[Federal Register Volume 69, Number 221 (Wednesday, November 17, 2004)]
[Notices]
[Pages 67351-67356]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 04-25501]


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ENVIRONMENTAL PROTECTION AGENCY

[OPP-2004-0357; FRL-7686-6]


Fenbuconazole; 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 extending time-
limited tolerances for residues of a certain pesticide chemical in or 
on various food commodities.

DATES: Comments, identified by docket identification (ID) number OPP-
2004-0357, must be received on or before December 17, 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: J. R. Tomerlin, Registration Division 
(7505C), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone 
number: (703) 305-0598; 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:
     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-2004-0357. 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. 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

[[Page 67352]]

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-2004-0357. 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-2004-0357. 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-2004-0357.
    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-2004-0357. 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.


[[Page 67353]]


    Dated: November 3, 2004.
Lois Rossi,
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.

Dow AgroSciences LLC

PP 1F3989, 1F3995, and 2F4154.

    EPA has received pesticide petitions (1F3989, 1F3995, and 2F4154) 
from Dow AgroSciences LLC, 9330 Zionsville Road, Indianapolis, IN 46268 
proposing, pursuant to section 408(d) of the Federal Food, Drug, and 
Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180.480 
by extending the time-limited tolerances for the combined residues of 
fenbuconazole (alpha-(2-(4-chlorophenyl)-ethyl)-alpha-phenyl-3-(1H-
1,2,4-triazole)-1-propanenitrile) and its metabolites cis-and trans-5-
(4-chlorophenyl)-dihydro-3-phenyl-3-(1H-1,2,4-triazole-1-ylmethyl)-2-
3H-furanone in or on the raw agricultural commodity fruit, stone, group 
12 (except plum, prune) at 2.0 parts per million (ppm); pecan at 0.1 
ppm; banana at 0.3 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 metabolism of fenbuconazole in plants is 
adequately understood for the purpose of these tolerances. Plant 
metabolism was evaluated in three diverse crops - wheat, peaches and 
peanuts. The route of metabolism is similar in all crop groups and 
proceeds with three main pathways. Oxidation at the benzylic carbon 
(pathway 1) led to the ketone and the lactone as metabolites. Oxidation 
or nucleophilic substitution on the carbon next to the triazole ring 
(pathway 2) led to triazole alanine (TA) and triazole acetic acid (TAA) 
presumably through free triazole. Metabolic pathway 3 produced the 
phenolic metabolite RH-4911, and led to the glucose conjugates found in 
all crops.
    2. Analytical method. An adequate enforcement method is available 
for the established and proposed tolerances. Quantitation of 
fenbuconazole residues (and lactones RH-9129 and RH-9130) at an 
analytical sensitivity of 0.01 milligrams/kilogram (mg/kg) is 
accomplished by soxhlet extraction of samples in methanol, partitioning 
into methylene chloride, redissolving in toluene, cleanup on silica 
gel, and gas liquid chromatography using nitrogen specific thermionic 
detection.
    3. Magnitude of residues--i. Stone fruit-peaches. Ten field trials 
were conducted on peaches. Seven to 10 applications were made at the 
maximum use rate of 0.1 pounds of active ingredient per acre (lb ai/
acre) per application, and fruit was harvested on the last day of 
application. The highest field residue value was 0.51 ppm, and the 
average field residue value was 0.36 ppm.
    ii. Stone fruit-cherries. Eleven field trials were conducted on 
cherries. Five to 6 applications were made at the maximum use rate of 
0.1 lb ai/acre per application, and fruit was harvested on the last day 
of application. The highest field residue value was 0.63 ppm, and the 
average field residue value was 0.43 ppm.
    iii. Stone fruit-apricots. Four field trials were conducted on 
apricots. Six applications were made at the maximum use rate of 0.125 
lb ai/acre per application, and fruit was harvested on the last day of 
application. The field residue values in four samples measured were 
0.17, 0.23, 0.27, and 0.28 ppm.
    iv. Pecans. Four field trials were conducted in pecans. Eight to 10 
applications were made at the maximum use rate of 0.125 lb ai/acre per 
application, and nuts were harvested 28 days after the last 
application. Field residue values in nutmeat for all four trials were 
<0.01 ppm.
    v. Bananas. Eighteen field trials were conducted on bagged bananas, 
which are typically used in commerce. Eight applications (5 and 7 
applications in two trials) were made at the maximum use rate of 0.09 
lb ai/acre per application and bananas were harvested on the last day 
of application. The highest field residue value in whole fruit or in 
pulp and peel combined was 0.062 ppm. The average field residue value 
in whole fruit or in pulp and peel combined was 0.03 ppm. The results 
of these studies support the proposed permanent tolerances for 
fenbuconazole on stone fruit, pecans, and bananas.

