Document ID: EPA-HQ-OPP-2003-0001-0001
Agency: epa
Document Type: Notice
Title: Lactofen; Notice of Filing Pesticide Petition to Establish Tolerances for Certain Pesticide Chemicals in or on Food
Posted Date: 2003-01-29T05:00Z

4475
Federal
Register
/
Vol.
68,
No.
19
/
Wednesday,
January
29,
2003
/
Notices
100%
of
the
RfD
because
the
RfD
represents
the
level
at
or
below
which
daily
aggregate
dietary
exposure
over
a
lifetime
will
not
pose
appreciable
risks
to
human
health.
Despite
the
potential
for
exposure
to
S­
metolachlor
in
drinking
water
and
from
non­
dietary,
non­
occupational
exposures,
the
assessment
presented
above
demonstrates
that
the
high
levels
of
safety
exist
for
current
and
proposed
uses
of
S­
metolachlor;
it
is
not
expected
that
aggregate
exposure
from
all
sources
will
exceed
100%
of
the
RfD.
Therefore,
one
can
conclude
there
is
a
reasonable
certainty
that
no
harm
will
result
from
aggregate
exposure
to
S­
metolachlor.
2.
Infants
and
children.
FFDCA
section
408
provides
that
EPA
may
apply
an
additional
safety
factor
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
prenatal
and
postnatal
toxicity
and
the
completeness
of
the
database.
Based
on
the
current
toxicological
data
requirements,
the
database
relative
to
prenatal
and
postnatal
effects
for
children
is
complete.
A
full
consideration
of
the
available
reproductive
toxicity
data
supporting
Smetolachlor
demonstrates
no
increased
sensitivity
to
infants
and
children.
Therefore,
it
is
concluded
that
an
additional
uncertainty
factor
is
not
warranted
to
protect
the
health
of
infants
and
children
and
that
the
cRfD
at
0.1
mg/
kg/
day
is
appropriate
for
assessing
aggregate
risk
to
infants
and
children
from
use
of
S­
metolachlor.
Based
on
the
aggregate
assessment
described
above,
the
percent
of
the
cRfD
that
will
be
utilized
by
aggregate
exposure
to
residues
of
S­
metolachlor
is
less
than
0.2%
for
non­
nursing
infants
and
children
1
to
6
years
old,
and
0.1%
for
children
7
to
12
years
old.
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD
because
the
RfD
represents
the
level
at
or
below
which
daily
aggregate
dietary
exposure
over
a
lifetime
will
not
pose
appreciable
risks
to
human
health.
Despite
the
potential
for
exposure
to
S­
metolachlor
in
drinking
water
and
from
non­
dietary,
non­
occuptional
exposure,
the
assessment
described
above
demonstrates
that
it
is
not
expected
that
aggregate
exposure
from
all
sources
provides
for
a
large
margin
of
safety
and
will
exceed
100%
of
the
RfD.
Therefore,
based
on
the
completeness
and
reliability
of
the
toxicity
data
and
the
exposure
assessment,
it
is
concluded
there
is
a
reasonable
certainty
that
no
harm
will
result
to
infants
and
children
from
aggregate
exposure
to
Smetolachlor
residues.
F.
International
Tolerances
There
are
no
Codex
Alimentarius
Commission
maximum
residue
levels
(
MRL's)
established
for
residues
of
Smetolachlor
in
or
on
raw
agricultural
commodities.
[
FR
Doc.
03
 
2019
Filed
1
 
28
 
03;
8:
45
am]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
OPP
 
2003
 
0001;
FRL
 
7287
 
6]

Lactofen;
Notice
of
Filing
Pesticide
Petitions
to
Establish
Tolerances
for
Certain
Pesticide
Chemicals
in
or
on
Food
AGENCY:
Environmental
Protection
Agency
(
EPA).
ACTION:
Notice.

SUMMARY:
This
notice
announces
the
initial
filing
of
pesticide
petitions
proposing
the
establishment
of
regulations
for
residues
of
certain
pesticide
chemicals
in
or
on
various
food
commodities.
DATES:
Comments,
identified
by
docket
ID
number
OPP
 
2003
 
0001,
must
be
received
on
or
before
February
28,
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:
Joanne
I.
Miller,
Registration
Division
(
7505C),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460
 
0001;
telephone
number:
(
703)
305
 
6224;
e­
mail
address:
miller.
joanne@
epamail.
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
categories
and
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
the
table
could
also
be
affected.
The
North
American
Industrial
Classification
System
(
NAICS)
codes
have
been
provided
to
assist
you
and
others
in
determining
whether
or
not
this
action
might
apply
to
certain
entities.
If
you
have
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
 
0001.
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
EPA's
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
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E:\
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29JAN1.
SGM
29JAN1
4476
Federal
Register
/
Vol.
68,
No.
19
/
Wednesday,
January
29,
2003
/
Notices
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
 
0001.
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
 
0001.
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
 
0001.
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
 
0001.
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.

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January
29,
2003
/
Notices
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
pesticide
petitions
as
follows
proposing
the
establishment
and/
or
amendment
of
regulations
for
residues
of
certain
pesticide
chemicals
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
these
petitions
contain
data
or
information
regarding
the
elements
set
forth
in
FFDCA
section
408d)
2);
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
support
granting
of
the
petitions.
Additional
data
may
be
needed
before
EPA
rules
on
the
petitions.

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

Dated:
January
17,
2003.
Debra
Edwards,
Acting
Director,
Registration
Division,
Office
of
Pesticide
Programs.

