48377
Federal
Register
/
Vol.
68,
No.
156
/
Wednesday,
August
13,
2003
/
Notices
toxicological
endpoint
for
short­
term
dermal
risks
is
the
NOEL
of
100
mg/
kg/
day
from
a
21
 
day
dermal
toxicity
study
in
rabbits.
No
acute
oral
hazard
has
been
identified
following
an
acute
exposure
to
S­
metolachlor
and,
therefore,
no
nondietary
assessment
is
needed.
The
short­
term
dermal
postapplication
risks
for
adults
and
children
are
acceptable,
ranging
from
520
to
870.
These
risk
estimates
exceed
the
EPA's
level
of
concern
for
S­
metolachlor
(
all
MOEs
are
greater
than
100).
Aggregate
exposure.
(
Drinking
Water
and
Dietary
Exposure).
Using
the
total
MOE
equation
for
the
determination
of
aggregate
chronic
exposure
(
food
and
drinking
water
only)
resulted
in
an
aggregate
MOET
of
>
4,000
for
the
most
sensitive
subpopulation,
non­
nursing
infants.
For
this
particular
subpopulation,
there
are
no
non­
dietary
exposure
contributions
to
the
MOET
aggregate
value.

D.
Cumulative
Effects
EPA
has
examined
the
common
mechanism
potential
for
S­
metolachlor
and
has
concluded
that
S­
metolachlor
should
not
be
included
with
some
pesticides
that
comprise
the
class
of
chloroacetanilides
included
in
a
``
Common
Mechanism
Group.''
Therefore,
a
cumulative
assessment
is
not
necessary
for
S­
metolachlor.

E.
Safety
Determination
1.
U.
S.
population.
Based
on
the
aggregate
assessment
described
above
and
the
completeness
and
reliability
of
the
toxicity
data,
it
is
concluded
that
aggregate
exposure
to
S­
metolachlor
(
including
the
proposed
uses)
in
food
will
utilize
less
than
0.1
percent
of
the
cRfD
for
the
U.
S.
population.
EPA
generally
has
no
concern
for
exposures
below
100
percent
of
the
RfD
because
the
RfD
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
S­
metolachlor
in
drinking
water
and
from
non­
dietary,
non­
occupational
exposures,
the
assessment
presented
above
demonstrates
that
the
high
levels
of
safety
exist
for
current
and
proposed
uses
of
S­
metolachlor;
it
is
not
expected
that
aggregate
exposure
from
all
sources
will
exceed
100%
of
the
RfD.
Therefore,
one
can
conclude
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
S­
metolachlor.
2.
Infants
and
children.
[
FFDCA
section
408
provides
that
EPA
may
apply
an
additional
safety
factor
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
pre­
and
post­
natal
toxicity
and
the
completeness
of
the
database.
Based
on
the
current
toxicological
data
requirements,
the
database
relative
to
pre­
and
post­
natal
effects
for
children
is
complete.
A
full
consideration
of
the
available
reproductive
toxicity
data
supporting
Smetolachlor
demonstrates
no
increased
sensitivity
to
infants
and
children.
Therefore,
it
is
concluded
that
an
additional
uncertainty
factor
is
not
warranted
to
protect
the
health
of
infants
and
children
and
that
the
cRfD
at
0.1
mg/
kg/
day
is
appropriate
for
assessing
aggregate
risk
to
infants
and
children
from
use
of
S­
metolachlor.
Based
on
the
aggregate
assessment
described
above,
the
percent
of
the
cRfD
that
will
be
utilized
by
aggregate
exposure
to
residues
of
S­
metolachlor
is
less
than
0.7
percent
for
all
children
subpopulations.
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD
because
the
RfD
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
Smetolachlor
in
drinking
water
and
from
non­
dietary,
non­
occupational
exposure,
the
assessment
described
above
demonstrates
that
it
is
not
expected
that
aggregate
exposure
from
all
sources
provides
for
a
large
margin
of
safety
and
will
exceed
100%
of
the
RfD.
Therefore,
based
on
the
completeness
and
reliability
of
the
toxicity
data
and
the
exposure
assessment,
it
is
concluded
there
is
a
reasonable
certainty
that
no
harm
will
result
to
infants
and
children
from
aggregate
exposure
to
Smetolachlor
residues.

F.
International
Tolerances
There
are
no
Codex
Alimentarius
Commission
(
CODEX)
maximum
residue
levels
(
MRL's)
established
for
residues
of
S­
metolachlor
in
or
on
raw
agricultural
commodities.

[
FR
Doc.
03
 
20643
Filed
8
 
12
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0271;
FRL
 
7322
 
6]

Etoxazole;
Notice
of
Filing
a
Pesticide
Petition
to
Establish
a
Tolerance
for
a
Certain
Pesticide
Chemical
in
or
on
Food
AGENCY:
Environmental
Protection
Agency
(
EPA).
ACTION:
Notice.

SUMMARY:
This
notice
announces
the
initial
filing
of
a
pesticide
petition
proposing
the
establishment
of
regulations
for
residues
of
a
certain
pesticide
chemical
in
or
on
various
food
commodities.
DATES:
Comments,
identified
by
docket
ID
number
OPP
 
2003
 
0271,
must
be
received
on
or
before
September
12,
2003.

ADDRESSES:
Comments
may
be
submitted
electronically,
by
mail,
or
through
hand
delivery/
courier.
Follow
the
detailed
instructions
as
provided
in
Unit
I.
of
the
SUPPLEMENTARY
INFORMATION.

FOR
FURTHER
INFORMATION
CONTACT:
Daniel
Kenny,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001;
telephone
number:
(
703)
305
 
7546;
e­
mail
address:
kenny.
dan@
epa.
gov.

SUPPLEMENTARY
INFORMATION:

I.
General
Information
A.
Does
this
Action
Apply
to
Me?

You
may
be
potentially
affected
by
this
action
if
you
are
an
agricultural
producer,
food
manufacturer,
or
pesticide
manufacturer.
Potentially
affected
entities
may
include,
but
are
not
limited
to:
 
Crop
Production
(
NAICS
111)
 
Animal
Production
(
NAICS
112)
 
Food
Manufacturing
(
NAICS
311)
 
Pesticide
Manufacturing
(
NAICS
32532)]
This
listing
is
not
intended
to
be
exhaustive,
but
rather
provides
a
guide
for
readers
regarding
entities
likely
to
be
affected
by
this
action.
Other
types
of
entities
not
listed
in
this
unit
could
also
be
affected.
The
North
American
Industrial
Classification
System
(
NAICS)
codes
have
been
provided
to
assist
you
and
others
in
determining
whether
this
action
might
apply
to
certain
entities.
If
you
have
any
questions
regarding
the
applicability
of
this
action
to
a
particular
entity,
consult
the
person
listed
under
FOR
FURTHER
INFORMATION
CONTACT.

