Summary
of
Petitions
The
petitioner
summary
of
the
pesticide
petitions
is
printed
below
as
required
by
section
408(
d)(
3)
of
the
FFDCA.
The
summary
of
the
petitions
was
prepared
by
the
petitioner
and
represents
the
view
of
the
petitioner.
EPA
is
publishing
the
petition
summary
verbatim
without
editing
it
in
any
way.
The
petition
summary
announces
the
availability
of
a
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)

2E6501
EPA
has
received
pesticide
petition
(
2E6501)
from
the
IR­
4
Project,
Rutgers
University
Technology
Centre
of
New
Jersey,
681
U.
S.
Highway
1
South,
North
Brunswick,
New
Jersey
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
180.355
by
establishing
tolerances
for
the
combined
residues
of
the
herbicide
bentazon
(
3­
isopropyl­
1H­
2,1,3­
benzothiadiazin­
4(
3H)­
one
2,2­
dioxide)
and
its
6­
and
8­
hydroxy
metabolites
in
or
on
the
raw
agricultural
commodities
peaches
and
nectarines
at
0.05
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.
The
qualitative
nature
of
the
residue
in
plants
is
adequately
understood.
Bentazon
is
rapidly
metabolized,
conjugated
and
incorporated
into
natural
plant
constituents.
Metabolism
involves
the
hydroxylation
of
bentazon
at
the
6­
and
8­
position.
The
terminal
residues
of
regulatory
concern
are
bentazon,
6­
hydroxy
bentazon,
and
8­
hydroxy
bentazon
(
as
specified
in
40
CFR
180.355
(
a)).

2.
Analytical
method.
Adequate
enforcement
methods
are
available
for
the
determination
of
residues
of
bentazon
and
its
6­
and
8­
hydroxy
metabolites
in/
on
plant
commodities.
The
Pesticide
Analytical
Manual
(
PAM)
Vol.
II
lists
Method
II,
a
GLC
method
with
flame
photometric
detection
for
the
determination
of
bentazon
and
its
hydroxy
metabolites
in/
on
corn,
rice,
and
soybeans;
the
limit
of
detection
for
each
compound
is
0.05
ppm.
Method
III,
modified
from
Method
II,
is
available
for
the
determination
of
bentazon
and
its
hydroxy
metabolites
in/
on
peanuts
and
seed
and
pod
vegetables
with
a
limit
of
detection
of
0.05
ppm
for
each
compound.

3.
Magnitude
of
residues.
Nine
field
trials
in
peach
orchards
were
conducted
with
bentazon
in
1999
in
EPA
Regions
I
(
1
trial),
II
(
4
trials),
V
(
1
trial),
and
X
(
3
trials)
in
order
to
determine
the
magnitude
of
the
residue
in/
on
peaches.
Bentazon
was
applied
two
times
to
peaches
as
a
directed
spray
to
the
orchard
floor
at
a
rate
of
1.0
lb
ai/
A,
for
a
total
of
2.0
lb
ai/
A.
Applications
were
made
12
to
16
days
apart
and
marketable
peaches
were
collected
9
to
15
days
following
the
last
application.
Samples
were
analyzed
for
residues
of
bentazon
and
its
6­
OH
and
8­
OH
metabolites.
No
residues
above
the
lowest
level
of
method
validation
(
LLMV)
of
0.05
ppm
were
observed
for
bentazon,
6­
OH
bentazon
or
8­
OH
bentazon.

B.
Toxicological
Profile
1.
Acute
toxicity.
Acute
toxicity
data
for
bentazon
show
that
this
chemical
is
not
acutely
toxic
by
the
oral,
inhalation,
or
dermal
routes
of
exposure
(
Toxicity
Categories
III
and
IV).
It
is
moderately
irritating
to
the
eye
(
Toxicity
Category
II)
and
slightly
irritating
to
the
skin
(
Toxicity
Category
IV).
Bentazon
is
also
a
dermal
sensitizer.

