Document ID: EPA-HQ-OPP-2003-0057-0001
Agency: epa
Document Type: Notice
Title: Trifloxysulfuron-sodium; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food
Posted Date: 2003-03-21T05:00Z

13924
Federal
Register
/
Vol.
68,
No.
55
/
Friday,
March
21,
2003
/
Notices
exposures
are
expected
for
the
general
population.

D.
Cumulative
Effects
EPA
does
not
have,
at
this
time,
available
data
to
determine
whether
tralkoxydim
has
a
common
mechanism
of
toxicity
with
other
substances
or
how
to
include
this
pesticide
in
a
cumulative
risk
assessment.
Tralkoxydim
is
structurally
a
cyclohexanedione.
Unlike
other
pesticides
for
which
EPA
has
followed
a
cumulative
risk
approach
based
on
a
common
mechanism
of
toxicity,
tralkoxydim
does
not
appear
to
produce
a
toxic
metabolite
produced
by
other
substances.
For
the
purposes
of
these
tolerances
action,
therefore,
EPA
has
not
assumed
that
tralkoxydim
has
a
common
mechanism
of
toxicity
with
other
substances.

E.
Safety
Determination
1.
U.
S.
population
 
i.
Acute
risk.
The
acute
dietary
analysis
based
on
the
NOAEL
of
30
mg/
kg/
day
from
the
rat
developmental
study
using
the
DEEM
computer
program
estimates
that
the
distribution
of
single­
day
exposures
utilizes
0.02%
of
acute
RfD.
The
drinking
water
level
of
comparisons
(
DWLOCs)
for
acute
exposure
to
tralkoxydim
in
drinking
water
calculated
for
females
13
+
years
old
was
9,000
ppb.
The
estimated
average
concentration
in
surface
water
for
tralkoxydim
is
9
ppb.
EPA's
acute
DWLOC
is
well
above
the
estimated
exposures
for
tralkoxydim
in
water
for
the
subgroup
of
concern.
For
ground
water,
the
estimated
environmental
concentrations
(
EEC's)
using
the
SCIGROW
model
were
all
less
than
1
ppb.
ii.
Chronic
risk.
A
DEEM
chronic
exposure
analysis
showed
that
exposure
from
tolerance
level
residues
in
or
on
wheat,
and
barley
for
children
1
to
6
years
old
(
the
subgroup
with
the
highest
exposure)
would
be
1.4%
of
the
RfD.
The
exposure
for
the
general
U.
S.
population
would
be
less
than
1%
of
the
RfD.
The
DWLOCs
for
chronic
exposure
to
tralkoxydim
in
drinking
water
calculated
for
U.
S.
population
was
150
ppb
and
for
children
(
1
to
6
years
old)
the
DWLOC
was
50
ppb.
The
estimated
average
concentration
in
surface
water
for
tralkoxydim
is
9
ppb.
EPA's
chronic
DWLOC
is
above
the
estimated
exposures
for
tralkoxydim
in
water
for
the
U.
S.
population
and
the
subgroup
of
concern.
Conservative
model
estimates
SCI­
GROW
of
the
concentrations
of
tralkoxydim
in
ground
water
indicate
that
exposure
will
be
minimal.
iii.
Cancer
risk.
A
DWLOC
for
cancer
was
calculated
as
1
ppb.
The
estimated
concentration
in
surface
water
and
ground
water
for
tralkoxydim
for
chronic
exposure
are
0.9
ppb,
2.8
ppb,
(
the
56
 
day
concentration)/
3,
and
0.1
ppb,
respectively.
The
model
exposure
estimates
are
less
than
the
cancer
DWLOC.
EPA
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
tralkoxydim
residues.
2.
Infants
and
children.
The
Agency
concluded
that
an
extra
safety
factor
to
protect
infants
and
children
is
not
needed
based
on
the
following
considerations:
The
toxicology
data
base
is
complete
for
the
assessment
of
special
sensitivity
of
infants
and
children.
The
developmental
and
reproductive
toxicity
data
do
not
indicate
increased
susceptibility
of
rats
or
rabbits
to
in
utero
and/
or
postnatal
exposure.
The
NOAEL
used
in
deriving
the
RfD
is
based
on
changes
in
liver
function
and
morphology
in
male
adult
dogs
(
not
developmental
or
neurotoxic
effects)
after
chronic
exposure
and
thus
are
not
relevant
for
enhanced
sensitivity
to
infants
and
children.
Unrefined
dietary
exposure
estimates
(
assuming
all
commodities
contain
tolerance
level
residues)
overestimate
dietary
exposure.
Model
data
used
for
ground
water
and
surface
water
source
drinking
water
exposure
assessments
result
in
estimates
considered
to
be
upper­
bound
concentrations.
There
are
no
registered
uses
for
tralkoxydim
that
could
result
in
residential
exposures.
EPA
concludes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
to
children
from
aggregate
exposure
to
tralkoxydim
residues.

F.
International
Tolerances
There
are
no
codex
Alimentarius
Commission
(
Codex)
or
Mexican
maximum
residue
levels
for
tralkoxydim
at
this
time.
[
FR
Doc.
03
 
6823
Filed
3
 
20
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0057;
FRL
 
7296
 
6]

Trifloxysulfuron­
sodium;
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
 
0057,
must
be
received
on
or
before
April
21,
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:
James
A.
Tompkins,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001;
telephone
number:
(
703)
305
 
5697;
e­
mail
address:
tompkins.
jim@
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
 
0057.
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
VerDate
Jan<
31>
2003
18:
05
Mar
20,
2003
Jkt
200001
PO
00000
Frm
00033
Fmt
4703
Sfmt
4703
E:\
FR\
FM\
21MRN1.
SGM
21MRN1
13925
Federal
Register
/
Vol.
68,
No.
55
/
Friday,
March
21,
2003
/
Notices
#
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
 
0057.
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
 
0057.
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
 
0057.
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
 
0057.
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
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/
Vol.
68,
No.
55
/
Friday,
March
21,
2003
/
Notices
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.

