63170 Federal Register / Vol. 62, No. 228 / Wednesday, November 26, 1997 / Notices

C. Mammalian Toxicological Profile

Bacillus thuringiensis proteins have

been used commercially for more than

30 years without any evidence for

adverse health effects. Bacillus

thuringiensis mode-of-action can be

divided into a series of critical steps:

ingestion by the insect, specific binding

to brush border membrane receptors,

membrane insertion, and pore formation

thus destroying the midgut lining and

causing death of the insect. Bacillus

thuringiensis proteins do not bind or

cause these types of effects to

mammalian gut membranes. The

extensive mammalian toxicity studies

performed to support the safety of

Bacillus thuringiensis - containing

pesticides clearly demonstrate that the

tested isolates are not toxic or

pathogenic (McClintock, et al., 1995,

Pestic. Sci. 45:95–105). Although

Bacillus thuringiensis strains have been

used for decades as sprayable microbial

products, no confirmed cases of allergic

reactions have been documented,

despite dermal, oral and inhalation

exposures. A reference to this is made

by the EPA in a Federal Register notice,

dated August 16, 1995 (60 FR 42443)

(FRL–4971–3).

The Cry9C protein insecticidal modeof-action is apparently similar to that of

the well known Cry1A proteins. In

addition to the safe history of Bacillus

thuringiensis proteins outlined above,

several other studies were performed to

evaluate mammalian safety of the Cry9C

protein. An acute toxicological study

was performed with mice, which

demonstrated that the Cry9C protein

had an LD50 >6,500 mg/kg. A test for in

vitro digestibility under simulated

gastric conditions showed that the

Cry9C protein found in bacteria and the

protein produced in plants was stable

for 4 hours when exposed to simulated

gastric juice. However, an amino acid

sequence homology search performed

using three different data banks (against

135,867 sequences) only found

homology to other related Bacillus

thuringiensis proteins. To determine

possible short stretch homology, an 8-

amino acid homology search was also

performed. Except with the Bacillus

thuringiensis proteins, no identical 8-

amino acid peptide sequences could be

detected in the searches. Therefore, it is

unlikely that Cry9C protein would have

significant allergenic potential.

The Cry9C protein or metabolites of

the protein are not expected to interact

with the immune or endocrine system,

since the protein sequence does not

match any known allergens or

hormones. Since proteins, in general,

are not known to be carcinogenic it is

unlikely that the Cry9C protein would

have carcinogenic properties.

All living organisms contain DNA and

there are no examples of nucleic acids

causing any toxicological effects from

dietary consumption. The genetic

material necessary for the production of

the Cry9C protein in plants includes the

genetic construct that encodes the

Cry9C protein and all other necessary

genetic elements for it’s expression.

These elements include: a promotor,

polylinker sequences, leader sequences

and terminators and none of which are

expected to cause any toxicological

effects.

Taken together, the data supports the

lack of mammalian toxicological effects

for the plant-pesticide Bacillus

thuringiensis subsp. tolworthi Cry9C

protein and the genetic material

necessary for the production of this

protein in corn for feed use only.

D. Aggregate Exposure

Since the Cry9C protein is expressed

in plant tissues, dermal or inhalation

will be negligible to non-existent.

Drinking water is unlikely to be

contaminated with Cry9C protein due to

the rapid degradation of plant materials

in the soil. Furthermore, no direct

human dietary exposure to Cry9C

protein will occur since this request is

for animal feed use only.

E. Cumulative Effects

The unique mode-of-action of Bt

proteins in general, coupled with the

lack of mammalian toxicity for the

Cry9C protein provides no basis for the

expectation of cumulative effects with

other compounds.

F. Safety Determination

Bt microbial pesticides containing Cry

proteins have been applied for more

than 30 years to food and feed crops

consumed by the US population. There

have been no human safety problems

attributed to Cry proteins. The extensive

mammalian toxicity studies performed

to support the safety of Bacillus

thuringiensis - containing pesticides

clearly demonstrate that the tested

isolates are not toxic or pathogenic

(McClintock, et al., 1995, Pestic. Sci.

