Document ID: EPA-HQ-OPP-2005-0537-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-03-22T05:00Z

Summary
of
Petitions
The
petitioner
summary
of
the
pesticide
petitions
is
printed
below
as
required
by
FFDCA
section
408
(
d)
(
3).
The
summary
of
the
petitions
is
prepared
by
the
petitioner
and
represents
the
view
of
the
petitioner.
The
petition
summary
announces
the
availability
of
the
description
of
the
analytical
methods
available
to
EPA
for
the
detection
and
measurement
of
the
pesticide
chemical
residues
or
an
explanation
of
why
no
such
method
is
needed.

Interregional
Research
Project
Number
4
(
IR­
4)

PP#
3E6564,
3E6565
and
5E6914
EPA
has
received
pesticide
petitions
(
PP#
3E6564,
3E6565
and
5E6914)
from
IR­
4,
681
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
180.345
by
establishing
tolerances
for
combined
residues
of
the
herbicide,
ethofumesate
(
2­
ethoxy
­
2,
3­
dihydro­
3,
3­
dimethyl­
5­
benzofuranyl
methanesulfonate)
and
its
metabolites
NC
8493
and
NC
9607
(
both
calculated
as
the
parent
compound)]
in
or
on
the
raw
agricultural
commodities:
carrots
at
10
parts
per
million
(
ppm)
(
PP
3E6565),
garden
beets
tops
at
4
ppm,
garden
beet
roots
at
0.5
ppm
(
PP
3E6564),
onion
dry
bulb
at
0.3
ppm
(
PP
5E6914),
garlic
bulb
at
0.3
ppm
(
PP
5E6914),
and
shallots
at
0.3
ppm
(
PP
5E6914).
Note
that
the
carrots
tolerance
requested
by
IR­
4
is
with
regional
restriction,
for
use
in
Washington
and
Oregon
only.
EPA
has
determined
that
the
petitions
contain
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.
This
notice
includes
a
summary
of
the
petitions
prepared
by
Bayer
CropScience,
P.
O.
Box
12014,
2
T.
W.
Alexander
Drive,
Research
Triangle
Park,
NC
27709.

A.
Residue
Chemistry
1.
Plant
metabolism.
The
metabolism
of
ethofumesate
in
plants
is
adequately
understood.
Studies
have
been
conducted
in
sugar
beet,
annual
ryegrass,
cabbage,
wheat
and
radish,
all
showing
similar
route
of
metabolism
for
ethofumesate.
The
major
metabolites
are
NC
8493,
NC
9607
(
the
lactone
analogue),
NC
20645
(
the
carboxy
analogue)
together
with
small
amounts
of
the
unchanged
parent.
Metabolite
NC
20645
exists
in
equilibrium
with
NC
9607
and
all
recovered
NC
20645
were
derivatized
and
reported
as
NC
9607.
From
the
studies,
the
residues
of
concern
are
the
combined
residues
of
ethofumesate
and
its
metabolites
NC
8493
and
NC
9607.]

2.
Analytical
method.
Analytical
methods
have
been
developed
and
validated
for
the
determination
of
ethofumesate
and
its
metabolites
NC
9607,
and
NC
8493
in
sugar
beet
(
roots
and
tops),
meat
and
milk.
The
method
has
also
been
shown
to
capture
NC
20645
as
NC
9607
in
sugar
beet
and
milk.
Therefore,
reported
residues
of
NC
9607
include
any
NC
20645
that
may
be
present.
Ethofumesate
and
its
related
residues
are
extracted
in
a
two­
part
process
and
quantified
using
gas
chromatography
equipped
with
flame
photometric
detector
(
GC­
NPD)
operated
in
sulfur
mode.
The
method
limit
of
quantification
is
0.05
ppm.
Therefore,
adequate
analytical
methodology
is
available
for
enforcement
purposes
and
it
allows
detection
of
residues
at
or
above
the
proposed
tolerances.

