EPA
Registration
Division
contact:
Barbara
Madden,
(
703)
305­
6463
Interregional
Research
Project
#
4
(
IR­
4)

PP#
4E6885
and
0E6204
Summary
of
Petitions
EPA
has
received
pesticide
petitions
(
4E6885
and
0E6204)
from
Interregional
Research
Project
Number
4
(
IR­
4),
681
U.
S.
Highway
#
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
180.412
by
establishing
a
tolerance
for
residues
of
sethoxydim
(
2­[
1­(
ethoxyimino)
butyl]­
5­[
2­(
ethylthio)
propyl]­
3­
hydroxy­
2­
cyclohexen­
1­
one)
and
its
metabolites
containing
the
2­
cyclohexen­
1­
one
moiety
(
calculated
as
the
herbicide).
The
following
tolerances
are
proposed:
borage,
seed
5
ppm;
borage,
meal
40
ppm;
borage,
oil
40
ppm;
buckwheat,
grain
20
ppm;
buckwheat
flour,
20
ppm;
dill,
fresh
leaves
10
ppm;
dill
dried
leaves
10
ppm;
okra
4
ppm;
radish,
tops
5
ppm;
and
vegetable,
root,
except
sugar
beet,
subgroup
4
ppm
(
PP#
4E6885)
and
turnip,
tops
at
5.0
ppm
(
0E6204).
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
Plant
metabolism.
The
qualitative
nature
of
the
residues
in
plants
and
animals
is
adequately
understood
for
the
purposes
of
registration.

2.
Analytical
method.
Analytical
methods
for
detecting
levels
of
sethoxydim
and
its
metabolites
in
or
on
food
with
a
limit
of
detection
that
allows
monitoring
of
food
with
residues
at
or
above
the
level
in
these
tolerances
were
submitted
to
EPA.
The
proposed
analytical
method
involves
extraction,
partition,
and
clean­
up.
Samples
are
then
analyzed
by
gas
chromotagraphy
with
sulfur­
specific
flame
photometric
detection.
The
limit
of
quantitation
is
0.05
ppm.

3.
Magnitude
of
residues.
Borage
residue
field
trials
were
conducted
in
two
locations
in
EPA
Region
5,
using
two
applications
of
sethoxdyim
with
a
total
seasonal
application
rate
of
1
lb
a.
i./
A
and
pre­
harvest
interval(
s)
of
23
to
27
days.
The
results
from
these
trials
showed
maximum
total
residues
of
sethoxydim
and
its
metabolites
of
3.49
ppm
in
borage
seed.
Concentration
of
sethoxydim
residues
in
meal
and
oil
samples
is
assumed
to
behave
similarly
to
that
in
canola.
Buckwheat
field
residue
trials
were
conducted
in
five
locations
across
four
regions
where
the
crop
is
grown.
Two
applications
of
sethoxydim
were
made
at
each
field
site
with
total
seasonal
application
rates
of
1
lb
a.
i./
A
and
pre­
harvest
interval(
s)
of
19
to
22
days.
Harvested
samples
were
tested
for
residues
of
sethoxydim
and
its
metabolites,
resulting
in
maximum
residues
of
13.74
ppm
in
buckwheat
seed.
There
was
no
concentration
of
residues
in
buckwheat
groats.
Three
sethoxydim
residue
field
trials
were
conducted
in
dill
in
Region
11,
with
a
total
seasonal
application
rate
of
1.0
lb
a.
i./
A
and
a
pre­
harvest
interval(
s)
of
13­
14
days.
Residue
analyses
in
fresh
dill
leaves
and
stems
resulted
in
maximum
residues
of
6.9
ppm.
The
maximum
total
residue
of
sethoxydim
in
dried
dill
leaves
was
4.71
ppm.
Residues
did
not
concentrate
in
processed
dill
oil.
Six
residue
field
trials
were
conducted
in
okra
throughout
five
regions,
using
3
applications
at
total
seasonal
application
rates
of
1
lb
a.
i./
A
and
pre­
harvest
interval(
s)
of
13
to
14
days.
The
maximum
total
residues
of
sethoxydim
and
its
metabolites
were
1.32
ppm.
Six
residue
field
trials
were
conducted
in
radish
tops
across
five
regions,
using
one
application
of
sethoxydim
at
0.5
lb
a.
i./
A
and
preharvest
interval
of
14
days.
The
maximum
total
residues
of
sethoxydim
and
its
metabolites
were
3.62
ppm
in
radish
tops,
and
0.69
ppm
in
radish
roots.
EPA
has
previously
established
a
tolerance
for
residues
of
sethoxydim
and
its
metabolites
in
carrots,
supporting
a
tolerance
in
vegetable,
root,
except
sugar
beet,
subgroup.