B.
How
Can
I
Get
Copies
of
this
Document
and
Other
Related
Information?

1.
Docket.
EPA
has
established
an
official
public
docket
for
this
action
under
docket
ID
number
OPP
 
2003
 
0271.
The
official
public
docket
consists
of
the
documents
specifically
referenced
in
this
action,
any
public
comments
received,
and
other
information
related
to
this
action.
Although,
a
part
of
the
official
docket,
the
public
docket
does
not
include
Confidential
Business
Information
(
CBI)
or
other
information
whose
disclosure
is
restricted
by
statute.
The
official
public
docket
is
the
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/
Vol.
68,
No.
156
/
Wednesday,
August
13,
2003
/
Notices
collection
of
materials
that
is
available
for
public
viewing
at
the
Public
Information
and
Records
Integrity
Branch
(
PIRIB),
Rm.
119,
Crystal
Mall
#
2,
1921
Jefferson
Davis
Hwy.,
Arlington,
VA.
This
docket
facility
is
open
from
8:
30
a.
m.
to
4
p.
m.,
Monday
through
Friday,
excluding
legal
holidays.
The
docket
telephone
number
is
(
703)
305
 
5805.
2.
Electronic
access.
You
may
access
this
Federal
Register
document
electronically
through
the
EPA
Internet
under
the
``
Federal
Register''
listings
at
http://
www.
epa.
gov/
fedrgstr/.
An
electronic
version
of
the
public
docket
is
available
through
EPA's
electronic
public
docket
and
comment
system,
EPA
Dockets.
You
may
use
EPA
Dockets
at
http://
www.
epa.
gov/
edocket/
to
submit
or
view
public
comments,
access
the
index
listing
of
the
contents
of
the
official
public
docket,
and
to
access
those
documents
in
the
public
docket
that
are
available
electronically.
Although,
not
all
docket
materials
may
be
available
electronically,
you
may
still
access
any
of
the
publicly
available
docket
materials
through
the
docket
facility
identified
in
Unit
I.
B.
1.
Once
in
the
system,
select
``
search,''
then
key
in
the
appropriate
docket
ID
number.
Certain
types
of
information
will
not
be
placed
in
the
EPA
Dockets.
Information
claimed
as
CBI
and
other
information
whose
disclosure
is
restricted
by
statute,
which
is
not
included
in
the
official
public
docket,
will
not
be
available
for
public
viewing
in
EPA's
electronic
public
docket.
EPA's
policy
is
that
copyrighted
material
will
not
be
placed
in
EPA's
electronic
public
docket
but
will
be
available
only
in
printed,
paper
form
in
the
official
public
docket.
To
the
extent
feasible,
publicly
available
docket
materials
will
be
made
available
in
EPA's
electronic
public
docket.
When
a
document
is
selected
from
the
index
list
in
EPA
dockets,
the
system
will
identify
whether
the
document
is
available
for
viewing
in
EPA's
electronic
public
docket.
Although,
not
all
docket
materials
may
be
available
electronically,
you
may
still
access
any
of
the
publicly
available
docket
materials
through
the
docket
facility
identified
in
Unit
I.
B.
EPA
intends
to
work
towards
providing
electronic
access
to
all
of
the
publicly
available
docket
materials
through
EPA's
electronic
public
docket.
For
public
commenters,
it
is
important
to
note
that
EPA's
policy
is
that
public
comments,
whether
submitted
electronically
or
on
paper,
will
be
made
available
for
public
viewing
in
EPA's
electronic
public
docket
as
EPA
receives
them
and
without
change,
unless
the
comment
contains
copyrighted
material,
CBI,
or
other
information
whose
disclosure
is
restricted
by
statute.
When
EPA
identifies
a
comment
containing
copyrighted
material,
EPA
will
provide
a
reference
to
that
material
in
the
version
of
the
comment
that
is
placed
in
EPA's
electronic
public
docket.
The
entire
printed
comment,
including
the
copyrighted
material,
will
be
available
in
the
public
docket.
Public
comments
submitted
on
computer
disks
that
are
mailed
or
delivered
to
the
docket
will
be
transferred
to
EPA's
electronic
public
docket.
Public
comments
that
are
mailed
or
delivered
to
the
docket
will
be
scanned
and
placed
in
EPA's
electronic
public
docket.
Where
practical,
physical
objects
will
be
photographed,
and
the
photograph
will
be
placed
in
EPA's
electronic
public
docket
along
with
a
brief
description
written
by
the
docket
staff.

C.
How
and
to
Whom
Do
I
Submit
Comments?
You
may
submit
comments
electronically,
by
mail,
or
through
hand
delivery/
courier.
To
ensure
proper
receipt
by
EPA,
identify
the
appropriate
docket
ID
number
in
the
subject
line
on
the
first
page
of
your
comment.
Please
ensure
that
your
comments
are
submitted
within
the
specified
comment
period.
Comments
received
after
the
close
of
the
comment
period
will
be
marked
``
late.''
EPA
is
not
required
to
consider
these
late
comments.
If
you
wish
to
submit
CBI
or
information
that
is
otherwise
protected
by
statute,
please
follow
the
instructions
in
Unit
I.
D.
Do
not
use
EPA
dockets
or
e­
mail
to
submit
CBI
or
information
protected
by
statute.
1.
Electronically.
If
you
submit
an
electronic
comment
as
prescribed
in
this
unit,
EPA
recommends
that
you
include
your
name,
mailing
address,
and
an
email
address
or
other
contact
information
in
the
body
of
your
comment.
Also,
include
this
contact
information
on
the
outside
of
any
disk
or
CD
ROM
you
submit,
and
in
any
cover
letter
accompanying
the
disk
or
CD
ROM.
This
ensures
that
you
can
be
identified
as
the
submitter
of
the
comment
and
allows
EPA
to
contact
you
in
case
EPA
cannot
read
your
comment
due
to
technical
difficulties
or
needs
further
information
on
the
substance
of
your
comment.
EPA's
policy
is
that
EPA
will
not
edit
your
comment,
and
any
identifying
or
contact
information
provided
in
the
body
of
a
comment
will
be
included
as
part
of
the
comment
that
is
placed
in
the
official
public
docket,
and
made
available
in
EPA's
electronic
public
docket.
If
EPA
cannot
read
your
comment
due
to
technical
difficulties
and
cannot
contact
you
for
clarification,
EPA
may
not
be
able
to
consider
your
comment.
i.
EPA
Dockets.
Your
use
of
EPA's
electronic
public
docket
to
submit
comments
to
EPA
electronically
is
EPA's
preferred
method
for
receiving
comments.
Go
directly
to
EPA
Dockets
at
http://
www.
epa.
gov/
edocket,
and
follow
the
online
instructions
for
submitting
comments.
Once
in
the
system,
select
``
search,''
and
then
key
in
docket
ID
number
OPP
 
2003
 
0271.
The
system
is
an``
anonymous
access''
system,
which
means
EPA
will
not
know
your
identity,
e­
mail
address,
or
other
contact
information
unless
you
provide
it
in
the
body
of
your
comment.
ii.
E­
mail.
Comments
may
be
sent
by
e­
mail
to
opp­
docket@
epa.
gov,
Attention:
Docket
ID
number
OPP
 
2003
 
0271.
In
contrast
to
EPA's
electronic
public
docket,
EPA's
e­
mail
system
is
not
an
``
anonymous
access''
system.
If
you
send
an
e­
mail
comment
directly
to
the
docket
without
going
through
EPA's
electronic
public
docket,
EPA's
e­
mail
system
automatically
captures
your
e­
mail
address.
E­
mail
addresses
that
are
automatically
captured
by
EPA's
e­
mail
system
are
included
as
part
of
the
comment
that
is
placed
in
the
official
public
docket,
and
made
available
in
EPA's
electronic
public
docket.
iii.
Disk
or
CD
ROM.
You
may
submit
comments
on
a
disk
or
CD
ROM
that
you
mail
to
the
mailing
address
identified
in
Unit
I.
C.
2.
These
electronic
submissions
will
be
accepted
in
WordPerfect
or
ASCII
file
format.
Avoid
the
use
of
special
characters
and
any
form
of
encryption.
2.
By
mail.
Send
your
comments
to:
Public
Information
and
Records
Integrity
Branch
(
PIRIB)
(
7502C),
Office
of
Pesticide
Programs
(
OPP),
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001,
Attention:
Docket
ID
Number
OPP
 
