[Federal Register Volume 68, Number 43 (Wednesday, March 5, 2003)]
[Notices]
[Pages 10464-10469]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-5034]


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ENVIRONMENTAL PROTECTION AGENCY

[OPP-2003-0027; FRL-7291-1]


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-2003-0027, must be 
received on or before April 4, 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: 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 are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
Potentially affected entities may include, but are not limited to:

[[Page 10465]]

    [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-2003-0027. 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-2003-0027 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-2003-0027. 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

[[Page 10466]]

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-2003-0027.
    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-2003-0027. 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 the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a. 
EPA has determined that this petition contains data or information 
regarding the elements set forth in FFDCA section 408(d)(2); however, 
EPA has not fully evaluated the sufficiency of the submitted data at 
this time or whether the data support granting of the petition. 
Additional data may be needed before EPA rules on the petition.

List of Subjects

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

    Dated: February 11, 2003.
Debra Edwards,
Acting Director, Registration Division, Office of Pesticide Programs.

Summary of Petition

    The petitioner's 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 views 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.

 Bayer CropScience

 PP 0E6074

    EPA has received a pesticide petition (0E6074) from Bayer 
CropScience, 2 T.W. Alexander Drive, PO Box 12014, Research Triangle 
Park, NC 27709 proposing, pursuant to section 408(d) of the FFDCA, 21 
U.S.C. 346a(d), to amend 40 CFR 180.472, by establishing an import 
tolerance for residues of imidacloprid, [(1-[6-chloro-3-pyridinyl) 
methyl]-N-nitro-2-imidazolidinimine) and its metabolites containing the 
6-chloropyridinyl moiety, all expressed as 1-[(6-chloro-3-
pyridinyl)methyl]-N-nitro-2-imidazolidinimine] in or on the raw 
agricultural commodity (RAC): Banana at 0.01 parts per million (ppm). 
EPA has determined that the petition contains data or information 
regarding the elements set forth in section 408(d)(2) of the FFDCA; 
however, EPA has not fully evaluated the sufficiency of the submitted 
data at this time or whether the data supports granting of the 
petition. Additional data may be needed before EPA rules on the 
petition.

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 it 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 chromatography 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. For bananas, Bayer conducted 12 residue 
crop field trials to evaluate the quantity of imidacloprid expected in 
bananas from applications of Confidor 70 WG and Confidor 350 SC. Trials 
were conducted at eight sites in the Caribbean coastal area of Central 
America and 4 sites in

[[Page 10467]]

the Pacific coastal area of Ecuador. Imidacloprid residues in banana 
whole fruit were quantitated by GC using a mass selective detector. The 
limit of quantitation (LOQ) was 0.01 ppm. The highest average field 
trial (HAFT) was 0.01 ppm in bananas.

B. Toxicological Profile

    1. Acute toxicity. The acute oral LD50 values for 
imidacloprid technical ranged from 424 milligrams/kilograms (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 
LC50 was <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 lowest observed 
adverse effect level (LOAEL) = 42 mg/kg body weight day (bwt/day).
    2. Genotoxicty. Mutagenicity studies 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 milligrams/kilograms of 
body weight/day (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 LOAEL was 10 mg/kg bwt/day 
lowest dose tested (LDT) based on decreased body weight gain; a NOAEL 
was not established. For developmental toxicity, the NOAEL was 30 mg/kg 
bwt/day and the LOAEL was 100 mg/kg bwt/day based on increased wavy 
ribs master record identification (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 LOAEL 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 LOAEL 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 LOAEL was 750 ppm (52 mg/kg bwt/day), based on 
decreases in body weight in both sexes in both generations. Based on 
these factors, EPA recommended that the Data Evaluation Record should 
be revised to indicate the parental/systemic/reproductive NOAEL and 
LOAEL 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 mg/kg bwt/day (LD), 6 
hours/day, 5 days/week for 3 weeks. No dermal or systemic toxicity was 
seen. For systemic and dermal toxicity, the NOAEL was <1,000 mg/kg bwt/
day, a LOAEL 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 LOAEL 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/m3 (MRID No. 422730-01).
     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 LOAEL 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 LOAEL 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 LOAEL (MRID No. 42273002).
    6. Animal metabolism. The metabolism 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 imidacloprid. 
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 10468]]

