Document ID: EPA-HQ-OPP-2003-0027-0001
Agency: epa
Document Type: Notice
Title: Imidacloprid; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food
Posted Date: 2003-03-05T05:00Z

10464
Federal
Register
/
Vol.
68,
No.
43
/
Wednesday,
March
5,
2003
/
Notices
population
utilizing
0.1%
of
the
RfD.
A
Tier
3
chronic
analysis
was
done
using
the
DEEMTM
software,
Version
7.76
(
Novigen
Sciences,
Inc.).
The
1994
 
96,
1998
CSFII
consumption
data
from
USDA
were
used.
Average
anticipated
residue
values
were
calculated
from
the
appropriate
field
trial
studies
conducted
for
pyrimethanil.
The
average
residue
values
were
adjusted
by
the
projected
PCT
at
product
maturity.
Concentration
factors
derived
from
processing
studies
were
included
where
appropriate.
Secondary
residues
were
calculated
using
theoretical
dietary
burdens
derived
from
sensible
diets
for
beef
and
dairy
cattle
and
tissue
to
feed
ratios
from
the
ruminant
feeding
study.
ii.
Drinking
water.
U.
S.
EPA's
Standard
Operating
Procedure
(
SOP)
for
Drinking
Water
Exposure
and
Risk
Assessments
was
followed
to
perform
the
Tier
1
drinking
water
assessment.
This
SOP
uses
a
variety
of
tools
to
conduct
drinking
water
assessments,
including
water
models
such
as
Screening
Concentration
in
Ground
Water
(
SCI­
GROW),
FIRST,
Pesticide
Root
Zone
Model
(
PRZMS)/
EXAMS,
and
monitoring
data.
If
monitoring
data
are
not
available
then
the
models
are
used
to
predict
potential
residues
in
surface
and
ground
water
and
the
highest
levels
(
whether
ground
or
surface)
are
assumed
to
be
the
drinking
water
residue.
In
the
case
of
pyrimethanil,
monitoring
data
are
not
available.
SCI­
GROW
and
FIRST
were
used
to
estimate
a
drinking
water
residue.
Calculation
of
the
Drinking
Water
Estimate
Concentration
(
DWEC)
for
surface
water
for
the
worst
case
pyrimethanil
use
scenario
results
in
an
acute
DWEC
of
122
parts
per
billion
(
ppb)
and
a
chronic
DWEC
of
37
ppb.
DWLOCs
calculated
based
on
the
acute
and
chronic
risk
assessments
described
above
are
many
fold
higher
than
these
conservative
DWECs.
The
adult
acute
and
chronic
DWLOCs
are
10,146
ppb
and
5,944
ppb
respectively.
Children's
acute
and
chronic
DWLOCs
are
2,762
ppb
and
1,695
ppb
respectively.
2.
Non­
dietary
exposure.
Pyrimethanil
products
are
not
labeled
for
residential
uses
(
food
or
non­
food),
thereby
eliminating
the
potential
for
residential
exposure
or
non­
occupational
exposure.

D.
Cumulative
Effects
Section
408(
b)(
2)(
D)(
v)
requires
that,
when
considering
whether
to
establish,
modify,
or
revoke
a
tolerance,
the
Agency
consider
``
available
information''
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
``
other
substances
that
have
a
common
mechanism
of
toxicity.''
There
are
no
available
data
to
determine
whether
pyrimethanil
has
a
common
mechanism
of
toxicity
with
other
substances
or
how
to
include
this
pesticide
in
a
cumulative
risk
assessment.
Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
pyrimethanil
does
not
appear
to
form
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
the
tolerance
petition
and
this
reduced
risk
rationale,
therefore,
it
has
been
assumed
that
pyrimethanil
does
not
have
a
common
mechanism
of
toxicity
with
other
substances.

E.
Safety
Determination
1.
U.
S.
population.
Using
the
assumptions
and
data
described
above,
based
on
the
completeness
and
reliability
of
the
toxicity
data,
it
is
concluded
that
dietary
risk
from
the
proposed
uses
of
pyrimethanil
are
acceptable
for
all
populations
examined.
Chronic
exposure
for
the
U.
S.
population
utilizes
0.1%
(
0.00015
mg/
kg
bwt/
day)
of
the
cRfD.
Acute
exposure
for
the
U.
S.
population
utilizes
3.4%
(
0.01012
mg/
kg
bwt/
day)
of
the
aRfD.
The
most
highly
exposed
population
of
children
1
 
