
the
eye
toxicity
category
for
dimethomorph
technical
is
Category
III
(
slightly­
to­
moderately
irritating)]
2.
Genotoxicty.
[
i.
Salmonella
reverse
gene
mutation
assays
(
2
studies)
were
negative
up
to
a
limit
dose
of
5,000
µ
g/
plate.
Chinese
hamster
lung
V79
cells
were
negative
for
mutations
at
the
HGPRT
locus
at
up
to
toxic
doses
in
two
studies.
ii.
Two
Chinese
hamster
lung
(
V79
cells)
structural
chromosomal
studies
were
reportedly
positive
for
chromosomal
aberrations
at
the
highest
dose
tested
(
HDT)
(
160
µ
g/
ml/­
S9;
170
µ
g/
ml/+
S9).
However,
dimethomorph
induced
only
a
weak
response
in
increasing
chromosome
aberrations
in
this
test
system.
In
addition,
these
results
were
not
confirmed
in
two
micronucleus
tests
under
in
vivo
conditions.
iii.
Structural
Chromosomal
Aberration
studies
were
weakly
positive
in
human
lymphocytic
cultures,
but
only
in
S9
activated
cultures
treated
at
422
µ
g/
ml,
the
highest
dose
tested
(
HDT),
which
was
strongly
cytotoxic.
No
increase
in
chromosomal
aberrations
was
observed
in
the
absence
of
S9
activation
at
all
doses.
Furthermore,
the
positive
clastogenic
response
observed
under
the
in
vitro
conditions
was
not
confirmed
in
two
in
vivo
micronucleus
assays.
iv.
Micronucleus
assay
(
2
studies)
indicated
that
dimethomorph
was
negative
for
inducing
micronuclei
in
bone
marrow
cells
of
mice
following
i.
p.
administration
of
doses
up
to
200
mg/
kg
or
oral
doses
up
to
the
limit
dose
of
5,000
mg/
kg.
Thus,
dimethomorph
was
found
to
be
negative
in
these
studies
for
causing
cytogenic
damage
in
vivo.
v.
Dimethomorph
was
negative
for
inducing
unscheduled
DNA
synthesis,
in
cultured
rat
liver
cells,
at
doses
up
to
250
µ
g/
ml,
a
weakly
cytotoxic
level.
Dimethomorph
was
negative
for
transformation
in
Syrian
hamster
embryo
cells
treated,
in
the
presence
and
absence
of
activation,
up
to
cytotoxic
concentrations
(
265
µ
g/
ml/+
S9;
50
µ
g/
ml/­
S9).]

3.
Reproductive
and
developmental
toxicity.
[
i.
A
rat
developmental
toxicity
study
with
a
Lowest­
Observed­
Effect
Level
(
LOEL)
for
maternal
toxicity
of
160
mg/
kg/
day
and
a
No­
Observed­
Effect
Level
(
NOEL)
for
maternal
toxicity
of
60
mg/
kg/
day.
The
NOEL
for
developmental
toxicity
is
60
mg/
kg/
day.
Dimethomorph
is
not
teratogenic
in
the
Sprague­
Dawley
rat.
ii.
A
rabbit
development
toxicity
study
with
a
LOEL
for
maternal
toxicity
of
650
mg/
kg/
day
and
a
NOEL
for
maternal
toxicity
of
300
mg/
kg/
day.
The
NOEL
for
developmental
toxicity
is
650
mg/
kg/
day,
the
highest
dose
tested.
Dimethomorph
is
not
teratogenic
in
the
New
Zealand
white
rabbit.
iii.
A
two­
generation
rat
reproduction
study
with
a
LOEL
for
parental
systemic
toxicity
of
1000
ppm,
or
approximately
80
mg/
kg/
day,
and
a
NOEL
for
parental
systemic
toxicity
of
300
ppm,
or
approximately
24
mg/
kg/
day.
The
NOEL
for
fertility
and
reproductive
function
was
1000
ppm,
the
highest
concentration
tested,
or
approximately
80
mg/
kg
b.
w./
day.]

4.
Subchronic
toxicity.
[
i.
A
90­
day
dietary
study
in
Sprague­
Dawley
rats
with
a
NOEL
of
greater
than
or
equal
to
1000
ppm,
the
highest
concentration
tested,
or
approximately
73
mg/
kg/
day
for
males
and
82
mg/
kg/
day
for
females.
ii.
A
90­
day
dog
dietary
study
with
a
NOEL
of
450
ppm,
or
approximately
15
mg/
kg/
day,
and
a
LOEL
of
1350
ppm,
or
approximately
43
mg/
kg/
day.]

