Dinotefuran; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food

Note: EPA no longer updates this information, but it may be useful as a reference or resource.

[Federal Register: July 2, 2003 (Volume 68, Number 127)]
[Notices]
[Page 39547-39554]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr02jy03-66]

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ENVIRONMENTAL PROTECTION AGENCY
[OPP-2003-0211; FRL-7312-8]

Dinotefuran; 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.

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SUMMARY: This notice announces the initial filing of a pesticide
petition proposing the establishment of regulations for residues of a
certain pesticide chemical in or on various food commodities.

DATES: Comments, identified by docket ID number OPP-2003-0211, must be
received on or before August 1, 2003.

ADDRESSES: Comments may be submitted electronically, by mail, or
through hand delivery/courier. Follow the detailed instructions as
provided in Unit I. of the SUPPLEMENTARY INFORMATION.

FOR FURTHER INFORMATION CONTACT: Rita Kumar, Registration Division
(7505C), Office of Pesticide Programs, Environmental Protection Agency,
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone
number: (703) 308-8291; e-mail address: kumar.rita@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 identification (ID) number OPP-2003-0211. The
official public docket consists of the documents specifically
referenced in this action, any public comments received, and other
information related to this action. Although a part of the official
docket, the public docket does not include Confidential Business
Information (CBI) or other information whose disclosure is restricted
by statute. The official public docket is the collection of materials
that is available for public viewing at the Public Information and
Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall #2,
1921 Jefferson Davis Hwy., Arlington, VA. This docket facility is open
from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal
holidays. The docket telephone number is (703) 305-5805.
2. Electronic access. You may access this Federal Register document
electronically through the EPA Internet under the ``Federal Register''
listings at http://www.epa.gov/fedrgstr/.
An electronic version of the public docket is available through
EPA's electronic public docket and comment system, EPA Dockets. You may
use EPA Dockets at http://www.regulations.gov/ to submit or view public
comments, access the index listing of the contents of the official
public docket, and to access those documents in the public docket that
are available electronically. Although not all docket materials may be
available electronically, you may still access any of the publicly
available docket materials through the docket facility identified in
Unit I.B.1. Once in the system, select ``search,'' then key in the
appropriate docket ID number.
Certain types of information will not be placed in EPA's Dockets.
Information claimed as CBI and other information whose disclosure is
restricted by statute, which is not included in the official public
docket, will not be available for public viewing in EPA's electronic
public docket. EPA's policy is that copyrighted material will not be
placed in EPA's electronic public docket but will be available only in
printed, paper form in the official public docket. To the extent
feasible, publicly available docket materials will be made available in
EPA's electronic public docket. When a document is selected from the
index list in EPA Dockets, the system will identify whether the
document is available for viewing in EPA's electronic public docket.
Although not all docket materials may be available electronically, you
may still access any of the publicly available docket materials through
the docket facility identified in Unit I.B. EPA intends to work towards
providing electronic access to all of the publicly available docket
materials through EPA's electronic public docket.
For public commenters, it is important to note that EPA's policy is
that public comments, whether submitted electronically or in paper,
will be made available for public viewing in EPA's electronic public
docket as EPA receives them and without change, unless the comment
contains copyrighted material, CBI, or other information whose
disclosure is restricted by statute. When EPA identifies a comment
containing copyrighted material, EPA will provide a reference to that
material in the version of the comment that is placed in EPA's
electronic public docket. The entire printed comment, including the
copyrighted material, will be available in the public docket.
Public comments submitted on computer disks that are mailed or
delivered to the docket will be transferred to EPA's electronic public
docket. Public comments that are mailed or delivered to the docket will
be scanned and placed in EPA's electronic public docket. Where
practical, physical objects will be photographed, and the photograph
will be placed in EPA's electronic public docket along with a brief
description written by the docket staff.

C. How and to Whom Do I Submit Comments?

You may submit comments electronically, by mail, or through hand
delivery/courier. To ensure proper receipt by EPA, identify the
appropriate docket ID number in the subject line on the first page of
your comment. Please ensure that your comments are submitted within the
specified comment period. Comments received after the close of the
comment period will be marked ``late.'' EPA is not required to consider
these late comments. If you wish to submit CBI or information that is
otherwise protected by statute, please follow the instructions in Unit
I.D. Do not use EPA Dockets or e-mail to submit CBI or information
protected by statute.
1. Electronically. If you submit an electronic comment as
prescribed in this

[[Page 39548]]

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-2003-0211. The system is an ``anonymous access'' system, which
means EPA will not know your identity, e-mail address, or other contact
information unless you provide it in the body of your comment.
ii. E-mail. Comments may be sent by e-mail to opp-docket@epa.gov,
Attention: Docket ID Number OPP-2003-0211. In contrast to EPA's
electronic public docket, EPA's e-mail system is not an ``anonymous
access'' system. If you send an e-mail comment directly to the docket
without going through EPA's electronic public docket, EPA's e-mail
system automatically captures your e-mail address. E-mail addresses
that are automatically captured by EPA's e-mail system are included as
part of the comment that is placed in the official public docket, and
made available in EPA's electronic public docket.
iii. Disk or CD ROM. You may submit comments on a disk or CD ROM
that you mail to the mailing address identified in Unit I.C.2. These
electronic submissions will be accepted in WordPerfect or ASCII file
format. Avoid the use of special characters and any form of encryption.
2. By mail. Send your comments to: Public Information and Records
Integrity Branch (PIRIB) (7502C), Office of Pesticide Programs (OPP),
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001, Attention: Docket ID Number OPP-2003-0211.
3. By hand delivery or courier. Deliver your comments to: Public
Information and Records Integrity Branch (PIRIB), Office of Pesticide
Programs (OPP), Environmental Protection Agency, Rm. 119, Crystal Mall
#2, 1921 Jefferson Davis Hwy., Arlington, VA, Attention: Docket
ID Number OPP-2003-0211. Such deliveries are only accepted during the
docket's normal hours of operation as identified in Unit I.B.1.