Summaries
of
Petitions
The
petitioner's
summaries
of
the
pesticide
petitions
are
printed
below
as
required
by
FFDCA
section
408(
d)(
3).
The
summaries
of
the
petitions
were
prepared
by
the
petitioner
and
represent
the
views
of
the
petitioner.
The
petitions
summaries
announce
the
availability
of
a
description
of
the
analytical
methods
available
to
EPA
for
the
detection
and
measurement
of
the
pesticide
chemicals
residues
or
an
explanation
of
why
no
such
method
is
needed.

Valent
U.
S.
A.
Corporation
PP
8F3591
and
PP
9F3798
EPA
has
received
pesticide
petitions
(
8F3591
and
9F3798)
from
Valent
U.
S.
A.
Corporation,
1333
North
California
Boulevard,
Suite
600,
Walnut
Creek,
California
94596
 
8025
proposing,
pursuant
to
section
408(
d)
of
the
FFDCA,
21
U.
S.
C.
346a(
d),
to
amend
40
CFR
180.432
by
establishing
tolerances
for
residues
of
the
herbicide
lactofen,
1­(
carboethoxy)
ethyl
5­[
2­
chloro­
4­(
trifluoromethyl)
phenoxy]­
2­
nitrobenzoate,
in
or
on
the
raw
agricultural
commodities
(
RACs)
cottonseed
at
0.01
part
per
million
(
ppm),
cotton
gin
byproducts
at
0.02
ppm,
and
peanut
nutmeats
at
0.01
ppm.
EPA
has
determined
that
the
petitions
contain
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
petitions.
Additional
data
may
be
needed
before
EPA
rules
on
the
petitions.

A.
Residue
Chemistry
1.
Plant
metabolism.
The
nature
of
the
residue
in
plants
is
adequately
understood
based
on
plant
metabolism
studies
on
cotton,
peanut,
soybean,
and
tomato.
The
Health
Effects
Division
(
HED)
Metabolism
Assessment
Review
Committee
(
MARC)
met
on
April
4,
2000,
considered
all
of
the
metabolism
studies
submitted
to
date
and
concluded
that
only
the
parent
compound
needs
to
be
regulated
for
plant
commodities,
provided
that
pre­
harvest
intervals
exceed
45
days.
2.
Analytical
method.
Adequate
analytical
methodology
is
available
for
detecting
and
measuring
levels
of
lactofen
in
or
on
RACs
with
a
limit
of
detection
(
LOD)
that
allows
monitoring
of
food
with
residues
at
or
above
the
level
of
the
proposed
tolerances.
The
method,
RM
 
28D,
has
been
successfully
radio
validated
in
conjunction
with
a
tomato
metabolism
study
and
has
undergone
a
successful
independent
laboratory
validation
trial.
This
method
was
also
successfully
validated
by
EPA's
Analytical
Chemistry
Laboratory
using
peanut
nutmeats
and
cottonseed.
In
general,
the
analytical
method
has
a
LOD
of
0.005
ppm
and
limit
of
quantitation
(
LOQ)
of
0.01
ppm
in
crops.
3.
Magnitude
of
residues.
Adequate
lactofen
residue
data
are
available
for
cotton
and
peanuts.
An
adequate
number
of
field
trials
distributed
throughout
cotton
and
peanut
growing
areas
of
the
United
States
have
been
conducted
on
these
crops
to
determine
lactofen
residues
resulting
from
the
application
of
lactofen
at
the
maximum
labeled
or
proposed
use
rate.
i.
Cotton.
Residues
of
lactofen
were
each
<
0.01
ppm,
in/
on
cottonseed
(
n=
14)
harvested
59
 
127
days
following
a
single
postemergence
soil­
directed
application
of
lactofen
at
0.4
lb
active
ingredient
per
acre
(
lb
active
ingredient/
acre)
(
2x
the
single
application
rate)
and
in/
on
cottonseed
(
n=
10)
harvested
23
 
108
days
following
the
last
of
two
postemergence
directed
applications
at
0.4
lb
active
ingredient/
acre
application
(
2x
the
maximum
seasonal
rate).
With
one
exception,
residues
of
lactofen
were
also
each
<
0.01
ppm,
in/
on
cotton
gin
byproducts
(
gin
trash)
(
n=
11)
derived
from
cotton
harvested
69
 
108
days
following
two
applications
at
0.2
lb
active
ingredient/
acre.
One
gin
trash
sample
bore
residues
of
lactofen
at
0.03
ppm,
but
confirmatory
analyses
of
this
sample
detected
lactofen
at
<
0.01
 
0.02
ppm,
and
residues
of
lactofen
were
<
0.01
ppm,
in
the
duplicate
treated
sample
from
the
same
trial.
In
a
single
processing
study,
residues
of
lactofen
were
<
0.01
ppm,
in/
on
cottonseed
harvested
76
days
following
the
last
of
two
directed
applications
of
lactofen
at
0.6
lb
active
ingredient/
acre
application
(
1.2
lb
active
ingredient/
acre/
season,
3x
rate).
Residues
of
lactofen
were
<
0.01
ppm
in
samples
of
meal,
hulls,
oil,
(
crude
and
refined)
and
soapstock.
All
these
data
support
proposed
tolerance
for
lactofen
in/
on
cottonseed
at
0.01
ppm,
and
in/
on
cotton,
gin
byproducts
at
0.02
ppm.
No
separate
tolerances
are
needed
for
cotton
processed
commodities.
ii.
Peanuts.
In
8
field
trials,
residues
of
lactofen
were
each
<
0.01
ppm,
in/
on
16
samples
of
peanut
nutmeats
and
hulls
harvested
65
 
71
days
following
the
last
of
2
broadcast
applications
of
lactofen
totaling
0.45
lb
active
ingredient/
acre
(
1x
the
maximum
proposed
rate).
Residues
of
lactofen
were
also
<
0.01
ppm,
in/
on
peanut
nutmeats
and
hulls
from
2
trials
conducted
at
2x
and
5x
the
maximum
seasonal
rate.
In
a
processing
study,
residues
of
lactofen
were
<
0.01
ppm
in
meal,
oil,
crude
and
refined,
and
soapstock
processed
from
nutmeats
treated
at
3x
and
5x
the
maximum
proposed
use
rates.
All
these
data
support
proposed
tolerance
for
lactofen
in/
on
peanut
nutmeats
at
0.01
ppm.
No
separate
tolerances
are
needed
for
peanut
processed
commodities.