6
utilizes
only
0.3%
of
the
cRfD
and
7.9%
of
the
aRfD.
The
actual
exposures
are
likely
to
be
much
less
as
more
realistic
data
and
models
are
developed.
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD
(
acute
or
chronic),
because
the
RfD
represents
the
level
at
or
below
which
exposure
will
not
pose
appreciable
risk
to
human
health.
DWLOC
for
adults
both
acute
(
10,146
ppb)
and
chronic
(
5,944
ppb)
are
several
orders
of
magnitude
above
the
conservative
DWEC
for
acute
(
122
ppb)
and
chronic
(
37
ppb)
worst
case
scenarios.
Therefore,
there
is
a
reasonable
certainty
that
no
harm
will
occur
to
the
U.
S.
population
from
aggregate
exposure
(
food
and
drinking
water)
to
residues
of
pyrimethanil.
2.
Infants
and
children.
The
relevant
toxicity
studies
as
discussed
in
the
toxicology
section
above
show
no
extra
sensitivity
of
infants
and
children
to
pyrimethanil,
therefore,
the
FQPA
safety
factor
can
be
removed.
Using
the
assumptions
and
data
described
in
the
exposure
section
above,
it
is
concluded
that
dietary
risk
from
the
proposed
uses
of
pyrimethanil
are
acceptable
for
all
infant
and
children
sub­
populations
examined.
The
most
highly
exposed
sub­
population
was
children
1
 
6
for
both
the
chronic
and
acute
analyses.
The
sub­
population
children
1
 
6
utilizes
0.3%
(
0.00047
mg/
kg
bwt/
day)
of
the
cRfD
and
7.9%
(
0.02377
mg/
kg
bwt/
day)
of
the
aRfD.
All
other
infant
and
children
populations
have
less
exposure.
The
chronic
and
acute
drinking
water
levels
of
concern
for
children
(
1,695
ppb
and
2,762
ppb
respectively)
are
well
above
the
conservative
DWEC
for
chronic
and
acute
scenarios.
The
chronic
DWEC
is
37
ppb
and
the
acute
DWEC
is
122
ppb.
Therefore,
there
is
a
reasonable
certainty
that
no
harm
will
occur
to
infants
and
children
from
aggregate
exposure
to
residues
of
pyrimethanil.

F.
International
Tolerances
Maximum
residue
limits
for
pyrimethanil
have
not
been
established
by
the
Codex
Alimentarius
Commission.

[
FR
Doc.
03
 
5032
Filed
3
 
4
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0027;
FRL
 
7291
 
1]

Imidacloprid;
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
 
0027,
must
be
received
on
or
before
April
4,
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:
Dani
Daniel,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001;
telephone
number:
(
703)
305
 
5409;
e­
mail
address:
daniel.
dani@
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:

VerDate
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21:
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2003
Jkt
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10465
Federal
Register
/
Vol.
68,
No.
43
/
Wednesday,
March
5,
2003
/
Notices
 
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
identification
(
ID)
number
OPP
 
2003
 
0027.
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
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
 
0027
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
 
0027.
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
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/
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5,
2003
/
Notices
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
 
0027.
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
 
0027.
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.
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:
February
11,
2003.
Debra
Edwards,
Acting
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
the
petitioner
and
represents
the
views
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.

Bayer
CropScience
PP
0E6074
EPA
has
received
a
pesticide
petition
(
0E6074)
from
Bayer
CropScience,
2
T.
W.
Alexander
Drive,
PO
Box
12014,
Research
Triangle
Park,
NC
27709
proposing,
pursuant
to
section
408(
d)
of
the
FFDCA,
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
180.472,
by
establishing
an
import
tolerance
for
residues
of
imidacloprid,
[(
1­[
6­
chloro­
3­
pyridinyl)
methyl]­
N­
nitro­
2­
imidazolidinimine)
and
its
metabolites
containing
the
6­
chloropyridinyl
moiety,
all
expressed
as
1­[(
6­
chloro­
3­
pyridinyl)
methyl]­
Nnitro
2­
imidazolidinimine]
in
or
on
the
raw
agricultural
commodity
(
RAC):
Banana
at
0.01
parts
per
million
(
ppm).
EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408(
d)(
2)
of
the
FFDCA;
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
supports
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

