Document ID: EPA-HQ-OPP-2006-0512-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-07-12T04:00Z

[
Federal
Register:
2006
(
Volume
,
Number
)]
[
Notices]
[
Page
]

­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­

ENVIRONMENTAL
PROTECTION
AGENCY
[
]

Pirimicarb:
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
pesticide
petitions
proposing
the
establishment
of
regulations
for
residues
of
a
certain
pesticide
chemical
in
or
on
various
food
commodities.

DATES:
Comments,
identified
by
docket
identification
(
ID)
number
OPP­
xxxxxx,
must
be
received
on
or
before
xxxxxx,
2006.

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:
George
LaRocca,
Registration
Division
(
7504P),
Office
of
Pesticide
Programs,
Environmental
Protection
Agency,
1200
Pennsylvania
Ave.,
NW.,
Washington,
DC
20460­
0001;
telephone
number:
(
703)
305­
6100;
e­
mail
address:
mailto:
larocca.
george@
epa.
gov.

SUPPLEMENTARY
INFORMATION:

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

You
may
be
potentially
affected
by
this
action
if
you
are
an
agricultural
producer,
food
manufacturer,
or
pesticide
manufacturer.
Potentially
affected
entities
may
include,
but
are
not
limited
to:
*
Industry
(
NAICS
code
111)
*
Crop
production
(
NAICS
code
112)
*
Animal
production
(
NAICS
code
311)
*
Food
manufacturing
(
NAICS
code
32532)
2
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
xxxxxx.
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.
Xxx,
One
Potomac
Yard,
2777
S.
Crystal
Drive,
Arlington,
VA
22202.
This
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.
1.
EPA
intends
to
work
towards
providing
electronic
access
to
all
of
the
publicly
available
docket
materials
through
EPA's
electronic
public
docket.
3
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.
When
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
e­
mail
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
xxxxxx.
The
system
is
an
  
anonymous
access''
system,
which
means
EPA
will
not
know
your
identity,
email
address,
or
other
contact
information
unless
you
provide
it
in
the
body
of
your
comment.
4
ii.
E­
mail.
Comments
may
be
sent
by
e­
mail
to:
opp­
docket@
epa.
gov
Attention:
Docket
ID
number
OPP­
xxxxxx.
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
xxxxxx.
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.
xxx,
One
Potomac
Yard,
2777
S.
Crystal
Drive,
Arlington,
VA.
Attention:
Docket
ID
number
OPP­
xxxxxx
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.
5
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
pesticide
petitions
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
these
pesticide
petitions
contain
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
these
pesticide
petitions.
Additional
data
may
be
needed
before
EPA
rules
on
the
pesticide
petitions.

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

Dated:
xxxxxxxx,
2006
xxxxxxxxx
Acting
Director,
Registration
Division,
Office
of
Pesticide
Programs.

Summary
of
Petition
The
petitioner's
summary
of
the
pesticide
petitions,
PP
2E6388,
PP
2E6509,
and
PP
0E6102,
is
printed
below
as
required
by
FFDCA
section
408(
d)(
3).
The
summary
of
the
pesticide
petitions
was
prepared
by
Syngenta
Crop
Protection,
Inc.
and
Interregional
Research
Project
Number
4
and
represents
the
view
of
the
pesticide
petitioners.
The
summary
of
the
pesticide
petitions
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.

Interregional
Research
Project
Number
4
PP
2E6388
(
Asparagus);
PP
2E6509
(
Leaf
Petioles
Subgroup)
and
PP
0E6102
(
Hops)
6
EPA
has
received
a
pesticide
petition
from
the
International
Research
Project
No.
4
(
IR­
4)
who
are,
on
behalf
of
Syngenta
Crop
Protection,
Inc,
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
combined
residues
of
pirimicarb
2­
(
dimethylamino)­
5,6­
dimethyl­
4­
pyrimidinyl
dimethylcarbamate
(
9Cl)
and
its
two
carbamate
metabolites:
desmethyl
pirimicarb
and
desmethylformamido
pirimicarb,
expressed
as
desmethyl
pirimicarb
in
or
on
the
raw
agricultural
commodities:
asparagus
at
0.01
ppm
,
hops
at
4.0
ppm,
and
the
leaf
petioles
subgroup
at
1.0
ppm.
EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408(
d)(
2)
of
the
FFDCA;
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
supports
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

EPA
has
determined
that
the
petition
contains
data
or
information
regarding
the
elements
set
forth
in
section
408(
d)(
2)
of
the
FFDCA;
however,
EPA
has
not
fully
evaluated
the
sufficiency
of
the
submitted
data
at
this
time
or
whether
the
data
supports
granting
of
the
petition.
Additional
data
may
be
needed
before
EPA
rules
on
the
petition.