5.
Chronic
toxicity.
[
i.
A
2­
year
chronic
toxicity
study
in
Sprague­
Dawley
rats
with
a
NOEL
of
200
ppm
or
approximately
9
mg/
kg/
day
for
males
and
12
mg/
kg/
day
for
females.
The
LOEL
for
systemic
toxicity
is
750
ppm,
or
approximately
36
mg/
kg/
day
for
males
and
58
mg/
kg/
day
for
females.
ii.
A
1­
year
chronic
toxicity
study
in
dogs
with
a
NOEL
of
450
ppm,
or
approximately
14.7
mg/
kg/
day
and
a
LOEL
of
1350,
or
approximately
44.6
mg/
kg/
day.
iii.
A
2­
year
oncogenicity
study
in
Sprague­
Dawley
rats
with
a
NOEL
for
systemic
toxicity
of
200
ppm,
or
approximately
9
mg/
kg/
day
for
males
and
11
mg/
kg/
day
for
females.
The
LOEL
for
systemic
toxicity
was
750
ppm,
or
approximately
34
mg/
kg/
day
for
males
and
46
mg/
kg/
day
for
females.
There
was
no
evidence
of
increased
incidence
of
neoplastic
lesions
in
treated
animals.
The
NOEL
for
oncogenicity
is
2000
ppm,
the
highest
concentration
tested,
or
approximately
95
mg/
kg/
day
for
males
and
132
mg/
kg/
day
for
females.
iv.
A
2­
year
oncogenicity
study
in
CD­
1
mice
with
a
NOEL
for
systemic
toxicity
of
100
mg/
kg/
day
and
a
LOEL
of
1,000
mg/
kg/
day.
There
was
no
evidence
of
increased
incidence
of
neoplastic
lesions
in
treated
animals.
The
NOEL
for
oncogenicity
is
1,000
mg/
kg/
day,
the
highest
dose
tested.]

6.
Animal
metabolism.
[
Results
from
the
livestock
and
rat
metabolism
studies
show
that
orally
administered
dimethomorph
was
rapidly
excreted
by
the
animals.
The
principal
route
of
elimination
is
the
feces.]

7.
Metabolite
toxicology.
[
There
were
no
metabolites
identified
in
plant
or
animal
commodities
which
require
regulation.]

8.
Endocrine
disruption.
[
Collective
organ
weights
and
histopathological
findings
from
the
two­
generation
reproduction
study
in
rats,
as
well
as
from
the
subchronic
and
chronic
toxicity
studies
in
two
or
more
animal
species,
demonstrate
no
apparent
estrogenic
effects
or
effects
on
the
endocrine
system.
There
is
no
information
available
that
suggests
that
dimethomorph
technical
would
be
associated
with
endocrine
effects.]

C.
Aggregate
Exposure
1.
Dietary
exposure.
[
An
assessment
was
conducted
to
evaluate
the
potential
risk
due
to
chronic
dietary
exposure
of
the
U.
S.
population
and
sub­
populations
to
residues
of
dimethomorph.
Tolerance
values
have
previously
been
established
for
grape;
grape,
raisin;
hop,
dried
cones;
lettuce,
head;
lettuce,
leaf;
potato,
wet
peel;
vegetable,
bulb,
group
3;
and
vegetable,
cucurbit,
group
9
and
are
listed
in
U.
S.
40
CFR
§
180.493.
The
EPA
recently
established
additional
tolerances
for
dimethomorph
in
brassica,
leafy
greens,
subgroup
5B;
taro,
corm;
taro,
leaves;,
and
vegetable,
fruiting,
group
8
and
are
listed
in
the
Federal
Register,
Volume
168,
No.
188
page
55826.
This
analysis
included
the
crops
with
established
tolerance
values
and
proposed
crop
tolerances
for
Brassica,
head
and
stem,
subgroup
5A.
The
proposed
tolerance
for
subgroup
5A
is
2.0
ppm.]

i.
Food.
[
Acute
Dietary
Exposure
Assessment
An
acute
assessment
was
not
needed
since
the
U.
S.
EPA
Toxicological
Endpoint
Selection
(
TES)
Committees
had
previously
evaluated
the
dimethomorph
toxicity
data,
including
developmental
and
maternal
toxicity
in
the
developmental
toxicity
studies
and
determined
there
was
no
toxicologic
endpoints
for
acute
dietary
exposure
and
a
quantitative
acute
dietary
exposure
and
risk
assessment
were
not
required.