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
10,
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
Syngenta
Crop
Protection,
Inc,
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.

Syngenta
Crop
Protection,
Inc.

PP
1F6280
EPA
has
received
a
pesticide
petition
(
1F6280)
from
Syngenta
Crop
Protection,
Inc.,
Greensboro,
NC
27419
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
trifloxysulfuron­
sodium
in
or
on
the
raw
agricultural
commodities
sugarcane
at
0.01
parts
per
million
(
ppm),
cottonseed
at
0.05
ppm,
cotton
by­
products
at
1.0
ppm,
citrus
at
0.01,
almond
hulls
at
0.01
ppm,
almond
nut
meat
at
0.01
ppm,
and
tomatoes
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
support
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

A.
Residue
Chemistry
1.
Plant
metabolism.
The
primary
metabolic
pathways
of
trifloxysulfuronsodium
in
plants
(
cotton,
sugarcane
and
citrus)
were
similar
to
those
described
for
animals,
with
certain
extensions
of
the
pathway
in
plants.
The
metabolism
of
trifloxysulfuron­
sodium
is
well
characterized
in
plants
and
animals
and
the
data
is
adequate
for
tolerance
setting
purposes.
The
metabolism
profile
in
plants
and
animals
supports
the
use
of
an
analytical
enforcement
method
that
accounts
for
parent
trifloxysulfuronsodium
The
multiple
other
metabolites
formed
in
plants
and
animals
are
considered
of
equal
or
lesser
toxicity
than
parent
compound.
2.
Analytical
method.
Syngenta
Crop
Protection,
Inc.
has
submitted
practical
analytical
methodology
for
detecting
and
measuring
levels
of
trifloxysulfuron­
sodium
in
or
on
raw
agricultural
commodities.
This
method
is
based
on
crop
specific
cleanup
procedures
and
determination
by
liquid
chromatography
with
a
ultraviolet
(
UV/
Vis)
detector.
The
limit
of
detection
(
LOD)
for
each
analyte
of
this
method
is
2
nanograms
of
trifloxysulfuron­
sodium.
The
limit
of
quantitation
(
LOQ),
as
demonstrated
by
acceptable
recoveries
from
fortified
control
samples,
is
0.01
ppm
for
each
substrate.
3.
Magnitude
of
residues.
A
residue
program
was
performed
with
trifloxysulfuron­
sodium
on
a
full
geography
to
support
use
on
cotton,
sugarcane,
citrus,
and
almonds.
Adequate
residue
trials
were
performed
to
support
the
proposed
use
on
tomatoes.

B.
Toxicological
Profile
1.
Acute
toxicity.
Trifloxysulfuronsodium
has
low
acute
toxicity.
The
oral
LD50
in
rats
is
>
5,000
millgrams/
kilogram
(
mg/
kg)
for
males
and
females
combined.
The
rat
dermal
LD50
is
>
2,000
mg/
kg
and
the
rat
inhalation
LC50
is
>
5.03
milligrams/
liter
(
mg/
L)
air.
Trifloxysulfuron­
sodium
is
not
a
skin
sensitizer
in
guinea
pigs
and
is
considered
to
have
slight
dermal
or
eye
irritation
in
rabbits.
End­
use
formulations
of
Trifloxysulfuronsodium
have
similar
low
acute
toxicity
profiles.
2.
Genotoxicity.
Trifloxysulfuronsodium
has
been
tested
for
its
potential
to
induce
gene
mutation
and
chromosomal
changes
in
five
different
test
systems.
Trifloxysulfuron­
sodium
technical
did
not
induce
point
mutations
in
bacteria
(
Ames
assay
in
Salmonella
typhimurium
or
Escherichia
coli)
or
in
cultured
mammalian
cells
(
Chinese
hamster
V79)
and
was
not
genotoxic
in
an
in­
vitro
unscheduled
DNA
synthesis
assay
in
rat
hepatocytes.
Chromosome
aberrations
were
not
observed
in
an
in­
vitro
test
using
Chinese
hamster
ovary
cells
and
there
were
no
clastogenic
or
aneugenic
effects
on
mouse
bone
marrow
cell
in­
vivo
in
a
mouse
micronucleus
test.
These
studies
show
that
trifloxysulfuronsodium
is
not
genotoxic.

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Vol.
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No.
55
/
Friday,
March
21,
2003
/
Notices
3.
Reproductive
and
developmental
toxicity.
Data
from
developmental
toxicity
studies
in
the
rat
and
rabbit
and
a
two­
generation
reproduction
study
in
the
rat
have
been
considered.
In
rabbit
(
0,
50,
100,
250,
500
mg/
kg/
day)
and
rat
(
0,
30,
300,
1,000
mg/
kg/
day)
teratology
studies
there
was
no
evidence
of
teratogenicity.
Maternal
toxicity
was
seen
at
500
mg/
kg/
day
and
250
mg/
kg/
day
as
evidenced
by
deaths
and
premature
sacrifices.
For
the
control
(
50,
100,
and
250
mg/
kg)
groups,
preimplantation
losses,
number
of
implantation
sites,
and
postimplantation
losses
were
not
affected
by
treatment.
The
findings
after
fetal
post
mortem
examination
and
fetal
visceral
examination
revealed
no
treatment
related
effects.
Similarly,
there
were
no
skeletal
malformations
in
this
study
and
the
incidence
of
anomalies
and
variations
were
not
affected
by
treatment.
In
conclusion,
the
no
observed
adverse
effect
levels
(
NOAEL)
for
maternal
toxicity
was
100
mg/
kg/
day
and
the
NOAEL
for
fetal
toxicity
was
250
mg/
kg/
day.
There
was
no
indication
of
embryotoxic,
fetotoxic
or
teratogenic
potential
for
trifloxysulfuron­
sodium
in
rabbits.
In
the
rat
teratology
study,
300
and
1,000
mg/
kg/
day
caused
maternal
toxicity
consisting
of
reduced
body
weight
and
food
consumption.
Developmental
toxicity
was
secondary
to
maternal
toxicity
and
consisted
of
slightly
reduced
fetal
body
weights
and
an
increase
in
minor
skeletal
anomalies
and
variations.
The
NOAELs
for
maternal
and
developmental
toxicity
were
both
30
mg/
kg/
day.
Trifloxysulfuron­
sodium
was
not
embryotoxic,
fetotoxic
or
teratogenic
in
rats
when
tested
under
the
conditions
of
this
study.
In
a
rat
multigeneration
study,
trifloxysulfuron­
sodium
technical
was
administered
in
feed
at
concentrations
of
0,
500,
1,000,
8,000
or
12,000
ppm.
The
dose
in
mg/
kg/
day
spans
a
wide
range
over
the
duration
of
the
study
as
animals
gain
weight
and
go
through
gestation
and
lactation.
The
ranges
are
24
 
