[Federal Register Volume 69, Number 87 (Wednesday, May 5, 2004)]
[Notices]
[Pages 25095-25100]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-10103]


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ENVIRONMENTAL PROTECTION AGENCY

[OPP-2004-0106; FRL-7355-1]


Imidacloprid; 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-2004-0106, must be 
received on or before June 4, 2004.

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: Dani Daniel, Registration Division 
(7505C), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone 
number: (703) 305-5409; 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 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)

[[Page 25096]]

     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-2004-0106. 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 the EPA Dockets. 
Information claimed as CBI and other information whose disclosure is 
restricted by statute, which is not included in the official public 
docket, will not be available for public viewing in EPA's electronic 
public docket. EPA's policy is that copyrighted material will not be 
placed in EPA's electronic public docket but will be available only in 
printed, paper form in the official public docket. To the extent 
feasible, publicly available docket materials will be made available in 
EPA's electronic public docket. When a document is selected from the 
index list in EPA Dockets, the system will identify whether the 
document is available for viewing in EPA's electronic public docket. 
Although not all docket materials may be available electronically, you 
may still access any of the publicly available docket materials through 
the docket facility identified in Unit I.B. EPA intends to work towards 
providing electronic access to all of the publicly available docket 
materials through EPA's electronic public docket.
    For public commenters, it is important to note that EPA's policy is 
that public comments, whether submitted electronically or in paper, 
will be made available for public viewing in EPA's electronic public 
docket as EPA receives them and without change, unless the comment 
contains copyrighted material, CBI, or other information whose 
disclosure is restricted by statute. When EPA identifies a comment 
containing copyrighted material, EPA will provide a reference to that 
material in the version of the comment that is placed in EPA's 
electronic public docket. The entire printed comment, including the 
copyrighted material, will be available in the public docket.
    Public comments submitted on computer disks that are mailed or 
delivered to the docket will be transferred to EPA's electronic public 
docket. Public comments that are mailed or delivered to the docket will 
be scanned and placed in EPA's electronic public docket. Where 
practical, physical objects will be photographed, and the photograph 
will be placed in EPA's electronic public docket along with a brief 
description written by the docket staff.

C. How and to Whom Do I Submit Comments?

    You may submit comments electronically, by mail, or through hand 
delivery/courier. To ensure proper receipt by EPA, identify the 
appropriate docket ID number in the subject line on the first page of 
your comment. Please ensure that your comments are submitted within the 
specified comment period. Comments received after the close of the 
comment period will be marked ``late.'' EPA is not required to consider 
these late comments. If you wish to submit CBI or information that is 
otherwise protected by statute, please follow the instructions in Unit 
I.D. Do not use EPA Dockets or e-mail to submit CBI or information 
protected by statute.
    1. Electronically. If you submit an electronic comment as 
prescribed in this unit, EPA recommends that you include your name, 
mailing address, and an e-mail address or other contact information in 
the body of your comment. Also include this contact information on the 
outside of any disk or CD ROM you submit, and in any cover letter 
accompanying the disk or CD ROM. This ensures that you can be 
identified as the submitter of the comment and allows EPA to contact 
you in case EPA cannot read your comment due to technical difficulties 
or needs further information on the substance of your comment. EPA's 
policy is that EPA will not edit your comment, and any identifying or 
contact information provided in the body of a comment will be included 
as part of the comment that is placed in the official public docket, 
and made available in EPA's electronic public docket. If EPA cannot 
read your comment due to technical difficulties and cannot contact you 
for clarification, EPA may not be able to consider your comment.
    i. EPA Dockets. Your use of EPA's electronic public docket to 
submit comments to EPA electronically is EPA's preferred method for 
receiving comments. Go directly to EPA Dockets at 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-2004-0106. 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-2004-0106. 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

[[Page 25097]]

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-2004-0106.
    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-2004-0106. 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 a pesticide petition as follows proposing the 
establishment and/or amendment of regulations for residues of a certain 
pesticide chemical in or on various food commodities under section 408 
of FFDCA, 21 U.S.C. 346a. EPA has determined that this petition 
contains data or information regarding the elements set forth in FFDCA 
section 408(d)(2); however, EPA has not fully evaluated the sufficiency 
of the submitted data at this time or whether the data support granting 
of the petition. Additional data may be needed before EPA rules on the 
petition.