45:95–105). The lack of mammalian

toxicity of the Cry9C protein provides

support for our request of a temporary

exemption from the requirement of a

tolerance set forth in this petition. Nondietary exposure of infants, children or

the US population in general, to the

Cry9C protein expressed in corn plant

materials, are not expected due to the

uses of this product for animal feed use

only.

G. Existing Tolerances

No tolerances or tolerance exemptions

have been granted for the Bacillus

thuringiensis subsp. tolworthi Cry9C

and the genetic material necessary for

the production of this protein in corn

for feed use only. (Michael

Mendelsohn)

[FR Doc. 97–31131 Filed 11–25–97; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[PF–779; FRL–5755–6]

Notice of Filing of Pesticide Petition

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 the

docket control number PF–779, must be

received on or before December 26,

1997.

ADDRESSES: By mail submit written

comments to: Public Information and

Records Integrity Branch, Information

Resources and Services Division

(7502C), Office of Pesticides 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.

Comments and data may also be

submitted electronically to: oppdocket@epamail.epa.gov. Follow the

instructions under ‘‘SUPPLEMENTARY

INFORMATION.’’ No confidential

business information should be

submitted through e-mail.

Information submitted as a comment

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.,
Federal Register / Vol. 62, No. 228 / Wednesday, November 26, 1997 / Notices 63171

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: James Tompkins, Registration

Division (7505C) Office of Pesticide

Programs, Environmental Protection

Agency, 401 M St., SW., Washington,

DC 20460. Office location and telephone

number: Rm. 265, CM #2, 1921 Jefferson

Davis Highway, Arlington, VA 22202,

(703) 305-7801; e-mail:

tompkins.james@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: 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 supports granting of the

petition. Additional data may be needed

before EPA rules on the petition.

The official record for this notice of

filing, as well as the public version, has

been established for this notice of filing

under docket control number [PF–779]

(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 official

record is located at the address in

‘‘ADDRESSES’’ at the beginning of this

document.

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. Comment and data will

also be accepted on disks in

Wordperfect 5.1 file format or ASCII file

format. All comments and data in

electronic form must be identified by

the docket number [PF–779] and

appropriate petition number. Electronic

comments on notice may be filed online

at many Federal Depository Libraries.

List of Subjects

Environmental protection,

Agricultural commodities, Food

additives, Feed additives, Pesticides and

pests, Reporting and recordkeeping

requirements.

Dated: November 4, 1997

James Jones,

Acting Director, Registration Division, Office

of Pesticide Programs.

Summaries of Petitions

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 petitioners and

represent the views of the petitioners.

EPA is publishing the petition

summaries verbatim without editing

them in any way. The petition summary

announces the availability of a

description of the analytical methods

available to EPA for the detection and

measurement of the pesticide chemical

residues or an explanation of why no

such method is needed.

Rhone-Poulenc Ag Company

PP 3F4233

EPA has received a pesticide petition

(PP 3F4233) from Rhone-Poulenc Ag

Company, 2 Alexander Drive, Research

Triangle Park, NC 27709, proposing

pursuant to section 408(d) of the Federal

Food, Drug and Cosmetic Act, 21 U.S.C.

346a(d), to amend 40 CFR part 180 to

extend the current time-limited

tolerances for bromoxynil and its

metabolite DBHA (3,5-dibromo-4-

hydroxybenzoic acid) resulting from the

application of octanoic and heptanoic

acid esters of bromoxynil to cotton in or

on the raw agricultural commodities

undelinted cottonseed at 7 parts per

million (ppm), cotton gin byproducts at

50 ppm, and cotton hulls at 21 ppm for

a 1–year period and to increase the

current acreage limitation from 3% to

10% of the U. S. cotton acreage

(1,300,000 acres). EPA has determined

that the petition contains data or

information regarding the elements set

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

however, EPA has not fully evaluated

the sufficiency of the submitted data at

this time or whether the data supports

granting of the petition. Additional data

may be needed before EPA rules on the

petition.