B.
Toxicological
Profile
1.
Acute
toxicity.
Sethoxydim
has
favorable
acute
toxicity.
The
acute
toxicity
studies
place
technical
sethoxydim
in
toxicity
category
III
for
acute
oral,
dermal
and
inhalation
toxicity.
Sethoxydim
is
category
IV
for
both
eye
and
skin
irritation,
and
it
is
not
a
dermal
sensitizer.

2.
Genotoxicty.
Sethoxydim
was
negative
for
inducing
mutations
in
both
an
in
vitro
Ames
test
and
an
in
vitro
mammalian
cell
mutation
assay.
Sethoxydim
also
demonstrated
no
chromosomal
effects
in
an
in
vivo
sister
chromatid
exhange
(
Chinese
hamster
bone
marrow)
assay.
An
additional
in
vitro
study
investigating
unscheduled
DNA
synthesis
showed
no
effects.
In
total,
sethoxydim
has
been
tested
in
five
genetic
toxicology
assays
consisting
of
in
vitro
and
in
vivo
studies.
It
can
be
stated
that
sethoxydim
did
not
show
any
mutagenic,
clastogenic
or
other
genotoxic
activity
when
tested
under
the
conditions
of
the
studies
mentioned
above.
Therefore,
sethoxydim
does
not
pose
a
genotoxic
hazard
to
humans.

3.
Reproductive
and
developmental
toxicity.
The
reproductive
and
developmental
toxicity
of
sethoxydim
was
investigated
in
a
2­
generation
rat
reproduction
study
as
well
as
in
rat
and
rabbit
developmental
toxicity
studies.
In
the
reproduction
study,
a
decreased
pup
body
weight
and
tail
abnormalities
were
observed
at
the
highest
dose
tested.
There
were
no
effects
on
reproduction
or
evidence
of
parental
toxicity.
The
NOAEL
is
>
150
mg/
kg
bw/
day
for
reproductive
toxicity
and
30
mg/
kg
bw/
day
for
developmental
toxicity.

In
the
rat
study,
maternal
toxicity
observed
at
the
two
highest
doses
consisted
of
some
clinical
signs
including
irregular
gait
and
decreased
activity.
Developmental
changes
were
also
noted
at
the
two
highest
doses
and
consisted
of
decreased
fetal
weights,
tail
abnormalities
and
skeletal
variations.
The
maternal
and
developmental
NOAEL's
were
180
mg/
kg
bw/
day.

In
the
rabbit
teratology
study,
maternal
toxicity
observed
at
high
dose
consisted
of
decreased
food
consumption
and
body
weight
gain.
An
increased
incidence
of
incompletely
ossified
6th
sternebrae
was
the
only
sign
of
developmental
toxicity.
The
NOAEL
for
both
maternal
and
developmental
toxicity
was
320
mg/
kg
bw.

4.
Subchronic
toxicity.
The
subchronic
toxicity
of
sethoxydim
was
investigated
in
90­
day
feeding
studies
with
rats
and
mice,
a
six­
month
feeding
study
in
dogs
and
a
21­
day
dermal
administration
study
in
rats
and
a
4­
week
inhalation
study
in
rats.
Generally,
mild
toxicity
was
observed.
At
high
dose
levels
in
feeding
studies,
general
findings
were
decreased
food
consumption
and
body
weight
gain
and
liver
changes
indicative
of
an
adaptive
response
to
treatment.
In
addition,
hemosiderosis
of
the
spleen
was
observed
at
the
highest
dose
tested
in
dogs.
The
lowest
NOAEL
in
the
subchronic
feeding
studies
was
20
mg/
kg
bw/
day
in
the
90­
day
dog
study.

In
the
21­
day
repeat
dose
dermal
study,
no
systemic
effects
were
noted
up
to
the
highest
dose
tested
of
1000
mg/
kg
bw/
day.
The
4­
week
inhalation
toxicity
study
had
a
NOEC
of
0.3
mg/
l
based
on
increased
liver
weight,
clinical
chemistry
and
liver
histopathology
at
2.4
mg/
l.

5.
Chronic
toxicity.
The
NOAEL
in
the
chronic
dog
study
was
17.5
mg/
kg
bw/
day
based
on
effects
observed
at
the
high
dose
consisting
of
increased
hemosiderosis
in
the
spleen
and
depressed
myeloid
erythropoiesis
in
the
sternal
bone
marrow,
increased
absolute
and
relative
liver
weights
and
increased
serum
liver
enzymes.