2.
Genotoxicty.
Bentazon
was
not
mutagenic
in
the
tests
for
gene
mutations,
which
were
reverse
mutation
assays
in
S.
typhimurium
and
in
E.
coli
WP2
uvrA
as
well
as
forward
mutation
assays
with
in
vitro
Chinese
hamster
ovary
cell
(
HGPRT)
cultures.
Bentazon
was
also
negative
in
the
mouse
micronucleus
test
for
assessing
structural
chromosomal
aberrations
and
the
unscheduled
DNA
synthesis
assay
with
primary
mouse
hepatocytes
for
detecting
DNA
damage.

3.
Reproductive
and
developmental
toxicity.
A
developmental
study
in
rats
was
conducted
at
doses
of
0,
40,
100,
or
250
mg/
kg/
day.
The
maternal
NOAEL
(
no
observed
adverse
effect
level)
is
250
mg/
kg/
day,
HDT
(
highest
dose
tested).
The
maternal
LOAEL
(
lowest
observed
adverse
effect
level)
is
greater
than
250
mg/
kg/
day.
The
developmental
NOAEL
is
100
mg/
kg/
day.
The
developmental
LOAEL
is
250
mg/
kg/
day,
based
on
increased
postimplantation
loss,
skeletal
variations
(
incomplete
or
absent
ossification
in
the
phalangeal
nucleii
of
the
extremities,
the
sternebrae
and
cervical
vertebrae),
and
reduced
body
weights
or
fetuses
surviving
to
day
21.
A
developmental
study
in
rabbits
was
conducted
at
doses
of
0,
75,
150,
or
375
mg/
kg/
day.
The
maternal/
developmental
NOAEL
is
150
mg/
kg/
day.
The
maternal/
developmental
LOAEL
is
375
mg/
kg/
day
(
HDT),
based
on
doe
with
partial
abortion,
embryonic
resorptions,
and
no
living
fetuses.
A
2­
generation
reproduction
toxicity
study
in
rats
was
conducted
at
doses
of
0,
200,
800,
or
3,200
ppm;
equivalent
to
0,
15,
62,
or
249
mg/
kg/
day.
The
parental
systemic
NOAEL
is
62
mg/
kg/
day.
The
parental
systemic
LOAEL
is
249
mg/
kg/
day,
based
on
increased
incidences
of
kidney
mineralization
and
liver
microgranuloma.
The
reproductive
NOAEL
is
15
mg/
kg/
day.
The
reproductive
LOAEL
is
62
mg/
kg/
day,
based
on
reduced
pup
growth
(
body
weight
gain)
during
lactation.

4.
Subchronic
toxicity.
A
21­
day
dermal
toxicity
study
in
rabbits
was
conducted
at
doses
of
0,
250,
500,
or
1,000
mg/
kg/
day.
The
NOAEL
is
1,000
mg/
kg/
day
(
HDT).
The
LOAEL
is
greater
than
1,000
mg/
kg/
day.
A
13­
week
feeding
study
in
rats
was
conducted
at
doses
of
0,
400,
1,200,
or
3,600
ppm;
equivalent
to
0,
25.3,
77.8,
or
243.3
mg/
kg/
day
for
males
and
0,
28.9,
86.1,
or
258.3
mg/
kg/
day
for
females.
The
NOAEL
is
77.8
mg/
kg/
day.
The
LOAEL
is
243.3
mg/
kg/
day
for
males
and
258.3
mg/
kg/
day
for
females
based
on
depressed
mean
body
weights
in
females,
a
slight
increase
in
food
consumption
in
males,
increased
thromboplastin
and
prothrombin
times
(
males
only),
and
increased
kidney
and
liver
weights.

