11850
Federal
Register
/
Vol.
68,
No.
48
/
Wednesday,
March
12,
2003
/
Notices
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,
tebufenozide
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
this
tolerance
petition,
Dow
AgroSciences
has
not
assumed
that
tebufenozide
has
a
common
mechanism
of
toxicity
with
other
substances.

E.
Safety
Determination
1.
U.
S.
population.
Using
the
exposure
assumptions
previously
described,
and
taking
into
account
the
completeness
and
reliability
of
the
toxicity
data,
Dow
AgroSciences
has
concluded
that
dietary
(
food
only)
exposure
to
tebufenozide
will
utilize
21%
of
the
chronic
population
adjusted
dose
(
cPAD)
for
the
U.
S.
population.
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
cPAD.
Submitted
environmental
fate
studies
suggest
that
tebufenozide
is
moderately
persistent
to
persistent
and
mobile;
thus,
tebufenozide
could
potentially
leach
to
ground
water
and
runoff
to
surface
water
under
certain
environmental
conditions.
The
modeling
data
for
tebufenozide
indicate
levels
less
than
the
Agency's
DWLOCs.
There
are
no
chronic
non­
occupational/
residential
exposures
expected
for
tebufenozide.
Therefore,
Dow
AgroSciences
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
adults,
infants
and
children
from
chronic
aggregate
exposure
to
tebufenozide
residues.
2.
Infants
and
children.
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
inter­
and
intra­
species
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.
Using
the
exposure
assumptions
previously
described,
and
taking
into
account
the
completeness
and
reliability
of
the
toxicity
data,
the
dietary
(
food
only)
exposure
to
tebufenozide
will
utilize
51%
of
the
cPAD
for
the
most
highly
exposed
population
subgroup
(
children
1
 
6
years
old).
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
cPAD.
Despite
the
potential
for
exposure
to
tebufenozide
in
drinking
water
and
from
non­
dietary
nonoccupational
exposure,
Dow
AgroSciences
does
not
expect
the
aggregate
exposure
to
exceed
100%
of
the
RfD.

F.
International
Tolerances
Codex
maximum
residue
levels
have
been
established
for
residues
of
tebufenozide
in/
on
pome
fruit
(
1.0
ppm),
husked
rice
(
0.1
ppm)
and
walnut
(
0.05
ppm).
Tebufenozide
is
registered
in
Canada,
and
a
tolerance
for
residues
in/
on
apples
is
established
at
1.0
ppm.
EPA
has
set
the
pome
fruit
tolerance
at
1.5
ppm
based
on
U.
S.
field
residue
trials.

[
FR
Doc.
03
 
5912
Filed
3
 
11
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0022;
FRL
 
7295
 
9]

Dimethenamid;
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
 
0022,
must
be
received
on
or
before
April
11,
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:
Sidney
Jackson,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001;
telephone
number:
(
703)
305
 
7610;
e­
mail
address:
jackson.
sidney@
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:
 
Industry
(
NAICS
111),
e.
g.,
Crop
production.
 
Industry
(
NAICS
112),
e.
g.,
Animal
production.
 
Industry
(
NAICS
311),
e.
g.,
Food
manufacturing.
 
Industry
(
NAICS
32532),
e.
g.,
Pesticide
manufacturing.
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.
To
determine
whether
you
or
your
business
may
be
affected
by
this
action,
you
should
carefully
examine
the
applicability
provisions
in
Unit
I.
A.
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
identification
(
ID)
number
OPP
 
2003
 
0022.
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
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
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Federal
Register
/
Vol.
68,
No.
48
/
Wednesday,
March
12,
2003
/
Notices
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
in
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
 
0022.
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
 
0022.
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
 
0022.
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
 
0022.
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
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.

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Register
/
Vol.
68,
No.
48
/
Wednesday,
March
12,
2003
/
Notices
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:
March
4,
2003.
Debra
Edwards,
Acting
Director,
Registration
Division,
Office
of
Pesticide
Programs.

Summary
of
Petition
The
petitioner
summary
of
the
pesticide
petition
is
printed
below
as
required
by
FFDCA
section
408(
d)(
3).
The
summary
of
the
petition
was
prepared
by
the
petitioner
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.