B. Toxicological Profile

    1. Acute toxicity. Fenbuconazole is practically non-toxic after 
administration by the oral and dermal routes, and was not significantly 
toxic to rats after a 4 hour inhalation exposure. Fenbuconazole is 
classified as not irritating to skin and inconsequentially irritating 
to the eyes. It is not a skin sensitizer.
    2. Genotoxicty. Fenbuconazole was negative (non-mutagenic) in an 
Ames assay with and without hepatic enzyme activation. Fenbuconazole 
was negative in a hypoxanthine guanine phosphoribosyl transferase 
(HGPRT) gene mutation assay using Chinese hamster ovary (CHO) cells in 
culture when tested with and without hepatic enzyme activation. In 
isolated rat hepatocytes, fenbuconazole did not induce unscheduled DNA 
synthesis (UDS) or repair. Fenbuconazole did not produce chromosome 
effects in rats in vivo. On the basis of the results from this battery 
of tests, it is concluded that fenbuconazole is not mutagenic or 
genotoxic.
    3. Reproductive and developmental toxicity.--i. Developmental 
toxicity in the rat. In the developmental study in rats, the maternal 
(systemic) no observed adverse effect level (NOAEL) was 30 (mg/kg/day) 
based on decreases in body weight and body weight gain at the lowest 
observed adverse effect level (LOAEL) of 75 mg/kg/day. The 
developmental (fetal) NOAEL was 30 mg/kg/day based on an increase in 
post implantation loss and a significant decrease in the number of live 
fetuses per dam at the LOAEL of 75 mg/kg/day.
    ii. Developmental toxicity in the rabbit. In the developmental 
study in rabbits, the maternal (systemic) NOAEL was 10 mg/kg/day based 
on decreased body weight gain at the LOAEL of 30 mg/kg/day. The 
developmental (fetal) NOAEL was 30 mg/kg/day based on increased 
resorptions at the LOAEL of 60 mg/kg/day.
    iii. Reproductive toxicity. In the 2-generation reproduction 
toxicity study in rats, the maternal (systemic) NOAEL was 4 mg/kg/day 
based on decreased body weight and food consumption, increased number 
of dams delivering nonviable offspring, and increases in adrenal and 
thyroid weights at the LOAEL of 40 mg/kg/day. The reproductive (pup) 
NOAEL was 40 mg/kg/day, the highest dose tested.
    4. Subchronic toxicity.--i. Rat 90-day oral study. A subchronic 
feeding study in rats conducted for 13 weeks resulted in a NOAEL of 80 
ppm (5.1 and 6.3 mg/

