6780 Federal Register / Vol. 62, No. 30 / Thursday, February 13, 1997 / Notices

Dated: February 6, 1997.

Janet L. Anderson,

Director, Biopesticides and Pollution

Prevention Division, Office of Pesticide

Programs.

[FR Doc. 97–3517 Filed 2–12–97; 8:45 am]

BILLING CODE 6560–50–F

[PF-708; FRL-5587-3]

ISK Biosciences Corporation;

Pesticide Tolerance Petition Filing

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice of filing.

SUMMARY: This notice announces the

filing of a pesticide petition proposing

the establishment of a regulation for

residues of chlorothalonil in or on

almonds and almond hulls. The notice

includes a summary of the petition

prepared by the petitioner, ISK

Biosciences Corporation.

DATES: Comments, identified by the

docket number [PF-708], must be

received on or before March 17, 1997.

ADDRESSES: By mail, submit written

comments to: Public Response and

Program Resources Branch, Field

Operations Division (7506C), Office of

Pesticide Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC 20460. In person, bring

comments to Rm. 1132, CM #2, 1921

Jefferson Davis Highway, Arlington, VA.

Comments and data may also be

submitted electronically by sending

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

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

docket number [PF-708]. Electronic

comments on this notice of filing may

be filed online at many Federal

Depository Libraries. Additional

information on electronic submissions

can be found in Unit II. of this

document.

Information submitted as comments

concerning this document may be

claimed confidential by marking any

part or all of that information as

‘‘Confidential Business Information’’

(CBI). CBI should not be submitted

through e-mail. Information marked as

CBI will not be disclosed except in

accordance with procedures set forth in

40 CFR part 2. A copy of the comment

that does not contain CBI must be

submitted for inclusion in the public

record. Information not marked

confidential may be disclosed publicly

by EPA without prior notice. All written

comments will be available for public

inspection in Rm. 1132 at the address

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

Monday through Friday, excluding legal

holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Cynthia Giles-Parker, Product

Manager (PM 22), Registration Division

(7505C), Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location, telephone number, and

e-mail address: Crystal Mall #2, Room

229, 1921 Jefferson Davis Highway,

Arlington, VA, 703-305-7740, e-mail:

giles-parker.cynthia@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: EPA has

received a pesticide petition (PP

5F4558), originally published in the

Federal Register on November 15, 1995

(60 FR 57419) (FRL-4971-5), from ISK

Biosciences Corporation (‘‘ISK’’), 5966

Heisley Road, P.O. Box 8000, Mentor,

Ohio 44061, 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 180.275 by

establishing tolerances for residues of

the fungicide chlorothalonil and its

metabolite, 4-hydroxy-2,5,6-

trichloroisophthalonitrile (SDS-3701) in

or on the raw agricultural commodity

(RAC) almonds (nutmeats) at 0.05 parts

per million (ppm) and almond hulls at

1.0 ppm. The proposed analytical

method is by electron capture gas

chromatography. 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.

As required by section 408(d) of the

FFDCA, as recently amended by the

Food Quality Protection Act (FQPA)

Pub. L. 104-170, ISK included in the

petition a summary of the petition and

authorization for the summary to be

published in the Federal Register in a

notice of receipt of the petition. The

summary represents the views of ISK.

EPA is in the process of evaluating the

petition. As required by section

408(d)(3) of the FFDCA, EPA is

including the summary as a part of this

notice of filing. EPA has made minor

edits to the summary for the purpose of

clarity.

I. Petition Summary

A. Residue Chemistry Data

1. Plant/animal metabolism. The

nature of the residue of chlorothalonil

in plants and animals, including

ruminants, is well understood.

Chlorothalonil is not systemic in plants.

Any chlorothalonil residue found on

almond nutmeats occurs as a surface

residue from transfer of the residue

during harvesting and shelling

operations. Chlorothalonil is rapidly

metabolized in the ruminant and is not

transferred to meat and milk from the

dietary consumption by animals.

Furthermore, chlorothalonil is not stable

in meat or milk.

2. Analytical method. An adequate

analytical method (gas chromatography)

is available for enforcement purposes.

The method is listed in the Pesticide

Analytical Manual, Vol. II (PAM II).

3. Magnitude of the residues. Residue

data from studies conducted with

almonds support a tolerance of 0.05

ppm for combined residues of

chlorothalonil and its metabolite, 4-

hydroxy-2,5,6-trichloroisophthalonitrile

in/on almond nutmeats and 1.0 ppm in/

on almond hulls. Residues of

chlorothalonil on plants are surface

residues. Nutmeats are not systemically

exposed to chlorothalonil since

chlorothalonil is not a systemic

fungicide in plants. Chlorothalonil

residues are not directly translocated to

the nutmeats, but residues from the

hulls that contaminate the almond

shells during harvest may be transferred

to the nutmeats during the shelling

process.