PP
0E6196
EPA
has
received
a
pesticide
petition
(
PP
0E6196)
from
the
Interregional
Research
Project
No.
4
(
IR
 
4),
Technology
Centre
of
New
Jersey,
Rutgers,
the
State
University
of
New
Jersey,
681
U.
S.
Highway
#
1
South,
North
Brunswick,
NJ
08902
 
3390
proposing,
pursuant
to
section
408(
d)
of
the
FFDCA,
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
part
180.464
by
establishing
tolerances
for
residues
of
dimethenamid,
(
R,
S)­
2­
chloro­
N­[(
1­
methyl­
2­
methoxy)
ethyl]­
N­(
2,4­
dimethyl­
thien­
3­
yl)­
acetamide
in
or
on
the
raw
agricultural
commodities
beet,
garden,
roots
at
0.01
parts
per
million
(
ppm);
beet,
garden,
tops
at
0.01
ppm;
beet,
sugar,
roots
at
0.01
ppm;
beet,
sugar,
tops
at
0.01
ppm;
garlic,
dry
bulb
at
0.01
ppm;
horseradish
at
0.01
ppm;
onion,
dry
bulb
at
0.01
ppm,
shallot,
dry
bulb
at
0.01
ppm;
and
tuberous
and
corm
vegetables
subgroup
(
Crop
group
1C)
at
0.01
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.
This
petition
summary
was
prepared
by
the
registrant,
BASF
Corporation,
P.
O.
Box
13528,
Research
Triangle
Park,
NC
27709
 
3528.

A.
Residue
Chemistry
1.
Plant
and
animal
metabolism.
BASF
Corporation
notes
that
metabolism
in
plants
and
animals
is
understood.
2.
Analytical
method.
The
proposed
analytical
method
uses
extraction
and
clean­
up
followed
by
quantification
with
capillary
column
gas
chromatography
(
GC)
using
thermionic
nitrogen
specific
detector.
A
GC/
mass
spectrocopy
(
MS)
method
for
identification
is
also
available.
This
method
is
not
selective
towards
the
dimethenamid
isomer
and
is
therefore
valid
for
residues
from
both
dimethenamid
and
the
enriched
dimethenamid­
P.
Tolerances
are
proposed
based
on
a
non­
isomer
specific
basis.
3.
Magnitude
of
residues.
For
onion,
magnitude
of
the
residue
data
are
based
on
applications
with
dimethenamid.
Residue
trials
were
conducted
at
8
locations
in
California,
Michigan,
New
York,
Oregon,
Texas,
Washington,
and
Wisconsin.
Treatments
were
made
at
1.5
lbs
active
ingredient/
acre
(
ai/
A)
30
or
45
days
before
harvest.
No
residues
above
the
limit
of
quantitation
(
LOQ)
of
0.01
ppm
were
detected
in
dry
bulb
onion.
Residue
data
from
dry
bulb
onion
will
be
used
as
surrogate
data
for
dry
bulb
garlic
and
shallots.
For
sugar
beet,
magnitude
of
the
residue
data
are
based
on
dimethenamid­
P
applications
to
sugar
beet
at
0.98
lb
ai/
A.
Dimethenamid­
P
is
the
biologically
active
isomer
from
the
racemic
dimethenamid
mixture.
The
method
measures
both
dimethenamid
and
dimethenamid­
P,
so
the
sugar
beet
residue
determinations
for
dimethenamid­
P
are
considered
representative
of
the
proposed
treatments
with
dimethenamid.
No
residues
were
detected
in
sugar
beet
roots
or
tops
from
a
testing
program
conducted
in
12
locations
across
8
states.
Data
from
processing
studies
indicate
that
no
residues
are
detected
in
the
roots
even
at
exaggerated
rates
of
3.15
lbs
ai/
A.
The
limit
of
quantitation
is
0.01
ppm.
The
sugar
beet
trials
also
support
the
tolerances
for
table
beet.
For
the
tuberous
and
corm
vegetable
subgroup,
magnitude
of
the
residue
data
for
potatoes
are
based
on
applications
with
dimethenamid­
P.
Residue
trials
were
conducted
at
17
locations
in
California,
Colorado,
Florida,
Idaho,
Michigan,
New
Jersey,
North
Carolina,
Oregon,
Pennsylvania,
Washington,
and
Wisconsin.
Treatments
were
made
at
1.25
lbs
ai/
A
40
days
before
harvest.
No
residues
above
the
LOQ
of
0.01
ppm
were
detected
in
potato
tubers.
Data
from
processing
studies
indicate
that
no
residues
are
detected
in
the
tubers
even
at
exaggerated
rates
of
12.5
lbs
ai/
A.
Residue
data
from
potato
tubers
will
be
used
as
surrogate
data
for
horseradish.
BASF
believes
that
due
to
the
low
levels
of
residue
in
the
RAC's,
tolerances
in
animals
are
not
required.

