Flucarbazone-sodium; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food, 43412-43417 [05-14736]
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Federal Register / Vol. 70, No. 143 / Wednesday, July 27, 2005 / Notices
Office of Pesticide Programs (OPP),
Environmental Protection Agency, Rm.
119, Crystal Mall #2, 1801 S. Bell St.,
Arlington, VA, Attention: Docket ID
Number OPP–2005–0167. 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
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or by e-mail. You may claim
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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
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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
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information claimed as CBI, a copy of
the comment that does not contain the
information claimed as CBI must be
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docket and EPA’s electronic public
docket. If you submit the copy that does
not contain CBI on disk or CD ROM,
mark the outside of the disk or CD ROM
clearly that it does not contain CBI.
Information not marked as CBI will be
included in the public docket and EPA’s
electronic public docket without prior
notice. If you have any questions about
CBI or the procedures for claiming CBI,
please consult the person listed under
FOR FURTHER INFORMATION CONTACT.
E. What Should I Consider as I Prepare
My Comments for EPA?
You may find the following
suggestions helpful for preparing your
comments:
1. Explain your views as clearly as
possible.
2. Describe any assumptions that you
used.
3. Provide copies of any technical
information and/or data you used that
support your views.
4. If you estimate potential burden or
costs, explain how you arrived at the
estimate that you provide.
5. Provide specific examples to
illustrate your concerns.
6. Offer alternative ways to improve
the registration activity.
7. Make sure to submit your
comments by the deadline in this
notice.
8. To ensure proper receipt by EPA,
be sure to identify the docket ID number
assigned to this action in the subject
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line on the first page of your response.
You may also provide the name, date,
and Federal Register citation.
II. Registration Applications
EPA received applications as follows
to register pesticide products containing
active ingredients not included in any
previously registered products pursuant
to the provision of section 3(c)(4) of
FIFRA. Notice of receipt of these
applications does not imply a decision
by the Agency on the applications.
Products Containing Active Ingredients
not Included in any Previously
Registered Products
1. File symbol: 82100–R. Applicant:
PQ Corporation, P.O. Box 840, Valley
Forge, PA 19482–0840. Product name:
AgSilr 25. Type of product: Biochemical
pesticide. Active ingredient: Potassium
silicate at 29.1%. Proposed
classification/Use: Fungicide, miticide
and insecticide.
2. File symbol: 82100–E. Applicant:
PQ Corporation, P.O. Box 840, Valley
Forge, PA 19482–0840. Product name:
Technical Potassium Silicate. Type of
product: Biochemical pesticide. Active
ingredient: Potassium silicate at 100%.
Proposed classification/Use: Fungicide,
miticide and insecticide.
List of Subjects
Environmental protection, Pesticides
and pests.
Dated: July 11, 2005.
Janet L. Andersen,
Director, Biopesticides and Pollution
Prevention Division, Office of Pesticide
Programs.
[FR Doc. 05–14881 Filed 7–26–05; 8:45 am]
BILLING CODE 6560–50–S
ENVIRONMENTAL PROTECTION
AGENCY
[OPP–2005–0139; FRL–7727–2]
Flucarbazone-sodium; Notice of Filing
a Pesticide Petition to Establish a
Tolerance for a Certain Pesticide
Chemical in or on Food
Environmental Protection
Agency (EPA).
ACTION: Notice.
AGENCY:
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
identification (ID) number OPP–2005–
0139, must be received on or before
August 26, 2005.
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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: Jim
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:
ADDRESSES:
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–2005–
0139. 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, 1801 S. Bell St., Arlington, VA. This
docket facility is open from 8:30 a.m. to
4 p.m., Monday through Friday,
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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
https://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 https://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.
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
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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
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at https://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–2005–0139. 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–
2005–0139. 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–2005–0139.
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, 1801 S. Bell St.,
Arlington, VA, Attention: Docket ID
Number OPP–2005–0139. 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
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disclosed except in accordance with
procedures set forth in 40 CFR part 2.
In addition to one complete version of
the comment that includes any
information claimed as CBI, a copy of
the comment that does not contain the
information claimed as CBI must be
submitted for inclusion in the public
docket and EPA’s electronic public
docket. If you submit the copy that does
not contain CBI on disk or CD ROM,
mark the outside of the disk or CD ROM
clearly that it does not contain CBI.
Information not marked as CBI will be
included in the public docket and EPA’s
electronic public docket without prior
notice. If you have any questions about
CBI or the procedures for claiming CBI,
please consult the person listed under
FOR FURTHER INFORMATION CONTACT.
E. What Should I Consider as I Prepare
My Comments for EPA?
You may find the following
suggestions helpful for preparing your
comments:
1. Explain your views as clearly as
possible.
2. Describe any assumptions that you
used.
3. Provide copies of any technical
information and/or data you used that
support your views.
4. If you estimate potential burden or
costs, explain how you arrived at the
estimate that you provide.
5. Provide specific examples to
illustrate your concerns.
6. Make sure to submit your
comments by the deadline in this
notice.
7. To ensure proper receipt by EPA,
be sure to identify the docket ID number
assigned to this action in the subject
line on the first page of your response.
You may also provide the name, date,
and Federal Register citation.
List of Subjects
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Parts per million
Environmental protection,
Agricultural commodities, Feed
additives, Food additives, Pesticides
and pests, Reporting and recordkeeping
requirements.
Meat and meat byproducts except
liver (cattle, goats,
sheep, horses,
hogs)
0.01
Dated: July 18, 2005.
Donald R. Stubbs,
Acting Director, Registration Division, Office
of Pesticide Programs.
Liver (cattle, goats,
sheep, horses,
hogs)
1.50
Summary of Petition
The petitioner summary of the
pesticide petition is printed below as
required by FFDCA section 408(d)(3).
The summary of the petition was
prepared by the petitioner and
represents the view of the petitioner.
The petition summary announces the
availability of a description of the
analytical methods available to EPA for
the detection and measurement of the
pesticide chemical residues or an
explanation of why no such method is
needed.
Arvesta Corporation
PP 5F6949
EPA has received a pesticide petition
(PP 5F6949) from Arvesta Corporation,
100 First Street, Suite 1700, San
Francisco, CA 94105, proposing,
pursuant to section 408(d) of the
FFDCA, 21 U.S.C. 346a(d), to amend 40
CFR part 180 by establishing a tolerance
for residues of flucarbazone-sodium:
4,5-dihydro-3-methoxy-4-methyl-5-oxoN-[[2(trifluoromethoxy)phenyl]sulfonyl]-1H1,2,4-triazole 1-carboxamide, sodium
salt; and its N-desmethyl metabolite in
or on the raw agricultural commodities
(RACs):
Commodity
Parts per million
Wheat, forage
0.30
Wheat, grain
0.01
Wheat, hay
0.10
Wheat, straw
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.