3.
Magnitude
of
residues.
Carrots
 
IR
4
received
requests
from
Washington
and
Oregon
for
the
use
of
ethofumesate
on
carrots.
In
support
of
the
requests,
magnitude
of
residue
data
were
collected
from
three
field
trials
in
Washington.
Samples
were
analyzed
for
residues
of
ethofumesate
and
its
metabolites
NC
9607
and
NC
8493
(
results
for
NC
8493
were
reported
as
NC
8906,
a
derivative
of
NC
8493).
In
treated
carrot
samples,
the
highest
total
residues
measured
for
the
three
analytes
ranged
from
3.9
ppm
to
6.3
ppm.
The
data
support
the
proposed
10
ppm
tolerance
for
the
carrot
roots.

Beets,
garden
 
IR
4
received
requests
from
New
York
and
Oregon
for
the
use
of
ethofumesate
on
garden
beet.
In
support
of
the
requests,
magnitude
of
residue
data
were
collected
from
a
total
of
six
field
trials
conducted
in
Texas,
Oregon,
New
York,
Wisconsin,
Michigan,
and
Washington.
Samples
were
analyzed
for
residues
of
ethofumesate
and
metabolites
NC
9607
and
NC
8493.
In
treated
samples
for
the
beet
tops,
the
highest
total
residues
measured
for
the
three
analytes
ranged
from
about
1.0
ppm
to
3.8
ppm.
The
total
residues
on
the
beet
roots
ranged
from
none
detectable
(
below
the
lowest
level
of
method
validation
of
0.05
ppm
for
each
of
the
three
analytes)
to
a
sum
residue
value
of
about
0.25
ppm.
The
data
support
the
proposed
tolerances
for
the
garden
beet
tops
(
4
ppm)
and
the
garden
beet
roots
(
0.5
ppm).

Onion
dry
bulb,
garlic
bulb,
shallot
bulb
 
IR
4
received
requests
from
Oregon,
Colorado,
Idaho,
North
Dakota,
Washington,
California,
Arizona,
New
Mexico,
and
Michigan
for
the
use
of
ethofumesate
on
dry
bulb
onions.
In
support
of
the
requests,
magnitude
of
residue
data
were
collected
from
a
total
of
10
field
trials
conducted
in
California,
Idaho,
Oregon,
New
York,
Texas,
Washington,
Michigan,
and
Colorado.
Samples
were
analyzed
for
residues
of
ethofumesate
and
metabolites
NC
9607
and
NC
8906
(
a
derivative
of
NC
8493
metabolite).
In
treated
samples
for
the
dry
bulb
onions,
the
total
residues
measured
for
the
three
analytes
ranged
from
none
detectable
(
below
the
lowest
level
of
method
validation
of
0.05
ppm
for
each
of
the
three
analytes)
to
a
sum
residue
value
of
about
0.196
ppm.
The
data
support
the
proposed
tolerances
of
0.4
ppm
for
the
dry
bulb
onion,
garlic
bulb,
and
shallot
bulb.

B.
Toxicological
Profile
1.
Acute
toxicity.
Ethofumesate
is
of
low
acute
toxicity
placing
the
active
ingredient
in
Toxicity
Category
III
and
IV.
Ethofumesate
is
non­
irritating
to
the
eyes
and
skin
and
is
not
a
skin
sensitizer.

2.
Genotoxicty.
Ethofumesate
has
been
evaluated
through
a
full
battery
of
mutagenicity
assays.
Ethofumesate
was
not
mutagenic
or
genotoxic
in
any
assay
in
either
the
presence
or
absence
of
metabolic
activation.