A. Residue Chemistry

1. Plant metabolism. The nature of the

bromoxynil residue in bromoxyniltolerant cotton is considered to be

adequately understood. The two major

components of the terminal residue are

parent bromoxynil and the metabolite

3,5-dibromo-4-hydroxybenzoic acid

(DBHA).

2. Analytical method. Adequate

analytical methodologies for both parent

bromoxynil and the DBHA are available

for enforcement purposes. The method

involves sample reflux in methanolic

KOH, partitioning with ether/hexane

and analysis by Gas Chromatography.

Limits of quantitation allow monitoring

of residues in cotton commodities at or

above tolerance levels. Multiresidue

testing with DBHA has been conducted

and submitted to FDA.

3. Magnitude of residues. Available

magnitude of the residue data from a 60

day phi crop field residue study

conducted at a maximum application

rate of 4.5 lb active ingredient/acre

indicate that the currently established

time-limited tolerances for bromoxynil

and DBHA will not be exceeded when

Buctril 4EC herbicide is used according

to approved label directions.

B. Toxicological Profile

1. Acute toxicity. A complete battery

of acute toxicity studies for bromoxynil

(phenol) has been conducted. The acute

oral toxicity study in rats resulted in a

LD50 of 81 milligrams/kilogram (mg/kg)

(males) and a LD50 of 93 mg/kg

(females). The acute dermal toxicity

study in rabbits resulted in a LD50 of

>2,000 mg/kg for both males and

females. The acute inhalation study in

rats resulted in a LC50 of 0.269

milligram/liter (mg/L) for males and

0.150 for females. The primary eye

irritation study showed corneal opacity

resolved within 3 days, iritis resolved

within 4 days and conjuctival irritation

which persisted for 10 days. There was

no irritation in the primary dermal

irritation study and the dermal

sensitization study in guinea pigs was

negative.

2. Genotoxicty. Mutagenicity studies

conducted include an unscheduled

DNA synthesis study-rat primary

hepatocytes (negative); in vitro

transformation assay-mouse cells

(negative); sister chromosomal exchange

study-CHO cells (negative); forward

mutation study-mouse lymphoma cells

(negative without activation and

positive with activation); DNA repair

test-E. Coli (positive); in vitro

chromosomal aberration (negative

without activation and positive with

activation); two separate micronucleus

assays (both negative); forward

mutation-CHO cells (negative); and

Salmonella typhimurium reverse

mutation assay (negative with and

without activation). Rhone-Poulenc

considers bromoxynil (phenol) and

DBHA to be non-mutagenic.

3. Reproductive and developmental

toxicity. A teratology study was

conducted with rats administered

(orally) bromoxynil phenol at dose

levels of 0, 4, 12.5, or 40 mg/kg/day. The

maternal no-observed-effect level

(NOEL) and lowest-observed-effect level
63172 Federal Register / Vol. 62, No. 228 / Wednesday, November 26, 1997 / Notices

(LEL) are 12.5 and 40 mg/kg/day

respectively. The developmental NOEL

and LEL are 4.0 and 12.5 mg/kg/day,

respectively. Maternal body weights and

food consumption were reduced in the

high dose group. Fetal effects observed

were reduced body weight, with

associtaed decreases in ossification. An

increase in 14th ribs was observed in

the mid and high dose levels. A

teratology study was conducted with

rats administered (orally) bromoxynil

phenol at dose levels of 0, 5, 15, or 35

mg/kg/day. The maternal NOEL and

LEL are 5.0 and 15 mg/kg/day,

respectively. The fetotoxicity and

developmental NOEL and LEL are less

than 5 and 5 mg/kg/day, respectively.

Significant maternal mortality and

decreased body weight gain were

associated with the high dose,

indicating that the maximum tolerance

dose was exceeded. Decreases in

maternal body weight gain were also

observed in the mid and low dose

levels. At the mid-dose level a

statistically significant increase in the

number of fetuses with supernumerary

ribs, a common fetal variant was

observed. A teratology study was

conducted with rats administered

(orally) bromoxynil phenol at dose

levels of 0, 1.7, 5, or 15 mg/kg/day. The

maternal NOEL and LEL are 5 and 15

mg/kg/day, respectively. The

developmental NOEL and LEL are 5 and

15 mg/kg/day, respectively. This study

was classified as unacceptable,

primarily due to reporting deficiendies.

