[Federal Register Volume 70, Number 119 (Wednesday, June 22, 2005)]
[Notices]
[Pages 36155-36159]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 05-12079]


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ENVIRONMENTAL PROTECTION AGENCY

[OPP-2005-0105; FRL-7710-1]


Fenpropimorph; 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 reannounces the filing of a pesticide petition 
proposing the establishment of regulations for residues of a certain 
pesticide chemical in or on various food commodities.

DATES: Comments, identified by docket identification (ID) number OPP-
2005-0105, must be received on or before July 22, 2005.

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

FOR FURTHER INFORMATION CONTACT: Mary L. Waller, Registration Division 
(7505C), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone 
number: (703) 308-9354; 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)
     Food manufacturing (NAICS 311)
     Pesticide manufacturing (NAICS 32532)
    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in this unit could also be 
affected. The North American Industrial Classification System (NAICS) 
codes have been provided to assist you and others in determining 
whether this action might apply to certain entities. If you have any 
questions regarding the applicability of this action to a particular 
entity, consult the person listed under FOR FURTHER INFORMATION 
CONTACT.

B. How Can I Get Copies of this Document and Other Related Information?

    1. Docket. EPA has established an official public docket for this 
action under docket ID number OPP-2005-0105. The official public docket 
consists of the documents specifically referenced in this action, any 
public comments received, and other information related to this action. 
Although a part of the official docket, the public docket does not 
include Confidential Business Information (CBI) or other information 
whose disclosure is restricted by statute. The official public docket 
is the collection of materials that is available for public viewing at 
the Public Information and Records Integrity Branch (PIRIB), Rm. 119, 
Crystal Mall 2, 1801 S. Bell St., Arlington, VA. This docket 
facility is open from 8:30 a.m. to 4 p.m., Monday through Friday, 
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.1. EPA intends to work 
towards providing electronic access to all of the publicly available 
docket materials through EPA's electronic public docket.
    For public commenters, it is important to note that EPA's policy is 
that public comments, whether submitted electronically or in paper, 
will be made available for public viewing in EPA's electronic public 
docket as EPA receives them and without change, unless the comment 
contains copyrighted material, CBI, or other information whose 
disclosure is restricted by statute. When EPA identifies a comment 
containing copyrighted material, EPA will provide a reference to that 
material in the version of the comment that is placed in EPA's 
electronic public docket. The entire printed comment, including the 
copyrighted material, will be available in the public docket.
    Public comments submitted on computer disks that are mailed or 
delivered to the docket will be transferred to EPA's electronic public 
docket. Public comments that are mailed or delivered to the docket will 
be scanned and placed in EPA's electronic public docket. Where 
practical, physical objects will be photographed, and the photograph 
will be placed in EPA's electronic public docket along with a brief 
description written by the docket staff.

C. How and to Whom Do I Submit Comments?

    You may submit comments electronically, by mail, or through hand 
delivery/courier. To ensure proper receipt by EPA, identify the 
appropriate docket ID number in the subject line on the first page of 
your comment. Please ensure that your comments are

[[Page 36156]]

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-2005-0105. 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-2005-0105. In contrast to EPA's 
electronic public docket, EPA's e-mail system is not an ``anonymous 
access'' system. If you send an e-mail comment directly to the docket 
without going through EPA's electronic public docket, EPA's e-mail 
system automatically captures your e-mail address. E-mail addresses 
that are automatically captured by EPA's e-mail system are included as 
part of the comment that is placed in the official public docket, and 
made available in EPA's electronic public docket.
    iii. Disk or CD ROM. You may submit comments on a disk or CD ROM 
that you mail to the mailing address identified in Unit I.C.2. These 
electronic submissions will be accepted in WordPerfect or ASCII file 
format. Avoid the use of special characters and any form of encryption.
    2. By mail. Send your comments to: Public Information and Records 
Integrity Branch (PIRIB) (7502C), Office of Pesticide Programs (OPP), 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460-0001, Attention: Docket ID Number OPP-2005-0105.
    3. By hand delivery or courier. Deliver your comments to: Public 
Information and Records Integrity Branch (PIRIB), Office of Pesticide 
Programs (OPP), Environmental Protection Agency, Rm. 119, Crystal Mall 
2, 1801 S. Bell St., Arlington, VA, Attention: Docket ID 
Number OPP-2005-0105. 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: May 27, 2005.
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

[[Page 36157]]

pesticide chemical residues or an explanation of why no such method is 
needed.