In
a
rat
chronic/
oncogenicity
study,
sethoxydim
was
administered
at
doses
up
to
143
mg/
kg
bw
/
day
in
males
and
204
mg/
kg
bw/
day
in
females.
Body
weight
gain
decreases
and
liver
toxicity
in
the
form
of
hepatocellular
hypertrophy
were
observed
at
the
higher
doses
tested.
The
NOAEL's
for
the
chronic/
oncogenicity
study
in
rats
were
12
mg/
kg
bw/
day
in
males
and
66
mg/
kg
bw/
day
in
females.
There
was
no
evidence
of
carcinogenicity
in
rats.

Sethoxydim
was
also
tested
for
oncogenic
potential
in
mice.
Body
weight
gains
were
decreased
in
both
sexes
at
the
high
dose.
In
addition,
liver
toxicity
occurred
at
the
two
highest
doses
tested
in
males.
This
included
an
early
onset
of
liver
effects
including
hepatocellular
hypertrophy
and
fatty
degeneration.
The
NOAEL's
are
13.8
mg/
kg
bw/
day
for
males
and
44
mg/
kg
bw/
day
for
females.
There
was
no
evidence
that
sethoxydim
produced
a
carcinogenic
effect
in
mice.

6.
Animal
metabolism.
In
a
rat
metabolism
study
with
sethoxydim,
excretion
was
shown
to
be
extremely
rapid
and
tissue
accumulation
was
negligible.
Of
the
administered
dose,
78%
was
excreted
in
urine
and
20.1%
in
feces.
Sethoxydim
is
extensively
metabolized
with
very
little
excretion
of
parent.

7.
Metabolite
toxicology.
The
most
abundant
plant
metabolites
for
sethoxydim
are
hydroxy
derivatives.
Additional
toxicology
studies
were
conducted
on
5­
OH­
MSO2,
as
a
surrogate
for
all
hydroxy
metabolites.
Based
on
these
data,
it
was
concluded
that
the
toxicological
potency
of
the
plant
hydroxy
metabolites
is
likely
to
be
equal
to
or
less
than
that
of
the
parent
compound.
8.
Endocrine
disruption.
No
specific
tests
have
been
conducted
with
sethoxydim
to
determine
whether
the
chemical
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
a
naturally
occurring
estrogen
or
other
endocrine
effects.
However,
there
were
no
significant
findings
in
other
relevant
toxicity
studies
(
i.
e.,
subchronic
and
chronic
toxicity,
teratology
and
multi­
generation
reproductive
studies)
which
would
suggest
that
sethoxydim
produces
endocrine­
related
effects.

C.
Aggregate
Exposure
The
sethoxydim
chronic
reference
dose
(
cRfD)
is
0.14
mg/
kg
bw/
day
based
on
the
NOAEL
of
14
mg/
kg
bw/
day
in
the
mouse
oncogenicity
study
and
a
100X
safety
factor.
The
acute
reference
dose
(
aRfD)
is
1.8
mg/
kg
b.
w./
day
for
the
general
population
and
females
of
child
bearing
age,
based
on
a
NOAEL
from
the
rat
developmental
toxicity
study
of
180
mg/
kg
bw/
day
and
a
100X
safety
factor.

The
EPA
determined
that
the
FQPA
safety
factor
(
in
the
form
of
a
database
uncertainty
factor)
should
be
retained
at
10X
for
both
acute
and
chronic
risk
assessments.
This
is
based
on
the
lack
of
subchronic
and
developmental
neurotoxicity
studies
and
evidence
of
developmental
(
tail)
abnormalities
in
the
rat
developmental
and
reproductive
studies.
This
results
in
an
acute
PAD
of
0.18
mg/
kg
bw/
day
and
a
chronic
PAD
of
0.014
mg/
kg
bw/
day.

BASF
has
will
submit
a
position
document
to
the
EPA
that
indicates
a
3X
FQPA
safety
factor
is
protective
of
children
while
the
requested
subchronic
and
developmental
neurotoxicity
studies
are
being
conducted.
This
results
in
a
calculated
acute
PAD
of
0.6
mg/
kg
bw/
day
and
a
chronic
PAD
of
0.05
mg/
kg
bw/
day.