70,
48
 
137,
400
 
1,133,
608
 
1,755
for
males
and
32
 
100,
60
 
199,
500
 
1,557,
792
 
2,374
for
females
at
the
500,
1,000,
8,000,
and
12,000
ppm
dietary
level,
respectively.
Trifloxysulfuron­
sodium
had
no
effect
on
reproductive
parameters.
Parental
body
weight
gain
and
food
consumption
were
reduced
at
12,000
ppm
in
both
sexes
and
at
8,000
ppm
in
males
only.
In
addition,
there
was
an
increased
relative
liver
weight
and
an
increased
incidence
of
hepatocellular
hypertrophy
at
12,000
ppm
in
both
sexes
of
adults
and
at
8,000
ppm
in
adult
males
only.
Offspring
body
weights
were
reduced
in
males
and
females
greater
than
or
equal
to
8,000
ppm.
In
conclusion,
the
NOAEL
for
systemic
toxicity
in
both
sexes
and
both
generations
was
1,000
ppm.
The
mean
dose
in
mg/
kg/
day
for
all
weekly
means
for
both
sexes,
both
generations,
all
time
points
at
this
dietary
level
was
83.4
mg/
kg/
day.
There
were
no
effects
on
the
reproductive
parameters
and
the
NOAEL
for
reproductive
toxicity
was
>
12,000
ppm.
Offspring
effects
were
observed
only
at
dose
levels
that
produced
parental
toxicity.
Thus,
there
is
no
evidence
that
developing
offspring
are
more
sensitive
than
adults
to
the
effects
of
trifloxysulfuron­
sodium,
and
it
is
concluded,
that
trifloxysulfuronsodium
does
not
cause
developmental
or
reproductive
toxicity.
4.
Subchronic
toxicity.
Trifloxysulfuron­
sodium
technical
was
evaluated
in
a
number
of
subchronic
studies.
In
a
3
 
month
rat
feeding
study
the
NOAEL
was
65.7
mg/
kg
with
hematologic
and
liver
effects
noted.
In
a
3
 
month
mouse
feeding
study,
the
NOAEL
was
67.9
mg/
kg.
Effects
seen
were
adaptive
liver
effects.
In
a
3
 
month
feeding
study
in
dogs
the
NOAEL
was
19.6
mg/
kg
and
hematopoietic
and
liver
effects
were
seen.
In
a
28
 
day
dermal
(
rat)
study,
the
NOAEL
was
100
mg/
kg.
In
this
study
only
body
weight
effects
were
noted,
and
only
occurred
at
1,000
mg/
kg.
5.
Chronic
toxicity.
Trifloxysulfuronsodium
technical
was
not
oncogenic
in
rats
or
mice.
In
a
12
 
month
feeding
study
in
dogs
fed
diets
containing
trifloxysulfuron­
sodium
that
resulted
in
average
(
sexes
combined)
daily
test
substance
intakes
of
0,
1.67,
6.71,
15.0,
48.2
or
122
mg/
kg/
day,
all
animals
survived.
In
life
observations,
food
consumption,
eye
and
neurological
examinations,
and
urine
profiles
were
not
affected
by
treatment.
Macroscopic
and
microscopic
examinations
revealed
no
findings
that
were
considered
to
be
treatment
related
and
indicative
of
systemic
toxicity.
The
body
weight
gain
was
decreased
by
16%
in
males
at
122
mg/
kg/
day.
The
33%
decrease
at
48.2
mg/
kg/
day
was
mainly
due
to
one
male
that
gained
significantly
less
weight
than
the
other
animals
of
this
group.
There
was
a
tendency
for
a
decrease
in
the
erythrocyte
count,
hemoglobin
concentration
and
hematocrit
for
both
sexes
at
122
mg/
kg/
day
at
the
end
of
treatment,
and
for
males
throughout
the
treatment
period.
In
female
dogs
treated
with
48.2
and
122
mg/
kg/
day,
the
mean
absolute
and
relative
liver
weights
were
increased,
and
a
tendency
for
an
increase
in
relative
liver
weight
was
noted
for
males
at
the
same
dose
levels.
The
maximum
tolerance
dose
(
MTD)
was
achieved
at
122
mg/
kg/
day
based
on
the
decrease
in
the
body
weight
gain
in
males
at
48.2
and
122
mg/
kg/
day.
Administration
of
trifloxysulfuronsodium
to
dogs
for
12
months
caused
a
tendency
for
decrease
in
red
blood
cell
parameters
in
both
sexes
at
122
mg/
kg/
day.
There
was
neither
histopathological
nor
functional
evidence
for
compound
related
neurotoxicity.
Based
on
the
effects
at
48.2
and
122
mg/
kg/
day,
the
NOAEL
was
established
at
15.0
mg/
kg/
day
for
males
and
14.9
mg/
kg/
day
for
females.
In
an
18
 