A.
Residue
Chemistry
1.
Plant
metabolism.
The
nature
of
the
imidacloprid
residue
in
plants
and
livestock
is
adequately
understood.
The
residues
of
concern
are
combined
residues
of
imidacloprid
and
it
metabolites
containing
the
6­
chloropyridinyl
moiety,
all
calculated
as
imidacloprid.
2.
Analytical
method.
The
analytical
method
is
a
common
moiety
method
for
imidacloprid
and
its
metabolites
containing
the
6­
chloropyridinyl
moiety
using
a
permanganate
oxidation,
silyl
derivatization,
and
capillary
gas
chromatography
mass
spectrometry
(
GCMS
selective
ion
monitoring.
This
method
has
successfully
passed
a
petition
method
validation
in
EPA
labs.
There
is
a
confirmatory
method
specifically
for
imidacloprid
and
several
metabolites
utilizing
GC/
MS
and
high
performance
liquid
chromatography
ultraviolet
(
HPLC­
UV)
which
has
been
validated
by
EPA
as
well.
Imidacloprid
and
its
metabolites
are
stable
for
at
least
24
months
in
the
commodities
when
frozen.
3.
Magnitude
of
residues.
For
bananas,
Bayer
conducted
12
residue
crop
field
trials
to
evaluate
the
quantity
of
imidacloprid
expected
in
bananas
from
applications
of
Confidor
70
WG
and
Confidor
350
SC.
Trials
were
conducted
at
eight
sites
in
the
Caribbean
coastal
area
of
Central
America
and
4
sites
in
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2003
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Notices
the
Pacific
coastal
area
of
Ecuador.
Imidacloprid
residues
in
banana
whole
fruit
were
quantitated
by
GC
using
a
mass
selective
detector.
The
limit
of
quantitation
(
LOQ)
was
0.01
ppm.
The
highest
average
field
trial
(
HAFT)
was
0.01
ppm
in
bananas.

B.
Toxicological
Profile
1.
Acute
toxicity.
The
acute
oral
LD50
values
for
imidacloprid
technical
ranged
from
424
milligrams/
kilograms
(
mg/
kg)
in
the
male
rat
and
<
450
mg/
kg
in
the
female
rat.
The
acute
dermal
LD50
was
<
5,000
mg/
kg
in
the
rat.
The
4
 