1.
Dietary
exposure.
An
assessment
was
conducted
to
evaluate
the
potential
risk
due
to
acute
and
chronic
dietary
exposure
of
the
U.
S.
population
and
sub­
populations
to
residues
of
sethoxydim
and
its
metabolites
containing
the
2­
cyclohexen­
1­
one
moiety.
Tolerance
values
have
previously
been
established
and
are
listed
in
U.
S.
40
CFR
§
180.412.
This
analysis
included
the
crops
with
established
tolerance
values
and
proposed
crop
tolerances
for
borage,
seed
at
5.0
ppm;
borage,
meal
at
40
ppm;
borage,
oil
at
40
ppm;
buckwheat,
grain
at
20
ppm;
buckwheat,
flour
at
20
ppm;
dill,
fresh
leaves
at
10
ppm;
and
dill,
dried
leaves
at
10
ppm;
okra
at
4
ppm;
radish,
tops
at
5
ppm;
and
vegetable,
root,
except
sugar
beet,
subgroup
at
4
ppm.

i.
Food.
Acute
Dietary
Exposure
Assessment
For
crops
which
have
an
existing
tolerance,
the
acute
dietary
exposure
was
calculated
by
the
EPA
and
published
in
the
Sethoxydim
Final
Rule,
Federal
Register
vol.
68,
No.
188,
September
29,2003.
The
EPA
used
tolerance
level
residues
for
most
crops,
but
field
trial
data
was
used
for
apples,
pears,
and
other
pomefruit,
grapes,
oranges,
potatoes,
strawberries,
peaches,
succulent
green
peas,
succulent
green
beans,
and
succulent
lima
beans.
Empirical
processing
data
was
used
for
apples,
grapes,
tomatoes,
and
oranges.
The
processing
factors
for
orange
juice
was
used
for
other
citrus
juices.
Percent
crop
treated
data
were
used
for
most
crops.
For
the
new
crops
listed
in
this
notice
of
filing,
the
acute
assessment
was
conducted
using
tolerance
level
residues
and
100%
crop
treated
factors.

The
acute
population
adjusted
dose
(
aPAD)
used
for
US
and
all
sub­
populations
is
0.18
mg/
kg
bw/
day.
Using
the
exposure
assumptions
discussed
above,
the
acute
dietary
exposure
from
food
is
53.8
%
aPAD
for
the
US
population.
The
two
most
highly
exposured
subpopulations
were
children
1­
2
years
old
and
children
3­
5
years
old.
The
%
aPAD
utilized
by
children
1­
2
years
and
children
3­
5
years
old
was
approximately
92%.
The
results
of
the
acute
dietary
assessment
are
presented
in
Table
1.

Table
1.
Results
for
Sethoxydim
Acute
Dietary
Exposure
Analysis.
Population
Subgroups
Exposure
Estimate
(
mg/
kg
bw/
day)
%
aPAD
U.
S.
Population
0.096814
53.8
Children
1­
2
years
0.166136
92.3
Children
3­
5
years
0.166317
92.4
Chronic
Dietary
Exposure
Assessment
For
crops
which
have
an
existing
tolerance,
the
chronic
dietary
exposure
was
calculated
by
the
EPA
and
published
in
the
Sethoxydim
Final
Rule,
Federal
Register
vol.
68,
No.
188,
September
29,2003.
The
EPA
used
tolerance
level
residues
for
all
crops
and
percent
crop
treated
data
were
used
for
most
crops.
Anticipated
residues
were
used
for
meat
and
milk.
For
the
new
crops
listed
in
this
notice
of
filing,
the
chronic
assessment
was
conducted
using
tolerance
level
residues
and
100%
crop
treated
factors.

The
chronic
population
adjusted
dose
(
cPAD)
used
for
US
and
all
sub­
populations
is
0.014
mg/
kg
bw/
day.
Using
the
exposure
assumptions
discussed
above,
sethoxydim
chronic
dietary
exposure
from
food
for
the
US
population
was
28.3%
of
the
cPAD.
The
most
highly
exposure
population
sub
group
was
infants
(<
1
year
old)
at
75.5%
cPAD.
The
results
of
the
chronic
dietary
assessment
are
presented
in
Table
2.

Table
2.
Summary
of
Chronic
Dietary
Exposure
Assessment
considering
crops
with
established
and
proposed
tolerances
for
Sethoxydim.
Population
Subgroups
Exposure
Estimate
(
mg/
kg
b.
w./
day)
%
cPAD
U.
S.
Population
0.003962
28.3
All
Infants
(<
1
yr
old)
0.010569
75.5
]

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
estimated
drinking
water
concentrations
(
EDWCs)
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.