A.
Residue
Chemistry
1.
Plant
metabolism.
Studies
of
the
nature
of
residues
in
3
diverse
crops,
potatoes,
apples,
and
lettuce,
have
demonstrated
that
pirimicarb
undergoes
very
extensive
metabolism,
with
the
residues
of
concern
in
primary
crops
being
both
pirimicarb
and
its
carbamate
metabolites.
Syngenta
Crop
Protection,
Inc.
proposes
that
combined
residues
of
pirimicarb,
2­(
dimethylamino)­
5,6­
dimethyl­
4­
pyrimidinyl
dimethylcarbamate
(
9Cl),
and
its
two
carbamate
metabolites
(
desmethyl
pirimicarb
and
desmethylformamido
pirimicarb)
expressed
as
desmethyl
pirimicarb
are
to
be
included
in
the
tolerance.

2.
Analytical
Method.
The
analytical
enforcement
method
uses
Gas
Chromatography
equipped
with
a
thermionic
nitrogen
specific
detector.
Crop
samples
are
macerated
with
methanol
and
then
filtered.
After
filtration,
the
methanol
is
evaporated
and
the
samples
resuspended
and
partitioned
with
hexane
and
hydrochloric
acid.
The
samples
are
left
overnight
to
allow
conversion
of
the
desmethylforamido
pirimicarb
metabolite
to
the
desmethyl
pirimicarb
metabolite.
The
hexane
layer
is
discarded
and
the
acidic
aqueous
layer
is
further
partitioned
with
ethyl
acetate.
Sodium
hydroxide
is
added
to
the
aqueous
layer
and
pirimicarb
and
its
carbamate
metabolites
are
extracted
with
dichloromethane.
This
method
has
been
validated
by
an
independent
laboratory,
with
a
limit
of
detection
of
7
0.01
ppm.

3.
Magnitude
of
residues.

Hops:
Three
field
trials
were
conducted
in
hops:
one
each
in
Idaho,
Oregon,
and
Washington.
Pirimor
50
 
DF
was
applied
2
times
at
an
interval
of
21(
 
2)
days
and
harvests
were
7(
 
1)
days
and
14(
 
1)
days
after
the
second
application.
There
were
some
exceptions
that
had
no
impact
on
the
proposed
tolerance:
in
the
Idaho
trial,
the
second
sampling
was
22
days
after
the
first
harvest
date
and
in
the
Washington
trials
the
application
rate
was
approximately
6%
and
10%
higher
than
the
intended
rate.
Combined
residues
of
pirimicarb
and
its
metabolites
in
hop
cones
harvested
6­
8
days
after
the
second
application
were
highest
in
the
Washington
samples,
at
approx.
3.1
ppm.
Combined
residues
of
pirimicarb
and
its
metabolites
in
hop
cones
harvested
14­
15
days
after
the
second
application
were
also
highest
in
the
Washington
samples,
at
approx.
2.2
ppm.
The
second
harvest
in
the
Idaho
trial
at
22
days
after
the
last
application
produced
a
combined
residue
of
approx.
0.8
ppm.
Asparagus:
Trials
were
conducted
in
California
(
3
trials),
Washington
(
2
trials),
Wisconsin
(
2
trials),
and
New
Jersey.
Asparagus
plots
were
treated
3
times
after
the
last
harvest
with
Pirimor
®
50
DF
at
approx.
0.25
lb
ai/
A,
except
in
the
two
trials
conducted
in
Washington
in
which
the
application
rate
was
approx.
0.2
lb
ai/
A
which
is
the
proposed
application
rate
.
Spear
samples
were
taken
the
following
growing
season
for
analysis
to
determine
the
magnitude
of
combined
residues
of
pirimicarb
and
its
metabolites.
No
residues
of
pirimicarb
or
its
carbamate
metabolites
above
the
limit
of
quantitation
(
0.01
ppm)
were
found
in
any
of
the
treated
samples
from
this
study.
Leaf
Petioles
Subgroup:
Celery
is
the
representative
commodity
for
the
leaf
petioles
subgroup.
Crop
residue
field
trials
were
conducted
in
celery
in
California
(
3
trials),
Florida
(
2
trials),
Oregon
(
2
trials),
Ohio,
and
Ontario,
Canada.
Pirimor
®
50­
DF
was
applied
as
a
foliar
spray
at
approx.
0.25
lb
ai/
acre
three
times
at
intervals
of
6­
8
days.
There
were
some
exceptions:
in
the
Ontario
trial,
the
treatment
intervals
were
7
and
9
days,
and
the
first
application
was
0.313
lb
ai/
acre,
in
one
of
the
Florida
trials
(
FL16),
a
total
of
five
applications
were
made
because
the
crop
was
not
ready
for
harvest
after
the
first
three
sprays.
In
all
of
the
trials,
treated
and
untreated
samples
were
collected
2­
3
days
after
the
last
application.
Residues
of
pirimicarb
were
in
the
range
0.0533­
0.703
ppm.
Desmethyl
pirimicarb
residues
were
in
the
range
0.0230­
0.858.
No
detectable
residues
of
R238177
were
found
in
any
of
the
treated
samples.
The
highest
residues
were
found
in
samples
from
trial
FL16,
in
which
5
applications
were
made.
The
residue
data
support
application
of
Pirimor
50­
DF
at
0.5
lb
(
0.25
lb
active)
per
acre
up
to
a
maximum
of
0.75
lb
ai/
A
per
year
with
a
3
day
PHI.

