Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices 38535

DEPARTMENT OF ENERGY

Federal Energy Regulatory

Commission

[Docket No. CP00–381–000]

Williams Gas Pipelines Central, Inc.;

Notice of Request Under Blanket

Authorization

June 15, 2000.

Take notice that on June 7, 2000,

Williams Gas Pipelines Central, Inc.

(Williams), P.O. Box 20008, Owensboro,

Kentucky 42304, filed in Docket No.

CP00–381–000 a request pursuant to

sections 157.205 and 157.211 of the

Commission’s Regulations (18 CFR

157.205 and 157.211) under the Natural

Gas Act (NGA) for authorization to

construct and operate delivery point

facilities for service to Quivira Realty,

Inc. (Quivira), in Johnson County,

Kansas, under Quivira’s blanket

certificate issued in Docket No. CP82–

479–000, pursuant to section 7 of the

NGA, all as more fully set forth in the

application which is on file with the

Commission and open to public

inspection. This filing may be viewed

on the web at http://www.ferc.fed..us/

online/htm (call 202–208–2222 for

assistance).

Williams requests authorization to

construct and operate delivery point

facilities to serve Quivira, which

requires the gas for residential air

conditioning use. It is stated that

Williams will use the facilities to

transport up to 12 Dt equivalent of

natural gas per day on a firm basis

pursuant to section 284.223 of the

Commission’s regulations. Williams

estimates the cost of the facilities at

$9,100 and states that it would be

reimbursed for the cost by Quivira. It is

asserted that Williams has sufficient

capacity to render the proposed service

without detriment or disadvantage to its

other existing customers and that

Williams’ tariff does not prohibit the

addition of delivery point facilities. It is

further asserted that the proposal will

have no significant impact on Williams’

peak day and annual deliveries. Any questions regarding the

application may be directed to David N.

Roberts, Manager of Certificates and

Tariffs, at (270) 688–6712, Williams Gas

Pipelines Central, Inc., P.O. Box 20008,

Owensboro, Kentucky 42304. Any person or the Commission’s staff

may, within 45 days after issuance of

the instant notice by the Commission,

file pursuant to Rule 214 of the

Commission’s Procedural Rules (18 CFR

385.214) a motion to intervene or notice

of intervention and pursuant to section

157.205 of the Regulations under the

NGA (18 CFR 157.205) a protest to the

request. If no protest is filed within the

time allowed therefor, the proposed

activity shall be deemed to be

authorized effective the day after the

time allowed for filing a protest. If a

protest is filed and not withdrawn

within 30 days after the time allowed

for filing a protest, the instant request

shall be treated as an application for

authorization pursuant to Section 7 of

the NGA.

Linwood A. Watson, Jr.,

Acting Secretary.

[FR Doc. 00–15570 Filed 6–20–00; 8:45 am]

BILLING CODE 6717–01–M

ENVIRONMENTAL PROTECTION

AGENCY

[PF–945; FRL–6558–9]

Notice of Filing a Pesticide Petition To

Establish a Tolerance for Certain

Pesticide Chemicals in or on Food

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: This notice announces the

initial filing of pesticide petitions

proposing the establishment of

regulations for residues of certain

pesticide chemicals in or on various

food commodities.

DATES: Comments, identified by docket

control number PF–945, must be

received on or before July 21, 2000.

ADDRESSES: Comments may be

submitted by mail, electronically, or in

person. Please follow the detailed

instructions for each method as

provided in Unit I.C. of the

‘‘SUPPLEMENTARY INFORMATION.’’

To ensure proper receipt by EPA, it is

imperative that you identify docket

control number PF–945 in the subject

line on the first page of your response.

FOR FURTHER INFORMATION CONTACT: By

mail: Shaja R. Brothers, Registration

Division (7505C), Office of Pesticide

Programs, Environmental Protection

Agency, Ariel Rios Bldg., 1200

Pennsylvania Ave., NW., Washington,

DC 20460; telephone number: (703)

308–3194; e-mail address:

brothers.shaja@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

You may be affected by this action if

you are an agricultural producer, food

manufacturer or pesticide manufacturer.

Potentially affected categories and

entities may include, but are not limited

to:

CategoriesNAICS

codes

Examples of potentially affected entities

Industry 111 Crop production

112 Animal production

311 Food manufacturing

32532 Pesticide manufacturing

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 the table could also

be affected. The North American

Industrial Classification System

(NAICS) codes have been provided to

assist you and others in determining

whether or not this action might apply

to certain entities. If you have 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 Additional

Information, Including Copies of this

Document and Other Related

Documents?

1. Electronically. You may obtain

electronic copies of this document, and

certain other related documents that

might be available electronically, from

the EPA Internet Home Page at http://

www.epa.gov/. To access this

document, on the Home Page select

‘‘Laws and Regulations’’ and then look

up the entry for this document under

the ‘‘Federal Register—Environmental

Documents.’’ You can also go directly to

the Federal Register listings at http://

www.epa.gov/fedrgstr/.

2. In person. The Agency has

established an official record for this

action under docket control number PF–

945. The official record consists of the

documents specifically referenced in

this action, any public comments

received during an applicable comment

period, and other information related to

this action, including any information

claimed as confidential business

information (CBI). This official record

includes the documents that are

physically located in the docket, as well

as the documents that are referenced in

those documents. The public version of

the official record does not include any

information claimed as CBI. The public

version of the official record, which

includes printed, paper versions of any

electronic comments submitted during

an applicable comment period, is

available for inspection in the Public

Information and Records Integrity

Branch (PIRIB), Rm. 119, Crystal Mall

#2, 1921 Jefferson Davis Highway,

Arlington, VA, from 8:30 a.m. to 4 p.m.,

38536 Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices

Monday through Friday, excluding legal

holidays. The PIRIB telephone number

is (703) 305–5805.

C. How and to Whom Do I Submit

Comments?

You may submit comments through

the mail, in person, or electronically. To

ensure proper receipt by EPA, it is

imperative that you identify docket

control number PF–945 in the subject

line on the first page of your response.

1. By mail. Submit your comments to:

Public Information and Records

Integrity Branch (PIRIB), Information

Resources and Services Division

(7502C), Office of Pesticide Programs

(OPP), Environmental Protection

Agency, 1200 Pennsylvania Ave., NW.,

Washington, DC 20460.

2. In person or by courier. Deliver

your comments to: Public Information

and Records Integrity Branch (PIRIB),

Information Resources and Services

Division (7502C), Office of Pesticide

Programs (OPP), Environmental

Protection Agency, Rm. 119, Crystal

Mall #2, 1921 Jefferson Davis Highway,

Arlington, VA. The PIRIB is open from

8:30 a.m. to 4 p.m., Monday through

Friday, excluding legal holidays. The

PIRIB telephone number is (703) 305–

5805.

3. Electronically. You may submit

your comments electronically by e-mail

to: ‘‘opp-docket@epa.gov,’’ or you can

submit a computer disk as described

above. Do not submit any information

electronically that you consider to be

CBI. Avoid the use of special characters

and any form of encryption. Electronic

submissions will be accepted in

Wordperfect 6.1/8.0 or ASCII file

format. All comments in electronic form

must be identified by docket control

number PF–945. Electronic comments

may also be filed online at many Federal

Depository Libraries.