B.
Toxicological
Profile
1.
Acute
toxicity.
Lactofen
has
very
low
acute
toxicity.
The
acute
oral
LD50
is
5.96
gram/
kilogram/
body
weight
(
g/
kg/
bwt)
toxicity
category
IV,
the
acute
dermal
LD50
is
>
2.0
g/
kg/
bwt
toxicity
category
III
and
the
acute
inhalation
LD50
is
>
6.3
milligrams/
liter
(
mg/
L)
toxicity
category
IV.
Lactofen
is
not
a
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19
/
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29,
2003
/
Notices
skin
sensitizer
but
is
a
very
slight
dermal
irritant.
2.
Genotoxicity.
Lactofen
has
very
little
mutagenic
or
genotoxic
activity.
While
a
positive
mutagenic
response
was
reported
in
one
trial
of
a
Salmonella
typhimurium/
mammalian
microsome
mutagenicity
assay,
this
response
was
not
repeated
in
the
second
assay
conducted.
In
addition,
lactofen
did
not
appear
to
induce
chromosomal
aberrations,
unscheduled
deoxyribonucleic
acid
(
DNA)
synthesis
or
inhibit
DNA
repair.
3.
Reproductive
and
developmental
toxicity.
Reproduction
and
teratology
studies
indicate
that
adverse
effects,
including
embryotoxicity,
occur
only
at
doses
that
are
also
maternally
toxic.
Since
lactofen
causes
effects
only
at
levels
which
also
produce
systemic
toxicity,
the
compound
is
not
a
reproductive
hazard.
In
a
2
 
generation
reproduction
study
in
rats,
decreased
pup
weight
and
decreased
absolute
and
relative
weights
of
the
spleen
were
first
reported
at
approximately
26.2
milligrams/
kilogram/
day
(
mg/
kg/
day)
(
based
on
dose
administered
to
the
parental
group).
The
same
dose
level
elicited
mortality
and
decreased
male
fertility
in
the
parental
groups.
The
no
observed
adversed
effect
level
(
NOAEL)
for
both
systemic
and
reproductive
toxicity
in
this
study
was
2.6
mg/
kg/
day.
In
the
developmental
toxicity
study
in
rats,
effects
were
observed
at
the
150
mg/
kg/
day
dose
level
consisting
of
decreases
in
fetal
weight
as
well
as
skeletal
abnormalities.
This
dose
level
also
elicited
signs
of
toxicity
in
the
parental
group.
The
NOAEL
for
this
study
was
50
mg/
kg/
day.
Based
on
this
NOAEL
and
an
uncertainty
factor
(
UF)
of
100,
the
acute
reference
dose
(
RfD)
for
lactofen
has
been
set
at
0.50
mg/
kg/
day.
Two
developmental
toxicity
studies
were
conducted
in
rabbits.
In
the
first
study,
pregnant
rabbits
were
administered
oral
doses
of
0,
5,
15,
or
50
mg/
kg
bwt/
day
lactofen
technical
on
days
6
 
18
of
gestation.
Maternal
toxicity
(
clinical
signs
and
reduced
weight
gain)
and
developmental
effects
(
increased
embryonic
death,
decreased
litter
size
and
increased
post­
implantation
loss)
were
reported
at
15
and
50
mg/
kg.
The
Agency
concluded
that
the
data
were
insufficient
to
establish
a
clear
NOAEL.
In
the
second
rabbit
developmental
toxicity
study,
pregnant
rabbits
were
exposed
to
0,
1,
4,
or
20
mg/
kg
bwt/
day
oral
doses
on
days
6
 
18
of
gestation.
Maternal
toxicity
(
reduced
food
consumption)
was
observed
at
20
mg/
kg
bwt/
day,
but
no
developmental
effects
were
observed
at
any
dose.
Therefore,
the
maternal
NOAEL
was
4
mg/
kg
bwt/
day
and
the
developmental
NOAEL
was
greater
than
20
mg/
kg
bwt/
day.
4.
Subchronic
toxicity
 
i.
Rats
4
 
week.
Male
and
female
rats
were
fed
diets
containing
lactofen
technical
at
concentrations
of
0,
200,
1,000,
5,000,
and
10,000
ppm,
for
4
weeks.
A
slight
increase
in
spleen
weight
was
the
basis
for
a
lowest
observed
adversed
effect
level
(
LOAEL)
of
200
ppm,
lowest
dose
tested
(
LDT).
At
doses
of
1,000
ppm,
or
higher,
the
following
findings
were
reported:
clinical
signs
of
toxicity;
decreased
red
blood
cell
(
RBC),
hemoglobin,
hematocrit,
and
increased
white
blood
cell
(
WBC);
increased
relative
liver
and
spleen
weights;
and
necrosis
and
pigmentation
of
hepatocytes.
At
10,000
ppm,
severe
toxic
signs
were
observed
by
day
7
and
all
animals
were
dead
or
killed
in
extremis
by
day
11.
Hypocellularity
of
the
spleen,
thymus,
and
bone
marrow
was
also
observed
in
animals
exposed
to
10,000
ppm.
ii.
Rats
3
 