5.
Chronic
toxicity.
A
chronic
feeding
study
in
dogs
was
conducted
at
doses
of
0,
100,
400,
or
1,600
ppm;
equivalent
to
0,
3.2,
13.1,
or
52.3
mg/
kg/
day.
The
NOAEL
is
3.2
mg/
kg/
day.
The
LOAEL
is
13.1
mg/
kg/
day
based
on
a
dose­
dependent
presence
of
feces
with
red
areas
in
dogs
at
13.1
mg/
kg/
day
(
400
ppm)
and
52.3
mg/
kg/
day
(
1600
ppm)
and
slight
to
severe
anemia
at
the
high
dose.
A
chronic
feeding/
carcinogenicity
study
in
rats
was
conducted
at
doses
of
0,
200,
800,
or
4,000
ppm;
equivalent
to
0,
9,
35,
or
180
mg/
kg/
day
in
males
and
0,
11,
45,
or
244
mg/
kg/
day
in
females.
The
NOAEL
is
9/
11
mg/
kg/
day,
in
males/
females.
The
LOAEL
is
35/
45
mg/
kg/
day,
in
males/
females,
based
on
increased
water
consumption,
changes
in
urinalysis
and
hematology/
coagulation
parameters,
and
decreased
absolute
and
relative
thyroid
weight.
No
evidence
of
carcinogenicity
was
observed.
An
oncogenicity
study
in
mice
was
conducted
at
doses
of
0,
100,
400,
or
2000
ppm;
equivalent
to
0,
12,
47,
or
242
mg/
kg/
day
in
males
and
0,
12,
48,
or
275
mg/
kg/
day
in
females.
The
NOAEL
is
12
mg/
kg/
day.
The
LOAEL
is
47/
48
mg/
kg/
day
in
males/
females,
based
on
increased
prothrombin
time,
increased
liver
and
kidney
weights,
calcification
of
the
tunica
albuginea,
and
islet
cell
hyperplasia
of
the
pancreas.
No
evidence
of
carcinogenicity
was
observed.

6.
Animal
metabolism.
A
rat
metabolism
study
with
oral
dosing
showed
that
parent
bentazon
was
the
major
metabolite
found
in
urine,
amounting
to
77.37­
91.02%
of
the
dose.
Another
metabolism
study
demonstrated
that
the
absorption
and
excretion
of
bentazon
or
its
sodium
salt
in
male
rats
after
oral
administration
is
rapid
and
essentially
equivalent.
No
sex
differences
in
the
absorption,
metabolism
or
excretion
of
sodium
bentazon
are
apparent
based
on
equivalent
excretion
half­
lives
(
4
hours),
pattern
of
excretion
(
greater
than
90%
in
urine)
or
urinary
metabolite
identification
(
greater
than
80%
as
free
acid).
A
dermal
penetration
study
in
rats
was
conducted
at
doses
of
0.12,
1.2,
12,
or
120
mg/
kg.
Single
topical
application
of
radioactive
sodium
bentazon
did
not
appear
to
significantly
penetrate
the
skin
since
a
maximum
of
only
1­
2%
of
the
radioactivity
was
recovered
(
primarily
in
the
urine)
at
72
hours.
Negligible
amounts
of
dermally
applied
radioactivity
were
retained
in
the
liver,
kidneys,
G.
I.
tract
and
carcass.
For
risk
assessment
purposes,
dermal
penetration
is
estimated
to
be
1­
2%.

7.
Metabolite
toxicology.
There
are
no
metabolites
of
toxicological
significance
to
mammals.

8.
Endocrine
disruption.
No
special
studies
investigating
potential
estrogenic
or
endocrine
effects
of
bentazon
have
been
conducted.
However,
the
standard
battery
of
required
studies
has
been
completed.
These
studies
include
an
evaluation
of
the
potential
effects
on
reproduction
and
development,
and
an
evaluation
of
the
pathology
exposure.
These
studies
are
generally
considered
to
be
sufficient
to
detect
any
endocrine
effects
but
no
such
effects
of
the
endocrine
organs
following
repeated
or
long­
term
were
noted
in
any
of
the
studies.