D. How Should I Handle CBI That I

Want to Submit to the Agency?

Do not submit any information

electronically that you consider to be

CBI. You may claim information that

you submit to EPA in response to this

document as CBI by marking any part or

all of that information as 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

version of the official record.

Information not marked confidential

will be included in the public version

of the official record without prior

notice. If you have any questions about

CBI or the procedures for claiming CBI,

please consult the person identified

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 control

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 pesticide petitions

as follows proposing the establishment

and/or amendment of regulations for

residues of certain pesticide chemicals

in or on various food commodities

under section 408 of the Federal Food,

Drug, and Comestic Act (FFDCA), 21

U.S.C. 346a. EPA has determined that

these petitions contain 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 support granting of the

petitions. Additional data may be

needed before EPA rules on the

petitions.

List of Subjects

Environmental protection,

Agricultural commodities, Feed

additives, Food additives, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: June 2, 2000.

Peter Caulkins,

Acting Director, Registration Division, Office

of Pesticide Programs.

Summaries of Petitions

The petitioner summaries of the

pesticide petitions are printed below as

required by section 408(d)(3) of the

FFDCA. The summaries of the petitions

were prepared by the petitioner and

represents the view of the petitioner.

The petition summaries announce 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.

I. Interregional Research Project

Number 4

9E6026

EPA has received pesticide petition

9E6026 from the Interregional Research

Project Number 4 (IR–4), New Jersey

Agricultural Experiment Station,

Rutgers University, New Brunswick,

New Jersey 08903, 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 paraquat in or on the raw

agricultural commodity (RAC) endive at

0.05 parts per million (ppm). EPA has

determined that the petition contains

data or information regarding the

elements set forth in section 408(d)(2) of

the FFDCA; however, EPA has not fully

evaluated the sufficiency of the

submitted data at this time or whether

the data support granting of the petition.

Additional data may be needed before

EPA rules on the petition. This notice

includes a summary of the petition

prepared by Zeneca Ag Products, the

registrant, 1800 Concord Pike. P.O. Box

15458, Wilmington, DE 19850–5458.

A. Residue Chemistry

1. Plant metabolism. The qualitative

nature of the residues in plants is

adequately understood based on studies

depicting the metabolism of paraquat in

carrots and lettuce following preemergence treatments and in potatoes

and soybeans following desiccant

treatment. The residue of concern in

plants is the parent chemical, paraquat.

2. Analytical method. An adequate

analytical method (spectrometric

method) has been accepted and

published in the Pesticide Analytical

Manual (PAM Vol. II) for the

enforcement of tolerances in plant

commodities.

B. Toxicological Profile

1. Acute toxicity. Acute toxicity

studies conducted with the 45.6%

paraquat dichloride technical

concentrate give the following results:

oral lethal dose (LD)50 in the rat of 344

milligrams/kilograms (mg/kg) males and

283 mg/kg females Category II; dermal

LD50 in the rat of >2,000 mg/kg for

Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices 38537

males and females (Category III); the

primary eye irritation study showed

corneal involvement with clearing

within 17-days (Category II); and dermal

irritation of slight erythema and edema

at 72 hours (Category IV). Paraquat is

not a dermal sensitizer. Acute

inhalation studies conducted pursuant

to EPA guideline with aerosolized

sprays result in lethal concentration

(LC)50 of 0.6 to 1.4 μg paraquat cation/

L (Category I). However, since paraquat

dichloride has no measurable vapor

pressure; and hydraulic spray droplets

are too large to be respirable, inhalation

exposure is not a concern in practice.

2. Genotoxicity. Paraquat dichloride

was not mutagenic in the Ames test

using Salmonella typhinurium strains

TA1535, TA1538, TA98, and TA100; the

chromosomal aberrations in the bone

marrow test system; or in the dominant

lethal mutagenicity study with CD–1

mice. Additionally, paraquat dichloride

was negative for unscheduled DNA

synthesis in rat hepatocyctes in vitro

and in vivo. Paraquat was weakly

positive in the mouse lymphoma cell

assay only in the presence of metabolic

activation. Paraquat dichloride was

weakly positive in mammalian cells

(lymphocytes) and positive in the sister

chromatid exchange (SCE) assay in

chinese hamster lung fibroblasts.

Paraquat is non-mutagenic.

3. Reproductive and developmental

toxicity. A 3-generation reproduction

study in rats fed diets containing 0, 25,

75, and 150 ppm (0, 1.25, 3.75, or 7.5

mg of paraquat cation/kg/day,

respectively) showed no effect on body

weight gain, food consumption and

utilization, fertility and length of

gestation of the F0, F1, and F2 parents

at any dose. The no observed adverse

effect level (NOAEL) and lowest

observed adverse effect level (LOAEL)

for systemic toxicity are 25 ppm (1.25

mg/kg/day) and 75 ppm (3.75 mg/kg/

day), respectively, expressed as

paraquat cation, based on high mortality

due to lung damage. The NOAEL for

reproductive toxicity is ≥150 ppm 7.5

mg/kg/day; highest dose tested (HDT)

expressed as paraquat cation, as there

were no reproductive effects observed.

Two developmental toxicity studies

were conducted in rats given gavage

doses of 0, 1, 5, or 10 mg/kg/day and 0,

1, 3, or 8 mg/kg/day, respectively,

expressed as paraquat cation. In the first

study, the NOAEL for maternal toxicity

was 1 mg/kg/day based on clinical signs

of toxicity and decreased body weight

gain at 5 mg/kg/day (the LOAEL). The

NOAEL for developmental toxicity was

set at 5 mg/kg/day based on delayed

ossification of the forelimb and

hindlimb digits. In the second study, the

maternal and developmental NOAEL is

8 mg/kg/day HDT as there were no

effects observed at any dose level. Based

on both studies, the overall NOAEL for

maternal and developmental toxicity is

at least 3 mg/kg/day.

Two developmental toxicity studies

were conducted in mice given gavage

doses of 0, 1, 5, or 10 mg/kg/day and 0,

7.5, 15, or 25 mg/kg/day paraquat ion,

respectively. In the first study the

NOAEL and LOAEL for maternal

toxicity are 5 mg/kg/day and 10 mg/kg/

day, respectively, based on reductions

in body weight gain and death (rangefinding study). The NOAEL and LOAEL

for developmental toxicity are 5 mg/kg/

day and 10 mg/kg/day, respectively

based on an increased number of litters

and fetuses with partial ossification of

the 4th sternebra at 10 mg/kg/day HDT.

Both the maternal and developmental

NOAELs are at 15 mg/kg/day in the

second study. The maternal LOAEL of

25 mg paraquat cation/kg/day is based

on death, decreases in body weight and

body weight gain, and other clinical

signs. The developmental LOAEL of 25

mg/kg/day is based on decreases in

mean fetal weights, retarded ossification

and other skeletal effects. According to

the registrant, Paraquat dichloride is not

a developmental toxin and the

developmental/maternal NOAEL should

be based on the second study and is 15

mg/kg/day.

