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

EPA
Registration
Division
contact:
[
insert
name
and
telephone
number
with
area
code]

INSTRUCTIONS:
Please
utilize
this
outline
in
preparing
tolerance
petition
documents.
In
cases
where
the
outline
element
does
not
apply
please
insert
"
NARemove
and
maintain
the
outline.
The
comment
notes
that
appear
on
the
left
margin
represent
hidden
typesetting
codes
designed
to
expedite
the
processing
of
the
Federal
Register
document.
Please
do
not
remove
or
alter
these
comment
notes
or
change
the
margins,
font,
or
format
in
your
document.
Simply
replace
the
instructions
that
appear
in
italics
and
brackets,
i.
e.,
"[
insert
company
name],"
with
the
information
specific
to
your
action.]

TEMPLATE:

[
IR­
4]

[
Insert
petition
number]

EPA
has
received
a
pesticide
petition
([
insert
petition
number])
from
[
IR­
4],
[
681
U.
S.
Highway
#
1
South,
North
Brunswick,
NJ
08902]
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.

(
Options
(
pick
one)

1.
by
establishing
a
tolerance
for
residues
of
2.
to
establish
an
exemption
from
the
requirement
of
a
tolerance
for
[
the
fungicide
trifloxystrobin
and
the
free
form
of
its
acid
metabolite
(
CGA 
32113)]
in
or
on
the
raw
agricultural
commodity
[
asparagus]
at
[
0.07]
parts
per
million
(
ppm);
[
papaya]
at
[
0.4]
ppm;
[
black
sapote]
at
[
0.4]
ppm;
[
canistel]
at
[
0.4]
ppm;
[
mamey
sapote]
at
[
0.4]
ppm;
[
mango]
at
[
0.4]
ppm;
[
sapodilla]
at
[
0.4]
ppm;
[
star
apple]
at
[
0.4]
ppm;
[
radish,
root]
at
[
0.2]
ppm;
and
[
radish,
tops]
at
[
20]
ppm.
EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408
(
d)(
2)
of
the
FDDCA;
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
metabolism
of
trifloxystrobin
in
plants
(
cucumbers,
apples,
wheat,
sugar
beets
and
peanuts)
is
well
understood.
Identified
metabolic
pathways
are
substantially
similar
in
plants
and
animals
(
goat,
rat
and
hen).
EPA
has
determined
that
trifloxystrobin
parent
and
its
metabolite
CGA­
321113
are
the
residue
of
concern
for
tolerance
setting
purposes.]

2.
Analytical
method.
[
A
practical
analytical
methodology
for
detecting
and
measuring
levels
of
trifloxystrobin
in
or
on
raw
agricultural
commodities
has
been
submitted.
The
limit
of
detection
(
LOD)
for
each
analyte
of
this
method
is
0.08
ng
injected,
and
the
limit
of
quantitation
(
LOQ)
is
0.02
ppm.
The
method
is
based
on
crop
specific
cleanup
procedures
and
determination
by
gas
chromatography
with
nitrogen­
phosphorus
detection.]

3.
Magnitude
of
residues.
[
ASPARAGUS
IR­
4
received
requests
from
the
states
of
California,
Idaho,
Michigan
and
Tennessee
for
the
use
of
Trifloxystrobin
on
asparagus.
To
support
this
request,
magnitude
of
residue
data
were
collected
from
five
field
trials
from
California,
Idaho,
Michigan,
New
Jersey,
and
Washington.
In
each
trial,
3
foliar
applications
of
the
test
substance
13
to
15
days
apart
were
made
to
the
treated
plots.
The
application
rates
ranged
from
0.123
to
0.134
lb
a.
i./
A
per
application
for
a
total
rate
range
of
0.374
to
0.386
lb
ai/
A
per
season
All
applications
were
made
to
the
ferns
in
the
fall.
The
ferns
were
mowed
after
senescing
prior
to
the
emergence
of
new
spears
in
the
spring.
The
new
spears
were
harvested
in
the
spring
as
done
commercially.
Sampling
started
in
the
untreated
control
plot
and
ended
in
the
treated
plot.
At
all
the
field
trials,
samples
were
harvested
92
 
100
days
after
the
last
application
in
the
CA
trials
and
167
 
188
days
after
the
last
application
at
the
other
trials.