Chronic
Dietary
Exposure
Assessment
A
Tier
1
chronic
dietary
exposure
assessment
was
conducted
assuming
tolerance
level
residues
and
100%
crop
treated
factors
for
all
registered
and
proposed
crops.
The
EPA
Food
Commodity
Ingredient
Database
(
FCID)
was
also
used
in
Exponent's
Dietary
Exposure
Evaluation
Module
(
DEEM­
FCID)
software.
Inadvertent
residues
in
animal
commodities
(
i.
e.
meat,
meat
byproducts,
milk,
eggs)
were
not
considered
as
a
result
of
grain
forage
since
studies
have
shown
dimethomorph
does
not
accumulate
in
animal
tissues
or
milk
and
tolerance
values
for
these
commodities
are
not
required
by
the
EPA.

Dietary
exposure
estimates
were
compared
against
the
established
dimethomorph
chronic
Population
Adjusted
Dose
(
cPAD)
of
0.11
mg/
kg
b.
w./
day
for
all
populations.
Results
of
the
chronic
dietary
assessments
are
listed
in
the
table
below.
The
estimated
chronic
dietary
exposure
from
crops
(
both
established
and
proposed
tolerances)
was
less
than
16.0
%
of
the
cPAD
for
all
subpopulations.
Additional
refinements
such
as
the
use
of
anticipated
residues
would
further
reduce
the
estimated
chronic
dietary
exposure.
The
results
in
the
Table
below
demonstrate
that
there
are
no
safety
concerns
for
any
subpopulation
based
on
established
and
new
uses,
and
that
the
results
clearly
meet
the
FQPA
standard
of
reasonable
certainty
of
no
harm.

Table
1.
Summary
of
Chronic
Dietary
Exposure
Assessment
considering
crops
with
established
and
proposed
tolerances
for
Dimethomorph.
Population
Subgroups
Exposure
Estimate
(
mg/
kg
b.
w./
day)
%
cPAD
U.
S.
Population
0.007113
6.5
All
Infants
(<
1
yr
old)
0.004183
3.8
Children
1­
2
years
0.016758
15.2
Children
3­
5
years
0.013179
12.0
Children
6
 
12
years
0.007767
7.1
Youth
13­
19
years
0.005788
5.3
Females
13­
49
years
0.006111
5.6
Adults
20­
49
years
0.006555
6.0
Adults
50+
years
0.00626
5.6
%
cPAD
=
percent
of
chronic
population
adjusted
dose
Exposure
estimates
based
on
tolerance
values,
percent
crop
treated
values
for
established
crop
tolerances,
100%
CT
for
crops
with
proposed
tolerances
]

ii.
Drinking
water.
[
Since
the
models
used
are
considered
to
be
screening
tools
in
the
risk
assessment
process,
the
Agency
does
not
use
estimated
environmental
concentrations
(
EECs)
from
these
models
to
quantify
drinking
water
exposure
and
risk
as
a
%
RfD
or
%
PAD.
Instead,
drinking
water
levels
of
comparison
(
DWLOCs)
are
calculated
and
used
as
points
of
comparison
against
the
model
estimates
of
a
pesticide's
concentration
in
water.
A
DWLOC
is
the
theoretical
upper
allowable
limit
of
a
pesticide's
concentration
in
drinking
water
and
is
calculated
with
considering
the
aggregate
exposure
to
a
pesticide
from
food
and
residential
uses.
A
DWLOC
will
vary
depending
on
the
toxic
endpoint,
drinking
water
consumption,
body
weights,
and
pesticide
uses.

Different
populations
will
have
different
DWLOCs.
If
the
DWLOC
is
greater
than
the
model
water
concentrations,
the
EPA
concludes
that
exposure
from
drinking
water
is
not
a
risk
issue.
The
modeled
water
concentration
is
obtained
from
PRZM/
EXAMS
model
for
surface
water
and
SCIGROW
for
groundwater.
The
values
used
for
comparison
to
the
DWLOC
are
the
maximum
concentrations
for
any
use.
When
the
EEC's
are
less
than
the
calculated
DWLOCs,
EPA
concludes
with
reasonable
certainty
that
exposures
to
the
pesticide
in
drinking
water
would
not
result
in
unacceptable
levels
of
aggregate
human
health
risk.