4. Subchronic toxicity. A 90-day

feeding study was conducted in dogs

fed doses of 0, 7, 20, 60, or 120 ppm

with a NOAEL of 20 ppm based on lung

effects such as alveolitis and alveolar

collapse seen at the LOAEL of 60 ppm.

In a 21-day inhalation toxicity study,

rats were exposed to respirable aerosols

of paraquat at doses of 0, 0.01, 0.1, 0.5,

or 1.0 μg/L with a NOAEL of 0.01 μg/

L and a LOAEL of 0.10 μg/L based on

histopathological changes to the

epithelium of the larynx and nasal

discharge.

5. Chronic toxicity. A 12-month

feeding study was conducted in dogs

fed dose levels of 0, 15, 30, or 50 ppm,

expressed as paraquat cation. These

levels corresponded to 0, 0.45, 0.93, or

1.51 mg of paraquat cation/kg/day,

respectively, in male dogs or 0, 0.48,

1.00, or 1.58 mg of paraquat cation/kg/

day, respectively for female dogs. There

was a dose-related increase in the

severity and extent of chronic

pneumonitis in the mid-dose and highdose male and female dogs. This effect

was also noted in the low-dose male

group, but was minimal when compared

with the male controls. The systemic

NOAEL is 15 ppm (0.45 mg/kg/day for

males and 0.48 mg/kg/day for females,

expressed as parquet cation). The

systemic LOAEL is 30 ppm (0.93 mg/kg/

day for males and 1.00 mg/kg/day for

females, expressed as paraquat cation).

In a 2-year chronic feeding/

carcinogenicity study, rats were fed

doses of paraquat dichloride at 0, 25, 75,

or 150 ppm which correspond to 0, 1.25,

3.75, or 7.5 mg of paraquat cation/kg/

day. Paraquat enhanced the

development of ocular lesions in all of

the treated groups. The predominant

lesions detected opthalmoscopically

were lenticular opacities and cataracts.

At test week 103, dose-related

statistically significant (P<0.001)

increases in the incidence of ocular

lesions were observed only in the middose and high-dose male and female

groups. Based on these findings, the

NOAEL (approximate) and the LOAEL

for systemic toxicity, for both sexes, are

25 ppm (1.25 mg/kg/day) and 75 ppm

(3.75 mg/kg/day), respectively.

In another 2-year chronic feeding/

carcinogenicity study, rats were dosed

at 0, 6, 30, 100, or 300 ppm, expressed

as paraquat dichloride (nominal

concentrations), equivalent to 0, 0.25,

1.26, 4.15, or 12.25 mg/kg/day,

respectively (males) and 0, 0.30, 1.5,

5.12, or 15.29 mg/kg/day respectively

(females), expressed as paraquat

dichloride. The incidence of ocular

changes were low and not caused by

paraquat in this study. The systemic

NOAEL is 100 ppm of paraquat

dichloride (4.15 and 5.12 mg/kg/day, for

males and females, respectively); or 3.0

mg/kg/day (males) and 3.7 mg/kg/day

(females), expressed as paraquat cation.

The systemic LOAEL is 300 ppm of

paraquat dichloride (12.25 and 15.29

mg/kg/day, for males and females,

respectively); or 9.0 mg/kg/day (males)

and 11.2 mg/kg/day (females), expressed

as paraquat cation.

A chronic feeding/carcinogenicity

study was conducted in rats fed dose

levels of 0, 25, 75, or 150 ppm,

expressed as paraquat cation (nominal

concentrations). These doses

corresponded to 0, 1.25, 3.75, or 7.5 mg

paraquat cation/kg/day, respectively.

There was uncertain evidence of

carcinogenicity (squamous cell

carcinomas in the head region; ears,

nasal cavity, oral cavity and skin) in

males at 7.5 mg/kg/day HDT with a

systemic NOAEL of 1.25 mg/kg/day.

Upon submission of additional data to

EPA, the incidence of pulmonary

adenomas and carcinomas was well

within historical ranges and it was

determined that paraquat was not

carcinogenic in the lungs and head

region of the rat.

In another chronic feeding/

carcinogenicity study, rats were fed

dose levels of 0, 6, 30, 100, or 300 ppm,

38538 Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices

expressed as paraquat dichloride. There

were no carcinogenic findings in this

study at the HDT. In a 2-year chronic

feeding/concinogenicity study, SPF

Swiss derived mice were fed paraquat

dichloride at dose levels of 0, 12.5, 37.5,

or 100/125 ppm, expressed as paraquat

cation. These rates correspond to 0,

1.87, 5.62, and 15 mg/kg/day as cation.

Because no toxic signs appeared after 35

weeks of dosing, the 100 ppm level was

increased to 125 ppm at week 36. There

were no carcinogenic effects observed in

this study. The systemic NOAEL for

both sexes is 12.5 ppm (1.87 mg/kg/day)

and the systemic LOAEL is 37.5 ppm

(5.6 mg/kg/day), each expressed as

paraquat cation based on renal tubular

degeneration in males and weight loss

and decreased food intake in females.

Paraquat is classified Category E for

carcinogenicity (no evidence of

carcinogenicity in animal studies).

6. Animal metabolism. The qualitative

nature of the residue in animals is

adequately understood based on the

combined studies conducted with

ruminants (goats and cows), swine, and

poultry. The residue of concern in eggs,

milk, and poultry, and livestock tissues

is the parent, paraquat.

C. Aggregate Exposure

In examining aggregate exposure,

FQPA directs EPA to take into account

available information concerning

exposures from the pesticide residue in

food and all other exposures for which

there is reliable information. These

other sources of exposure include

drinking water, and non-occupational

exposures, e.g., to pesticides used in

and around the home. For estimating

acute and chronic risks the Agency

considers aggregate exposures from the

diet and from drinking water. Exposures

from uses in and around the home that

may be short term, intermediate, or

other durations may also be aggregated

as appropriate for specific chemicals.

1. Dietary exposure. For purposes of

assessing the potential dietary exposure

under the proposed tolerance, Zeneca

has estimated aggregate exposure based

on the tolerance levels of 0.05 ppm, 0.3

ppm, 0.05 ppm, and 0.05 ppm in or on

globe artichokes, dry peas, persimmons,

endive and from all other established

tolerances. Percent crop treated was also

incorporated into the assessment to

derive an upper bound anticipated

residue contribution (ARC). The

registrant has concluded that there are

no acute endpoints of concern for

paraquat, and an acute aggregate

assessment is not required. The chronic

population adjusted dose (cPAD) for

chronic dietary assessments is 0.0045

mg/kg/day, based on a NOAEL of 0.45

mg/kg/day from a 1-year dog study and

the addition of a standard uncertainty

factor of 100.

i. Food.— a. Chronic dietary

assessment. A chronic dietary exposure

analysis was performed using current

and reassessed tolerance level residues,

contributions from the proposed

tolerance for use on globe artichoke, dry

peas, persimmons, endive, and current

percent crop treated information to

estimate the ARC for the general

population and 22 subgroups. The

tolerance in globe artichoke resulted in

an ARC of 0.0000001 mg/kg/day

(0.002% of the cPAD) for the general

population. The resulting ARC for the

general U.S. population from all

established uses is 0.000367 mg/kg/day

(8.2% of the cPAD). For children ages 1

to 6, the most highly exposed subgroup,

the resulting ARC is 0.001077 mg/kg/

day (23.9% of the cPAD).

b. Acute dietary assessment. The

registrant has determined that current

data on paraquat shows no acute dietary

endpoint of concern. Therefore, an acute

dietary risk assessment was not

conducted for paraquat.

ii. Drinking water. The registration

eligibility document (RED) for paraquat

has stated the following:

Paraquat is not expected to be a

contaminant of groundwater. Paraquat

dichloride binds strongly to soil clay

particles and it did not leach from the

surface in terrestrial field dissipation

studies. There were, however,

detections of paraquat in drinking water

wells from two states cited in the

pesticides in groundwater data base

(1991). These detections are not

considered to be representative of

normal paraquat use. Therefore,

paraquat is not expected to be a

groundwater contaminant or concern

based on normal use patterns.