BASF Corporation

PP 7E4874

    EPA has received a pesticide petition (PP 7E4874) from BASF 
Corporation, 26 Davis Drive, Research Triangle Park, NC 27709-3528, 
proposing pursuant to section 408(d) of the FFDCA, 21 U.S.C. 346a(d), 
to amend 40 CFR part 180 by establishing a tolerance for residues of 
fenpropimorph, (+)-cis-4-(3-((4-tert-butylphenyl))-2-methylpropyl)-2,6-
dimethylmorpholine in or on the raw agricultural commodity banana at 
1.5 parts per million (ppm) of which no more than 0.3 ppm is found in 
the pulp. This petition was previously published in the Federal 
Register on December 7, 1998 (63 FR 67476) (FRL-6047-2), identified by 
the docket control number PF-848. 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 results of the banana metabolism study 
indicate that fenpropimorph constitutes the total toxic residue. All 
other significant portions of the total radioactive residue are due to 
natural products, predominately carbohydrates. Therefore, for 
regulatory purposes, the residue of concern determined by the 
analytical method consists only of fenpropimorph.
    2. Analytical method. The method of analysis includes extraction, 
liquid/liquid partition, column clean-up, and quantitation by gas 
chromatography/nitrogen-phosphorus detector. The overall fortification 
recoveries from the unpeeled, whole banana, and the peeled (pulp) 
samples together averaged 87.1%  9.3% (N=76).
    3. Magnitude of residues. Fifteen crop residue trials were 
conducted in the banana growing regions of Mexico, South and Central 
America including three sites in Colombia, four sites in Costa Rica, 
four sites in Ecuador, one site in Guatemala, two sites in Honduras, 
and one site in Mexico. Four sequential applications were made at the 
target rate of 545 gram/hectares (g/ha) to both bagged and unbagged 
bananas at each site. Fruit from both the bagged and unbagged 
treatments were harvested at 0 days following the last application.
    Whole fruit (peel and pulp) samples and pulp only samples were 
analyzed for all treatments at all sites. Under typical practices, 
bagged banana residues in the whole fruit ranged from the limit of 
quantitation (LOQ) 0.050 milligrams/kilogram (mg/kg) to a maximum of 
0.4 mg/kg. Banana pulp residues from bagged bananas ranged from the < 
LOQ (0.050 mg/kg to 0.20 mg/kg and averaged 0.0518 mg/kg). The average 
value was calculated by assuming all values below the LOQ were equal to 
one-half the < LOQ or 0.025 mg/kg. Under worst-case practices, unbagged 
bananas residues in the whole fruit ranged from < the LOQ (0.050 mg/kg 
to a maximum of 1.4 mg/kg). Banana pulp residues from unbagged bananas 
ranged from < the LOQ (0.050 mg/kg to 0.43 mg/kg and averaged 0.1149 
mg/kg). The average value was calculated by assuming all values below 
the LOQ were equal to one-half the LOQ or 0.025 mg/kg.