[[Page 67354]]

kg/day in males and females, respectively). The only effect observed at 
80 ppm was minimal centrilobular hypertrophy (seen in one male) and 
hepatocytic centrilobular vacuolation (3 males) with no concomitant 
increase in liver weight or clinical chemistry correlates and no 
analogous effects in females. As such, these observations are not 
considered to be adverse. Increased liver weight, hepatic hypertrophy, 
thyroid hypertrophy, and decreased body weight were observed at the 
higher doses of 400 and 1,600 ppm.
    ii. Dog 90-day oral study. A subchronic feeding study in dogs 
conducted for 13 weeks resulted in a NOAEL of 100 ppm (3.3 and 3.5 mg/
kg/ day in males and females, respectively). At the LOAEL of 400 ppm, 
increased liver weight, clinical chemistry parameters, and liver 
hypertrophy (males) were observed.
    iii. Rat 4-week dermal study. In a 21-day dermal toxicity in the 
rat study, the NOAEL was greater than 1,000 mg/kg/day, with no effects 
seen at this limit dose.
    5. Chronic toxicity.--i. Dog. A 1-year feeding study in dogs 
resulted in a NOAEL of 15 ppm (0.62 mg/kg/day) for females and 150 ppm 
(5.2 mg/kg/day) for males. Decreased body weight, increased liver 
weight, liver hypertrophy, and pigment in the liver were observed at 
the LOAEL of 150 and 1,200 ppm in females and males, respectively.
    ii. Mouse. A 78-week chronic/oncogenicity study was conducted in 
male and female mice at 0, 10, 200 (males only), 650, and 1,300 ppm 
(females only). The NOAEL was 10 ppm (1.4 mg/kg/day), and the LOAEL was 
200 ppm (26.3 mg/kg/day) for males and 650 ppm (104.6 mg/kg/day) for 
females based on increased liver weight and histopathological effects 
on the liver, which were consistent with chronic enzyme induction. 
There was no statistically significant increase of any tumor type in 
males. However, there was a statistically significant increase in 
combined liver adenomas and carcinomas in females at the high dose only 
(1,300 ppm; 208.8 mg/kg/day). There were no liver tumors in the control 
females, and liver tumor incidences in the high-dose females just 
exceeded the historical control range. In ancillary mode-of-action 
studies in female mice, the increased tumor incidence was associated 
with changes in several parameters in mouse liver following high doses 
of fenbuconazole, including an increase in P450 enzymes (predominately 
of the CYP 2B type), an increase in cell proliferation, an increase in 
hepatocyte hypertrophy, and an increase in liver weight. Changes in 
these liver parameters, as well as the occurrence of the low incidence 
of liver tumors, were non-linear with respect to dose (i.e., effects 
were observed only at high dietary doses of fenbuconazole). Similar 
findings have been shown with several pharmaceuticals, including 
phenobarbital, which is not carcinogenic in humans. The non-linear dose 
response relationship observed with respect to liver changes (including 
the low incidence of tumors) in the mouse indicates that these findings 
should be carefully considered in deciding the relevance of high-dose 
animal tumors to human dietary exposure.
    iii. Rat. A 24-month chronic/oncogenicity study in male and female 
rats was conducted at 0, 8, 80, and 800 ppm fenbuconazole, and a second 
24-month chronic/oncogenicity study was conducted in male rats at 0, 
800, and 1,600 ppm. The NOAEL was 80 ppm (3 and 4 mg/kg/day in males 
and females, respectively), and the LOAEL was 800 ppm (31 and 43 mg/kg/
day in males and females, respectively) based on decreased body weight, 
increased liver and thyroid weights, and liver and thyroid hypertrophy. 
Fenbuconazole produced a minimal but statistically significant increase 
in the incidence of combined thyroid follicular cell benign and 
malignant tumors. These findings occurred only in male rats following 
life-time ingestion of very high levels (800 and 1,600 ppm in the diet) 
of fenbuconazole.
    iv. Carcinogenicity. The Agency has concluded that the available 
data provide limited evidence of the carcinogenicity of fenbuconazole 
in both mice and rats and has classified fenbuconazole as a Group C 
carcinogen (possible human carcinogen with limited evidence of 
carcinogenicity in animals) in accordance with Agency guidelines, 
published in the Federal Register (51 FR 33992, September 24, 1986), 
and recommended that for the purpose of risk characterization a low-
dose extrapolation model applied to the experimental animal tumor data 
should be used for quantification of human risk (Q1*). EPA's 26Feb98 
Hazard Identification Assessment Review Committee (HIARC) report 
concluded that 0.00359 (mg/kg/day)-1 is the appropriate q* 
for fenbuconazole; this q* is based on the fenbuconazole mouse liver 
tumor data, along with a power surface area scaling factor.
    6. Animal metabolism. The absorption, distribution, excretion, and 
metabolism of fenbuconazole in rats, goats, and hens were investigated. 
Following oral administration, fenbuconazole was completely and rapidly 
absorbed, extensively metabolized by oxidation/hydroxylation and 
conjugation, and rapidly and essentially completely excreted, 
predominately in the feces. Fenbuconazole did not accumulate in 
tissues.
    7. Metabolite toxicology. There are no toxicological concerns for 
fenbuconazole based on differential metabolic pathways in plants and 
animals. Triazole fungicides are known to produce three common 
metabolites, 1,2,4-triazole, triazolylalanine and triazole acetic acid. 
To support the extension of existing parent triazole-derivative 
fungicide tolerances, EPA conducted an interim human health assessment 
for aggregate exposure to 1,2,4-triazole. This interim assessment was 
summarized in the Federal Register notice of August 4, 2004 (69 FR 
47005) (FRL-7352-1) and titled Propiconazole; Time-Limited Pesticide 
Tolerances. EPA concluded that for all exposure durations and 
population subgroups, aggregate exposures to 1,2,4-triazole are not 
expected to exceed its level of concern.
    8. Endocrine disruption. The mammalian endocrine system includes 
estrogen and androgens as well as other hormonal systems. Fenbuconazole 
is not known to interfere with reproductive hormones; thus, 
fenbuconazole should not be considered to be estrogenic or androgenic. 
There are no known instances of proven or alleged adverse reproductive 
or developmental effects to people, domestic animals, or wildlife as a 
result of exposure to fenbuconazole or its residues.