List of Subjects

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

    Dated: April 26, 2004.
Betty Shackleford,
Acting Director, Registration Division, Office of Pesticide Programs.

Summary of Petition

    The petitioner summary of the pesticide petition is printed below 
as required by FFDCA section 408(d)(3). The summary of the petition was 
prepared by the petitioner and represents the view of the petitioner. 
The petition summary announces the availability of a description of the 
analytical methods available to EPA for the detection and measurement 
of the pesticide chemical residues or an explanation of why no such 
method is needed.

Gustafson LLC

4F6825

    EPA has received a pesticide petition (4F6825) from Gustafson LLC, 
1400 Preston Road, Suite 400, Plano, TX 75093 proposing, pursuant to 
section 408(d) of FFDCA, 21 U.S.C. 346a(d), to amend 40 CFR part 180 by 
establishing a tolerance for residues of imidacloprid, 1-[(6-chloro-3-
pyridinyl)methyl]-N-nitro-2-imidazolidinimine in or on the raw 
agricultural commodity soybean, seed at 1.0 parts per million (ppm) and 
the processed commodity soybean, meal at 2.5 ppm. EPA has determined 
that the petition contains data or information regarding the elements 
set forth in section 408(d)(2) of the FFDCA; however, EPA has not fully 
evaluated the sufficiency of the submitted data at this time or whether 
the data support granting of the petition. Additional data may be 
needed before EPA rules on the petition.

A. Residue Chemistry

    1. Plant metabolism. The nature of the imidacloprid residue in 
plants and livestock is adequately understood. The residues of concern 
are combined residues of imidacloprid and its metabolites containing 
the 6-chloropyridinyl moiety, all calculated as imidacloprid.
    2. Analytical method. The analytical method is a common moiety 
method for imidacloprid and its metabolites containing the 6-
chloropyridinyl moiety using a permanganate oxidation, silyl 
derivatization, and capillary gas chromatography/mass spectrometry (GC-
MS) selective ion monitoring. This method has successfully passed a 
petition method validation in EPA labs. There is a confirmatory method 
specifically for imidacloprid and several metabolites utilizing GC/MS 
and high performance liquid chromotography/ultraviolet (HPLC-UV) which 
has been validated by EPA as well. Imidacloprid and its metabolites are 
stable for at least 24 months in the commodities when frozen.
    3. Magnitude of residues. Gustafson conducted three residue crop 
field trials to evaluate the quantity of imidacloprid expected in 
soybeans from application of Gaucho. Trials were conducted in three 
states. Imidacloprid residues in soybean seed were quantitated by gas 
chromatography using a mass selective detector. The limit of 
quantitation (LOQ) was 0.05 ppm. The average field result was 0.277 
ppm. In a 10x processing study with soybean, the average residue in 
soybean meal was 0.947 ppm. The concentration factor for soybean meal 
is 2.2x.

[[Page 25098]]