month.
Lactofen
technical
was
fed
to
male
and
female
rats
at
dietary
concentrations
of
0,
40,
200,
and
1,000
ppm,
for
13
weeks.
Histopathological
changes
in
the
liver
and
significant
changes
in
clinical
chemistry
associated
with
the
liver
were
observed
in
rats
exposed
to
1,000
ppm,
dosage.
Decreased
RBC,
hemoglobin
and
hematocrit
values
were
also
observed
at
1,000
ppm.
The
NOAEL
in
this
study
was
200
ppm,
14.1
mg/
kg/
day.
iii.
Dogs
4
 
week.
In
a
range
finding
study
lactofen
technical
was
fed
in
the
diet
of
dogs
at
0,
1,000,
3,000,
and
10,000
ppm,
for
4
weeks.
Toxic
effects
noted
in
dogs
fed
10,000
ppm,
included
decreased
RBC
count
and
hemocrit,
and
increased
blood
urea
nitrogen
(
BUN)
and
serum
glutamic­
pyruvic
transaminase
(
SGPT).
Food
palatability
problems
led
to
greatly
decreased
feed
consumption
at
higher
dosages.
The
NOAEL
appeared
to
be
1,000
ppm.
iv.
Mice
3
 
month.
Groups
of
male
and
female
mice
were
fed
diets
containing
lactofen
technical
at
concentrations
of
0,
40,
200,
1,000,
5,000,
and
10,000
for
13
weeks.
At
week
5,
the
dosage
of
the
40
ppm,
groups
was
increased
to
2,000
ppm.
Treatment
related
mortality
occurred
at
dosages
above
1,000
ppm.
The
LOAEL
was
200
ppm,
28.6
mg/
kg/
day
based
on:
 
Increased
WBC;
decreased
hematocrit,
hemoglobin
and
RBC.
 
Increased
alkaline
phosphatase,
serum
glutamic­
oxloacetic
transaminase
(
SGOT),
SGPT,
cholesterol
and
total
serum
protein
levels.
 
Increased
weights
or
enlargement
of
the
spleen,
liver,
adrenals,
heart,
and
kidney;
histopathological
changes
of
the
liver,
kidney,
thymus,
spleen,
ovaries,
and
testes.
In
general,
effects
were
slight
in
the
200
ppm
groups,
and
moderate
to
severe
in
the
1,000
ppm
groups.
v.
Peroxisome
proliferation.
Butler
et
al
(
1988)
studied
the
effects
of
lactofen
on
peroxisome
proliferation
in
mice
exposed
for
7
weeks
to
dietary
concentrations
of
2,
10,
50,
and
250
ppm.
Liver­
weight
to
body­
weight
ratio,
liver
catalase,
liver
acyl­
CoA
oxidase,
liver
cell
cytoplasmic
eosinophilia,
nuclear,
and
cellular
size,
and
peroxisomal
staining
were
increased
by
the
tumorigenic
dose
of
lactofen,
i.
e.
250
ppm.
Lower
doses
of
lactofen
had
little
to
no
effect
on
these
parameters.
This
study
indicates
that
lactofen
induces
peroxisome
proliferation
and
further,
that
50
ppm,
7
mg/
kg/
day,
a
dose
which
is
not
tumorigenic,
would
be
considered
a
threshold
dose
in
mice
for
peroxisome
proliferation
produced
by
lactofen.
A
subchronic
study
conducted
in
chimpanzees
(
Couch
and
Erickson
1986),
indicated
no
effect
on
clinical
chemistry
or
histological
endpoints
that
would
suggest
liver
toxicity
or
peroxisome
proliferation
at
doses
up
to
75
mg/
kg
bwt/
day
administered
for
93
days.
Therefore,
Valent
believes
that
75
mg/
kg
bwt/
day
is
a
clear
NOAEL
for
peroxisome
proliferation
observed
in
a
species
closely
related
to
man.
On
January
17,
2001,
the
Mechanism
of
Toxicity
Assessment
Review
Committee
(
MTARC)
reviewed
the
merits
of
the
toxicological
data
supporting
peroxisome
proliferation
as
the
proposed
mode
of
action
for
lactofen.
Based
on
the
weight­
of­
evidence
from
guideline,
as
well
as
mechanistic
studies,
the
MTARC
concluded
that
there
are
sufficient
data
to
classify
lactofen
as
a
non­
genotoxic
hepatocarcinogen
in
rodents
with
peroxisome
proliferation
being
a
plausible
mode
of
action.
5.
Chronic
toxicity.
Lactofen
causes
adverse
health
effects
when
administered
to
animals
for
extended
periods
of
time.
These
effects
include
proliferative
changes
in
the
liver,
spleen,
and
kidney;
hematological
changes;
and
blood
biochemistry
changes.
i.
Mouse
18
 
month.
In
a
dietary
18
 
month
oncogenicity
study
in
mice
at
dosages
of
10,
50,
and
250
ppm,
lactofen
technical,
an
increase
in
liver
adenomas
and
carcinomas,
cataracts,
and
liver
pigmentation
was
observed
at
250
ppm,
a
dose
that
clearly
exceeded
the
maximum
tolerance
dose
(
MTD).
The
lowest
dose,
10
ppm,
1.4
mg/
kg/
day,
was
the
LOAEL
based
on
increased
liver
weight
and
hepatocytomegaly.