B.
Toxicological
Profile
1.
Acute
toxicity.
Like
other
N­
methyl
carbamate
insecticides,
pirimicarb
induces
toxic
signs
that
are
characteristic
of
cholinesterase
inhibition.
These
effects
are
rapidly
reversed
when
exposure
ceases
and
recovery
is
usually
complete.
The
acute
toxicity
of
technical
pirimicarb
is
classified
as
acute
toxicity
Category
II
based
on
the
acute
oral
toxicity
in
the
rat.
8
Pirimicarb
Technical
Toxicity
Summary:

Toxicity
Test
Results
Toxicity
Category
Acute
Oral
Rat
LD50
152
mg/
kg
(
m),
142
mg/
kg
(
f)
II
Acute
Dermal
Rat
LD50
>
1000
mg/
kg
(
f)
III
Acute
Inhalation
Rat
0.95
mg/
L
(
m);
0.86
mg/
L
(
f)
III
Eye
Irritation
Rabbit
Non­
irritant
IV
Skin
Irritation
Rabbit
slight
irritant
IV
Skin
Sensitization
moderate
may
cause
allergic
reaction
The
acute
toxicity
of
the
formulated
product,
Pirimor
®
50­
DF
is
classified
as
acute
toxicity
Category
II
based
on
acute
oral
toxicity
in
the
rat
and
eye
irritation
in
the
rabbit.

Formulated
Material
(
PIRIMOR
®
50­
DF)
Toxicity
Summary:

Toxicity
Test
Results
Toxicity
Category
Acute
Oral
Rat
LD50
87
mg/
kg
II
Acute
Dermal
Rat
LD50
>
2000
mg/
kg
III
Acute
Inhalation
Rat
1.7
mg/
L
(
f)
III
Eye
Irritation
Rabbit
moderate
irritant
II
Skin
Irritation
Rabbit
slight
irritant
IV
Skin
Sensitization
not
a
sensitizer
­­­­­­­