Commodity
0.05
And combined residues of
flucarbazone-sodium and its metabolites
converted to 2(trifluoromethoxy)benzene sulfonamide
and calculated as flucarbazone-sodium
in or on the raw agricultural
commodities:
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Milk
Frm 00025
Parts per million
0.005
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EPA has determined that the petition
contains data or information regarding
the elements set forth in section
408(d)(2) of the FFDCA; however, EPA
has not fully evaluated the sufficiency
of the submitted data at this time or
whether the data supports granting of
the petition. Additional data may be
needed before EPA rules on the petition.
A. Residue Chemistry
1. Plant metabolism. The metabolism
of flucarbazone-sodium in wheat was
rapid and extensive. Little or no parent
flucarbazone-sodium was found in the
RACs. A primary metabolic pathway in
wheat involved the N-demethylation of
flucarbazone-sodium to give Ndesmethyl flucarbazone-sodium. Ndesmethyl flucarbazone-sodium was
found in all of the wheat RACs. The Ndesmethyl flucarbazone-sodium was
then either hydrolyzed or conjugated
with glucose. Another primary
metabolic pathway was hydrolysis of
flucarbazone-sodium yielding sulfonic
acid and sulfonamide which were
isolated, and N,O-dimethyl triazolinone
which was not isolated. Other
metabolites were then subsequently
formed by oxidative reactions,
hydrolytic reactions, and conjugation.
2. Analytical method—i. Plants. The
proposed tolerance expression is parent
flucarbazone-sodium and N-desmethyl
flucarbazone-sodium. An analytical
method was developed to measure these
two analytes in plant matrices. This
method was validated in wheat tissues.
The flucarbazone-sodium and Ndesmethyl flucarbazone-sodium
residues are extracted from the wheat
samples with 0.05 M NH4OH by
accelerated solvent extraction (ASE).
The extracts are purified by a
combination of C-18 solid phase
extraction (SPE) and ethylene diamineN-propyl (PSA) spe. The resultant
analytes are detected by liquid
chromatography/tandem mass
spectroscopy (lc/ms/ms) and quantified
against known amounts of deuterated
internal standards. The method limit of
quantitation (LOQ) is 0.01 milligram/
kilogram (mg/kg) of either analyte in all
wheat matrices. The method limit of
detection (LOD) is 0.005 mg/kg of either
analyte in all wheat matrices.
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ii. Animals. An analytical method was
developed to measure the residues of
flucarbazone-sodium in animal tissues
and milk. Since the flucarbazonesodium-related residues were present in
ruminant tissues as a mixture of bound,
conjugated, and unconjugated residues,
a method was developed that
simultaneously extracted and
hydrolyzed the majority of the
flucarbazone-sodium-related residues to
flucarbazone-sodium sulfonamide. The
flucarbazone-sodium residues are
simultaneously hydrolyzed to
flucarbazone-sodium sulfonamide and
extracted from the animal tissues and
milk by heating with 8% trifluoroacetic
acid (TFA) in water. The analysis of fat
was complicated by the large quantities
of lipids that were released during
hydrolysis and extraction. Therefore,
the flucarbazone-sodium residues are
extracted into acetonitrile/water (9:1)
before they are hydrolyzed to
flucarbazone-sodium sulfonamide. After
conversion to flucarbazone-sodium
sulfonamide, the residues are purified
and partitioned. The residues are
detected by lc/ms/ms and quantified
against known amounts of deuterated
internal standards. The LOQ in the
tissues and milk is 0.020 and 0.005 mg/
kg, respectively. The estimated LOD (3x
highest background response) in the
liver, muscle, and milk is 0.014, 0.002,
and 0.004 mg/kg, respectively. The
recoveries of flucarbazone-sodium were
determined in all tissues and milk after
fortification with flucarbazone-sodium.
The average recoveries of flucarbazonesodium from liver fortified at 0.020 and
0.100 mg/kg were 104 and 100%,
respectively. The average recoveries of
flucarbazone-sodium from muscle
fortified at 0.020 and 0.100 mg/kg were
97 and 102%, respectively. In milk, the
average recoveries of flucarbazonesodium at fortifications of 0.005, 0.010,
and 0.050 mg/kg were 111 (after
correction for background in the control
samples, the average recovery was
92%), 97 and 91%, respectively. An
independent laboratory validation of the
analytical method was performed. The
method was successfully validated
indicating that the method could be
satisfactorily run by following the
written procedure.
3. Magnitude of residues. Field trials
were conducted with wheat at 36
locations to evaluate the quantity of
flucarbazone-sodium residues in wheat
forage, hay, straw, and grain following
treatment with flucarbazone-sodium
70WG at a rate of 30 grams active
ingredient/hectacre (g ai/ha). The
highest average field trial (HAFT)
residue detected in forage, hay, and
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straw were 0.27, 0.08, and 0.04 mg/kg,
respectively. Residues of flucarbazonesodium were <0.01 mg/kg in wheat
grain.
B. Toxicological Profile
1. Acute toxicity—i. Flucarbazonesodium is not toxic to fasted rats
following a single oral administration.
The oral lethal dose (LD50) is >5,000 mg/
kg body weight (bwt) for males and
females.
ii. Flucarbazone-sodium is not toxic
to rats following a single dermal
application. The dermal LD50 is >5,000
milligrams/kilogram/body weight (mg/
kg/bwt) for males and females.
iii. An acute inhalation study with
rats showed low toxicity with a 4–hour
dust aerosol lethal concentration (LC50)
>5,130 mg/m3 air for males and females.
iv. An eye irritation study in rabbits
showed only very slight, reversible
irritation.
v. A dermal irritation study in rabbits
showed flucarbazone-sodium is not
irritating to skin.
vi. Flucarbazone-sodium has no skin
sensitizing potential under the
conditions of the maximization test in
guinea pigs.
2. Genotoxicity. The genotoxic action
of flucarbazone-sodium was studied in
bacteria and mammalian cells with the
aid of various in vitro test systems
(Salmonella microsome test,
hypoxanthine guanine phophoribosyl
transferase (HGPRT) test with Chinese
hamster V79 cells, cytogenetic study
with Chinese hamster V79 cells, and
unscheduled DNA synthesis test) and in
one in vivo test (micronucleus test).
None of the tests revealed any evidence
of a mutagenic or genotoxic potential of
flucarbazone-sodium. The compound
did not induce point mutation, DNA
damage, or chromosome aberration.