C.
Aggregate
Exposure
1.
Dietary
exposure­­
i.
Food
In
1999,
EPA
evaluated
the
hazard
and
exposure
data
for
bentazon
and
recommended
that
the
FQPA
safety
factor
be
retained
at
10X
in
assessing
the
risk
posed
by
this
chemical
because
there
was
evidence
of
increased
susceptibility
in
the
developmental
toxicity
study
in
rats
and
in
the
two­
generation
reproduction
toxicity
study
in
rats.
The
10X
FQPA
Safety
Factor
is
applicable
to
females
13­
50
years
old
for
acute
dietary
and
residential
exposure
assessments
and
to
all
population
subgroups
for
chronic
dietary
and
residential
exposure
assessments.
The
acute
and
chronic
Population
Adjusted
Doses
(
aPAD
and
cPAD,
respectively)
are
modification
of
the
acute
and
chronic
RfDs
to
include
the
FQPA
safety
factor.
The
acute
or
chronic
PAD
is
equal
to
the
acute
or
chronic
RfD
divided
by
the
FQPA
safety
factor.
Acute
and
chronic
dietary
exposure
analyses
for
bentazon
were
performed
using
the
Dietary
Exposure
Evaluation
Model
(
DEEM)
which
incorporates
data
generated
in
the
USDA
1989­
1992
Nationwide
Continuing
Surveys
of
Food
Intake
by
Individuals
(
CSII).
For
the
acute
analysis,
tolerance
level
residues
were
used
and
100%
crop
treated
(
CT)
was
assumed
for
all
commodities
(
Tier
I)
for
the
females
13­
50
years
old
subgroup
(
the
subpopulation
of
concern).
For
all
the
females
13­
50
years
old
subgroup,
5%
or
less
of
the
aPAD
is
occupied
by
dietary
exposure
from
food.
Results
of
the
acute
analysis
indicate
that
the
acute
dietary
risk
residues
in
food
associated
with
existing
and
proposed
uses
of
bentazon
do
not
exceed
EPA's
level
of
concern.
A
refined
chronic
dietary
exposure
analysis
(
Tier
3)
was
performed
using
anticipated
and
tolerance
level
residues
for
commodities
for
the
general
U.
S.
population
and
all
population
subgroups.
For
the
chronic
analysis,
percent
crop
treated
information
was
used
for
several
commodities.
The
percent
chronic
population
adjusted
dose
(%
cPADs)
for
all
subgroups
were
less
than
100%,
with
the
highest
being
28%
for
the
children
1­
6
years
subgroup.
Results
of
the
chronic
analysis
indicate
that
the
chronic
dietary
risk
from
residues
in
food
associated
with
the
existing
and
proposed
uses
of
bentazon
do
not
exceed
EPA's
level
of
concern.
ii.
Drinking
water.
SCI­
GROW
(
Screening
Concentration
in
Ground
Water)
modeling
indicates
that
bentazon
residue
(
bentazon
+
its
metabolite,
2­
amino­
N­
isopropyl
benzamide
[
AIBA])
concentrations
in
groundwater
used
as
drinking
water
are
not
likely
to
exceed
4.25
ppb.
The
other
regulated
bentazon
metabolites
(
6­
hydroxy
and
8­
hydroxy
bentazon)
have
not
been
found
in
environmental
fate
studies.
Limited
monitoring
data
indicated
a
range
of
bentazon
concentrations
(
excluding
degradation
products)
in
groundwater
of
20
to
120
ppb.
Because
monitoring
data
indicate
a
higher
concentration
than
the
SCI­
GROW
screening
model,
EPA
used
the
20
ppb
as
the
environmental
exposure
concentration
(
EEC)
for
both
acute
and
chronic
scenarios.
The
EEC
for
surface
water
(
from
EPA's
Pesticide
Root
Zone
Model­
EXAMS
modeling)
is
41
ppb
for
the
peak
(
acute)
and
8
ppb
for
the
36­
year
annual
mean
(
chronic).
The
surface
and
ground
water
estimates
were
used
to
compare
against
back­
calculated
drinking
water
levels
of
comparison
(
DWLOCs)
for
aggregate
risk
assessments.
For
the
acute
exposure
scenario,
the
DWLOC
is
2800
ppb
for
females
(
13+/
nursing).
For
the
chronic
exposure
scenario,
the
DWLOCs
are
95,
82,
22,
94,
and
95
ppb
for
the
US
population,
females
(
13+/
nursing),
children
(
1­
6
years),
Hispanics
and
males
(
13­
19
years),
respectively.
2.
Non­
dietary
exposure.
Because
bentazon
is
registered
for
consumer
use
on
turf
and
ornamentals,
there
is
potential
for
residential
exposure
to
adult
applicators
and
adults
and
children
entering
recreational
and
residential
areas
treated
with
bentazon.
Short­
