Document ID: EPA-HQ-OPP-2006-0073-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-03-01T05:00Z

FILE
NAME:
company.
wpt
(
7/
1/
2005)
(
xml)
Template
Number
P25
COMPANY
FEDERAL
REGISTER
DOCUMENT
SUBMISSION
TEMPLATE
(
1/
1/
2005)

EPA
Registration
Division
contact:
[
Shaja
R.
Brothers,
703­
308­
3194]

TEMPLATE:

[
Interregional
Research
Project
#
4
(
IR­
4),
and
Syngenta
Crop
Protection,
Inc.]

[
PP
6E4653,
PP
1E6228
and
PP
1F5068]

EPA
has
received
a
pesticide
petition
([
PP
6E4653
and
PP
1E6228])
from
[
Interregional
Research
Project
#
4
(
IR­
4),
681
US
Highway
#
1
South,
North
Brunswick,
NJ
08902­
3390]
on
behalf
of
Syngenta
Crop
Protection,
Inc.],
[
P.
O.
Box
18300,
Greensboro,
NC
27410]
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
[
sodium
salt
of
fomesafen,
5­[
2­
cloro­
4­(
trifluoromethyl)
phenoxy]­
N­(
methylsulfonyl)­
2­
nitrobenzamide]
in
or
on
the
raw
agricultural
commodities
[
snap
beans
and
dry
beans]
at
[
0.025]
parts
per
million
(
ppm).

EPA
has
also
received
a
pesticide
petition
([
PP
1F5068])
from
[
Syngenta
Crop
Protection,
Inc.],
[
P.
O.
Box
18300,
Greensboro,
NC
27410]
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
[
sodium
salt
of
fomesafen,
5­[
2­
cloro­
4­
(
trifluoromethyl)
phenoxy]­
N­(
methylsulfonyl)­
2­
nitrobenzamide]
in
or
on
the
raw
agricultural
commodities
[
cotton
seed
and
cotton
by­
products]
at
[
0.025]
parts
per
million
(
ppm).

EPA
has
determined
that
these
petitions
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.
Cotton
and
soybean
metabolism
studies
were
conducted
using
14Clabeled
fomesafen.
The
major
degradation
pathway
of
fomesafen
in
cotton
and
soybean
plants
involves
ether
cleavage
followed
by
cystine
conjugation.
The
major
portion
of
the
applied
chemical
is
comprised
of
unchanged
fomesafen.
Metabolites,
if
present
are
<
0.01
mg/
kg.
Very
little
translocation
from
treated
foliage
tissue
occurs.
The
nature
of
the
residue
is
adequately
2
understood.

2.
Analytical
method.
An
analytical
method
using
chemical
derivatization
followed
by
gas
chromatography
with
Nitrogen­
Phosphorus
detection
(
NPD)
has
been
developed
and
validated
for
residues
of
fomesafen
in
snap/
dry
beans,
cotton
seed
and
cotton
gin
byproducts,
as
well
as
for
other
crops.
After
homogenization,
the
samples
are
extracted
with
acidified
acetonitrile.
After
addition
of
water
and
additional
acid,
the
extract
was
submitted
to
liquid/
liquid
partition.
The
residue
is
transferred
to
dichloromethane,
followed
by
acetone
and
derivatized
with
iodomethane
in
the
presence
of
anhydrous
potassium
carbonate.
A
silica
gel
column
cleanup
is
done,
with
dichloromethane:
hexane
as
the
eluent.
The
final
extract
is
transferred
to
toluene
and
analyzed
by
GC­
NPD.
The
limit
of
quantitation
is
0.025
ppm.

3.
Magnitude
of
residues.
No
residues
of
fomesafen
are
detected
in
the
snap
bean
field
residue
trials.
Seven
magnitude
of
the
residue
trials
were
conducted
by
IR­
4
in
Regions
I,
II,
III,
and
V,
for
a
regional
label
for
snap
beans.
Five
typically
cultivated
varieties
of
snap
beans
were
used
in
the
trials.
Results
demonstrated
that
when
fomesafen
is
applied
as
a
single
pre/
early
bloom
application
at
the
maximum
use
rate
of
0.375
lb.
ai/
A
(
0.25
lb
a.
i./
A
in
Florida)
and
with
a
24
­
34
day
PHI,
no
residues
of
fomesafen
were
detected
at
the
limit
of
quantitation
of
0.025
ppm,
which
is
the
limit
for
the
analytical
method
described
above.
In
addition,
Zeneca
Ag
Products
conducted
five
magnitude
of
the
residue
trials
during
1999
to
supplement
the
data
in
order
to
complete
the
number
of
trials
required
for
a
national
label
for
use
of
fomesafen
on
snap
beans.
These
trials
also
showed
that
there
were
no
residues
above
the
limit
of
quantitation
of
0.02
mg/
kg.