2.
Genotoxicity.
Pirimicarb
has
been
evaluated
for
genotoxicity
and
mutagenicity.
As
reported
in
the
EPA's
Cancer
Assessment
Review
Committee
(
CARC)
report
for
pirimicarb
(
July
13,
2005),
pirimicarb
was
not
mutagenic
in
bacteria
and
did
not
induce
a
clastogenic
response
in
mammalian
cell
in
vitro
or
micronuclei
in
the
bone
marrow
of
treated
mice.
However,
there
was
a
positive
response
in
an
in
vitro
mammaliancell
gene
mutation
assayy
with
L5178Y
mouse
lymphoma
cells;
mutagenic
activity
was
reproducible,
confined
to
the
S9­
activated
portion
of
the
assay,
concentrated­
related
and
occurred
at
severly
cytotoxic
levels
(
causing
10%
survival)
to
levels
where
>
50%
of
the
cells
survived.
3.
Reproductive
and
developmental
toxicity.
Pirimicarb
was
not
teratogenic
to
rats
when
tested
in
a
study
using
oral
gavage
dose
levels
of
0,
10,
25
and
75
mg/
kg/
day.
Fetotoxicity
in
the
presence
of
maternal
toxicity
was
observed
at
75
mg/
kg/
day,
but
there
9
were
no
effects
on
mother
or
fetus
at
a
dose
level
of
25
mg/
kg/
day.
The
overall
NOEL
for
fetotoxicity
was
therefore
25
mg/
kg/
day
in
the
rat.
Pirimicarb
was
not
teratogenic
in
the
rabbit
when
tested
in
a
study
using
oral
gavage
dose
levels
of
0,
2,
10
or
60
mg/
kg/
day.
Maternal
toxicity
was
observed
at
60
mg/
kg/
day,
but
there
were
no
effects
on
the
fetus
at
any
dose
level.
There
was
no
evidence
of
fetotoxicity
or
teratogenicity
in
the
rabbit
at
doses
up
to
and
including
a
maternally
toxic
dose
of
60
mg/
kg/
day.
Neither
study
showed
effects
on
the
fetus
in
the
absence
of
effects
on
the
mother,
and
thus
there
was
no
evidence
of
enhanced
fetal
susceptibility
to
pirimicarb.
Pirimicarb
showed
no
evidence
of
reproductive
toxicity
to
rats
in
a
2
generation
reproductive
toxicity
study
using
dose
levels
of
0,
50,
200
or
750
ppm.
There
were
no
effects
on
reproductive
parameters
at
750
ppm
(
88
mg/
kg/
day),
the
highest
dose
tested
(
HDT)

4.
Subchronic
toxicity.
a.
Rat:
90­
day
feeding
studies.
In
a
number
of
repeat
dose
studies,
male
and
female
rats
were
fed
diets
containing
0,
175,
250,
or
750
ppm
of
pirimicarb
for
a
period
of
56
­
90
days.
There
were
no
adverse
clinical,
hematological,
or
pathological
effects.
The
only
effect
was
a
reduction
in
body
weight
gain
that
was
clearly
evident
in
2
studiesat
750
ppm;
in
another
study
slight
effects
were
seen
at
250
ppm.
The
NOEL
for
subchronic
toxicity
in
the
rat
was
concluded
to
be
175
ppm
(
17.5
mg/
kg/
day).

b
Dog:
90­
day
feeding
study
Groups
of
4
male
and
4
female
beagle
dogs
were
dosed
with
pirimicarb
by
capsule
at
0,
0.4
or
1.8
mg/
kg/
day
as
an
oral
dose
for
a
period
of
at
least
90
days;
a
further
group
received
pirimicarb
at
4
mg/
kg/
day
for
180
days.
There
were
no
adverse
clinical
or
pathological
effects,
but
the
animals
receiving
4
mg/
kg/
day
showed
evidence
of
increased
erythropoetic
activity
in
the
bone
marrow.
The
NOEL
in
this
study
was
1.8
mg/
kg/
day.

c.
Rat:
21­
day
dermal
study.
Pirimicarb
was
assessed
for
its
sub­
acute
dermal
toxicity
in
the
rat.
.
Over
a
period
of
21
days
groups
of
5
male
and
5
female
rats
received15,
6­
hour
dermal
applications
of
pirimicarb
applied
as
a
paste
in
deionized
water
at
dosages
of
40,
200,
or
1000
mg/
kg
.
There
were
no
signs
of
skin
irritation
and
no
indications
of
systemic
toxicity.
Test
animals
that
received
the
1000
mg/
kg
dose
showed
a
small
reduction
in
brain
cholinesterase.
The
NOAEL
was
200
mg/
kg.