A teratology study was conducted with

rabbits administered (orally) bromoxynil

phenol at dose levels of 0, 15, 30, or 60

mg/kg/day. The maternal NOEL and

LEL are 15 and 30 mg/kg/day,

respectively. The developmental NOEL

and LEL are less than 15 and 15 mg/kg/

day, respectively. Significant body

weight gain decrements were reported at

the two highest dose levels along with

observed decreases in food

consumption. The severe maternal

toxicity among high dose dams was

associated with fetoxicity and

teratogenicity. A slight, nonsignificant

increase in supernumerary ribs was

reported at the mid and low dose levels.

A teratology study was conducted with

mice administered (orally) bromoxynil

phenol at dose levels of 0, 11, 32, or 96

mg/kg/day. Maternal mortality was

observed at 32 and 96 mg/kg/day. Fetal

body weight was decreased at the top

dose level, associated with a decrease in

caudal vertebral ossification and an

increase in supernumerary ribs. The

maternal NOEL and LEL are 11 and 32

mg/kg/day respectivel. The

developmental NOEL and LEL are 32

and 96 mg/kg/day, respectively.

A reproduction study was conducted

with rats administered (orally)

bromoxynil phenol at dose levels of 0.

0.8, 4, or 21 mg/kg/day in the diet. The

systemic adult rat NOEL is 4 mg/kg/day

and the LEL is 21 mg/kg/day. The

reproductive NOEL is 21 mg/kg/day,

and the LEL is greater than 21 mg/kg/

day. The postnatal developmental NOEL

is 4 mg/kg/day, and the LEL is 21 mg/

kg/day. Body weight gain decrements

were reported. However, no adverse

effects on fertility, fecundity,

reproductive performance or pre and

postnatal development were observed.

A reproduction study was conducted

with rats administered (orally)

bromoxynil phenol at dose levels of 0,

1.5, 5, or 15 mg/kg/day in the diet. The

systemic rat NOEL is 1.5 mg/kg/day,

and the LEL is is 5 mg/kg/day. The

reproductive NOEL is 15 mg/kg/day,

and the LEL is greater than 15 mg/kg/

day. The offspring developmental NOEL

is 5 mg/kg/day and the LEL is 15 mg/

kg/day. Body weight gain decrements

were reported. However, no adverse

effects on fertility, fecundity,

reproductive performance or pre and

postnatal development were observed.

Based on the studies discussed above,

it is concluded that bromoxynil is not

teratogenic at doses that are not

maternally toxic. In addition,

bromoxynil is not considered a

reproductive toxicant and shows no

evidence of endocrine effects.

4. Subchronic toxicity. In a 12–week

range-finding study, bromoxynil

(phenol) was administered in the diets

of male and female CD-1 mice at dose

levels of 0, 1.3, 3.9, 13, 39, 130, or 390

mg/kg/day. For male mice, the NOEL is

3.9 mg/kg/day and the LOEL is 13 mg/

kg/day based on increased liver weights

and hepatocellular hypertrophy. In

female mice, the NOEL is 13 mg/kg/day

and the LOEL is 39 mg/kg/day based on

increased liver weights, hepatocellular

hypertrophy, hepatocellular

degeneration, and hepatocellular

vacuolization. In a 13–week subchronic

feeding study, bromoxynil (phenol) was

administered in the diet to male and

female Sprague-Dawley rats at dose

levels of 0, 28, 58, or 168 mg/kg/day.

For male rats, the NOEL is 28 mg/kg/day

and the LOEL is 58 mg/kg/day based on

decreased body weight gain, increased

ALT and increased alkaline

phosphatase. For female rats, no NOEL

was determined in this study and the

LOEL is 35 mg/kg/day based on

decreased body weight gain. In a 13–

week range-finding study, bromoxynil

(phenol) was administered orally to

male and female dogs at doses of 0, 1,

5, 8, 12, 16, 20, 30, 40, or 50 mg/kg/day.