C. Aggregate Exposure

    1. Dietary exposure--i. Food. Dietary exposure assessments for 
fenbuconazole were conducted using the Dietary Exposure Evaluation 
Model (DEEM) software with the Food Commodity Intake Database (DEEM-
FCID, version 2) which incorporates food consumption data as reported 
in the Continuing Survey of Food Intake by Individuals (CSFII) Survey 
1994-1996, and 1998. These exposure assessments include all existing 
uses under section 3 registrations (stone fruit except plums or prunes, 
pecans and bananas) and section 18 registrations (grapefruit, 
blueberry, and meat and meat by-products resulting from grapefruit pulp 
as animal feedstuff). The assessments were performed in two levels. In 
the first assessment (Level 1), a Tier 1 analysis was conducted with 
the assumption that 100% of the crops would be treated with 
fenbuconazole and that residues would be present at

[[Page 67355]]

the tolerance levels. In the second assessment (Level 2), residues at 
tolerance levels were still assumed but the percent crop treated (PCT) 
was adjusted using the 4 or 5 year average for chronic assessment and 
the highest PCT for acute assessment. PCT values were based on data 
available for apricot, cherry, peach, grapefruit and pecan from the 
Doane database. Additionally, the default processing factors were used 
for all processed commodities except citrus oil. The tolerance of 35 
ppm was used for citrus oil based on the residue data in grapefruit.
    a. Acute dietary exposure. Although no acute adverse effect was 
observed as a result of exposure to a single dose, EPA has established 
an acute reference dose (aRfD) for the purpose of the acute dietary 
assessment. This aRfD was set at 0.3 mg/kg/day for females 13+ years 
old, the population sub-group of concern. This was based on the 
developmental rat toxicity study with a NOAEL of 30 mg/kg/day and an 
uncertainty factor of 100. The 100-fold safety factor includes 
intraspecies and interspecies variations. Using the above assumptions 
for Level 1 assessment, the food exposure for females 13+ years old at 
the 95th percentile was estimated to be less than 0.005 mg/
kg/day which utilized less that 2% of the aRfD. For the level 2 
assessment, the estimated food exposure at the 99.99th percentile was 
less than 0.003 mg/kg/day which utilizes less than 1.0% of the RfD.
    b. Chronic dietary exposure. EPA has established a chronic 
reference dose (cRfD) for fenbuconazole at 0.03 mg/kg/day for all 
population subgroups. The cRfD is based on the 2-year combined chronic 
feeding-carcinogenicity study in rats with a NOAEL of 3.03 and 4.02 mg/
kg/day in males and females respectively, and an uncertainty factor of 
100. The 100-fold safety factor includes intraspecies and interspecies 
variations. No additional FQPA safety factor is required. The food 
exposure for the overall U.S. population was estimated to be 0.000552 
mg/kg/day which utilizes less then 2% of the cRfD. The population 
subgroup with the highest potential for exposure was non-nursing 
infants at 10.6% of the cRfD with estimated food exposure of 0.003185 
mg/kg/day. For the level 2 assessment, the estimated food exposure 
drops to 0.6% of the cRfD for the general population and 2.8% of the 
cRfD for non-nursing infants.
    c. Cancer dietary exposure. EPA has classified fenbuconazole as a 
Group C carcinogen (possible human carcinogen with limited evidence of 
carcinogenicity in animals) and has established a Q1* of 0.00359 (mg/
kg/day)-1 in human equivalents. Using the above assumptions 