and
intermediate­
term
exposure
and
risk.
The
handler
exposure
is
expected
to
be
short­
term
while
the
post­
application
exposure
is
expected
for
both
the
short­
and
intermediate­
term.
However,
since
there
is
no
short­
term
dermal
endpoint,
the
residential
post­
application
exposure
cannot
be
aggregated
with
the
handler
exposure.
Short­
term,
non­
dietary
ingestion
exposure
for
toddlers
is
not
a
concern
because
it
was
determined
that
there
is
no
acute
dietary
or
oral
endpoint
applicable
to
infants
and
children.
However,
intermediate­
term,
non­
dietary
ingestion
exposure
to
toddlers
playing
on
treated
turf
is
possible
and
was
assessed
using
the
intermediateterm
endpoint
identified
from
the
one­
year
dog
feeding
study.
Intermediate­
term
exposure
is
not
expected
for
the
ornamental
use.
The
level
of
concern
for
residential
exposures
to
bentazon
is
for
MOE's
less
than
1,000.
There
are
no
chemical­
specific
or
site­
specific
data
available
to
determine
the
potential
risks
associated
with
residential
exposures
from
handling
bentazon.
Therefore,
the
exposure
estimates
are
based
on
assumptions
and
generic
data
as
specified
by
the
December
18,
1997
Draft
HED
Standard
Operating
Procedures
(
SOPs)
for
Residential
Exposure
Assessments.
Because
bentazon
is
applied
no
more
than
twice
per
year,
only
short­
term
exposure
is
expected
for
the
residential
handler.
Because
a
dermal
endpoint
of
concern
for
the
short­
term
duration
was
not
identified,
only
inhalation
exposure
estimates
are
relevant.
Assuming
that
a
homeowner
treats
his
lawn
and
ornamental
plants
on
the
same
day,
the
aggregate
inhalation
short­
term
MOE
is
500,000
for
the
residential
handler.
This
estimate
indicates
that
the
potential
handler
risks
from
residential
uses
of
bentazon
do
not
exceed
EPA's
level
of
concern.
Environmental
fate
data
indicate
that
bentazon
is
moderately
resistant
to
degradation
(
t1/
2
=
24­
65
days).
Due
to
the
length
of
time
bentazon
is
expected
to
remain
in
the
environment,
both
short­
and
intermediate­
term
residential
post­
application
exposures
are
expected.
For
toddlers
playing
on
treated
turf,
the
oral
intermediate­
term
endpoint
was
used
to
assess
toddler
incidental
ingestion
exposures.
Based
on
the
residential
use
pattern,
no
long­
term
post­
application
residential
exposure
is
expected.
Short­
term,
non­
dietary
oral
exposures
to
the
toddler
were
not
assessed
because
the
subgroup
of
concern
was
identified
as
females
13­
50
years
old.
This
endpoint
is
not
applicable
to
the
infant
and
children
population
subgroups.
Intermediate­
term,
post­
application
exposure
is
not
expected
from
the
ornamental
use
of
bentazon.
Changes
to
the
Residential
SOPs
have
been
proposed
that
alter
the
residential
post­
application
scenario
assumptions.
The
proposed
assumptions
are
expected
to
better
represent
residential
exposure
and
are
still
considered
to
be
high­
end,
screening
level
assumptions.
Therefore,
the
proposed
assumptions
are
used
to
calculate
exposure
estimates.
The
dermal
post­
application
exposure
from
the
turfgrass
use
for
the
adult
results
in
an
MOE
of
9,100.
The
MOEs
for
post­
application
exposures
for
the
toddler
are
calculated
as
6,400
and
3,500
for
dermal
and
hand­
to­
mouth
exposures,
respectively.
The
aggregate
intermediate
MOE
for
post­
application
residential
exposure
to
toddlers
is
2,200.
Therefore,
all
residential
post­
application
exposure
estimates
are
well
below
EPA's
level
of
concern.
Because
these
estimates
were
calculated
using
screening­
level
assumptions,
it
is
believed
that
the
actual
risks
will
be
lower.
For
the
intermediate­
term,
typical
lawn
maintenance
practices
such
as
mowing
and
watering
are
expected
to
expedite
the
dissipation
of
bentazon
on
turfgrass.
Therefore,
with
less
residue
available,
potential
incidental
hand­
to­
mouth
exposures
are
expected
to
be
substantially
lower.