B. Toxicological Profile

    Based on review of the available data, BASF believes the reference 
dose (RfD) for fenpropimorph will be based on a 2-year feeding study in 
rats with a threshold no observed adverse effect level (NOAEL) of 0.3 
milligrams/kilogram/day (mg/kg/day). Using an uncertainty factor of 
100, the RfD is calculated to be 0.003 mg/kg/day. A summary of the 
available mammalian toxicology data is given in the following sections.
    1. Acute toxicity. Based on available acute toxicity data, 
fenpropimorph does not pose any acute toxicity risks. These studies are 
not required for an import tolerance, but we have provided the 
following information to demonstrate that fenpropimorph is not an acute 
toxicant. The acute toxicity studies place technical fenpropimorph in 
acute toxicity category III for acute oral, dermal, inhalation, and 
skin irritation; and in acute toxicity category IV for eye irritation 
and the technical material is not a skin sensitizer.
    2. Genotoxicty. The following genotoxicity tests were performed 
with fenpropimorph: A modified Ames Test (2 studies; point mutation) - 
Negative; In Vitro CHO/HPRT Mammalian Cell Mutation Assay (1 study; 
point mutation) - Negative; In Vitro Cytogenetic test in Chinese 
Hamster V79 cells (1 study; chromosome aberrations) - non-activated 
negative, activated equivocal; In Vitro Cytogenetics-Human lymphocytes 
(1 study; chromosome aberrations) - Negative; In Vivo Mouse 
Micronucleus Assay (2 studies; chromosome aberrations) - Negative; In 
Vitro UDS Test Using Rat Hepatocytes (1 study; DNA damage and repair): 
Negative; In Vivo dominant lethal test in mice (1 study; chromosome 
aberrations in germ cells) - Negative. Fenpropimorph has been tested in 
a total of nine genetic toxicology assays. These assays were performed 
both in vitro and in vivo. The weight of the evidence from these nine 
studies indicates that fenpropimorph is not genotoxic.
    3.Reproductive and developmental toxicity -- i. A developmental 
prenatal toxicity study was conducted via oral gavage in rats at doses 
of 0, 2.5, 10, 40, and 160 mg/kg/day from day 6 to 15 of gestation with 
a developmental toxicity NOAEL of 40 mg/kg/day and a maternal toxicity 
NOAEL of 10 mg/kg/day based on the following: (a) Signs of maternal 
toxicity, in the form of decreased body weights (bwt) and/or clinical 
signs observed at dose levels > 40 mg/kg/day; (b) maternal animals in 
the 160 mg/kg/day dose group showed an increased incidence of vaginal 
bleeding from day 10 to 19 of gestation and increased placental weight; 
(c) maternal animals in the 160 mg/kg/day dose group showed an increase 
in the number of resorptions as compared to controls; (d) decreases in 
fetal body weights and size and number of viable fetus were observed at 
160 milligrams/kilogram body weight/day (mg/kg bwt/day); (e) a 
significant number of fetuses had a finding of cleft palate at 160 mg/
kg bwt/day; and (f) litters from animals treated at the lower doses 
remained entirely unaffected.
    ii. A perinatal developmental toxicity study was conducted via oral 
gavage in rats at doses of 0, 2.5, 10, 40, and 160 mg/kg/day from 
gestation day 15 to day 21 post partum with a developmental and 
maternal toxicity NOAEL of 40 mg/kg/day based on the following: (a) 
Four high dose maternal animals died on days 1 to 6 after delivery; (b) 
signs of maternal toxicity, in the form of decreased body weight and/or 
clinical signs observed at the top dose level; (c) at birth, body 
weight was significantly reduced in the pups of the top dose group; (d) 
the brood care at the top dose group animals was generally 
unsatisfactory and led to a high perinatal mortality of the fetuses 
with only 30 viable fetuses left on day 1 post partum, the dead fetuses 
showed no increased incidence of malformations; (e) the few surviving 
pups of the dams at the 160 mg/kg/day dose group showed decreases in 
fetal body weight and size was retarded, no disturbances were found in 
the functional and behavioral tests that were conducted on