5.
Neurotoxicity.
i.
Acute
neurotoxicity.
In
an
acute
neurotoxicity
study,
pirimicarb
was
administered
as
a
single
oral
dose
at
levels
of
0,
10,
40,
or
110
mg/
kg
body
weight.
The
animals
were
observed
up
to
14
days.
A
neurotoxicity
screening
battery
of
tests
including
a
functional
observational
battery
and
quantitative
measurement
of
motor
activity
was
evaluated
one
week
prior
to
the
study,
and
on
days
1,
8,
and
15.
Administration
of
110
mg/
kg
resulted
in
early
mortalities
and
adverse
clinical
signs.
Brain
neurotoxic
esterase
activity
was
not
affected
by
treatment.
Changes
at
the
40
mg/
kg
dose
were
transient
and
not
accompanied
by
biologically
significant
reductions
in
brain
or
erythrocyte
cholinesterase
activity.
It
is
concluded
that
pirimicarb
shows
reversible
clinical
signs
of
neurotoxicity
following
administration
of
a
single
oral
dose
of
110
mg/
kg.
The
NOEL
for
clinical
signs
of
transient
acute
neurotoxicity
is
40
mg/
kg/
day.
The
NOEL
for
this
study
is
10
mg/
kg/
day
10
ii.
Subchronic
neurotoxicity.
A
subchronic
rat
neurotoxicity
study
was
performed
in
which
pirimicarb
was
fed
to
rats
at
levels
of
0,
75,
250,
and
1000
ppm
for
90
days.
A
neurotoxicity
screening
battery
of
tests,
including
a
functional
observational
battery
and
a
quantitative
assessment
of
motor
activity
was
evaluated
in
weeks
1,
5,
9,
and
14.
After
90
days
neurotoxic
esterase
activity
in
the
brain
and
histopathological
assessment
were
performed
.
Reduced
growth
and
food
consumption/
utilization
were
observed
at
250
and
1000
ppm.
There
were
no
treatment­
related
effects
on
the
functional
observational
battery,
motor
activity,
cholinesterase,
neurotoxic
esterase
activities
and
neuropathology.
The
NOEL
for
subchronic
neurotoxicity
was
1000
ppm
(
approximately
81
mg/
kg/
day).

6.
Chronic
toxicity.
In
two
chronic
feeding
studies,
dogs
were
dosed
at
levels
up
to
25
mg/
kg/
day
for
either
1
or
2
years.
Pirimicarb
produced
hemolytic
anemia
or
related
hematological
changes
in
a
very
small
proportion
of
dogs.
Prolonged
administration
of
pirimicarb
was
required
to
produce
this
effect
and
it
was
reversible
when
exposure
to
pirimicarb
ceased.
This
effect
was
not
observed
in
toxicity
studies
in
the
rat
and
mouse.
A
clear
NOEL
of
3.5
mg/
kg/
day
was
established
based
on
hematological
changes
in
all
of
the
available
studies.

As
reported
in
the
EPA's
Cancer
Assesssment
Review
Committee
(
CARC)
report
for
pirmicarb
(
July
2005),
three
carcinogenicity
studies
were
conducted
with
pirimicarb:
one
rat
study
and
two
mice
studies.
In
a
2­
year
rat
chronic
toxicity
pirimicarb
was
fed
for
up
to
two
years
at
0,
75,
250
and
750
ppm.
The
maximum
tolerated
dose
was
750
ppm,
with
no
carcinogenic
response
over
2
years.
A
NOEL
was
established
at
250
ppm
(
12.3
mg/
kg/
day).

In
one
mouse
carcinogenicity
study,
mice
were
fed
pirimicarb
at
0,
200,
400,
and
1600
ppm.
The
CARC
considered
the
resulting
male
and
female
liver
and
lung
tumors,
and
the
female
ovarian
papillary
and
mammary
gland
tumors
to
be
treatment
related.

In
the
other
mouse
carcinogenicity
study
mice
were
fed
pirimicarb
at
0,
50,
200,
and
700
ppm.
It
was
concluded
that
there
was
an
increase
of
incidence
of
benign
lung
tumors
in
female
mice
at
the
top
dose
of
700
ppm
only.
The
EPA
categorized
pirmicarb
as
"
likely
to
be
carcinogenic
to
humans"
based
on
multiple
benign
and/
or
malignant
tumors
in
mice.
The
CARC
recommended
that
a
linear
low­
dose
extrapolation
approach
(
Q1*)
be
used
to
estimate
human
cancer
risk.
Based
on
the
tumor
response
in
mice
the
Q1*
was
determined
to
be
3.526
x
10­
2
6.
Animal
metabolism.
Studies
in
the
rat
and
dog
with
radiolabeled
pirimicarb
demonstrated
that
following
oral
administration,
pirimicarb
is
well
absorbed,
extensively
metabolized,
and
the
metabolites
are
rapidly
eliminated.
Metabolism
following
a
single
oral
dose
is
quantitatively
similar
in
rats
and
dogs
and
there
is
no
evidence
of
bioaccumulation.

7.
Metabolite
toxicology.
Pirimicarb
and
its
carbamate
metabolites
are
associated
with
acute
effects
of
cholinesterase
inhibition.