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; uses pending with EPA in the 2003 work plan including 
dry beans, peas, bushberries, lingonberry, juneberries, salal, carrots, 
turnips, okra, cranberries, artichoke (globe), watercress, beet roots, 
leaves of root and tuber vegetables, stone fruit, mamey sapote, guava, 
feijoa, jaboticaba, wax jambu, starfruit, passion fruit, acerola, 
strawberry, cucumber (greenhouse), and tomato (greenhouse), this import 
tolerance petition on bananas; and active and proposed section 18 uses 
on blueberries, cranberries, table beets, strawberries, turnips.
    Novigen Sciences, Inc.'s Dietary Exposure Evaluation Model 
(DEEMTM), which is licensed to Bayer, was used to estimate 
the chronic and acute dietary exposure. This software uses the food 
consumption data from the 1994-1998 Department of Agriculture (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, the LOAEL from an acute 
neurotoxicity study. Based on an uncertainty factor (UF) of 10x for 
inter-species and 10x for intra-species the acute reference dose (aRfD) 
= 0.42 mg/kg bwt/day. EPA has determined that an additional 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 margin of 
exposure (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 inter-species 
and 10x for intra-species. EPA has determined that an additional UF for 
FQPA (reduced to 3x) applies to all population subgroups for chronic 
risk. Application of the additional 3x safety factor results in a 
chronic population adjusted dose (cPAD) of 0.019 mg/kg bwt/day. 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 active ingredient/acre 
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 limit of 
detection (LOD)/LOQ values were used for all non-detected values 
(values below the sensitivity of the method). Bayer's acute Monte Carlo 
dietary exposure assessment estimated percent of the aPAD and 
corresponding 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 7.73% of the aPAD at the 99.9th 
percentile. The most highly exposed population subgroup, children (1-6 
years), had an exposure equal to 16.42% 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. Bayer's chronic 
dietary exposure estimated the percent of the 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 1.4% of the 
cPAD. The most highly exposed population subgroup, children (1-6 
years), had an exposure equal to 3.0% 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 of 
April 10, 2001 (66 FR 18554) (FRL-6777-6), calculated acute and chronic 
DWLOCs and compared them with the EECs for surface and ground water. 
Based on this comparison, they determined that acute exposure and 
chronic exposure would not be expected to exceed the aPAD and cPAD, 
respectively. It is not expected that the additional exposure from the 
minor crops pending in EPA's 2003 work plan would significantly change 
EPA's water assessment.
    2. Non-dietary exposure--i. Residential turf. Bayer 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 NOAEL 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 [mu]g/cm2 and for 
5-year old children from 5.1 - 33.5 [mu]g/cm2. This compares 
with the average imidacloprid transferable residue level of 0.080 
[mu]g/cm2 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 and Bayer. Data 
indicate that the MOS 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% 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 
NOAEL of 5.5 mg/m3, it is apparent that exposure to 
imidacloprid from smoking (direct and/or indirect exposure) would not 
be significant.

[[Page 10469]]

    iv. Pet treatment. Human exposure from the use of imidacloprid to 
treat dogs and cats for fleas has been addressed by EPA with the 
conclusion that due to the fact that imidacloprid is not an inhalation 
or dermal toxicant and that while dermal absorption data are not 
available, 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 post-natal 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.
    FFDCA section 408 provides that EPA shall apply an additional 
tenfold margin of safety for infants and children in the case of 
threshold effects to account for prenatal and postnatal toxicity and 
the completeness of the data base unless EPA determines that a 
different MOS will be safe for infants and children. MOS are 
incorporated into EPA risk assessments either directly through use of a 
MOE analysis or through using uncertainty (safety) factors (UF) in 
calculating a dose level that poses no appreciable risk to humans. EPA 
believes that reliable data support using the standard UF (usually 100 
for combined inter-species and intra-species variability) and not the 
additional tenfold MOE/UF when EPA has a complete data base under 
existing guidelines and when the severity of the effect in infants or 
children or the potency or unusual toxic properties of a compound do 
not raise concerns regarding the adequacy of the standard MOE/UF.
    Although developmental toxicity studies showed no increased 
sensitivity in fetuses as compared to maternal animals following in 
utero exposures in rats and rabbits, no increased sensitivity in pups 
as compared to adults was seen in the 2-generation reproduction 
toxicity study in rats, and the toxicology data base is complete as to 
core requirements, EPA has determined that the additional safety factor 
for the protection of infants and children will be retained but reduced 
to 3x based on the following weight-of-the-evidence considerations 
relating to potential sensitivity and completeness of the data:
    i. There is concern for structure activity relationship. 
Imidacloprid, a chloronicotinyl compound, is an analog to nicotine and 
studies in the published literature suggests that nicotine, when 
administered causes developmental toxicity, including functional 
deficits, in animals and/or humans that are exposed in utero.
    ii. There is evidence that imidacloprid administration causes 
neurotoxicity following a single oral dose in the acute study and 
alterations in brain weight in rats in the 2-year carcinogenicity 
study.
    iii. The concern for structure activity relationship along with the 
evidence of neurotoxicity dictates the need of a developmental 
neurotoxicity study for assessment of potential alterations on 
functional development. Because a developmental neurotoxicity study 
potentially relates to both acute and chronic effects in both the 
mother and the fetus, EPA has applied the additional UF for FQPA for 
all population subgroups, and in both acute and chronic risk 
assessments.
    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 7.73% of the aPAD at the 99.9th percentile 
and 1.4% 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 16.42% of the aPAD at the 
99.9th percentile and 3.0% of the cPAD for the most 
sensitive population subgroup, children 1-6 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 any crops pending in EPA's 2003 work plan.
[FR Doc. 03-5034 Filed 3-4-03; 8:45 am]
BILLING CODE 6560-50-S