hour
rat
inhalation
LC50
was
<
5.33
mg/
L.
Imidacloprid
was
not
irritating
to
rabbit
skin
or
eyes.
Imidacloprid
did
not
cause
skin
sensitization
in
guinea
pigs.
In
an
acute
neurotoxicity
study
the
lowest
observed
adverse
effect
level
(
LOAEL)
=
42
mg/
kg
body
weight
day
(
bwt/
day).
2.
Genotoxicty.
Mutagenicity
studies
have
demonstrated
that
imidacloprid
is
non­
mutagenic
both
in
vivo
and
in
vitro.
3.
Reproductive
and
developmental
toxicity.
In
a
developmental
toxicity
study
with
Sprague­
Dawley
rats,
groups
of
pregnant
animals
(
25/
group)
received
oral
administration
of
imidacloprid
(
94.2%)
at
0,
10,
30,
or
100
mg/
kg
bwt/
day
during
gestation
days
6
through
16.
Maternal
toxicity
was
manifested
as
decreased
body
weight
gain
at
all
dose
levels
and
reduced
food
consumption
at
100
milligrams/
kilograms
of
body
weight/
day
(
mg/
kg
bwt/
day.
No
treatment­
related
effects
were
seen
in
any
of
the
reproductive
parameters
(
i.
e.,
Cesarean
section
evaluation).
At
100
mg/
kg
bwt/
day,
developmental
toxicity
manifested
as
wavy
ribs
(
fetus
=
7/
149
in
treated
vs.
2/
158
in
controls
and
litters,
4/
25
vs.
1/
25).
For
maternal
toxicity,
the
LOAEL
was
10
mg/
kg
bwt/
day
lowest
dose
tested
(
LDT)
based
on
decreased
body
weight
gain;
a
NOAEL
was
not
established.
For
developmental
toxicity,
the
NOAEL
was
30
mg/
kg
bwt/
day
and
the
LOAEL
was
100
mg/
kg
bwt/
day
based
on
increased
wavy
ribs
master
record
identification
(
MRID
No.
42256338).
In
a
developmental
toxicity
study
with
Chinchilla
rabbits,
groups
of
16
pregnant
does
were
given
oral
doses
of
imidacloprid
(
94.2%)
at
0,
8,
24,
or
72
mg/
kg
bwt/
day
during
gestation
days
6
through
18.
For
maternal
toxicity,
the
NOAEL
was
24
mg/
kg
bwt/
day
and
the
LOAEL
was
72
mg/
kg
bwt/
day
based
on
mortality,
decreased
body
weight
gain,
increased
resorptions,
and
increased
abortions.
For
developmental
toxicity,
the
NOAEL
was
24
mg/
kg
bwt/
day
and
the
LOAEL
was
72
mg/
kg
bwt/
day
based
on
decreased
fetal
body
weight,
increased
resorptions,
and
increased
skeletal
abnormalities
(
MRID
No.
42256339).
In
a
2­
generation
reproductive
toxicity
study,
imidacloprid
(
95.3%)
was
administered
to
Wistar/
Han
rats
at
dietary
levels
of
0,
100,
250,
or
700
ppm
(
0,
7.3,
18.3,
or
52.0
mg/
kg
bwt/
day
for
males
and
0,
8.0,
20.5,
or
57.4
mg/
kg
bwt/
day
for
females)
(
MRID
No.
42256340,
Doc.
No.
010537).
For
parental/
systemic/
reproductive
toxicity,
the
NOAEL
was
250
ppm
(
18.3
mg/
kg
bwt/
day)
and
the
LOAEL
was
750
ppm
(
52
mg/
kg
bwt/
day),
based
on
decreases
in
body
weight
in
both
sexes
in
both
generations.
Based
on
these
factors,
EPA
recommended
that
the
Data
Evaluation
Record
should
be
revised
to
indicate
the
parental/
systemic/
reproductive
NOAEL
and
LOAEL
to
be
250
and
700
ppm,
respectively,
based
upon
the
body
weight
decrements
observed
in
both
sexes
in
both
generations.
4.
Subchronic
toxicity.
In
a
dermal
toxicity
study,
groups
of
five
male
and
five
female
New
Zealand
white
rabbits
received
repeated
dermal
applications
of
imidacloprid
(
95%)
at
1,000
mg/
kg
bwt/
day
(
LD),
6
hours/
day,
5
days/
week
for
3
weeks.
No
dermal
or
systemic
toxicity
was
seen.
For
systemic
and
dermal
toxicity,
the
NOAEL
was
<
1,000
mg/
kg
bwt/
day,
a
LOAEL
was
not
established
(
MRID
No.
42256329).
In
an
oral
toxicity
study,
groups
of
Fischer
344
rats
(
12/
sex/
dose)
were
fed
diets
containing
imidacloprid
(
98.8%)
at
0,
150,
1,000,
or
3,000
ppm
(
0,
9.3,
63.3,
or
196
mg/
kg
bwt/
day
in
males
and
0,
10.5,
69.3
or
213
mg/
kg
bwt/
day
in
females,
respectively)
for
90
days.
No
treatment­
related
effects
were
seen
at
150
ppm.
Treatment­
related
effects
included
decreases
in
body
weight
gain
during
the
first
4
weeks
of
the
study
at
1,000
ppm
(
22%
in
males
and
18%
in
females)
and
3,000
ppm
(
50%
in
males
and
25%
in
females)
with
an
associated
decrease
in
forelimb
grip
strength
especially
in
males.
The
NOAEL
was
150
ppm
(
9.3
and
10.5
mg/
kg
bwt/
day
in
males
and
females,
respectively)
and
the
LOAEL
was
1,000
ppm
(
63.3
and
69.3
mg/
kg
bwt/
day
in
males
and
females,
respectively)
(
MRID
No.
43286401).
In
a
rat
inhalation
study
(
28
 
day
study
in
which
rats
were
exposed
6
hours/
day,
5
days/
week
for
4
weeks),
the
NOAEL
for
imidacloprid
was
5.5
mg/
m3
(
MRID
No.
422730
 
01).
5.
Chronic
toxicity.
In
a
chronic
toxicity
study,
groups
of
beagle
dogs
(
4/
sex/
dose)
were
fed
diets
containing
imidacloprid
(
94.9%)
at
0,
200
or
1,250/
2,500
ppm
(
0,
6.1,
15
or
41/
72
mg/
kg
bwt/
day,
respectively)
for
52
weeks.
The
1,250
ppm
dose
was
increased
to
2,500
ppm
from
week
17
onwards.
The
threshold
NOAEL
was
1,250
ppm
(
41
mg/
kg
bwt/
day).
The
LOAEL
was
2,500
ppm
(
72
mg/
kg
bwt/
day)
based
on
increased
cytochrome­
P­
450
levels
in
both
sexes
and
was
considered
to
be
a
threshold
dose.
Due
to
the
lack
of
toxicity
at
1,250
ppm,
a
LOAEL
was
not
established
in
this
study
following
the
dose
increase
to
the
2,500
ppm
level,
toxicity
was
observed,
thus
making
1,250
ppm
the
threshold
NOAEL
and
2,500
ppm
the
threshold
LOAEL
(
MRID
No.
42273002).
6.
Animal
metabolism.
The
metabolism
imidacloprid
in
rats
was
reported
in
seven
studies.
These
data
show
that
imidacloprid
was
rapidly
absorbed
and
eliminated
in
the
excreta
(
90%
of
the
dose
within
24
hours),
demonstrating
no
biologically
significant
differences
between
sexes,
dose
levels,
or
route
of
administration.
Elimination
was
mainly
renal
(
70
 