month
oncogenicity
study,
mice
were
fed
diets
containing
trifloxysulfuron­
sodium
that
resulted
in
average
(
sexes
combined)
daily
test
substance
intakes
of
0,
5.84,
24.3,
116,
and
836
mg/
kg/
day.
Treatment
had
no
adverse
effect
on
appearance
or
behavior.
Survival
in
treated
animals
was
comparable
to
controls.
There
were
no
effects
on
organ
weights,
and
there
were
no
macroscopic
or
microscopic
findings
indicative
of
treatment­
related
systemic
toxicity.
Trifloxysulfuronsodium
was
not
carcinogenic
in
the
mouse.
Body
weight
gain
in
females
at
836
mg/
kg/
day
was
decreased
by
21%
compared
to
controls
after
3
months
and
16%
after
18
months.
Food
consumption
was
decreased
in
this
group
by
8%.
The
MTD
was
achieved
at
836
mg/
kg/
day
based
on
a
decrease
in
body
weight
gain
of
greater
than
15%
throughout
the
study.
Trifloxysulfuronsodium
was
not
carcinogenic
in
the
mouse.
Based
on
the
findings
at
836
mg/
kg/
day,
the
NOAEL
for
chronic
toxicity
was
established
at
121
mg/
kg/
day
for
males
and
112
mg/
kg/
day
for
females.
In
a
2
 
year
chronic
toxicity
and
carcinogenicity
study,
rats
were
fed
diets
containing
trifloxysulfuronsodium
that
resulted
in
average
(
sexes
combined)
daily
test
substance
intakes
of
0,
2.08,
22.0,
91.0
or
464
mg/
kg/
day.
Clinical
signs,
survival,
eye
examinations,
blood
chemistry,
urinalysis,
and
water
consumption
were
not
adversely
affected
by
treatment.
Survival
in
high
dose
females
was
greater
than
80%,
than
in
controls
of
60%.
There
were
no
treatment­
related
findings
at
the
12
 
month
interim
or
terminal
necropsy.
A
treatment­
related
decrease
in
body
weight
gain
(
17%
decrease
compared
to
controls)
was
seen
in
both
females
and
males
at
464
mg/
kg/
day
(
10,000
ppm),
which
was
considered
to
be
the
maximum
tolerated
dose
(
MTD).
Overall
food
consumption
was
decreased
by
6%
in
males
or
9%
in
females
at
464
mg/
kg/
day.
At
the
interim
and
terminal
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Notices
sacrifices,
mean
carcass
weights
were
lower
in
males
(
9%
and
13%,
respectively)
and
females
(
17%
and
12%,
respectively)
for
the
464
mg/
kg/
day
group.
At
terminal
sacrifice,
the
testes
to
body
weight
ratio
was
increased
by
19%
in
the
464
mg/
kg/
day
group.
Microscopical
examination
revealed
a
non­
dose
responsive
increase
in
the
incidence
of
kidney
tubular
atrophy
in
the
two
top
dose
groups
of
female
rats,
and
an
increase
in
Leydig
cell
hyperplasia
in
high
dose
males
only.
Both
treatment­
related
lesions
occurred
late
in
age/
treatment,
and
were
not
seen
in
animals
sacrificed
in
the
initial
year
of
the
study.
Neither
lesion
showed
an
increase
in
severity
(
only
incidence)
or
a
progression
of
the
lesion.
Both
lesions
are
commonly
seen
in
high
incidence
in
aged
control
rats;
26%
of
control
females
showed
renal
tubular
atrophy,
and
22%
of
control
males
showed
Leydig
cell
hyperplasia.
The
control
incidence
in
10
studies
was
less
than
10%,
suggesting
that
the
animals
in
this
study
were
particularly
susceptible
to
this
lesion.
There
were
no
data
from
other
measured
parameters
in
this
study
that
suggest
kidney
or
testis
as
target
organs,
therefore
indicating
that
these
lesions
are
high­
dose,
long­
term
effects.
In
conclusion,
the
MTD
was
reached
or
exceeded
at
464
mg/
kg/
day
for
the
2
 
year
rat
feeding
study.
The
NOAEL
in
males
was
82.6
mg/
kg/
day
based
on
the
increased
incidence
of
Leydig
cell
hyperplasia,
and
23.7
mg/
kg/
day
in
females
based
on
the
increased
incidence
of
kidney
tubular
atrophy.
There
was
no
evidence
of
a
carcinogenic
effect
after
2
years
of
treatment
with
trifloxysulfuron­
sodium
in
rats.
6.
Animal
metabolism.
Metabolism
in
rats
proceeded
primarily
via
three
concurrent
metabolic
pathways
(
typical
sulfonylurea
chemistry:
Oxidative
odemethylation
hydroxylation
of
the
pyrimidine
ring
and
Smiles
rearrangement
of
the
sulfonylurea.
Hydrolysis
of
the
sulfonylurea
and
oxidative
O­
demethylation
are
minor
pathways
in
the
rat.
Parent
compound
was
the
major
residue
in
the
rat.
The
metabolite
pattern
in
urine
and
feces
extracts
of
dogs
is
similar
to
that
of
rats.
Trifloxysulfuron­
sodium
was
the
major
component
detected
in
extracts
of
urine
and
feces
for
dogs,
as
in
the
rats.
In
hens
and
goats,
the
metabolite
profile
was
very
similar
to
that
observed
in
the
rat.
7.
Metabolite
toxicology.
The
metabolism
profile
for
trifloxysulfuronsodium
supports
the
use
of
an
analytical
enforcement
method
that
accounts
for
parent
trifloxysulfuron­
sodium.
Other
metabolites
are
considered
of
equal
or
lesser
toxicity
than
parent
compound.
8.
Endocrine
disruption.
Trifloxysulfuron­
sodium
does
not
belong
to
a
class
of
chemicals
known
or
suspected
of
having
adverse
effects
on
the
endocrine
system.
There
is
no
evidence
that
trifloxysulfuron­
sodium
has
any
effect
on
endocrine
function
in
development
or
reproduction
studies.
Furthermore,
histological
investigation
of
endocrine
organs
in
chronic
dog,
mouse,
and
rat
studies
did
not
indicate
that
the
endocrine
system
is
targeted
by
trifloxysulfuron­
sodium.
9.
Neurotoxicity.
In
an
acute
range
finding
neurotoxicity
study
in
which
rats
received
a
single
oral
dose
of
2,000
or
3,500
mg/
kg
trifloxysulfuron­
sodium,
there
were
no
effects
on
clinical
signs,
body
weight
and
food
consumption,
or
parameters
in
an
abbreviated
functional
observational
battery
(
FOB).
Therefore,
the
time
to
peak
effect
for
FOB
and
motor
activity
testing
was
based
on
a
blood
kinetic
study.
In
this
study,
trifloxysulfuron­
sodium
induced
peak
plasma
levels
at
1
 