The
samples
were
analyzed
using
the
Cornell
Analytical
Method
titled,
"
Residue
Analysis
of
Trifloxystrobin
(
CGA­
279202
and
CGA­
321113)
on
Asparagus
by
GCMS
Detection."
The
LOD
for
the
method
was
calculated
to
be
0.025
ppm
and
the
LOQ
was
calculated
to
be
0.076
ppm
for
trifloxystrobin
and
the
LOD
and
LOQ
were
calculated
to
be
0.006
ppm
and
0.019
ppm
respectively
for
CGA321113.
No
detectable
residues
of
Trifloxystrobin
or
CGA321113
were
found
in
any
of
the
treated
or
untreated
samples
(
LLMV
=
0.05
ppm
for
trifloxystrobin
and
0.02
ppm
for
CGA321113).

PAPAYA
IR­
4
received
requests
from
the
state
of
Hawaii
and
territory
of
Puerto
Rico
for
the
use
of
Trifloxystrobin
on
papaya.
To
support
this
request,
magnitude
of
residue
data
were
collected
from
four
field
trials
located
Florida
and
Hawaii.
At
each
trial,
4
foliar
applications
of
the
test
substance
7
to
8
days
apart
were
made
to
the
treated
plots.
The
application
rates
ranged
from
0.125
to
0.135
lb
a.
i./
A
per
application
for
a
total
rate
range
of
0.506
to
0.521
lb
ai/
A
per
season.
The
papaya
fruit
were
harvested
simulating
commercial
practices
on
the
day
of
last
application.

Samples
were
analyzed
at
the
IR­
4
North
Central
Region
Leader
Laboratory
at
Michigan
State
University.
The
method
used
for
the
analysis
was
adapted
from
the
reference
method:
"
Analytical
Method
for
Determination
of
Residues
CGA­
279202
and
the
Acid
Metabolite
CGA­
321113
in
Crops
and
Animal
Substrates
by
Gas
Chromatography."
The
LOD
for
the
method
was
calculated
to
be
0.009
ppm
and
the
LOQ
was
calculated
to
be
0.027
ppm
for
trifloxystrobin
and
the
LOD
and
LOQ
were
calculated
to
be
0.008
ppm
and
0.023
ppm
respectively
for
CGA321113.
Residues
of
Trifloxystrobin
in
the
treated
papaya
samples
ranged
from
0.07
ppm
to
0.28
ppm.
Residues
of
Trifloxystrobin
acid
metabolite
in
the
treated
samples
from
the
two
FL
trials
were
<
0.02
ppm
however,
for
the
two
HI
trials,
the
residues
were
reported
as
0.03
ppm
to
0.04
ppm.

RADISH
IR­
4
received
requests
from
the
states
of
California,
New
Jersey,
and
New
York
for
the
use
of
trifloxystrobin
on
radish.
To
support
this
request,
magnitude
of
residue
data
were
collected
from
six
field
trials
located
in
the
states
of
California,
Florida,
New
York,
Oregon,
and
Wisconsin.
In
each
trial,
two
foliar
directed
applications
of
the
test
substance
7
to
8
days
apart
were
made
to
each
of
the
treated
plots.
The
application
rates
ranged
from
0.125
to
0.132
lb
a.
i./
A
per
application
for
a
total
rate
range
of
0.251
to
0.264
lb
ai/
A
per
season.
All
applications
were
made
using
appropriate
spray
equipment,
and
the
spray
volume
was
sufficient
to
provide
adequate
dispersal
of
the
test
substance.
In
all
the
field
trials,
radish
tops
(
leaves)
and
root
RAC
samples
were
harvested
by
hand,
6­
8
days
after
the
last
application
The
samples
were
analyzed
using
the
Cornell
Analytical
Laboratory
method
entitled
"
Residue
Analysis
of
Trifloxystrobin
on
Radish
(
Roots
and
Tops)
by
GC/
MS
Detection,
Version
#
3."
For
tops,
the
method
limit
of
detection
(
LOD)
was
calculated
to
be
0.01
ppm
and
0.007
ppm
for
trifloxystrobin
and
CGA­
321113,
respectively,
and
the
limit
of
quantitation
(
LOQ)
was
calculated
to
be
0.030
ppm
and
0.021
ppm
for
trifloxystrobin
and
CGA­
321113,
respectively.
For
roots,
the
method
LOD
was
calculated
to
be
0.010
ppm
and
0.007
ppm
for
trifloxystrobin
and
CGA­
321113,
respectively,
and
the
LOQ
was
calculated
to
be
0.029
ppm
and
0.021
ppm
for
trifloxystrobin
and
CGA­
321113,
respectively.
For
radish
tops,
the
combined
residues
of
trifloxystrobin
and
CGA­
321113
were
0.15
­
7.33
ppm.
For
radish
roots,
the
combined
residues
of
trifloxystrobin
and
CGA­
321113
were
<
0.04
­
0.08
ppm.]