3. Reproductive and developmental
toxicity. In a 2–generation reproduction
study, Wistar rats were administered
dietary levels of flucarbazone-sodium at
levels of 0, 50, 4,000, and 20,000/12,000
parts per million (ppm) (dose reduction
week 6). The no observed adverse effect
levels (NOAELs) for reproductive
parameters was established at 4,000
ppm, based on slight reduction in pup
weight development at 12,000 ppm. The
NOAELs established for parental males
and females were 4,000 and 50 ppm,
respectively.
i. A developmental toxicity study was
conducted with Sprague-Dawley rats via
oral gavage of flucarbazone-sodium at
levels of 0, 100, 300, and 1,000
milligrams/kilogram body weight/day
(mg/kg bwt/day) on days 6 through 19
of gestation. There were no signs of
maternal toxicity, embryotoxicity,
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43415
fetotoxicity, or teratogenicity at the level
of 1,000 mg/kg bwt/day. Therefore, the
maternal and developmental NOAELs
for rats were established at >1,000 mg/
kg bwt/day, the limit dose for this study
type.
ii. Himalayan rabbits were
administered flucarbazone-sodium at
levels of 0, 100, 300, 500, or 1,000 mg/
kg/bwt by oral gavage days 6 through 28
post coitum in a test for developmental
toxicity. A maternal NOAEL of 100 mg/
kg bwt/day was established based on
clinical findings, body weight loss,
decreased feed consumption,
gastrointestinal changes, increased liver
weights, and fatty liver changes at 300
mg/kg bwt/day. The gestation rate
NOAEL of 100 mg/kg bwt/day was
based on one abortion (assessed as
secondary due to maternal toxicity) at
300 mg/kg bwt/day. The NOAEL for
fetal parameters of 300 mg/kg bwt/day
was based on decreased fetal weights
and delayed ossification at 500 mg/kg
bwt/day. No teratogenic potential of
flucarbazone-sodium was evident in
rabbits.
4. Subchronic toxicity—i. A 28–day
dermal rabbit study established a
systemic NOAEL of >1,000 mg/kg bwt/
day (the dermal limit dose) for males
and females. The local dermal effects,
skin thickening, seen at 1,000 mg/kg
were regarded as a result of mechanical
friction and of no toxicological
relevance.
ii. A 90–day rat feeding study defined
a NOAEL at 250 ppm (17.6 mg/kg bwt/
day) for males and 1,000 ppm (101.7
mg/kg bwt/day) for females based on a
decreased spleen weight in males at
1,000 ppm and on immunologic changes
at 4,000 ppm in females.
iii. A 90–day feeding study with male
and female B6C3F1 mice established a
NOAEL of 7,000 ppm (equivalent to
>2,083, and 3,051 mg/kg bwt/day for
males and females, respectively). The
dose of 7,000 ppm was the HDT.
iv. A 90–day dog feeding study at
levels of 0, 1,000, 5,000, and 50,000
ppm established a NOAEL of 1,000 ppm
(equivalent to 33.8 mg/kg bwt/day in
males and 35.2 mg/kg bwt/day in
females) based on decreased thyroxine
levels and increased thyroxine-binding
capacity, macroscopic and microscopic
effects on the gastric mucosa and an
eosinophilic hepatocellular cytoplasm
occurring at 5,000 ppm and above. The
liver enzyme induction at 1,000 ppm
was assessed as a slight adaptive
response in the detoxification process of
flucarbazone-sodium but not as an
adverse effect, due to the absence of
clinical chemical changes that would
indicate liver damage and due to the
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absence of any histopathologic liver
changes at this dietary level.
v. A 28–day (6 hours/day; 5 days/
week) subacute inhalation toxicity study
was conducted with male and female
Wistar rats exposed to mean actual
concentrations of 5.2, 30.0, 180.1 and
513.3 mg/m3 air. A NOAEL of 5.2 mg/
m3 air was established based on
histopathological changes observed at
30 mg/m3 air and above.
5. Chronic toxicity—i. A 2–year
chronic toxicity/oncogenicity study was
conducted with male and female Wistar
rats at dietary levels of 0, 2.5, 7.5, 125,
and 1,000 mg/kg bwt. A NOAEL of 125
mg/kg was established based on
increased food consumption (both
sexes) and lower body weights (females)
at 1,000 mg/kg. No carcinogenic
potential was indicated.
ii. B6C3F1 mice were administered
flucarbazone-sodium via the diet at
levels of 0, 50, 1,000, and 7,000 ppm in
a 2–year carcinogenicity study. The
NOAEL was established in males and
females at 1,000 ppm (equivalent to 275
and 459 mg/kg bwt/day, respectively)
based on reduced body weight gain in
both sexes and on increased feed
consumption in males at the 7,000 ppm
level. No carcinogenic potential was
indicated.
iii. A 1–year feeding study in dogs at
levels of 0, 200, 1,000, and 5,000 ppm
established a NOAEL of 1,000 ppm for
males (equal to 35.9 mg/kg bwt/day)
based on decreased body weight
development, increased ALAT- and
ASAT-levels and slightly increased Ndemethylase levels. The NOAEL of
1,000 ppm for females (equal to 37.1
mg/kg bwt/day) was based on body
weight gain depression, increased Ndemethylase levels, decreased T4 levels,
and marginally increased liver weight.
6. Animal metabolism. Flucarbazonesodium was metabolized via two
pathways. The major pathway involved
the hydrolysis of the urea linkage
forming sulfonamide and N,Odimethyltriazolinone. The sulfonamide
was shown to be the major metabolite in
the blood, fat, liver, and muscle at 4 to
6 hours following oral administration of
phenyl-UL-14C flucarbazone-sodium.
The sulfonamide was conjugated with
glucuronic acid or acetate sulfonamide
N-glucuronide or N-acetyl sulfonamide
or hydroxylated and then conjugated
with glucuronic acid to form
hydroxysulfonamide-O-glucuronide
prior to elimination in the urine. A
minor pathway involved Ndemethylation of flucarbazone-sodium
to form N-desmethyl flucarbazonesodium followed by hydrolysis to form
the sulfonamide and Omethyltriazolinone. Demethylation of
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N,Odimethyltriazolinone led to the
formation of N-methyltriazolinone, Omethyltriazolinone, and ultimately,
urazole; methyl urethane was probably
formed from the cleavage of Omethyltriazolinone.
7. Metabolite toxicology—i. The
animal and plant metabolite
flucarbazone-sodium sulfonamide
(trifluoromethoxysulfonamide) has a
low acute oral toxicity (LD50 >2,000 mg/
kg/bwt) in fasted rats.
ii. The plant metabolite flucarbazonesodium sulfonamide lactate conjugate
has no acute oral toxicity (NOAEL:
5,000 mg/kg/bwt) in fasted rats.
iii. The plant metabolite flucarbazonesodium sulfonamide alanine has no
acute oral toxicity (NOAEL: 5,000 mg/
kg/bwt) in fasted rats.
iv. The soil metabolite O-desmethyl
flucarbazone-sodium has an acute oral
LD50 value in fasted male and female
rats of >2,500 - <5,000 mg/kg bwt.
v. The plant, animal, and soil
metabolite, MKH 10868 (flucarbazonesodium sulfonic acid Na-salt), has no
acute oral toxicity (LD50 >5,000 mg/kg
bwt) in fasted male and female rats.
vi. MKH 10868 was considered nonmutagenic with and without S9 mix in
the plate incorporation as well as in the
preincubation modification of the
Salmonella/microsome test.
8. Endocrine disruption. There is no
evidence to suggest that flucarbazonesodium has an effect on the endocrine
system. Studies in this data base include
evaluation of the potential effects on
reproduction and development, and an
evaluation of the pathology of the
endocrine organs following short- and
long-term exposure. These studies
revealed no endocrine effects due to
flucarbazone-sodium.
9. Other studies—i. An acute
neurotoxicity screening study in rats
established an overall NOAEL for males
and females of 500 mg/kg based on
transient neurobehavioral effects.
