Federal Register / Vol. 62, No. 38 / Wednesday, February 26, 1997 / Notices 8737

food or drinking water is anticipated by

using Pseudomonas fluorescens PRA-25

as a seed treatment.

2. Non-dietary exposure such as lawn

care, topical insect repellents, etc. is not

anticipated since this microbial

pesticide does not have these uses.

3. Occupational exposure will be

mitigated through the use of proper

personal protective equipment.

E. Cumulative Exposure

Biological control agents of this type

generally work by out competing

disease organisms, thus, not having a

toxic mode of action that can be shared.

Other exposure can occur since other

strains of Pseudomonas fluorescens are

registered as microbial pesticides. Good

Bugs, Inc. believes that human exposure

from use of Pseudomonas fluorescens

PRA-25 as a seed treatment is expected

to be negligible.

F. Safety Determination

Good Bugs, Inc. believes that the

safety of the U.S. population and that of

infants and children will not be

adversely affected by the use of

Pseudomonas cepacia PRA-25 as a

vegetable seed treatment. Strain PRA-25

is a naturally occurring strain originally

isolated from the rhizosphere of a pea.

G. Existing Tolerances

1. Tolerance exemptions have been

granted for other strains of

Pseudomonas fluorescens.

2. International tolerance exemptions

have been granted for other strains of

Pseudomonas fluorescens.

II. Public Record

Interested persons are invited to

submit comments on the notice of filing.

Comments must bear a notation

indicating the document control

number, [PF-711].

A record has been established for this

notice under docket number [PF-711]

including comments and data submitted

electronically as described below). A

public version of this record, including

printed, paper versions of electronic

comments, which does not include any

information claimed as CBI, is available

for inspection from 8:30 a.m. to 4 p.m.,

Monday through Friday, excluding legal

holidays. The public record is located in

Room 1132 of the Public Response and

Program Resources Branch, Field

Operations Division (7506C), Office of

Pesticide Programs, Environmental

Protection Agency, Crystal Mall #2,

1921 Jefferson Davis Highway,

Arlington, VA.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption.

The official record for this

rulemaking, as well as the public

version, as described above will be kept

in paper form. Accordingly, EPA will

transfer all comments received

electronically into printed, paper form

as they are received and will place the

paper copies in the official rulemaking

record which will also include all

comments submitted directly in writing.

The official rulemaking record is the

paper record maintained at the address

in ‘‘ADDRESSES’’ at the beginning of

this document.

List of subjects

Environmental protection,

Administrative practice and procedure,

Agricultural commodities, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: February 11, 1997.

Janet L. Andersen,

Director, Biopesticides and Pollution

Prevention Division, Office of Pesticide

Programs.

[FR Doc. 97–4630 Filed 2–25–97; 8:45 am]

BILLING CODE 6560–50–F

[PF–701; FRL–5585–2]

Rhone-Poulenc Ag Company;

Pesticide Tolerance Petition Filing

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice of filing.

SUMMARY: This notice announces the

filing of a pesticide petition proposing

the establishment of a tolerance for

residues of isoxaflutole in or on field

corn. This notice contains a summary of

the petition prepared by the petitioner,

Rhone-Poulenc Ag Company.

DATES: Comments, identified by the

docket control number [PF–701], must

be received on or before, March 28,

1997.

ADDRESSES: By mail, submit written

comments to Public Response and

Program Resources Branch, Field

Operations Division (7506C), Office of

Pesticide Programs, Environmental

Protection Agency, 401 M St. SW.,

Washington, DC 20460. In person, bring

comments to Rm. 1132, CM#2, 1921

Jefferson Davis Highway, Arlington, VA

22202.

Comments and data may also be

submitted electronically by sending

electronic mail (e-mail) to: oppdocket@epamail.epa.gov. Electronic

comments must be submitted as an

ASCII file avoiding the use of special

characters and any form of encryption.

Comments and data will also be

accepted on disks in WordPerfect in 5.1

file format or ASCII file format. All

comments and data in electronic form

must be identified by the docket number

[PF–701]. Electronic comments on this

notice may be filed online at many

Federal Depository Libraries. Additional

information on electronic submissions

can be found in Unit II of this

document.