2
hours
post­
dose,
and
levels
were
almost
zero
at
24
hours.
In
an
acute
neurotoxicity
study
in
rats,
trifloxysulfuron­
sodium
was
administered
by
gavage
at
0
or
2,000
mg/
kg.
Mortality,
body
weight
development
and
food
consumption
were
not
affected
by
treatment.
Neither
clinical
signs
nor
changes
in
observation
and
functional
test
conducted
as
part
of
the
FOB
were
observed.
Reduced
horizontal
and
vertical
motor
activity
were
observed
in
males
and
females
only
at
the
time
of
peak
effect
(
1
 
2
hours
post­
dosing).
There
were
no
persistent
signs
of
toxicity
and
no
histopathological
evidence
of
neurotoxicity.
In
a
second
acute
neurotoxicity
study
in
rats,
trifloxysulfuron­
sodium
was
administered
by
gavage
at
0,
200,
600
and
2,000
mg/
kg.
Mortality,
body
weight
development
and
food
consumption
were
not
affected
by
treatment.
There
were
no
effects
on
clinical
signs
or
on
parameters
in
the
FOB.
During
the
peak
plasma
period
(
1
 
2
hours
post­
dosing),
motor
activity
parameters
of
the
males
were
comparable
to
the
control
while
females
tended
to
be
slightly
less
active.
Based
on
the
results
of
this
study,
Trifloxysulfuron­
sodium
was
devoid
of
neurotoxic
effects.
Due
to
the
slightly
reduced
motor
activity
in
top
dose
females,
the
NOAEL
was
established
at
600
mg/
kg.
In
a
90
 
day
subchronic
neurotoxicity
study
in
rats,
trifloxysulfuron­
sodium
was
not
neurotoxic
when
administered
in
the
diet
for
13
weeks
at
concentrations
resulting
in
average
daily
test
substance
intakes
of
0,
112,
472,
or
967
mg/
kg/
day
for
males
or
0,
134,
553
or
1,128
mg/
kg/
day
for
females.
There
were
no
treatment­
related
deaths
or
clinical
signs.
Effects
on
body
weight
development
and
food
consumption
indicated
systemic
toxicity
in
males
at
doses
472
mg/
kg/
day
and
in
females
at
1,128
mg/
kg/
day.
There
were
no
treatment­
related
neurobehavioral
or
motor
activity
effects,
no
macroscopic
findings,
and
no
microscopic
findings
in
central
or
peripheral
nervous
tissue.
In
the
absence
of
any
functional
or
morphological
changes
in
the
nervous
system
at
any
of
the
dose
levels
tested,
trifloxysulfuron­
sodium
is
considered
devoid
of
neurotoxic
potential
when
administered
to
rats
for
90
days.
Based
on
body
weight
effects,
the
NOAEL
was
established
at
112
mg/
kg/
day
for
male
rats
and
553
mg/
kg/
day
for
female
rats.

C.
Aggregate
Exposure
1.
Dietary
exposure.
Dietary
exposure
from
trifloxysulfuron­
sodium
potentially
exists
through
both
food
commodities
and
drinking
water.
Each
exposure
pathway
is
addressed
below.
i.
Food.
Chronic
dietary
exposure
to
trifloxysulfuron­
sodium
was
estimated
based
on
proposed
tolerance­
based
residue
values
and
the
assumption
that
100%
of
all
planted
acres
were
treated.
The
assessment
included
cotton,
processed
cotton
fractions,
sugarcane
and
associated
processed
commodities,
citrus,
almonds
and
tomatoes.
Chronic
exposure
for
all
populations
was
compared
to
a
reference
dose
(
RfD)
of
0.15
milligrams/
kilogram/
body
weight/
day
(
mg/
kg/
bwt/
day)
based
on
a
no
observed
adverse
effect
level
(
NOAEL)
of
14.9
mg/
kg/
bwt/
day
from
a
1
 
year
study
in
dogs
and
a
100X
uncertainty
factor.
The
analysis
was
conducted
using
the
dietary
exposure
evaluation
model
(
DEEMTM)
and
the
USDA's
1994
 