Evidence of toxicity was only slight at
a limit dose of 2,000 mg/kg and
complete recovery occurred within 7
days following treatment.
ii. A subchronic neurotoxicity
screening study in rats established an
overall NOAEL of 2,000 ppm for males
(equal to 147 mg/kg bwt/day) and
20,000 ppm (equal to 1,736 mg/kg bwt/
day) for females based on a slight
decrease in body weight and food
consumption. The NOAEL for
microscopic lesions was 20,000 ppm for
males and females, the highest dose
tested (HDT). There was no evidence of
neurotoxicity at any dietary level.
iii. A plaque-forming-cell assay (to
investigate immunotoxicological
potential) was performed on rats after a
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4–week dietary exposure. The NOAEL
of 20,000 ppm (equivalent to 2,205 and
2,556mg/kg bwt/day in males and
females, respectively) was based on the
lack of specific effects in the HGT.
iv. The immunotoxicity potential of
flucarbazone-sodium was additionally
investigated in antibody plaque-cell
forming assays and in assays examining
splenic T-cells, B-cells, and NK-cells
after 4–week dietary administrations in
male and female rats at levels up to and
including 1,000 mg/kg bwt/day. There
was no statistically significant effect on
the humoral immune system and no
effects on splenic cell populations, cellmediated immune response, or the
innate immune response in males or
females. The NOAEL for
immunotoxicity from these studies was
1,000 mg/kg bwt/day, the
immunotoxicity limit dose.
C. Aggregate Exposure
1. Dietary exposure—i. Food.
Estimates of chronic dietary exposure to
residues of flucarbazone-sodium
utilized the proposed tolerance-level
residues for wheat forage, wheat hay,
wheat straw, wheat grain, meat, liver,
and milk of 0.30, 0.10, 0.05, 0.01, 0.01,
1.50, and 0.005 ppm, respectively. Other
assumptions were that 100% of the
target crop would be treated with
flucarbazone-sodium and that no loss of
residue would occur due to processing
and/or cooking. A chronic reference
dose (RfD) of 0.36 milligrams/kilogram/
day (mg/kg/day) was assumed based on
the NOAEL of 35.9 mg/kg/day from the
one year dog feeding study. A safety
factor of 100 was used based on
interspecies extrapolation (10x) and
intraspecies variability (10x). Using
these conservative assumptions, dietary
residues of flucarbazone-sodium
contribute 0.006659 mg/kg/day (2% of
the RfD) for children 1-6 years, the most
sensitive sub-population. For the U.S.
population, the exposure was 0.002891
mg/kg/day (1% of the RfD). For acute
dietary exposure, the same conservative
assumptions were made. Based on the
NOAEL of 300 mg/kg/day from the
rabbit developmental toxicity study, an
acute RfD of 3.0 mg/kg/day was used to
calculate the acute dietary risk to the
most exposed subgroup: females, 13 to
50 years old. The acute dietary exposure
from food to flucarbazone-sodium will
occupy <1% of the RfD for females, 13
to 50 years old.
ii. Drinking water. Given the postemergence application pattern, low use
rates and rapid soil degradation of
flucarbazone-sodium, the risk of ground
and surface water contamination and
exposure via drinking water is
negligible. The surface water model
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generic expected environment
concentration (GENEEC) and the ground
water model (SCI-GROW) were used to
determine whether drinking water from
surface or ground water sources
represented a worst-case exposure
scenario. These models predict residues
of flucarbazone-sodium would be higher
in surface water. Assuming a worst-case
GENEEC scenario where residues of
flucarbazone-sodium occur in surface
water used for drinking water at the
highest predicted acute and chronic
concentrations, the risk from exposure
to residues of flucarbazone-sodium are
well within EPA’s acceptable limits.
The GENEEC model predicted an
acute surface water concentration of
flucarbazone-sodium of 1.45 µg/L.
Assuming a 70 kilogram (kg) adult
drinks 2 liters/day containing 1.45 µg/L,
the acute exposure would be 0.0000414
mg/kg/day for adults. Assuming a 10 kg
child drinks 1 liter/day containing 1.45
µg/L, the exposure would be 0.000145
mg/kg/day. Based on the NOAEL of 300
mg/kg/day from the rabbit
developmental toxicity study and
assuming a safety of 100 (10x for
interaspecies variability and 10x for
interspecies extrapolation), the MOE for
adults of 72,500 and for children of
20,700 do not exceed EPA’s level of
concern for adults or children. This
assessment is based on the GENEEC
highest predicted acute concentration of
flucarbazone-sodium in drinking water
using worst-case assumptions.
Using GENEEC, the highest predicted
chronic (60–day exposure)
concentration of flucarbazone-sodium
was 1.44 µg/L. EPA interim policy
recommends that the 60–day GENEEC
value to be divided by an adjustment
factor of 3 to obtain a value for chronic
risk assessment calculations. Therefore,
a surface water value of 0.48 µg/L was
used for chronic risk assessment.
Assuming a 70 kg adult consumes 2
liters (L) of water per day containing
0.48 µg/L of flucarbazone-sodium
residues for a period of 70 years, less
than 0.004% of the RfD was consumed
from residues of flucarbazone-sodium in
surface water used for drinking water
(worst-case scenario). For a 10 kg child
drinking 1 L of water per day containing
0.48 µg/L of flucarbazone-sodium
residues, only 0.01% of the RfD was
consumed by drinking water.
2. Non-dietary exposure. There are no
current non-food uses for flucarbazonesodium registered under the Federal
Insecticide,Fungicide, and Rodenticide
Act (FIFRA), as amended. No non-food
uses are proposed for flucarbazonesodium. No non-dietary exposures are
expected for the general population.
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D. Cumulative Effects
Flucarbazone-sodium falls into the
category of sulfonamide herbicides.
There is no information to suggest that
any of this class of herbicides has a
common mechanism of mammalian
toxicity or even produce similar effects
so it is not appropriate to combine
exposures of flucarbazone-sodium with
other herbicides. Arvesta Corporation is
considering only the potential risk of
flucarbazone-sodium.
E. Safety Determination
1. U.S. population. As presented
previously, the exposure of the U.S.
general population to flucarbazonesodium is low, and the risks, based on
comparisons to the reference dose, are
minimal. The margins of safety from the
use of flucarbazone-sodium are well
within EPA’s acceptable limits. Arvesta
Corporation concludes that there is a
reasonable certainty that no harm will
result to the U.S. population from
aggregate exposure to flucarbazonesodium residues.
2. Infants and children. The complete
toxicological data base including the
developmental toxicity and 2–
generation reproduction studies were
considered in assessing the potential for
additional sensitivity of infants and
children to residues of flucarbazonesodium. The developmental toxicity
studies in rats and rabbits revealed no
increased sensitivity of rats or rabbits to
in-utero exposure to flucarbazonesodium. The 2–generation reproduction
study did not reveal any increased
sensitivity of rats to in-utero or
postnatal exposure to flucarbazonesodium. Furthermore, none of the other
toxicology studies revealed any data
demonstrating that young animals were
more sensitive to flucarbazone-sodium
than adult animals. The data taken
collectively clearly demonstrate that
application of a Food Quality Protection
Act (FQPA) uncertainty factor for
increased sensitivity of infants and
children is not necessary for
flucarbazone-sodium.