3.
Reproductive
and
developmental
toxicity.
i.
Teratology
­
Rat
Groups
of
24
time­
mated
female
rats
received
ethofumesate
by
daily
oral
gavage
at
dose
levels
of
0,
10,
100,
or
1000
mg/
kg/
day
from
day
6
to
day
15
of
gestation.
All
dams
survived
the
study
and
no
adverse
effects
on
uterine/
implantation
and
fetal
values
or
on
the
incidence
of
fetal
defects
were
detected
at
any
dose
level.
NOEL
(
dam):
100
mg/
kg
/
day,
based
on
body
weight,
food
and
water
effects
at
1000
mg/
kg/
day.
NOEL
(
fetus):
1000
mg/
kg
/
day,
based
on
the
absence
of
effects
at
the
highest
dose
tested
in
the
study.

ii.
Teratology
­
Rabbit
Groups
of
16
mated
female
New
Zealand
White
rabbits
were
dosed
with
ethofumesate
orally
by
gavage
at
0,
300,
600,
or
1200
mg/
kg/
day
from
day
7
to
19
of
gestation.
Administration
of
ethofumesate
led
to
maternal
toxicity
at
1200
mg/
kg/
day,
which
was
characterized
by
reduced
body
weight
gain,
food
consumption,
and
abortion
in
one
animal.
There
was,
however,
no
indication
of
an
adverse
effect
on
embryonic
or
fetal
development
at
this
dose.
There
were
no
significant
maternal
and
fetal
effects
at
doses
of
300
and
600
mg/
kg/
day.
NOEL
(
dams):
600
mg/
kg/
day,
based
on
maternal
toxic
effects
at
1200
mg/
kg/
day.
NOEL
(
offspring):
1200
mg/
kg/
day,
based
on
the
absence
of
effects
at
the
highest
dose
tested
in
the
study.

iii.
Two­
Generation
Reproduction
­
Rat
Groups
of
25
males
and
25
females
Sprague­
Dawley
rats
were
dosed
with
ethofumesate
at
0,
3000,
10000,
and
30000
ppm
in
the
diet
to
assess
reproductive
performance
over
two
successive
generations.
There
were
no
treatment
related
mortalities
or
clinical
observations.
Mating
performance,
fertility,
vaginal
smear
patterns,
and
macroscopic
or
microscopic
findings
were
not
affected
by
ethofumesate.
Pup
body
weights,
pup
development,
and
litter
size
at
3000
ppm
were
not
affected
by
ethofumesate.
Pup
survival,
clinical
conditions,
and
necropsy
findings
were
not
affected
by
treatment.
NOEL
(
all
generations):
3000
ppm,
corresponding
to
overall
245
and
296
mg/
kg/
day
in
males
and
females,
respectively,
based
on
reduction
in
body
weight
gain
at
10000
ppm.

4.
Subchronic
toxicity.

i.
90
Day
Dietary
­
Rat
Groups
of
ten
male
and
ten
female
Sprague­
Dawley
CD
rats
received
ethofumesate
in
the
diet
at
dose
levels
of
0,
300,
3000,
or
30000
ppm
for
13
weeks.
There
were
no
deaths
or
treatmentrelated
clinical
findings
during
the
course
of
the
study.
At
30000
ppm
reduced
body
weight
gain
(
in
females
and
in
males
to
a
lesser
extent),
lower
food
consumption
(
in
females)
and
utilization
(
in
both
sexes),
and
marginally
increased
water
consumption
(
in
males)
were
recorded.
Increased
liver
weights
were
recorded
in
males
and
females.
Increased
kidney
weights
occurred
among
males
with
an
associated
incidence
of
irregular
renal
cortical
scarring
at
post­
mortem
examination.
NOEL:
3000
ppm,
corresponding
to
190
and
230
mg/
kg/
day
in
males
and
females,
respectively,
based
on
the
reduction
in
body
weight
and
minor
biochemical
disturbances
and
kidney
changes
recorded
at
30000
ppm.

ii.
90
Day
oral
­
Dog
Groups
of
four
male
and
four
female
Beagle
dogs
received
ethofumesate
once
daily
by
gavage
at
0,
250,
750,
or
1500
mg/
kg/
day
for
13
weeks.
There
were
no
treatment­
related
clinical
signs,
ocular
changes,
organ
weight
changes,
or
hematological
changes.
Body
weights
and
body
weight
gains
were
unaffected
by
treatment
and
food
consumption
for
all
treated
groups
was
comparable
to
that
of
the
untreated
group.
NOEL:
250
and
750
mg/
kg/
day
in
males
and
females,
respectively,
based
on
the
minor
effects
on
clinical
chemistry
at
750
and
1500
mg/
kg/
day
in
males
and
females,
respectively.