96
Continuing
Survey
of
Food
Intake
by
Individuals
(
CSFII).
Secondary
residues
in
animal
commodities
were
not
considered
in
this
evaluation
since
calculations
showed
that
transfer
from
livestock
and
poultry
was
minimal
and
would
result
in
residue
levels
significantly
below
current
analytical
method
capabilities.
Chronic
exposure
to
trifloxysulfuron­
sodium
was
found
to
be
essentially
zero
with
less
than
0.1%
of
the
RfD
utilized
for
all
populations.
These
exposure
calculations
are
conservative
in
that
100%
of
the
crop
was
assumed
as
treated
and
tolerancebased
residue
levels
were
entered
into
the
dietary
model.
Acute
dietary
assessments
were
conducted
for
trifloxysulfuron­
sodium
using
proposed
tolerance­
based
residue
values
and
the
assumption
that
100%
of
all
planted
acres
were
treated.
The
assessment
included
cotton,
processed
cotton
fractions,
sugarcane
and
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Notices
associated
processed
commodities,
citrus,
almonds
and
tomatoes.
Acute
exposure
to
the
female
population
(
13
 
50
years
old)
was
compared
to
a
RfD
of
0.30
mg/
kg/
bwt/
day
based
on
a
NOAEL
of
30
mg/
kg/
bwt/
day
from
a
rat
teratology
study
and
a
100X
uncertainty
factor.
Acute
exposure
to
the
general
population
and
all
other
population
subgroups
(
including
infants
and
children)
was
compared
to
a
RfD
of
6.0
mg/
kg/
bwt/
day
based
on
a
NOAEL
of
600
mg/
kg/
bwt/
day
from
an
acute
neurotoxicity
study
in
rats
and
a
100X
uncertainty
factor.
The
analyses
were
conducted
using
the
Dietary
Exposure
Evaluation
Model
(
DEEMTM)
from
Novigen
Sciences
and
the
USDA's
1994
 
96
CSFII.
Secondary
residues
in
animal
commodities
were
not
considered
in
this
evaluation
since
calculations
showed
that
transfer
from
livestock
and
poultry
was
minimal
and
would
result
in
residue
levels
significantly
below
current
analytical
method
capabilities.
The
acute
exposures
are
presented
at
the
99.9th
percentile
of
exposure
although
the
Agency
accepts
the
95th
percentile
when
conservative
Tier
I
estimates
are
made
(
tolerance­
based
residues
and
100%
crop
treated
assumptions).
Even
at
the
99.9th
percentile,
exposure
and
subsequent
risk
was
found
to
be
0.2%
of
the
acute
reference
dose
(
aRfD)
for
the
female
population
(
13
 
19
years
not
pregnant
or
nursing)
and
essentially
zero
with
less
than
0.1%
of
the
aRfD
utilized
for
all
other
populations.
These
exposure
calculations
are
conservative
in
that
100%
of
the
crop
was
assumed
as
treated,
and
tolerance­
based
residue
levels
were
entered
into
the
dietary
model.
ii.
Drinking
water.
For
chronic
exposure
in
water,
the
estimated
maximum
concentrations
of
trifloxysulfuron­
sodium
in
surface
water
at
day
56/
3
was
0.35
parts
per
billion
(
ppb)
generic
expected
environmental
concentration
(
GENEEC)
(
sugarcane)
and
0.051
ppb
in
ground
water
(
SCIGROW
(
turf).
The
chronic
drinking
water
levels
of
concern
(
DWLOC)
values
were
calculated
and
compared
to
these
estimated
water
concentrations.
From
the
chronic
dietary
exposure
analysis,
an
exposure
estimate
of
0.000015
mg/
kg/
day
was
determined
for
the
U.
S.
population
and
less
than
or
equal
to
0.000037
mg/
kg/
day
for
all
subgroups.
Using
this
information,
chronic
drinking
water
levels
of
concern
(
DWLOCchronic)
were
calculated
for
trifloxysulfuronsodium
The
trifloxysulfuron­
sodium
estimated
ground
water
(
0.051
ppb)
and
surface
water
(
0.35
ppb)
concentrations
do
not
exceed
the
calculated
chronic
DWLOC
values
(
µ
g/
L):
1,500
to
5,250).
Therefore,
trifloxysulfuron­
sodium
exposures
would
not
exceed
the
exposure
allowable
by
the
chronic
risk
cup.
The
estimated
maximum
proposed
rates
for
the
``
worst
case''
estimation
of
the
proposed
use
concentrations
of
trifloxysulfuron­
sodium
in
surface
water
at
Peak
Day
 
0
was
2.56
ppb
GENEEC
(
sugarcane)
and
0.051
ppb
in
ground
water
(
SCI­
GROW)
(
turf).
The
acute
DWLOC
values
were
calculated
and
compared
to
these
estimated
water
concentrations.
From
the
acute
dietary
exposure
analysis,
the
lowest
margin
of
exposure
(
MOE)
from
the
use
of
trifloxysulfuronsodium
was
at
the
95th
percentile
for
the
U.
S.
population
and
all
population
subgroups.
This
indicates
a
food
exposure
of
less
than
or
equal
to
0.00016
mg/
kg/
day
for
all
populations.
Based
on
the
EPA's
``
Interim
Guidance
for
Conducting
Drinking
Water
Exposure
and
Risk
Assessments''
document
(
draft
12/
2/
97),
acute
drinking
water
levels
of
concern
(
DWLOCacute)
were
calculated
for
trifloxysulfuron­
sodium.
The
lowest
acceptable
MOE
for
any
pesticide
is
100.
This
value
was
used
in
the
DWLOC
calculations.
Based
on
this
analysis,
trifloxysulfuron­
sodium
estimated
surface
water
(
2.56
ppb)
and
ground
water
(
0.051
ppb)
concentrations,
for
sugarcane,
do
not
exceed
the
calculated
acute
DWLOC
values
(
µ
g/
L:
8997
to
209,965).
Therefore,
trifloxysulfuronsodium
exposures
would
not
exceed
the
exposure
allowable
by
the
risk
cup.
2.
Non­
dietary
exposure.
The
acute
MOE
for
children
ingesting
pesticidetreated
turf
exceeds
190
million.
The
risk
estimate
does
not
exceed
the
level
of
concern
(
MOE
=
100),
indicating
there
are
no
oral
exposure
concerns
for
children
ingesting
trifloxysulfuronsodium
treated
turf.