F. International Tolerances
A default Maximum Residue Limit
(MRL) of 0.01 ppm has been established
in Canada for residues of flucarbazonesodium and its N-desmethyl metabolite
on wheat grain. This value is consistent
with the tolerance being proposed in the
United States on wheat grain. There are
no harmonized MRLs at the European
Union level and no Codex MRLs for this
compound on wheat at present.
Therefore, no compatibility issues exist
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43417
with Codex in regard to the proposed
U.S. tolerances.
[FR Doc. 05–14736 Filed 7–26–05; 8:45 am]
BILLING CODE 6560–50–S
ENVIRONMENTAL PROTECTION
AGENCY
[OPP–2005–0166; FRL–7719–5]
Potassium Silicate; Notice of Filing a
Pesticide Petition to Establish a
Tolerance for a Certain Pesticide
Chemical in or on Food
Environmental Protection
Agency (EPA).
ACTION: Notice.
AGENCY:
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
identification (ID) number OPP–2005–
0166, must be received on or before
August 26, 2005.
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:
Carol E. Frazer, Biopesticides and
Pollution Prevention Division (7511C),
Office of Pesticide Programs,
Environmental Protection Agency, 1200
Pennsylvania Ave., NW., Washington,
DC 20460–0001; telephone number:
(703) 308–8810; e-mail
address:frazer.carol@epa.gov.
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does this Action Apply to Me?
You may be potentially affected by
this action if you an agricultural
producer, food manufacturer, or
pesticide manufacturer. Potentially
affected entities may include, but are
not limited to:
• Crop production (NAICS code 111)
• Animal production (NAICS code
112)
• Food manufacturing (NAICS code
311)
• Pesticide manufacturing (NAICS
code 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
E:\FR\FM\27JYN1.SGM
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]]>Agencies
[Federal Register Volume 70, Number 143 (Wednesday, July 27, 2005)]
[Notices]
[Pages 43412-43417]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 05-14736]
-----------------------------------------------------------------------
ENVIRONMENTAL PROTECTION AGENCY
[OPP-2005-0139; FRL-7727-2]
Flucarbazone-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 identification (ID) number OPP-
2005-0139, must be received on or before August 26, 2005.
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: Jim 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-2005-0139. 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, 1801 S. Bell St., Arlington, VA. This docket
facility is open from 8:30 a.m. to 4 p.m., Monday through Friday,
[[Page 43413]]
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 https://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 https://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.
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 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 https://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-2005-0139. 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-2005-0139. 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-2005-0139.
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, 1801 S. Bell St., Arlington, VA, Attention: Docket ID
Number OPP-2005-0139. 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
[[Page 43414]]
disclosed except in accordance with procedures set forth in 40 CFR part
2.
In addition to one complete version of the comment that includes
any information claimed as CBI, a copy of the comment that does not
contain the information claimed as CBI must be submitted for inclusion
in the public docket and EPA's electronic public docket. If you submit
the copy that does not contain CBI on disk or CD ROM, mark the outside
of the disk or CD ROM clearly that it does not contain CBI. Information
not marked as CBI will be included in the public docket and EPA's
electronic public docket without prior notice. If you have any
questions about CBI or the procedures for claiming CBI, please consult
the person listed under FOR FURTHER INFORMATION CONTACT.
E. What Should I Consider as I Prepare My Comments for EPA?
You may find the following suggestions helpful for preparing your
comments:
1. Explain your views as clearly as possible.
2. Describe any assumptions that you used.
3. Provide copies of any technical information and/or data you
used that support your views.
4. If you estimate potential burden or costs, explain how you
arrived at the estimate that you provide.
5. Provide specific examples to illustrate your concerns.
6. Make sure to submit your comments by the deadline in this
notice.
7. To ensure proper receipt by EPA, be sure to identify the docket
ID number assigned to this action in the subject line on the first page
of your response. You may also provide the name, date, and Federal
Register citation.
II. What Action is the Agency Taking?
EPA has received a pesticide petition as follows proposing the
establishment and/or amendment of regulations for residues of a certain
pesticide chemical in or on various food commodities under section 408
of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a.
EPA has determined that this petition contains data or information
regarding the elements set forth in FFDCA section 408(d)(2); however,
EPA has not fully evaluated the sufficiency of the submitted data at
this time or whether the data support granting of the petition.
Additional data may be needed before EPA rules on the petition.
List of Subjects
Environmental protection, Agricultural commodities, Feed additives,
Food additives, Pesticides and pests, Reporting and recordkeeping
requirements.
Dated: July 18, 2005.
Donald R. Stubbs,
Acting Director, Registration Division, Office of Pesticide Programs.
Summary of Petition
The petitioner summary of the pesticide petition is printed below
as required by FFDCA section 408(d)(3). The summary of the petition was
prepared by the petitioner and represents the view of the petitioner.
The petition summary announces the availability of a description of the
analytical methods available to EPA for the detection and measurement
of the pesticide chemical residues or an explanation of why no such
method is needed.
Arvesta Corporation
PP 5F6949
EPA has received a pesticide petition (PP 5F6949) from Arvesta
Corporation, 100 First Street, Suite 1700, San Francisco, CA 94105,
proposing, pursuant to section 408(d) of the FFDCA, 21 U.S.C. 346a(d),
to amend 40 CFR part 180 by establishing a tolerance for residues of
flucarbazone-sodium: 4,5-dihydro-3-methoxy-4-methyl-5-oxo-N-[[2-
(trifluoromethoxy)phenyl]sulfonyl]-1H-1,2,4-triazole 1-carboxamide,
sodium salt; and its N-desmethyl metabolite in or on the raw
agricultural commodities (RACs):
------------------------------------------------------------------------
Commodity Parts per million
------------------------------------------------------------------------
Wheat, forage 0.30
-------------------------------------------
Wheat, grain 0.01
-------------------------------------------
Wheat, hay 0.10
-------------------------------------------
Wheat, straw 0.05
------------------------------------------------------------------------
And combined residues of flucarbazone-sodium and its metabolites
converted to 2-(trifluoromethoxy)benzene sulfonamide and calculated as
flucarbazone-sodium in or on the raw agricultural commodities:
------------------------------------------------------------------------
Commodity Parts per million
------------------------------------------------------------------------
Milk 0.005
-------------------------------------------
Meat and meat byproducts except liver 0.01
(cattle, goats, sheep, horses, hogs)
-------------------------------------------
Liver (cattle, goats, sheep, horses, hogs) 1.50
------------------------------------------------------------------------
EPA has determined that the petition contains data or information
regarding the elements set forth in section 408(d)(2) of the FFDCA;
however, EPA has not fully evaluated the sufficiency of the submitted
data at this time or whether the data supports granting of the
petition. Additional data may be needed before EPA rules on the
petition.