iii.
90
Day
Dietary
­
Mouse
Groups
of
ten
male
and
ten
female
CD­
1
mice
received
ethofumesate
in
the
diet
at
concentrations
of
0,
300,
3000
or
10000
ppm
for
13
weeks.
No
treatment­
related
clinical
signs
were
observed
and
there
was
no
treatment­
related
effect
on
body
weight
gain.
Food
consumption
of
treated
groups
was
similar
to
that
of
controls.
There
were
no
treatmentrelated
macroscopic
post­
mortem
findings
or
histological
changes.
NOEL:
10000
ppm,
corresponding
to
2054
and
3103
mg/
kg/
day
for
males
and
females,
respectively,
based
on
the
absence
of
toxic
effects
at
the
highest
dose
tested
in
the
study.

5.
Chronic
toxicity.

i.
Chronic
Toxicity
­
Dog
Groups
of
eight
male
and
eight
female
beagle
dogs
received
technical
ethofumesate
at
dietary
concentrations
of
0,
800,
4000
or
20000
ppm
for
104
weeks.
At
termination,
liver
weights
were
increased
in
both
sexes
at
the
highest
dose
level
but
there
was
no
associated
histopathological
change.
No
observed
adverse
effect
level:
4000
ppm,
corresponding
to
118
and
109
mg/
kg/
day
for
males
and
females,
respectively,
based
on
liver
weight
and
clinical
chemistry
changes
at
20000
ppm.

ii.
Combined
Chronic
Toxicity/
Oncogenicity
­
Rat
Groups
of
50
male
and
50
female
Sprague­
Dawley
rats
were
dosed
daily
for
104
weeks
with
ethofumesate
via
the
diet
at
0,
2000,
7000
or
20000
ppm.
In
males
receiving
20000
ppm
reduced
body
weight
gain
and
reduced
food
consumption
were
recorded.
At
the
same
dose
in
females
reduced
body
weight
gain,
increased
liver
weight,
and
histological
changes
in
liver
were
seen.
Reduced
body
weight
gain
(
females
only)
was
seen
at
7000
ppm.
No
effects
considered
to
be
of
toxicological
significance
were
recorded
in
males
and
females
receiving
2000
ppm.
NOEL:
2000
ppm,
corresponding
to
113
and
143
mg/
kg/
day
in
males
and
females,
respectively.

iii.
Oncogenicity
­
Mouse
Groups
of
50
male
and
50
female
CD­
1
mice
received
ethofumesate
in
the
diet
at
0,
1000,
3000
or
10000
ppm
for
80
weeks.
The
only
treatment­
related
changes
observed
were
increased
liver
weights
in
all
treated
female
groups.
In
the
absence
of
histopathological
changes
in
this
organ,
this
effect
was
not
considered
to
be
of
toxicological
significance
at
any
dose
level
and
especially
at
1000
ppm
where
the
increase
was
only
slightly
more
than
10%.
NOEL:
1000
ppm,
corresponding
to
161
and
204
mg/
kg/
day
in
males
and
females,
respectively,
based
the
liver
weight
changes
at
3000
ppm.
6.
Animal
metabolism.
The
metabolism
of
ethofumesate
has
been
extensively
studied
in
rats,
ruminants
and
hens.
Studies
with
radiolabelled
ethofumesate
in
the
rat
show
that
the
compound
is
rapidly
and
extensively
absorbed.
Ethofumesate
is
extensively
metabolised
mostly
to
the
water
soluble
metabolite
NC
20645
(
the
carboxy
analogue)
that
is
excreted
mainly
in
the
urine.
At
higher
dose
levels
there
was
an
increase
in
excretion
via
the
faeces.
Most
of
the
administered
radiolabel
was
eliminated
from
the
body
within
the
first
24
hours
after
dosing.
Tissue
residue
levels
five
or
seven
days
after
dosing
were
very
low.
Even
at
the
high
dose
levels
(
100
or
500
mg/
kg)
maximum
levels
were
below
1
mg/
kg
in
most
tissues.
There
was
no
evidence
of
selective
accumulation
in
any
tissue
or
organ.
Three
studies
conducted
with
repeated
dietary
treatments
showed
no
significant
effect
on
the
absorption,
distribution,
metabolism
and
excretion
in
the
rat.
A
dairy
cow
was
orally
dosed
twice
daily
with
[
14C]­
ethofumesate
with
a
mean
daily
dose
of
2.94
g
(
equivalent
to
5.0
mg/
kg
body
weight)
for
four
consecutive
days.
This
dose
was
equivalent
to
an
exposure
of
274
ppm
in
the
diet.
Radioactive
residues
were
detectable
in
all
edible
tissues
at
between
0.033
and
1.863
mg
equivalents/
kg
tissue.
In
milk,
residue
levels
rose
rapidly
reaching
a
maximum
of
0.134
mg
equivalents/
kg
at
32
hours
post
administration
of
the
initial
dose.
The
highest
residue
levels
were
found
in
the
kidney
at
1.863
mg
equivalents/
kg,
followed
by
the
liver
at
0.661
mg/
equivalents/
kg.
In
most
tissues
the
major
component
seen
was
the
unchanged
parent
compound
with
small
quantities
of
metabolites
NC
8493,
NC
9607
(
the
lactone
analogue)
and
NC
20645.