80%
of
the
dose)
and
fecal
(
17
 
25%).
The
major
part
of
the
fecal
activity
originated
in
the
bile.
Total
body
accumulation
after
48
hours
consisted
of
0.5%
of
the
radioactivity
with
the
liver,
kidney,
lung,
skin
and
plasma
being
the
major
sites
of
accumulation.
Therefore,
bioaccumulation
of
imidacloprid
is
low
in
rats.
Maximum
plasma
concentration
was
reached
between
1.1
and
2.5
hours.
Two
major
routes
of
biotransformation
were
proposed
for
imidacloprid.
The
first
route
included
an
oxidative
cleavage
of
the
parent
compound
rendering
6­
chloronicotinic
acid
and
its
glycine
conjugate.
Dechlorination
of
this
metabolite
formed
the
6­
hydroxynicotinic
acid
and
its
mercapturic
acid
derivative.
The
second
route
included
the
hydroxylation
followed
by
elimination
of
water
of
the
parent
compound
rendering
imidacloprid.
A
comparison
between
[
methylene­
14C]­
imidacloprid
and
[
imidazolidine­
4,5­
14C]­
imidacloprid
showed
that
while
the
rate
of
excretion
was
similar,
the
renal
portion
was
higher
with
the
imidazolidine­
labeled
compound.
In
addition,
accumulation
in
tissues
was
generally
higher
with
the
imidazolidine­
labeled
compound.
A
comparison
between
imidacloprid
and
one
of
its
metabolites,
WAK
3839,
showed
that
the
total
elimination
was
the
same
for
both
compounds.
The
proposed
metabolic
pathways
for
these
two
compounds
were
different.
WAK
3839
was
formed
following
pretreatment
(
repeated
dosing)
of
imidacloprid.
7.
Endocrine
disruption.
The
toxicology
data
base
for
imidacloprid
is
current
and
complete.
Studies
in
this
data
base
include
evaluation
of
the
potential
effects
on
reproduction
and
development,
and
an
evaluation
of
the
pathology
of
the
endocrine
organs
following
short­
term
or
long­
term
exposure.
These
studies
revealed
no
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Notices
primary
endocrine
effects
due
to
imidacloprid.

C.
Aggregate
Exposure
1.
Dietary
exposure.
Assessments
were
conducted
to
evaluate
potential
risks
due
to
chronic
and
acute
dietary
exposure
of
the
U.
S.
population
and
selected
population
subgroups
to
residues
of
imidacloprid.
These
analyses
cover
all
registered
crops
including
rotational
crops;
uses
pending
with
EPA
in
the
2003
work
plan
including
dry
beans,
peas,
bushberries,
lingonberry,
juneberries,
salal,
carrots,
turnips,
okra,
cranberries,
artichoke
(
globe),
watercress,
beet
roots,
leaves
of
root
and
tuber
vegetables,
stone
fruit,
mamey
sapote,
guava,
feijoa,
jaboticaba,
wax
jambu,
starfruit,
passion
fruit,
acerola,
strawberry,
cucumber
(
greenhouse),
and
tomato
(
greenhouse),
this
import
tolerance
petition
on
bananas;
and
active
and
proposed
section
18
uses
on
blueberries,
cranberries,
table
beets,
strawberries,
turnips.
Novigen
Sciences,
Inc.'
s
Dietary
Exposure
Evaluation
Model
(
DEEMTM),
which
is
licensed
to
Bayer,
was
used
to
estimate
the
chronic
and
acute
dietary
exposure.
This
software
uses
the
food
consumption
data
from
the
1994
 