Based
on
the
FIRST
and
SCIGROW
models,
the
EDWCs
of
sethoxydim
for
acute
exposure
are
estimated
to
be
100.0
ug/
L
(
ppb)
in
surface
water
and
1.0
ug/
L
in
ground
water.
The
EDWCs
for
chronic
exposure
are
estimated
to
be
20.0
ug/
L
in
surface
water
and
1.0
ug/
L
in
ground
water.

Acute
Aggregate
Exposure
and
Risk
(
Food
and
water)
The
aggregate
acute
risk
includes
residues
of
sethoxydim
from
food
and
water.
Exposures
from
residential
uses
are
not
included
in
the
acute
aggregate
assessment.
The
estimated
peak
concentrations
of
sethoxydim
in
surface
and
ground
water
are
lower
than
the
DWLOCs
for
all
sub­
populations
(
Table
3).
The
results
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
3.
Acute
Drinking
Water
Levels
of
Comparison
for
Sethoxydim
Population
Subgroup
aPAD
(
mg/
kg/
day)
Food
Exp
(
mg/
kg/
day)
Max.
Water
Exp
(
mg/
kg/
day)
Acute
Ground
Water
EDWC
(
ug/
L)
Acute
Surface
Water
EDWC
(
ug/
L)
DWLOC
(
ug/
L)

U.
S.
Population
0.18
0.096814
0.083186
2912
Children
1­
2
years
0.18
0.166136
0.013864
1.0
100
139
Children
3­
5
years
0.18
0.166317
0.013683
137
Chronic
Aggregate
Exposure
and
Risk
(
food
and
water)
The
aggregate
chronic
risk
includes
residues
of
sethoxydim
from
food
and
water.
Exposures
from
residential
uses
are
not
included
in
the
chronic
aggregate
assessment.
The
estimated
peak
concentrations
of
sethoxydim
in
surface
and
ground
water
are
lower
than
the
DWLOCs
for
all
sub­
populations
(
Table
5).
The
results
demonstrate
that
there
are
no
safety
concerns
based
on
established
and
new
uses,
and
that
the
results
clearly
meet
the
FQPA
standard
of
reasonable
certainty
of
no
harm.

Table
5.
Chronic
Drinking
Water
Levels
of
Comparison
for
Sethoxydim
Population
Subgroup
cPAD
(
mg/
kg/
day)
Food
Exp
(
mg/
kg/
day)
Max.
Water
Exp
(
mg/
kg/
day)
Acute
Ground
Water
EDWC
(
ug/
L)
Acute
Surface
Water
EDWC
(
ug/
L)
DWLOC
(
ug/
L)

U.
S.
Population
0.014
0.003962
0.010038
351
All
Infants
(<
1
yr
old)
0.014
0.010569
0.003431
1.0
20.0
34
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.
Sethoxydim
is
only
used
for
spot
treatment
in
residential
environments.
The
EPA
has
stated
that
exposure
from
spot
treatment
is
negligible
and
a
exposure
risk
assessment
is
not
required.
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
sethoxydim.

2.
Non­
dietary
exposure.
Sethoxydim
is
only
used
for
spot
treatment
in
gardens,
flower
beds,
recreational
areas,
and
around
building
and
structures.
The
EPA
has
determined
that
for
sethoxydim,
the
quantification
of
dermal
exposure
risk
assessment
is
not
required
because
of
lack
of
dermal
and
prenatal
toxicity
in
rabbits,
and
the
low
dermal
absorption
of
sethoxydim.
The
EPA
has
also
stated
that
the
residential
post­
application
exposure
from
spot
treatment
is
negligible.
Therefore
based
on
the
lack
of
dermal
toxicity
and
negligible
exposure
potential,
a
non­
dietary
exposure
assessment
was
not
conducted.
D.
Cumulative
Effects
The
EPA
is
currently
developing
methodology
to
perform
cumulative
risk
assessments.
At
this
time,
there
is
no
available
data
to
determine
whether
sethoxydim
has
a
common
mechanism
of
toxicity
with
other
substances
or
how
to
include
this
pesticide
in
a
cumulative
risk
assessment.
Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
sethoxydim
does
not
appear
to
produce
a
toxic
metabolite
common
to
other
substances.

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
sethoxydim
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
sethoxydim
residues.

F.
International
Tolerances
There
are
no
codex
maximum
residue
limits
or
tolerances
for
sethoxydim
in
borage,
buckwheat,
dill,
okra,
radish
tops,
or
vegetable,
root,
except
sugar
beet,
subgroup.