No
residues
of
fomesafen
were
detected
in
the
dry
bean
field
residue
trials.
Three
magnitude
of
the
residue
trials
were
conducted
by
IR­
4
in
Regions
I
and
V
for
a
regional
label
for
dry
beans.
These
regions
correspond
to
the
major
dry
bean
producing
area
of
the
United
States.
Three
typically
cultivated
varieties
of
dry
beans
were
used
in
the
trials.
Results
demonstrated
that
when
fomesafen
is
applied
as
a
single
early
post­
emergence
to
early­
bloom
growth
stage,
no
residues
of
fomesafen
were
detected
at
the
limit
of
quantitation
of
0.026
ppm.

No
residues
of
fomesafen
are
detected
in
the
cotton
field
residue
trials.
Twelve
magnitude
of
the
residue
trials
were
conducted
during
1997
in
the
United
States
to
produce
samples
of
cotton
undelinted
seed
and
cotton
gin
byproducts
for
residue
analysis.
One
application
of
Reflex
at
0.05
lb
ai/
A
was
made
at
the
following
representative
proposed
timing:
broadcast
surface,
or
broadcast
preplant
incorporated,
or
post­
directed
to
bottom
of
the
cotton
plan
at
late
layby.
A
1.0
lb
ai/
A
rate
was
applied
broadcast,
preplant
incorporated
just
prior
to
planting.
The
samples
from
each
trial
of
undelinted
seed
and
gin
byproducts
were
analyzed
for
fomesafen.
No
residues
were
detected
at
the
limits
of
quantitation
(
LOQ),
except
for
one
gin
byproduct
sample
with
a
residue
exactly
at
the
LOQ.
The
LOQ
in
undelinted
seed
and
gin
byproducts
were
0.025
ppm
and
0.02
ppm,
respectively.
3
4
Cotton
processing
study:
A
study
was
conducted
to
produce
samples
of
undelinted
seed,
hulls,
meal,
and
refined
oil
from
the
processing
of
cotton
seed
collected
from
a
field
plot
treated
once
at
2.5
lb
ai/
A,
a
5X
exaggerated
maximum
label
rate
of
Reflex.
There
was
no
fomesafen
detected
at
the
LOQ
of
0.025
ppm
in
samples
of
undelinted
seed
at
the
5X
exaggerated
rate.
Since
it
has
been
shown
that
no
residues
above
the
LOQ
were
detected
in
the
magnitude
of
residue
trials
described
above,
it
was
concluded
that
analysis
of
processed
commodities
for
the
hulls,
meal,
and
refined
oil
is
not
necessary.

B.
Toxicological
Profile
1.
Acute
toxicity.
The
acute
toxicity
profile
of
technical
fomesafen
is
low
by
oral
and
dermal
routes.
Acute
oral
LD50
is
1250
mg/
kg
in
male
rats,
acute
dermal
LD
50
is
greater
than
1000
mg/
kg,
fomesafen
is
a
moderate
eye
irritant,
mild
skin
irritant,
and
a
dermal
sensitizer.

Similarly
the
formulated
fomesafen
(
REFLEX)
is
of
low
oral,
dermal
and
inhalation
toxicity
but
is
classed
as
Category
I
toxicity
based
on
the
highest
hazard,
severe
eye
irritancy
for
the
formulated
product.

