Federal Register / Vol. 69, No. 223 / Friday, November 19, 2004 / Notices 67731

ENVIRONMENTAL PROTECTION 

AGENCY

[OPP–2004–0363; FRL–7686–5]

Pinoxaden; 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.

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 

identification (ID) number OPP–2004–

0363, must be received on or before 

December 20, 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: Jim 

Tompkins, Registration Division 

(7505C), Office of Pesticide Programs, 

Environmental Protection Agency, 1200 

Pennsylvania Ave., NW., Washington, 

DC 20460–0001; telephone number: 

(703) 305–5697; e-mail address: 

tompkins.jim@epa.gov.

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–

0363. 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 

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 

handdelivery/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 email 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 

67732 Federal Register / Vol. 69, No. 223 / Friday, November 19, 2004 / Notices 

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 totechnical 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–2004–0363. 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 opp-docket@epa.gov, 

Attention: Docket ID Number OPP–

2004–0363. Incontrast 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 diskor 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–2004–0363.

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–2004–0363. 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 theelements 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 supports 

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: November 3, 2004

Lois Rossi,

Director, Registration Division, Office of 

PesticidePrograms.

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.

Syngenta Crop Protection

EPA has received a pesticide petition 

4F6817 from Syngenta Crop Protection, 

Inc., P.O. Box 18300, Greensboro, North 

Carolina, 27419–8300 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 by establishing a tolerance for 

residues of pinoxaden in or on the raw 

agricultural commodities (RAC) wheat 

grain at 0.70 parts per million (ppm), 

wheat, forage at 3.0 ppm, wheat, hay at 

1.75 ppm, wheat, straw at 1.5 ppm, 

barley, grain at 0.70 ppm, barley, hay at 

1.25 ppm, and barley, straw at 0.60 

ppm. EPA has determined that the 

petition contains data or information 

regarding the elements set forth in 

section 408(d)(2) of the FFDCA; 

Federal Register / Vol. 69, No. 223 / Friday, November 19, 2004 / Notices 67733

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. Metabolism of 

pinoxaden was studied in wheat using 

radiolabeled pinoxaden. The 

metabolism in plants is well understood 

and the data is adequate for selection of 

residues of concern for tolerance setting 

purposes. The metabolic profile in 

plants supports the use of an analytical 

method that accounts for parent 

pinoxaden and its major metabolites.

2. Analytical method. Syngenta Crop 

Protection, Inc., has submitted practical 

analytical methodology for detecting 

and measuring levels of pinoxaden and 

its three major metabolites. The method 

is based upon commodity specific 

cleanup procedures and High 

Performance Liquid Chromatography 

(HPLC) determination with triple stage 

quadruple mass spectrometry (LC/MS/

MS). The limit of quantitation (LOQ), as 

demonstrated by the lowest acceptable 

recovery samples, is 0.01 ppm for grain, 

and 0.02 ppm for forage, hay, and straw.

3. Magnitude of residues. A 

magnitude of the residueprogram was 

performed with pinoxaden on full 

guideline geography to support uses on 

all types of wheat, and barley crops.

B. Toxicological Profile

1. Acute toxicity. Pinoxaden technical 

and the end-use formulation have very 

low acute toxicity by oral, dermal, and 

inhalation exposure routes. For 

pinoxaden technical, the oral LD50 in 

rats is >5,000 millgrams/kilogram (mg/

kg). The rat dermal LD50 is >2,000 mg/

kg and the rat inhalation LC50 is 5.22 

milligrams/liter (mg/L) air. Pinoxaden 

technical is irritating to the eye and 

non-irritating to the skin. The end-use 

formulation is mildly to moderately 

irritating to the eye and skin, the oral 

LD50 in rats is 3,129 mg/kg, the rat 

dermal LD50 is >2,000 mg/kg and the rat 

inhalation LC50 is >5 mg/L. Neither the 

technical nor the formulation are skin 

sensitizers.