2003
 
0271.
3.
By
hand
delivery
or
courier.
Deliver
your
comments
to:
Public
Information
and
Records
Integrity
Branch
(
PIRIB),
Office
of
Pesticide
Programs
(
OPP),
Environmental
Protection
Agency,
Rm.
119,
Crystal
Mall
#
2,
1921
Jefferson
Davis
Hwy.,
Arlington,
VA,
Attention:
Docket
ID
number
OPP
 
2003
 
0271.
Such
deliveries
are
only
accepted
during
the
docket's
normal
hours
of
operation
as
identified
in
Unit
I.
B.
1.

D.
How
Should
I
Submit
CBI
to
the
Agency?
Do
not
submit
information
that
you
consider
to
be
CBI
electronically
through
EPA's
electronic
public
docket
or
by
e­
mail.
You
may
claim
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13AUN1.
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13AUN1
48379
Federal
Register
/
Vol.
68,
No.
156
/
Wednesday,
August
13,
2003
/
Notices
information
that
you
submit
to
EPA
as
CBI
by
marking
any
part
or
all
of
that
information
as
CBI
(
if
you
submit
CBI
on
disk
or
CD
ROM,
mark
the
outside
of
the
disk
or
CD
ROM
as
CBI
and
then
identify
electronically
within
the
disk
or
CD
ROM
the
specific
information
that
is
CBI).
Information
so
marked
will
not
be
disclosed
except
in
accordance
with
procedures
set
forth
in
40
CFR
part
2.
In
addition
to
one
complete
version
of
the
comment
that
includes
any
information
claimed
as
CBI,
a
copy
of
the
comment
that
does
not
contain
the
information
claimed
as
CBI
must
be
submitted
for
inclusion
in
the
public
docket
and
EPA's
electronic
public
docket.
If
you
submit
the
copy
that
does
not
contain
CBI
on
disk
or
CD
ROM,
mark
the
outside
of
the
disk
or
CD
ROM
clearly
that
it
does
not
contain
CBI.
Information
not
marked
as
CBI
will
be
included
in
the
public
docket
and
EPA's
electronic
public
docket
without
prior
notice.
If
you
have
any
questions
about
CBI
or
the
procedures
for
claiming
CBI,
please
consult
the
person
listed
under
FOR
FURTHER
INFORMATION
CONTACT.

E.
What
Should
I
Consider
as
I
Prepare
My
Comments
for
EPA?

You
may
find
the
following
suggestions
helpful
for
preparing
your
comments:
1.
Explain
your
views
as
clearly
as
possible.
2.
Describe
any
assumptions
that
you
used.
3.
Provide
copies
of
any
technical
information
and/
or
data
you
used
that
support
your
views.
4.
If
you
estimate
potential
burden
or
costs,
explain
how
you
arrived
at
the
estimate
that
you
provide.
5.
Provide
specific
examples
to
illustrate
your
concerns.
6.
Make
sure
to
submit
your
comments
by
the
deadline
in
this
notice.
7.
To
ensure
proper
receipt
by
EPA,
be
sure
to
identify
the
docket
ID
number
assigned
to
this
action
in
the
subject
line
on
the
first
page
of
your
response.
You
may
also
provide
the
name,
date,
and
Federal
Register
citation.

II.
What
Action
is
the
Agency
Taking?

EPA
has
received
a
pesticide
petition
as
follows
proposing
the
establishment
and/
or
amendment
of
regulations
for
residues
of
a
certain
pesticide
chemical
in
or
on
various
food
commodities
under
section
408
of
the
Federal
Food,
Drug,
and
Cosmetic
Act
(
FFDCA),
21
U.
S.
C.
346a.
EPA
has
determined
that
this
petition
contains
data
or
information
regarding
the
elements
set
forth
in
FFDCA
section
408(
d)(
2);
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
support
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

List
of
Subjects
Environmental
protection,
Agricultural
commodities,
Feed
additives,
Food
additives,
Pesticides
and
pests,
Reporting
and
recordkeeping
requirements.

Dated:
August
6,
2003.
Debra
Edwards,
Director,
Registration
Division,
Office
of
Pesticide
Programs.

Summary
of
Petition
The
petitioner's
summary
of
the
pesticide
petition
is
printed
below
as
required
by
FFDCA
section
408(
d)(
3).
The
summary
of
the
petition
was
prepared
by
Valent
U.
S.
A.
Corporation
and
represents
the
view
of
the
petitioner.
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.

Valent
U.
S.
A.
Corporation
PP
2F6420
EPA
has
received
a
pesticide
petition
(
2F6420)
from
Valent
U.
S.
A.
Corporation,
1333
North
California
Blvd.,
Suite
600,
Walnut
Creek,
CA
94596
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
etoxazole
in
or
on
the
raw
agricultural
commodity
pome
fruit
(
Crop
Group
11)
at
0.2
parts
per
million
(
ppm),
apple
wet
pomace
at
1.0
ppm,
strawberry
at
0.5
ppm,
cottonseed
at
0.05
ppm,
cotton,
gin
byproducts
(
gin
trash)
at
1.0
ppm,
and
oranges
at
0.10
ppm
(
to
support
the
importation
of
mandarin
oranges
into
the
U.
S.).
As
residues
in
processed
commodities
fed
to
animals
may
be
transferred
to
milk
and
edible
tissue
of
ruminants,
tolerances
are
also
proposed
for
animal
fat
at
0.03
ppm
and
milk
fat
at
0.04
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.
Metabolism
of
14C­
etoxazole
labeled
in
the
tbutylphenyl
difluorophenyl,
or
oxazole
rings
has
been
studied
in
apples,
cotton,
oranges,
and
eggplants.
Etoxazole
was
rapidly
and
extensively
metabolized
to
many
metabolites
in
all
plants.
Even
with
exaggerated
treatment,
individual
metabolites
and
parent
were
only
found
at
very
low
concentrations.
Comparisons
of
metabolites
detected
and
quantified
from
plants
and
animals
show
that
there
are
no
significant
aglycones
in
plants
which
are
not
also
present
in
the
excreta
or
tissues
of
animals.
The
residue
of
concern
is
best
defined
as
the
parent
etoxazole.
2.
Analytical
method.
Practical
analytical
methods
for
detecting
and
measuring
levels
of
etoxazole
have
been
developed
and
validated
in/
on
all
appropriate
agricultural
commodities
and
respective
processing
fractions.
The
extraction
methodology
has
been
validated
using
aged
radiochemical
residue
samples
from
14C­
metabolism
studies.
The
enforcement
methods
have
been
validated
in
cottonseed,
cotton
gin
trash,
and
in
fresh
mandarin
oranges
at
independent
laboratories.
The
LOQ
of
etoxazole
in
these
methods
is
0.01
ppm
in
mandarin
oranges
and
cottonseed
and
0.2
ppm
in
cotton
gin
trash,
which
will
allow
monitoring
of
food
with
residues
at
the
levels
proposed
for
the
tolerances.
Methods
have
also
been
developed
and
validated
for
determining
etoxazole
in
animal
samples.
The
LOQ
of
etoxazole
in
these
methods
is
0.02
ppm
in
milk
fat
and
beef
fat.
3.
Magnitude
of
residues.
An
extensive
crop
residue
program
has
been
conducted
for
etoxazole
in
all
major
growing
regions
of
the
United
States
for
the
following
crops:
apples
and
pears
(
representing
pome
fruits),
strawberries,
and
cotton.
Residue
trials
have
also
been
conducted
for
etoxazole
in
Europe
to
support
the
importation
of
mandarin
oranges
into
the
U.
S.
The
results
of
these
studies
can
be
summarized
as
follows:
 
For
pome
fruit,
the
maximum
etoxazole
residues
from
two
applications
at
0.135
lbs.
active
ingredient/
acre/
treatment,
are
0.07
ppm
for
apples
and
0.11
for
pears
harvested
28
days
after
application.
 