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2003
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Federal
Register
/
Vol.
68,
No.
48
/
Wednesday,
March
12,
2003
/
Notices
B.
Toxicological
Profile
1.
Acute
toxicity.
Based
on
available
acute
toxicity
data,
dimethenamid
and
dimethenamid­
P
do
not
pose
an
acute
dietary
risk.
The
acute
toxicity
studies
place
both
technical
materials
in
acute
toxicity
category
II
for
acute
oral;
in
acute
toxicity
category
III
for
acute
dermal,
inhalation,
and
eye;
and
in
acute
toxicity
category
IV
for
dermal
irritation.
The
technical
materials
are
a
positive
skin
sensitizer.
2.
Genotoxicity.
The
following
testing
was
performed
with
dimethenamid
for
genotoxicity.
A
modified
ames
test:
Negative;
in
vitro
CHO/
HGPRT
mammalian
cell
mutation
assay:
Negative;
in
vitro
cytogentics
­
CHO
cells
(
1
study;
chromosome
aberrations):
Weakly
positive;
in
vitro
UDS
test
using
rat
hepatocytes
(
3
studies;
DNA
damage
and
repair):
2
negative;
1
equivocally
positive,
mouse
micronucleus
assay
(
2
studies;
chromosome
aberrations):
Negative,
rat
dominant
lethal
assay:
1
study
equivocally
positive,
1
study
negative.
Overall
dimethenamid
has
been
tested
in
14
genetic
toxicology
assays.
The
weight
of
the
evidence
demonstrates
that
dimethenamid
is
not
genotoxic.
The
following
testing
was
performed
with
dimethenamid­
P
for
genotoxicity.
A
modified
ames
test
(
3
studies;
point
mutation):
Negative;
in
vitro
CHO/
HGPRT
mammalian
cell
mutation
assay
(
1
study;
point
mutation):
Negative;
in
vitro
cytogentics
­
CHO
cells
(
1
study;
chromosome
aberrations):
Negative;
in
vitro
UDS
test
using
rat
hepatocytes
(
1
study;
DNA
damage
and
repair):
Negative;
mouse
micronucleus
assay
(
1
study;
chromosome
aberrations):
Negative.
Dimethenamid­
P
has
been
tested
in
a
total
of
7
genetic
toxicology
assays.
These
assays
were
performed
both
in
vitro
and
in
vivo
and
multiple
assays
were
conducted
for
each
of
the
three
EPA
Guideline
requirement
categories.
Based
on
the
data
presented
above,
the
data
indicates
that
dimethenamid­
P
does
not
induce
gene
mutations,
is
not
clastogenic
and
does
not
induce
other
effects
indicative
of
genotoxicity.
Therefore,
BASF
concludes
that
dimethenamid­
P
does
not
pose
a
mutagenic
hazard
to
humans.
3.
Reproductive
and
developmental
toxicity
 