Information submitted as a comments

concerning this document may be

claimed confidential by marking any

part or all of that information as

‘‘Confidential Business Information’’

(CBI). CBI should not be submitted

through e-mail. Information marked as

CBI will not be disclosed except in

accordance with procedures set forth in

40 CFR part 2. A copy of the comment

that does not contain CBI must be

submitted for inclusion in the public

record. Information not marked

confidential may be disclosed publicly

by EPA without prior notice. All written

comments will be available for public

inspection in Rm. 1132 at the address

given above, from 8:30 a.m. to 4 p.m.,

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT:

Joanne Miller, Product Manager (PM)

23, Registration Division (7505C), Office

of Pesticide Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC. Office location,

telephone number and e-mail address:

Rm. 237, Crystal Mall #2, 1921 Jefferson

Davis Highway, Arlington, VA, 703–

305–6224, e-mail:

miller.joanne@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: EPA has

received a pesticide petition (PP

6F4664) from Rhone-Poulenc Ag

Company, P.O. Box 12014, 2 T.W.

Alexander Drive, Research Triangle

Park, NC 27709, 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 the

combined residues of the herbicide

isoxaflutole [5-cyclopropyl-4-(2-

methylsulfonyl-4-trifluoromethyl

benzoyl) isoxazole] and its metabolites

1-(2-methylsulfonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropylpropan-1,3-dione and 2-

methylsulphonyl-4-trifluoromethyl

benzoic acid, calculated as the parent

compound, in or on the raw agricultural

commodity field corn at 0.20 parts per

million (ppm), field corn, fodder, at 0.50

ppm, field corn, forage at 1.0 ppm; and
8738 Federal Register / Vol. 62, No. 38 / Wednesday, February 26, 1997 / Notices

establishing a tolerance for combined

residues of the herbicide isoxaflutole [5-

cyclopropyl-4-(2-methylsulfonyl-4-

trifluoromethyl benzoyl)isoxazole] and

its metabolite 1-(2-methylsulfonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropylpropan-1,3-dione,

calculated as the parent compound, in

or on the liver of cattle, goat, hogs,

horses, poultry and sheep at 0.40 ppm,

meat byproducts (except liver) of cattle,

goat, hogs, horses, and sheep at 0.2 ppm

and milk at 0.02 ppm. The proposed

analytical method is gas

chromatography. EPA has determined

that the petition contains data or

information regarding the elements set

forth in 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 petitions. Additional data may be

needed before EPA rules on the

petitions.

As required by section 408(d) of the

FFDCA, as recently amended by the

Food Quality Protection Act (FQPA)

Rhone-Poulenc included in the petition

a summary of the petition and

authorization for the summary to be

published in the Federal Register in a

notice of receipt of the petition. The

summary represents the views of RhonePoulenc; EPA is in the process of

evaluating the petition. As required by

section 408(d)(3) EPA is including the

summary as a part of this notice of

filing. EPA may have made minor edits

to the summary for the purpose of

clarity.

I. Petition Summary

A. Isoxaflutole Uses

Isoxaflutole is the first compound in

a new class of isoxazole herbicides.

Weeds found resistant to other

herbicides are not cross resistant to

isoxaflutole. The unique mode of action,

which disrupts pigment biosynthesis in

susceptible plants, of isoxaflutole

provides excellent selective control for

a wide spectrum of grass and broadleaf

weeds at low use rates.

Isoxaflutole will be used on field corn

to control broadleafs (including Kochia,

lambsquarters, mallow, mustard,

nightshade, pigweed, ragweed,

smartweed, velvetleaf, and waterhemp);

grasses (including barnyardgrass,

cupgrass, foxtails, Panicum and wild

proso millet).

Isoxaflutole will be applied in either

conventional, conservation tillage, or

no-till crop management systems and

may be applied either pre-plant, preplant incorporated or preemergence for

use in field corn production. The

product controls emerging weeds and

also has postemergent burn-down

activity to small exposed weeds.

Application rates for isoxaflutole alone

range from 0.035 to 0.14 pounds active

ingredient per acre dependent on soil

texture. Combinations of isoxaflutole

with up to one-half rates of other

herbicides improves control of several

annual grasses and dramatically reduces

total herbicide volume usage in

comparison with current agronomic

practices. Applications can be made up

to 14 days before planting field corn in

either conventional or no-till situations.

Isoxaflutole is formulated as a 75

percent water dispersible granule and

will be marketed under the trade name

of ‘‘BALANCE’’.

B. Isoxaflutole Safety

Rhone-Poulenc Ag Company has

submitted 41 separate toxicology studies

in support of tolerances for isoxaflutole.