D.
Cumulative
Effects
The
potential
for
cumulative
effects
of
trifloxysulfuron­
sodium
and
other
substances
that
have
a
common
mechanism
of
toxicity
has
also
been
considered.
Trifloxysulfuron­
sodium
is
a
member
of
the
class
of
herbicides
designated
as
sulfonylureas.
There
is
no
reliable
information
to
indicate
that
toxic
effects
produced
by
trifloxysulfuron­
sodium
would
be
cumulative
with
those
of
any
other
chemical
including
another
pesticide.
Therefore,
Syngenta
believes
it
is
appropriate
to
consider
only
the
potential
risks
of
trifloxysulfuronsodium
in
an
aggregate
risk
assessment.
E.
Safety
Determination
1.
U.
S.
population.
In
assessing
the
potential
for
additional
sensitivity
of
infants
and
children
to
residues
of
trifloxysulfuron­
sodium,
data
from
developmental
toxicity
studies
in
the
rat
and
rabbit
and
a
two­
generation
reproduction
study
in
the
rat
have
been
considered.
2.
Infants
and
children.
In
assessing
the
potential
for
additional
sensitivity
of
infants
and
children
to
residues
of
trifloxysulfuron­
sodium,
data
from
developmental
toxicity
studies
in
the
rat
and
rabbit
and
a
two­
generation
reproduction
study
in
the
rat
have
been
considered.
In
rabbit
(
0,
50,
100,
250,
500
mg/
kg/
day)
and
rat
(
0,
30,
300,
1,000
mg/
kg/
day)
teratology
studies
there
was
no
evidence
of
teratogenicity.
Delayed
fetal
development
was
apparent
only
at
maternally
toxic
doses
of
trifloxysulfuron­
sodium
technical
in
rats.
In
rabbits,
500
mg/
kg/
day
was
clearly
toxic
to
does
and
at
250
mg/
kg/
day,
lesser
toxicity
was
seen.
For
the
control
(
50,
100,
and
250
mg/
kg)
groups,
pre­
implantation
losses,
number
of
implantation
sites,
and
postimplantation
losses
were
not
affected
by
treatment.
The
findings
after
fetal
post
mortem
examination
and
fetal
visceral
examination
revealed
no
treatment
related
effects.
Similarly,
there
were
no
skeletal
malformations
in
this
study
and
the
incidence
of
anomalies
and
variations
were
not
affected
by
treatment.
The
no
observed
adverse
effect
levels
(
NOAEL)
for
maternal
toxicity
was
100
mg/
kg/
day
and
the
NOAEL
for
fetal
toxicity
was
250
mg/
kg/
day.
There
was
no
indication
of
embryotoxic,
fetotoxic,
or
teratogenic
potential
for
trifloxysulfuron­
sodium
in
rabbits.
In
the
rat
teratology
study
developmental
toxicity
was
secondary
to
maternal
toxicity
and
consisted
of
slightly
reduced
fetal
body
weights
and
an
increase
in
minor
skeletal
anomalies
and
variations.
The
NOAELs
for
maternal
and
developmental
toxicity
were
both
30
mg/
kg/
day.
Trifloxysulfuron­
sodium
was
not
embryotoxic,
fetotoxic,
or
teratogenic
in
rats
when
tested
under
the
conditions
of
this
study.
In
a
rat
multigeneration
study,
trifloxysulfuron­
sodium
had
no
effect
on
reproductive
parameters.
The
NOAEL
for
systemic
toxicity
in
both
sexes
and
both
generations
was
1,000
ppm.
The
mean
dose
in
mg/
kg/
day
for
all
weekly
means
for
both
sexes,
both
generations,
all
time
points
at
this
dietary
level
was
83.4
mg/
kg/
day.
There
were
no
effects
on
the
reproductive
parameters
and
the
NOAEL
for
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/
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68,
No.
55
/
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March
21,
2003
/
Notices
reproductive
toxicity
was
>
12,000
ppm.
Offspring
effects
were
not
observed
at
dose
levels
that
did
not
produce
parental
toxicity.
There
is
no
evidence
that
developing
offspring
are
more
sensitive
than
adults
to
the
effects
of
trifloxysulfuron­
sodium.
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
prenatal
and
postnatal
toxicity
and
the
completeness
of
the
data
base.
Based
on
the
current
toxicological
requirements,
the
data
base
for
trifloxysulfuronsodium
relative
to
prenatal
and
postnatal
effects
for
children
is
complete.
Further,
for
trifloxysulfuronsodium
the
developmental
studies
showed
no
increased
sensitivity
in
fetuses
as
compared
to
maternal
animals
following
in­
utero
exposures
in
rats
and
rabbits,
and
no
increased
sensitivity
in
pups
as
compared
to
the
adults
in
the
multi­
generation
reproductive
toxicity
study.
Therefore,
it
is
concluded
that
an
additional
uncertainty
factor
is
not
warranted
to
protect
the
health
of
infants
and
children
and
that
a
RfD
of
0.15
mg/
kg/
day
is
appropriate
for
assessing
aggregate
risk
to
infants
and
children
of
trifloxysulfuron­
sodium.
Assuming
tolerance
level
residues
and
100%
of
crops
treated,
less
than
0.1%
of
the
trifloxysulfuron­
sodium
chronic
RfD
is
utilized
in
the
population
subgroup
all
infants
(>
1
year
old).
Therefore,
based
on
the
completeness
and
reliability
of
the
toxicity
data
base,
Syngenta
concludes
that
there
is
reasonable
certainty
that
no
harm
will
result
to
infants
and
children
from
aggregate
exposure
to
trifloxysulfuronsodium
residues.