B. Toxicological Profile

    1. Acute toxicity. The acute oral lethal dose (LD)50 
values for imidacloprid technical ranged from 424 milligrams/kilogram 
(mg/kg) in the male rat and >450 mg/kg in the female rat. The acute 
dermal LD50 was >5,000 mg/kg in the rat. The 4-hour rat 
inhalation lethal concentration (LC)50 was greater 5.33 mg/
L. Imidacloprid was not irritating to rabbit skin or eyes. Imidacloprid 
did not cause skin sensitization in guinea pigs. In an acute 
neurotoxicity study the LOEL = 42 milligrams/kilogram body weight/day 
(mg/kg bwt/day).
    2. Genotoxicty. Mutagenicity studies as shown below have 
demonstrated that imidacloprid is non-mutagenic both in vivo and in 
vitro.
    3.Reproductive and developmental toxicity. In a developmental 
toxicity study with Sprague-Dawley rats, groups of pregnant animals 
(25/group) received oral administration of imidacloprid (94.2%) at 0, 
10, 30, or 100 mg/kg bwt/day during gestation days 6 through 16. 
Maternal toxicity was manifested as decreased body weight gain at all 
dose levels and reduced food consumption at 100 mg/kg bwt/day. No 
treatment-related effects were seen in any of the reproductive 
parameters (i.e., Cesarean section evaluation). At 100 mg/kg bwt/day, 
developmental toxicity manifested as wavy ribs (fetus =7/149 in treated 
vs. 2/158 in controls and litters, 4/25 vs. 1/25). For maternal 
toxicity, the lowest observed effect level (LOEL) was 10 mg/kg bwt/day 
(LDT) based on decreased body weight gain; a no observed adverse effect 
level (NOAEL) was not established. For developmental toxicity, the 
NOAEL was 30 mg/kg bwt/day and the LOEL was 100 mg/kg bwt/day based on 
increased wavy ribs (MRID No. 42256338).
    In a developmental toxicity study with Chinchilla rabbits, groups 
of 16 pregnant does were given oral doses of imidacloprid (94.2%) at 0, 
8, 24, or 72 mg/kg bwt/day during gestation days 6 through 18. For 
maternal toxicity, the NOAEL was 24 mg/kg bwt/day and the LOEL was 72 
mg/kg bwt/day based on mortality, decreased body weight gain, increased 
resorptions, and increased abortions. For developmental toxicity, the 
NOAEL was 24 mg/kg bwt/day and the LOEL was 72 mg/kg bwt/day based on 
decreased fetal body weight, increased resorptions, and increased 
skeletal abnormalities (MRID No. 42256339).
    In a 2-generation reproductive toxicity study, imidacloprid (95.3%) 
was administered to Wistar/Han rats at dietary levels of 0, 100, 250, 
or 700 ppm (0, 7.3, 18.3, or 52.0 mg/kg bwt/day for males and 0, 8.0, 
20.5, or 57.4 mg/kg bwt/day for females) (MRID No. 42256340, Doc. No. 
010537). For parental/systemic/reproductive toxicity, the NOAEL was 250 
ppm (18.3 mg/kg bwt/day) and the LOEL was 750 ppm (52 mg/kg bwt/day), 
based on decreases in body weight in both sexes in both generations. 
Based on these factors, the EPA/OPP/HED Hazard Identification 
Assessment Review Committee (HIARC) recommended that the Data 
Evaluation Record should be revised to indicate the parental/systemic/
reproductive NOAEL and LOEL to be 250 and 700 ppm, respectively, based 
upon the body weight decrements observed in both sexes in both 
generations.
    4. Subchronic toxicity. In a dermal toxicity study, groups of five 
male and five female New Zealand White rabbits received repeated dermal 
applications of imidacloprid (95%) at 1,000 milligrams/kilogram (mg/kg) 
body weight/day (bwt/day) (Limit Dose), 6 hours/day, 5 days/week for 3 
weeks. No dermal or systemic toxicity was seen. For systemic and dermal 
toxicity, the NOAEL was greater 1,000 mg/kg bwt/day; a LOEL was not 
established (MRID No. 42256329).
    In an oral toxicity study, groups of Fischer 344 rats (12/sex/dose) 
were fed diets containing imidacloprid (98.8%) at 0, 150, 1,000, or 