The
results
of
an
apple
processing
study
indicate
that
etoxazole
residues
do
not
concentrate
in
apple
juice,
but
do
concentrate
in
wet
apple
pomace
with
an
average
concentration
factor
of
5.7x.
 
The
maximum
etoxazole
residue
in
strawberries
harvested
one
day
following
the
last
of
two
treatments
at
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13AUN1.
SGM
13AUN1
48380
Federal
Register
/
Vol.
68,
No.
156
/
Wednesday,
August
13,
2003
/
Notices
0.135
lbs.
active
ingredient/
acre/
treatment
is
0.32
ppm.
 
The
maximum
expected
etoxazole
residues
in
cottonseed
and
cotton
gin
trash
from
two
applications
at
0.045
lbs.
active
ingredient/
acre/
treatment
applied
28
days
before
harvest
are
0.02
ppm
and
0.60
ppm,
respectively.
Cotton
gin
trash
was
also
analyzed
for
metabolite
R
 
3
but
was
detected
in
samples
from
only
one
of
seven
test
sites
at
a
level
only
slightly
above
the
0.10
ppm
limit
of
detection
(
LOD)
(
mean
residue
was
0.13
ppm).
Therefore,
no
tolerance
is
being
proposed
for
metabolite
R
 
3
in
cotton
gin
trash.
 
The
results
of
a
cotton
processing
study
indicate
that
etoxazole
does
not
concentrate
in
hulls,
meal,
or
oil.
 
Following
a
single
application
to
mandarin
oranges
of
0.05
lbs.
active
ingredient/
acre,
the
maximum
etoxazole
residues
in
whole
fruit
harvested
14
days
after
application
is
0.05
ppm.
 
No
processing
of
mandarins
was
required
because
only
fresh
or
canned
mandarins
will
be
imported
for
direct
consumption.
Separate
analysis
of
mandarin
peel
and
pulp
from
residue
field
trials
demonstrated
that
etoxazole
residues
are
confined
to
the
peel.
Canned
mandarins
that
contain
only
mandarin
pulp
would
therefore
not
be
expected
to
contain
detectable
residues
of
etoxazole.
These
field
trial
data
are
adequate
to
support
proposed
tolerances
of
0.2
ppm
for
pome
fruit;
1.0
ppm
for
wet
apple
pomace;
0.5
ppm
for
strawberries;
0.05
ppm
for
cottonseed;
1.0
ppm
in
cotton
gin
trash;
and
0.1
ppm
in
oranges.
Apple
pomace
and
all
cotton
commodities
are
significant
feed
items
for
beef
and
dairy
cattle
and
results
of
a
goat
metabolism
study
suggest
the
possibility
that
etoxazole
residues
in
feed
may
transfer
to
edible
tissues
and
milk.
Therefore,
a
cow
feeding
study
was
conducted
with
etoxazole
to
determine
the
level
of
secondary
residues
and
the
need
for
corresponding
tolerances.
Etoxazole
was
detected
in
fat
and
cream
only
and
Valent
is
therefore
proposing
tolerances
of
0.03
ppm
in
the
fat
of
animals
and
0.04
ppm
in
milk
fat.
Cotton
meal
is
the
only
commodity
under
consideration
that
is
used
as
a
poultry
feed
item
and
the
results
of
the
cotton
processing
study
indicate
that
etoxazole
residues
in
this
commodity
are
very
low.
Additionally,
the
results
of
a
hen
metabolism
study
demonstrated
very
low
potential
for
residues
in
feed
to
transfer
to
poultry
tissues
or
eggs.
Therefore,
no
hen
residue
feeding
study
was
performed
and
tolerances
are
not
proposed
for
secondary
residues
in
poultry
commodities.
B.
Toxicological
Profile
A
full
battery
of
toxicology
testing,
including
studies
of
acute,
chronic,
oncogenicity,
developmental,
mutagenicity,
and
reproductive
effects
has
been
completed
for
etoxazole.
The
acute
toxicity
of
etoxazole
is
low
by
all
routes.
Etoxazole
is
not
a
developmental
or
reproductive
toxicant,
and
is
not
mutagenic
or
oncogenic.
The
toxicology
reports
for
etoxazole
have
not
yet
been
reviewed
by
EPA
and
thus,
the
Agency
has
not
yet
established
toxic
endpoints
of
concern,
specifically
chronic
and
acute
oral
toxicity
endpoints
for
the
compound.
For
the
purpose
of
dietary
risk
analysis,
Valent
proposes
0.04
mg/
kg
bwt/
day
as
the
chronic
Population
Adjusted
Dose
(
cPAD)
and
an
acute
Population
Adjusted
Dose
(
aPAD)
of
2
mg/
kg
bwt/
day.
The
cPAD
is
based
on
a
chronic
endpoint
of
4
mg/
kg
bw/
day
NOEL
for
males
from
the
rat
chronic/
oncogenicity
feeding
study
and
an
uncertainty
factor
of
100.
The
aPAD
is
based
on
the
200
mg/
kg
bwt/
day
NOEL
from
the
rabbit
developmental
toxicity
study
and
an
uncertainty
factor
of
100.
Valent
is
unable
to
identify
toxicity
endpoints
of
concern
for
acute,
shortterm
or
chronic
human
exposures
by
any
route
other
than
oral.
1.
Acute
toxicity.
The
acute
toxicity
of
technical
grade
etoxazole
is
low
by
all
routes.
The
battery
of
acute
toxicity
studies
place
etoxazole
in
Toxicity
Category
III.
The
oral
LD50
in
the
rat
was
greater
than
5
grams/
kilogram
(
g/
kg),
the
dermal
LD50
was
greater
than
2.0
g/
kg,
and
the
inhalation
LC50
in
the
rat
was
greater
than
1.09
milligrams/
liter
(
mg/
L).
Etoxazole
technical
was
not
an
irritant
to
eyes
or
skin
and
was
not
a
skin
sensitizer.
2.
Genotoxicty.
Etoxazole
was
evaluated
and
found
to
be
negative
in
an
Ames
reverse
mutation
assay,
a
chromosome
aberration
assay,
a
micronucleus
assay,
and
an
unscheduled
DNA
synthesis
(
UDS)
assay.
Etoxazole
produced
a
positive
result
in
the
mouse
lymphoma
gene
mutation
assay
but
only
in
the
presence
of
metabolic
activation.
Etoxazole
does
not
present
a
genetic
hazard.
3.
Reproductive
and
developmental
toxicity.
 