For males, no NOEL was determined

and the LOEL is 1 mg/kg/day based on

decreased body weight gain. For

females, the NOEL is 1 mg/kg/day and

the the LOEL is 5 mg/kg/day based on

decreased body weight gain, panting

and liquid feces. In a 21 day subchronic

dermal study, bromoxynil (phenol) was

applied to skin of male and female New

Zealand white rabbits at doses of 0, 30,

300, or 1,000 mg/kg/day for 6 hours/

day, 5 days/week. Treatment produced

no observable dermal or systemic

toxicity, therefore the NOEL is 1,000

mg/kg/day.

5. Chronic toxicity. A 1–year oral

study was conducted with dogs

administered bromoxynil (phenol) at

dose levels of 0, 0.1, 0.3, 1.5, and 7.5

mg/kg/day in capsules. The NOEL/LEL

is 1.5 mg/kg/day for both females and

males based on decreased body weight

gain, decreased RBC count, decreased

hemoglobin, decreased PCV, and

increased liver weights. The chronic dog

study was determined by RhonePoulenc to be the most appropriate

study for setting the Reference Dose

(RfD) of 0.015 mg/kg/day (includes a

hundredfold safety factor).

A 2–year combined chronic toxicity/

carcinogenicity study was conducted

with rats administered (oral) dosages of

0, 60, 190, or 600 ppm (0, 2.6, 8.2, or

28 mg/kg/day in males; 0, 3.3, 11.0, or

41 mg/kg/day in females) bromoxynil

phenol in the diet. In males the noobserved-effect-level (NOEL) for

systemic toxicity is 2.6 mg/kg/day, and

the lowest-effect-level (LEL) is 8.2 mg/

kg/day. In females, the NOEL is 3.3 mg/

kg/day, and the LEL is 11.0 mg/kg/day.

This study did not demonstrate any

increase in tumor incidences in either

male or female rats.

A 2–year combined feeding/

carcinogenicity study was conducted

with rats administered bromoxynil

phenol in the diet at dose levels of 0, 10,

30, or 100 ppm (0, 0.5, 1.5, or 5 mg/kg/

day). In both males and females, the

NOEL and LOEL for systemic toxicity

was 5 mg/kg/day and >5 mg/kg/day,

respectively. At the highest dose tested,

increased liver weights were observed at

12 months, but not at 24 months. This

study was considered negative for

carcinogenicity. An 18 month

carcinogenicity study was conducted

with mice administered bromoxynil

phenol at dose levels of 0, 10, 30, or 100

ppm (0, 1.3, 3.9, or 13 mg/kg/day) in the

diet. For males, dose related increases in

hyperplastic nodules and liver

adenomas/carcinomas were observed

which were statistically significant at

the 100 ppm. Increased relative liver

weights were also observed. In females,
Federal Register / Vol. 62, No. 228 / Wednesday, November 26, 1997 / Notices 63173

increased absolute liver weights and

relative liver and kidney weights were

observed. The study was considered

negative for carcinogenicity for females.

An 18 month carcinogenicity study was

conducted with mice administered

bromoxynil phenol at dose levels of 0,

20, 75, or 300 ppm (0, 3.1, 12 or 46 mg/

kg/day in males and 0, 3.7, 14, or 53 mg/

kg/day in females). Mice given 300 ppm

had significantly increased absolute and

relative liver weights. Histopathology of

the liver revealed increased

hepatocellular hypertrophy,

hepatocellular degeneration, necrosis of

individual hepatocytes, and pigment

accumulation in hepatocytes and

Kupffer cells. Male mice had

statistically significant increased

numbers of hepatocellular adenomas

and carcinomas at 20 ppm, but not 75

ppm. In contrast, no significant increase

in tumor incidence was observed for

female mice by pair-wise analysis. The

trend test was significant for adenomas

or carcinomas in females, only at

p<0.05, not p<0.01 as would be

appropriate for this type of tumor. The

trend is due entirely to the high dose

group and therefore is of questionable

validity. It is concluded that bromoxynil

is a weak, single sex, single species,

non-metastic, single target organ

carcinogen, inducing hepatocellular

tumors in male mice exposed to 300

ppm for 18 months. These tumors and

associated histopathological findings are

consistent with secondary mechanisms

such as peroxisome proliferation, a

mechanism known to have marked

species differences and questionable

relevance for humans. It is the opinion

of Rhone-Poulenc that the data are not

suitable for quantitative risk assessment.