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Notices
ii.
Rat
24
 
month.
In
a
2
 
year
chronic
feeding/
oncogenicity
study
of
lactofen
technical
in
rats
at
dosages
of
0,
500,
1,000
ppm;
and
2,000
ppm,
in
the
diet,
an
increase
in
liver
neoplastic
nodules
and
foci
of
cellular
alteration
was
observed
in
both
sexes
at
2,000
ppm.
The
NOAEL
for
systemic
toxicity
is
500
ppm,
2
mg/
kg/
day
based
on
kidney
and
liver
pigmentation.
iii.
Dog
12
 
month.
In
a
1
 
year
study
in
dogs
exposed
to
40,
200,
and
1,000
ppm;
week
1
 
17
or
3,000
ppm;
week
18
 
52
lactofen
technical
in
their
diet,
the
NOAEL
was
determined
to
be
200
ppm,
(
0.79
mg/
kg/
day)
based
on
renal
dysfunction
and
decreased
RBC,
hemoglobin
hematocrit
and
cholesterol
observed
at
1,000/
3,000
ppm.
Based
on
this
NOAEL
and
an
uncertainty
factor
(
UF)
of
100,
the
chronic
RfD
for
lactofen
has
been
set
at
0.008
mg/
kg/
day.
iv.
Carcinogenicity.
As
a
member
of
the
diphenyl
ether
chemical
family,
lactofen
is
structurally
related
to
four
other
chemicals
that
are
oncogenic
in
rodents:
 
Sodium
acifluorfen
(
acifluorfen
is
a
lactofen
metabolite),
nitrofen,
oxyfluorfen,
and
fomesafen.
 
Sodium
acifluorfen
produces
hepatocellular
adenomas
and
carcinomas
in
mice
but
is
negative
in
rats.
 
Nitrofen
produces
hepatocellular
carcinomas
in
mice
and
pancreatic
carcinomas
in
rats.
 
Oxyfluorfen
produces
marginally
positive
liver
tumors
in
mice
but
is
negative
in
rats.
 
Fomesafen
produces
hepatocellular
adenomas
and
carcinomas
in
mice.
The
Cancer
Peer
Review
Committee
(
CPRC)
evaluated
the
relevant
data
on
the
carcinogenic
potential
of
lactofen
in
1987
and
classified
lactofen
as
a
B2
carcinogen
Probable
Human
Carcinogen
and
assigned
a
Cancer
Potency
Factor
(
Q1*)
of
1.7
x
10­
1
mg/
kg/
day­
1,
based
on
a
interspecies
scaling
factor
of
0.67.
This
Q1*
has
since
been
reduced
to
1.19
x
10­
1
mg/
kg/
day­
1
based
on
recent
EPA
guidance
indicating
that
0.75
is
a
more
appropriate
interspecies
scaling
factor.
The
B2
classification
is
based
on
an
increase
in
the
combined
incidence
of
liver
adenomas
and
carcinomas
in
mice
and
increases
in
liver
neoplastic
nodules
and
foci
of
cellular
alteration
(
possible
precursor
of
tumors)
in
rats.
In
1996,
and
1999,
EPA
proposed
new
cancer
risk
assessment
guidelines
which
state
that
nonmutagenic
carcinogens
known
to
cause
cancer
via
a
threshold
mechanism,
such
as
peroxisome
proliferation,
could
be
assessed
using
a
nonlinear
margin
of
exposure
(
MOE)
approach
rather
than
the
Q1
*
method.
EPA
has
recently
determined
that
lactofen
acts
via
a
peroxisome
proliferation
mechanism
and
is
currently
reevaluating
its
approach
to
the
quantification
of
the
cancer
risk
for
lactofen.
6.
Animal
metabolism.
In
a
rat
metabolism
study,
lactofen
was
shown
to
metabolize
to
acifluorfen,
5­[
2­
chloro­
4­(
trifluoromethyl)
phenoxy]­
2­
nitrobenzoate,
which
was
eliminated
via
both
urine
and
feces.
While
lactofen
was
the
primary
compound
found
in
the
feces,
acifluorfen
accounted
for
>
90%
of
the
radioactivity
in
the
urine.
Negligible
amounts
of
the
administered
radioactivity
were
found
in
any
tissue
with
less
than
0.8%
of
the
administered
radioactivity
being
found
in
the
liver
one
of
the
main
target
organs.
7.
Metabolite
toxicology.
Acifluorfen
is
also
a
hydrolytic
metabolite
of
lactofen.
The
sodium
salt
of
this
benzoic
acid
is
the
registered
herbicide,
sodium
acifluorfen.
This
product
has
a
complete
data
base
supporting
registration
with
a
RfD
of
0.013
mg/
kg/
day
and
a
Q1*
of
5.30
x
10­
2
mg/
kg/
day­
1.
Because
lactofen
and
its
metabolites
are
not
retained
in
the
body,
the
potential
for
acute
toxicity
from
in
situ
formed
metabolites
is
low.
The
potential
for
chronic
toxicity
of
lactofen
metabolites
has
been
adequately
addressed
by
an
extensive
battery
of
lactofen
chronic
toxicity
testing.
8.
Endocrine
disruption.
No
special
studies
to
investigate
the
potential
for
estrogenic
or
other
endocrine
effects
of
lactofen
have
been
performed.
However,
a
large
and
detailed
toxicology
data
base
exists
for
the
compound
including
studies
acceptable
to
the
Agency
in
all
required
categories.
These
studies
include
evaluations
of
reproduction
and
reproductive
toxicity
and
detailed
pathology
and
histology
of
endocrine
organs
following
repeated
or
long­
term
exposure.
These
studies
are
considered
capable
of
revealing
endocrine
effects
and
no
such
effects
were
observed.