3,000 ppm (0, 9.3, 63.3, or 196 mg/kg bwt/day in males and 0, 10.5, 
69.3 or 213 mg/kg bwt/day in females, respectively) for 90 days. No 
treatment-related effects were seen at 150 ppm. Treatment-related 
effects included decreases in body weight gain during the first 4 weeks 
of the study at 1,000 ppm (22% in males and 18% in females) and 3,000 
ppm (50% in males and 25% in females) with an associated decrease in 
forelimb grip strength especially in males. The NOAEL was 150 ppm (9.3 
and 10.5 mg/kg bwt/day in males and females, respectively) and the LOEL 
was 1,000 ppm (63.3 and 69.3 mg/kg bwt/day in males and females, 
respectively) (MRID No. 43286401).
    In a rat inhalation study (28-day study in which rats were exposed 
6 hours/day, 5 days/week for 4 weeks), the NOAEL for imidacloprid was 
5.5 mg/m\3\ (MRID No. 42273001).
    5.Chronic toxicity. In a chronic toxicity study, groups of beagle 
dogs (4/sex/dose) were fed diets containing imidacloprid (94.9%) at 0, 
200 or 1,250/2,500 ppm (0, 6.1, 15 or 41/72 mg/kg bwt/day, 
respectively) for 52 weeks. The 1,250 ppm dose was increased to 2,500 
ppm from week 17 onwards. The threshold NOAEL was 1,250 ppm (41 mg/kg 
bwt/day). The LOEL was 2,500 ppm (72 mg/kg bwt/day) based on increased 
cytochrome-P-450 levels in both sexes and was considered to be a 
threshold dose. Due to the lack of toxicity at 1,250 ppm, a LOEL was 
not established in this study; following the dose increase to the 2,500 
ppm level, toxicity was observed, thus making 1,250 ppm the threshold 
NOAEL and 2,500 ppm the threshold LOEL (MRID No. 42273002).
    6. Animal metabolism. The metabolism of NTN 33893 (imidacloprid) in 
rats was reported in seven studies. These data show that imidacloprid 
was rapidly absorbed and eliminated in the excreta (90% of the dose 
within 24 hours), demonstrating no biologically significant differences 
between sexes, dose levels, or route of administration. Elimination was 
mainly renal (70%-80% of the dose) and fecal (17%-25%). The major part 
of the fecal activity originated in the bile. Total body accumulation 
after 48 hours consisted of 0.5% of the radioactivity with the liver, 
kidney, lung, skin and plasma being the major sites of accumulation. 
Therefore, bioaccumulation of imidacloprid is low in rats. Maximum 
plasma concentration was reached between 1.1 and 2.5 hours. Two major 
routes of biotransformation were proposed for imidacloprid. The first 
route included an oxidative cleavage of the parent compound rendering 
6-chloronicotinic acid and its glycine conjugate. Dechlorination of 
this metabolite formed the 6-hydroxynicotinic acid and its mercapturic 
acid derivative. The second route included the hydroxylation followed 
by elimination of water of the parent compound rendering NTN 35884. A 
comparison between [methylene-14C]-imidacloprid and [imidazolidine-4,5-
14C]-imidacloprid showed that while the rate of excretion was similar, 
the renal portion was higher with the imidazolidine-labeled compound. 
In addition, accumulation in tissues was generally higher with the 
imidazolidine-labeled compound.
    A comparison between imidacloprid and one of its metabolites, WAK 
3839, showed that the total elimination was the same for both 
compounds. The proposed metabolic pathways for these two compounds were 
different. WAK 3839 was formed following pretreatment (repeated dosing) 
of imidacloprid.
    7. Endocrine disruption. The toxicology data base for imidacloprid 
is current and complete. Studies in this data base include evaluation 
of the potential effects on reproduction and development, and an 
evaluation of the pathology of the endocrine organs following short-
term or long-term exposure. These studies revealed no