i.
Rat.
A
developmental
rat
study
using
dimethenamid
via
oral
gavage
resulted
in
dosages
of
0,
50,
215,
and
425
milligram
per
kilogram
(
mg/
kg)/
day
with
a
development
toxicity
no
observed
adverse
effect
level
(
NOAEL)
of
215
mg/
kg/
day
and
a
maternal
toxicity
of
50
mg/
kg/
day
based
on
the
following:
(
1)
Signs
of
maternal
toxicity,
in
the
form
of
reduced
body
weight
gain
and
food
consumption,
increased
liver
weight
and
clinical
observations
were
observed
at
dose
levels
>
215
mg/
kg/
day
with
an
increase
in
effects
to
the
upper
dose
level;
(
2)
at
the
=
215
mg/
kg/
day
dose
levels
slight
decreases
in
fetal
body
weights
were
observed
which
are
not
indicative
a
teratogenic
effect;
and
(
3)
at
the
425
mg/
kg/
day
dose
level
a
slight
increase
in
resorptions
was
observed,
and
two
fetuses
had
incomplete
ossified
manubria.
These
effects
are
not
indicative
of
a
teratogenic
effect.
A
developmental
rat
study
using
dimethenamid­
P
via
oral
gavage
resulted
in
dosages
of
0,
25,
150,
and
300
mg/
kg/
day
with
a
development
toxicity
NOAEL
of
25
mg/
kg/
day
and
a
maternal
toxicity
of
25
mg/
kg/
day
based
on
based
on
the
following:
(
1)
Signs
of
maternal
toxicity,
in
the
form
of
decreased
body
weights
and
food
consumption
were
observed
at
dose
levels
>
150
mg/
kg/
day
with
an
increase
in
effects
to
the
upper
dose
level;
(
2)
at
the
150
mg/
kg/
day
dose
level
slight
decreases
in
fetal
body
weights
and
retarded
ossification
of
the
pelvis
pubis
were
observed
which
are
not
indicative
a
teratogenic
effect;
and
(
3)
at
the
300
mg/
kg/
day
dose
level
slight
decreases
in
fetal
body
weights,
microphthalmia
in
two
fetuses/
two
litters,
distended
ureters,
and
retarded
ossification
of
the
2nd
sternal
centra
and
pelvis
pubis
were
observed,
similarly,
these
effects
are
not
indicative
of
a
teratogenic
effect.
ii.
Rabbits.
A
developmental
study
in
rabbits
using
dimethenamid
via
oral
gavage
resulted
in
dosages
of
0,
37.5,
75,
and
150
mg/
kg/
day
(
HDT)
with
a
development
toxicity
NOAEL
of
75
mg/
kg/
day
and
a
maternal
toxicity
of
37.5
mg/
kg/
day
based
on:
(
1)
Decreased
body
weight,
food
consumption,
and
absorption/
premature
delivery
in
the
75
and
150
mg/
kg/
day
dose
groups;
and
(
2)
effects
on
fetal
development
were
a
low
incidence
of
absorption/
premature
delivery
and
hyoid
angulated
changes
in
the
150
mg/
kg/
day
dose
group
which
are
not
are
indicative
of
a
teratogenic
effect.
iii.
Two­
generation
reproduction
­
rats.
A
two­
generation
reproduction
study
using
dimethenamid
with
rats
fed
dosages
of
0,
7.5,
38,
and
155
mg/
kg/
day
(
average
mg/
kg/
day
dose
levels
for
both
male
and
female
rats)
with
a
reproductive
NOAEL
of
38
mg/
kg/
day
and
with
a
parental
NOAEL
of
38
mg/
kg/
day
based
on:
(
1)
Parental
toxicity
as
evident
by
reduction
in
body
weight
and
food
consumption
and
significant
increases
in
absolute
and/
or
relative
liver
weights
in
both
males
and
female
rats
in
the
155
mg/
kg/
day
dose
group;
and
(
2)
significant
reductions
in
pup
weight
during
lactation
were
observed
in
the
150
mg/
kg/
day
dose
group.
No
changes
in
pregnancy
rates,
fertility
or
length
of
gestation
were
observed
at
all
dose
levels
tested.
4.
Chronic
feeding
and
carcinogenicity.
The
established
reference
dose
(
RfD)
for
dimethenamid
and
dimethenamid­
P
is
based
on
a
2­
year
feeding
study
in
rats
with
dimethenamid,
with
a
threshold
NOAEL
of
5.1
mg/
kg/
day.
Using
an
uncertainty
factor
of
100,
the
RfD
is
calculated
to
be
0.05
mg/
kg/
day.
The
following
are
summaries
of
the
pertinent
toxicity
data
supporting
dimethenamid
tolerances:
i.
Chronic
feeding
­
nonrodent.
A
1­
year
feeding
study
in
dogs
fed
dimethenamid
at
dosages
of
0,
2,
9.6,
or
49
mg/
kg/
day
with
a
NOAEL
of
9.6
mg/
kg/
day
based
on
the
following
effects:
(
1)
Slight
decreases
in
body
weights
for
both
the
high
dose
male
and
female
dogs
as
compared
to
controls;
(
2)
a
variable
degree
of
periportal
hepatocyte
vacuolation
in
the
high­
dose
male
and
female
dogs;
(
3)
minimal
or
mild
hepatocyte
enlargement
was
similarly
observed
in
the
high­
dose
dogs;
and
(
4)
the
liver
changes
at
the
high­
dose
group
correlated
with
increase
in
serum
alkaline
phosphatase
activity
and
cholesterol
levels
and
increased
liver­
tobody
weight
ratios
in
both
male
and
female
dogs.
ii.
Chronic
feeding/
carcinogenicity
­
rat.
A
combined
chronic
feeding/
carcinogenicity
study
using
dimethenamid
was
performed
in
rats
being
fed
dosages
of
0,