D. How Should I Submit CBI to the Agency?

Do not submit information that you consider to be CBI
electronically through EPA's electronic public docket or by e-mail. You
may claim information that you submit to EPA as CBI by marking any part
or all of that information as CBI (if you submit CBI on disk or CD ROM,
mark the outside of the disk or CD ROM as CBI and then identify
electronically within the disk or CD ROM the specific information that
is CBI). Information so marked will not be disclosed except in
accordance with procedures set forth in 40 CFR part 2.
In addition to one complete version of the comment that includes
any information claimed as CBI, a copy of the comment that does not
contain the information claimed as CBI must be submitted for inclusion
in the public docket and EPA's electronic public docket. If you submit
the copy that does not contain CBI on disk or CD ROM, mark the outside
of the disk or CD ROM clearly that it does not contain CBI. Information
not marked as CBI will be included in the public docket and EPA's
electronic public docket without prior notice. If you have any
questions about CBI or the procedures for claiming CBI, please consult
the person listed under FOR FURTHER INFORMATION CONTACT.

E. What Should I Consider as I Prepare My Comments for EPA?

You may find the following suggestions helpful for preparing your
comments:
1. Explain your views as clearly as possible.
2. Describe any assumptions that you used.
3. Provide copies of any technical information and/or data you used
that support your views.
4. If you estimate potential burden or costs, explain how you
arrived at the estimate that you provide.
5. Provide specific examples to illustrate your concerns.
6. Make sure to submit your comments by the deadline in this
notice.
7. To ensure proper receipt by EPA, be sure to identify the docket
ID number assigned to this action in the subject line on the first page
of your response. You may also provide the name, date, and Federal
Register citation.

II. What Action is the Agency Taking?

EPA has received 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 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 the petitions.
Additional data may be needed before EPA rules on the petitions.

List of Subjects

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

Dated: June 20, 2003.
Debra Edwards,
Director, Registration Division, Office of Pesticide Programs.

Summary of Petition

The petitioner's summary of the pesticide petitions is printed
below as required by FFDCA section 408(d)(3). The summary of the
petitions was prepared by the petitioner and represents the view of the
petitioner. The petitions 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.

Mitsui Chemicals, Inc.

PP 2F6427 and 3F6566

EPA has received pesticide petitions (2F6427 and 3F6566) from
Mitsui Chemicals, Inc., Chiyoda-ku, Tokyo, Japan, proposing pursuant to
section 408(d) of the FFDCA, 21 U.S.C. 346a(d), to amend 40 CFR part
180 by establishing tolerances for residues of dinotefuran, (RS)-1-
methyl-2-nitro-3-(tetrahydro-3-furylmethyl)guanidine and its major
metabolites, 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine,

[[Page 39549]]

and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea, in or on fruiting
vegetables, leafy vegetables, head and stem brassica vegetables,
cotton, cucurbits, grapes, and potato. The tolerances are set at the
following value: Fruiting vegetables, 0.7 part per million (ppm); leafy
vegetables, 5.0 ppm; tomato paste, 1.0 ppm; cucurbits, 0.5 ppm; head
and stem brassica vegetables, 1.4 ppm; grape, 0.8 ppm; raisin, 2.5 ppm;
potato, 0.05 ppm; chips, 0.10 ppm; granules, 0.15 ppm; cotton seed
undelinted at 0.2 ppm, and cotton gin byproducts at 7.0 ppm. Tolerances
for meat, milk, and byproducts is set at 0.05 ppm. This new active
ingredient has been accepted by EPA as a reduced risk chemical. EPA has
determined that the petitions contains data or information regarding
the elements set forth in section 408(d)(2) of the FFDCA; however, EPA
has not fully evaluated the sufficiency of the submitted data at this
time or whether the data support granting of the petitions. Additional
data may be needed before EPA rules on the petitions.