According to Rhone-Poulenc,

isoxaflutole is not acutely toxic and

produces minimal skin and eye

irritation. Further, isoxaflutole is not

genotoxic, teratogenic nor a

reproductive toxin.

The following mammalian toxicity

studies have been conducted to support

the tolerance of isoxaflutole:

A rat acute oral study with an LD50 of

greater than 5,000 milligrams/kilogram

(mg/kg).

A rabbit acute dermal LD50 of greater

than 2,000 mg/kg.

A rat acute inhalation of LC50 of

greater than 5.23 milligram/litre (mg/L).

A primary eye irritation study in the

rabbit which showed minimal irritation.

A primary dermal irritation study in

the rabbit which showed minimal

irritation.

A primary dermal sensitization study

in the guinea pig which showed no

sensitization.

An acute neurotoxicity study

conducted in rats administered a single

dose at 0, 125, 500 or 2,000 mg/kg with

a no observed effect level (NOEL) of

2,000 mg/kg (limit dose) and no

treatment-related effects at any dose.

A 90–day subchronic neurotoxicity

study in rats administered at dose levels

of 0, 25, 250 or 750 milligrams/kilogram

of body weight per day (mg/kg bwt/day)

with NOEL of 750 mg/kg/day. This dose

is also the Lowest Effect Level (LEL) for

non-neurotoxic effects based on a

significant decrease in mean body

weight gain.

A 12–month feeding study in dogs

administered at levels of 0, 240, 1,200,

12,000 or 30,000 ppm with NOEL of

1,200 ppm based on slight changes in

liver and kidney weights in the absence

of any associated histopathological

changes.

A 24–month chronic feeding/

oncogenicity study in rats administered

at levels of 0.5, 2, 20 or 500 mg/kg bwt/

day) with an overall NOEL of 2.0 mg/

kg/day based on non-neoplastic changes

in the cornea, sciatic nerve, thigh

muscle, thyroid and liver observed at 20

mg/kg/day. An increased incidence of

hepatocellular adenomas and

carcinomas was observed at 500 mg/kg

bwt/day for males and females. In

addition, most of the 500 mg/kg/day

males with liver tumors also had

follicular cell adenomas in the thyroid.

An oncogenicity study in mice

administered 0, 25, 500 and 7,000 ppm

with a NOEL of 25 ppm based on a

slight effect on liver weight and body

weight gain at the LEL of 500 ppm. An

increased incidence of hepatocellular

adenomas and carcinomas was observed

at 7,000 ppm in both sexes. Increased

liver weight, non-neoplastic cellular

changes in the liver, and amyloidosis in

the duodenum, ileum, jejunum,

kidneys, heart ventricle, mesenteric

lymph node, and thyroid were also

observed at 7,000 ppm.

A developmental toxicity study in rats

administered at doses of 0, 10, 100 or

500 mg/kg bwt/day on gestation days 6

through 15 with a maternal NOEL of 100

mg/kg/day based on salivation and

lower body weight, body weight gain

and food consumption observed at 500

mg/kg/day and a fetal NOEL of 10 mg/

kg/day based on growth retardation and

increased incidences of vertebral and rib

anomalies and subcutaneous edema

observed at 100 mg/kg/day.

A developmental toxicity study in

rabbits administered at levels of 0, 5, 20

or 100 mg/kg bwt/day on gestation days

6 through 19 with a maternal NOEL of

20 mg/kg/day based on no weight gain

and decreased food consumption

observed at 100 mg/kg/day and fetal

NOEL of 5 mg/kg/day based on growth

retardation and increased incidences of

rib and vertebral anomalies noted at 20

mg/kg/day.

A 2 generation reproduction study in

rats fed at dose levels of 0, 0.5, 2, 20 or

500 mg/kg bwt/day with a NOEL for

postnatal development and parental

toxicity of 2 mg/kg/day based on

increased liver weight and

hepatocellular hypertrophy in F0 and

F1 adults and a slightly lower viability

index for F1 pups at 20 mg/kg/day. No

adverse effects on mating or fertility

indices and gestation, live birth or

weaning indices were noted in any

generation.

Mutagenicity—Ames Assay. Negative

with and without metabolic activation.

Mouse lymphoma. Negative with and

without metabolic activation.
Federal Register / Vol. 62, No. 38 / Wednesday, February 26, 1997 / Notices 8739

In-vivo Mouse Micronucleus Assay.