i.
Rat
developmental
study.
Etoxazole
did
not
produce
developmental
toxicity
in
rats.
Etoxazole
technical
was
administered
by
oral
gavage
to
pregnant
rats
at
dosage
levels
of
40,
200,
and
1,000
mg/
kg/
day
on
days
6
through
15
of
gestation.
There
were
no
mortalities
or
treatment­
related
adverse
effects
in
any
dose
group.
Food
consumption
was
slightly
decreased
in
dams
during
the
dosing
period
for
the
1,000
mg/
kg/
day
group.
On
cesarean
section
evaluation
there
was
no
differences
in
number
of
corpora
lutea,
number
of
live
and
dead
fetuses,
percent
resorption,
placental
weight,
fetal
weight
or
sex
ratio
in
the
dams
and
no
treatment­
related
external,
visceral
or
skeletal
malformations
noted
in
any
of
the
fetuses.
It
was
concluded
that
the
maternal
no
observed
adverse
effect
level
(
NOAEL)
was
200
mg/
kg/
day,
based
on
decreased
food
consumption
at
1,000
mg/
kg/
day.
The
developmental
NOAEL
was
1,000
mg/
kg/
day,
the
highest
dose
tested.
ii.
Rabbit
developmental
study.
Etoxazole
did
not
produce
developmental
toxicity
in
rabbits.
Etoxazole
technical
was
administered
by
oral
gavage
to
pregnant
rabbits
at
dosage
levels
of
40,
200,
and
1,000
mg/
kg/
day
on
days
6
through
18
of
gestation.
No
treatment­
related
adverse
effects
were
found
on
maternal
rabbits
in
the
40
and
200
mg/
kg/
day
groups.
One
high
dose
rabbit
died
but
it
is
unclear
whether
this
death
was
attributed
to
treatment.
Decreased
body
weight,
body
weight
gain,
food
consumption
and
enlarged
liver
were
noted
at
1,000
mg/
kg/
day.
Cesarean
section
findings
showed
that
there
was
no
differences
in
number
of
corpora
lutea,
number
of
live
and
dead
fetuses,
percent
resorptions,
placental
weight,
fetal
weight
and
sex
ratio
in
the
dams
and
showed
no
treatment­
related
malformations
(
external,
visceral,
skeletal)
in
any
of
the
fetuses.
A
statistically
significant
increased
incidence
of
27
presacral
vertebrae
with
13th
ribs
was
observed
in
fetuses
at
1,000
mg/
kg/
day
compared
with
controls.
This
finding
was
within
historical
control
range
for
fetal
incidence
but
above
the
historical
control
range
for
litter
incidence.
No
dose
response
was
evident
and
the
variation
is
considered
to
be
equivocally
treatment
related.
The
NOAEL
for
maternal
and
developmental
toxicity
was
200
mg/
kg/
day
based
on
decreased
body
weight
and
body
weight
gain,
decreased
food
consumption,
and
liver
enlargement
at
1,000
mg/
kg/
day.
The
NOAEL
for
developmental
toxicity
was
200
mg/
kg/
day
based
on
statistically
significant
increased
incidence
of
27
presacral
vertebrae
with
13th
ribs
in
fetuses
at
1,000
mg/
kg/
day.
iii.
Rat
reproduction
study.
Etoxazole
showed
no
effects
on
reproduction
in
a
two­
generation
rat
study.
Etoxazole
technical
was
fed
to
two
generations
of
male
and
female
Sprague
Dawley
rats
at
dietary
concentrations
of
80,
400,
and
2,000
ppm.
No
treatment­
related
adverse
effects
were
observed
in
the
80
and
400
ppm
groups
for
any
parameter.
In
the
2,000
ppm
group,
relative
liver
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weights
were
increased
in
the
F0
and
F1
parental
males.
No
adverse
reproductive
effects
were
noted
at
any
dose
level
in
the
incidence
of
normal
estrous
cycle,
mating
index,
fertility
and
gestation
indices,
the
number
of
implantation
sites,
and
duration
of
gestation
in
F0
and
F1
parental
animals.
For
the
offspring,
it
was
noted
that
at
2,000
ppm,
the
viability
index
on
lactation
Day
4
was
significantly
lower
in
the
F1
pups
and
body
weights
were
lowered
in
pups
during
the
latter
half
of
the
lactation
period.
For
the
F0
and
F1
pups
of
the
80
and
400
ppm
groups,
there
were
no
treatment­
related
adverse
effects
observed
for
any
parameter,
i.
e.
mean
number
of
pups
delivered,
sex
ratio,
viability
indices
on
lactation
days
0,
4
and
21,
clinical
signs,
body
weights
and
gross
pathological
findings.
The
parental
NOAEL
was
400
ppm
(
17.0
mg/
kg/
day)
based
on
the
effects
on
relative
liver
weight
in
males
at
2,000
ppm.
The
pup
NOAEL
was
400
ppm
(
37.9
mg/
kg/
day)
based
on
decreased
viability
on
lactation
Day
4
and
decreased
body
weight
at
2,000
ppm
in
the
F1
pups.
The
reproductive
NOAEL
was
2,000
ppm
(
86.4
mg/
kg/
day),
the
highest
dose
tested.
4.
Subchronic
toxicity.
Subchronic
toxicity
studies
conducted
with
etoxazole
technical
in
the
rat
(
oral
and
dermal),
mouse
and
dog
indicate
a
low
level
of
toxicity.
Effects
observed
at
high
dose
levels
consisted
primarily
of
anemia
and
histological
changes
in
the
adrenal
gland,
liver
and
kidneys.
i.
Rat
feeding
study:
A
90
 
day
subchronic
toxicity
study
was
conducted
in
rats,
with
dietary
intake
levels
of
100,
300,
1,000
and
3,000
ppm
etoxazole
technical.
The
NOAEL
was
100
ppm
for
males
and
300
ppm
for
females
based
on
increased
incidence
of
hepatocellular
swelling
at
1,000
ppm
and
3,000
ppm.
ii.
Mouse
feeding
study.
A
90
 
day
subchronic
toxicity
study
was
conducted
in
mice,
with
dietary
intake
levels
of
100,
400,
1,600,
and
6,400
ppm
etoxazole
technical.
The
NOAEL
was
400
ppm
for
males
and
1,600
ppm
for
females
based
on
increased
alkaline
phosphatase
activity,
increased
liver
weights,
and
increased
incidence
of
hepatocellular
swelling
at
6,400
ppm
(
both
sexes)
and
at
1,600
ppm
in
males
and
enlarged
livers
in
females
at
6,400
ppm.
iii.
Dog
feeding
study.
Etoxazole
technical
was
fed
to
male
and
female
Beagle
dogs
for
13
weeks
at
dietary
concentrations
of
200,
2,000,
and
10,000
ppm.
The
NOAEL
was
200
ppm
(
5.3
mg/
kg/
day)
based
on
clinical
signs,
clinical
pathology
changes,
liver
weight
effects
and
histopathological
changes
at
2,000
and
10,000
ppm.
iv.
Repeated
dose
dermal
study.
A
28
 