A. Residue Chemistry

1. Plant metabolism. The primary metabolic pathways of dinotefuran
in plants (rice, apple, potato, oilseed, rape, and lettuce) were
similar to those described for animals, with certain extensions of the
pathway in plants. Parent compound, dinotefuran, and two metabolites,
1-methyl-3-(tetrahydro-3-furymethyl)guanidine and 1-methyl-3-
(tetrahydro-3-furymethyl)-urea were major metabolites in all crops. The
metabolism of dinotefuran in plants and animals is understood for the
purposes of the proposed tolerances. Parent dinotefuran and the
metabolites, 1-methyl-3-(tetrahydro-3-furymethyl)guanidine and 1-
methyl-3-(tetrahydro-3-furymethyl)-urea are the residues of concern for
tolerance setting purposes.
2. Analytical method. Mitsui Chemicals, Inc., has submitted
practical analytical methodology for detecting and measuring levels of
dinotefuran and its metabolites, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
in or on raw agricultural commodities (RACs). The high performance
liquid chromotography (HPLC) method was validated for determination of,
dinotefuran, 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-
methyl-3-(tetrahydro-3-furylmethyl)-urea in or on tomatoes, peppers,
cucurbits, brassica, grapes, potatoes, and lettuce for raw agricultural
commodity matrices and in or on tomato paste, puree, grape juice,
raisins, potato chips, granules, and wet peel for processed commodity
matrices. After extraction with a water/acetonitrile mixture and clean
up with hexane and extraction columns, concentrations of dinotefuran
and its metabolites were quantified after HPLC separation by mass
spectrometry/molecular size (MS/MS) detection. The limit of
quantitation (LOQ) was 0.01 ppm for all matrices.
The HPLC method was validated for the determination of dinotefuran
and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea in or on cotton
(undelinted seed, gin trash, meal, hulls, refined oil), and leafy
vegetables. After extraction with a water/acetonitrile mixture and
clean up dinotefuran, 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine,
and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea were quantified after
HPLC separation by MS/MS detection. For undelinted seed, gin trash,
meal, and hulls, a LOQ of 0.05 milligram/kilogram (mg/kg) and a working
range from 0.05 to 0.50 mg/kg were successfully validated for
dinotefuran, 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-
methyl-3-(tetrahydro-3-furylmethyl)-urea. For refined oil, a LOQ of
0.01 mg/kg and a working range from 0.01 to 0.10 mg/kg were
successfully validated for dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea.
An HPLC method was validated for the determination of dinotefuran, 1-
methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-
(tetrahydro-3-furylmethyl)-urea, in lettuce. After extraction with
water/acetonitrile mixture and clean-up, dinotefuran was quantified
after HPLC separation by ultraviolet ray (UV) detection, 1-methyl-3-
(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea by MSD. A LOQ 0.010 mg/kg and a working range from
0.01 to 5.00 mg/kg were successfully validated from dinotefuran, 1-
methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-
(tetrahydro-3-furylmethyl)-urea. All of the above methods have been
independently validated.
3. Magnitude of residues. Crops in residue trials were treated at
maximum label rates and harvested at the specified minimum treatment to
harvest intervals. The residue method for dinotefuran, 1-methyl-3-
(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea, in all components utilized HPLC separation with MS/
MS detection.
For cucurbit vegetables (crop group 9), residue trials were
conducted for each of the three representative crops, cucumbers,
melons, and squash. The proposed tolerance in or on cucurbit vegetables
for combined residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
is 0.5 ppm. The maximum combined residue found for the representative
cucurbit vegetable crops was 0.44 ppm for a melon sample.
For leafy vegetables (crop group 4), residue trials were conducted
for each of the four representative crops, celery, leaf lettuce, head
lettuce, and spinach, at six locations. The proposed tolerance in or on
leafy vegetables for combined residues of dinotefuran, 1-methyl-3-
(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea, is 5.0 ppm. The maximum combined residue found for
the representative leafy vegetable crops was 4.36 ppm for a spinach
sample.
Residue trials for cotton were conducted at 13 locations and
undelinted cotton seed samples were collected and analyzed. Cotton gin
byproducts (gin trash) samples were obtained for 7 of the locations.
Processing studies with analyses of cotton seed meal, hulls, and oil
were performed with cotton seed harvested at two locations that were
both treated with 5X the maximum label rate. The proposed tolerance for
combined residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
in or on cotton seed undelinted is 0.2 ppm. All cotton seed residue
samples had combined residues of less than 0.2 ppm. The proposed
tolerance for cotton gin byproducts is 7.0 ppm for combined residues of
dinotefuran and its two major metabolites. The maximum combined
residues for cotton gin byproducts in these trials was 6.4 ppm.
Processing studies established that residues of dinotefuran and its
metabolites, 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-
methyl-3-(tetrahydro-3-furylmethyl)-urea, did not concentrate in cotton
seed meal, oil, or hulls. Therefore, tolerances are not proposed for
these processing fractions.
Residue trials for grapes were conducted at 13 locations and 2
grape juice and raisin processing studies were performed with grapes
from exaggerated treatment rate applications. The proposed tolerance
for combined residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
in or on grapes is 0.8 ppm. The maximum combined residue for an
individual grape residue sample was 0.73 ppm and the highest average
field trial (HAFT) for grapes had

[[Page 39550]]