for Level 1 assessment, the food exposure was estimated to be 0.00552 
mg/kg/day with a cancer risk estimate of 1.98 x 10-6. Using 
the refinements of PCT in the Level 2 assessment results in a more 
realistic cancer risk assessment of 6.9 x 10-7 and a food 
exposure of 0.000191 mg/kg/day.
    ii. Drinking water. The estimated drinking water concentration was 
calculated using the Pesticide Root Zone/Exposure Analysis Modeling 
System (PRZM/EXAMS) which predicts and annual average of 0.22 ppb. 
These results are considered a conservative assessment of possible 
concentration of fenbuconazole in drinking water. Using this value of 
0.22 ppb, for dietary consumption of water in the DEEM-FCID chronic 
analysis results in the exposure from drinking water to be 
insignificant at <0.1% of the cRfD for all population subgroups. 
Additionally in a later assessment the Agency used (Generic Estimated 
Environmental Concentration) GENEEC and (Screening Concentration in 
Ground Water) SCI-GROW models to estimate the environmental 
concentrations (EECs) for surface water and ground water. The EECs for 
fenbuconazole are 6.7 ppb for acute and 3.6 ppb for chronic exposure. 
Since the EECs in ground water are much lower than the EECs in surface 
water, conservatively only the surface water EECs were used for 
comparison with the drinking water levels of comparison (DWLOC). DWLOC 
is a theoretical upper limit on a pesticide's concentration in drinking 
water in light of total aggregate exposure to a pesticide in food, and 
from residential uses. DWLOC is not a regulatory standard for drinking 
water, but is used as a point of comparison against the estimated 
potential concentrations in groundwater or surface water. It is 
calculated by subtracting the food dietary exposure (from DEEM 
analysis) from the RfD and then expressed as [mu]g/L using default body 
weights (70 kg for adult and 10 kg for infants) and drinking water 
consumption (2 L/day for adults and 1 L/day for children). The acute 
DWLOC for females 13 years and older (population sub-group of concern) 
was calculated to be 8,915 [mu]g/L. The chronic DWLOC for the general 
U.S. population and non-nursing infants (population sub-group of 
concern) was calculated to be 1,043 [mu]g/L and 292 [mu]g/L, 
respectively. The cancer DWLOC is the concentration in drinking water 
that results in a negligible cancer risk of 1 x 10-6. Using 
the Level 2 assessment, the estimated chronic food exposure is 0.000191 
mg/kg/day for the general U.S. population. Assuming a negligible cancer 
risk of 1 x 10-6 and the Q1* of 0.00359 (mg/kg/
day)-1, the maximum allowable water exposure is 0.00009 mg/
kg/day resulting in a calculated cancer DWLOC of 3 [mu]g/L. When 
comparing the EEC to the cancer DWLOC, the Agency policy states that a 
factor of 3 will be applied to GENEEC modeled values because the 
estimated environmental concentration is derived from a 56-day average 
value and not a longer-term average. Applying a factor of 3, the EEC is 
1.2 [mu]g/L which is less than the calculated cancer DWLOC of 3 [mu]g/
L. The DWLOCs are substantially greater than the estimated residue 
concentration in ground water or surface water, therefore, exposure to 
fenbuconazole would not result in unacceptable levels of aggregate 
human health risk.
    2. Non-dietary exposure. Fenbuconazole is not currently registered 
for use on any sites that would result in residential exposure. Thus, 
the risk from non-dietary exposure would be considered negligible.