[[Page 36158]]

the surviving pups; (f) at necropsy, all dams showed comparable number 
of implantations and the animals sacrificed as scheduled revealed no 
treatment-related changes and also the mean organ weights were similar 
in treated and untreated groups; and (g) litters from animals treated 
at the lower doses remained entirely unaffected and no pathological 
findings were also noted in these pups.
    iii. A series of two developmental toxicity studies were conducted 
via gavage with rabbits. In the first study, rabbits were treated at 
dose levels of 0, 2.4, 12, 36, and 60 mg/kg/day and in the second study 
the dose levels were 0, 7.5, 15, and 30 mg/kg/day. Considering both 
studies, the maternal and developmental toxicity NOAEL's were 15 mg/kg/
day based on the following: (a) Severe clinical signs and/or mortality 
were observed at dose levels > 30 mg/kg/day; (b) decreased body weight, 
food consumption, and absorption/premature delivery in the 36 and 60 
mg/kg/day dose groups which survived to the end of the studies; (c) 
fetal effects consisted of a high number of dead fetuses and several 
gross malformations (pseudo ancylosis, syndactylia, micromelia, aplasia 
of the twelfth rib) at the highest dose tested; and (d) pseudo 
ancylosis was also seen in 1 fetus from the 12 mg/kg/day dose group and 
in 6 fetuses in the 36 mg/kg/day dose level, but this finding is known 
to occur spontaneously in rabbits of this strain used and the 
contractures usually normalize during early stages of life. Due to the 
severe maternal effect at the high dose level (HDL), these effects were 
not considered to represent a specific teratogenic effect of the 
treatment.
    iv. A 2-generation reproduction study was conducted with rats fed 
dosages of 0, 0.625, 1.25, and 2.5 mg/kg/day average mg/kg/day dose 
levels for both male and female rats with a reproductive NOAEL of 2.5 
mg/kg/day and with a parental NOAEL of 2.5 mg/kg/day based on: (a) 
Significant body weight changes in adults; (b) no effects were observed 
on parameters of fertility and gestation, or macro- or 
histopathological changes for the parental F0 and 
F1 animals at all dose levels tested; (c) in the 
F1 litters, a slight increased incidence of stillborn pups, 
unfolding of the ear, and slight reduced body weight development during 
lactation were observed in the 2.5 mg/kg/day dose level group, but this 
was not reproduced in the F2 litters; and (d) in the 
F2 litters, no treatment-related effects were observed at 
all dose levels tested.
    4. Subchronic toxicity. The short-term toxicity of fenpropimorph 
was investigated in an oral 28-day range-finding study in rats as well 
as in 3-month studies in rats and dogs. In addition, the short-term 
toxicity following dermal exposure was determined in a 21-day study in 
rabbits and the short-term inhalation toxicity was studied in a 28-day 
inhalation study in rats.
    The signs of toxicity observed in rats and dogs tested orally were 
overall similar with the liver as the target organ. The effects 
observed typically included the increase in one or more serum liver 
enzymes, changes in cholesterol and increased liver weight. No 
pathological changes were observed in any organ. Plasma cholinesterase 
was decreased in the highest doses tested in rats. Brain and RBC 
cholinesterase were unaffected by treatment.
    Severe dermal irritation with repeated dosing limited the highest 
dose tested for 3 weeks in rabbits to 8.5 mg/kg bwt/day. No substance-
related systemic findings were detected up to the highest dose. Rats 
were exposed via inhalation for 28 days at concentrations up to 160 mg/
m3. The NOAEL was determined to be 10 mg/m3 based 
on serum liver enzyme and cholesterol changes and reduced plasma 
cholinesterase at higher concentrations.
    5.Chronic toxicity --i. A combined chronic feeding/oncogenicity 