F.
International
Tolerances
There
are
no
Codex
MRLs
established
for
residues
of
trifloxysulfuron­
sodium
on
cottonseed,
cotton
byproducts,
citrus,
almonds,
sugarcane
or
tomatoes.

[
FR
Doc.
03
 
6822
Filed
3
 
20
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
FRL
 
7471
 
2]

Strategic
Plan
for
North
American
Cooperation
in
the
Conservation
of
Biodiversity
 
Draft
for
Public
Review
AGENCY:
Environmental
Protection
Agency
(
EPA).
ACTION:
Notice
of
availability.

SUMMARY:
Comments
are
requested
on
the
final
draft
of
the
Strategic
Plan
for
North
American
Cooperation
in
the
Conservation
of
Biodiversity
(
Strategic
Plan).
The
Strategic
Plan
has
been
prepared
by
the
Secretariat
of
the
Commission
for
Environmental
Cooperation
(
CEC),
under
the
North
American
Agreement
on
Environmental
Cooperation,
in
coordination
with
representatives
from
Canada,
Mexico,
and
the
United
States.
The
Strategic
Plan
will
be
used
to
guide
the
CEC
Council,
its
Biodiversity
Conservation
Working
Group,
and
the
CEC
Secretariat
in
their
work
with
stakeholders
in
cooperatively
defining
and
implementing
mutually
beneficial
biodiversity
conservation
activities
in
North
America.
Comments
will
be
categorized
and
responses
will
be
developed
for
each
category.
Responses
to
comment
categories
will
be
published
in
the
Federal
Register
within
45
days
of
the
closing
date
for
comments.
Changes
to
the
final
draft
of
the
Strategic
Plan,
to
be
made
in
response
to
comments,
will
be
discussed
with
representatives
from
Canada,
Mexico
and
the
CEC
Secretariat.

DATES:
Written
comments
will
be
accepted
for
30
calendar
days.
Please
submit
or
postmark
written
comments
on
the
final
draft
document
by
April
21,
2003.

ADDRESSES:
Comments
should
be
sent
to
Patrick
Cotter,
Office
of
International
Affairs
(
2260R),
U.
S.
Environmental
Protection
Agency,
and
1300
Pennsylvania
Avenue,
NW.,
Washington,
DC
20004.
Faxed
comments
should
be
sent
to
Patrick
Cotter
at
(
202)
565
 
2409.
Comments
can
also
be
sent
by
email
to
Cotter.
Patrick@
epa.
gov.
Access
to
the
Document:
The
complete
text
of
the
final
draft
document,
in
English,
is
available
through
a
link
on
the
EPA
Office
of
International
Affair's
Web
site
at:
http://
www.
epa.
gov/
international/
trade/
index.
html,
or
you
may
access
the
document
directly
on
the
CEC's
Web
site
at:
http://
www.
cec.
org/
pubs_
docs/
documents/
index.
cfm?
varlan=
english&
ID=
1088.
Copies
of
the
final
draft
document
can
be
obtained
in
electronic
or
hard
copy
format
by
request
from
Patrick
Cotter
at
the
above
mailing
address,
email
address
or
by
calling
(
202)
564
 
6414.

FOR
FURTHER
INFORMATION
CONTACT:
Patrick
Cotter
by
telephone
at
(
202)
564
 
6414
or
by
email
at
Cotter.
Patrick@
epa.
gov.
Dated:
March
17,
2003.
Dona
M.
Harris,
Acting
Director,
Office
of
Management
Operations,
Office
of
International
Affairs.
[
FR
Doc.
03
 
6818
Filed
3
 
20
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
P
DEPARTMENT
OF
HEALTH
AND
HUMAN
SERVICES
Food
and
Drug
Administration
[
Docket
No.
02N
 
0281]

Agency
Information
Collection
Activities;
Announcement
of
OMB
Approval;
General
Administrative
Procedures:
Citizen
Petitions;
Petition
for
Reconsideration
or
Stay
of
Action;
Advisory
Opinions
AGENCY:
Food
and
Drug
Administration,
HHS.

ACTION:
Notice.

SUMMARY:
The
Food
and
Drug
Administration
(
FDA)
is
announcing
that
a
collection
of
information
entitled
``
General
Administrative
Procedures:
Citizen
Petitions;
Petition
for
Reconsideration
or
Stay
of
Action;
Advisory
Opinions''
has
been
approved
by
the
Office
of
Management
and
Budget
(
OMB)
under
the
Paperwork
Reduction
Act
of
1995.

FOR
FURTHER
INFORMATION
CONTACT:
JonnaLynn
P.
Capezzuto,
Office
of
Information
Resources
Management
(
HFA
 
250),
Food
and
Drug
Administration,
5600
Fishers
Lane,
Rockville,
MD
20857,
301
 
827
 
4659.

SUPPLEMENTARY
INFORMATION:
In
the
Federal
Register
of
December
18,
2002
(
67
FR
77498),
the
agency
announced
that
the
proposed
information
collection
had
been
submitted
to
OMB
for
review
and
clearance
under
44
U.
S.
C.
3507.
An
agency
may
not
conduct
or
sponsor,
and
a
person
is
not
required
to
respond
to,
a
collection
of
information
unless
it
displays
a
currently
valid
OMB
control
number.
OMB
has
now
approved
the
information
collection
and
has
assigned
OMB
control
number
0910
 
0183.
The
approval
expires
on
March
31,
2006.
A
copy
of
the
supporting
statement
for
this
information
collection
is
available
on
the
Internet
at
http://
www.
fda.
gov/
ohrms/
dockets.

Dated:
March
14,
2003.
William
K.
Hubbard,
Associate
Commissioner
for
Policy
and
Planning.
[
FR
Doc.
03
 
6739
Filed
3
 
20
 
03;
8:
45
am]

BILLING
CODE
4160
 
01
 
S
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