day
dermal
toxicity
study
was
conducted
in
rats
at
dose
levels
of
30,
100,
and
1,000
mg/
kg.
There
were
no
treatment
related
changes
in
any
of
the
parameters
monitored.
The
NOAEL
was
1,000
mg/
kg,
the
highest
dose
tested.
5.
Chronic
toxicity.
Etoxazole
technical
has
been
tested
in
chronic
studies
with
dogs,
rats
and
mice.
Valent
proposes
a
chronic
oral
endpoint
of
4
mg/
kg
bwt/
day,
based
on
the
NOAEL
for
male
rats
in
a
two­
year
chronic
toxicity
oncogenicity
feeding
study.
i.
Dog
chronic
feeding
study.
Etoxazole
technical
was
fed
to
male
and
female
beagle
dogs
for
one
year
at
dietary
concentrations
of
200,
1,000,
and
5,000
ppm.
The
NOAEL
was
200
ppm
(
4.6
mg/
kg/
day
for
males
and
4.79
mg/
kg/
day
for
females)
based
on
increased
absolute
and
relative
liver
weights
with
corresponding
histopathological
changes
in
the
liver
at
1,000
and
5,000
ppm.
ii.
Rat
chronic
feeding/
oncogenicity
study.
Etoxazole
was
not
oncogenic
in
rats
in
either
of
two
chronic
feeding
studies
conducted.
In
the
first
study,
etoxazole
technical
was
fed
to
male
and
female
Sprague
Dawley
rats
for
two
years
at
dietary
concentrations
of
4,
16,
and
64
mg/
kg/
day.
A
trend
toward
decreased
body
weight
gain
for
males
at
64
mg/
kg/
day
in
the
latter
half
of
the
study
was
observed.
Hemotology
and
clinical
chemistry
changes,
increased
liver
weights
and
hepatic
enlargement
at
16
mg/
kg/
day
or
above
were
observed.
Testicular
masses,
centrilobular
hepatocellular
swelling
and
testicular
interstitial
(
Leydig)
cell
tumors
occurred
at
or
above
16
mg/
kg/
day.
The
interstitial
(
Leydig)
cell
tumors
were
believed
to
be
incidental.
The
NOAEL
was
4
mg/
kg/
day
for
males
and
16
mg/
kg/
day
for
females.
Because
an
MTD
level
was
not
achieved
in
this
study,
a
second
study
was
conducted
in
which
etoxazole
technical
was
fed
to
male
and
female
Sprague
Dawley
rats
for
two
years
at
dietary
concentrations
of
50,
5,000,
and
10,000
ppm.
In
this
study,
decreased
mortality,
bodyweight
and
food
consumption/
efficiency
(
females)
at
10,000
ppm
was
observed.
Hematological,
clinical,
and
histopathological
changes
of
the
incisors,
and
increased
liver
weights
occurred
in
both
sexes
at
5,000
and
10,000
ppm.
Centrilobular
hepatocellular
hypertrophy
was
observed
in
both
sexes
at
10,000
ppm.
The
interstitial
(
Leydig)
cell
tumors
observed
in
the
first
study,
were
not
observed
in
the
repeat
study.
The
NOAEL
in
the
repeat
study
was
50
ppm
(
1.8
mg/
kg/
day).
iii.
Mouse
oncogenicity
study.
Etoxazole
was
not
oncogenic
in
either
of
two
mouse
oncogenicity
studies
conducted.
In
the
first
study,
etoxazole
technical
was
fed
to
male
and
female
CD­
1
mice
for
18
months
at
dietary
concentrations
of
15,
60,
and
240
mg/
kg/
day.
Increased
liver
weights
occurred
in
females
at
the
highest
dose
tested.
Histopathology
parameters
were
altered
for
males
at
240
mg/
kg/
day.
No
neoplastic
lesions
were
observed
at
any
dose
level.
The
NOAEL
was
60
mg/
kg/
day.
Since
the
toxicity
in
this
study
was
minimal
and
did
not
meet
the
definition
of
MTD,
a
second
study
was
conducted
at
dose
levels
of
2,250
and
4,500
ppm
etoxazole.
There
were
no
effects
in
any
group
on
clinical
observations,
mortality,
body
weight,
food
consumption
or
hematology.
Females
showed
a
significant
elevation
in
relative
liver
weight
after
52
weeks
of
treatment
at
4,500
ppm.
In
histopathology,
a
significantly
higher
incidence
of
centrilobular
hepatocellular
fatty
change
was
observed
in
males
in
the
4,500
ppm
group
necropsied
after
78
weeks
of
treatment.
There
were
no
treatmentrelated
changes
in
either
sex
of
the
2,250
ppm
dose
group.
No
increase
in
neoplastic
lesions
were
observed
in
any
treated
group
of
either
sex.
Therefore,
it
was
concluded
that
the
no
observed
effect
level
is
2,250
ppm
(
242
mg/
kg/
day
for
the
males
and
243
mg/
kg/
day
for
the
females).
6.
Animal
metabolism.
The
absorption,
tissue
distribution,
metabolism
and
excretion
of
etoxazole
were
studied
in
rats
after
single
oral
doses
of
5
or
500
mg/
kg,
and
after
14
daily
oral
doses
at
5
mg/
kg.
Etoxazole,
labeled
in
both
the
t­
butylphenyl
ring
and
the
oxazole
ring
were
used
in
this
study.
For
both
single
dose
groups,
most
(
94
 
97%)
of
the
administered
radiolabel
was
excreted
in
the
urine
and
feces
within
seven
days
after
dosing.
Most
of
this
excretion
occurred
in
the
first
48
hours
after
dosing.
Maximum
plasma
concentrations
occurred
2
 
4
hours
after
dosing,
with
half­
lives
ranging
from
53
 
89
hours
at
the
low
dose
and
7
 
44
hours
at
the
high
dose.
Plasma
levels
were
significantly
lower
in
females.
Concentrations
of
radioactivity
were
significantly
higher
in
the
tissues
of
male
rats
compared
to
females.
The
highest
concentrations
occurred
at
3
hours
after
dosing
and
were
greatest
in
the
gastrointestinal
tract
and
tissues
such
as
liver
and
kidneys,
which
are
responsible
for
metabolism
and
excretion.
By
168
hours,
the
concentration
in
most
tissues
was
below
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Notices
the
concentration
in
the
corresponding
plasma,
with
only
the
liver
and
fat
having
significant
levels
of
radioactivity.
After
multiple
doses,
peak
concentrations
of
radioactivity
in
tissues
occurred
2
hours
after
dosing
and
then
declined.
The
distribution
of
radioactivity
showed
a
similar
profile
to
those
found
after
single
oral
doses
but
were
significantly
higher,
indicating
some
accumulation.
Etoxazole
was
extensively
metabolized
by
rats.
The
main
metabolic
reactions
in
rats
were
postulated
to
be
hydroxylation
of
the
4,5­
hydrooxazole
ring
followed
by
cleavage
of
the
molecule
and
hydroxylation
of
the
t­
butyl
side
chain.
7.
Metabolite
toxicology.
In
an
oral
toxicity
limit
test
in
rats,
the
oral
LD50
of
metabolite
R­
3
was
estimated
to
be
greater
than
5
g/
kg
for
both
male
and
female
rats.
No
treatment
related
body
weight
changes
and
no
treatment
related
macroscopic
abnormalities
were
observed
in
this
study.
In
another
test,
the
oral
toxicity
of
metabolite
R­
7
(
as
the
HCl
salt)
was
assessed.
The
oral
LD50
of
this
metabolite
was
also
estimated
to
be
greater
than
5
g/
kg
for
both
male
and
female
rats.
No
treatment
related
macroscopic
abnormalities
were
observed
in
this
test
although
some
clinical
signs
were
observed
within
six
minutes
of
dosing.
Mutagenicity
screens
were
performed
with
metabolite
R­
3
and
metabolite
R­
7
(
as
the
HCl
salt).
Neither
metabolite
was
mutagenic
when
tested
with
multiple
strains
of
two
bacterial
cultures
(
Salmonella
typhimurium
and
Escherichia
coli).
8.
Endocrine
disruption.
No
special
studies
to
investigate
the
potential
for
estrogenic
or
other
endocrine
effects
of
etoxazole
have
been
performed.
However,
as
summarized
above,
a
large
and
detailed
toxicology
data
base
exists
for
the
compound
including
studies
in
all
required
categories.
These
studies
include
acute,
sub­
chronic,
chronic,
developmental,
and
reproductive
toxicology
studies
including
detailed
histology
and
histopathology
of
numerous
tissues,
including
endocrine
organs,
following
repeated
or
long
term
exposures.
These
studies
are
considered
capable
of
revealing
endocrine
effects.
The
results
of
all
of
these
studies
show
no
evidence
of
any
endocrine­
mediated
effects
and
no
pathology
of
the
endocrine
organs.
Consequently,
it
is
concluded
that
etoxazole
does
not
possess
estrogenic
or
endocrine
disrupting
properties.