8.
Endocrine
disruption.
Pirimicarb
shows
no
evidence
of
hormonal
effects.
Therefore
there
is
no
evidence
of
endocrine
disruption.
There
are
no
toxicity
endpoints
involving
reproductive
organs
in
either
male
or
female
animals
in
any
of
these
studies.
11
C.
Aggregate
Exposure
1.
Dietary
exposure.
Currently
there
are
no
food
use
tolerances
established
for
pirmicarb;
the
current
EPA­
approved
use
for
pirmicarb
is
limited
to
alfalfa
grown
for
seed
and
is
classified
as
a
non­
food
use.
Syngenta
Crop
Protection,
Inc.
has
already
filed
a
petition
for
tolerances
for
pirimicarb
in
or
on
apples,
lettuce
and
potatoes.
The
purpose
of
this
Notice
of
Filing
is
to
include
the
petition
for
tolerances
for
pirimicarb
in
or
on
asparagus,
the
leaf
petioles
subgroup
4B,
and
hops.

Using
the
Dietary
Exposure
Evaluation
Model
(
DEEM­
FCIDTM
version
2.03)
from
Exponent,
acute
(
Tier
1)
and
chronic
(
Tier
III)
dietary
exposure
was
evaluated
for
pirimicarb
in
apples,
asparagus,
the
leaf
petioles
subgroup,
lettuce,
hops,
and
potatoes
All
consumption
data
for
these
assessments
was
taken
from
the
USDA's
Continuing
survey
of
Food
Intake
by
individuals
(
CSFII)
with
the
1994­
96
consumption
database
and
the
Supplemental
CSFII
children's
survey
(
1998)
consumption
database.
The
percent
crop
treated
in
the
acute
exposure
assessment
was
assumed
to
be
100%
for
all
comodities.
For
the
chronic
exposure
assessments,
residue
values
were
taken
from
field
trials
in
which
pirimicarb
was
applied
at
the
maximum
intended
use
rate
and
samples
were
harvested
at
the
minimum
pre­
harvest
interval
(
PHI).
Average
field
trial
residue
values
were
entered
into
the
DEEM­
FCIDTM
software
with
an
adjustment
for
the
predicted
percent
of
the
crop
that
would
be
treated.
Secondary
residues
in
animal
commodities
were
not
included
in
these
exposure
assessments
based
on
the
lack
of
residue
in
potentially
fed
commodities
(
apples
and
potatoes)
and
the
absence
of
either
pirimicarb
or
any
other
metabolite
containing
the
carbamate
functionality
at
detectable
limits
in
the
animal
metabolism
studies.
Drinking
water
estimates
were
incorporated
directly
into
the
dietary
exposure
assessment
using
the
higher
of
the
estimated
drinking
water
concentrations
(
EDWCs)
for
surface
and
ground
water.

i.
Food.
Acute
Exposure:
The
Tier
I
pirimicarb
acute
dietary
risk
assessment
was
performed
for
all
population
subgroups
with
acute
exposure.
For
this
assessment
the
following
were
used:
acute
reference
dose
of
0.010
mg/
kg/
day
based
on
a
rat
neurotoxicity
study
with
a
no
observable
adverse
effect
level
(
NOAEL)
of
10
mg/
kg/
day,
an
uncertainty
factor
of
100X
for
intra­
and
interspecies
variations,
and
an
FQPA
safety
factor
of
10X
for
lack
of
a
developmental
neurotoxicity
study.