B.
Toxicological
Profile
1.
Acute
toxicity.
[
Studies
conducted
with
the
technical
material
of
trifloxystrobin:

rat
acute
oral
toxicity
study
with
a
LD50
>
5000
mg/
kg
mouse
acute
oral
toxicity
study
with
a
LD50
>
5000
mg/
kg
rabbit
acute
dermal
toxicity
study
with
a
LD50
>
2000
mg/
kg
rat
acute
dermal
toxicity
study
with
a
LD50
>
2000
mg/
kg
rat
acute
inhalation
toxicity
study
with
a
LC50
>
4.65
mg/
L
rabbit
eye
irritation
study
showing
slight
irritation
(
Category
III)
rabbit
dermal
irritation
study
showing
slight
irritation
(
Category
IV)
Guinea
pig
dermal
sensitization
study
with
the
Buehler's
method
showing
negative
findings
Guinea
pig
dermal
sensitization
study
with
the
Maximization
method
showing
some
positive
findings.]

2.
Genotoxicty.
[
No
genotoxic
activity
is
expected
of
trifloxystrobin
under
invivo
or
physiological
conditions.
The
compound
has
been
tested
for
its
potential
to
induce
gene
mutation
and
chromosomal
changes
in
five
different
test
systems.
The
only
positive
finding
was
seen
in
the
in
vitro
test
system
(
Chinese
hamster
V79
cells)
as
a
slight
increase
in
mutant
frequency
at
a
very
narrow
range
(
250
­
278
Fg/
ml)
of
cytotoxic
and
precipitating
concentrations
(
compound
solubility
in
water
was
reported
to
be
0.61
Fg/
ml;
precipitate
was
visually
noted
in
culture
medium
at
150
Fg/
ml).
The
chemical
was
found
to
be
non­
mutagenic
in
the
in
vivo
system
or
all
other
in
vitro
systems.
Consequently,
the
limited
gene
mutation
activity
in
the
V79
cell
line
is
considered
a
nonspecific
effect
under
non­
physiological
in
vitro
conditions
and
not
indicative
of
a
real
mutagenic
hazard.]

3.
Reproductive
and
developmental
toxicity.
[
FFDCA
section
408
provides
that
EPA
may
apply
an
additional
safety
factor
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
pre­
and
post­
natal
toxicity
and
the
completeness
of
the
database.
Based
on
the
current
toxicological
data
requirements,
the
database
on
trifloxystrobin
relative
to
pre­
and
post­
natal
effects
for
children
is
complete.

In
assessing
the
potential
for
additional
sensitivity
of
infants
and
children
to
residues
of
trifloxystrobin,
data
were
considered
from
teratogenicity
studies
in
the
rat
and
the
rabbit
and
a
2­
generation
reproduction
studies
in
the
rat.
The
teratogenicity
studies
are
designed
to
evaluate
adverse
effects
on
the
developing
embryo
as
a
result
of
chemical
exposure
during
the
period
of
organogenesis.
Reproduction
studies
provide
information
on
effects
from
chemical
exposure
on
the
reproductive
capability
of
mating
animals
and
systemic
and
developmental
toxicity
from
in­
utero
exposure.

In
the
rat
teratology
study,
reductions
in
body
weight
gain
and
food
consumption
were
observed
in
the
dam
at
$
100
mg/
kg.
No
teratogenic
effects
or
any
other
effects
were
seen
on
pregnancy
or
fetal
parameters
except
for
the
increased
incidence
of
enlarged
thymus,
which
is
a
type
of
variation,
at
1000
mg/
kg.
The
developmental
NOEL
was
100
mg/
kg.