A. Residue Chemistry
1. Plant metabolism. The metabolism of flucarbazone-sodium in wheat
was rapid and extensive. Little or no parent flucarbazone-sodium was
found in the RACs. A primary metabolic pathway in wheat involved the N-
demethylation of flucarbazone-sodium to give N-desmethyl flucarbazone-
sodium. N-desmethyl flucarbazone-sodium was found in all of the wheat
RACs. The N-desmethyl flucarbazone-sodium was then either hydrolyzed or
conjugated with glucose. Another primary metabolic pathway was
hydrolysis of flucarbazone-sodium yielding sulfonic acid and
sulfonamide which were isolated, and N,O-dimethyl triazolinone which
was not isolated. Other metabolites were then subsequently formed by
oxidative reactions, hydrolytic reactions, and conjugation.
2. Analytical method--i. Plants. The proposed tolerance expression
is parent flucarbazone-sodium and N-desmethyl flucarbazone-sodium. An
analytical method was developed to measure these two analytes in plant
matrices. This method was validated in wheat tissues. The flucarbazone-
sodium and N-desmethyl flucarbazone-sodium residues are extracted from
the wheat samples with 0.05 M NH4OH by accelerated solvent
extraction (ASE). The extracts are purified by a combination of C-18
solid phase extraction (SPE) and ethylene diamine-N-propyl (PSA) spe.
The resultant analytes are detected by liquid chromatography/tandem
mass spectroscopy (lc/ms/ms) and quantified against known amounts of
deuterated internal standards. The method limit of quantitation (LOQ)
is 0.01 milligram/kilogram (mg/kg) of either analyte in all wheat
matrices. The method limit of detection (LOD) is 0.005 mg/kg of either
analyte in all wheat matrices.
[[Page 43415]]
ii. Animals. An analytical method was developed to measure the
residues of flucarbazone-sodium in animal tissues and milk. Since the
flucarbazone-sodium-related residues were present in ruminant tissues
as a mixture of bound, conjugated, and unconjugated residues, a method
was developed that simultaneously extracted and hydrolyzed the majority
of the flucarbazone-sodium-related residues to flucarbazone-sodium
sulfonamide. The flucarbazone-sodium residues are simultaneously
hydrolyzed to flucarbazone-sodium sulfonamide and extracted from the
animal tissues and milk by heating with 8% trifluoroacetic acid (TFA)
in water. The analysis of fat was complicated by the large quantities
of lipids that were released during hydrolysis and extraction.
Therefore, the flucarbazone-sodium residues are extracted into
acetonitrile/water (9:1) before they are hydrolyzed to flucarbazone-
sodium sulfonamide. After conversion to flucarbazone-sodium
sulfonamide, the residues are purified and partitioned. The residues
are detected by lc/ms/ms and quantified against known amounts of
deuterated internal standards. The LOQ in the tissues and milk is 0.020
and 0.005 mg/kg, respectively. The estimated LOD (3x highest background
response) in the liver, muscle, and milk is 0.014, 0.002, and 0.004 mg/
kg, respectively. The recoveries of flucarbazone-sodium were determined
in all tissues and milk after fortification with flucarbazone-sodium.
The average recoveries of flucarbazone-sodium from liver fortified at
0.020 and 0.100 mg/kg were 104 and 100%, respectively. The average
recoveries of flucarbazone-sodium from muscle fortified at 0.020 and
0.100 mg/kg were 97 and 102%, respectively. In milk, the average
recoveries of flucarbazone-sodium at fortifications of 0.005, 0.010,
and 0.050 mg/kg were 111 (after correction for background in the
control samples, the average recovery was 92%), 97 and 91%,
respectively. An independent laboratory validation of the analytical
method was performed. The method was successfully validated indicating
that the method could be satisfactorily run by following the written
procedure.
3. Magnitude of residues. Field trials were conducted with wheat at
36 locations to evaluate the quantity of flucarbazone-sodium residues
in wheat forage, hay, straw, and grain following treatment with
flucarbazone-sodium 70WG at a rate of 30 grams active ingredient/
hectacre (g ai/ha). The highest average field trial (HAFT) residue
detected in forage, hay, and straw were 0.27, 0.08, and 0.04 mg/kg,
respectively. Residues of flucarbazone-sodium were <0.01 mg/kg in wheat
grain.
B. Toxicological Profile
1. Acute toxicity--i. Flucarbazone-sodium is not toxic to fasted
rats following a single oral administration. The oral lethal dose
(LD50) is >5,000 mg/kg body weight (bwt) for males and
females.
ii. Flucarbazone-sodium is not toxic to rats following a single
dermal application. The dermal LD50 is >5,000 milligrams/
kilogram/body weight (mg/kg/bwt) for males and females.
iii. An acute inhalation study with rats showed low toxicity with a
4-hour dust aerosol lethal concentration (LC50) >5,130 mg/
m3 air for males and females.
iv. An eye irritation study in rabbits showed only very slight,
reversible irritation.
v. A dermal irritation study in rabbits showed flucarbazone-sodium
is not irritating to skin.
vi. Flucarbazone-sodium has no skin sensitizing potential under the
conditions of the maximization test in guinea pigs.
2. Genotoxicity. The genotoxic action of flucarbazone-sodium was
studied in bacteria and mammalian cells with the aid of various in
vitro test systems (Salmonella microsome test, hypoxanthine guanine
phophoribosyl transferase (HGPRT) test with Chinese hamster V79 cells,
cytogenetic study with Chinese hamster V79 cells, and unscheduled DNA
synthesis test) and in one in vivo test (micronucleus test). None of
the tests revealed any evidence of a mutagenic or genotoxic potential
of flucarbazone-sodium. The compound did not induce point mutation, DNA
damage, or chromosome aberration.
3. Reproductive and developmental toxicity. In a 2-generation
reproduction study, Wistar rats were administered dietary levels of
flucarbazone-sodium at levels of 0, 50, 4,000, and 20,000/12,000 parts
per million (ppm) (dose reduction week 6). The no observed adverse
effect levels (NOAELs) for reproductive parameters was established at
4,000 ppm, based on slight reduction in pup weight development at
12,000 ppm. The NOAELs established for parental males and females were
4,000 and 50 ppm, respectively.
i. A developmental toxicity study was conducted with Sprague-Dawley
rats via oral gavage of flucarbazone-sodium at levels of 0, 100, 300,
and 1,000 milligrams/kilogram body weight/day (mg/kg bwt/day) on days 6
through 19 of gestation. There were no signs of maternal toxicity,
embryotoxicity, fetotoxicity, or teratogenicity at the level of 1,000
mg/kg bwt/day. Therefore, the maternal and developmental NOAELs for
rats were established at >1,000 mg/kg bwt/day, the limit dose for this
study type.
ii. Himalayan rabbits were administered flucarbazone-sodium at
levels of 0, 100, 300, 500, or 1,000 mg/kg/bwt by oral gavage days 6
through 28 post coitum in a test for developmental toxicity. A maternal
NOAEL of 100 mg/kg bwt/day was established based on clinical findings,
body weight loss, decreased feed consumption, gastrointestinal changes,
increased liver weights, and fatty liver changes at 300 mg/kg bwt/day.