C.
Aggregate
Exposure
1.
Dietary
exposure.
A
full
battery
of
toxicology
testing,
including
studies
of
acute,
chronic,
oncogenicity,
developmental,
mutagenicity,
and
reproductive
effects
is
available
for
lactofen.
For
the
following
risk
assessments,
the
NOAEL
from
the
chronic
oral
toxicity
study
in
dogs,
0.79
mg/
kg/
day,
was
selected
as
the
chronic
oral
toxicity
endpoint.
Based
on
this
NOAEL,
and
an
UF
of
100,
the
chronic
RfD
and
the
chronic
population
adjusted
dose
(
cPAD)
for
lactofen
has
been
set
at
0.008
mg/
kg/
day.
The
NOAEL
from
the
rat
developmental
study,
50
mg/
kg/
day,
was
selected
as
the
acute
oral
toxicity
endpoint.
Based
on
this
NOAEL
and
an
UF
of
100,
the
acute
RfD
for
lactofen
has
been
set
at
0.50
mg/
kg/
day.
An
acute
adjusted
dose
(
aPAD)
of
0.17
mg/
kg/
day
was
calculated
using
this
endpoint
and
an
additional
Food
Quality
Protection
Act
(
FQPA)
safety
factor
of
3.
This
aPAD
will
only
be
used
to
assess
acute
exposures
to
the
females
13
to
50
year
old
population
subgroup
since
it
is
derived
from
a
developmental
toxicity
endpoint.
No
other
acute
endpoints
were
identified
to
assess
acute
exposures
to
other
populations.
i.
Food.
Dietary
risk
was
considered
for
the
currently
registered
uses
of
lactofen
on
soybeans,
snap
beans,
and
cotton
and
for
the
pending
use
on
peanuts.
Dietary
risk
assessments
were
done
using
the
Dietary
Exposure
Evaluation
Model
(
DEEMTM),
which
incorporates
consumption
data
generated
in
U.
S.
Department
of
Agriculture
(
USDA)
Continuing
Surveys
of
Food
Intakes
by
Individuals
(
CSFII),
1989
 
1992.
For
chronic
dietary
risk
assessments,
the
3
 
day
average
of
consumption
for
each
subpopulation
is
combined
with
residues
in
commodities
to
determine
average
exposure
in
mg/
kg/
day.
For
refined
acute
dietary
risk
assessments,
the
entire
distribution
of
consumption
events
for
individuals
is
multiplied
by
a
distribution
of
residues
to
obtain
a
distribution
of
exposures
in
mg/
kg/
day.
This
is
a
probabilistic
analysis,
referred
to
as
``
Monte
Carlo,''
and
the
risk
is
reported
at
the
99.9th
percentile
of
exposure.
Food
monitoring
data
are
not
available
from
Food
and
Drug
Administration
(
FDA)
or
USDA
for
residues
of
lactofen.
Therefore,
only
field
trial
data
were
used.
A
value
of
one­
half
the
LOQ,
0.005
ppm,
was
used
to
represent
the
residues
in
all
treated
commodities.
Percent
crop
treated
(
PCT)
were
incorporated
for
soybeans
and
snap
beans,
as
reliable
usage
information
was
available
for
these
commodities.
The
estimated
risk
from
food
is
presented
in
the
following
table:

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Notices
TABLE
1.
 
DIETARY
EXPOSURE
AND
RISK
TO
LACTOFEN
FROM
FOOD
SOURCES
Population
Acute
Endpoint
Chronic
Endpoint
Cancer
Endpoint2
Exposure
mg/
kg/
day
%
aPAD
Exposure
mg/
kg/
day
%
aPAD
Exposure
mg/
kg/
day
Risk
U.
S.
population
NA1
NA
1
x
10­
6
<
0.1
1
x
10­
6
8
x
10­
8
Females
13
to
50
2
x
10­
6
<
0.1
<
1
x
10­
6
<
0.1
NA
NA
Children
1
to
6
NA1
NA
2
x
10­
6
<
0.1
NA
NA
1Acute
endpoint
applies
only
to
females
of
childbearing
age.
2Cancer
risk
is
generally
reported
for
the
U.
S.
population.