In
the
rabbit
teratology
study,
body
weight
loss
and
dramatically
reduced
food
consumption
were
observed
in
the
dam
at
$
250
mg/
kg.
No
teratogenic
effects
or
any
other
effects
were
seen
on
pregnancy
or
fetal
parameters
except
for
the
increase
in
skeletal
anomaly
of
fused
sternebrae­
3
and
­
4
at
the
top
dose
level
of
500
mg/
kg.
This
finding
is
regarded
as
a
marginal
effect
on
skeletal
development
that
could
have
resulted
from
the
40­
65%
lower
food
intake
during
treatment
at
this
dose
level.
The
developmental
NOEL
was
250
mg/
kg.

In
the
2­
generation
rat
reproduction
study,
body
weight
gain
and
food
consumption
were
decreased
at
$
750
ppm,
especially
in
females
during
lactation.
Consequently,
the
reduced
pup
weight
gain
during
lactation
($
750
ppm)
and
the
slight
delay
in
eye
opening
(
1500
ppm)
are
judged
to
be
a
secondary
effect
of
maternal
toxicity.
No
other
fetal
effects
or
any
reproductive
changes
were
noted.
The
low
developmental
NOEL,
50
ppm
(
5
mg/
kg),
seen
in
this
study
was
probably
due
to
the
lack
of
intermediate
dose
levels
between
50
and
750
ppm.
Based
on
an
evaluation
of
the
dose­
response
relationship
for
pup
weight
at
750
ppm
and
1500
ppm,
the
NOEL
should
have
been
nearly
ten­
fold
higher
if
such
a
dose
was
available.

Based
on
all
these
teratology
and
reproduction
studies,
the
lowest
NOEL
for
developmental
toxicity
is
5
mg/
kg
while
the
lowest
NOEL
in
the
subchronic
and
chronic
studies
is
2.5
mg/
kg/
day
(
from
the
rat
chronic
study).
Therefore,
no
additional
sensitivity
for
infants
and
children
to
trifloxystrobin
is
suggested
by
the
data
base.]

4.
Subchronic
toxicity.
[
In
subchronic
studies,
several
mortality
related
changes
were
reported
for
the
top
dose
in
dogs
(
500
mg/
kg)
and
rats
(
800
mg/
kg).
At
these
dose
levels,
excessive
toxicity
has
resulted
in
body
weight
loss
and
mortality
with
the
associated
and
nonspecific
changes
in
several
organs
(
such
as
atrophy
in
the
thymus,
pancreas,
bone
marrow,
lymph
node,
and
spleen)
which
are
not
considered
specific
target
organs
for
the
test
compound.
In
the
dog,
specific
effects
were
limited
to
hepatocellular
hypertrophy
at
$
150
mg/
kg
and
hyperplasia
of
the
epithelium
of
the
gall
bladder
at
500
mg/
kg.
Target
organ
effects
in
the
rat
were
noted
as
hepatocellular
hypertrophy
($
200
mg/
kg)
and
the
related
liver
weight
increase
($
50
mg/
kg).
In
the
mouse,
target
organ
effects
included
single
cell
necrosis
($
300
mg/
kg)
and
hypertrophy
(
1050
mg/
kg)
in
the
liver
and
extramedullary
hematopoiesis
($
300
mg/
kg)
and
hemosiderosis
in
the
spleen
(
1050
mg/
kg).

In
general,
definitive
target
organ
toxicity,
mostly
in
the
liver,
was
seen
at
high
feeding
levels
of
over
100
mg/
kg
for
an
extended
treatment
period.
At
LOEL,
no
serious
toxicity
was
observed
other
than
mostly
non­
specific
effects
including
a
reduction
in
body
weight
and
food
consumption
or
liver
hypertrophy.]

5.
Chronic
toxicity.
[
The
liver
appears
to
be
the
major
primary
target
organ
based
on
the
chronic
studies
conducted
in
mice,
rats,
and
dogs.
It
was
identified
as
a
target
organ
in
both
the
mouse
and
the
dog
studies
with
trifloxystrobin.
However,
no
liver
effect
was
seen
in
the
chronic
rat
study
which
produced
the
lowest
NOEL
of
2.5
mg/
kg
based
on
reduced
body
weight
gain
and
food
consumption
seen
at
higher
dose
levels.