2. Genotoxicty. Pinoxaden has been 

tested for its potential to induce gene 

mutation and chromosomal changes in 

six different test systems. Pinoxaden 

technical was negative in a bacterial 

gene mutation assay, a mouse 

lymphoma mammalian cell mutation 

assay and an unscheduled DNA 

synthesis (UDS) assay in rat 

hepatocytes. In in vitro tests for 

chromosome aberrations in Chinese 

hamster ovary cells, a small dose related 

increase was observed at dose levels 

that produced cytotoxicity. To assess 

the biological significance of this single 

positive in vitro finding, two in vivo

tests were performed. When tested in a 

micronucleus test in bone marrow cells 

of the mouse at dose levels up to a limit 

dose of 2,000 mg/kg, pinoxaden did not 

induce micronuclei, and produced no 

significant toxicity in the animals. In an 

in vivo UDS study in rats, pinoxaden 

was negative in this assay for DNA 

repair. Based on the complete database, 

it is concluded that pinoxaden is not 

genotoxic.

3. Reproductive and developmental 

toxicity. Pinoxadenproduced no 

evidence of reproductive toxicity. In a 

rat multi-generation reproduction study, 

pinoxaden technical was administered 

orally by gavage to rats at dosages of 0, 

10, 50, 250, and 500 mg/kg/day over two 

generations. At 500 mg/kg, parental 

toxicity was observed as decreased body 

weight gain (F0 males) and kidney 

pathology accompanied by increased 

water consumption (F0 and F1 males 

and females.) At 500 mg/kg/day, F1 and 

F2 pups had lower body weight gain 

during lactation. Changes in organ 

weights were seen in pups at this dose 

level, but no treatment-related adverse 

findings were observed for pups ineither 

generation upon histologic examination. 

At 10, 50 and 250 mg/kg/day, there was 

no indication of any adverse effects of 

treatment. On the basis of the results 

obtained in this study, the no observed 

adverse effect level (NOAEL) for both 

sexes and generations was 250 mg/kg/

day. There were no effects on the 

reproductive parameters and the 

NOAEL for reproductive toxicity was 

>500 mg/kg/day. Offspring effects were 

minor and were observed only at dose 

levels that produced parental toxicity. 

There were no indications of any 

differences in sensitivity to pinoxaden 

exposure between the different 

generations or between parental animals 

andoffspring, and it is concluded that 

pinoxaden does not cause reproductive 

toxicity.

In a rat teratogenicity study, 

pinoxaden technical was administered 

by gavage to 24 pregnant rats per group 

at dose levels of 0, 3, 30, 300 or 800 mg/

kg/day from days 6 through 20 of 

gestation. Maternal body weight gain 

was significantly reduced at the top two 

dose levels compared to controls. There 

was no effect of treatment on the 

number of implantation sites, postimplantation loss, live litter size, and 

sex ratios, and no significant findings 

were observed in the maternal animals 

upon necropsy. Gravid uterus weights, 

carcass weights and net weight change 

from day 6 post coitum were 

significantly reduced at the top dose 

level. In the presence of the maternal 

toxicity, mean fetal body weights were 

reduced at 800 mg/kg/day, and slightly 

reduced ossification was observed at 

both 800 and 300 mg/kg bw/day. There 

were no treatment-related external or 

visceral observations in the fetuses. 

Pinoxaden, was not teratogenic in rats 

when tested under the conditions of this 

study. The no observed effect level 

(NOEL) for both maternal and 

developmental toxicity was 30 mg/kg/

day.

Pinoxaden, was evaluated in rabbit 

developmental toxicity studies. In an 

initial guideline rabbit study, pinoxaden 

technical was administered by gavage to 

pregnant rabbits at dose levels of 0, 10, 

30, and 100 mg/kg/day from days 7 

through 28 of gestation. Maternal body 

weight gain was significantly reduced at 

100 mg/kg/day. Fetal body weight was 

reduced at the 100 mg/kg dose level. A 

second guideline developmental 

toxicity study was conducted in the 

rabbit at 0, 10, 30, and 100 mg/kg/day. 