Three
laying
hens
were
orally
dosed
with
[
14C]­
ethofumesate
at
1.50
mg
per
bird
per
day
for
ten
consecutive
days.
The
dose
was
equivalent
to
about
12
ppm
in
the
diet.
Following
administration
of
the
first
dose
of
ethofumesate,
elimination
of
the
dosed
radioactivity
was
rapid
with
82%
recovered
within
24
hours.
Residue
levels
of
ethofumesate
and/
or
its
metabolites
in
the
edible
tissues
of
the
hen
were
low,
with
residue
range
from
0.002
(
egg
whites)
to
0.095
mg
(
liver)
equivalents/
kg
tissue.
Analysis
of
the
nature
of
the
residues
showed
that
unchanged
ethofumesate
was
present
in
all
tissues
and
was
the
major
residue
identified
in
the
egg
yolks,
fat
and
skin.
NC
20645
was
the
major
residue
identified
in
the
muscle
and
liver
and
was
also
present
in
the
skin
and
egg
yolks.
NC
9607
was
present
in
all
tissues.

7.
Endocrine
disruption.
No
special
studies
have
been
conducted
to
investigate
the
potential
of
ethofumesate
to
induce
estrogenic
or
other
endocrine
effects.
However,
no
evidence
of
estrogenic
or
other
endocrine
effects
has
been
noted
in
any
of
the
standard
toxicology
studies
that
have
been
conducted
with
this
product
and
there
is
no
reason
to
suspect
that
any
such
effects
would
be
likely.

C.
Aggregate
Exposure
1.
Dietary
exposure.

i.
Food.
Tier
1
dietary
risk
assessments
were
conducted
for
acute
and
chronic
exposures.
Dietary
exposure
estimates
were
based
on
tolerances
that
have
been
established
(
40
CFR
180.345)
for
combined
residues
of
ethofumesate
and
metabolites
in
or
on
sugar
beets
and
the
proposed
tolerances
for
minor
crops
use
in
onions,
garlic
and
shallots
(
0.4
ppm),
carrots
(
10.0
ppm)
and
garden
beets
(
0.5
ppm).
It
was
assumed
that
100%
of
the
crops
were
treated
with
ethofumesate.
Dietary
exposure
estimates
were
calculated
using
the
Dietary
Exposure
Evaluation
Model
software
(
DEEM
 