The
compound
did
not
cause
any
treatment­
related
increase
in
general
tumor
incidence,
any
elevated
incidence
of
rare
tumors,
or
shortened
time
to
the
development
of
palpable
or
rapidly
lethal
tumors
in
the
18­
month
mouse
and
the
24­
month
rat
studies.
Dosages
in
both
studies
were
sufficient
for
identifying
a
cancer
risk.
In
the
absence
of
carcinogenicity,
a
Reference
Dose
approach
is
appropriate
for
quantitation
of
human
risks.]

6.
Animal
metabolism.
[
Trifloxystrobin
is
moderately
absorbed
from
the
gastrointestinal
tract
of
rats
and
is
rapidly
distributed.
Subsequent
to
a
single
oral
dose,
the
half
life
of
elimination
is
about
2
days
and
excretion
is
primarily
via
bile.
Trifloxystrobin
is
extensively
metabolized
by
the
rat
into
about
35
metabolites,
but
the
primary
actions
are
on
the
methyl
ester
(
hydrolysis
into
an
acid),
the
methoxyimino
group
(
O­
demethylation),
and
the
methyl
side
chain
(
oxidation
to
a
primary
alcohol).
Metabolism
is
dose
dependent
as
it
was
almost
complete
at
low
doses
but
only
about
60%
complete
at
high
doses.

In
the
goat,
elimination
of
orally
administered
trifloxystrobin
is
primarily
via
the
feces.
The
major
residues
were
the
parent
compound
and
the
acid
metabolite
(
CGA­
321113)
plus
its
conjugates.
In
the
hen,
trifloxystrobin
is
found
as
the
major
compound
in
tissues
and
in
the
excreta,
but
hydroxylation
of
the
trifluormethylphenyl
moiety
and
other
transformations,
including
methyl
ester
hydrolysis
and
demethylation
of
the
methoxyimino
group,
are
also
seen.
In
conclusion,
the
major
pathways
of
metabolism
in
the
rat,
goat,
and
hen
are
the
same.]

7.
Metabolite
toxicology.
[
Metabolism
of
trifloxystrobin
has
been
well
characterized
in
plants,
soil,
and
animals.
In
plants
and
soil,
photolytically
induced
isomerization
results
in
a
few
minor
metabolites
not
seen
in
the
rat;
however,
most
of
the
applied
materials
remained
as
parent
compound
as
shown
in
the
apple
and
cucumber
studies.
All
quantitatively
major
plant
and/
or
soil
metabolites
were
also
seen
in
the
rat.
The
toxicity
of
the
major
acid
metabolite,
CGA­
321113
(
formed
by
hydrolysis
of
the
methyl
ester),
has
been
evaluated
in
cultured
rat
hepatocytes
and
found
to
be
20­
times
less
cytotoxic
than
the
parent
compound.
Additional
toxicity
studies
were
conducted
for
several
minor
metabolites
seen
uniquely
in
plants
and/
or
soil.
The
studies
indicate
that
these
metabolites,
including
CGA­
357261,
CGA­
373466,
and
NOA­
414412,
are
not
mutagenic
to
bacteria
and
are
of
low
acute
toxicity
(
LD50
>
2000
mg/
kg).
In
conclusion,
the
metabolism
and
toxicity
profiles
support
the
use
of
an
analytical
enforcement
method
that
accounts
for
parent
trifloxystrobin.]

8.
Endocrine
disruption.
[
Trifloxystrobin
does
not
belong
to
a
class
of
chemicals
known
for
having
adverse
effects
on
the
endocrine
system.
Developmental
toxicity
studies
in
rats
and
rabbits
and
reproduction
study
in
rats
gave
no
indication
that
trifloxystrobin
might
have
any
effects
on
endocrine
function
related
to
development
and
reproduction.
The
subchronic
and
chronic
studies
also
showed
no
evidence
of
a
long­
term
effect
related
to
the
endocrine
system.]

C.
Aggregate
Exposure
1.
Dietary
exposure.
[
Assessments,
using
the
DEEM
FCID
Version
2.0,
1994­
1996,98
CSFII
software,
were
conducted
to
evaluate
potential
risks
due
to
chronic
and
acute
dietary
(
food
and
water)
exposure
of
the
U.
S.
population
and
selected
population
subgroups
to
residues
of
trifloxystrobin.
These
analyses
cover
all
registered
crops
plus
the
pending
uses
on
asparagus,
radish,
and
the
tropical
crops
papaya,
black
sapote,
canistel,
mamey
sapote,
mango,
sapodilla,
and
star
apple.