Negative.

In-vitro Cytogenetics Human

Lymphocyte Assay. Negative in the

presence and absence of metabolic

activation.

A metabolism study in the rat which

demonstrates that the majority of the

total radioactivity (TRR) is excreted

within 24 to 48 hours through the urine

and feces. Isoxaflutole is metabolized

primarily via hydrolysis to the 1-(2-

methylsulfonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropylpropan-1,3-dione (RPA

202248) followed by either reduction of

the cyanonitrile group to form RPA

205834 or further hydrolysis to 2-

methylsulphonyl-4-trifluoromethyl

benzoic acid (RPA 203328). The RPA

202248 is the major metabolite excreted

while RPA 203328 is the most polar.

Thus, the acute oral toxicity and

mutagenic potential of these two

metabolites were assessed.

In the acute oral toxicity studies, RPA

203328 had an oral LD50 greater than

5,000 mg/kg while RPA 202248 had an

oral LD50 greater than 2,000 mg/kg in

fasted rats. At 5,000 mg/kg, RPA 202248

produced 40 percent mortality in both

male and female rats. In Ames assays,

both RPA 202248 and RPA 203328 were

found to be devoid of mutagenic activity

in the absence and presence of

metabolic activation.

In the 28-day rat study, RPA 203328

was administered continuously in the

diet at levels of 0, 150, 500, 5,000, and

15,000 ppm (10 rats/sex/group). No

mortalities or treatment-related clinical

signs were observed during the study.

No effects were observed on body

weight, food consumption, hematology,

clinical chemistry, urinalysis, or

ophthalmoscopy. Further, no changes in

organ weight or histopathology were

noted at any level. The NOEL of 15,000

ppm is equivalent to 1,120 mg/kg/day in

males and 1,270 mg/kg/day in females.

C. Chronic Dietary Effects

Based upon all available data, the

lowest NOEL of 2.0 mg/kg/day was

observed in the chronic rat study. Using

this NOEL and a safety factor of 100, a

theoretical Reference Dose (RfD) of 0.02

mg/kg/day is obtained. The only

pending registration for isoxaflutole is

for use in/on field corn. A chronic

dietary risk assessment using the

maximum residue limits proposed in

this petition, and a 100 percent crop

treated shows that this use represents

1.8, 4.8, 5.3, and 3.3 percent of the RfD

for the whole U.S. population, for nonnursing infants less than 1 year old, for

children aged 1 to 6 years, and for

children aged 7 to 12 years,

respectively. Realizing that isoxaflutole

is likely to achieve only a 25 percent

market share at maturity, less than 1.5

percent of the RfD is reached for all

segments of the population. Thus,

Rhone-Poulenc believes that the

anticipated dietary exposure to

isoxaflutole is well below the theoretical

RfD of 0.02 mg/kg/day and is negligible

for all segments of the population

including infants and children.

Isoxaflutole presents a minimal acute

hazard. The acute oral NOEL is at least

1,000–fold higher than lowest chronic

NOEL of 2 mg/kg/day indicating that

acute exposure is unlikely to constitute

any significant dietary risk. Further, as

field corn is generally not directly

consumed, no significant acute dietary

exposure is likely to occur.

D. Aggregate Exposure

The FQPA of 1996 lists three other

potential sources of exposure to the

general population that must be

addressed. These are pesticides in

drinking water, exposure from nonoccupational sources, and the potential

cumulative effect of pesticides with

similar toxicological modes of action.

These exposures for isoxaflutole are

discussed below.

1. Drinking water. There is no

established maximum contaminant level

(MCL) or health advisory level (HAL) for

isoxaflutole nor its primary metabolite,

1-(2-methylsulphonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropane-1,3-dione. In the field

dissipation study, the half-life for

isoxaflutole was up to 3.0 days and for

1-(2-methylsulphonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropane-1,3-dione was 16 days

under actual field conditions. Residues

were only found in the uppermost

depths (above 12 inches). Based upon

the data generated by this study,

isoxaflutole and its primary metabolite

have a low potential for reaching

groundwater. Under actual use

conditions, neither compound is

expected to be present at toxicologically

significant concentrations in ground

water due to the low application rate

(maximum use rate 0.14 lbs. per acre)

and the low acute toxicity of each

compound. Therefore, Rhone-Poulenc

does not anticipate the presence of

isoxaflutole residues in drinking water.