[[Page 25099]]

primary endocrine effects due to imidacloprid.

C. Aggregate Exposure

    1. Dietary exposure. Assessments were conducted to evaluate 
potential risks due to chronic and acute dietary exposure of the U.S. 
population and selected population subgroups to residues of 
imidacloprid. These analyses cover all registered crops including 
rotational crops and soybean uses, and section 18 uses on blueberries, 
cranberries, table beets, strawberries, turnips. Novigen Sciences, 
Inc.'s Dietary Exposure Evaluation Model (DEEM\TM\, Version 7.81), 
which is licensed to Bayer CropScience, was used to estimate the 
chronic and acute dietary exposure (Tier 3) on behalf of Gustafson LLC. 
This software uses the food consumption data from the 1994-1998 USDA 
Continuing Surveys of Food Intake by Individuals (CSFII 1994-1998).
    The endpoint for acute dietary risk assessments is based on 
neurotoxicity characterized by decreases in motor or locomotor activity 
in female rats at 42 mg/kg bwt/day (LOEL) from an acute neurotoxicity 
study. Based on an uncertainty factor of 10x for interspecies and 10x 
for intraspecies the acute reference dose (aRfD) = 0.42 mg/kg bwt/day. 
EPA has determined that an additional uncertainty factor (UF) for FQPA 
(reduced to 3x) applies to all population subgroups for acute risk. 
Application of the additional 3x safety factor results in an acute 
population adjusted dose (aPAD) 0.14 mg/kg bwt/day or a MOE of 300.
    For chronic dietary analyses, EPA has established the reference 
dose (RfD) for imidacloprid at 0.057 mg/kg/day based on a NOAEL of 5.7 
mg/kg bwt/day from a rat chronic toxicity carcinogenicity study and 
uncertainty factors of 10x for interspecies and 10x for intraspecies. A 
chronic population adjusted dose (cPAD) of 0.057 mg/kg bwt/day was 
determined.
    Results from the acute and chronic dietary exposure analyses 
described below demonstrate a reasonable certainty that no harm to the 
overall U.S. population or any population subgroup will result from the 
use of imidacloprid on currently registered and pending uses.
    i. Food. Acute and chronic (Tier 3) risk assessments were made 
using the results of field trials conducted at maximum label 
application rates and the shortest pre-harvest intervals. For some of 
the vegetable crops, these residue data were collected at 1.5x or 
greater than the maximum label rate of 0.5 lb ai/A per season. In 
addition, no adjustments were made to account for dissipation of 
residues during storage, transportation from the field to the consumer, 
washing or peeling. Therefore, the actual dietary exposure will be less 
than that presented here.
    For the chronic analysis, mean field trial residues were 
calculated. For the acute Monte Carlo analysis, the entire distribution 
of residue field trial data was used for the ``non-blended'' and 
``partially blended'' foods as determined by EPA's HED SOP 99.6. For 
the foods considered as ``blended'' by EPA'S HED SOP 99.6, mean field 
trial residue data were used. As allowed in EPA's draft guidance for 
submission of probabilistic human health exposure assessments one half 
LOD/LOQ values were used for all non-detected values (values below the 
sensitivity of the method).
    a. Acute. Bayer CropScience's acute Monte Carlo dietary exposure 
assessment estimated percent of the aPAD and corresponding margins of 
exposure (MOE) for the overall U.S. population (all seasons), and 
various subpopulations. In this analysis, the exposure for the total 
U.S. population was equal to 7.8% of the aPAD at the 99.9th percentile. 
The most highly exposed population subgroup, children (1-2 years), had 
an exposure equal to 20.9% of the aPAD at the 99.9th percentile. 
Therefore, the acute dietary exposure estimates are below EPA's level 
of concern for the overall U.S. population as well as the various 
subpopulations.
    b. Chronic. Bayer CropScience's chronic dietary exposure estimated 
the percent of the chronic population adjusted dose (cPAD) for the 
overall U.S. population (all seasons) and various subpopulations. In 
this analysis, the exposure for the total U.S. population was equal to 
0.5% of the cPAD. The most highly exposed population subgroup, children 
(1-2 years), had an exposure equal to 1.5% of the cPAD. Therefore, the 
chronic exposure estimates are below EPA's level of concern for the 
overall U.S. population as well as the various subpopulations.
    ii. Drinking water. EPA, as published in the Federal Register (66 
FR 18554) (FRL-6777-6), calculated acute and chronic drinking water 
levels of concerns (DWLOCs) and compared them with the EECs for surface 
water and ground water. Based on this comparison, EPA determined that 
acute exposure and chronic exposure would not be expected to exceed the 
aPAD and cPAD, respectively.
    2. Non-dietary exposure--i. Residential turf. Bayer CropScience has 
conducted an exposure study to address the potential exposures of 
adults and children from contact with imidacloprid treated turf. The 
population considered to have the greatest potential exposure from 
contact with pesticide-treated turf soon after pesticides are applied 
are young children. Margins of safety (MOS) of 7,587-41,546 for 10-year 
old children and 6,859-45,249 for 5-year old children were estimated by 
comparing dermal exposure doses to the imidacloprid no observable 
effect level of 1,000 mg/kg/day established in a 15-day dermal toxicity 
study in rabbits. The estimated safe residue levels of imidacloprid on 
treated turf for 10-year old children ranged from 5.6-38.2 g/cm\2\ and 
for 5-year old children from 5.1-33.5 g/cm\2\. This compares with the 
average imidacloprid transferable residue level of 0.080 g/cm\2\ 
present immediately after the sprays have dried. These data indicate 
that children can safely contact imidacloprid-treated turf as soon 
after application as the spray has dried.
    ii. Termiticide. Imidacloprid is registered as a termiticide. Due 
to the nature of the treatment for termites, exposure would be limited 
to that from inhalation and was evaluated by EPA's Occupational and 
Residential Exposure Branch (OREB) and Bayer. Data indicate that the 
Margins of Safety for the worst case exposures for adults and infants 
occupying a treated building who are exposed continuously (24 hours/
day) are 8.0 x 10\7\ and 2.4 x 10\8\, respectively; and exposure can 
thus be considered negligible.
    iii. Tobacco smoke. Studies have been conducted to determine 
residues in tobacco and the resulting smoke following treatment. 
Residues of imidacloprid in cured tobacco following treatment were a 
maximum of 31 ppm (7 ppm in fresh leaves). When this tobacco was burned 
in a pyrolysis study only 2% percent of the initial residue was 
recovered in the resulting smoke (main stream plus side stream). This 
would result in an inhalation exposure to imidacloprid from smoking of 
approximately 0.0005 mg per cigarette. Using the measured subacute rat 
inhalation NOEL of 5.5 mg/m\3\, it is apparent that exposure to 
imidacloprid from smoking (direct and/or indirect exposure) would not 
be significant.
    iv. Pet treatment. Human exposure from the use of imidacloprid to 
treat dogs and cats for fleas has been addressed by EPA's Occupational 
and Exposure Branch (OREB) who have concluded that due to the fact that 
imidacloprid is not an inhalation or dermal toxicant and that while 
dermal absorption data are not available,