1998
Department
of
Agriculture
(
USDA)
continuing
surveys
of
food
intake
by
individuals
(
CSFII)
1994
 
1998.
The
endpoint
for
acute
dietary
risk
assessments
is
based
on
neurotoxicity
characterized
by
decreases
in
motor
or
locomotor
activity
in
female
rats
at
42
mg/
kg
bwt/
day,
the
LOAEL
from
an
acute
neurotoxicity
study.
Based
on
an
uncertainty
factor
(
UF)
of
10x
for
interspecies
and
10x
for
intra­
species
the
acute
reference
dose
(
aRfD)
=
0.42
mg/
kg
bwt/
day.
EPA
has
determined
that
an
additional
UF
for
FQPA
(
reduced
to
3x)
applies
to
all
population
subgroups
for
acute
risk.
Application
of
the
additional
3x
safety
factor
results
in
an
acute
population
adjusted
dose
(
aPAD)
0.14
mg/
kg
bwt/
day
or
a
margin
of
exposure
(
MOE)
of
300.
For
chronic
dietary
analyses,
EPA
has
established
the
reference
dose
(
RfD)
for
imidacloprid
at
0.057
mg/
kg/
day
based
on
a
NOAEL
of
5.7
mg/
kg
bwt/
day
from
a
rat
chronic
toxicity
carcinogenicity
study
and
uncertainty
factors
of
10x
for
interspecies
and
10x
for
intra­
species.
EPA
has
determined
that
an
additional
UF
for
FQPA
(
reduced
to
3x)
applies
to
all
population
subgroups
for
chronic
risk.
Application
of
the
additional
3x
safety
factor
results
in
a
chronic
population
adjusted
dose
(
cPAD)
of
0.019
mg/
kg
bwt/
day.
Results
from
the
acute
and
chronic
dietary
exposure
analyses
described
below
demonstrate
a
reasonable
certainty
that
no
harm
to
the
overall
U.
S.
population
or
any
population
subgroup
will
result
from
the
use
of
imidacloprid
on
currently
registered
and
pending
uses.
i.
Food.
Acute
and
chronic
(
tier
3)
risk
assessments
were
made
using
the
results
of
field
trials
conducted
at
maximum
label
application
rates
and
the
shortest
pre­
harvest
intervals.
For
some
of
the
vegetable
crops,
these
residue
data
were
collected
at
1.5x
or
greater
than
the
maximum
label
rate
of
0.5
lb
active
ingredient/
acre
per
season.
In
addition,
no
adjustments
were
made
to
account
for
dissipation
of
residues
during
storage,
transportation
from
the
field
to
the
consumer,
washing
or
peeling.
Therefore,
the
actual
dietary
exposure
will
be
less
than
that
presented
here.
For
the
chronic
analysis,
mean
field
trial
residues
were
calculated.
For
the
acute
Monte
Carlo
analysis,
the
entire
distribution
of
residue
field
trial
data
was
used
for
the
``
non­
blended''
and
``
partially
blended''
foods
as
determined
by
EPA's
HED
SOP
99.6.
For
the
foods
considered
as
``
blended''
by
EPA'S
HED
SOP
99.6,
mean
field
trial
residue
data
were
used.
As
allowed
in
EPA's
draft
guidance
for
submission
of
probabilistic
human
health
exposure
assessments
one
half
limit
of
detection
(
LOD)/
LOQ
values
were
used
for
all
non­
detected
values
(
values
below
the
sensitivity
of
the
method).
Bayer's
acute
Monte
Carlo
dietary
exposure
assessment
estimated
percent
of
the
aPAD
and
corresponding
MOE
for
the
overall
U.
S.
population,
(
all
seasons),
and
various
subpopulations.
In
this
analysis,
the
exposure
for
the
total
U.
S.
population
was
equal
to
7.73%
of
the
aPAD
at
the
99.9th
percentile.
The
most
highly
exposed
population
subgroup,
children
(
1
 
6
years),
had
an
exposure
equal
to
16.42%
of
the
aPAD
at
the
99.9th
percentile.
Therefore,
the
acute
dietary
exposure
estimates
are
below
EPA's
level
of
concern
for
the
overall
U.
S.
population
as
well
as
the
various
subpopulations.
Bayer's
chronic
dietary
exposure
estimated
the
percent
of
the
cPAD
for
the
overall
U.
S.
population
(
all
seasons)
and
various
subpopulations.
In
this
analysis,
the
exposure
for
the
total
U.
S.
population
was
equal
to
1.4%
of
the
cPAD.
The
most
highly
exposed
population
subgroup,
children
(
1­
6
years),
had
an
exposure
equal
to
3.0%
of
the
cPAD.
Therefore,
the
chronic
exposure
estimates
are
below
EPA's
level
of
concern
for
the
overall
U.
S.
population
as
well
as
the
various
subpopulations.
ii.
Drinking
water.
EPA,
as
published
in
the
Federal
Register
of
April
10,
2001
(
66
FR
18554)
(
FRL
 