2.
Genotoxicity.
Fomesafen
tested
negative
in
assay
systems
for
gene
mutation,
structural
chromosome
aberration
and
other
genotoxic
effects.
In
one
older
in
vivo
cytogenicity
test,
fomesafen
did
produce
a
weak
clastogenic
response
in
the
rat
bone
marrow
when
the
analysis
of
the
data
was
undertaken
with
gap­
type
aberrations
both
included
and
excluded.
The
guidelines
for
metaphase
study
evaluations,
and
the
significance
to
be
ascribed
to
gap­
type
aberrations
has
evolved
since
these
studies
were
conducted.
The
current
view
among
cytogeneticists
is
that
gap­
type
aberrations
(
small
discontinuities
in
the
staining
of
the
chromosomes,
as
distinct
from
breaks),
do
not
indicate
significant
chromosomal
damage
and
should
be
excluded
from
the
evaluation
of
such
assays.
Additional
data
to
clarify
the
genotoxic
potential
of
fomesafen
were
developed,
including
a
bone
marrow
micronucleus
assay
in
the
mouse
(
negative)
and
a
more
recent
in
vivo
cytogenetic
assay
in
rat
bone
marrow
that
was
conducted
to
current
standards
(
negative).
The
complete
set
of
cytogenic
data,
including
a
review
by
an
external
consultant,
support
the
conclusion
that
fomesafen
is
not
genotoxic.

3.
Reproductive
and
developmental
toxicity.
Rat.
In
a
2­
generation
reproduction
study,
male
and
female
rats
were
treated
with
diet
containing
fomesafen
at
0,
50,
250
and
1000
ppm,
corresponding
to
achieved
dose
levels
of
0,
2.5,
12.5
and
50
mg/
kg/
day.
Two
different
litters
(
A
and
B)
were
produced
in
each
of
two
generations
(
F1
and
F2).
The
parental
(
systemic)
NOAEL
was
12.5
mg/
kg/
day
(
250
ppm),
based
on
decreased
body
weight
and
liver
histopathology
at
the
LOAEL
of
50
mg/
kg/
day
(
1000
ppm).
The
NOAEL
for
both
reproductive
effects
and
offspring
effects
was
12.5
mg/
kg/
day
(
250
ppm),
based
on
reductions
in
the
proportion
of
pups
born
live
and
the
proportion
surviving
to
day
22
at
50
mg/
kg/
day
(
1000
ppm;
reproductive
LOAEL)
and
5
based
on
significant
reduction
in
litter
weight
gain
at
50
mg/
kg/
day
(
1000
ppm;
offspring
LOAEL).
This
is
the
same
value
as
the
NOAEL
for
parental
toxicity,
and
therefore,
there
is
no
indication
of
increased
sensitivity
of
offspring
to
fomesafen
in
a
2­
generation
reproduction
study
in
rats.

Two
developmental
toxicity
studies
were
conducted
for
fomesafen
in
rats.
In
the
first
study
rats
were
given
oral
doses
of
fomesafen
at
0,
50,
100,
or
200
mg/
kg/
day
on
gestation
days
6
to
15.
An
increase
in
post­
implantation
loss
was
seen
at
the
maternally
toxic
dose
of
200
mg/
kg/
day
(
clinical
toxicity
and
reduction
in
body
weight
gain).
There
was
also
an
increase
in
all
treated
groups
of
the
incidence
of
extra
ribs
and
partial
ossification
of
the
calcaneum.
Incidences
of
these
skeletal
variations
were
not
dose­
related,
and
comparison
with
historic
control
values
indicated
that
they
were
related
to
an
unusually
low
incidence
for
the
control
group
and
therefore
they
were
not
treatment­
related
effects.
A
second
study
was
conducted
at
lower
doses
(
0,
1.0,
7.5
and
50
mg/
kg/
day)
and
showed
no
maternal
or
fetal
effects.
The
systemic
(
maternal)
and
developmental
NOEL
for
fomesafen
is
100
mg/
kg/
day,
based
on
maternal
toxicity
and
increased
postimplantation
loss
at
200
mg/
kg/
day.

Rabbit.
A
developmental
toxicity
study
in
rabbits
given
oral
doses
of
0,
2.5,
10,
or
40
mg/
kg/
day
on
gestation
days
6
to
18
revealed
no
developmental
toxicity.
The
NOEL
for
maternal
systemic
effects
(
stomach
mucosal
erosion
and
death)
was
10
mg/
kg/
day,
and
the
developmental
NOEL
was
40
mg/
kg/
day
(
HDT).

4.
Subchronic
toxicity.
In
a
90­
day
oral
rat
study
at
dietary
levels
of
0,
1,
5,
100
and
1000
ppm,
the
fomesafen
NOEL
was
0.25
mg/
kg/
day
(
5
ppm),
based
on
a
transient
reduction
in
plasma
triglyceride
and
cholesterol
levels,
hyalinization
of
hepatocytes
and
increase
in
peroxisomes
in
the
liver
at
100
ppm
in
males.