ii.
Drinking
water.
Environmental
fate
properties
indicate
that
lactofen
is
not
very
persistent
or
mobile.
Hydrolysis
half­
lives
are
10.7,
4.6,
and
<
1.0
days
at
pH
5,
7,
and
9
at
40
°
C,
respectively.
This
temperature
most
likely
exceeds
temperatures
that
lactofen
would
be
expected
to
be
exposed
to
under
normal
conditions,
thus
the
hydrolysis
rates
are
probably
slower.
Aerobic
soil
metabolism
half­
lives
range
from
1
to
3
days.
Lactofen
has
a
low
probability
to
contaminate
drinking
water
because
it
has
a
short
half­
life
(
3
days
or
less)
and
high
binding
potential(
Koc>
1,000).
Limited
data
suggest
that
lactofen
conversion
to
acifluorfen
in
water
is
approximately
52%.
The
HED
MARC
has
concluded
that
the
residues
of
concern
in
drinking
water
are
acifluorfen
and
amino
acifluorfen.
Insufficient
information
is
available
to
estimate
the
amino
acifluorfen
concentration
in
water,
but
it
is
likely
to
be
less
than
that
of
acifluorfen.
Laboratory
studies
have
shown
that
acifluorfen
reaches
its
maximum
concentration
of
53.3%
of
applied
lactofen
at
7
days
following
application
and
it
is
most
likely
to
form
under
the
soil
surface.
Thus,
the
formed
acifluorfen
is
not
subject
to
drift,
erosion,
or
runoff
forces
that
contribute
to
surface
water
contamination.
Surface
water,
however,
could
be
contaminated
with
acifluorfen
from
lactofen
applications
via
spray
drift.
The
registrant
also
has
conducted
two
prospective
ground
water
studies
which
showed
that
neither
lactofen
nor
acifluorfen
from
lactofen
applications
contaminate
ground
water.
Therefore,
in
the
following
discussion,
the
potential
exposure
to
lactofen
from
drinking
water
will
address
only
potential
surface
water
contamination
with
lactofen
and
acifluorfen.
The
Tier
II
estimated
environmental
concentration
(
EEC)
assessment
in
surface
water
uses
a
single
site,
or
multiple
single
sites,
which
represents
a
high­
end
exposure
scenario
from
pesticide
use
on
a
particular
crop
or
non­
crop
use
site.
The
EEC's
for
lactofen
were
generated
for
the
standard
Mississippi
cotton
scenario.
The
Agency
has
implemented
the
concept
of
index
reservoirs
(
IR)
and
the
PCT
area
to
better
estimate
potential
residue
level
in
drinking
water
sources.
The
scenarios
used
with
EPA
pesticide
root
zone
model
(
PRZM)
and
exposure
analysis
modeling
systems
(
EXAMS)
to
estimate
lactofen
in
the
``
standard
pond''
were
rerun
with
the
IR
for
the
cotton
and
soybean
scenarios.
The
Agency
has
estimated
that
the
PCT
area
for
the
Mississippi
cotton
scenario
is
0.20
(
20%).
The
Office
of
Pesticide
Programs
(
OPP)
has
calculated
drinking
water
levels
of
comparison
(
DWLOCs)
for
acute
and
chronic
exposure
to
lactofen
and
acifluorfen
from
applications
of
lactofen
in
surface
water.
To
calculate
the
DWLOC
for
acute
exposure,
the
acute
dietary
food
exposure
from
the
DEEMTM
analysis
was
subtracted
from
the
aPAD.
To
calculate
the
DWLOC
for
chronic
(
non­
cancer)
exposure,
the
chronic
dietary
food
exposure
from
the
DEEMTM
analysis
was
subtracted
from
the
cPAD
to
obtain
the
acceptable
chronic
non­
cancer
exposure
to
lactofen
and
acifluorfen
in
drinking
water.
A
DWLOC
cancer
was
calculated
in
a
similar
manner,
assuming
a
negligible
risk
of
1
x
10­
6.
Assumptions
used
in
calculating
the
DWLOCs
include
70
kg
bwt
for
the
U.
S.
population,
60
kg
bwt
for
adult
females,
10
kg
bwt
for
children,
2
liters
of
water
consumption
per
day
for
adults,
and
1
liter
consumption
for
children.

TABLE
2.
 
DIETARY
EXPOSURE
AND
RISK
TO
LACTOFEN
FROM
DRINKING
WATER
Population
Acute
Endpoint
Chronic
Endpoint
Cancer
Endpoint2
Exposure
µ
g/
L
DWLOC
µ
g/
L
Exposure
µ
g/
L
DWLOC
µ
g/
L
Exposure
µ
g/
L
DWLOC
µ
g/
L
U.
S.
population
NA1
NA
0.022
280
0.012
0.3
Females
13
to
50
0.62
5,100
0.022
240
­
­

Children
1
to
6
NA1
NA
0.022
80
­
­

1
Acute
endpoint
applies
only
to
females
of
childbearing
age.
2
Cancer
risk
is
generally
reported
for
the
U.
S.
population.

TABLE
3.
 
DIETARY
EXPOSURE
AND
RISK
TO
ACIFLUORFEN1
FROM
DRINKING
WATER
Population
Acute
Endpoint
Chronic
Endpoint
Cancer
Endpoint3
Exposure
µ
g/
L
DWLOC
µ
g/
L
Exposure
µ
g/
L
DWLOC
µ
g/
L
Exposure
µ
g/
L
DWLOC
µ
g/
L
U.
S.
population
NA2
NA
0.99
140
0.34
0.7
Females
13
to
50
4.9
600
0.99
120
­
­

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29,
2003
/
Notices
TABLE
3.
 
DIETARY
EXPOSURE
AND
RISK
TO
ACIFLUORFEN1
FROM
DRINKING
WATER
 
Continued
Population
Acute
Endpoint
Chronic
Endpoint
Cancer
Endpoint3
Exposure
µ
g/
L
DWLOC
µ
g/
L
Exposure
µ
g/
L
DWLOC
µ
g/
L
Exposure
µ
g/
L
DWLOC
µ
g/
L
Children
1
to
6
NA2
NA
0.99
40
­
­

1
Acifluorfen
derived
from
applications
of
lactofen.
2
Acute
endpoint
applies
only
to
females
of
childbearing
age.
3
Cancer
risk
is
generally
reported
for
the
U.
S.
population.

HED
has
a
concern
if
the
DWLOC
for
any
scenario
is
below
the
estimated
environmental
concentration
from
the
models.
All
of
the
DWLOCs
shown
in
the
tables
above
exceed
the
estimated
EECs.
2.
Non­
dietary
exposure.
Lactofen
is
proposed
only
for
agricultural
uses
and
no
home
owner
or
turf
uses.
Thus,
no
non­
dietary
risk
assessment
is
needed.