The gestation rate NOAEL of 100 mg/kg bwt/day was based on one abortion
(assessed as secondary due to maternal toxicity) at 300 mg/kg bwt/day.
The NOAEL for fetal parameters of 300 mg/kg bwt/day was based on
decreased fetal weights and delayed ossification at 500 mg/kg bwt/day.
No teratogenic potential of flucarbazone-sodium was evident in rabbits.
4. Subchronic toxicity--i. A 28-day dermal rabbit study established
a systemic NOAEL of >1,000 mg/kg bwt/day (the dermal limit dose) for
males and females. The local dermal effects, skin thickening, seen at
1,000 mg/kg were regarded as a result of mechanical friction and of no
toxicological relevance.
ii. A 90-day rat feeding study defined a NOAEL at 250 ppm (17.6 mg/
kg bwt/day) for males and 1,000 ppm (101.7 mg/kg bwt/day) for females
based on a decreased spleen weight in males at 1,000 ppm and on
immunologic changes at 4,000 ppm in females.
iii. A 90-day feeding study with male and female B6C3F1 mice
established a NOAEL of 7,000 ppm (equivalent to >2,083, and 3,051 mg/kg
bwt/day for males and females, respectively). The dose of 7,000 ppm was
the HDT.
iv. A 90-day dog feeding study at levels of 0, 1,000, 5,000, and
50,000 ppm established a NOAEL of 1,000 ppm (equivalent to 33.8 mg/kg
bwt/day in males and 35.2 mg/kg bwt/day in females) based on decreased
thyroxine levels and increased thyroxine-binding capacity, macroscopic
and microscopic effects on the gastric mucosa and an eosinophilic
hepatocellular cytoplasm occurring at 5,000 ppm and above. The liver
enzyme induction at 1,000 ppm was assessed as a slight adaptive
response in the detoxification process of flucarbazone-sodium but not
as an adverse effect, due to the absence of clinical chemical changes
that would indicate liver damage and due to the
[[Page 43416]]
absence of any histopathologic liver changes at this dietary level.
v. A 28-day (6 hours/day; 5 days/week) subacute inhalation toxicity
study was conducted with male and female Wistar rats exposed to mean
actual concentrations of 5.2, 30.0, 180.1 and 513.3 mg/m3
air. A NOAEL of 5.2 mg/m3 air was established based on
histopathological changes observed at 30 mg/m3 air and
above.
5. Chronic toxicity--i. A 2-year chronic toxicity/oncogenicity
study was conducted with male and female Wistar rats at dietary levels
of 0, 2.5, 7.5, 125, and 1,000 mg/kg bwt. A NOAEL of 125 mg/kg was
established based on increased food consumption (both sexes) and lower
body weights (females) at 1,000 mg/kg. No carcinogenic potential was
indicated.
ii. B6C3F1 mice were administered flucarbazone-sodium via the diet
at levels of 0, 50, 1,000, and 7,000 ppm in a 2-year carcinogenicity
study. The NOAEL was established in males and females at 1,000 ppm
(equivalent to 275 and 459 mg/kg bwt/day, respectively) based on
reduced body weight gain in both sexes and on increased feed
consumption in males at the 7,000 ppm level. No carcinogenic potential
was indicated.
iii. A 1-year feeding study in dogs at levels of 0, 200, 1,000, and
5,000 ppm established a NOAEL of 1,000 ppm for males (equal to 35.9 mg/
kg bwt/day) based on decreased body weight development, increased ALAT-
and ASAT-levels and slightly increased N-demethylase levels. The NOAEL
of 1,000 ppm for females (equal to 37.1 mg/kg bwt/day) was based on
body weight gain depression, increased N-demethylase levels, decreased
T4 levels, and marginally increased liver weight.
6. Animal metabolism. Flucarbazone-sodium was metabolized via two
pathways. The major pathway involved the hydrolysis of the urea linkage
forming sulfonamide and N,O-dimethyltriazolinone. The sulfonamide was
shown to be the major metabolite in the blood, fat, liver, and muscle
at 4 to 6 hours following oral administration of phenyl-UL-14C
flucarbazone-sodium. The sulfonamide was conjugated with glucuronic
acid or acetate sulfonamide N-glucuronide or N-acetyl sulfonamide or
hydroxylated and then conjugated with glucuronic acid to form
hydroxysulfonamide-O-glucuronide prior to elimination in the urine. A
minor pathway involved N-demethylation of flucarbazone-sodium to form
N-desmethyl flucarbazone-sodium followed by hydrolysis to form the
sulfonamide and O-methyltriazolinone. Demethylation of
N,Odimethyltriazolinone led to the formation of N-methyltriazolinone,
O-methyltriazolinone, and ultimately, urazole; methyl urethane was
probably formed from the cleavage of O-methyltriazolinone.
7. Metabolite toxicology--i. The animal and plant metabolite
flucarbazone-sodium sulfonamide (trifluoromethoxysulfonamide) has a low
acute oral toxicity (LD50 >2,000 mg/kg/bwt) in fasted rats.
ii. The plant metabolite flucarbazone-sodium sulfonamide lactate
conjugate has no acute oral toxicity (NOAEL: 5,000 mg/kg/bwt) in fasted
rats.
iii. The plant metabolite flucarbazone-sodium sulfonamide alanine
has no acute oral toxicity (NOAEL: 5,000 mg/kg/bwt) in fasted rats.
iv. The soil metabolite O-desmethyl flucarbazone-sodium has an
acute oral LD50 value in fasted male and female rats of
>2,500 - <5,000 mg/kg bwt.
v. The plant, animal, and soil metabolite, MKH 10868 (flucarbazone-
sodium sulfonic acid Na-salt), has no acute oral toxicity
(LD50 >5,000 mg/kg bwt) in fasted male and female rats.
vi. MKH 10868 was considered non-mutagenic with and without S9 mix
in the plate incorporation as well as in the preincubation modification
of the Salmonella/microsome test.
8. Endocrine disruption. There is no evidence to suggest that
flucarbazone-sodium has an effect on the endocrine system. Studies in
this data base include evaluation of the potential effects on
reproduction and development, and an evaluation of the pathology of the
endocrine organs following short- and long-term exposure. These studies
revealed no endocrine effects due to flucarbazone-sodium.
9. Other studies--i. An acute neurotoxicity screening study in rats
established an overall NOAEL for males and females of 500 mg/kg based
on transient neurobehavioral effects. Evidence of toxicity was only
slight at a limit dose of 2,000 mg/kg and complete recovery occurred
within 7 days following treatment.
ii. A subchronic neurotoxicity screening study in rats established
an overall NOAEL of 2,000 ppm for males (equal to 147 mg/kg bwt/day)
and 20,000 ppm (equal to 1,736 mg/kg bwt/day) for females based on a
slight decrease in body weight and food consumption. The NOAEL for
microscopic lesions was 20,000 ppm for males and females, the highest
dose tested (HDT). There was no evidence of neurotoxicity at any
dietary level.
iii. A plaque-forming-cell assay (to investigate
immunotoxicological potential) was performed on rats after a 4-week
dietary exposure. The NOAEL of 20,000 ppm (equivalent to 2,205 and
2,556mg/kg bwt/day in males and females, respectively) was based on the
lack of specific effects in the HGT.
iv. The immunotoxicity potential of flucarbazone-sodium was
additionally investigated in antibody plaque-cell forming assays and in
assays examining splenic T-cells, B-cells, and NK-cells after 4-week
dietary administrations in male and female rats at levels up to and
including 1,000 mg/kg bwt/day. There was no statistically significant
effect on the humoral immune system and no effects on splenic cell
populations, cell-mediated immune response, or the innate immune
response in males or females. The NOAEL for immunotoxicity from these
studies was 1,000 mg/kg bwt/day, the immunotoxicity limit dose.