In
a
26­
week
oral
dog
study
at
dose
levels
of
0,
0.1,
1
and
25
mg/
kg/
day,
there
were
no
deaths,
no
clinical
signs
of
toxicity,
and
no
treatment­
related
variations
in
body
weight.
The
NOEL
was
1
mg/
kg/
day
based
on
slight
hematology
effects,
reduction
in
plasma
triglyceride
and
cholesterol
levels,
a
small
increase
in
liver
weight
(
males),
and
increased
kidney
weights
(
females)
at
25
mg/
kg/
day.

5.
Chronic
toxicity.
2­
year
rat
study.
There
was
no
evidence
of
tumor
induction
in
the
rat
following
dietary
exposure
to
fomesafen
at
levels
up
to
1000
ppm.
The
NOEL
for
systemic
toxicity
was
100
ppm
(
5
mg/
kg/
day)
based
on
decreased
body
weight
(
males),
increased
liver
weights,
micropathology
changes
to
the
liver
consistent
with
peroxisome
proliferation,
and
decreased
plasma
cholesterol
and
trigycerides
at
1000
ppm.

2­
year
mouse
study.
In
a
2­
year
oncogenicity
study
in
mice,
the
NOEL
was
10
ppm
(
1
mg/
kg/
day).
Effects
seen
at
the
LOAEL
of
100
ppm
included
increased
food
consumption
(
males),
6
changes
in
selected
clinical
chemistry
parameters,
increased
liver
weights,
histological
changes
to
the
liver
consistent
with
peroxisome
proliferation,
and
an
increase
in
hepatocellular
adenomas
and
carcinomas.
Through
a
series
of
mechanistic
studies,
the
mode
of
action
for
liver
tumor
formation
by
fomesafen
in
mice
has
been
established
as
PPAR­
alpha
activation
(
peroxisome
proliferation),
which
would
not
be
operative
in
humans
exposed
to
fomesafen.
The
weight
of
evidence
indicates
that
liver
tumors
resulting
from
fomesafen
and
other
PPAR­
alpha
agonists
are
rodent­
specific
and
are
unlikely
to
indicate
oncogenic
risk
to
humans.

6.
Animal
metabolism.
Fomesafen
is
not
readily
metabolized.
Rats
dosed
500
mg/
kg
excrete
up
to
95%
of
fomesafen
unchanged
in
urine.
Metabolism
is
restricted
to
substitution
on
the
benzamide
ring
moiety
in
rats.
Similarly
in
the
lactating
goat
and
poultry
metabolism
studies,
fomesafen
was
excreted
primarily
unchanged
in
urine
and
feces.
There
were
no
significant
residues
in
the
meat,
milk,
eggs,
or
meat
by­
products
of
either
the
goat
or
poultry.
Analysis
of
urine
and
feces
indicated
that
the
major
metabolic
pathway
of
fomesafen
is
reduction
to
5­(
2­
chloro­
a,
a,
a,
trifluoro­
4­
tolyloxy)­
N­
methylsulphonyl
anthranilamide,
followed
by
further
metabolism
to
5­(
2­
chloro­
a,
a,
a,­
trifluoro­
4­
tolyloxy)
anthranilic
acid.

7.
Metabolite
toxicology.
Fomesafen
remains
primarily
unchanged
in
both
plants
and
animals,
so
metabolite
toxicology
is
not
a
concern.
In
plants,
some
metabolism
occurs
due
to
ether
bond
cleavage
(
catalyzed
by
glutathione
transferase)
to
form
a
phenol
and
a
cystine
conjugate.
These
metabolites
are
not
toxicologically
active.

8.
Endocrine
disruption.
There
is
no
indication
of
endocrine
disruption
potential
from
the
fomesafen
toxicology
data.
There
is
no
hormonal
disruption
and
no
evidence
of
developmental
or
reproductive
toxicity
in
the
absence
of
maternal
toxicity.
Furthermore,
the
chemical
structure
of
fomesafen
is
unlikely
to
disrupt
mammalian
hormones.