5.1,
36,
and
80
mg/
kg/
day
(
males)
and
0,
6.8,
49,
and
109
mg/
kg/
day
(
females)
with
a
NOAEL
of
5.1
mg/
kg/
day
(
males)
and
6.8
mg/
kg/
day
(
females)
based
on
the
following
effects:
(
1)
Decreased
body
weights
in
both
males
and
female
rat
at
dose
levels
>
36
mg/
kg/
day
dose
groups
with
a
slight
progression
of
severity
to
the
upper
level;
(
2)
decreased
food
consumption
in
both
males
and
female
rats
at
dose
levels
>
36
mg/
kg/
day
dose
groups
with
a
slight
progression
of
severity
to
the
upper
dose
level;
(
3)
minimal
hematological
and
clinical
chemistry
value
changes
at
dose
levels
>
36
mg/
kg/
day
dose
groups
with
very
slight
increase
of
severity
at
the
higher
dose
tested;
(
4)
increased
absolute
liver
weights
for
females
at
dose
levels
>
49
mg/
kg/
day;
(
5)
microscopic
findings
were
observed
in
the
liver,
parathyroid,
and
stomach
of
high­
dose
males,
only,
and
ovaries
of
high­
dose
females;
and
(
6)
an
increased
incidence
of
benign
and
malignant
tumors
of
the
liver
at
the
highest
dose
level
tested.
The
liver
tumors
observed
in
this
study
occurred
at
an
incidence
which
was
slightly
beyond
the
historical
control
range
for
this
tumor
type,
and
occurred
at
the
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maximum
tolerated
dose
(
MTD).
Given
the
lack
of
structural
activity
relationship
(
SAR)
and
the
lack
of
mutagenicity
discussed
in
section
B.
2.,
it
is
BASFs
opinion
that
dimethenamid­
P
should
not
be
considered
a
biologically
relevant
carcinogen
in
rats
and
the
assessment
is
made
that
the
results
of
this
carcinogenicity
study
do
not
indicate
a
carcinogenic
potential
of
the
test
substance
for
humans.
iii.
Carcinogenicity
­
mice.
A
carcinogenicity
study
using
dimethenamid
in
mice
fed
dosages
of
0,
3.8,
41,
205,
and
431
(
HDT)
mg/
kg/
day
(
males)
and
0,
4.1,
41,
200,
and
411
(
HDT)
mg/
kg/
day
(
females)
with
a
NOAEL
of
41
mg/
kg/
day
for
male
and
female
mice
based
on
the
following
effects:
(
1)
Decreased
body
weights
and
food
consumption
were
observed
in
both
males
and
female
mice
at
the
highest
dose
tested;
(
2)
increased
liver
weights
were
observed
for
male
and
female
mice
at
the
highest
dose
tested
at
an
interim
sacrifice
and
increased
weights
for
kidney
and
liver
were
observed
for
female
mice
at
dose
levels
>
200
mg/
kg/
day
at
terminal
sacrifice;
(
3)
microscopic
findings
were
observed
in
the
liver
and
stomach
for
both
male
and
female
mice
at
the
upper
dose
levels;
(
4)
concerning
the
finding
in
the
stomach,
EPA
has
determined
that
this
finding
was
attributed
to
irritation
of
the
material
and
the
finding
was
not
toxicology
significant;
and
(
4)
no
increased
incidence
of
neoplasms
occurred
at
any
dose
levels
tested
in
this
study.
EPA
has
concluded
that
this
product
is
not
carcinogenic
under
the
conditions
of
this
study.
Dimethenamid
is
considered
not
to
be
carcinogenic
in
mice
by
BASF.
In
the
rat
carcinogenicity
study,
a
slight
increase
in
liver
tumors
was
observed
in
males,
only,
at
the
highest
dose
tested.
The
liver
tumors
observed
in
this
study
occurred
at
an
incidence
that
was
slightly
beyond
the
historical
control
range
for
this
tumor
type,
and
occurred
at
the
MTD.
Dimethenamid
shares
no
common
mechanisms
with
other
compounds
in
the
chloroacetanilide
class
of
compounds.
It
is
BASF's
opinion
that
dimethenamid
and
dimethenamid­
P
should
not
to
be
considered
biologically
relevant
carcinogens
in
rats
and
the
assessment
is
made
that
the
results
of
this
carcinogenicity
study
do
not
indicate
a
carcinogenic
potential
of
these
substances
for
humans.
However,
EPA
has
determined
that
dimethenamid
is
considered
to
be
a
Group
C
carcinogen
­
possible
human
carcinogen
­
based
on
the
judgment
of
the
EPA
Carcinogenicity
Peer
Review
Committee
assessment.
Also,
the
Committee
determined
for
risk
assessment
purposes,
the
RfD
approach
should
be
used
to
quantify
human
risk.
BASF
agrees
with
the
Agency
that
the
RfD
approach
for
human
risk
assessment
is
valid.
5.
Endocrine
disruption.
No
specific
tests
have
been
performed
with
dimethenamid­
P
or
dimethenamid
to
determine
whether
the
chemical
may
have
an
effect
in
humans
that
is
similar
to
an
effect
produced
by
naturally
occurring
estrogen
or
other
endocrine
effects.
However,
there
are
no
significant
findings
in
other
relevant
toxicity
studies,
i.
e.
teratology
and
multi­
generation
reproductive
studies,
that
would
suggest
the
dimethenamid
produces
endocrine
related
effects.