A threshold safety factor approach is

more appropriate and is commonly used

for single sex, single species carcinogens

such as bromoxynil that are thought to

work through secondary mechanisms.

For the purposes of this tolerance

petition, risk assessments have been

performed using a low dose linear

extrapolation model (Q1* is 1.03 × 10-1).

6. Animal metabolism. Results of a

bromoxynil metabolism study with the

rat (octanoate) demonstrated that 2 mg/

kg of radiolabeled bromoxynil octanoate

was rapidly absorbed, hydrolyzed to

bromoxynil phenol, distributed, and

excreted in rats following repeated oral

administration. The urine was the major

route of excretion, representing 80.24%

of the administered dose in males and

67.91% in females at 7 days postdosing. Tissue distribution was similar

for both sexes with the highest

radioactivity recovered in the liver and

kidney. Similar results were obtained in

a separate rat metabolism study

conducted with bromoxynil heptanoate.

7. Metabolite toxicology. DBHA (3,5-

dibromo-4-hydroxybenzoic acid) is a

major plant metabolite of bromoxynil

only in bromoxynil-resistant transgenic

cotton. Acute oral toxicity testing with

DBHA in rats resulted in an LD50 of

>2,000 mg/kg. Acute dermal toxicity

testing with DBHA in rabbits resulted in

an LD50 of >2,000 mg/kg. The primary

dermal irritation study with DBHA in

rabbits indicated DBHA to be a slight

irritant, and DBHA was not a dermal

sensitizer in Guinea pigs. Mutagenicity

studies conducted with DBHA include a

Salmonella typhimurium reverse

mutation assay (negative with and

without activation); micronucleus assay

(negative); and TK∂/- mouse lymphoma

assay (negative with and without

metabolic activation). In subchronic

feeding studies in the rat, DBHA was

administered by oral gavage to groups of

Sprague-Dawley rats for 28 days at dose

levels of 25, 50, 100 and 250 mg/kg/day.

No toxicologically meaningful changes

were observed in any of the parameters

measured in this study. The NOEL and

LEL for this study were 250 and >250

mg/kg/day, respectively.

C. Aggregate Exposure

1. Dietary (food) exposure. For the

purpose of estimating the potential

human dietary exposure resulting from

bromoxynil use on cotton under the

existing tolerances, anticipated residues

of bromoxynil and DBHA were used.

Anticipated residue values of 1.44 ppm

(cottonseed), 8.74 ppm (cotton gin

trash), and 0.43 ppm (cottonseed meal)

were derived by taking the mean residue

values from available crop field trials

conducted at the 4.5 lb/A broadcast rate

and adjusting by a factor of 0.333 to

extrapolate to the current 1.5 lb/A

application rate. Adjusting these values

for % dry matter and the proposed 10%

of crop treated results in anticipated

cotton feedstuff residue values of 0.14

ppm (cottonseed), 0.87 ppm (cotton gin

trash), and 0.043 ppm (cottonseed

meal). Based on the use of these

exposure data and a unit risk (Q1* (mg/

kg/day)-1, of bromoxynil of 1.03 × 10-1,

the upper-bound human risk estimate

for the general (U.S.) population

represented by all sources of

bromoxynil exposure, including use on

up to 10% of the U.S. treated acreage is

approximately 2 × 10-6.