study was performed in rats being fed doses of 0, 0.2, 0.3, 1.7, and 
8.8 mg/kg/day (males) and 0, 0.2, 0.4, 2.1, and 11.2 mg/kg/day 
(females) with a NOAEL of 0.3 mg/kg/day (males) and 0.4 mg/kg/day 
(females) based on the following effects: (a) Decreased body weights 
were observed in both male and female rats at dose levels > 1.7 mg/kg/
day; (b) decreased food consumption in female rats at the 11.2 mg/kg/
day; (c) significantly lower activities of plasma cholinesterase were 
noted in male and female rats in the high dose whereas no effect was 
found for red blood cell and brain cholinesterase values; (d) at 
terminal sacrifice, reduced activities of brain cholinesterase were 
detected in males, only, at the 1.7 and 8.8 mg/kg/day dose levels 
groups tested; (e) increased liver weights for females at dose levels > 
2.1 mg/kg/day and in males of the top dose group; (f) microscopic 
findings were observed in the liver of male and female rats in both 
sexes of the two highest dose groups consisting of enlargement of the 
centriobular hepatocytes and increased incidences of multinucleate 
hepatocytes; and (g) no increased incidence of neoplasms occurred at 
any dose levels tested in this study.
    ii. A carcinogenicity study in mice fed doses of 0, 0.5, 3.0, 16, 
and 106 mg/kg/day (males) and 0, 0.5, 3.5, 17, and 118 HDT mg/kg/day 
(females) with a NOAEL of 3.0 and 3.5 mg/kg/day for male and female 
mice, respectively, based on the following effects: (a) Decreased body 
weights were observed with no effect on food consumption in both male 
and female mice at the highest dose tested; (b) decreased 
cholinesterase activities were observed in red blood cells for female 
mice in the 17 and 118 mg/kg/day dose level tested at terminal 
sacrifice; (c) at the high dose, increased liver weights were observed 
for female mice at terminal sacrifice and in males at interim sacrifice 
after 52 weeks; and (d) no increased incidence of neoplasms occurred at 
any dose levels tested in this study.
    iii. A 1 year feeding study in dogs fed doses of 0, 0.8, 3.2, or 
12.7 mg/kg/day with a NOAEL of 3.2 mg/kg/day based on the following 
effects: (a) No changes in body weights nor food consumption for both 
the high dose male and female dogs were observed at all tested dose 
levels as compared to controls; (b) blood biochemistry values were 
slightly increased in high dose males (alkaline phosphatase) and 
females (alanine aminotransferase); (c) the cholininesterase from 
plasma, red blood cells, and brain showed comparable activities in 
treated and untreated dogs; and (d) neither organ weight analyses nor 
macro- and histopathological examinations demonstrated any treatment-
related effects as compared to controls.
    6. Animal metabolism. Fenpropimorph was well absorbed orally (>90%) 
and extensively metabolized by rats. Excretion was rapid (plasma half-
life of 16-24 hours) occurring by urine and bile. By 48 hours after 
treatment, essentially all of the administered dose was eliminated by 
all routes. Levels in tissues were small and rapidly declined, and 
there was no evidence for a bioaccumulation potential. Fenpropimorph 
was eliminated exclusively in the form of metabolites. Significant 
amounts of the metabolites were in conjugated form.
    7. Metabolite toxicology. There were no metabolites identified in 
plant commodities which require regulation.
    8. Endocrine disruption. No specific tests have been performed with 
fenpropimorph to determine whether the chemical may have an effect in 
humans that is similar to an effect produced by naturally occurring 
estrogen or other endocrine effects. However, there are significant 
findings in other relevant toxicity studies, i.e., teratology, and 
multi-generation reproductive studies, that would suggest fenpropimorph 
produces endocrine-related effects.