C.
Aggregate
Exposure
1.
Dietary
exposure.
A
full
battery
of
toxicology
testing
including
studies
of
acute,
chronic,
oncogenicity,
developmental,
mutagenicity,
and
reproductive
effects
is
available
for
etoxazole.
EPA
has
not
had
the
opportunity
to
review
all
of
the
toxicity
studies
on
etoxazole
and
has
not
established
toxic
endpoints.
Thus,
in
these
risk
assessments
Valent
proposes
as
the
chronic
oral
toxic
endpoint
the
NOAEL
for
males
from
the
rat
chronic/
oncogenicity
feeding
study,
4
mg/
kg/
day.
To
assess
the
chronic
risk
to
the
U.
S.
population
from
exposure
to
etoxazole,
the
daily
chronic
exposures
were
compared
against
an
estimated
chronic
population
adjusted
dose
(
cPAD)
of
0.04
mg/
kg
bwt/
day.
This
endpoint
is
derived
from
the
NOAEL
from
the
2
 
year
chronic
rat
study
by
applying
an
uncertainty
factor
of
100
to
account
for
intraspecies
and
interspecies
variations.
There
is
no
evidence
that
any
additional
safety
factors
are
needed
to
further
protect
vulnerable
subpopulations.
The
proposed
acute
oral
toxic
endpoint
is
the
NOAEL
from
the
rabbit
oral
developmental
toxicity
study,
200
mg/
kg/
day.
To
assess
the
acute
risk
to
the
U.
S.
population
from
exposure
to
etoxazole,
acute
exposures
were
compared
against
an
estimated
acute
population
adjusted
dose
(
aPAD)
of
2
mg/
kg
bwt/
day.
This
endpoint
is
derived
from
the
NOAEL
from
the
rabbit
oral
developmental
toxicity
study
by
applying
an
uncertainty
factor
of
100
to
account
for
intraspecies
and
interspecies
variations.
Based
on
dietary,
drinking
water,
and
nonoccupational
exposure
assessments,
there
is
reasonable
certainty
of
no
harm
to
the
U.
S.
population,
any
population
subgroup,
or
infants
and
children
from
short­
term
or
chronic
exposure
to
etoxazole.
i.
Food.
Dietary
exposure
was
estimated
using
DEEMTM,
proposed
tolerances,
and
assuming
100%
crop
treated.
Results
of
the
acute
analysis
demonstrate
that
estimated
exposure
is
0.5%
or
less
of
the
estimated
aPAD
(
at
the
95th
percentile)
for
all
population
groups
examined.
Acute
dietary
exposure
for
the
overall
U.
S.
population
was
estimated
to
be
0.002572
mg/
kg
bwt/
day
at
the
95th
percentile
of
exposure
(
0.13%
of
the
aPAD).
Chronic
dietary
exposure
was
estimated
for
the
overall
U.
S.
population
and
25
population
sub
groups.
Daily
exposure
for
the
overall
U.
S.
population
was
estimated
to
be
0.000574
mg/
kg
bwt/
day,
representing
1.4%
of
the
estimated
cPAD.
Daily
exposure
for
the
most
highly
exposed
population
subgroup,
children
1
 
6
years
of
age,
was
estimated
to
be
0.002293
mg/
kg
bwt/
day,
or
5.7%
of
the
estimated
cPAD.
ii.
Drinking
water.
Since
etoxazole
is
applied
outdoors
to
growing
agricultural
crops,
the
potential
exists
for
the
parent
or
its
metabolites
to
reach
ground
or
surface
water
that
may
be
used
for
drinking
water.
But,
because
of
the
physical
properties
of
etoxazole,
it
is
unlikely
that
etoxazole
or
its
metabolites
can
leach
to
potable
groundwater.
Although,
relatively
stable
to
hydrolysis,
etoxazole
undergoes
fairly
rapid
photolysis,
degrades
fairly
readily
in
soil
and
is
immobile
in
all
soil
types
examined.
To
quantify
potential
exposure
from
drinking
water,
FIRST
and
SCI­
GROW
models
were
used
to
estimate
surface
and
groundwater
residues.
Estimated
surface
water
residues
were
much
higher
than
estimated
groundwater
residues
and
therefore
the
surface
residues
were
used
as
the
drinking
water
environmental
concentration
(
DWEC).
The
peak
(
acute)
concentration
predicted
in
the
simulated
pond
water
was
estimated
to
be
2.47
ppb
and
the
annual
average
(
chronic)
concentration
predicted
in
the
simulated
pond
water
was
estimated
to
be
1.93
ppb.
To
assess
the
contribution
to
the
dietary
risk
from
exposure
to
drinking
water
containing
residues
of
etoxazole,
these
DWEC's
are
compared
to
drinking
water
levels
of
comparison
(
DWLOC's),
the
maximum
drinking
water
concentration
allowed
before
combined
water,
dietary,
and
other
exposures
will
exceed
the
population
adjusted
doses.
If
the
DWLOC
is
greater
than
the
DWEC,
then
overall
exposure
will
not
exceed
the
population
adjusted
doses
and
combined
exposure
from
water
and
food
is
considered
to
be
acceptable.
Acute
DWLOC's
for
etoxazole
range
from
19,900
to
69,910
ppb
and
chronic
DWLOC's
range
from
377
to1380
ppb
for
all
U.
S.
population
subgroups
examined.
Since
these
DWLOC's
exceed
the
modeled
acute
and
chronic
DWEC
surface
water
residues
by
a
wide
margin,
Valent
concludes
that
exposure
to
potential
residues
in
drinking
water
is
negligible
and
that
aggregate
(
food
and
water)
exposure
to
etoxazole
residues
will
be
acceptable.
2.
Non­
dietary
exposure.
Etoxazole
is
proposed
only
for
agricultural
uses
and
no
homeowner
or
turf
uses.
Thus,
no
non­
dietary
risk
assessment
is
needed.

D.
Cumulative
Effects
Section
408(
b)(
2)(
D)(
v)
requires
that
the
Agency
must
consider
``
available
information''
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
``
other
substances
that
have
a
common
mechanism
of
toxicity.''
Available
information
in
this
context
include
not
only
toxicity,
chemistry,
and
exposure
data,
but
also
scientific
policies
and
methodologies
for
understanding
common
mechanisms
of
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Federal
Register
/
Vol.
68,
No.
156
/
Wednesday,
August
13,
2003
/
Notices
toxicity
and
conducting
cumulative
risk
assessments.
For
most
pesticides,
although,
the
Agency
has
some
information
in
its
files
that
may
turn
out
to
be
helpful
in
eventually
determining
whether
a
pesticide
shares
a
common
mechanism
of
toxicity
with
any
other
substances,
EPA
does
not
at
this
time
have
the
methodologies
to
resolve
the
complex
scientific
issues
concerning
common
mechanism
of
toxicity
in
a
meaningful
way.
In
consideration
of
potential
cumulative
effects
of
etoxazole
and
other
substances
that
may
have
a
common
mechanism
of
toxicity,
there
are
currently
no
available
data
or
other
reliable
information
indicating
that
any
toxic
effects
produced
by
etoxazole
would
be
cumulative
with
those
of
other
chemical
compounds.
Thus,
only
the
potential
risks
of
etoxazole
have
been
considered
in
this
assessment
of
aggregate
exposure
and
effects.
Valent
will
submit
information
for
EPA
to
consider
concerning
potential
cumulative
effects
of
etoxazole
consistent
with
the
schedule
established
by
EPA
at
62
Federal
Register
42020
(
Aug.
4,
1997)
and
other
subsequent
EPA
publications
pursuant
to
the
Food
Quality
Protection
Act.