Due to its persistent nature, paraquat

could potentially be found in surface

water systems associated with soil

particles carried by erosion, however,

paraquat is immobile in most soils, and

at very high application rates (50–

1000X), there was no desorption of

paraquat from soils. Based on paraquat’s

normal use patterns and unique

environmental fate characteristics,

exposures to paraquat in drinking water

are not expected to be obtained from

surface water sources. Therefore, the

only exposures considered in aggregate

risk assessment for paraquat is chronic

dietary.

2. Non-dietary exposure. Paraquat

dichloride has no residential or other

non-occupational uses that might result

in non-occupational, non-dietary

exposure for the general population.

Paraquat products are restricted use, for

use by certified applicators only, which

means the general public cannot buy or

use paraquat products.

D. Cumulative Effects

In assessing the potential risk from

cumulative effects of paraquat and other

chemical substances, the Agency has

considered structural similarities that

exist between paraquat and other

bipyridylium compounds such as diquat

dibromide. Examination of the

toxicology data bases of paraquat and

diquat dibromide, indicates that the two

compounds have clearly different target

organs. Based on available data, the

registrant does not believe that the toxic

effects produced by paraquat would be

cumulative with those of diquat

dibromide.

E. Safety Determination

1. U.S. population. Based on the

paraquat RED, the only exposure route

of concern for paraquat is chronic

dietary. Using the conservation

assumptions presented earlier, EPA has

established a cPAD of 0.0045 mg/kg/

day. This was based on the NOAEL for

the 1-year dog study of 0.45 mg/kg/day

and employed a 100-fold uncertainty

factor. Results of this aggregate exposure

assessment, which includes EPA’s

reassessment of tolerances for existing

crops and the tolerance for use on globe

artichokes, dry peas, persimmons, and

endive utilize 8.2% of the cPAD.

Generally, exposures below 100% of the

cPAD are of no concern because it

represents the level at or below which

daily aggregate dietary exposure over a

lifetime will not pose appreciable risk to

human health. Thus, the registrant has

concluded that there is reasonable

certainty that no harm will result from

aggregate exposures to paraquat

residues.

2. Infants and children. Zeneca has

determined that the established

tolerances for paraquat, with

amendments and changes as specified

in this notice, meet the safety standards

under the FQPA amendments to section

408(b)(2)(C) for infants and children.

The safety determination for infants and

children considers the factors noted

above for the general population, but

also takes into account the possibility of

increased dietary exposure due to

specific consumption patterns of infants

and children, as well as the possibility

of increased susceptibility to the toxic

effects of paraquat residues in this

population subgroup.

In determining whether or not infants

and children are particularly susceptible

to toxic effects from paraquat residues,

Zeneca considered the completeness of

the data base for developmental and

Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices 38539

reproductive effects, the nature and

severity of the effects observed, and

other information.

Based on the current data

requirements, paraquat has a complete

data base for developmental and

reproductive toxicity. In the

developmental studies, effects were

seen (delayed ossification in the

forelimb and hindlimb digits) in the

fetuses only at the same or higher dose

levels than effects in the mother. In the

reproduction study, no effects on

reproductive performance were seen.

Also because the NOAELs from the

developmental and reproduction studies

were equal to or greater than the NOAEL

used for establishing the cPAD, the

registrant concluded that it is unlikely

that there is additional risk concern for

immature or developing organisms.

Finally, there is no epidemiological

information suggesting special

sensitivity of infants and children to

paraquat. Therefore, the registrant found

that an additional safety factor for

infants and children is not warranted for

paraquat.

Zeneca estimates that paraquat

residues in the diet of non-nursing

infants (less than 1 year) account for

17.6% of the cPAD and 23.9% of the

cPAD for children aged 1 to 6 years.

Further, residues in drinking water are

not expected. Therefore, Zeneca has

determined that there is reasonable

certainty that dietary exposure to

paraquat will not cause harm to infants

and children.

F. International Tolerances

There is no approved CODEX

maximum residue level (MRL)

established for residues of paraquat on

endive.

II. Interregional Research Project

Number 4

0E6090

EPA has received a pesticide petition

0E6090 from the Interregional Research

Project Number 4 (IR–4); Rutgers

University, New Brunswick, NJ, 08903-

0231 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

Fosetyl-Al in or on the raw agricultural

commodity (RAC) cranberries at 0.5

parts per million (ppm). EPA has

determined that the petition contains

data or information regarding the

elements set forth in section 408(d)(2) of

the FFDCA; however, EPA has not fully

evaluated the sufficiency of the

submitted data at this time or whether

the data support granting of the petition.

Additional data may be needed before

EPA rules on the petition. This notice

includes a summary of the petition

prepared by Aventis CropScience the

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

Alexander Drive, Research Triangle

Park, NC, 27709.

A. Residue Chemistry

1. Plant metabolism. The metabolism

of fosetyl-Al in plants is adequately

understood. Adequate data on the

nature of the residues in plants,

including identification of major

metabolites and degradates of fosetyl-Al,

are available. Radiolabeled studies on

the uptake, translocation and

metabolism in plants show that the

chemical proceeds through hydrolytic

cleavage of the ethyl ester. The major

residues are fosetyl-Al, phosphorus

acid, and ethanol. The tolerances are

established for the parent only, that is

fosetyl-Al.

2. Analytical method. Adequate

methods are available for enforcement

purposes. There are two analytical

methods acceptable for determining

residues of fosetyl-Al in plants: a gas

chromatography method is available for

enforcement of tolerance in pineapple

and is listed as method I in pesticide

analytical manual (PAM), Vol. II; a gas

chromatography/phosphorus specific

flame photometric detector (FPD-P)

method (Aventis CropScience method

no. 163) for citrus has undergone a

successful method tryout on oranges

and has been sent to the Food and Drug

Adminstration (FDA) for inclusion in

PAM as method II.

3. Magnitude of residues. Field trials

were conducted in EPA regions 1 (MA),

2 (NJ), 5 (WI), and 12 (OR). All field trial

sites consisted of 1 untreated control

plot and 1 treated plot. Each treated plot

received four foliar spray applications of

fosetyl-Al at a rate of 4.0 lb active

ingredient per acre (ai/A) # 5% each, for

a total of approximately 16 lb ai/A. The

first application was made at

approximately 93 days prior to harvest

and subsequent applications were made

at approximately 30-day intervals.

Samples were collected at 3 or 4 days

after the last application in all trials.