[[Page 36159]]

C. Aggregate Exposure

    1. Dietary exposure. A dietary assessment was conducted to evaluate 
the potential risk due to chronic dietary exposure of the U.S. 
population and all sub-populations to residues of fenpropimorph. 
Fenpropimorph is not registered in the United States so no tolerances 
have previously been established.
    This dietary analysis was conducted to evaluate the proposed import 
tolerance for banana pulp at 0.3 ppm. The dietary assessment was 
conducted using tolerance level residues, default processing factors, 
and 100% crop treated factors. These assumptions are conservative 
because it assumes all bananas imported into the United States will be 
at tolerance level and 100% of all the import bananas will have been 
treated with fenpropimorph. Inadvertent residues in animal commodities 
(i.e., meat, meat byproducts, milk, eggs) were not considered because 
imported bananas will not be used as an animal feed commodity.
    i. Food. Acute dietary exposure assessment for fenpropimorph. BASF 
believes there is no concern regarding acute dietary risk since the 
available toxicity data do not indicate any evidence of significant 
toxicity from a 1 day or single, event exposure by the oral route.
    ii. Chronic dietary exposure assessment.Achronic assessment was 
conducted for all subpopulations. The chronic dietary exposure 
assessment was conducted using the Dietary Exposure Evaluation Model 
software with Food Commodity Intake Database (DEEM-FCID). The chronic 
population adjusted dose (cPAD) used for all subpopulations was 0.003 
mg/kg bwt/day. Using the exposure assumptions discussed above, 
fenpropimorph chronic dietary exposure from food is less than 19% cPAD 
for all subpopulations. The most highly exposed subpopulation was 
children 1-2 years old and utilized 18.4 % of the cPAD. The results of 
the chronic dietary assessment are presented in Table 1.

  Table 1.-- Summary of Chronic Dietary Exposure Assessment Considering
    Crops With Established and Proposed Tolerances for Fenpropimorph.
------------------------------------------------------------------------
                                   Exposure Estimate
      Population Subgroups          (mg/kg bw/day)           %cPAD
------------------------------------------------------------------------
U.S. population                   0.0001140           3.8
---------------------------------
All Infants                       0.0004320           14.4
---------------------------------
Children (1-2 years)              0.0005520           18.4
---------------------------------
Children (3-5 years)              0.0002880           9.6
---------------------------------
Children (6-12 years)             0.0001200           4.0
---------------------------------
Females (13-19 years)             0.0000720           2.4
---------------------------------
Youth (13-19 years)               0.0000480           1.6
------------------------------------------------------------------------

    Results of the chronic dietary exposure analysis demonstrate a 
reasonable certainty that no harm to the general U.S. population or any 
subpopulation would results from importing bananas treated with 
fenpropimorph.
    iii. Drinking water. Fenpropimorph is not registered for use within 
the United States and therefore exposure through drinking water will 
not occur.
    An aggregate exposure assessment for fenpropimorph is not needed 
because the only exposure to fenpropimorph will occur from the dietary 
food route. Fenpropimorph is not registered within the United States 
for any uses. The dietary assessment conducted above demonstrates that 
there are no safety concerns for any subpopulation, and that the 
results clearly meet the FQPA standard of reasonable certainty of no 
harm.
    2. Non-dietary exposure. Fenpropimorph is not registered for use 
within the United States. Thus, residential exposure is not possible.

D. Cumulative Effects

    Section 408(b)(2)(D)(v) requires that, when considering whether to 
establish, modify, or revoke a tolerance, the Agency consider 
``available information'' concerning the cumulative effects of a 
particular pesticide's residues and other substances that have a common 
mechanism of toxicity. Results for toxicity studies indicate that toxic 
effects produced by fenpropimorph would not be cumulative with those of 
any other chemical.

E. Safety Determination

    1. U.S. population. Based on this risk assessment, BASF concludes 
that there is a reasonable certainty that no harm will result to the 
general population from the aggregate exposure to fenpropimorph 
residues.
    2. Infants and children. Based on this risk assessment, BASF 
concludes that there is a reasonable certainty that no harm will result 
to infants or children from the aggregate exposure to fenpropimorph.

F. International Tolerances

    A maximum residue level has not been established under Codex 
Alimentarius Commission for fenpropimorph in bananas.

[FR Doc. 05-12079 Filed 6-21-05; 8:45 am]
BILLING CODE 6560-50-S