C. Aggregate Exposure
1. Dietary exposure--i. Food. Estimates of chronic dietary exposure
to residues of flucarbazone-sodium utilized the proposed tolerance-
level residues for wheat forage, wheat hay, wheat straw, wheat grain,
meat, liver, and milk of 0.30, 0.10, 0.05, 0.01, 0.01, 1.50, and 0.005
ppm, respectively. Other assumptions were that 100% of the target crop
would be treated with flucarbazone-sodium and that no loss of residue
would occur due to processing and/or cooking. A chronic reference dose
(RfD) of 0.36 milligrams/kilogram/day (mg/kg/day) was assumed based on
the NOAEL of 35.9 mg/kg/day from the one year dog feeding study. A
safety factor of 100 was used based on interspecies extrapolation (10x)
and intraspecies variability (10x). Using these conservative
assumptions, dietary residues of flucarbazone-sodium contribute
0.006659 mg/kg/day (2% of the RfD) for children 1-6 years, the most
sensitive sub-population. For the U.S. population, the exposure was
0.002891 mg/kg/day (1% of the RfD). For acute dietary exposure, the
same conservative assumptions were made. Based on the NOAEL of 300 mg/
kg/day from the rabbit developmental toxicity study, an acute RfD of
3.0 mg/kg/day was used to calculate the acute dietary risk to the most
exposed subgroup: females, 13 to 50 years old. The acute dietary
exposure from food to flucarbazone-sodium will occupy <1% of the RfD
for females, 13 to 50 years old.
ii. Drinking water. Given the post-emergence application pattern,
low use rates and rapid soil degradation of flucarbazone-sodium, the
risk of ground and surface water contamination and exposure via
drinking water is negligible. The surface water model
[[Page 43417]]
generic expected environment concentration (GENEEC) and the ground
water model (SCI-GROW) were used to determine whether drinking water
from surface or ground water sources represented a worst-case exposure
scenario. These models predict residues of flucarbazone-sodium would be
higher in surface water. Assuming a worst-case GENEEC scenario where
residues of flucarbazone-sodium occur in surface water used for
drinking water at the highest predicted acute and chronic
concentrations, the risk from exposure to residues of flucarbazone-
sodium are well within EPA's acceptable limits.
The GENEEC model predicted an acute surface water concentration of
flucarbazone-sodium of 1.45 [mu]g/L. Assuming a 70 kilogram (kg) adult
drinks 2 liters/day containing 1.45 [mu]g/L, the acute exposure would
be 0.0000414 mg/kg/day for adults. Assuming a 10 kg child drinks 1
liter/day containing 1.45 [mu]g/L, the exposure would be 0.000145 mg/
kg/day. Based on the NOAEL of 300 mg/kg/day from the rabbit
developmental toxicity study and assuming a safety of 100 (10x for
interaspecies variability and 10x for interspecies extrapolation), the
MOE for adults of 72,500 and for children of 20,700 do not exceed EPA's
level of concern for adults or children. This assessment is based on
the GENEEC highest predicted acute concentration of flucarbazone-sodium
in drinking water using worst-case assumptions.
Using GENEEC, the highest predicted chronic (60-day exposure)
concentration of flucarbazone-sodium was 1.44 [mu]g/L. EPA interim
policy recommends that the 60-day GENEEC value to be divided by an
adjustment factor of 3 to obtain a value for chronic risk assessment
calculations. Therefore, a surface water value of 0.48 [mu]g/L was used
for chronic risk assessment. Assuming a 70 kg adult consumes 2 liters
(L) of water per day containing 0.48 [mu]g/L of flucarbazone-sodium
residues for a period of 70 years, less than 0.004% of the RfD was
consumed from residues of flucarbazone-sodium in surface water used for
drinking water (worst-case scenario). For a 10 kg child drinking 1 L of
water per day containing 0.48 [mu]g/L of flucarbazone-sodium residues,
only 0.01% of the RfD was consumed by drinking water.
2. Non-dietary exposure. There are no current non-food uses for
flucarbazone-sodium registered under the Federal Insecticide,Fungicide,
and Rodenticide Act (FIFRA), as amended. No non-food uses are proposed
for flucarbazone-sodium. No non-dietary exposures are expected for the
general population.
D. Cumulative Effects
Flucarbazone-sodium falls into the category of sulfonamide
herbicides. There is no information to suggest that any of this class
of herbicides has a common mechanism of mammalian toxicity or even
produce similar effects so it is not appropriate to combine exposures
of flucarbazone-sodium with other herbicides. Arvesta Corporation is
considering only the potential risk of flucarbazone-sodium.
E. Safety Determination
1. U.S. population. As presented previously, the exposure of the
U.S. general population to flucarbazone-sodium is low, and the risks,
based on comparisons to the reference dose, are minimal. The margins of
safety from the use of flucarbazone-sodium are well within EPA's
acceptable limits. Arvesta Corporation concludes that there is a
reasonable certainty that no harm will result to the U.S. population
from aggregate exposure to flucarbazone-sodium residues.
2. Infants and children. The complete toxicological data base
including the developmental toxicity and 2-generation reproduction
studies were considered in assessing the potential for additional
sensitivity of infants and children to residues of flucarbazone-sodium.
The developmental toxicity studies in rats and rabbits revealed no
increased sensitivity of rats or rabbits to in-utero exposure to
flucarbazone-sodium. The 2-generation reproduction study did not reveal
any increased sensitivity of rats to in-utero or postnatal exposure to
flucarbazone-sodium. Furthermore, none of the other toxicology studies
revealed any data demonstrating that young animals were more sensitive
to flucarbazone-sodium than adult animals. The data taken collectively
clearly demonstrate that application of a Food Quality Protection Act
(FQPA) uncertainty factor for increased sensitivity of infants and
children is not necessary for flucarbazone-sodium.
F. International Tolerances
A default Maximum Residue Limit (MRL) of 0.01 ppm has been
established in Canada for residues of flucarbazone-sodium and its N-
desmethyl metabolite on wheat grain. This value is consistent with the
tolerance being proposed in the United States on wheat grain. There are
no harmonized MRLs at the European Union level and no Codex MRLs for
this compound on wheat at present. Therefore, no compatibility issues
exist with Codex in regard to the proposed U.S. tolerances.
[FR Doc. 05-14736 Filed 7-26-05; 8:45 am]
BILLING CODE 6560-50-S