B. Toxicological Profile

The following studies on file with the

Agency support this petition.

1. Acute toxicity. Acute toxicity

studies include an acute oral rat study

on technical chlorothalonil with an LD50

>10,000 milligram/kilogram (mg/kg), an

acute dermal toxicity study in the rabbit

with an LD50 >20,000 mg/kg, a 4-hour

inhalation study with finely ground

technical chlorothalonil resulting in a

LC50 of 0.092 mg/L (actual airborne

concentration), a primary eye irritation

study with irreversible eye effects in the

rabbit at 21 days, a primary dermal

irritation study showing technical

chlorothalonil is not a dermal irritant,

and a dermal sensitization study

showing technical chlorothalonil is not

a skin sensitizer.

2. Genotoxicity. The mutagenic

potential of chlorothalonil has been

evaluated in a large number of studies

covering a variety of endpoints. ISK

concludes that chlorothalonil is not

mutagenic.

Mutagenicity studies with

chlorothalonil include gene mutation

assays in bacterial and mammalian

cells; in vitro and in vivo chromosomal

aberration assays; DNA repair assays in

bacterial systems; and cell
Federal Register / Vol. 62, No. 30 / Thursday, February 13, 1997 / Notices 6781

transformation assays. All were negative

with the following two exceptions:

i. Chlorothalonil was positive in an in

vitro chromosomal aberration assay in

CHO cells without metabolic activation

but was negative with metabolic

activation.

ii. In vivo chromosomal aberration

studies in rats and mice were negative

and one study in the Chinese hamster

was equivocal. The results of this study

could not be confirmed in a subsequent

study at higher doses. The conclusion

was that chlorothalonil does not cause

chromosome aberrations in bone

marrow cells of the Chinese hamster. It

can be concluded that chlorothalonil

does not have clastogenic potential in

intact mammalian systems.

In bacterial DNA repair tests

chlorothalonil was negative in Bascillus

subtilis, but was positive in Salmonella

typhimurium. In an in vivo DNA

binding study in rats, with 14Cchlorothalonil, there was no covalent

binding of the radiolabel to the DNA of

the kidney, which is the target organ for

chlorothalonil toxicity in rodents.

3. Developmental and reproductive

toxicity. A developmental toxicity study

with rats given gavage doses of 0, 25,

100, and 400 mg/kg body weight (bwt)/

day from days 6 through 15 of gestation

resulted in a no observed effect level

(NOEL) for maternal toxicity of 100 mg/

kg/day based on increased mortality,

reduced body weight, and a slight

increase in early resorptions at the

highest dose. There were no

developmental effects observed at any

dose in this study.

A developmental toxicity study in

rabbits given gavage doses of 0, 5, 10, or

20 mg/kg/day on days 7 through 19 of

gestation resulted in a maternal NOEL of

10 mg/kg/day. Effects observed in the

dams in the high-dose group were

decreased body weight gain and

reduced food consumption. There were

no developmental effects observed in

this study.

A 2-generation reproduction study in

rats fed diets containing 0, 500, 1,500

and 3,000 ppm resulted in a

reproductive NOEL of 1,500 ppm

(equivalent to 115 mg/kg/day) based on

lower neonatal body weights by day 21.

There were no effects seen on any other

reproductive parameter at any dose

level in this study.

4. Subchronic toxicity. i. A 90-day

subchronic toxicity study was

conducted in rats at doses of 0, 1.5, 3.0,

10, and 40 mg/kg bwt. Treatment related

hyperplasia and hyperkeratosis of the

forestomach was observed at the two

highest dose levels. Although the initial

histopathological evaluation did not

demonstrate any nephrotoxicity, a

subsequent evaluation observed a

treatment-related increase in

hyperplasia of the proximal tubule

epithelium at 40 mg/kg bwt in the male

rats but not in the females. The NOEL

for renal histopathology was 10 mg/kg

bwt in males and 40 mg/kg bwt in

females.

ii. A 90-day oral toxicity study was

conducted in dogs with dose levels of

technical chlorothalonil of 15, 150, and

750 mg/kg bwt/day. The two highest

dosages resulted in lower body weight

gain in male dogs. The NOEL was 15

mg/kg/day. There were no macroscopic

or microscopic tissue alterations related

to chlorothalonil and there were no

signs of renal toxicity.

iii. Two 21-day dermal toxicity

studies have been conducted with

technical chlorothalonil. In the initial

study, doses of 50, 2.5, and 0.1 mg/kg

bwt/day were administered to rabbits.