C.
Aggregate
Exposure
1.
Dietary
exposure.
A
Tier
II
chronic
dietary
exposure
evaluation
was
made
for
fomesafen
using
the
Dietary
Exposure
Evaluation
Model
(
DEEM­
FCID
 
,
version
2.03)
from
Exponent.
These
exposure
assessments
included
fomesafen
use
on
soybeans
and
proposed
new
uses
on
cotton,
dry
beans
and
snap
beans.
Residue
data
was
taken
from
field
trials
where
fomesafen
was
applied
at
the
maximum
intended
use
rate
and
samples
were
harvested
at
the
minimum
pre­
harvest
interval
(
PHI)
to
obtain
maximum
residue
values.
Empirically
derived
processing
factors
for
processed
commodities
of
cotton
and
soybeans
(
all
1X)
were
used
in
these
assessments.
All
other
processing
factors
used
DEEM
 
(
version
7.87)
defaults.
Estimated
percent
crop
treated
(%
CT)
were
used
in
these
assessments.
Anticipated
residues
in
meat
and
milk
were
calculated
by
constructing
a
theoretical
worst­
case
diet.
Diets
7
constructed
for
these
assessments
consisted
of
a
nutritionally
balanced
mixture
of
feeds
(
typically
30%
protein
and
70%
carbohydrates.
Drinking
water
estimates
were
incorporated
directly
into
the
dietary
exposure
assessment
using
the
higher
of
the
estimated
drinking
water
concentrations
(
EDWCs)
for
surface
and
ground
water.

i.
Food.
Acute
Exposure.
Fomesafen
is
not
considered
to
be
acutely
toxic.
No
studies
that
would
suggest
an
appropriate
reference
dose
for
acute
exposures
are
present
in
the
available
toxicological
studies
for
fomesafen.

Chronic
Exposure.
The
fomesafen
chronic
dietary
risk
assessment
was
performed
for
all
population
subgroups
with
a
chronic
reference
dose
of
0.01
mg/
kg­
bw/
day
based
on
a
26­
week
feeding
study
in
dogs
with
a
no
observable
adverse
effect
level
(
NOAEL)
of
1.0
mg/
kg­
bw/
day
and
an
uncertainty
factor
of
100X.
The
100X
safety
factor
includes
intra­
and
inter­
species
variations.
No
additional
FQPA
safety
factor
was
applied.
For
the
purpose
of
aggregate
risk
assessment,
the
exposure
values
were
expressed
in
terms
of
margin
of
exposure
(
MOE),
which
was
calculated
by
dividing
the
NOAEL
by
the
exposure
for
each
population
subgroup.
In
addition,
exposure
was
expressed
as
a
percent
of
the
reference
dose
(%
RfD).
Chronic
dietary
(
food
only)
exposure
to
the
U.
S.
population
resulted
in
a
MOE
of
978,695
(
0.01%
of
the
chronic
RfD
of
0.01
mg/
kg­
bw/
day).
The
most
exposed
sub­
population
was
children
(
1­
2
years
old)
with
a
MOE
of
346,161
(
0.03%
of
the
chronic
RfD).
Since
the
benchmark
MOE
for
this
assessment
was
100
and
since
the
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
dietary
(
food
only)
exposure
to
residues
arising
from
the
current
and
proposed
tolerances
for
fomesafen.

Cancer.
A
Weight
of
Evidence
evaluation
has
established
that
the
mode
of
action
for
liver
tumor
formation
by
fomesafen
in
mice
is
via
PPAR­
alpha
activation
(
peroxisome
proliferation),
which
would
not
be
operative
in
humans.
Therefore,
fomesafen
is
not
likely
to
be
carcinogenic
in
humans,
and
no
cancer
risk
assessment
was
performed
for
fomesafen.

ii.
Drinking
water.
The
EPA
uses
the
screening
models
FIRST
or
PRZM/
EXAMS
to
estimate
potential
surface
water
concentrations
and
the
screening
model
SCI­
GROW
to
estimate
potential
ground
water
concentrations.
None
of
these
models
includes
consideration
of
the
impact
that
processing
(
mixing,
dilution,
or
treatment)
would
have
on
the
removal
of
pesticides
from
the
water
source
prior
to
distribution
as
drinking
water.
The
primary
use
of
these
models
is
to
provide
a
conservative
approximation
of
the
Estimated
Drinking
Water
Concentrations
(
EDWCs)
of
specific
pesticides
in
drinking
water.
These
models,
along
with
a
3­
year
prospective
ground
water
(
PGW)
study
were
used
by
Syngenta
to
provide
EDWCs
of
fomesafen
for
a
variety
of
crops
using
seasonal
loads
and
application
methods
according
to
the
current
and
proposed
labels.
Based
on
Tier
2
modeling
and
the
PGW
study
results,
Syngenta
determined
the
following
EDWCs
for
fomesafen:
0.07­
0.69
ppb
for
surface
water
and
1
ppb
for
ground
water.
Since
the
ground
water
EDWC
exceeds
the
surface
water
EDWCs,
8
the
ground
water
value
will
be
used
for
comparison
purposes
and
will
be
considered
to
be
protective
for
any
surface
water
concentration
concerns.