Fosetyl-Al residues in treated samples

ranged from <0.05 ppm to 0.35 ppm.

Data from this study support the

proposed tolerance of 0.5 ppm.

B. Toxicological Profile

1. Acute toxicity. A complete battery

of acute toxicity studies for fosetyl-Al

technical has been conducted. The

lethal dose LD50 from the acute oral rat

is 5.4 g/kg and the LD50 from an acute

dermal rabbit study is >2 g/kg. The LC50

for a rat inhalation study is >1.73 mg/

L. The acute oral rat and primary dermal

irritation studies indicate category IV

toxicity. A guinea pig dermal

sensitization study shows fosetyl-Al is

not a skin sensitizer. The primary eye

irritation study in rabbits shows fosetylAl to be an eye irritant with Category I

toxicity.

2. Genotoxicity. Fosetyl-Al is neither

mutagenic nor genotoxic. The genetic

toxicity potential of fosetyl-Al was

assessed in several assays. Eight

mutagenicity tests performed with

fosetyl-Al were negative. The tests

included two Ames assays with S.

typhimurium, two phase induction

assays using E. coli, two micronucleus

studies in mice, one DNA repair assay

using E. coli and one mutation assay in

Saccharomyces cereviseae.

3. Reproductive and developmental

toxicity. Fosetyl-Al is not a reproductive

toxicant and shows no evidence of

estrogenic or androgenic related effects.

i. In a 3-generation reproduction

study, fosetyl-Al was administered to

rats at dietary levels of 0, 6,000, 12,000,

or 24,000 ppm. No adverse effects on

reproductive performance or pup

survival were observed in any dose

group. The lowest observed adverse

effect level (LOAEL) was established at

12,000 ppm based on effects on animal

weights and urinary tract changes. The

no observed adverse effect level

(NOAEL) for all effects was 6,000 ppm.

ii. A developmental study in rats

dosed via oral gavage at 500, 1,000 or,

4,000 mg/kg/day showed a

developmental NOAEL of 1,000 mg/kg.

At 4,000 mg/kg, there was maternal

toxicity, as evidenced by effects on

animal weights, maternal deaths,

increased resorptions and delayed fetal

ossification.

iii. A rabbit developmental study

showed no toxic effects at oral doses up

to 500 mg/kg. Effects of fosetyl-Al on

fetal development were observed only

in the rat at a dose producing severe

maternal toxicity. In the absence of

maternal toxicity, no adverse effects on

fetal development were observed, i.e. at

1,000 mg/kg/day in rats or at 500 mg/

kg/day in rabbits.

4. Subchronic toxicity. In subchronic

studies, no significant toxicity was

observed even at doses exceeding the

limit of 1,000 mg/kg/day.

i. A 21-day dermal study in rabbits

showed mild to moderate skin irritation

and a NOAEL of 1.5 g/kg/day.

ii. A 90-day feeding study in rats

showed a NOAEL of >5,000 ppm; the

LOAEL was 25,000 ppm with

extramedullary hematopoiesis in the

spleen.

iii. A 90-day dog feeding study

showed a NOAEL of 10,000 ppm and a

38540 Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices

LOAEL at 50,000 ppm, at which the test

animals had a lower serum potassium

level than untreated animal.

5. Chronic toxicity. Chronic toxicity

studies have been conducted in dogs

and rats:

i. Dog. Fosetyl-Al was fed to dogs for

2-years at concentrations of 0, 10,000,

20,000, and 40,000 ppm. The NOAEL

was 10,000 ppm, equivalent to 250 mg/

kg/day. The LOAEL was 20,000 ppm

based on a slight degenerative effect on

the testes. These testicular changes, as

well as a few scattered clinical changes,

were seen in the high dose dogs. No

effects were observed in the urinary

tract.

ii. Rat. Fosetyl-Al was administered

via admixture in the diet to CD rats at

target levels of 0, 2,000, 8,000, and

30,000/40,000 ppm for approximately 2-

years. Based on these levels, respective

doses were 100, 400 and 2,000/1,500

mg/kg/day. After 2-weeks at 40,000

ppm, this dietary level was reduced to

30,000 ppm due to the occurrence of red

coloration of the urine and a decrease in

body weight gain. Although these

findings were no longer apparent after

week 2, analytical verification of dietary

levels revealed that the highest dietary

level ranged from approximately 38,000

to 61,000 ppm during the first 32-weeks

of the study. No significant differences

in body weight or food consumption

were noted at 2,000 or 8,000 ppm. No

biologically significant differences were

observed in ophthalmoscopy,

hematology, clinical chemistry, or

urinalysis for treated and control

animals. Calculi in the urinary bladder

were observed for several male and

female rats in the high dose group. Nonneoplastic findings consisted of

epithelial hyperplasia and inflammation

in the urinary bladders of males at

30,000/40,000 ppm. Increased

incidences of hydronephrosis,

inflammation, and epithelial

hyperplasia in the kidney were also

observed in males from the high dose

group. Females from the same group

exhibited increased incidences of

epithelial hyperplasia in the urinary

bladder and hydronephrosis in the

kidney. The NOAEL in the chronic rat

study was 8,000 ppm (400 mg/kg/day).

The lowest NOAEL for chronic effects

of fosetyl-Al is 10,000 ppm (250 mg/kg/

day) based on the dog study. This

NOAEL is based on minor changes at

20,000 ppm. In the rat, calculi in the

urinary bladder and related

histopathological changes in the bladder

and kidneys of males and females were

observed at 30,000/40,000 ppm.

6. Carcinogenicity. Long-term feeding

studies were conducted with technical

grade fosetyl-Al in mice and rats and

with monosodium phosphite, the

primary urinary metabolite of fosetyl-Al,

in rats. These studies, in addition to a

mechanistic study in rats, are described

below:

i. Rat. Fosetyl-Al was administered

via admixture in the diet to CD rats at

target levels of 0, 2,000, 8,000, and

30,000/40,000 ppm for approximately 2-

years. After 2-weeks at 40,000 ppm, this

dietary level was reduced to 30,000 ppm

due to the occurrence of red coloration

of the urine and a decrease in body

weight gain. Although these findings

were no longer apparent after Week 2,

analytical verification of dietary levels

revealed that the highest dietary level

ranged from approximately 38,000 to

61,000 ppm during the first 32-weeks of

the study. Calculi in the urinary bladder

were observed for several male and

female rats at 30,000/40,000 ppm.

Microscopic examination revealed

transitional cell carcinomas and

papillomas in the urinary bladders of

high dose males. In addition, a

statistically significant increase in

adrenal pheochromocytomas (benign

and malignant combined) was observed

in males at 8,000 and 30,000/40,000

ppm. The adrenal slides were

independently reread by two consulting

pathologists who found no significant

dose-related increases in the incidence

of pheochromocytomas or hyperplasia.