,
Exponent,
Inc.,
formerly
Novigen
Sciences,
Inc.,
Version
7.87)
and
the
1994­
1996
and
1998
USDA
Continuing
Survey
of
Food
Intake
by
Individuals
(
CSFII)
consumption
data
base.
An
acute
reference
dose
(
RfD)
of
6.0
mg/
kg/
day
was
used
for
the
acute
dietary
assessment
and
was
based
on
the
results
from
a
rabbit
teratology
study
(
NOEL
600
mg/
kg/
day)
and
an
uncertainty
factor
of
100
(
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation).
The
U.
S.
population
was
estimated
to
have
an
acute
dietary
exposure
of
0.010338
mg/
kg/
day
(
95th
percentile)
which
occupies
0.17%
of
the
acute
RfD.
The
most
highly
exposed
subpopulation
was
non­
nursing
infants
at
1.3%
(
0.079699
mg/
kg/
day)
of
the
acute
RfD.

Chronic
dietary
exposure
was
evaluated
using
a
reference
dose
(
RfD)
of
1.09
mg/
kg/
day,
based
on
the
results
from
a
chronic
dog
study
(
NOAEL
of
109
mg/
kg/
day)
and
an
uncertainty
factor
of
100
(
10X
for
interspecies
extrapolation
and
10X
for
intraspecies
variation).
Chronic
dietary
exposure
for
the
U.
S.
population
was
estimated
to
be
0.002060
mg/
kg/
day
which
occupies
0.2%
of
the
chronic
reference
dose.
The
most
highly
exposed
subpopulation
was
non­
nursing
infants
at
1.2%
(
0.012950
mg/
kg/
day)
of
the
chronic
reference
dose.
There
is
no
concern
for
exposures
occupying
100%
or
less
of
the
RfD.
Therefore,
the
acute
and
chronic
dietary
exposures
for
both
the
U.
S.
population
and
infants
and
children
are
well
within
acceptable
levels.

ii.
Drinking
water.
US
EPA's
Standard
Operating
Procedure
(
SOP)
for
Drinking
Water
Exposure
and
Risk
Assessments
was
used
to
perform
the
drinking
water
assessment.
This
SOP
uses
a
variety
of
tools
to
conduct
drinking
water
assessments.
These
tools
include
water
models
such
as
SCI­
GROW,
FIRST,
PRZMS/
EXAMS,
and
monitoring
data.
When
monitoring
data
is
not
available,
the
models
are
used
to
predict
potential
residues
in
surface
and
ground
water
and
the
highest
value
is
assumed
to
be
the
drinking
water
residue.
In
the
case
of
ethofumesate,
SCI­
GROW
and
PRZM/
EXAMS
models
were
used
to
estimate
a
water
residue.
The
estimated
concentrations
of
the
pesticide
in
surface
water
or
ground
water
were
calculated
and
then
compared
to
the
drinking
water
level
of
comparison
(
DWLOC).
The
DWLOC
is
the
concentration
of
a
pesticide
in
drinking
water
that
would
be
acceptable
as
an
upper
limit.
These
drinking
water
levels
of
comparison
estimates
are
based
on
conservative
dietary
(
food)
exposures
and
are
expected
to
be
much
higher
in
real
world
situations.

For
adults,
the
chronic
DWLOC
was
38,078
ppb
and
the
acute
DWLOC
was
209,637
ppb.
The
chronic
and
acute
DWLOCs
for
non­
nursing
infants
were
10,771
ppb
and
59,204
ppb,
respectively.
The
estimated
environmental
concentration
(
EEC)
for
the
worst
case
chronic
scenario
was
29
ppb
(
PRZM/
EXAMS)
and
the
acute
EEC
(
PRZM/
EXAMS)
was
158
ppb.
The
DWLOCs
are
substantially
greater
than
the
high­
end
estimated
exposure
from
the
surface
water
models
indicating
risk
from
potential
drinking
water
exposure
to
ethofumesate
is
well
within
acceptable
levels.