combined residues of 0.55 ppm. The proposed tolerance for raisins is
2.5 ppm for combined residues of dinotefuran and its two major
metabolites based on the average concentration factor of 4.0 for
processing grapes to raisins. The grape juice processing studies
established an average concentration factor of 1.3 for residues of
dinotefuran and its metabolites 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
because the product of multiplying the grape HAFT times the average
concentration factor for processing grapes into juice is less than the
proposed grape tolerance, a separate tolerance is not proposed for
grape juice.
For potatoes, residue trials were performed at 17 locations and 2
studies processing potatoes into chips, granules, and wet peel were
performed with potatoes that were treated with exaggerated application
rates. The proposed tolerance for combined residues of dinotefuran and
its metabolites 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-
methyl-3-(tetrahydro-3-furylmethyl)-urea, on potatoes is 0.05 ppm. The
maximum combined residues found on potatoes were less than 0.05 ppm
with maximum residues of dinotefuran less than 0.03 ppm. The HAFT
result was 0.04 ppm of combined residues. The average concentration
factors for processing potatoes into chips, granules, and wet peel were
2.2, 3.65, and less than 1 respectively. No separate tolerance is
proposed for wet peel. Based on the average concentration factors and
the HAFT, tolerances for combined residues of dinotefuran, 1-methyl-3-
(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea, are proposed for potato chips at 0.1 ppm and for
potato granules at 0.15 ppm.
For fruiting vegetables (crop group 8) residue trials were
conducted for the three representative commodities, tomatoes, bell
pepper, and non-bell pepper. The proposed tolerance for combined
residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
in or on fruiting vegetables is 0.7 ppm. The maximum combined residue
for the representative fruiting vegetables was 0.58 ppm on peppers. The
HAFT result for combined residues on tomatoes was 0.20 ppm. Three
studies for processing tomatoes into tomato puree and tomato paste were
performed with tomatoes that were treated at exaggerated application
rates. The average concentration factors determined in these studies
were 1.8 for processing tomatoes into puree and 4.8 for processing
tomatoes into paste. Since the product of the average concentration
factor for puree and the HAFT for tomatoes is less than the proposed
tolerance for fruiting vegetables, no separate tolerance is proposed
for tomato puree. A combined tolerance of 1.0 ppm is proposed for
tomato paste, based on the average concentration factor for processing
of 4.8 and the HAFT of 0.20 ppm for tomatoes.
For vegetables, brassica head, and stem crop subgroup (crop
subgroup 5-A), residue trials were conducted with three representative
crops, broccoli, cauliflower, and cabbage. The proposed tolerance for
combined residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
1-methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-
(tetrahydro-3-furylmethyl)-urea, on stem and head brassica vegetables
is 1.4 ppm. The maximum combined residue in field trials was 1.25 ppm
on broccoli.
Metabolism studies in livestock and poultry (nature of residue
studies with goats and hens), established that dinotefuran was rapidly
metabolized and excreted and that there was very little transmittal of
residues of dinotefuran and its metabolites to meat, milk, or eggs. For
goats fed 10 ppm of radiolabeled dinotefuran, the total radioactive
residues (TRR) in meat and milk were less than 0.05 ppm.
The maximum livestock dietary burden from feeding cotton
commodities and potatoes (which all contain residues at the proposed
tolerance levels) was 1.9 ppm for beef cattle and 1.9 ppm for dairy
cattle. To provide for the possible transmittal of the residues of
dinotefuran and its metabolites, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
in cattle and other livestock, tolerances are proposed for combined
residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea,
in milk at 0.05 ppm, in meat (from cattle, goats, hogs, horses, and
sheep) at 0.05 ppm and in meat byproducts, including fat, liver, and
kidney, (from cattle, goats, hogs, horses, and sheep) at 0.05 ppm.
These proposed tolerances are based on the results of a cow feeding
study where dairy cows received dosages of combined residues of
dinotefuran and its metabolites and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea, representing 5ppm (1X), 15 ppm (3X), and 50 ppm
(10X) in the daily diet. The dosages contained dinotefuran, 1-methyl-3-
(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea, in a 3:1:1 ratio, thus, the 5 ppm level contained 3
ppm of dinotefuran, 1 ppm of 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1 ppm of 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea. The dosing period was 29 to 30 days, whole milk,
skim milk, and cream were analyzed through the collection period and
meat, fat, and edible tissues were analyzed at conclusion of the dosing
period.
There were only low levels of residues transmitted to milk, meat,
fat, and edible tissues in the study. No dinotefuran residues (<0.01
ppm) were measured in milk from 5 ppm dosage cows. Maximum residues of
dinotefuran in milk were 0.012 ppm in the 3X level cows and 0.032 ppm
in the 10X level cows. No detectable residues of parent dinotefuran
were found in muscle, fat, or edible tissues from cows at any dosage
level. Milk, muscle, fat, and edible tissues were also analyzed for 1-
methyl-3-(tetrahydro-3-furylmethyl)guanidine, and 1-methyl-3-
(tetrahydro-3-furylmethyl)-urea, the two dinotefuran metabolites
included in the combined residues in the proposed tolerance expression.
Transmittal of quantifiable residues of 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine was found at the 1X dosage level with maximum
residues of 0.013 ppm of 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine
in milk and at the 10X level with 0.011 ppm of 1-methyl-3-(tetrahydro-
3-furylmethyl)guanidine in milk and 0.02 ppm of 1-methyl-3-(tetrahydro-
3-furylmethyl)guanidine in muscle, liver, and kidney. Quantifiable
residues of 1-methyl-3-(tetrahydro-3-furylmethyl)-urea were found in
the 1X dosage level, with 1-methyl-3-(tetrahydro-3-furylmethyl)-urea
residues up to 0.02 ppm in whole milk and 1-methyl-3-(tetrahydro-3-
furylmethyl)-urea residues of 0.011 to 0.012 in muscle, liver, and
kidney. The 1-methyl-3-(tetrahydro-3-furylmethyl)-urea residues
increased proportional to dosage with the 10X level having 1-methyl-3-
(tetrahydro-3-furylmethyl)-urea residues of up to 0.24 ppm in milk,
0.13 ppm in muscle, 0.07 ppm in fat, 0.12 ppm in liver, and 0.18 ppm in
kidney. In the cow feeding study at the 1X dosage level comprising
combined residues of dinotefuran, 1-methyl-3-(tetrahydro-3-
furylmethyl)guanidine, and 1-methyl-3-(tetrahydro-3-furylmethyl)-urea
of 5 ppm of diet, the total combined residues for milk, muscle, fat,
liver, and kidney were each less than 0.05 ppm. Since the maximum
theoretical combined

[[Page 39551]]

residues from the proposed uses of dinotefuran on cotton and potatoes
would be 1.9 ppm, for dairy and beef cattle, the proposed tolerances in
milk, meat, and meat byproducts, would be sufficient to provide for
potential transmittal of residues from livestock diets containing
residues of dinotefuran and its metabolites.
The maximum theoretical poultry dietary burden from feeding cotton
commodities containing residues of dinotefuran and its metabolites at
the proposed tolerance levels was calculated to be 0.09 ppm. Since the
TRR in meat and eggs from hens fed 10 ppm of radiolabeled dinotefuran
in the poultry metabolism study was less than 0.05 ppm it can be
concluded that there is no reasonable expectation of transmittal of
finite residues of dinotefuran and its metabolites to meat and eggs,
for poultry fed cotton commodities treated with dinotefuran. Therefore
no tolerances are proposed for combined residues of dinotefuran and its
metabolites in poultry or eggs.