The NOAEL for fosetyl-Al in the chronic

rat study was 8,000 ppm. A subsequent

mechanistic study in rats conducted

with dietary levels of 8,000, 30,000 and

50,000 ppm demonstrated that the

massive doses of 30,000 and 50,000

ppm fosetyl-Al alter calcium/

phosphorous homeostasis resulting in

severe acute renal injury, similar to that

observed in the chronic rat study, and

the formation of calculi in kidneys,

ureters, and bladder. Under conditions

of chronic exposure, these effects could

lead to the formation of bladder tumors

as seen in the chronic rat study. At

8,000 ppm, no evidence of renal injury

was observed, a result consistent with

the absence of bladder tumors. Thus, the

bladder tumors induced by fosetyl-Al

were the result of acute renal injury

followed by a chronic toxic reaction

rather than a true carcinogenic effect.

A carcinogenicity study in rats was

conducted with monosodium phosphite

administered via dietary mixture at

levels of 2,000, 8,000, and 32,000 ppm.

No evidence of carcinogenicity was

observed in this study.

ii. Mouse. A 2-year feeding/

carcinogenicity study was conducted in

mice fed diets containing fosetyl-Al at 0,

2,500, 10,000, or 20,000/30,000 ppm.

The 20,000 ppm dose was increased to

30,000 ppm during week 19 of the

study. The NOAEL for all effects was

20,000/30,000 ppm (3,000/4,500 mg/kg/

day). There were no carcinogenic effects

observed under the conditions of this

study.

7. Animal metabolism. Rat

metabolism studies showed that most of

the radiolabel rapidly appeared in

exhaled carbon dioxide. There was also

some radiolabel excreted in the urine as

phosphite, along with a smaller amount

as the unchanged parent compound. It

appears that fosetyl-Al is essentially

completely absorbed after ingestion and

extensively hydrolyzed to carbon

dioxide which is exhaled. The

phosphite is excreted in the urine

without further oxidation to phosphate.

Aluminum does not appear to be

absorbed to a significant extent from the

gastrointestinal trac.

8. Metabolite toxicology. There are no

metabolites of toxicological concern.

The tolerances are established for the

parent only, that is fosetyl-Al.

9. Endocrine disruption. No evidence

of estrogenic or androgenic effects were

noted in any study with fosetyl-Al. No

adverse effects on mating or fertility

indices and gestation, live birth, or

weaning indices were noted in a 3-

generation rat reproduction study at

doses well above EPA’s limit of 1,000

mg/kg/day. Therefore, Aventis

CropScience concludes that fosetyl-Al

does not have any effect on the

endocrine system.

C. Aggregate Exposure

1. Dietary exposure. EPA has

established the chronic reference dose

(RfD) for fosetyl-Al at 2.5 mg/kg/day.

This RfD is based on a NOAEL of 250

mg/kg/day from a 2-year feeding study

in dogs and the use of a 100 fold safety

factor to account for inter-species and

intra-species differences. No appropriate

endpoint attributable to a single dose

exposure was identified in oral toxicity

studies. Therefore, an acute RfD was not

established and there is no expectation

of acute risk. Since no dermal or

systemic toxicity was seen at the limit

dose following repeated dermal

applications in the 21-day toxicity study

using rats, no endpoint value was

calculated for short-and intermediateterm exposure and risk. The Agency has

concluded that fosetyl-Al is unlikely to

pose a carcinogenic hazard to humans.

Therefore, a cancer exposure and risk

assessment is not appropriate.

i. Food. For all currently registered

uses of fosetyl-Al, chronic food

exposure for various subgroups of the

U.S. population was estimated by EPA

through the use of the dietary exposure

evaluation model (DEEM) software. The

DEEM analysis evaluated the individual

Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices 38541

food consumption as reported by

respondents in the U. S. Department of

Agricultural (USDA) 1989–1991

nationwide continuing surveys of food

intake by individuals. As the risk

estimate was low for even the most

highly exposed subpopulation, no

anticipated residues were used. In the

surveys, 100% crop treated and

tolerance level residues were assumed

for all crops. The calculated potential

exposure for the U.S. population is

0.077 mg/kg/day resulting in utilization

of 3% of the chronic population

adjusted dose (cPAD). Potential

exposure for the most highly exposed

group, children (1–6 years), is 0.157 mg/

kg/day and corresponds to 6% of the

chronic cPAD. Aventis CropScience

anticipates that the incremental

exposure resulting from the proposed

use on cranberries will be minimal and

that dietary exposure for the proposed

tolerance in addition to all existing

tolerances for fosetyl-Al will be well

below the Agency’s level of concern.

ii. Drinking water. There is no

established maximum contaminant level

(MCL) or health advisory level for

fosetyl-Al. The potential for ground

water and/or surface water

contamination by fosetyl-Al and its

degradates is expected to be very low,

in most cases, due to the rapid

degradation of the compound in soil to

non-toxic degradates under both aerobic

and anaerobic conditions. Under aerobic

laboratory conditions, the half-life of

fosetyl-Al is between 1 and 1.5 hours in

loamy sand, silt loam and clay loam and

20 minutes in sandy loam soil. The

degradation proceeds through the

hydrolysis of the ethyl ester bond,

resulting in the formation of

phosphorous acid and ethanol. The

ethanol is further degraded into carbon

dioxide. Based on the short half-life of

fosetyl-Al and the known fate of

phosphates under anaerobic conditions,

EPA determined that an anaerobic soil

metabolism study was not necessary. An

anaerobic aquatic soil metabolism study

was conducted. When anaerobic

conditions were established by flooding

soil, the half-life was 40 hours with silty

clay loam and 14 hours with sandy loam

soil. Aventis CropScience expects that

potential fosetyl-Al residues in drinking

water are not a significant contribution

to aggregate exposure.

2. Non-dietary exposure. Fosetyl-Al is

currently registered for residential use

on turf and ornamental plants. Chronic

exposure is not expected for residential

uses. There is also no expectation of

acute risk. No appropriate endpoint

attributable to a single dose exposure

was identified in oral toxicity studies

and consequently, an acute RfD cannot

be calculated. No endpoint value is

calculable for short-term and

intermediate-term exposure and a risk

analysis cannot be performed since no

dermal or systemic toxicity was seen at

the limit dose following repeated

dermal applications in the 21-day

toxicity study using rats. The Agency

has previously concluded that fosetyl-Al

is unlikely to pose a carcinogenic

hazard to humans. Therefore, a cancer

exposure and risk assessment is not

appropriate. Thus, Aventis CropScience

concludes that the ornamental and turf

uses do not add significantly to the

aggregate exposure for fosetyl-Al.

D. Cumulative Effects

Effects associated with fosetyl-Al are

unlikely to be cumulative with any

other compound. The formation of

calculi and bladder tumors in rats are

the only significant toxicological effects

observed with fosetyl-Al. These effects

were observed in the rat only at a dose

which, not only exceeds estimated

human exposure by several orders of

magnitude, but is in excess of EPA’s

dose limit for carcinogenicity studies.

Therefore, an aggregate assessment

based on common mechanisms of

toxicity is not appropriate as exposure

to humans will be well below the levels

producing calculi and bladder tumors in

rats. Further, considering the rapid

elimination of fosetyl-Al in the rat

metabolism study, any effects associated

with fosetyl-Al are unlikely to be

cumulative with any other compound.

Based on these reasons, only the

potential risks of fosetyl-Al are

considered in the exposure assessment.