2. Non-occupational exposure.

Isoxaflutole is being proposed for use on

field corn only at this time. Thus, nonoccupational exposure to isoxaflutole

via dermal or inhalation routes does not

exist and dietary exposure is the only

consideration for risk assessment

purposes.

3. Common mechanism of action. No

other pesticides have been identified

which inhibit 4-HPPDase. The thyroid

and liver tumors observed with

isoxaflutole in the rodent studies are

most likely indirectly related to a

significant induction of the hepatic

microsomal enzymes PROD, BROD, and

UDPGT. While hepatic microsomal

enzyme induction in rodents is likely to

be produced by many other pesticides,

there is no data to indicate that these

effects would be cumulative with any

other pesticide. Considering the rapid

elimination of isoxaflutole in the animal

metabolism study, the effects associated

with isoxaflutole are unlikely to be

cumulative with any other compound.

Further, considering the known

sensitivity of the rat to the development

of thyroid lesions in response to an

imbalance of thyroid hormones and

rodents to the development of liver

tumors in response to the induction of

microsomal enzymes, occurrence of

these tumors via these mechanisms in

rodent studies have little if any practical

relevance for human cancer or risk

assessment. Epidemiological studies

support the position that neither thyroid

tumors observed in rats due to an

imbalance of thyroid hormones or liver

tumors observed in rodents exposed to

inducers of microsomal enzyme activity

are likely to occur in humans.

Therefore, only the potential risks

associated with exposure to isoxaflutole

are considered for this assessment.

E. Determination of Safety for Infants

and Children

Developmental toxicity (delayed

ossification and rib and vertebral

anomalies) were observed in the

developmental toxicity studies. The

NOELs were 10 mg/kg/day in rats and

5 mg/kg/day in rabbits. In a 2-generation

reproduction study, pups from the high

dose group of 500 mg/kg/day had

significantly lower weights and a

slightly lower viability index for both F1

and F2 litters and corneal lesions for F2

litters. Parental systemic toxicity for this

dose group consisted of lower weight

gain and food consumption, corneal

lesions, increased liver weight, and

hepatocellular hypertrophy. In addition,

a slightly lower viability index was

noted for F1 pups from the 20 mg/kg/

day dose group but not for F2 pups.

Parental systemic toxicity at 20 mg/kg/

day included increased liver weight and

hepatocellular hypertrophy.

Considering the conservative

exposure assumptions in setting the

tolerances and the dietary risk

assessment assuming 100 percent crop

treated, less than 5.5 percent of the RfD

is utilized for non-nursing infants,
8740 Federal Register / Vol. 62, No. 38 / Wednesday, February 26, 1997 / Notices

children 1 to 6 years old, and children

7 to 12 years old. No non-occupational

sources of exposure exist for

isoxaflutole. Therefore, based upon the

completeness and reliability of the

toxicity data and the conservative

exposure assessment, Rhone-Poulenc

believes that there is a reasonable

certainty that no harm will result to

infants and children from exposure to

the residues of isoxaflutole and no

additional uncertainty factor is

warranted.

F. Estrogenic Effects

No evidence of estrogenic or

androgenic effects were noted in any

study. No adverse effects on mating or

fertility indices and gestation, live birth,

or weaning indices were noted in the 2-

generation rat reproduction study. An

imbalance of thyroid hormones related

to the induction of UDPGT was noted in

rats. However, considering species

differences in the half-life of thyroid

hormones in rodent versus primates (12

to 24 hours in rat compared to 5 to 9

days in humans) and differences in the

responsiveness of thyroid cells to TSH,

thyroid hormone levels in humans are

unlikely to be affected by the extremely

low levels of isoxaflutole residues that

might be present in food. Therefore,

Rhone-Poulenc believes that

isoxaflutole is not likely to cause any

endocrine effects in most species

including humans.

G. Chemical Residue

The nature of the residue of

isoxaflutole in plants and animals is

considered understood. In plants, the

metabolism proceeds through the

hydrolysis of the isoxazole ring to form

the primary degradate, 1-(2-

methylsulphonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropane-1,3-dione, and further

hydrolysis yields the second metabolite,

2-methylsulphonyl-4-trifluromethyl

benzoic acid. In animals the metabolic

pathway is very similar and the

metabolites formed are primarily the 1-

(2-methylsulphonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropane-1,3-dione with two other

toxicologically insignificant minor

degradates.