Drinking
water
estimates
were
incorporated
directly
into
the
dietary
exposure
assessment
along
with
the
food
exposure
using
the
ground
water
EDWC
of
1
ppb.
Chronic
exposure
(
food
and
water)
to
the
U.
S.
population
resulted
in
a
MOE
of
45,
250
(
0.2%
of
the
chronic
RfD
of
0.01
mg/
kg­
bw/
day.
The
most
exposed
sub­
population
was
infants
(<
1
year
old)
with
a
MOE
of
14,041
(
0.7%
of
the
chronic
RfD
of
0.01
mg/
kg­
bw/
day).
Since
the
benchmark
MOE
for
this
assessment
was
100
and
since
the
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
dietary
(
food
and
drinking
water)
exposure
to
residues
arising
from
all
current
and
proposed
uses
of
fomesafen.

2.
Non­
dietary
exposure.
There
are
no
current
or
proposed
uses
of
fomesafen
that
would
result
in
residential
exposure.

D.
Cumulative
Effects
Cumulative
Exposure
to
Substances
with
a
Common
Mechanism
of
Toxicity.
Section
408(
b)(
2)(
D)(
v)
requires
that,
when
considering
whether
to
establish,
modify,
or
revoke
a
tolerance,
the
Agency
consider
"
available
information"
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
"
other
substances
that
have
a
common
mechanism
of
toxicity".
The
EPA
does
not
have,
at
this
time,
available
data
to
determine
whether
fomesafen
has
a
common
mechanism
of
toxicity
with
other
substances
or
how
to
include
this
pesticide
in
a
cumulative
risk
assessment.
For
purposes
of
this
tolerance
action,
the
EPA
has
not
assumed
that
fomesafen
has
a
common
mechanism
of
toxicity
with
other
substances.

E.
Safety
Determination
1.
U.
S.
population.
The
chronic
dietary
exposure
analysis
(
food
plus
water)
showed
that
exposure
from
all
established
and
proposed
uses
of
fomesafen
would
result
in
a
MOE
of
45,250
(
0.2%
of
the
chronic
RfD)
for
the
general
U.
S.
population.
Based
on
the
completeness
and
reliability
of
the
toxicity
data
supporting
these
petitions,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
residues
arising
from
all
current
and
proposed
fomesafen
uses,
including
anticipated
dietary
exposure
from
food,
water,
and
all
other
types
of
non­
occupational
exposures.

2.
Infants
and
children.
Using
the
conservative
assumptions
described
in
the
exposure
section
above,
and
based
on
the
completeness
and
reliability
of
the
toxicity
data,
the
chronic
aggregate
exposure
calculation
for
current
and
proposed
uses
of
fomesafen
provided
a
MOE
9
of
14,041
for
infants
<
1
year
old
(
the
most
sensitive
population
subgroup).
Since
the
aggregate
MOE
of
14,041
exceeds
the
benchmark
MOE
of
100,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
occur
to
infants
and
children
from
aggregate
exposure
to
residues
arising
from
all
current
and
proposed
fomesafen
uses,
including
anticipated
dietary
exposure
from
food,
water,
and
all
other
types
of
non­
occupational
exposures.

F.
International
Tolerances
There
are
no
Codex
maximum
residue
levels
(
MRLs)
established
for
residues
of
fomesafen
in
or
on
soybeans,
cotton,
dry
beans
or
snap
beans.
A
Canadian
tolerance
of
0.05
ppm
is
established
for
fomesafen
residues
in
or
on
soybeans,
dry
beans,
lima
beans,
and
snap
beans.
A
Mexican
tolerance
of
0.01
ppm
is
established
for
fomesafen
residues
in
or
on
"
beans".