Acute
Aggregate
Exposure
and
Risk
(
Food
and
water)

Since
the
U.
S.
EPA
Toxicological
Endpoint
Selection
(
TES)
Committees
has
evaluated
the
dimethomorph
toxicity
data
and
determined
there
was
no
toxicologic
endpoints
for
acute
dietary
exposure,
the
determination
of
an
acute
aggregate
exposure
and
risk
evaluation
was
not
required.

Chronic
Aggregate
Exposure
and
Risk
(
food
and
water)

Table
4.
Summary
of
chronic
drinking
water
levels
of
comparison
for
Dimethomorph
Population
Subgroup
Chronic
Food
Exposure
(
mg/
kg/
day
cPAD1
Maximum
Allowable
Water
Exposure
(
mg/
kg/
b.
w./
day)
DWLOC
(
ug/
L)
Sci­
Grow
ground
water
(
ug/
L)
GENEEC
surface
water
(
ug/
L)

US
Population
(
0­
1year)
0.007113
0.11
0.102887
3601
0.30
28.5
Infants
(<
1
yr
old)
0.004183
0.11
0.105817
1058
Children
(
1­
2
years)
0.016758
0.11
0.093242
932
Females
(
13­
49)
0.006111
0.11
0.103889
3117
Adults
(
20­
49)
0.006555
0.11
0.103445
3620
1
Inter/
inter
species
safety
factor
=
100
FQPA
safety
factor
=
1,
NOAEL
=
11
mg/
kg
bw/
day
The
results
in
the
summary
table
of
chronic
DWLOCs
demonstrate
that
there
are
no
safety
concerns
for
any
subpopulation
based
on
established
and
new
uses,
and
that
the
results
clearly
meet
the
FQPA
standard
of
reasonable
certainty
of
no
harm.

In
summary,
we
can
conclude
with
reasonable
certainty
that
no
harm
will
occur
from
chronic
aggregate
exposure
of
dimethomorph.

Short­
and
Intermediate
Term
Aggregate
Exposure
and
Risk
(
Food,
Water
and
Residential
Exposure)

Short­
and
intermediate­
term
aggregate
exposure
takes
into
account
residential
exposure
plus
chronic
exposure
from
food
and
water.
Dimethomorph
is
not
registered
for
use
on
any
sites
that
would
result
in
residential
exposure.
Therefore,
the
aggregate
risk
is
the
sum
from
chronic
food
and
water.
The
chronic
aggregate
risk
assessment
has
shown
that
there
is
no
concern
risk
concerns.
Therefore
we
can
conclude
with
reasonable
certainty
that
no
harm
will
occur
from
short­
term
aggregate
exposure
of
dimethomorph
residues.]

2.
Non­
dietary
exposure.
[
Dimethomorph
is
not
registered
for
use
on
any
sites
that
would
result
in
residential
exposure.
Therefore,
a
residential
exposure
and
risk
assessment
was
not
conducted]

D.
Cumulative
Effects
[
There
is
no
information
to
indicate
that
any
toxic
effects
produced
by
dimethomorph
would
be
cumulative
with
those
of
any
other
chemical.
The
fungicidal
mode
of
action
of
dimethomorph
is
unique;
dimethomorph
inhibits
cell
wall
formation
only
in
Oomycete
fungi.
The
result
is
lysis
of
the
cell
wall
that
kills
growing
cells
and
inhibits
spore
formation
in
mature
hyphae.
This
unique
mode
of
action
and
limited
pest
spectrum
suggest
that
there
is
little
or
no
potential
for
cumulative
toxic
effects
in
mammals.
In
addition,
the
toxicity
studies
submitted
to
support
this
petition
do
not
indicate
that
dimethomorph
is
a
particularly
toxic
compound.
No
toxic
end­
points
of
potential
concern
were
identified.]

E.
Safety
Determination
1.
U.
S.
population.
[
Based
on
this
risk
assessment,
BASF
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
the
general
population
from
the
aggregate
exposure
to
dimethomorph
residues.]
2.
Infants
and
children.
[
Based
on
this
risk
assessment,
BASF
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
infants
or
children
from
the
aggregate
exposure
to
dimethomorph
residues.]

F.
International
Tolerances
[
There
are
no
Canadian,
Mexican,
or
Codex
MRLs
established
for
dimethomorph
for
the
commodities
associated
with
this
request;
consequently,
a
discussion
of
international
harmonization
is
not
relevant.]