C.
Aggregate
Exposure
1.
Dietary
exposure
 
i.
Food.
BASF
has
reviewed
the
available
toxicology
database
to
determine
the
endpoints
of
concern.
For
dimethenamid
and
dimethenamid­
P,
BASF
believes
there
is
no
concern
regarding
an
acute
dietary
risk
since
the
available
data
do
not
indicate
any
evidence
of
significant
toxicity
from
a
1
day
or
single
event
exposure
by
the
oral
route.
For
the
purpose
of
assessing
the
potential
chronic
dietary
exposure,
BASF
has
estimated
aggregate
exposure
based
on
theoretical
maximum
residue
contribution
(
TMRC)
from
the
tolerance
of
dimethenamid
on
sweet
corn,
sorghum,
peanuts,
and
dry
beans
at
0.01
ppm
for
all
uses
stated,
respectively.
The
TMRC
is
a
``
worse
case''
estimate
of
dietary
exposure
since
it
is
assumed
that
100%
of
all
crops
for
which
the
tolerances
are
established
are
treated
and
that
pesticide
residues
are
always
found
at
tolerance
levels.
EPA
in
a
letter
issued
on
October
13,
1995,
for
dimethenamid,
determined
the
TMRC
for
the
crops
mentioned
in
section
C.
1.
to
be
0.076
and
0.341
microgram
(
ug)/
kg/
day
for
the
general
U.
S.
population
and
non­
nursing
infants
(<
1),
respectively.
Dimethenamid
treated
crops
using
the
TMRC
values
utilized
0.15%
and
0.683%
for
the
general
U.
S.
population
and
non­
nursing
infants
(<
1),
respectively,
of
the
RfD
(
0.05
mg/
kg/
day).
These
assessments
are
also
valid
for
dimethenamid­
P.
BASF
concurs
with
this
assessment.
The
addition
of
an
onion
tolerance
at
0.01
ppm
has
a
TMRC
of
0.0011
ug/
kg/
day
for
the
general
population
and
a
TMRC
of
0.0004
ug/
kg/
day
for
nonnursing
infants.
Sugar
beet
tolerances
at
0.01
ppm,
add
0.0033
ug/
kg/
day
to
the
TMRC
for
the
general
population
and
0.0013
ug/
kg/
day
to
the
TMRC
for
nonnursing
infants.
The
addition
of
table
beet
tops,
dry
bulb
garlic,
horseradish,
and
dry
bulb
shallot
is
negligible;
table
beet
root
tolerances
at
0.01
ppm
add
0.00022
ug/
kg/
day
to
the
TMRC
for
the
general
population
and
0.0019
ug/
kg/
day
to
the
TMRC
for
non­
nursing
infants.
The
addition
of
potato
tolerances
at
0.01
ppm
would
contribute
0.011
ug/
kg/
day
to
the
TMRC
for
the
general
population
and
0.014
ug/
kg/
day
to
the
TMRC
for
non­
nursing
infants.
The
addition
of
sweet
potato
tolerances
at
0.01
ppm
would
contribute
0.00039
ug/
kg/
day
to
the
TMRC
for
the
general
population
and
0.0029
ug/
kg/
day
to
the
TMRC
for
non­
nursing
infants.
The
total
RfD
utilization
from
all
uses,
both
registered
and
proposed,
is
0.18%
for
the
general
population,
and
0.72%
for
non­
nursing
infants.
Therefore,
based
on
the
completeness
and
reliability
of
the
toxicity
data,
and
the
exposure
assessment
discussed
in
section
C.
1.,
BASF
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
residues
of
dimethenamid
and
dimethenamid­
P,
including
all
anticipated
dietary
exposure.
ii.
Drinking
water.
Other
potential
sources
of
exposure
to
dimethenamid
for
the
general
population
are
residues
in
drinking
water
and
exposure
from
non­
occupational
sources.
In
a
dimethenamid­
P
environmental­
fate
risk
assessment
dated
December
1998,
EPA
calculated
the
following
maximum
concentrations
for
drinking
water:
Based
on
SCI­
GROW
model
calculations,
ground­
water
concentrations
were
expected
to
be
<
1.0
parts
per
billion
(
ppb).
Based
on
PRZM/
EXAMS
model
calculations
for
surface
water,
the
maximum
yearly
average
(
chronic)
concentration
was
5.4
ug/
l
from
a
Southeast
corn
scenario.
Using
these
values,
the
drinking
water
level
of
comparison
(
DWLOC)
and
the
aggregate
RfD
utilization
are
summarized
in
the
table
below.