2.
Non­
dietary
exposure.
Ethofumesate
is
an
active
ingredient
in
three
products:
Nortron 
SC
Herbicide,
Progress,
Herbicide,
and
Prograss,
Herbicide.
There
are
no
residential
uses
of
Nortron 
SC
Herbicide
or
Progress 
Herbicide.
Prograss
®
Herbicide
may
be
applied
to
residential
lawns
by
professional
lawn
care
operators.
It
is
not
intended
for
use
by
homeowners.
Therefore,
there
is
no
exposure
of
homeowners
to
ethofumesate
during
the
mixing,
loading,
and
application
of
Prograss
®
Herbicide
to
residential
lawns.
Post­
application
exposure
to
adults
and
toddlers
on
lawns
treated
with
Prograss
®
Herbicide
is
possible,
however.
Tier
I
residential
reentry
assessments
were
prepared
for
adults
and
toddlers
following
treatment
of
residential
lawns
with
Prograss
®
Herbicide.
Estimates
were
made
for
the
worst
case
scenario,
3
applications
of
Prograss
®
Herbicide
at
a
rate
of
3
lb
ai/
A
at
21
day
intervals.
Turf
transferable
residues
were
conservatively
estimated
using
EPA
default
assumptions
of
5%
of
application
rate
immediately
after
treatment,
and
10%
dissipation
per
day.

Using
these
assumptions,
the
residue
was
calculated
to
be
37.7
:
g/
cm2
immediately
after
the
third
treatment.
EPA
Standard
Operating
Procedures
(
SOPs)
for
Residential
Exposure
Assessment
were
used
to
complete
the
residential
exposure
estimates
for
adults
and
toddlers.
Exposure
of
adults
to
ethofumesate
is
from
the
dermal
route
only.
In
addition
to
dermal
exposure,
toddlers
may
have
oral
exposure
to
ethofumesate
during
post­
application
activities
on
treated
turf
via
hand­
to­
mouth,
object­
to­
mouth,
and
soil
ingestion
routes.
Risk
was
estimated
by
calculating
dermal
margins
of
exposure
(
MOEs)
for
adults
and
toddlers,
and
an
oral
MOE
for
toddlers.
Dermal
margins
of
exposure
(
MOEs)
were
based
on
a
rabbit
21/
22
day
dermal
no­
observable
adverse
effect
level
(
NOAEL)
of
1000
mg/
kg/
day.
Oral
MOEs
were
based
on
a
rat
90­
day
oral
NOAEL
of
190
mg/
kg/
day.
Dermal
MOEs
for
adults
and
toddlers
were
1280
and
765,
respectively.
The
oral
MOE
for
toddlers
was
3015.
The
combined
MOE
for
toddlers
from
dermal
and
oral
exposure
was
610.
MOEs
for
adult
and
toddler
activities
on
residential
lawns
following
treatment
with
the
maximum
application
of
Prograss
®
Herbicide
are
well
above
the
target
MOE
of
100
when
conservative
Tier
I
assumptions
were
used
in
the
assessment.
This
assessment
indicates
that
there
is
a
reasonable
certainty
of
no
harm
to
adults
or
toddlers
from
potential
residential
exposure
to
ethofumesate
after
application
to
homeowner
lawns.

D.
Cumulative
Effects.

There
is
no
reliable
information
to
indicate
that
toxic
effects
of
ethofumesate
would
be
cumulative
with
those
of
another
pesticide
chemical.
Thus,
it
is
appropriate
to
consider
only
the
potential
risks
of
ethofumesate
in
an
aggregate
exposure
assessment.