For
the
purpose
of
aggregate
risk
assessment,
the
exposure
values
were
expressed
in
terms
of
margin
of
exposure
(
MOE)
which
was
calculated
by
dividing
the
NOAEL
by
the
exposure
for
each
population
subgroup.
In
addition,
exposure
was
expressed
as
a
per
cent
of
the
reference
dose
(%
RfD).
Acute
dietary
(
food
only)
exposure
to
the
US
Population
resulted
in
an
MOE
of
11,660
(
9.6%
of
the
acute
RfD
of
0.010
mg/
kg/
day).
The
most
exposed
sub­
population
was
children
1­
2
years
old
with
an
MOE
of
10,071
(
9.9%
of
the
acute
RfD
of
0.010
mg/
kg/
day).
Since
the
benchmark
MOE
for
this
assessment
is
1,000
and
since
the
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
acute
dietary
(
food
only)
exposure
to
residue
arising
from
all
current
and
proposed
uses
of
pirimicarb.
12
Chronic
Exposure:
The
Tier
III
chronic
(
non­
cancer)
dietary
risk
assessment
for
pirimicarb
was
performed
for
all
population
subgroups.
The
following
values
were
used:
a
chronic
reference
dose
of
0.0035
mg/
kg/
day
based
on
a
chronic
feeding
study
in
the
dog
with
a
no
observable
adverse
effect
level
(
NOAEL)
of
3.5
mg/
kg/
day;
an
uncertainty
factor
of
100X
for
intra­
and
interspecies
variations,
and
an
FQPA
safety
factor
of
10X
based
on
the
lack
of
a
developmental
neurotoxicity
study.
For
the
purpose
of
aggregate
risk
assessment,
the
exposure
values
were
expressed
in
terms
of
margin
of
exposure
(
MOE)
which
was
calculated
by
dividing
the
NOAEL
by
the
exposure
for
each
population
subgroup.
In
addition,
exposure
was
expressed
as
a
percent
of
the
reference
dose
(
RfD).
Chronic
dietary
(
food
only)
exposure
to
the
US
population
resulted
in
an
MOE
of
429,721
(
0.2%
of
the
chronic
RfD
of
0.0035
mg/
kg/
day).
The
most
exposed
sub­
population
was
children
1­
2
years
old
with
an
MOE
of
216,761
(
0.5%
of
the
chronic
RfD
of
0.0035
mg/
kg/
day.
Since
the
benchmark
MOE
for
this
assessment
is
1,000
and
since
the
EPA
generally
has
no
concern
for
exposures
below
100%
of
the
RfD,
Syngenta
believes
that
there
is
a
reasonable
certainty
that
no
harm
will
result
from
chronic
(
non­
cancer)
dietary
(
food
only)
exposure
to
residues
arising
from
all
current
and
proposed
uses
of
pirimicarb.

Cancer
Exposure:
The
Tier
III
chronic
(
cancer)
dietary
risk
assessment
for
pirimicarb
was
performed
for
the
US
population
with
a
carcinogenic
potency
factor
(
Q1*)
of
0.03526
(
mg/
kg/
day)­
1
based
on
tumor
responses
in
mice.
Dietary
(
food
only)
cancer
exposure
to
pirimicarb
resulted
in
a
risk
of
2.88
x
10­
7.

ii.
Drinking
water.

Drinking
water
levels
of
comparison
(
DWLOC)
were
calculated
for
pirimicarb
for
adults
and
children
for
both
acute
and
chronic
exposures,
in
accordance
with
EPA's
Standard
Operating
Procedure
(
SOP)
for
Drinking
Water
Exposure
and
Risk
Assessments
(
11/
20/
97).
Drinking
water
exposure
from
surface
and
groundwater
for
pirimicarb
was
estimated
using
Tier
II
model
PRZM/
EXAMS
and
Tier
I
model
SCI­
GROW,
respectively.
The
exposure
estimates
and
DWLOCs
are
summarized
below:

Drinking
Water
Levels
of
Comparison
and
Acute
Exposure
Estimates
for
Pirimicarb
Population
Subgroup
SCI­
GROW
(
ug/
L)*
PRZM/
EXAMS
(
ug/
L)**
Acute
DWLOC
(
ug/
L)
Adult
­
US
Population
0.25
4.66
3385
Children
0.25
4.66
980
*
SCI­
GROW
estimate
based
on
highest
water
estimate
from
all
crop
uses
**
PRZM/
EXAMS
based
on
instantaneous
concentration
for
total
carbamate
residues
(
parent
+
metabolites)
13
Drinking
Water
Levels
of
Comparison
and
Chronic
Exposure
Estimates
for
Pirimicarb
Population
Subgroup
SCI­
GROW
(
ug/
L)*
PRZM/
EXAMS
(
ug/
L)**
Chronic
DWLOC
(
ug/
L)
Adult
­
US
Population
0.25
0.88
1225
Children
0.25
0.88
350
*
SCI­
GROW
estimate
based
on
highest
water
estimate
from
all
crop
uses
**
PRZM/
EXAMS
based
on
annualized
average
value
for
total
carbamate
residues
(
parent
+
metabolites)

Based
on
the
estimated
dietary
and
water
exposures
for
pirimicarb,
Syngenta
has
concluded
that
there
is
a
reasonable
certainty
of
no
harm
to
infants,
children
and
adults
resulting
from
potential
acute
or
chronic
aggregate
exposure
to
pirimicarb.

2.
Non­
dietary
exposure.
Pirimicarb
is
not
registered
for
either
indoor
or
outdoor
residential
uses.
Therefore
the
aggregate
risk
includes
drinking
water
and
food
exposure
only.