2. Drinking water. There is no

Maximum Concentration Level or

Health Advisory Level established for

bromoxynil under the Safe Drinking

Water Act. Based on field dissipation

studies demonstrating a short half-life of

bromoxynil in the environment (average

half-life of 3–7 days), bromoxynil

residues will degrade in soil before

residues can move downward into

ground water. Therefore, no significant

potential exists for bromoxynil residues

to be present in drinking water from

ground water. Likewise, contamination

of drinking water supplies from

bromoxynil movement through

agricultural surface runoff is considered

highly unlikely due to relatively low

application rates and rapid degradation

rates in soil. As demonstrated by

available monitoring data, normal

dilution and degradation processes will

greatly reduce concentrations in surface

water during movement from

agricultural ditches near fields into

streams of adequate size for use as

drinking water. It is the conclusion of

Rhone-Poulenc that the potential

bromoxynil exposure derived from any

use through drinking water is

insignificant and does not significantly

increase the aggregate risk assessment

above that estimated to occur through

food exposure alone.

3. Non-dietary exposure. The

potential for non-occupational exposure

to bromxynil among the general public

is insignificant. There are no residential

lawn or garden uses for bromoxynil

products where the general population

might be exposed via inhalation or

dermal routes. Turfgrass use is restricted

to non-residential areas. Exposure to

bromoxynil following application to

non-residential turfgrass is not likely to

be significant in either time or duration.

This use will therefore not significantly

add to the aggregate exposure.

D. Cumulative Effects

There are no reliable data suggesting

that any toxic effect that might be

caused by bromoxynil would be

cumulative with those of any other

compound. Further, bromoxynil does

not appear to produce a toxic metabolite

that is produced by other substances.

Therefore, consideration of potential

cumulative effects is not appropriate at

this time.

E. Safety Determination

1. U.S. population. Using the present

RfD for bromoxynil of 0.015 mg/kg/day,

it has been determined that aggregate

chronic exposure to bromoxynil from all

uses, including cotton, represents <1%

of the RfD for all population sub-groups.

A unit risk, Q1* (mg/kg/day)-1, of

bromoxynil of 1.03 × 10-1 in human

equivalents, has been calculated based

on mouse liver tumors. It is the opinion

of Rhone-Poulenc that the bromoxynil

data are not suitable for quantitative risk

assessment. A threshold safety factor

approach is more appropriate and is
63174 Federal Register / Vol. 62, No. 228 / Wednesday, November 26, 1997 / Notices

commonly used for single sex, single

species carcinogens such as bromoxynil

that are thought to work through

secondary mechanisms. Nevertheless,

the risk assessments filed with this

petition have been performed using

quantitative risk assessment

methodology. Accordingly, the upperbound risk estimate for the general U.S.

population represented by all sources of

bromoxynil exposure, including use of

bromoxynil on up to 10% of the U.S.

treated acreage is approximately 2 ×

10-6.

2. Infants and children. To estimate

acute dietary risk for systemic effects

other than developmental from food

sources, an MOE of 270 was calculated

using 1–day dietary exposure for infants

(the most highly exposed population

group) and a NOEL of 8 mg/kg/day

derived from a 13–week oral toxicity

study in dogs. It is concluded that

reliable data support use of the standard

hundredfold margin of exposure/safety

factor in assessing the risk to children.

The general U.S. population and all

population sub-groups are estimated to

be exposed at a level less than 1 percent

of the bromoxynil RfD of 0.015 mg/kg/

day. Both chronic and acute

assessments show no appreciable

threshold risks to children and the nonthreshold cancer risk is no greater than

negligible. Therefore, there is a

reasonable certainty that no harm will

result to infants and children from

aggregate exposure to bromoxynil.

Two multi-generation rodent

reproduction studies demonstrated that

there were no adverse effects on

reproductive performance, fertility,

fecundity, pup survival, or pup

development. Maternal and

developmental NOELs and LOELs were

comparable indicating no increase

susceptibility of developing organisms.

No evidence of endocrine effects were

noted in any study. It is therefore

concluded that bromoxynil poses no

additional risk for infants and children

and no additional uncertainty factor is

warranted.

F. International Tolerances

There are no Codex tolerances

established for bromoxynil residues,

therefore international compatibility is

not considered to be an issue at this

time.

[FR Doc. 97–30812 Filed 11–25–97; 8:45 am]

BILLING CODE 6560–50–F

ENVIRONMENTAL PROTECTION

AGENCY

[FRL–5927–7]

Proposed Settlement Pursuant to

Section 122(g) of the Comprehensive

Environmental Response,

Compensation, and Liability Act,

Regarding the Sealand Restoration

Superfund Site, Lisbon, New York

AGENCY: Environmental Protection

Agency.