E. Safety Determination

1. U.S. population. Chronic risk

estimates associated with exposure to

fosetyl-Al in food and water are

expected to be well below the Agency’s

level of concern. The DEEM chronic

exposure analysis previously performed

by the Agency for all currently

registered food uses showed that the

U.S. general population, 3% of the

cPAD is occupied by dietary (food)

exposure. For the most highly exposed

subgroup, children 1–6 years old, 6% of

the cPAD is occupied by dietary (food)

exposure. The contribution of fosetyl-Al

residues in surface and ground water to

chronic aggregate exposure is expected

to be minimal. The incremental

exposure resulting from the proposed

use on cranberries is also expected to be

negligible. Therefore, Aventis

CropScience concludes that there is a

reasonable certainty that no harm will

result from aggregate exposure to

fosetyl-Al residues.

2. Infants and children. No indication

of increased susceptibility of rat or

rabbit fetuses to in utero and/or

postnatal exposure was noted in the

developmental and reproductive

toxicity studies. The Agency has

previously determined that no

additional safety factor to protect infants

and children is necessary for this

product.

Using the conservative assumptions

described in the exposure section above

(unit II.C.), aggregate exposure to

fosetyl-Al from currently registered food

uses will utilize up to 6% of the cPAD

for infants and children. The

incremental exposure to fosetyl-Al

resulting from the proposed use on

cranberries is expected to be minimal

and even when considered in addition

to the potential for exposure to residues

in drinking water and from non-dietary,

non-occupational exposure, the

aggregate exposure to fosetyl-Al is not

expected to exceed 100% of the cPAD.

Aventis CropScience concludes that

there is a reasonable certainty that no

harm will result to infants and children

from aggregate exposure to fosetyl-Al

residues.

F. International Tolerances

There are presently no Codex

alimentarius commission maximum

residue levels established for residues of

fosetyl-Al.

III. Interregional Research Project

Number 4

8E5012

EPA has received a pesticide petition

8E5012 from the Interregional Research

Project Number 4 (IR–4), New Jersey

Agricultural Experiment Station, P.O.

Box 231 Rutgers University, New

Brunswick, NJ 08903 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 cyprodinil in or on the raw

agricultural commodities dry bulb

onion, green onion, and strawberries at

0.6, 4.0, and 5.0 parts per million (ppm).

A. Residue Chemistry

1. Plant metabolism. Novartis believes

the metabolism of cyprodinil has been

well characterized in plants. The

metabolism profile supports the use of

an analytical enforcement method that

accounts for only parent cyprodinil.

2. Analytical method. Analytical

method AG–631A is a practical

analytical method involving extraction,

filtration, and solid phase cleanup of

samples with analysis by high

performance liquid chromotography

38542 Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices

(HPLC) and ultra-violet ray (UV). The

limits of quantitation (LOQ) for various

commodities are as follows: fruit, grain,

juice-0.02 ppm; forage, fodder, straw0.05 ppm; and grapes-0.01 ppm.

3. Magnitude of residues. This

petition is supported by field trials

conducted on representative members of

the bulb vegetable crop grouping and

strawberries. All samples were analyzed

by residue method AG–631A to

determine the residues of cyprodinil. In

bulb vegetables, the maximum residue

found on representative commodities

were 3.9 ppm and 2.7 ppm, for green

onion and bulb onion, respectively. The

maximum residue found in strawberries

was 3.3 ppm. A tolerance of 5.0 ppm for

strawberries has been proposed.

B. Toxicological Profile

Cyprodinil appears to pose relatively

little human toxicity risk due to low use

rate, low risk to groundwater, low

dietary risk and low worker exposure.

The risk from acute dietary exposure to

cyprodinil is considered to be very low.

The mammalian toxicity studies that

have been conducted to support the

tolerances of cyprodinil are listed

below.

1. Acute toxicity. The following are

results from the acute toxicity tests

conducted on the technical material:

i. A rat acute oral study for cyprodinil

with a LD50 of 2,796 milligrams/

kilograms(mg/kg).

ii. A rat acute dermal study for

cyprodinil with a LD50 > 2,000 mg/kg.

iii. A rat inhalation study for

cyprodinil with a LC50 > 1.2 mg/liter air.

iv. A primary eye irritation study in

rabbits showing cyprodinil as minimally

irritating.

v. A primary dermal irritation study

in rabbits showing cyprodinil as slightly

irritating.

vi. A skin sensitization study in

guinea pigs showing cyprodinil as a

weak sensitizer.

2. Genotoxicity. The following are

results from the genotoxicity test:

i. In vitro gene mutation test. Ames

assay-negative; chinese hamster V79 cell

test-negative; rat hepatocyte DNA repair

test-negative.

ii. In vitro chromosome test. Chinese

hamster ovary cell cytogenetic testnegative.

iii. In vivo mutagenicity test. Mouse

bone marrow test-negative.

3. Reproductive and developmental

toxicity. Cyprodinil is not a

reproductive or developmental hazard,

as is demonstrated by the results of the

following studies:

i. Rat oral developmental. An oral

developmental study in the rat with a

maternal no observed adverse effect

level (NOAEL) of 200 mg/kg based on

reductions in body weight gain and food

consumption and a fetal NOAEL of 200

mg/kg based on decreased pup weight

and delayed skeletal growth at 1,000

mg/kg.

ii. Rabbit oral developmental study.

An oral developmental study in the

rabbit with a maternal NOAEL of 150

mg/kg based on reduction in body

weight gain and a fetal NOAEL of 400

mg/kg based on the absence of any fetal

effects.

iii. Rat 2-generation reproduction

study. A 2-generation reproduction

study in the rat with a systemic NOAEL

of 100 ppm and a fetal NOAEL of 1,000

ppm (100 mg/kg). A slight decrease in

pup weight at birth and subsequent

body weight gain during the lactation

phase was observed only at the

maternally toxic dose of 4,000 ppm

without any effects on reproduction and

fertility.

4. Subchronic toxicity. These tests are

summarized below:

i. A 28-day dermal study in the rat

with a NOAEL of 5 mg/kg based on

clinical signs.

ii. A 90-day feeding study in the dog

with a NOAEL of 1,500 ppm (37.5 mg/

kg) based on reduced food intake and

body weight.

iii. A 90-day feeding study in the

mouse with a NOAEL of 500 ppm (75

mg/kg) based on liver histologic

changes.

iv. A 90-day feeding study in the rat

with a NOAEL of 50 ppm (5 mg/kg)

based on hematologic and histologic

findings.

5. Chronic toxicity. The reference dose

(RfD) for cyprodinil is 0.0375 mg/kg/

day. This value is based on the systemic

NOAEL of 3.75 mg/kg/day in the rat

chronic feeding study with a 100-fold

safety factor to account for interspecies

extrapolation and intraspecies

variability.

i. A 12-month feeding study in the

dog with a NOAEL of 2,500 ppm (62.5

mg/kg) based on liver histologic

changes.

ii. An 18-month carcinogenicity

feeding study in the mouse with a

NOAEL of 2,000 ppm (300 mg/kg). The

maximum tolerated dose (MTD) was

5,000 ppm based on reduction in body

weight gain and no evidence of

carcinogenicity was seen.

iii. A 24-month chronic feeding/

carcinogenicity study in the rat with a

NOAEL of 75 ppm (3.75 mg/kg) based

on hematologic and histologic findings.