D.
Cumulative
Effects
Pirimicarb
is
a
member
of
the
N­
methyl
carbamate
class
of
chemistry.
These
carbamates'
common
mechanism
of
toxicity
is
the
inhibition
of
acetylcholinesterase.
The
EPA's
cumulative
risk
assessment
for
this
group
of
carbamates
is
in
progress
with
scheduled
completion
in
2006.

E.
Safety
Determination
1.
U.
S.
population.
Based
on
the
available
toxicity
data,
0.0035
mg/
kg/
day
is
the
chronic
reference
dose
based
on
a
chronic
feeding
study
in
the
dog
with
a
no
observable
adverse
effect
level
(
NOAEL)
of
3.5
mg/
kg/
day;
an
uncertainty
factor
of
100X
for
intra­
and
interspecies
variations,
and
an
FQPA
safety
factor
of
10X
based
on
the
lack
of
a
developmental
neurotoxicity
study.
The
acute
reference
dose
is
0.010
mg/
kg/
day
based
on
a
rat
neurotoxicity
study
with
a
no
observable
adverse
effect
level
(
NOAEL)
of
10
mg/
kg/
day,
an
uncertainty
factor
of
100X
for
intra­
and
interspecies
variations,
and
an
FQPA
safety
factor
of
10X
for
lack
of
a
developmental
neurotoxicity
study.
:
The
Tier
III
chronic
(
cancer)
dietary
risk
assessment
for
pirimicarb
was
performed
for
the
US
population
with
a
carcinogenic
potency
factor
(
Q1*)
of
0.03526
(
mg/
kg/
day)­
1
based
on
tumor
responses
in
mice.
Dietary
(
food
only)
cancer
exposure
to
pirimicarb
resulted
in
a
risk
of
2.88
x
10­
7.
Acute
dietary
(
food
only)
exposure
to
the
US
Population
resulted
in
9.6%
of
the
acute
RfD
of
0.010
mg/
kg/
day).
Chronic
dietary
(
food
only)
exposure
to
the
US
population
resulted
in
0.2%
of
the
chronic
RfD
of
0.0035
mg/
kg/
day.
Drinking
water
levels
of
comparison
(
DWLOC)
were
calculated
for
pirimicarb
for
adults
and
children
for
both
acute
and
chronic
exposures,
in
accordance
with
EPA's
Standard
Operating
Procedure
(
SOP)
for
Drinking
Water
Exposure
and
Risk
Assessments
(
11/
20/
97).
Drinking
water
exposure
from
surface
and
groundwater
for
pirimicarb
was
estimated
using
Tier
II
model
PRZM/
EXAMS
and
Tier
I
model
SCI­
GROW,
respectively
14
2.
Infants
and
children.
Developmental
toxicity
and
reproductive
toxicity
studies
have
not
shown
fetal
effects
other
than
mild
fetotoxicity
in
the
rat
(
reduced
fetus/
litter
weight
and
indications
of
delayed
development)
at
doses
which
were
also
toxic
to
the
mother.
There
was
no
evidence
in
these
studies
of
any
extra
susceptibility
of
the
fetus.
Neither
has
there
been
any
indication
of
any
particular
susceptibility
of
juvenile
animals.
Based
on
the
database,
there
is
no
reason
to
consider
human
infants
and
children
to
be
inherently
more
at
risk
of
toxicity
from
pirimicarb
than
adults.
Chronic
dietary
(
food
only)
exposure
for
most
exposed
sub­
population,
children
1­
2
years
old,
will
be
0.5%
of
the
chronic
RfD
of
0.0035
mg/
kg/
day.

FFDCA
section
408
provides
that
EPA
may
apply
an
additional
safety
factor
for
infants
and
children
in
the
case
of
threshold
effects
to
account
for
pre­
and
post­
natal
toxicity
and
the
completeness
of
the
database.
Based
on
the
current
toxicological
data
requirements,
the
database
relative
to
pre­
and
post­
natal
effects
for
children
is
complete.
No
additional
FQPA
safety
factor
is
required
for
pirimicarb.

F.
International
Tolerances
The
CODEX
maximum
residue
levels
for
pirimicarb
and
its
carbamate
metabolites
(
desmethyl
and
desmethyl
formamido
pirimicarb)
are:
potatoes
0.05
ppm,
lettuce
1.0
ppm,
and
apples
(
pome
fruit)
1.0
ppm.