U.
S.
population
(%
of
RfD)
Non­
nursing
infants
(%
of
RfD)

Chronic
dietary
exposure
0.18
0.72
Remainder
RfD
available
for
water
(%)
(
drinking
water
level
of
comparison)
99.82
99.32
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U.
S.
population
(%
of
RfD)
Non­
nursing
infants
(%
of
RfD)

SCI­
GROW
ground
water
estimation1
<
0.10
0.20
PRZM/
EXAMS
surface
water
estimation1
0.30
1.10
Total
of
RfD
used
by
diet
and
water
0.58
2.00
1Used
highest
values
predicted
from
the
model
for
all
agricultural
uses.
Assumes
2L/
day
and
70
kg
adult;
1L/
day
and
10
kg
infant.

2.
Non­
dietary
exposure.
For
nonoccupational
exposure,
dimethenamid/
dimethenamid­
P
is
not
registered
for
either
golf
course
or
homeowner
uses
which
could
contribute
to
``
non­
dietary
or
other
exposure.''

D.
Cumulative
Effects
BASF
has
considered
the
potential
for
cumulative
effects
of
dimethenamid
and
other
substances
that
have
a
common
mechanism
of
toxicity.
BASF
is
aware
of
several
other
chloroacetanilide
herbicides
that
have
been
considered
structurally
similar
to
dimethenamid,
these
being:
Acetochlor,
propachlor,
butachlor,
metolachlor,
and
alachlor.
However,
BASF
believes
that
consideration
of
a
common
mechanism
of
toxicity
to
these
products
is
not
appropriate
or
valid.
This
conclusion
was
based
on
the
presentation
EPA
made
to
the
EPA
FIFRA
Science
Advisory
Panel
(
SAP)
on
March
20,
1997.
The
title
of
the
presentation
was
``
Grouping
of
Chloroacetanilide
Pesticides
Based
on
a
Common
Mechanism
of
Toxicity.''
In
this
presentation
EPA
showed
the
structure
of
several
chloroacetanilides
that
included
dimethenamid.
BASF
is
identifying
Chlor
 
7
as
dimethenamid.
EPA
concluded
that
Chlor
 
7
should
not
be
considered
to
have
a
common
mechanism
to
the
other
chloroacetanilides
based
on
the
following
reasons:
 
Except
for
Chlor
 
7
all
other
members
of
this
case
study
have
a
potential
to
generate
a
quinone
imine.
The
quinone
imine
intermediate,
is
capable
of
reacting
with
macromolecules.
 