D.
Cumulative
Effects
There
is
no
available
data
to
determine
whether
bentazon
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,
bentazon
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
this
notice
of
filing,
therefore,
it
is
assumed
that
bentazon
does
not
have
a
common
mechanism
of
toxicity
with
other
substances.

E.
Safety
Determination
1.
U.
S.
Population.
Acute
risk
estimates
from
aggregate
exposure
to
bentazon
in
food
and
water
are
below
EPA's
level
of
concern.
For
Tier
1
acute
dietary
exposure
analysis,
it
was
assumed
that
100%
of
the
crops
treated
with
bentazon
and
that
residues
equaled
the
tolerance
level.
For
all
females
13­
50
years
old
subgroups,
less
than
or
equal
to
5%
of
the
aPAD
is
occupied
by
dietary
exposure
from
food.
The
acute
dietary
risk
from
food
associated
with
the
existing
and
proposed
uses
of
bentazon
is
below
EPA's
level
of
concern.
The
estimated
average
concentrations
of
bentazon
in
surface
and
ground
water
are
less
than
EPA's
levels
of
comparison
for
bentazon
in
drinking
water
as
a
contribution
to
acute
aggregate
exposure.
Chronic
(
Non­
Cancer)
Aggregate
Risk
estimates
are
below
EPA's
level
of
concern.
The
chronic
dietary
exposure
analysis
for
residues
in
food
incorporated
anticipated
and
tolerance
level
residues
for
commodities.
Percent
CT
information
was
used
for
several
commodities.
The
%
cPADs
for
all
subgroups
were
less
than
100%,
with
the
highest
being
28%
for
the
children
(
1­
6
years
old)
subgroup.
Thus,
the
chronic
dietary
risk
estimates
from
food
associated
with
existing
and
proposed
uses
of
bentazon
do
not
exceed
EPA's
level
of
concern.
For
ground
and
surface
water,
the
estimated
average
concentrations
of
bentazon
are
less
than
EPA's
levels
of
comparison
for
bentazon
in
drinking
water
as
a
contribution
to
chronic
aggregate
exposure.
Aggregate
short­
term
risk
estimates
are
below
EPA's
level
of
concern.
In
aggregating
short­
term
risk,
the
background
chronic
dietary
exposure
(
food
+
drinking
water)
and
short
term
inhalation
exposures
from
residential
uses
are
considered.
Because
a
dermal
endpoint
of
concern
for
the
short­
term
duration
was
not
identified,
only
inhalation
exposure
estimates
are
relevant
for
the
adult
handler.
Short­
term
inhalation
exposure
may
occur
for
a
homeowner
treating
turf
and
ornamentals
on
the
same
day.
The
total
short­
term
food
and
residential
aggregate
MOE
value
is
220,000.
As
this
MOE
is
greater
than
1,000,
the
short­
term
food
and
residential
aggregate
risk
estimate
is
below
EPA's
level
of
concern.
For
surface
and
ground
water,
the
estimated
average
concentrations
of
bentazon
are
less
than
EPA's
levels
of
comparison
for
bentazon
in
drinking
water
as
a
contribution
to
short­
term
aggregate
exposure.
Aggregate
intermediate­
term
risk
estimates
are
below
EPA's
level
of
concern
for
adults.
In
aggregating
intermediate­
term
risk,
the
background
chronic
dietary
exposure
(
food
+
drinking
water)
and
intermediate­
term
dermal
exposures
from
residential
uses
are
considered.
For
adults,
dermal
post­
application
exposures
may
result
from
dermal
contact
with
treated
turf.
For
adults,
the
total
food