6777
 
6),
calculated
acute
and
chronic
DWLOCs
and
compared
them
with
the
EECs
for
surface
and
ground
water.
Based
on
this
comparison,
they
determined
that
acute
exposure
and
chronic
exposure
would
not
be
expected
to
exceed
the
aPAD
and
cPAD,
respectively.
It
is
not
expected
that
the
additional
exposure
from
the
minor
crops
pending
in
EPA's
2003
work
plan
would
significantly
change
EPA's
water
assessment.
2.
Non­
dietary
exposure
 
i.
Residential
turf.
Bayer
has
conducted
an
exposure
study
to
address
the
potential
exposures
of
adults
and
children
from
contact
with
imidacloprid
treated
turf.
The
population
considered
to
have
the
greatest
potential
exposure
from
contact
with
pesticide
treated
turf
soon
after
pesticides
are
applied
are
young
children.
Margins
of
safety
(
MOS)
of
7,587
­
41,546
for
10
 
year
old
children
and
6,859
­
45,249
for
5
 
year
old
children
were
estimated
by
comparing
dermal
exposure
doses
to
the
imidacloprid
NOAEL
of
1,000
mg/
kg/
day
established
in
a
15
 
day
dermal
toxicity
study
in
rabbits.
The
estimated
safe
residue
levels
of
imidacloprid
on
treated
turf
for
10
 
year
old
children
ranged
from
5.6
­
38.2
µ
g/
cm2
and
for
5
 
year
old
children
from
5.1
­
33.5
µ
g/
cm2.
This
compares
with
the
average
imidacloprid
transferable
residue
level
of
0.080
µ
g/
cm2
present
immediately
after
the
sprays
have
dried.
These
data
indicate
that
children
can
safely
contact
imidacloprid­
treated
turf
as
soon
after
application
as
the
spray
has
dried.
ii.
Termiticide.
Imidacloprid
is
registered
as
a
termiticide.
Due
to
the
nature
of
the
treatment
for
termites,
exposure
would
be
limited
to
that
from
inhalation
and
was
evaluated
by
EPA
and
Bayer.
Data
indicate
that
the
MOS
for
the
worst
case
exposures
for
adults
and
infants
occupying
a
treated
building
who
are
exposed
continuously
(
24
hours/
day)
are
8.0
x
10­
7
and
2.4
x
10­
8,
respectively
­
and
exposure
can
thus
be
considered
negligible.
iii.
Tobacco.
Smoke
Studies
have
been
conducted
to
determine
residues
in
tobacco
and
the
resulting
smoke
following
treatment.
Residues
of
imidacloprid
in
cured
tobacco
following
treatment
were
a
maximum
of
31
ppm
(
7
ppm
in
fresh
leaves).
When
this
tobacco
was
burned
in
a
pyrolysis
study
only
2%
of
the
initial
residue
was
recovered
in
the
resulting
smoke
(
main
stream
plus
side
stream).
This
would
result
in
an
inhalation
exposure
to
imidacloprid
from
smoking
of
approximately
0.0005
mg
per
cigarette.
Using
the
measured
subacute
rat
inhalation
NOAEL
of
5.5
mg/
m3,
it
is
apparent
that
exposure
to
imidacloprid
from
smoking
(
direct
and/
or
indirect
exposure)
would
not
be
significant.

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Notices
iv.
Pet
treatment.
Human
exposure
from
the
use
of
imidacloprid
to
treat
dogs
and
cats
for
fleas
has
been
addressed
by
EPA
with
the
conclusion
that
due
to
the
fact
that
imidacloprid
is
not
an
inhalation
or
dermal
toxicant
and
that
while
dermal
absorption
data
are
not
available,
imidacloprid
is
not
considered
to
present
a
hazard
via
the
dermal
route.

D.
Cumulative
Effects
Imidacloprid
is
a
chloronicotinyl
insecticide.
At
this
time,
EPA
has
not
made
a
determination
that
imidacloprid
and
other
substances
that
may
have
a
common
mechanism
of
toxicity
would
have
cumulative
effects.
Therefore,
for
these
tolerance
petitions,
it
is
assumed
that
imidacloprid
does
not
have
a
common
mechanism
of
toxicity
with
other
substances
and
only
the
potential
risks
of
imidacloprid
in
its
aggregate
exposure
are
considered.