E.
Safety
Determination
1.
U.
S.
population.
 
i.
Acute
risk.
The
potential
acute
exposure
from
food
to
the
U.
S.
population
and
various
nonchild
infant
population
subgroups
are
estimated
to
be
0.06
to
0.13
%
of
the
proposed
aPAD.
Exposure
to
potential
acute
residues
in
drinking
water
is
expected
to
be
negligible,
as
acute
DWLOC's
are
substantially
higher
than
modeled
acute
DWEC's.
Based
on
this
assessment,
Valent
concludes
that
there
is
a
reasonable
certainty
that
no
harm
to
the
U.
S.
population
or
any
population
subgroup
will
result
from
acute
exposure
to
etoxazole.
ii.
Chronic
risk.
The
potential
chronic
exposure
from
food
to
the
U.
S.
population
and
various
non­
child/
infant
population
subgroups
are
estimated
to
be
0.7%
to
1.9%
of
the
proposed
cPAD.
Chronic
exposure
to
potential
residues
in
drinking
water
is
also
expected
to
be
negligible,
as
chronic
DWLOC's
are
substantially
higher
than
modeled
chronic
DWEC's.
Based
on
this
assessment,
Valent
concludes
that
there
is
a
reasonable
certainty
that
no
harm
to
the
U.
S.
population
or
any
population
subgroup
will
result
from
chronic
exposure
to
etoxazole.
2.
Infants
and
children.
 
i.
Safety
Factor
for
Infants
and
Children.
In
assessing
the
potential
for
additional
sensitivity
of
infants
and
children
to
residues
of
etoxazole,
FFDCA
section
408
provides
that
EPA
shall
apply
an
additional
margin
of
safety,
up
to
tenfold
for
added
protection
for
infants
and
children
in
the
case
of
threshold
effects
unless
EPA
determines
that
a
different
margin
of
safety
will
be
safe
for
infants
and
children.
The
toxicological
data
base
for
evaluating
prenatal
and
postnatal
toxicity
for
etoxazole
is
complete
with
respect
to
current
data
requirements.
There
are
no
special
prenatal
or
postnatal
toxicity
concerns
for
infants
and
children,
based
on
the
results
of
the
rat
and
rabbit
developmental
toxicity
studies
or
the
2­
generation
reproductive
toxicity
study
in
rats.
Valent
has
concluded
that
reliable
data
support
use
of
the
standard
100
 
fold
uncertainty
factor
and
that
an
additional
uncertainty
factor
is
not
needed
for
etoxazole
to
be
further
protective
of
infants
and
children.
ii.
Acute
risk.
The
potential
acute
exposure
from
food
to
infants
and
children
are
estimated
to
be
0.16
to
0.50
%
of
the
proposed
aPAD.
Exposure
to
potential
acute
residues
in
drinking
water
is
expected
to
be
negligible,
as
acute
DWLOC's
are
substantially
higher
than
modeled
acute
DWEC's.
Based
on
this
assessment,
Valent
concludes
that
there
is
a
reasonable
certainty
that
no
harm
to
infants
and
children
will
result
from
acute
exposure
to
etoxazole.
iii.
Chronic
risk.
The
potential
chronic
exposure
from
food
to
infants
and
children
are
estimated
to
be
2.1
to
5.7%
of
the
proposed
cPAD.
Chronic
exposure
to
potential
residues
in
drinking
water
is
expected
to
be
negligible,
as
chronic
DWLOC's
are
substantially
higher
than
modeled
DWEC's.
Based
on
this
assessment,
Valent
concludes
that
there
is
a
reasonable
certainty
that
no
harm
to
infants
and
children
will
result
from
chronic
exposure
to
etoxazole.
3.
Safety
determination
summary.
Aggregate
acute
or
chronic
dietary
exposure
to
various
sub­
populations
of
children
and
adults
demonstrate
acceptable
risk.
Acute
and
chronic
dietary
exposures
to
etoxazole
occupy
considerably
less
than
100%
of
the
appropriate
PAD.
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
acute
and
chronic
PAD's
because
these
represent
levels
at
or
below
which
daily
aggregate
dietary
exposure
over
a
lifetime
will
not
pose
appreciable
risks
to
human
health.
Chronic
and
acute
dietary
risk
to
children
from
etoxazole
should
not
be
of
concern.
Further,
etoxazole
has
only
agricultural
uses
and
no
other
uses,
such
as
indoor
pest
control,
homeowner
or
turf,
that
could
lead
to
unique,
enhanced
exposures
to
vulnerable
sub­
groups
of
the
population.
Valent
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
the
U.
S.
population
or
to
any
sub­
group
of
the
U.
S.
population,
including
infants
and
children,
from
aggregate
chronic
or
aggregate
acute
exposures
to
etoxazole
residues
resulting
from
proposed
uses.

F.
International
Tolerances
Etoxazole
has
not
been
evaluated
by
the
JMPR
and
there
are
no
Codex
Maximum
Residue
Limits
(
MRL)
for
etoxazole.
MRL
values
have
been
established
to
allow
the
following
uses
of
etoxazole
in
the
following
countries:
Turkey,
Israel,
South
Africa,
Japan,
France,
Taiwan,
and
Korea.
The
use
pattern
and
MRL's
are
similar
to
those
proposed
for
the
U.
S.

[
FR
Doc.
03
 
20642
Filed
8
 
12
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
FRL
 
7543
 
8]

Proposed
CERCLA
Section
122(
h)
Administrative
Agreement
for
Recovery
of
Response
Costs
for
the
Amenia
Town
Landfill
Superfund
Site,
Town
of
Amenia,
Dutchess
County,
NY
AGENCY:
Environmental
Protection
Agency.
ACTION:
Notice;
request
for
public
comment.

SUMMARY:
In
accordance
with
Section
122(
i)
of
the
Comprehensive
Environmental
Response,
Compensation,
and
Liability
Act
of
1980,
as
amended
(``
CERCLA''),
42
U.
S.
C.
9622(
i),
notice
is
hereby
given
by
the
U.
S.
Environmental
Protection
Agency
(``
EPA''),
Region
II,
of
a
proposed
administrative
agreement
pursuant
to
Section
122(
h)
of
CERCLA,
42
U.
S.
C.
9622(
h),
for
recovery
of
response
costs
concerning
the
Amenia
Town
Landfill
Superfund
Site
(``
Site'')
located
in
the
Town
of
Amenia,
Dutchess
County,
New
York.
The
settlement
requires
the
settling
parties,
Town
of
Amenia,
New
York;
Ashland,
Inc.;
BP
America
Inc.;
Curtiss­
Wright
Corporation;
International
Business
Machines
Corporation;
Alastair
B.
Martin;
Estate
of
Edith
Martin;
Metal
Improvement
Company,
Inc.;
Town
of
Sharon,
Connecticut;
Syngenta
Crop
Protection,
Inc.;
TBG
Services,
Inc.;
Unisys
Corporation;
and
Weyerhaeuser
Company
to
pay
$
361,873.17
in
reimbursement
of
EPA's
response
costs
at
the
Site.
The
settlement
includes
a
covenant
not
to
sue
the
settling
parties
pursuant
to
Section
107(
a)
of
CERCLA,
42
U.
S.
C.
9607(
a),
in
exchange
for
their
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