The NOEL for systemic effects was

greater than 50 mg/kg bwt/day and the

NOEL for dermal irritation was 0.1 mg/

kg bwt/day.

A subsequent 21-day dermal study

was conducted in male rats to

specifically evaluate the potential for

nephrotoxicity in this laboratory species

following dermal dosing. In this study

the doses were 60, 100, 250, and 600

mg/kg bwt/day. The NOEL for

nephrotoxicity was greater than 600 mg/

kg bwt/day.

5. Estrogenic effects. Based upon all of

the chronic toxicity, teratogenicity,

mutagenicity, and reproductive studies

conducted with chlorothalonil and its

metabolites, ISK concludes that there

were no results which indicate any

potential to cause estrogenic effects or

endocrine disruption. These effects

would have manifested themselves in

these studies as reproductive or

teratogenic effects or by producing

histopathological changes in estrogen

sensitive tissues such as the uterus,

mammary glands, or the testes. Thus,

ISK concludes based upon the in vivo

studies, that chlorothalonil does not

cause estrogenic effects.

6. Chronic toxicity. i. A 12-month

chronic oral toxicity study in Beagle

dogs was conducted with technical

chlorothalonil at dose levels of 15, 150,

and 500 mg/kg/day. The NOEL was 150

mg/kg/day based on lower blood

albumin levels at the highest dose.

There was no nephrotoxicity observed

at any dose in this study. This study

replaced an old outdated study that was

not conducted under current guidelines

and did not use the current technical

material.

ii. A chronic feeding/carcinogenicity

study with Fischer 344 rats fed diets

containing 0, 800, 1,600 or 3,500 ppm

(equivalent to 0, 40, 80 or 175 mg/kg

bwt/day) for 116 weeks in males or 129

weeks in females, resulted in a

statistically higher incidence of

combined renal adenomas and

carcinomas. At the high dose, which

was above the MTD, there was also a

statistically significant higher incidence

of tumors of the forestomach in female

rats.

iii. In a second chronic feeding/

carcinogenicity study with Fischer 344

rats, designed to define the NOEL for

tumors and the preneoplastic

hyperplasia, animals were fed diets

containing 0, 2, 4, 15 or 175 mg/kg/day.

The NOEL in this study, based on renal

tubular hyperplasia, was a nominal dose

of 2 mg/kg bwt/day. Because of the

potential for chlorothalonil to bind to

diet the 2 mg/kg bwt/day dose,

expressed as unbound chlorothalonil, is

1.8 mg/kg bwt/day. The NOEL for

hyperplasia and hyperkeratosis of the

forestomach was 4 mg/kg bwt/day or a

dose of 3.8 mg/kg bwt/day based on

unbound chlorothalonil.

iv. A 2-year carcinogenicity study,

conducted in CD-1 mice at dietary levels

of 0, 750, and 1,500 or 3,000 ppm

(equivalent to 0, 107, 214 or 428 mg/kg/

day), resulted in a statistically higher

incidence of squamous cell carcinomas

of the forestomach in both sexes and a

statistically higher incidence of

combined renal adenomas/carcinomas

in only the male mice receiving the low

dose. There were no renal tumors in any

female mouse in this study.

v. A 2-year carcinogenicity study, in

male CD-1 mice for the purpose of

establishing the NOEL for renal and

forestomach effects, was conducted at

dietary levels of 0, 10/15, 40, 175, or 750

ppm (equivalent to 0, 1.4/2.1, 5.7, 25 or

107 mg/kg/day). The NOEL for renal

effects was 40 ppm and the NOEL for

forestomach effects was 15 ppm. This

study did not duplicate the results from

the previous study where a statistically

higher incidence of renal tumors, when

compared to controls, was observed at

750 ppm.

In 1987, the Office of Pesticide

Programs’ Toxicology Branch Peer

Review Committee classified

chlorothalonil as a B2 (probable human

carcinogen) based on evidence of

carcinogenicity in the forestomach and

kidneys of rats and mice. The Agency

currently regulates chlorothalonil as a

B2 carcinogen although ISK has

provided a significant amount of

mechanistic data indicating that the

tumors result from a threshold

mechanism. A potency factor, Q1* (Q1
6782 Federal Register / Vol. 62, No. 30 / Thursday, February 13, 1997 / Notices

1‘‘Mechanistic Interpretation of the Oncogenicity

of Chlorothalonil in Rodents and an Assessment of

Human Relevance,’’ by Drs. C. F. Wilkinson and J.