E.
Safety
Determination
1.
U.
S.
population.
EPA
has
considered
data
from
developmental
toxicity
studies
in
the
rat
and
rabbit
and
a
2­
generation
reproduction
study
in
the
rat.
These
studies
are
discussed
under
section
A
(
Toxicology
Profile)
above.
The
developmental
toxicity
data
demonstrated
no
increased
sensitivity
of
rats
or
rabbits
to
in
utero
exposure
to
imidacloprid.
In
addition,
the
multigeneration
reproductive
toxicity
study
did
not
identify
any
increased
sensitivity
of
rats
to
in
utero
or
postnatal
exposure.
Parental
NOAELs
were
lower
or
equivalent
to
developmental
or
offspring
NOAELs.
The
developmental
toxicity
studies
are
designed
to
evaluate
adverse
effects
on
the
developing
organism
resulting
from
maternal
pesticide
exposure
during
gestation.
Reproduction
studies
provide
information
relating
to
effects
from
exposure
to
the
pesticide
on
the
reproductive
capability
of
mating
animals
and
data
on
systemic
toxicity.
FFDCA
section
408
provides
that
EPA
shall
apply
an
additional
tenfold
margin
of
safety
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
prenatal
and
postnatal
toxicity
and
the
completeness
of
the
data
base
unless
EPA
determines
that
a
different
MOS
will
be
safe
for
infants
and
children.
MOS
are
incorporated
into
EPA
risk
assessments
either
directly
through
use
of
a
MOE
analysis
or
through
using
uncertainty
(
safety)
factors
(
UF)
in
calculating
a
dose
level
that
poses
no
appreciable
risk
to
humans.
EPA
believes
that
reliable
data
support
using
the
standard
UF
(
usually
100
for
combined
inter­
species
and
intraspecies
variability)
and
not
the
additional
tenfold
MOE/
UF
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/
UF.
Although
developmental
toxicity
studies
showed
no
increased
sensitivity
in
fetuses
as
compared
to
maternal
animals
following
in
utero
exposures
in
rats
and
rabbits,
no
increased
sensitivity
in
pups
as
compared
to
adults
was
seen
in
the
2­
generation
reproduction
toxicity
study
in
rats,
and
the
toxicology
data
base
is
complete
as
to
core
requirements,
EPA
has
determined
that
the
additional
safety
factor
for
the
protection
of
infants
and
children
will
be
retained
but
reduced
to
3x
based
on
the
following
weight­
of­
the­
evidence
considerations
relating
to
potential
sensitivity
and
completeness
of
the
data:
i.
There
is
concern
for
structure
activity
relationship.
Imidacloprid,
a
chloronicotinyl
compound,
is
an
analog
to
nicotine
and
studies
in
the
published
literature
suggests
that
nicotine,
when
administered
causes
developmental
toxicity,
including
functional
deficits,
in
animals
and/
or
humans
that
are
exposed
in
utero.
ii.
There
is
evidence
that
imidacloprid
administration
causes
neurotoxicity
following
a
single
oral
dose
in
the
acute
study
and
alterations
in
brain
weight
in
rats
in
the
2
 
year
carcinogenicity
study.
iii.
The
concern
for
structure
activity
relationship
along
with
the
evidence
of
neurotoxicity
dictates
the
need
of
a
developmental
neurotoxicity
study
for
assessment
of
potential
alterations
on
functional
development.
Because
a
developmental
neurotoxicity
study
potentially
relates
to
both
acute
and
chronic
effects
in
both
the
mother
and
the
fetus,
EPA
has
applied
the
additional
UF
for
FQPA
for
all
population
subgroups,
and
in
both
acute
and
chronic
risk
assessments.
Based
on
the
exposure
assessments
described
above
and
on
the
completeness
and
reliability
of
the
toxicity
data,
it
can
be
concluded
that
the
dietary
exposure
estimates
from
all
label
and
pending
uses
of
imidacloprid
are
7.73%
of
the
aPAD
at
the
99.9th
percentile
and
1.4%
of
the
cPAD
for
the
U.
S.
population.
Thus,
it
can
be
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
imidacloprid
residues.
2.
Infants
and
children.
Based
on
the
exposure
assessments
described
above
for
the
safety
determination
of
the
U.
S.
population
and
on
the
completeness
and
reliability
of
the
toxicity
data,
it
can
be
concluded
that
the
dietary
exposure
estimates
from
all
label
and
pending
uses
of
imidacloprid
are
16.42%
of
the
aPAD
at
the
99.9th
percentile
and
3.0%
of
the
cPAD
for
the
most
sensitive
population
subgroup,
children
1
 
6
years.
Thus,
it
can
be
concluded
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
imidacloprid
residues.

F.
International
Tolerances
No
CODEX
Maximum
Residue
Levels
have
been
established
for
residues
of
imidacloprid
on
any
crops
pending
in
EPA's
2003
work
plan.
[
FR
Doc.
03
 
5034
Filed
3
 
4
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0047;
FRL
 
7294
 
5]

Trifloxystrobin;
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
 
0047,
must
be
received
on
or
before
April
4,
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:

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21:
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