Chlor
 
7
has
not
produced
nasal
nor
thyroid
tumors
in
rats,
thus
does
not
support
inclusion
in
the
group
for
a
common
mechanism
for
these
tumor
types.
For
liver
tumors,
Chlor
 
1,
Chlor
 
7,
Chlo
 
r5,
and
Chlor
 
6,
can
be
potentially
grouped
for
a
common
mechanism,
but
EPA
determined
that
there
is
no
knowledge
of
a
common
mechanism
of
toxicity
or
of
a
common
toxic
species
responsible
for
the
effect.
Therefore,
EPA
concluded
that
because
a
mechanism
can
not
be
postulated,
it
believes
that
sufficient
evidence
is
not
available
to
support
a
common
mechanism
for
this
tumor
type
with
these
materials.
Therefore,
BASF
agrees
with
the
position
put
forward
by
the
Agency
and
confirmed
by
the
SAP
that
a
common
mechanism
is
inappropriate
for
dimethenamid
(
Chlor
 
7)
and
the
other
chloroacetanilides
mentioned
in
section
D.
BASF
has
considered
only
the
potential
risks
of
dimethenamid
in
its
exposure
assessment.

E.
Safety
Determination
1.
U.
S.
population.
Using
the
exposure
assumptions
described
in
section
C.,
based
on
the
completeness
and
the
reliability
of
the
toxicity
data,
BASF
has
estimated
that
aggregate
exposure
to
dimethenamid
will
utilize
<
1%
of
the
RfD
(
0.05
mg/
kg/
day)
for
the
U.
S.
population.
EPA
generally
has
no
concern
for
exposure
below
100%
of
the
RfD.
Therefore,
based
on
the
completeness
and
reliability
of
the
toxicity
data,
and
the
exposure
assessment
discussed
in
sections
B.
and
C.,
BASF
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
residues
of
dimethenamid
including
all
anticipated
dietary
exposure
and
all
other
non­
occupational
exposures.
2.
Infants
and
children.
BASF
cites
results
of
developmental
toxicity
studies
reported
in
section
B.
3.
including:
 
Observed
developmental
toxicity
effects
in
rats
are
not
indicative
of
teratogenic
effect.
 
The
results
of
developmental
study
in
rabbits
also
demonstrated
that
dimethenamid
is
not
a
teratogenic
compound
and
has
a
development
toxicity
NOAEL
of
75
mg/
kg/
day
and
a
maternal
toxicity
of
37.5
mg/
kg/
day.
BASF
believes
that
these
test
results
demonstrate
that
the
rat
and
rabbit
are
similarly
sensitive
to
dimethenamid.
Additionally,
the
NOAEL
of
5
mg/
kg/
day
from
the
chronic
rat
study
used
to
set
the
RfD
is
7.5X
and
5X
lower
than
the
maternal
NOAELs
established
in
the
rabbit
and
rat
teratology
studies,
respectively.
The
developmental
effects
observed
in
either
the
rat
or
rabbit
occurred
only
at
maternally
toxic
doses.
Therefore,
BASF
concludes
that
no
additional
safety
factor
is
needed
for
children.
F.
International
Tolerances
A
maximum
residue
level
has
not
been
established
under
Codex
Alimentarius
Commission
for
dimethenamid
for
any
of
the
proposed
uses.

[
FR
Doc.
03
 
5914
Filed
3
 
11
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0043;
FRL
 
7292
 
5]

Extension
of
an
Experimental
Use
Permit
AGENCY:
Environmental
Protection
Agency
(
EPA).
ACTION:
Notice.

SUMMARY:
EPA
has
granted
an
extension
of
an
experimental
use
permit
(
EUP)
to
the
following
pesticide
applicant.
An
EUP
permits
use
of
a
pesticide
for
experimental
or
research
purposes
only
in
accordance
with
the
limitations
in
the
permit.

FOR
FURTHER
INFORMATION
CONTACT:
Ann
Sibold,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001;
telephone
number:
(
703)
305
 
6502;
e­
mail
address:
sibold.
ann@
epa.
gov.

SUPPLEMENTARY
INFORMATION:

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

This
action
is
directed
to
the
public
in
general.
Although
this
action
may
be
of
particular
interest
to
those
persons
who
conduct
or
sponsor
research
on
pesticides,
the
Agency
has
not
attempted
to
describe
all
the
specific
entities
that
may
be
affected
by
this
action.
If
you
have
any
questions
regarding
the
information
in
this
action,
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
identification
(
ID)
number
OPP
 
2003
 
0043.
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
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