An analytical method is available for

detecting and measuring levels of

isoxaflutole in field corn with a limit of

quantitation of 0.01 ppm. The method

involves hydrolysis of isoxaflutole to a

methyl ester for gas chromatography

analysis.

A total of 32 field corn trials were

conducted in 13 different states. The

maximum residues were 0.88 ppm in

forage, 1.1 ppm in silage, 0.40 ppm in

fodder and 0.11 ppm in grain. Based on

these data, the proposed tolerance levels

are adequate to cover residues likely to

be present from the proposed use of

isoxaflutole. Isoxaflutole residues do not

appear to concentrate in corn processed

commodities. Therefore, no food

additive tolerances are being proposed

for these processed commodities.

In animal feeding studies, quantifiable

residues in the cow were observed only

in liver (up to 0.8 ppm), kidney (up to

0.2 ppm) and milk (up to 0.03 ppm) at

the 46 ppm (10X) dietary burden level.

No residues were observed in fat or

muscle. In poultry, quantifiable residues

were observed only in the liver (up to

0.6 ppm) at the highest dose level of 1.8

ppm (10X dietary burden). No residues

of isoxaflutole nor its primary

metabolite, 1-(2-methylsulphonyl-4-

trifluoromethylphenyl)-2-cyano-3-

cyclopropane-1,3-dione, were observed

in eggs, meat, fat or muscle. Based on

these data and the expected (1X) dietary

burden in animal feed, the proposed

tolerance levels are adequate to cover

residues likely to be present in animal

tissues resulting from the corn feed

items of the animal’s diet.

II. Public Record

EPA invites interested persons to

submit comments on this notice of

filing. Comments must bear a

notification indicating the docket

control number [PF–701].

A record has been established for this

notice under docket control numbers

[PF–701] (including comments and data

submitted electronically as described

below). A public version of this record,

including printed, paper versions of

electronic comments, which does not

include any information claimed as CBI,

is available for inspection from 8:30

a.m. to 4 p.m., Monday through Friday,

excluding legal holidays. The public

record is located in Rm. 1132 of the

Public Response and Program Resources

Branch, Field Operations Division

(7506C), Office of Pesticide Programs,

Environmental Protection Agency,

Crystal Mall #2, 1921 Jefferson Davis

Highway, Arlington, VA.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as ASCII file avoiding the use

of special characters and any form of

encryption.

The official record for this notice, as

well as the public version, as described

above will be kept in paper form.

Accordingly, EPA will transfer all

comments received electronically into

printed, paper form as they are received

and will place the paper copies in the

official record which will also include

all comments submitted directly in

writing. The official record is the paper

record maintained at the Virginia

address in ‘‘ADDRESSES’’ at the

beginning of this document.

Authority: 21 U.S.C. 346a.

List of Subjects

Environmental Protection,

Administrative practice and procedure,

Agricultural commodities, Pesticide and

pest, Reporting and recordkeeping

requirements.

Dated: February 11, 1997.

Stephen L. Johnson,

Director, Registration Division, Office of

Pesticide Programs.

[FR Doc. 97–4628 Filed 2–25–97; 8:45 am]

BILLING CODE 6560–50–F

[OPP–00468; FRL–5587–4]

Pesticide Product Label System;

Notice of Availability

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: This notice announces the

availability of the new Pesticide Product

Label System on CD ROM which

supersedes and replaces the Compact

Label File on microfiche.

FOR FURTHER INFORMATION CONTACT: By

mail: BeWanda Alexander, Office of

Pesticide Programs (7502C),

Environmental Protection Agency, 401

M St., SW., Washington, DC 20460.

Office location for commercial courier

delivery and telephone number: Rm.

700N, Crystal Mall #2, 1921 Jefferson

Davis Highway, Arlington, VA, (703)

305–5259.

ADDRESSES: For specific address and

price information, refer to Unit II. of this

document.

SUPPLEMENTARY INFORMATION:

I. Introduction

The Pesticide Product Label System

(PPLS), a software product developed by

EPA’s Office of Pesticide Programs

(OPP), contains images of registered

pesticide product labels submitted by

pesticide registrants and accepted by

OPP since 1971.

The label images have been indexed

by company, product, and date. The

retrieval program allows the user to

search by registration number, which is

a combination of company number and

product number. Searches can be

conducted based on partial numbers if