and
residential
intermediate­
term
aggregate
MOE
is
7,600.
As
this
value
is
greater
than
1,000,
the
intermediate­
term
aggregate
risk
estimate
is
below
EPA's
level
of
concern.
For
surface
and
ground
water,
the
estimated
average
concentrations
of
bentazon
are
less
than
EPA's
levels
of
comparison
for
bentazon
in
drinking
water
as
a
contribution
to
intermediate­
term
aggregate
exposure.
A
cancer
risk
assessment
was
not
done.
Bentazon
is
classified
as
a
Group
E
chemical
(
evidence
of
non­
carcinogenicity
for
humans)
based
upon
lack
of
evidence
of
carcinogenicity
in
rats
and
mice.
Based
on
these
risk
assessments,
it
is
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
bentazon
residues.
2.
Infants
and
children.
In
assessing
the
potential
for
additional
sensitivity
of
infants
and
children
to
residues
of
bentazon,
data
from
developmental
toxicity
studies
in
the
rat
and
rabbit
and
a
2­
generation
reproduction
study
in
the
rat
are
considered.
The
developmental
toxicity
studies
are
designed
to
evaluate
adverse
effects
on
the
developing
organism
resulting
from
maternal
pesticide
exposure
during
gestation.
Reproduction
studies
provide
information
relating
to
effects
from
exposure
to
the
pesticide
on
the
reproductive
capability
of
mating
animals
and
data
on
systemic
toxicity.
FFDCA
section
408
provides
that
EPA
shall
apply
an
additional
tenfold
margin
of
safety
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
prenatal
and
postnatal
toxicity
and
the
completeness
of
the
data
base
unless
EPA
determines
that
a
different
margin
of
safety
will
be
safe
for
infants
and
children.
Margins
of
safety
are
incorporated
into
EPA
risk
assessments
either
directly
through
use
of
a
margin
of
exposure
(
MOE)
analysis
or
through
using
uncertainty
(
safety)
factors
in
calculating
a
dose
level
that
poses
no
appreciable
risk
to
humans.
EPA
believes
that
reliable
data
support
using
the
standard
uncertainty
factor
(
usually
100
for
combined
interspecies
and
intraspecies
variability)
and
not
the
additional
tenfold
MOE/
uncertainty
factor
when
EPA
has
a
complete
data
base
under
existing
guidelines
and
when
the
severity
of
the
effect
in
infants
or
children
or
the
potency
or
unusual
toxic
properties
of
a
compound
do
not
raise
concerns
regarding
the
adequacy
of
the
standard
MOE/
safety
factor.
The
toxicological
data
base
for
evaluating
prenatal
and
postnatal
toxicity
of
bentazon
is
complete
with
respect
to
current
data
requirements.
There
was
evidence
of
increased
susceptibility
following
in
utero
exposure
to
bentazon
in
the
prenatal
developmental
toxicity
study
in
rats
and
there
was
quantitative
evidence
of
increased
susceptibility
following
pre­
/
postnatal
exposure
to
bentazon
in
the
2­
generation
reproduction
study
in
rats.
There
is
a
complete
toxicity
data
base
for
bentazon
and
exposure
data
are
complete
or
are
estimated
based
on
data
that
reasonably
accounts
for
potential
exposures.
The
FQPA
Safety
Factor
for
protection
of
infants
and
children
will
be
retained
at
10x
for
bentazon
due
to
the
increased
pre­
/
postnatal
susceptibility.
The
FQPA
Safety
Factor
for
bentazon
is
applicable
to
females
13­