B. Toxicological Profile

1. Acute toxicity. Dinotefuran has low acute oral, dermal, and
inhalation toxicity. The oral lethal dose (LD)₅₀ in rats is
2,450 mg/kg, the dermal LD₅₀ is >2,000 mg/kg and the
inhalation 4-hour lethal concentration (LC)₅₀ is >4.09
milligrams/Liter (mg/L) air. Dinotefuran is not a skin sensitizer in
guinea pigs, but is slightly irritating to the skin and eyes of
rabbits. End-use formulations of dinotefuran have similar low acute
toxicity profiles.
2. Genotoxicity. Dinotefuran and its metabolites do not induce gene
mutations in bacterial and mammalian cells, chromosome aberrations in
mammalian cells or deoxyribonucleic acid (DNA) damage in bacterial
cells in in vitro test systems. Similarly, it does not exhibit a
clastogenic effect in vivo in the mouse micronucleus test. Therefore,
there is no evidence to suggest a genotoxic hazard at any of the three
main levels of genetic organization.
3. Reproductive and developmental toxicity. In rat and rabbit
developmental toxicity studies with dinotefuran, there was no evidence
of teratogenicity or other embryotoxic effects at the highest dose
levels, although maternal toxicity was evident. There were no
treatment-related effects on litter parameters at any dose level in
either species. In rats, 1,000 mg/kg produced decreased food
consumption, body weight gain, and increased water intake. In rabbits,
300 mg/kg produced hypoactivity, prone position, panting, flushing of
the nose and ears, tremors, reduced weight gain, food consumption, and
water intake. Necropsy revealed pale brown discoloration of liver and
gray/white plaques in the stomach at 125 and 300 mg/kg. The no adverse
effect level (NOAEL) values in maternal rats and rabbits were 300 and
52 mg/kg/day, respectively. The NOAEL values in rats and rabbits for
embryonic development and teratogenicity were the highest dose levels
administered, 1,000 and 300 mg/kg/day, respectively. In a 2-generation
study, parental animals of both sexes and both generations showed
reduced body weight gain and food consumption at the highest dose level
evaluated (10,000 ppm), but there was no effect of treatment at any
dose level in either generation on reproductive performance indicators.
There were no treatment-related effects at any dose level on the
histopathological appearance of the reproductive organs of either sex.
Similarly, there were no effects at any dose level in either generation
on quantitative ovarian histopathology or on sperm counts, motility and
morphology. Reduced spleen weight in probit dose extrapolation model
(P) generation animals and reduced thyroid weight in F1 generation
parental females were apparent at 10,000 ppm. F1 pup behavioral and
sexual development was unaffected by treatment at all dose levels but
pup weight gain during lactation was reduced at 10,000 ppm in both
generations. Furthermore, the spleen weight of F1 generation progeny
was reduced at 10,000 ppm. Based on reduced weight gain and food
consumption in parental animals at 10,000 ppm and reduced pre-weaning
weight gain in the offspring, the NOAEL value for parental animals and
offspring is 241 mg/kg.
4. Subchronic toxicity. Dinotefuran was evaluated in a 13-week oral
(diet) toxicity studies in rats, mice, and dogs. No specific target
organs were identified in any species. In the rat study, a NOAEL of 500
ppm (34/38 mg/kg/day for males and females) was established, based on
minimal growth retardation in females and adrenal cortical vacuolation
in males. A NOAEL was established at 5,000 ppm (336/384 mg/kg/day for
males/females) based on marked growth retardation at 25,000 ppm
(adrenal cortical vacuolation not adverse). In the mouse study, a NOAEL
of 25,000 ppm (4,442/5,414 mg/kg/day for males/females) was established
based on growth retardation at 50,000 ppm. In the dog study, a NOAEL of
8,000 ppm (307/323 mg/kg/day in males/females) was established based on
growth retardation. Dinotefuran was also evaluated for dermal and
inhalation toxicity for 4 weeks in rats. Daily inhalation exposure of
rats for 6 hours/day for 4 weeks did not elicit toxicologically
significant effects at any exposure concentration up to and including
the highest technically achievable concentration (2.08 mg/L) with a low
mass median aerodynamic diameter) (MMAD£+/-GSM of 2.03
[mu]m+/-3.60. Dinotefuran was well tolerated and there were no
treatment-related effects on clinical condition, hematology, and
clinical chemistry profiles, organ weights, macroscopic, and
microscopic pathology. Dermal application for 4 weeks at dose levels up
to 1,000 mg/kg/day did not elicit any local or systemic effects on any
of the parameters examined. Therefore, no target organs were identified
in the rat either by dermal or inhalation exposure.
5. Neurotoxicity. Dinotefuran did not produce any functional or
histomorphological evidence of neurotoxicity in acute (gavage) and 13-
week (dietary) neurotoxicity studies in rats. The NOAEL for
neurotoxicity in the acute study was 1,500 mg/kg, the highest dose
level administered. The NOAEL for neurotoxicity in the 13-week dietary
study was 50,000 ppm (3,413/3,806 mg/kg/day for males and females). The
NOAEL for all effects in this study was 5,000 ppm (327/400 mg/kg/day
for males and females) based on reduced body weight gain and food
consumption.
6. Chronic toxicity. Chronic toxicity studies with dinotefuran have
been conducted in rats, mice, and dogs. In common with the subchronic
studies in these species, no specific target organs could be
identified. In the 52-week dog study, a NOAEL of 559/512 mg/kg/day for
males/females was established based on decreased weight gain in both
sexes and decreased food consumption in females. In the 78-week mouse
study, a NOAEL of 345/441 mg/kg/day for males/females was established,
based on decreased weight gain and a decrease in circulating platelet
counts. In the 104-week rat study, a NOAEL of 991/127 mg/kg/day for
males/females was established. This was based on a decrease in weight
gain in females.
7. Carcinogenicity. The carcinogenic potential of dinotefuran has
been evaluated in rats and mice. Survival incidences in the
oncogenicity studies were unaffected by treatment at all dose levels.
There were no treatment-related effects on the nature and incidence of
neoplastic and adverse non-neoplastic histomorphological findings in
either species at any dose level. Therefore, the NOAEL values for all
effects, 991/127 mg/kg/day (male/female rats) and 345/441 mg/kg/day
(male/female mice) are based on reduced weight gain, and also