D.
Cumulative
Effects
Section
408(
b)(
2)(
D)(
v)
requires
that
the
Agency
must
consider
``
available
information''
concerning
the
cumulative
effects
of
a
particular
pesticide's
residues
and
``
other
substances
that
have
a
common
mechanism
of
toxicity.''
Available
information
in
this
context
include
not
only
toxicity,
chemistry,
and
exposure
data,
but
also
scientific
policies
and
methodologies
for
understanding
common
mechanisms
of
toxicity
and
conducting
cumulative
risk
assessments.
For
most
pesticides,
although
the
Agency
has
some
information
in
its
files
that
may
turn
out
to
be
helpful
in
eventually
determining
whether
a
pesticide
shares
a
common
mechanism
of
toxicity
with
any
other
substances,
EPA
does
not
at
this
time
have
the
methodologies
to
resolve
the
complex
scientific
issues
concerning
common
mechanism
of
toxicity
in
a
meaningful
way.
There
are
other
pesticidal
compounds
that
are
structurally
related
to
lactofen
and
have
similar
effects
on
animals.
In
consideration
of
potential
cumulative
effects
of
lactofen
and
other
substances
that
may
have
a
common
mechanism
of
toxicity,
there
are
currently
no
available
data
or
other
reliable
information
indicating
that
any
toxic
effects
produced
by
lactofen
would
be
cumulative
with
those
of
other
chemical
compounds.
Thus,
only
the
potential
risks
of
lactofen
have
been
considered
in
this
assessment
of
aggregate
exposure
and
effects.
Valent
will
submit
information
for
EPA
to
consider
concerning
potential
cumulative
effects
of
lactofen
consistent
with
the
schedule
established
by
EPA
in
the
Federal
Register
of
August
4,
1997
(
62
FR
42020)
(
FRL­
5734
 
6),
and
other
subsequent
EPA
publications
pursuant
to
FQPA.
E.
Safety
Determination
1.
U.
S.
population.
Water
is
not
expected
to
be
a
significant
source
of
exposure
for
lactofen,
as
it
degrades
quickly
in
the
environment
to
numerous
degradates,
including
acifluorfen.
EECs
for
lactofen
and
acifluorfen
are
well
below
the
DWLOC
for
chronic,
acute,
and
cancer
risk.
Therefore,
the
only
significant
source
of
human
exposure
to
lactofen
is
in
food.
Residues
of
lactofen
are
generally
non­
detectable
at
a
LOQ
of
0.005
ppm,
in
all
food
forms.
The
exposure
is
<
0.1%
of
the
acute
and
chronic
PAD
for
all
population
subgroups.
Exposure
is
generally
not
of
concern
if
it
is
less
than
100%
of
the
PAD.
The
estimated
cancer
risk
for
the
U.
S.
population
is
8
x
10­
8,
which
is
more
than
an
order
of
magnitude
less
than
the
risk
that
is
generally
considered
negligible
1
x
10­
6.
2.
Infants
and
children.
As
stated
above,
dietary
exposure
assessments,
including
drinking
water,
utilize
less
than
0.1%
of
the
acute
and
chronic
PADs
for
all
population
subgroups,
including
infants
and
children.
Reproduction
and
developmental
effects
have
been
found
in
toxicology
studies
for
lactofen
but
only
at
levels
that
were
also
maternally
toxic.
This
indicates
that
developing
animals
are
not
more
sensitive
than
adults.
FQPA
requires
an
additional
safety
factor
of
up
to
10
for
chemicals
which
present
special
risks
to
infants
or
children.
Lactofen
does
not
meet
the
criterion
for
application
of
an
additional
safety
factor
for
infants
and
children.
The
FQPA
Safety
Factor
Committee
met
on
March
13,
2000
to
evaluate
the
hazard
and
exposure
data
for
lactofen
and
recommended
that
FQPA,
safety
factor
for
protection
of
infants
and
children
should
be
reduced
to
3x
for
lactofen.
This
safety
factor
was
reduced
to
3x
by
The
FQPA,
Safety
Factor
Committee
because
available
data
provide
no
indication
of
quantitative
or
qualitative
increased
susceptibility
from
in
utero
and/
or
postnatal
exposure
to
lactofen
in
rats.
Information
on
the
reproduction
and
developmental
effects
caused
by
the
other
diphenyl
ether
herbicides
is
not
available
to
Valent.
Additional
time
is
needed
for
the
Agency
to
evaluate
the
need
for
an
additional
safety
factor
related
to
these
other
chemicals.
However,
even
if
an
additional
safety
factor
were
deemed
necessary,
the
dietary
exposures
are
still
expected
to
be
well
below
the
established
reference
doses.

F.
International
tolerances.

There
are
no
Codex
maximum
residue
limits
established
for
lactofen
on
cotton
or
peanut
commodities,
so
there
is
no
conflict
between
this
proposed
action
and
international
residue
limits.
[
FR
Doc.
03
 
2020
Filed
1
 
28
 
03;
8:
45
a
m]

BILLING
CODE
6560
 
50
 
S
ENVIRONMENTAL
PROTECTION
AGENCY
[
FRL
 
7445
 
4;
RCRA
 
2002
 
0029]

Land
Disposal
Restrictions:
Treatment
Standards
for
Mercury­
Bearing
Hazardous
Waste;
Notice
of
Data
Availability
AGENCY:
Environmental
Protection
Agency
(
EPA).
ACTION:
Notice
of
data
availability.

SUMMARY:
This
notice
of
data
availability
(
NODA)
makes
available
to
the
public
two
studies
conducted
on
the
treatment
of
mercury
wastes.
The
studies
were
initiated
to
help
evaluate
whether
EPA
could
propose
treatment
and
disposal
alternatives
to
the
current
land
disposal
restriction
(
LDR)
treatment
standard
of
mercury
retorting.
The
studies
were
performed
to
assess
conditions
that
affect
the
stability
of
waste
residues
resulting
from
the
treatment
of
high
mercury
(
greater
than
260
mg/
kg
total
mercury)
wastes.
This
NODA
also
makes
available
the
results
of
the
peer
review
of
these
studies.
As
a
result
of
our
investigation,
we
have
concluded
that
changes
to
our
national
regulations
are
impractical
at
this
time.
Additionally,
this
notice
also
provides
information
on
how
to
use
the
existing
treatability
variance
procedures
to
make
site­
specific
choices
on
alternatives
to
mercury
recovery.
The
treatability
studies
and
the
results
of
the
peer
review
are
presented
here
only
to
provide
information
 
we
are
not
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19:
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