E.
Safety
Determination.

1.
U.
S.
population.
Acute
dietary
exposure
for
the
U.
S.
population
to
residues
of
ethofumesate
from
current
and
proposed
uses
was
estimated
to
occupy
0.2%
of
the
acute
RfD,
which
is
well
below
levels
expected
to
pose
any
appreciable
risk
to
human
health.
Additionally,
the
acute
DWLOC
was
calculated
to
be
over
1300­
fold
greater
than
potential
ethofumesate
residues
predicted
in
drinking
water
by
the
water
models.
Therefore,
aggregate
acute
exposure
to
ethofumesate
for
proposed
and
current
uses
is
within
acceptable
levels.
Ethofumesate
may
be
applied
to
residential
lawns
by
professional
lawn
care
operators
which
may
result
in
postapplication
exposure
to
adults
on
lawns
treated
with
ethofumesate.
Aggregate
short­
term
exposures
were
determined
by
combining
chronic
dietary
(
food
and
water)
exposures
with
shortterm
residential
exposures.
The
short­
term
aggregate
MOE
for
the
general
population
of
adults
was
calculated
to
be
1235
which
is
well
above
the
acceptable
level
of
100.
Therefore,
aggregate
short­
term
exposure
and
risk
for
adults
is
expected
to
be
well
within
acceptable
levels.
Using
conservative
exposure
assumptions
previously
described,
chronic
dietary
exposure
to
residues
of
ethofumesate
from
current
and
proposed
uses
was
estimated
to
occupy
0.2%
of
the
chronic
RfD
for
the
general
U.
S.
population.
The
chronic
DWLOC
for
adults
was
calculated
to
be
over
1,300
fold
greater
that
potential
ethofumesate
residue
in
drinking
water
predicted
by
conservative
screening­
level
models.
Thus,
based
on
the
completeness
and
reliability
of
the
toxicity
data
and
the
conservative
exposure
assessment
it
is
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
the
general
U.
S.
population
from
acute,
short­
term
or
chronic
aggregate
exposures
to
ethofumesate
residues
from
current
and
proposed
uses.

2.
Infants
and
children.
Acute
dietary
exposure
for
the
infants
and
children
subpopulations
to
residues
of
ethofumesate
from
current
and
proposed
uses
was
estimated
to
occupy
1.3%
of
the
acute
RfD,
which
is
well
below
levels
expected
to
pose
any
appreciable
risk
to
human
health.
Additionally,
the
acute
DWLOC
was
calculated
to
be
over
375­
fold
greater
than
potential
ethofumesate
residues
predicted
in
drinking
water
by
the
water
models.
Therefore,
aggregate
acute
exposure
to
ethofumesate
for
proposed
and
current
uses
is
within
acceptable
levels.
Infants
and
children
may
experience
short­
term
dermal
and
oral
exposure
to
ethofumesate
as
a
result
of
postapplication
activities
on
treated
residential
turf.
Aggregate
short­
term
exposures
were
determined
by
combining
chronic
dietary
(
food
and
water)
exposures
with
short­
term
residential
exposures.
The
short­
term
aggregate
MOE
was
560
for
infants
and
children,
which
is
well
above
the
acceptable
level
of
100.
Using
conservative
exposure
assumptions
previously
described,
chronic
dietary
exposure
to
residues
of
ethofumesate
from
current
and
proposed
uses
was
estimated
to
occupy
1.2%
of
the
chronic
RfD
for
the
most
highly
exposed
subpopulation,
non­
nursing
infants
.
The
chronic
DWLOC
for
children
was
calculated
to
be
over
350
fold
greater
than
potential
ethofumesate
residues
in
drinking
water
predicted
by
conservative
screening­
level
models.
Thus,
based
on
the
completeness
and
reliability
of
the
toxicity
data
and
the
conservative
exposure
assessment
it
is
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
infants
and
children
from
acute,
short­
term
or
chronic
aggregate
exposures
to
ethofumesate
residues
from
current
and
proposed
uses.

F.
International
Tolerances.

CODEX
Maximum
Residue
Levels
(
MRL)
are
not
yet
established
for
ethofumesate.
European
Union
(
EU)
has
published
its
provisional
MRLs
for
ethofumesate
(
Directive
2003/
60/
EC
of
June
18,
2003).
These
MRLs
are
established
in
accordance
with
Article
4
(
1)(
f)
of
Directive
91/
414/
EEC;
unless
amended,
the
provisional
MRLs
will
become
definitive
with
effect
from
July
14,
2007.
The
EU
MRLs
are
for
crops
of
cereals,
meat/
milk/
poultry
commodities,
fresh/
dry
fruits
and
nuts,
fresh
vegetables
and
subgroups
(
e.
g.,
root
and
tuber
vegetables,
bulb
vegetables),
pulses,
oil
seed
crops,
potatoes,
tea,
and
hops.