[[Page 39552]]

on reduced numbers of platelets in mice.
8. Animal metabolism. In the rat, dinotefuran is rapidly and almost
completely absorbed from the gastrointestinal tract into the general
circulation, and is widely distributed throughout the tissues and
fluids of the body. Elimination is rapid, predominantly by urinary
excretion and almost complete within 7 days of administration. There is
no evidence for tissue accumulation. Dinotefuran is rapidly transferred
to maternal milk and widely distributed into fetal tissues but rapidly
eliminated from them. More than 90% of orally and intravenously
administered dinotefuran is eliminated as unchanged parent molecule,
which is also the major radioactive component in plasma, milk, bile,
and most tissues. The major route of metabolism is an initial enzymatic
hydroxylation of the tetrahydrofuran ring to form isomers of 6-hydroxy-
5-(2-hydroxyethyl)-1-methyl-1,3-diazinane-2-ylidine-N-nitroamine,
followed by further oxidation, reduction and acetylation of 6-hydroxy-
5-(2-hydroxyethyl)-1-methyl-1,3-diazinane-2-ylidine-N-nitroamine, to
produce possible isomers of 1-methyl-2-nitro-3-(2-oxotetrahydro-3-
furylmethyl)guanidine, 1-[4-hydroxy-2-(hydroxymethyl)butyl]-3-methyl-2-
nitroguanidine, 6-hydroxy-5-(2-hydroxyethyl)-1-methyl-1, 3-diazinane-2-
ylidene-N-nitroamine acetyl conjugate and 3-hydroxymethyl-4- (3-methyl-
2-nitroguanidine) butyric acid. Several minor pathways of metabolism of
dinotefuran were identified in animals. The absorption, distribution,
metabolism and elimination of dinotefuran is unaffected by sex and
treatment regimen. In hens and goats, the metabolite profile was
similar as in plant metabolism.
9. Metabolite toxicology. The metabolism profile for dinotefuran
supports the use of an analytical enforcement method that accounts for
parent dinotefuran, and 1-methyl-3-(tetrahydro-3-furymethyl)guanidine
and 1-methyl-3-(tetrahydro-3-furymethyl)-urea. Other metabolites are
considered of equal or lesser toxicity than parent compound.
10. Endocrine disruption. Dinotefuran does not belong to a class of
chemicals known or suspected of having adverse effects on the endocrine
system. There is no evidence that dinotefuran has any effect on
endocrine function in developmental or reproduction studies.
Furthermore, histological investigation of endocrine organs in chronic
dog, rat, and mouse studies did not indicate that the endocrine system
is targeted by dinotefuran.

C. Aggregate Exposure

1. Dietary exposure. Chronic dietary exposure assessments were
conducted using a Tier I approach. This Tier I assessment incorporated
tolerance level residues and 100% crop-treated in the EXP estimated
dietary intake trends evaluation system (EXPedite\TM\ system, Version
4.1). EXPedite\TM\ utilized the food consumption data derived from the
1994-1996 U.S. Department of Agriculture (USDA) Continuing Surveys of
Food Intake by Individuals (CSFII) with the 1998 supplemental
children's survey. The resulting exposures were compared to a RfD of
1.27 mg/kg/day, which was based on the female NOAEL of 127 mg/kg/day
from the 104-week rat study and a 100-fold uncertainty factor. Chronic
dietary exposure estimates for the overall U.S. population and 25
population subgroups are well below the chronic RfD. Results of these
analyses are summarized below.

Table 1.--Chronic Dietary Risk (DEEM\TM\) Analysis of Dinotefuran
------------------------------------------------------------------------
Population Subgroup Mg/Kg Bwt/Day %RfD
------------------------------------------------------------------------
U.S. population 0.004109 0.32%
------------------------------------------------------------------------
All infants (<1-year old) 0.002815 0.22%
------------------------------------------------------------------------
Non-nursing infants 0.003438 0.27%
------------------------------------------------------------------------
Children (1 to 6) 0.007247 0.57%
------------------------------------------------------------------------
Children (7 to 12) 0.004348 0.34%
------------------------------------------------------------------------
Females (13 to 50) 0.003350 0.26%
------------------------------------------------------------------------
Males 13+ years 0.003173 0.25%
------------------------------------------------------------------------