[[Page 25100]]

imidacloprid is not considered to present a hazard via the dermal 
route.

D. Cumulative Effects

    Imidacloprid is a chloronicotinyl insecticide. At this time, EPA 
has not made a determination that imidacloprid and other substances 
that may have a common mechanism of toxicity would have cumulative 
effects. Therefore, for these tolerance petitions, it is assumed that 
imidacloprid does not have a common mechanism of toxicity with other 
substances and only the potential risks of imidacloprid in its 
aggregate exposure are considered.

E. Safety Determination

    1. U.S. population. EPA has considered data from developmental 
toxicity studies in the rat and rabbit and a 2-generation reproduction 
study in the rat. These studies are discussed under section A 
(Toxicology Profile) above. The developmental toxicity data 
demonstrated no increased sensitivity of rats or rabbits to in utero 
exposure to imidacloprid. In addition, the multi-generation 
reproductive toxicity study did not identify any increased sensitivity 
of rats to in utero or postnatal exposure. Parental NOAELs were lower 
or equivalent to developmental or offspring NOAELs. The developmental 
toxicity studies are designed to evaluate adverse effects on the 
developing organism resulting from maternal pesticide exposure during 
gestation. Reproduction studies provide information relating to effects 
from exposure to the pesticide on the reproductive capability of mating 
animals and data on systemic toxicity.
    Based on the exposure assessments described above and on the 
completeness and reliability of the toxicity data, it can be concluded 
that the dietary exposure estimates from all label and pending uses of 
imidacloprid are 7.8% of the aPAD at the 99.9th percentile and 0.5% of 
the cPAD for the U.S. population. Thus, it can be concluded that there 
is a reasonable certainty that no harm will result from aggregate 
exposure to imidacloprid residues.
    2. Infants and children. Based on the exposure assessments 
described above for the safety determination of the U.S. population and 
on the completeness and reliability of the toxicity data, it can be 
concluded that the dietary exposure estimates from all label and 
pending uses of imidacloprid are 20.9% of the aPAD at the 99.9th 
percentile and 1.5% of the cPAD for the most sensitive population 
subgroup, children 1-2 years. Thus, it can be concluded that there is a 
reasonable certainty that no harm will result from aggregate exposure 
to imidacloprid residues.

F. International Tolerances

    No CODEX maximum residue levels have been established for residues 
of imidacloprid on soybean.
[FR Doc. 04-10103 Filed 5-4-04; 8:45 am]
BILLING CODE 6560-50-S