ACTION: Notice of proposed

administrative settlement and

opportunity for public comment.

SUMMARY: In accordance with section

122(i) of the Comprehensive

Environmental Response,

Compensation, and Liability Act of

1980, as amended (CERCLA), 42 U.S.C.

9622(i), the U.S. Environmental

Protection Agency (EPA), Region II,

announces a proposed administrative de

minimis settlement pursuant to section

122(g)(4) of CERCLA, 42 U.S.C.

9622(g)(4), relating to the Sealand

Restoration Superfund Site (Site). The

Site is located on Pray Road in the

Town of Lisbon, St. Lawrence County,

New York. This document is being

published pursuant to section 122(i) of

CERCLA to inform the public of the

proposed settlement and give it the

opportunity to comment. EPA will

consider any comments received during

the comment period and may withdraw

or withhold consent to the proposed

settlement if comments disclose facts or

considerations which indicate that the

proposed settlement is inappropriate,

improper, or inadequate.

The proposed de minimis settlement

between EPA and Westpoint Stevens

Inc., on behalf of former Cluett, Peabody

& Co. (Respondent) has been

memorialized in an Administrative

Order on Consent (Index Number

CERCLA–97–0215). This Order will

become effective after the close of the

public comment period, unless

comments received disclose facts or

considerations which indicate the

Agreement is inappropriate, improper,

or inadequate, and EPA, in accordance

with section 122(i)(3) of CERCLA,

modifies or withdraws its consent to the

Agreement. Under the Order, the

Respondent will be obligated to make

payments to the Hazardous Substance

Superfund in reimbursement of EPA’s

response costs relating to the Site, plus

a premium, based on documented

volumes of substances in EPA’s records

associated with the Site, totaling

$47,676.

Pursuant to CERCLA section

122(h)(1), the Order may not be issued

without the prior written approval of

the Attorney General or her designee. In

accordance with that requirement, the

Attorney General or her designee has

approved the proposed administrative

order in writing.

DATES: Comments must be provided on

or before December 26, 1997.

ADDRESSES: Comments should be

addressed to the U.S. Environmental

Protection Agency, Office of Regional

Counsel, New York/Caribbean

Superfund Branch, 17th Floor, 290

Broadway, New York, New York 10007–

1866, and should refer to: ‘‘Sealand

Restoration Superfund Site, U.S. EPA

Index No. CERCLA–97–0215’’. For a

copy of the settlement document,

contact the individual listed below.

FOR FURTHER INFORMATION CONTACT:

Elizabeth Davis, Assistant Regional

Counsel, New York/Caribbean

Superfund Branch, Office of Regional

Counsel, U.S. Environmental Protection

Agency, 17th Floor, 290 Broadway, New

York, New York 10007. Telephone:

(212) 637–3165.

Dated: November 4, 1997.

William J. Muszynski,

Acting Regional Administrator.

[FR Doc. 97–31137 Filed 11–25–97; 8:45 am]

BILLING CODE 6560–50–P

COUNCIL ON ENVIRONMENTAL

QUALITY

Notice of Meeting; Postponement

SUMMARY: The Council on

Environmental Quality (CEQ) is

postponing a public meeting it had

previously scheduled for December 2,

1997, to discuss development of a

memorandum of understanding on

coordinating environmental response

actions with natural resource restoration

under the Comprehensive

Environmental Response,

Compensation, and Liability Act and

other laws. 62 FR 51660 (October 2,

1997). CEQ intends to reschedule the

meeting for late January or early

February, 1998. CEQ will soon publish

another Federal Register notice

identifying the time, place, and agenda

for the meeting.

FOR FURTHER INFORMATION CONTACT:

Mary Morton at (202) 208–3302.

Bradley M. Campbell,

Associate Director.

[FR Doc. 97–31031 Filed 11–25–97; 8:45 am]

BILLING CODE 3125–01–M