There are no acute toxicity concerns with dinotefuran as there is
no toxicological endpoint attributable to a single exposure in the
dinotefuran toxicology data base, including the rat and rabbit
developmental studies. Therefore, only chronic dietary exposures have
been assessed.
2. Non-dietary exposure. Mitsui also requests registrations for the
use of dinotefuran on cats, turf, ornamentals, indoor foggers, and
ready to use sprays. Mitsui has considered potential non-dietary and
aggregate (non-dietary + dietary) exposures to adults, adult females,
and toddlers (1 to 3 years of age) for these uses.
Applicator and post-application exposures can result from dermal
and inhalation routes for both adults and toddlers. Additionally,
toddlers can be exposed through the post-application incidental
ingestion route via hand-to-mouth behavior. Based on the label
instructions and typical use patterns of these product types, only
short-term and intermediate-term exposure scenarios should be
considered for dinotefuran products. However, since there are no
toxicological endpoints attributable to a single or possible multiple
exposures in a very short duration, as in a short-term scenario, only
the intermediate-term exposure scenario has been evaluated for this
document.
Dermal exposures for applicator and post-application activities
were not assessed because the very high dermal NOAEL (>1,000 mg/kg/day)
for dinotefuran indicates that dermal exposures are not of concern.
Short-term oral (e.g., incidental ingestion) exposures for toddlers, as
mentioned above, were not assessed because there are no toxicological
endpoints attributable to a single exposure or multiple exposures
during a very short-term time frame in the dinotefuran toxicology data
base. Since the oral endpoint is used to calculate inhalation risks,
short-term inhalation exposures for toddlers and adults were also not
evaluated since there is no toxicological endpoint attributable to a
short-term endpoint. Intermediate-term inhalation exposures for
applicator and post-application activities also were not assessed
because the very high inhalation NOAEL (>7,000 mg/kg/day) for
dinotefuran indicates that inhalation exposures are not of concern.
Therefore, only intermediate-term oral (incidental ingestion) exposures
for toddlers were assessed. These exposures were assessed for each
individual dinotefuran product, as well as for the aggregation of all
products. In the aggregate assessment, it was assumed that the toddlers
would be exposed to residues resulting from the agricultural uses
(chronic dietary), all within 1-day.
These non-dietary assessments were conducted using equations and
default parameters from EPA's Residential Standard Operation Procedures
(SOPs) (EPA, 1997 and 2001) and maximum application rates. Although
these exposures are based on the intermediate-term time frame, the
residue on the day of application was used in the SOP equations in
order to maintain an extra level of conservatism. This assumption
implies that the toddlers are exposed to residue levels, which are
equivalent to levels resulting on the day of application, every day
over an intermediate-term time frame. The resulting oral and aggregate
exposures were compared to the NOAEL

[[Page 39553]]

of 307 mg/kg/day observed in the 13-week dog study. These risk
estimates (margin of exposures (MOE)) for toddlers (1 to 3 years of
age) are summarized below. From the results below, Mitsui concludes
there is reasonable certainty of no harm associated with the aggregate
(dietary + non-dietary) exposure to dinotefuran.

Table 2.--Intermediate-Term Aggregate MOEs
--------------------------------------------------------------------------------------------------------------------------------------------------------
Exposure Routes Dietary RTU Spray Fogger Turf Cat Aggregate
--------------------------------------------------------------------------------------------------------------------------------------------------------
Toddlers (1 to 3 years old)

Dietary 184,163 NA NA NA NA 184,163
--------------------------------------------------------------------------------------------------------------------------------------------------------
Incidental Ingestion NA 23,356 11,431 80,050 1,850 1,410
--------------------------------------------------------------------------------------------------------------------------------------------------------
Total 1,410
--------------------------------------------------------------------------------------------------------------------------------------------------------

3. Drinking water exposure. EPA uses the drinking water level of
comparison (DWLOC) as a theoretical upper limit on a pesticide's
concentration in drinking water when considering total aggregate
exposure to a pesticide in food, drinking water, and residential uses.
DWLOCs are not regulatory standards for drinking water; however, EPA
uses DWLOCs in the risk assessment process as a surrogate measure of
potential exposure from drinking water. In the absence of monitoring
data for pesticides, it is used as a point of comparison against
conservative model estimates of a pesticides concentration in water.
An estimate of the drinking water environmental concentration
(DWEC) in ground water and surface water for dinotefuran has been made
for this notice of filing. The DWEC of dinotefuran in ground water was
estimated to be 0.94 part per billion (ppb) using screening
concentration in ground water (SCI-GROW) (the screening model for
ground water), and the DWEC for surface water was estimated to be 6.24
ppb (for chronic and intermediate-term aggregate assessments) using
FQPA Index Reservoir Screening Tool (FIRST).
To calculate the DWLOC for chronic aggregate exposure relative to a
chronic toxicity endpoint, the chronic dietary food exposure from
EXPedite\TM\, as addressed above, was subtracted from the reference
dose (RfD) to obtain the acceptable chronic exposure to dinotefuran in
drinking water. DWLOCs, as presented below, were then calculated using
default body weights and drinking water consumption figures.