Maternal toxicity was observed at 30 

and at 100 mg/kg/day in the form of 

reduced overall weight gain compared 

to control animals. There was no effect 

of treatment on the number, growth or 

survival of the fetuses in utero and no 

evidence for an adverse effect on fetal 

development. There were no treatmentrelated fetal external, visceral or skeletal 

findings. In conclusion, the full set of 

studies indicated that pinoxaden is not 

teratogenic in rabbits. The maternal 

NOEL was 10 mg/kg/day, and the NOEL 

for developmental toxicity was 30 mg/

kg/day.

In conclusion, there is no evidence 

that developing offspring are more 

sensitive than adults to the effects of 

pinoxaden, and it is concluded, that 

pinoxaden does not cause primary 

developmental toxicity or reproductive 

toxicity.

4. Subchronic toxicity. Pinoxaden 

technical was evaluated in a number of 

subchronic studies. In a 3–month gavage 

study in rats the NOAEL was 300 mg/

kg, the highest dose tested. Higher doses 

in a 28–day rat study caused kidney 

toxicity at 600 mg/kg, with a NOAEL of 

300 mg/kg. In a 3–month gavage study 

in mice, the NOAEL was 100 mg/kg. 

Effects at higher dose levels involved 

reduced body weights at 1,000 mg/kg, 

reduced hemoglobin at doses greater 

than or equal to 400 mg/kg (females 

only) and renal tubule basophilia and 

increased water consumption in males 

at 1,000 mg/kg. In a 3–month study in 

dogs the NOAEL was 100 mg/kg, and 

inappetance, body weight loss and 

gastro-intestinal effects were seen at 250 

mg/kg. In a 28–day dermal (rat) study, 

67734 Federal Register / Vol. 69, No. 223 / Friday, November 19, 2004 / Notices 

the NOAEL was 1,000 mg/kg, the 

highest dose tested, and only a mild, 

low-grade inflammatory response at the 

treatment site was noted. In a 90–day 

subchronic neurotoxicity study in rats, 

pinoxaden was not neurotoxic when 

administered by gavage at dose levels of 

0, 10, 100 and 500 mg/kg/day. There 

were no treatment-related 

neurobehavioral or motor activity 

effects, no macroscopic findings and no 

microscopic findings in central or 

peripheral nervous tissue. In addition, 

pinoxaden was devoid of any acute 

neurotoxic effects when administered to 

rats at a single oral dose of up to 2,000 

mg/kg.

5. Chronic toxicity. Pinoxaden was 

not oncogenic in rats or mice. In a 2–

year combined carcinogenicity/chronic 

toxicity study in rats, pinoxaden 

technical was administered by daily 

gavage at dose levels of 0, 1, 10, 100, 

250, and 500 mg/kg/day. Toxicity was 

observed in the form of decreased body 

weight (500 and 250 mg/kg/day), 

depressed survival (500 and 250 mg/kg/

day males only), and kidney 

pathological changes (500, 250, and 100 

mg/kg/day). The kidney pathology was 

associated with changes in blood 

chemistry parameters and other 

associated effects. A minor and sporadic 

epithelial thickening of the duodenum 

was observed mainly at 250 and 500 

mg/kg. There was no evidence of a 

carcinogenic effect in this study. In 

conclusion, chronic treatment of 

pinoxaden to rats produced effects in 

only one major target organ at high dose 

levels, involving chronic progressive 

nephropathy and associated effects 

related to kidney toxicity. The NOEL 

was 10 mg/kg for males and females 

based on kidney effects at 100 mg/kg 

and above, and pinoxaden was not 

carcinogenic.

In an 18–month mouse oncogenicity 

study, pinoxaden technical was 

administered by gavage at dose levels of 

0, 5, 40, 300 and 750 mg/kg body. 

Toxicity was observed in the form of 

decreased body weight gain at 300 mg/

kg/day (females only) and 750 mg/kg/

day (males and females), decreased 

survival rates (40, 300 and 750 mg/kg/

day males), minor hematology effects 

(300 and 750 mg/kg), increased liver 

weights (300 and 750 mg/kg, with 

increased glycogen deposition) and 

increased kidney weights (750 mg/kg in 

females only). Increased epithelial 

thickening occurred in the small 

intestine of males and females at 300 

and 750 mg/kg. The reduced survival at 

the higher dose levels in males was a 

consequence of the gavage dosing 

procedure, as demonstrated by macroand micropathology evidence of lung 

involvement as the single major factor 

contributing to death. Other than 

increased mortality in males, there were 

no treatment-related effects at 40 mg/kg/

day. The NOEL for this study was 5 mg/

kg for both males and females, and 

pinoxaden was not carcinogenic.