The MTD was 2,000 ppm based on liver

histopathology and no evidence of

carcinogenicity was seen.

6. Animal metabolism. Ruminant

metabolism shows extensive

degradation following a pathway that is

similar to plants. Extrapolating from

goat studies, none of the metabolites,

including parent compound, will be

near the normal minimum range for

detection by analytical methods (0.01 to

0.05 ppm). Therefore, parent residues

will be proposed as an adequate marker

for total residues of cyprodinil in

animals. The analysis also demonstrates

that livestock tolerances are not

required in conjunction with this

petition.

7. Endocrine disruption. Cyprodinil

does not belong to a class of chemicals

known or suspected of having adverse

effects on the endocrine system.

Developmental toxicity studies in rats

and rabbits and a reproduction study in

rats gave no indication that cyprodinil

might have any effects on endocrine

function related to development and

reproduction. The chronic studies also

showed no evidence of a long-term

effect related to the endocrine system.

C. Aggregate Exposure

1. Dietary exposure—i. Food. For the

purposes of assessing the potential

dietary exposure under the proposed

tolerances, Novartis has estimated

aggregate exposure from the previously

established tolerances for the raw

agricultural commodities: almond

nutmeat at 0.02 (ppm), almond hulls at

0.05 ppm, grapes at 2.0 ppm, raisins at

3.0 ppm, pome fruit crops at 0.1 ppm,

wet apple pomace at 0.15 ppm, and

stone fruit crops at 2.0 ppm; and the

requested tolerances of strawberries at

5.0 ppm, dry bulb onion at 0.6 ppm, and

green onion at 4.0 ppm. The tier 1

chronic cyprodinil assessment

displayed below used tolerance values

listed in 40 CFR 180.532 for all

commodities; 100% market share was

assumed for all crops. Results of the

cyprodinil assessment are displayed

below as a percentage of the chronic

RfD.

Population Chronic RfD

U.S. Population ....... 11.5%

All infants (< 1 year) 24.6%

Nursing infants (< 1

year).

10.7%

Non-nursing infants

(< 1 year).

28.6%

Children (1–6 years) 31.1%

Children (7–12

years).

13.5%

ii. Drinking water. The potential for

exposure to cyprodinil through drinking

water (surface or ground water) is slight

due to the minimal level of this

chemical anticipated to reach these

Federal Register / Vol. 65, No. 120 / Wednesday, June 21, 2000 / Notices 38543

bodies of water. This expectation is

based on the rapid degradation of

cyprodinil and the recommended low

use rates that will further restrict the

amount of chemical available for

leaching or run-off.

2. Non-dietary exposure. Novartis

believes that the potential for nonoccupational exposure to the general

public is unlikely except for potential

residues in food crops discussed above.

The proposed uses for cyprodinil are for

agricultural crops and the product is not

used residentially in or around the

home.

D. Cumulative Effects

Consideration of a common

mechanism of toxicity is not appropriate

at this time since there is no information

to indicate that toxic effects produced

by cyprodinil would be cumulative with

those of any other chemicals.

Consequently, only the potential

exposure to cyprodinil is considered in

this risk assessment.

E. Safety Determination

1. U.S. population. For the U.S.

population (48 contiguous states)

chronic exposure was 11% of the RfD.

EPA usually 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.

Novartis concludes that there is a

reasonable certainty that no harm will

result from aggregate exposure to

cyprodinil.

2. Infants and children. Maximum

expected chronic exposure to cyprodinil

in the diets of the most sensitive subpopulations, for non-nursing infants

(<1–year old) and 31.1% of the RfD for

childern (1–6 years old) was calculated

to be 28.6% of the RfD.

F. International Tolerances

Codex maximum residue levels

(MRLs) have not been established for

residues.

[FR Doc. 00–15161 Filed 6–20–00; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[PF–942; FRL–6557–3]

Notice of Filing a Pesticide Petition to

Establish a Tolerance for Certain

Pesticide Chemicals 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

control number PF–942, must be

received on or before July 21, 2000.

ADDRESSES: Comments may be

submitted by mail, electronically, or in

person. Please follow the detailed

instructions for each method as

provided in Unit I.C. of the

‘‘SUPPLEMENTARY INFORMATION.’’

To ensure proper receipt by EPA, it is

imperative that you identify docket

control number PF–942 in the subject

line on the first page of your response.

FOR FURTHER INFORMATION CONTACT: By

mail: Richard J. Gebken, Registration

Support Branch, Registration Division

(7505C), Office of Pesticide Programs,

Environmental Protection Agency, Ariel

Rios Bldg., 1200 Pennsylvania Ave.,

NW., Washington, DC 20460; telephone

number: (703) 305–6701; e-mail address:

gebken.richard@epa.gov.

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

You may be affected by this action if

you are an agricultural producer, food

manufacturer or pesticide manufacturer.

Potentially affected categories and

entities may include, but are not limited

to:

Categories NAICS Examples of potentially affected entities

Industry 111 Crop production

112 Animal production

311 Food manufacturing

32532 Pesticide manufacturing

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 the table could also

be affected. The North American

Industrial Classification System

(NAICS) codes have been provided to

assist you and others in determining

whether or not this action might apply

to certain entities. If you have 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 Additional

Information, Including Copies of this

Document and Other Related

Documents?

1. Electronically. You may obtain

electronic copies of this document, and

certain other related documents that

might be available electronically, from

the EPA Internet Home Page at http://

www.epa.gov/. To access this

document, on the Home Page select

‘‘Laws and Regulations’’ and then look

up the entry for this document under

the ‘‘Federal Register—Environmental

Documents.’’ You can also go directly to

the Federal Register listings at http://

www.epa.gov/fedrgstr/.

2. In person. The Agency has

established an official record for this

action under docket control number PF–

942. The official record consists of the

documents specifically referenced in

this action, any public comments

received during an applicable comment

period, and other information related to

this action, including any information

claimed as confidential business

information (CBI). This official record

includes the documents that are

physically located in the docket, as well

as the documents that are referenced in

those documents. The public version of

the official record does not include any

information claimed as CBI. The public

version of the official record, which

includes printed, paper versions of any

electronic comments submitted during

an applicable comment period, is

available for inspection in the Public

Information and Records Integrity

Branch (PIRIB), Rm. 119, Crystal Mall

#2, 1921 Jefferson Davis Highway,

Arlington, VA, from 8:30 a.m. to 4 p.m.,

Monday through Friday, excluding legal

holidays. The PIRIB telephone number

is (703) 305–5805.

C. How and to Whom Do I Submit

Comments?

You may submit comments through

the mail, in person, or electronically. To

ensure proper receipt by EPA, it is

imperative that you identify docket

control number PF–942 in the subject

line on the first page of your response.

1. By mail. Submit your comments to:

Public Information and Records

Integrity Branch (PIRIB), Information

Resources and Services Division

(7502C), Office of Pesticide Programs

(OPP), Environmental Protection

Agency, Ariel Rios Bldg., 1200

Pennsylvania Ave., NW., Washington,

DC 20460.

2. In person or by courier. Deliver

your comments to: Public Information

and Records Integrity Branch (PIRIB),

Information Resources and Services