D. Cumulative Effects

    Fenbuconazole is a member of the triazole class of fungicides. At 
this time, EPA does not have available data to determine whether 
fenbuconazole exhibits a common mechanism of toxicity with other 
triazole fungicides. For purposes of this tolerance action, it is 
assumed that fenbuconazole does not have a mechanism of toxicity common 
with other substances and no cumulative risk is required.

E. Safety Determination

    1. U.S. population. Using the conservative exposure assumptions 
(Level 1/Tier 1) and taking into account the completeness and 
reliability of the toxicity data, the chronic dietary food exposure 
from all supported section 3 and section 18 registered uses will 
utilize 1.8% of the cRfD for the U.S. population. The major 
identifiable sub-group with the highest chronic food exposure is non-
nursing infants at 10.6% of the cRfD. EPA generally has no concern for 
exposures below 100% of the RfD because the RfD represents the level at 
or below which daily aggregate dietary exposure over a lifetime will 
not pose appreciable risks to human health. Thus, there is a reasonable 
certainty that no harm will result from aggregate exposure to 
fenbuconazole residues from the proposed uses. The acute dietary food 
exposure at the 95th percentile for females 13+ years, the 
population sub-group of concern, is <2% of the aRfD. Therefore, there 
is no

[[Page 67356]]

concern for acute exposure because the acute RfD represents the level 
at or below which a single daily exposure will not pose appreciable 
risk to human health. Additionally, the potential contribution of 
fenbuconazole residues in drinking water is expected to be minimal. 
Using a slight refinement for PCT, the cancer risk assessment is 6.9 x 
10-7. Generally the Agency has no concern for exposures that 
result in a cancer risk estimate below 1 x 10-6. Including 
the potential for exposure in drinking water, the cancer risk is not 
expected to exceed 1x 10-6 for the U.S. population as a 
whole.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of fenbuconazole, data 
from developmental toxicity studies in rats and rabbits and a 2-
generation reproduction study in the rat are considered. The 
developmental toxicity studies are designed to evaluate adverse effects 
on the developing organism resulting from pesticide exposure during 
prenatal development. Reproduction studies provide information relating 
to effects from exposure to the pesticide on the reproductive 
capability and potential systemic toxicity of mating animals and on 
various parameters associated with the well-being of offspring. The 
completeness and adequacy of the toxicity database is also considered. 
No indication of increased susceptibility to infants and children was 
noted in these studies for fenbuconazole. EPA has previously determined 
that no additional safety factor to protect infants and children is 
necessary for fenbuconazole and that the RfD of 0.03 mg/kg/day is 
appropriate for assessing risk to infants and children.

F. International Tolerances

    International CODEX values are established for apricot, banana, 
barley, barley straw and fodder, cattle fat, meat, milk and edible 
offal, cherries, cucumber, eggs, grapes, melon except watermelon, 
peach, plum, pome fruits, poultry fat, meat and edible offal, rape 
seed, rye, summer squash, sunflower, and wheat.
[FR Doc. 04-25501 Filed 11-16-04; 8:45 am]
BILLING CODE 6560-50-S