In a 12–month chronic oral toxicity 

study in dogs, pinoxaden technical was 

administered by capsule at dose levels 

of 0, 5, 25 or 125 mg/kg/day. At 25 and 

125 mg/kg/day, treatment-related 

clinical observations were limited to an 

increased incidence of salivation at 

dosing and minor gastrointestinal 

effects, which were not considered 

adverse. There were noadverse effects 

on body weights or food consumption. 

Minor changes in hematology and blood 

clinical chemistry parameters were 

observed at 25 and 125 mg/kg/day 

compared to control animals. However, 

due to the small magnitude of the effects 

and the absence of any treatment-related 

effects on organ weights or any 

pathology findings, these clinical 

pathology changes are considered to be 

of no toxicological significance. There 

were no treatment-related 

micropathology changes seen at any 

dose level. The NOAEL in this study 

was 125 mg/kg/day.

6. Animal metabolism. Animal 

metabolism of pinoxaden is well 

understood. Pinoxaden is rapidly 

absorbed and excreted when 

administered to rats, and tissue residues 

are extremely low, with no 

accumulation upon repeated dosing. 

Similar rapid absorption and excretion 

was seen in mice and rabbits. The 

metabolic pathway is similar in rodents, 

rabbits, goats and hens.

7. Metabolite toxicology. Toxicity of 

pinoxaden metabolites has been tested 

and is well understood. The 

toxicological profile of all metabolites 

supports the proposed definition of 

residue.

8. Endocrine disruption. Pinoxaden 

does not belong to a class of chemicals 

known or suspected of having adverse 

effects on the endocrine system. There 

is no evidence that pinoxaden has any 

effect on endocrine function in 

developmental or reproductive studies. 

Furthermore, histological investigation 

of endocrine organs in chronic dog, 

mouse, and rat studies did not indicate 

that the endocrine system is targeted by 

pinoxaden.

C. Aggregate Exposure

1. Dietary exposure. The potential for 

chronic and acute dietary exposure from 

pinoxaden through food and water 

sources is addressed below.

i. Food. Dietary (food) risk evaluations 

for pinoxaden were performed using 

field trial residues. A percent of crop 

treated value of 20% was estimated for 

wheat and barley based upon Syngenta’s 

estimates of economic, pest, and 

competitive pressures. Wheat and barley 

are the only RAC included in the 

assessment. For the chronic 

assessments, the average wheat and 

barley field trial residue values were 

utilized. For the acute assessment, the 

two highest field trial residues were 

averaged and this highest average field 

trial residue (HAFT) was used in the 

assessment for all non-blended and 

partially blended commodities. All 

dietary exposure evaluations were made 

using the Dietary Evaluation Model 

(DEEMTM, version 7.87) from Exponent, 

Inc. and the USDA’s Continuing Survey 

of Food Intake by Individuals (1994–96) 

with the supplemental 1998 children’s 

survey. Chronic exposure was compared 

to a chronic reference dose of 0.10 mg/

kg bw/day is based upon a NOAEL of 

10 mg/kg bw/day from the chronic rat 

study. The acute reference dose of 0.3 

mg/kg bw/day for the subpopulation of 

women 13–49 years of age is based upon 

the developmental NOAEL of 30 mg/kg/

day in developmental toxicity studies in 

rabbits. For all other subpopulations, 

the acute reference dose of 1.5 mg/kg 

bw/day is based upon a NOAEL for 

acute effects at 150 mg/kg/day in a range 

finding rabbit developmental toxicity 

study. A 100x uncertainty factor was 

assumed for both the chronic and acute 

assessments. The chronic exposures 

were expressed as a percent of a 

reference dose of 0.10 mg/kg bw/day. 