The
EPA
has
established
an
acute
Population
Adjusted
Dose
(
aPAD)
of
2.5
mg/
kg/
day
for
acute
dietary
risk
assessments
based
on
a
NOAEL
of
250
mg/
kg
bwt/
day
from
a
rabbit
developmental
toxicity
study
and
an
uncertainty
factor
or
100.
For
chronic
dietary
analyses,
the
EPA
established
a
chronic
Population
Adjusted
Dose
(
cPAD)
of
0.038
based
on
a
NOAEL
of
3.8
from
a
rat
reproductive
toxicity
study
and
and
uncertainty
factor
of
100.

Results
from
the
acute
and
chronic
dietary
exposure
analyses
described
below
demonstrate
a
reasonable
certainty
that
no
harm
to
the
overall
U.
S.
population
or
any
population
subgroup
will
result
from
the
use
of
trifloxystrobin
on
currently
registered
uses
plus
the
pending
uses
on
asparagus,
radish,
and
the
tropical
crops
papaya,
black
sapote,
canistel,
mamey
sapote,
mango,
sapodilla,
and
star
apple.]

i.
Food.
[
For
food,
a
Tier
1
acute
and
a
Tier
2
chronic
dietary
exposure
assessments
were
performed.
Acute
exposure,
expressed
at
the
95th
percentile
of
exposure,
was
0.64%
of
the
aPAD
for
females
13­
49
years
old
(
only
population
subgroup
of
concern).
The
chronic
exposure
was
5.3%
cPAD
for
the
total
US
population
and
17.6%
cPAD
for
the
most
sensitive
population,
children
1­
2
years
old.]

ii.
Drinking
Food.
[
Acute
and
chronic
exposure
estimates
from
water
are
included
in
the
exposure
values
given
above
for
food.
These
exposure
estimates
for
water
are
based
on
EPA's
surface
water
estimated
environmental
concentrations
(
EECs)
of
trifloxystrobin
and
CGA­
321113
for
acute
exposure
at
92
parts
per
billion
(
ppb)
and
for
chronic
exposures
at
50
ppb.
These
values
are
listed
in
the
Federal
Register
(
71
FR
15597).]

2.
Non­
dietary
exposure.
[
As
published
in
the
Federal
Register
(
71
FR
15597),
the
EPA
considered
chronic,
short
term
and
intermediate
term
risk
from
residential
uses
of
trifloxystrobin.
The
EPA
determined
that
the
risk
did
not
exceed
the
Agency's
level
of
concern.]

D.
Cumulative
Effects
[
EPA
has
determined,
as
published
in
the
Federal
Register
(
68
FR
53297),
that
unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
trifloxystrobin
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.
Therefore
EPA
has
not
assumed
that
trifloxystrobin
has
a
common
mechanism
of
toxicity
with
other
substances.]
E.
Safety
Determination
1.
U.
S.
population.
[
Based
on
the
information
supplied
under
Aggregate
Exposure
describe
above,
there
is
reasonable
certainty
that
exposure
from
trifloxystrobin
will
not
result
in
harm
to
the
adult
U.
S.
population.]

2.
Infants
and
children.
[
Based
on
the
information
supplied
under
Aggregate
Exposure
describe
above,
there
is
reasonable
certainty
that
exposure
from
trifloxystrobin
will
not
result
in
harm
to
infants
and
children.]

F.
International
Tolerances
[
No
Codex
MRLs
have
been
established
for
trifloxystrobin
on
the
pending
crops
asparagus,
radish,
and
the
tropical
crops
papaya,
black
sapote,
canistel,
mamey
sapote,
mango,
sapodilla,
and
star
apple.
No
MRLs
have
been
established
in
other
countries
for
asparagus.
MRLs
for
trifloxystrobin
have
been
established
for
the
following
pending
crops:
Radish:
Japan
Root
and
tuber
vegetables:
Spain
and
the
European
Community
Papaya:
Japan
Mango:
Japan,
Kenya,
and
Taiwan.]