Table 3.--Chronic Aggregate Drinking Water Assessment
--------------------------------------------------------------------------------------------------------------------------------------------------------
Maximum Water
Population Subgroup Dietary Mg/Kg Bwt/ Exposure Mg/Kg Bwt/ Kg Bwt SCI-GROW (ppb) FIRST (ppb) DWLOC (ppb)
Day Day
--------------------------------------------------------------------------------------------------------------------------------------------------------
U.S. population 0.004109 1.265891 70 0.94 6.24 44,306
--------------------------------------------------------------------------------------------------------------------------------------------------------
All infants (<1-year old) 0.002815 1.267185 10 0.94 6.24 12,672
--------------------------------------------------------------------------------------------------------------------------------------------------------
Non-nursing infants 0.003438 1.266562 10 0.94 6.24 12,666
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children (1 to 6) 0.007247 1.262753 20 0.94 6.24 25,255
--------------------------------------------------------------------------------------------------------------------------------------------------------
Children (7 to 12) 0.004348 1.265652 40 0.94 6.24 50,626
--------------------------------------------------------------------------------------------------------------------------------------------------------
Females (13 to 50) 0.003350 1.266650 60 0.94 6.24 38,000
--------------------------------------------------------------------------------------------------------------------------------------------------------
Males (13+ years) 0.003173 1.266827 70 0.94 6.24 44,339
--------------------------------------------------------------------------------------------------------------------------------------------------------
Chronic RfD used in assessments - 1.27 mg/kg bwt/day

The estimated average concentration of dinotefuran in surface water
is 6.24 ppb. This value is less than the lowest DWLOC for dinotefuran
as a contribution to chronic aggregate exposure (12,666 ppb for non-
nursing infants, the most highly exposed population group for the
chronic scenario). Therefore, taking into account the proposed uses, it
can be concluded with reasonable certainty that residues of dinotefuran
in food and drinking water will not result in unacceptable levels of
human health risk.
To calculate the DWLOC for the intermediate-term aggregate exposure
relative to a sub-chronic toxicity endpoint, the chronic dietary food
exposure from EXPedite\TM\ plus the intermediate-term non-dietary
exposures were subtracted from the NOAEL, divided by the target MOE
(100), to obtain the acceptable intermediate-term exposure to
dinotefuran in drinking water. DWLOCs, as presented below, were then
calculated using default body weights and drinking water consumption
figures.

[[Page 39554]]

Table 4.--Intermediate-term Aggregate Drinking Water Assessment
--------------------------------------------------------------------------------------------------------------------------------------------------------
NOAEL/MOE Mg/Kg/ Aggregate Exposure Maximum Water
Population Subgroup Day Mg/Kg/Day Exposure mg/kg/day SCI-GROW (ppb) FIRST (ppb) DWLOC (ppb)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Toddlers (1 to 3)\1\ 0.307 0.217 2.852 0.94 6.24 42,785
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Assume 70kg bodyweight

The estimated average concentration of dinotefuran in surface water
is 6.24 ppb. This value is less than the DWLOC for dinotefuran as a
contribution to intermediate-term aggregate exposure (42,785 ppb).
Therefore, taking into account the proposed uses, it can be concluded
with reasonable certainty that residues of dinotefuran in residential
environments and in food and drinking water will not result in
unacceptable levels of human health risk.

D. Cumulative Effects

The potential for cumulative effects of dinotefuran and other
substances that have a common mechanism of toxicity has also been
considered. Dinotefuran belongs to a pesticide chemical class known as
the neonicotinoids and subclass nitroguanadines. There is no reliable
information to indicate that toxic effects produced by dinotefuran
would be cumulative with those of any other chemical including another
pesticide. Therefore, Mitsui believes it is appropriate to consider
only the potential risks of dinotefuran in an aggregate risk
assessment.

E. Safety Determinations

1. U.S. population. Using the chronic exposure assumptions and the
proposed RfD described above, the dietary exposure to dinotefuran for
the U.S. population (48 states, all seasons) was calculated to be 0.32%
of the RfD of 1.27 mg/kg/day. The resulting DWLOC, 44,306 ppb, is much
greater than the estimated average concentration of dinotefuran in
surface water, 6.24 ppb. Therefore, taking into account the proposed
uses, it can be concluded with reasonable certainty that residues of
dinotefuran in residential environments and in food and drinking water
will not result in unacceptable levels of human health risk.
2. Infants and children. FFDCA section 407 provides that EPA shall
apply an additional safety factor for infants and children to account
for prenatal and postnatal toxicity and the completeness of the data
base. Only when there is no indication of increased sensitivity of
infants and children and when the data base is complete, may the extra
safety factor be removed. In the case of dinotefuran, the toxicology
data base is complete. There is no indication of increased sensitivity
in the data base overall, and specifically, there is no indication of
increased sensitivity in the developmental and multi-generation
reproductive toxicity studies. Therefore, Mitsui concludes that there
is no need for an additional safety factor; the RfD of 1.27 mg/kg/day
and sub-chronic NOAEL of 307 mg/kg/day are protective of infants and
children.
Using the chronic exposure assumptions and the proposed RfD
described above, the dietary exposure to dinotefuran for infants and
children (1 to 6 years) was calculated to be 0.57% of the reference
dose of 1.27 mg/kg bwt/day. The resulting DWLOC for non-nursing
infants, 12,666 ppb, is much greater than the estimated average
concentration of dinotefuran in surface water, 6.24 ppb.
Using the intermediate-term exposure assumptions and the proposed
NOAEL described above, the intermediate-term aggregate exposure to
dinotefuran for the toddlers (1 to 3 years) resulted in an MOE of
1,410. The resulting DWLOC, 42,785 ppb, is much greater than the
estimated average concentration of dinotefuran in surface water, 6.24
ppb. Therefore, taking into account the proposed uses, it can be
concluded with reasonable certainty that residues of dinotefuran in
residential environments and in food and drinking water will not result
in unacceptable levels of human health risk.

F. International Tolerances

No codex maximum residue levels have been established for residues
of dinotefuran on any crops at this time.

[FR Doc. 03-16737 Filed 7-1-03; 8:45 am]
BILLING CODE 6560-50-S

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Dinotefuran; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food

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