[Federal Register Volume 68, Number 127 (Wednesday, July 2, 2003)]
[Notices]
[Pages 39547-39554]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-16737]


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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: [email protected].

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:
    [sbull] Crop production (NAICS 111)
    [sbull] Animal production (NAICS 112)
    [sbull] Food manufacturing (NAICS 311)
    [sbull] 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.epa.gov/edocket/ to submit or view public 
comments, access the index listing of the contents of the official 
public docket, and to access those documents in the public docket that 
are available electronically. Although not all docket materials may be 
available electronically, you may still access any of the publicly 
available docket materials through the docket facility identified in 
Unit I.B.1. Once in the system, select ``search,'' then key in the 
appropriate docket ID number.
    Certain types of information will not be placed in EPA's Dockets. 
Information claimed as CBI and other information whose disclosure is 
restricted by statute, which is not included in the official public 
docket, will not be available for public viewing in EPA's electronic 
public docket. EPA's policy is that copyrighted material will not be 
placed in EPA's electronic public docket but will be available only in 
printed, paper 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 [email protected], 
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