50
years
old
only
for
acute
dietary
and
residential
exposure
assessments
because
increased
susceptibility
was
demonstrated
in
the
developmental
study
in
rats
which
is
designed
to
evaluate
chemical
effects
on
the
mother
and
fetus
from
the
time
of
implantation
of
the
fertilized
egg
in
the
uterus
through
the
end
of
gestation.
The
safety
factor
is
also
applicable
to
all
population
subgroups
for
chronic
dietary
and
residential
exposure
assessments
because
increased
susceptibility
was
demonstrated
in
the
2­
generation
reproduction
study
(
which
is
designed
to
assess
the
effects
of
the
pesticide
on
male
and
female
reproductive
processes,
from
egg
and
sperm
production
and
mating
through
pregnancy,
birth,
nursing,
growth
and
development,
and
maturation).
An
acute
endpoint
was
not
identified
and
this
risk
assessment
was
not
required.
Using
the
exposure
assumptions
described
in
this
unit,
it
was
concluded
that
aggregate
exposure
to
bentazon
from
food
will
utilize
28%
of
the
chronic
PAD
for
children
(
1­
6
years
old).
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
chronic
PAD
because
the
chronic
PAD
represents
the
level
at
or
below
which
daily
aggregate
dietary
exposure
over
a
lifetime
will
not
pose
appreciable
risks
to
human
health.
Despite
the
potential
for
exposure
to
bentazon
in
drinking
water
and
from
non­
dietary,
non­
occupational
exposure,
the
aggregate
exposure
is
not
expected
to
exceed
100%
of
the
chronic
PAD.
Although
bentazon
is
a
registered
herbicide
for
use
on
turf
and
ornamentals,
short­
term
non­
dietary
ingestion
exposure
for
toddlers
is
not
assessed
because
EPA
determined
that
there
is
no
acute
dietary
or
oral
endpoint
applicable
to
infants
and
children.
Aggregate
intermediate­
term
risk
estimates
are
below
EPA's
level
of
concern
for
infants
and
children.
In
aggregating
intermediate­
term
risk,
background
chronic
dietary
exposure
(
food
+
drinking
water)
and
intermediate­
term,
non­
dietary
oral
and
dermal
exposures
from
residential
uses
are
considered.
For
toddlers,
dermal
and
non­
dietary
oral
postapplication
exposures
may
result
from
dermal
contact
with
treated
turf
as
well
as
hand­
to­
mouth
transfer
of
residues
from
turfgrass.
For
infants
and
children,
the
total
food
and
residential
intermediate­
term
aggregate
MOE
is
2,000.
As
this
value
is
greater
than
1,000,
the
intermediate­
term
aggregate
risk
estimate
is
below
EPA's
level
of
concern.
For
surface
and
ground
water,
the
estimated
average
concentrations
of
bentazon
are
less
than
EPA's
levels
of
comparison
for
bentazon
in
drinking
water
as
a
contribution
to
intermediate­
term
aggregate
exposure.
Based
on
these
risk
assessments,
it
is
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
infants
and
children
from
aggregate
exposure
bentazon
to
residues.

F.
International
Tolerances
The
Commission
of
European
Communities
has
established
provisional
maximum
residue
level
for
bentazon
(
sum
of
bentazon
and
the
conjugates
6­
OH­
and
8­
OH­
bentazon
expressed
as
bentazon)
on
peaches
(
including
nectarines
and
similar
hybrids)
at
0.10
ppm.
There
is
no
Codex
proposal
for
limits
of
bentazon
in/
on
peaches.