The acute exposures (at the 99.9th 

percentile) were expressed as a percent 

of a reference dose of 0.3 mg/kg bw/day 

for women 13–49 years of age and 1.5 

mg/kg bw/day for all other 

subpopulations. Secondary residues in 

animal commodities were calculated by 

constructing diets for beef and dairy 

cattle, poultry and swine in order to 

calculate anticipated residues in meat, 

fat, milk and pork. The beef cattle diet 

was used to calculate meat, fat and 

organ meats residues. The dairy cattle 

diet was used to estimate residues in 

milk. The swine diet was used for 

secondary residues in pork commodities 

and the poultry diet was used for 

residues in poultry commodities. The 

chronic animal diet was calculated 

using averaged field trial residues where 

as the acute animal diet used averaged 

field trial residues on blended 

commodities such as grain and the 

HAFT on non-blended commodities 

such as hay, straw and forage. Beef 

(cattle and dairy) and swine transfer 

factors were derived from a lactating 

goat metabolism study, where the 

Federal Register / Vol. 69, No. 223 / Friday, November 19, 2004 / Notices 67735

animals were dosed with 121 ppm 

pinoxaden. Poultry transfer factors were 

derived from a hen metabolism study, 

where the animals were dosed with 97 

ppm pinoxaden.

The results were favorable in both 

acute and chronic assessment scenarios. 

Acute exposures at the (99.9th 

percentile) were 0.11% of the acute 

reference dose (0.3 mg/kg bw/day) for 

women 13–49 years of age, and less than 

0.05% for all other subpopulations. The 

chronic exposure values were negligible 

(<0.05% of the chronic reference dose of 

0.10 mg/kg bw/day for all 

subpopulations).

ii. Drinking water. The acute 

estimated environmental concentrations 

of pinoxaden (including the major 

degradates) in surface and ground water 

are 1.366 ppb (PRZM/EXAMS) and 

0.003234 ppb (SCI-GROW), respectively. 

The acute Population Adjusted Dose 

(aPAD) for pinoxaden (plus degradates) 

is 0.3 mg/kg bw/day for women 13–49 

years of age and 1.5 mg/kg bw/day for 

all other population subgroups. From 

the acute dietary exposure analysis, the 

highest acute food exposure from the 

uses of pinoxaden was 0.000509 mg/kg/

day at the 99.9th percentile for the 20–

49 years old subpopulation. Using this 

information, acute drinking water levels 

of comparison (DWLOC acute) were 

calculated for pinoxaden and the major 

degradates, ranging from 8,990 to 52,487 

ppb. Based on this analysis, pinoxaden 

(plus degradates) estimated 

environmental concentrations (EECs) do 

not exceed the calculated acute 

DWLOCs. The chronic estimated 

environmental concentration of 

pinoxaden (including the major 

degradates) in surface water is 0.21137 

ppb (annual average value from PRZM/

EXAMS). The chronic PAD for 

pinoxaden (plus degradates) is 0.10 mg/

kg bw/day. From the chronic dietary 

exposure analysis, the highest exposure 

estimate of 0.000047 mg/kg bw/day was 

determined for the children 1–2 years 

old subpopulation. Based on the EPA’s 

‘‘Interim Guidance for Conducting 

Drinking Water Exposure and Risk 

Assessments’’ document (62 FR 63662, 

December, 2, 1997), chronic DWLOC 

chronic were calculated for pinoxaden 

(plus degradates), ranging from 999.5 to 

2999.4 ppb. Based on this analysis, 

pinoxaden (plus degradates) EECs do 

not exceed the calculated chronic 

DWLOCs.

2. Non-dietary exposure. There are no 

sources ofnon-dietary exposure, as 

pinoxaden will be registered for 

agricultural uses only and will not be 

available for any residential or public 

uses.

D. Cumulative Effects

The potential for cumulative effects of 

pinoxaden and other substances that 

have a common mechanism of toxicity 

has also been considered. Pinoxaden, is 

a member of the new phenylpyrazolin 

class of herbicides. There is no reliable 

information to indicate that toxic effects 

produced by pinoxaden would be 

cumulative with those of any other 

chemical including another pesticide. 

Therefore, Syngenta believes it is 

appropriate toconsider only the 

potential risks of pinoxaden in an 

aggregate risk assessment.

E. Safety Determination

1. Infants and children. In assessing 

the potential for additional sensitivity of 

infants and children to residues of 

pinoxaden, data from developmental 

toxicity studies in the rat and rabbit and 

a two-generation reproduction study in 

the rat have been considered. In a multigeneration reproductive study, there 

were no indications of any differences 

in sensitivity to pinoxaden exposure 

between the different generations or 

between animals and offspring. The 

parental NOAEL for both sexes was 

considered to be 250 mg/kg/day. 

Offspring effects were not observed at 

dose levels that did not produce 

parental toxicity. Pinoxaden was not 

teratogenic and not directly toxic to the 

progeny in a developmental toxicity 

study in rats. The NOEL for both 

maternal and developmental toxicity 

was 30 mg/kg/day. Pinoxaden was not 

teratogenic in rabbits, and the maternal 

NOEL was 10 mg/kg/day. The NOEL for 

fetuses was 30 mg/kg/day. Since the 

NOEL for fetal effects was higher than 

the NOEL for maternal effects, there was 

no indication of a greater sensitivity of 

fetuses to pinoxaden administration. 

FFDCA section 408 provides that EPA 

may apply an additional safety factor for 

infants and children in the case of 

threshold effects to account for prenatal 

and postnatal toxicity and the 

completeness of the database. Based on 

the current toxicological requirements, 

the database for pinoxaden relative to 

prenatal and postnatal effects for 

children is complete. Further, the 

developmental studies showed no 

increased sensitivity in fetuses as 

compared to maternal animals following 

in utero exposures in rats and rabbits, 

and no increased sensitivity in pups as 

compared to the adults in the multigeneration reproductive toxicity study. 

Therefore, it is concluded that an 

additional uncertainty factor is not 

warranted to protect the health of 

infants and children and that RfDs of 0.3 

mg/kg/day (acute exposures to women 

13–50 yrs of age), 1.5 mg/kg/day (acute 

exposures to general population) and 

0.10 mg/kg/day (chronic expsoures) are 

appropriate for assessing aggregate risk 

to infants and children of pinoxaden. 

Chronic and acute aggregate exposures 

to all infants (<1 year old) is less than 

0.2% of the acute and chronic RfDs. 

Therefore, based on the completeness 

and reliability of the toxicity database, 

Syngenta concludes that there is 

reasonable certainty that no harm will 

result to infants and children from 

aggregate exposure to pinoxaden 

residues.

F. International Tolerances

There are no tolerances or maximum 

residue limits set for pinoxaden in any 

country at the time of this filing.

[FR Doc. 04–25714 Filed 11–18–04; 8:45 am]

BILLING CODE 6560–50–S

ENVIRONMENTAL PROTECTION 

AGENCY 

[FRL–7838–9] 

E–Docket ID No. ORD–2004–0003; 

Draft Proposed Sampling Program To 

Determine Extent of World Trade 

Center Impacts to the Indoor 

Environment

AGENCY: Environmental Protection 

Agency.

ACTION: Notice of Extension of Public 

Comment Period for Draft Proposed 

Sampling Program to Determine Extent 

of World Trade Center Impacts to the 

Indoor Environment. 

SUMMARY: On October 21, 2004, EPA 

published a Federal Register notice (69 

FR 61838) announcing the availability 

of the External Review Draft entitled, 

Draft Proposed Sampling Program to 

Determine Extent of World Trade Center 

Impacts to the Indoor Environment

(EPA/600/R–04/169A), and the 

beginning of a 30-day public comment 

period. At the request of members of the 

Lower Manhattan community and labor 

organizations who have said an 

extension is needed for them to 

formulate their comments, EPA is 

extending the public comment period 

until January 3, 2005. EPA will consider 

the public comment submissions in 

revising the document.

DATES: The public comment period will 

end on January 3, 2005. Technical 

comments should be in writing and 

must be postmarked by January 3, 2005.

ADDRESSES: The External Review Draft, 

Draft Proposed Sampling Program to 

Determine Extent of World Trade Center 

Impacts to the Indoor Environment, is