C. Killeen, Regulatory Toxicology and

Pharmacology 24: 69-84 (1996), Article No. 006.

star), of 0.00766 (mg/kg/day)1 has been

used by the Agency when conducting

mathematical modeling to estimate

carcinogenic risk to man. ISK believes

that because the nephrotoxicity seen in

the rat is due to a threshold mechanism,

any risk associated with chlorothalonil

can be managed using the margin of

safety (exposure) approach.

Numerous metabolism and toxicology

studies indicate that chlorothalonil is

non-genotoxic and produces a speciesspecific renal toxicity in the rat that

eventually may lead to tumor formation

through an epigenetic mechanism.

Studies comparing metabolism and

toxicological effects in dogs with those

in rats demonstrate that the renal effects

observed in the rat are due to the

exposure of the kidney of the rat to

significant levels of nephrotoxic thiol

metabolites of chlorothalonil. In the

dog, no thio metabolites are found and

there are no toxic effects seen in kidneys

of dogs dosed with high levels of

chlorothalonil.

7. Reference dose (RfD). The NOEL for

chlorothalonil in the rat is 1.8 mg/kg

bwt based on the nephrotoxicity

observed in the chronic rat study. The

NOEL in the dog was 15 mg/kg bwt in

the 90-day study and 150 mg/kg bwt

based on the 1-year study. NOEL for

maternal toxicity from developmental

studies are 10 mg/kg bwt in rabbits and

100 mg/kg bwt in the rat. The NOEL for

pup growth in the reproduction study

was 1,500 mg/kg bwt, which would be

most conservatively estimated as

equating to approximately 75 mg/kg

bwt. Data indicate that the

nephrotoxicity in the rat is produced

through a mechanism for which there is

a clear threshold. In a study which

measured cell turnover in the rat kidney

with proliferating cell nuclear antigen

(PCNA) immunohistochemical staining,

a NOEL was established at 1.5 mg/kg

bwt. Other chronic studies have

established the NOEL for hyperplasia in

the kidney to be 1.8 mg/kg bwt. If all the

available toxicity data in laboratory

animals are considered without regards

to its applicability to humans, the

lowest NOEL for any adverse effect

would be 1.5 mg/kg bwt/day. Because

the mechanism of toxicity which is

related to the tumor formation in the

kidney has been shown to have a

threshold, the use of the normal 100-

fold safety factor in conjunction with

the 1.5 mg/kg NOEL would produce a

reference dose which would provide

more than adequate safety for all of the

possible effects seen in any laboratory

animal.

In two recent reviews of

chlorothalonil by the Joint Meeting of

Pesticide Residue Experts (1990 and

1992) and the review by the World

Health Organization’s International

Program for Chemical Safety, these

esteemed groups concluded that the rat

was not the appropriate species to use

in consideration of the risk assessment

for man. They concluded that the dog

was the more appropriate species for

determination of subchronic and

chronic effects. If the toxicological data

for the dog were used, the NOEL would

be at least 15 mg/kg bwt, which is based

on the most recent 90-day study of the

dog.

Therefore, under the most

conservative scenario (using the

toxicological data in the rat), the

reference dose would be 1.8 mg/kg bwt/

day divided by a 100-fold safety factor

or 0.018 mg/kg bwt/day with a

threshold model being used for

carcinogenic risk assessment. In the

scenario that uses the toxicological data

of the dog, the reference dose would be

15 mg/kg bwt/day divided by a safety

factor of 100 or 0.15 mg/kg bwt/day.

C. Aggregate Exposure

The following is a description of the

likelihood of exposure to chlorothalonil

from various routes.

1. Dietary exposure.— i. Food. The

Agency’s Dietary Exposure Analysis

dated April 1, 1996, of ISK’s petition

(PP 5F4558), which requested tolerances

for chlorothalonil and its metabolite, 4-

hydroxy- 2,5,6-

trichloroisophthalonitrile (SDS-3701)

in/on almond nutmeats and almond

hulls, determined the dietary exposure

from the proposed new anticipated

residue contributed from almonds to be

0.000001 mg/kg bwt/day to the U.S.

population and also to children ages 1

to 6.

The Agency had calculated that the

exposure of the general population from

existing published tolerances for

chlorothalonil is 0.000133 mg/kg bwt/

day and 0.00021 mg/kg bwt/day for

infants and children ages 1 to 6.

Unfortunately, the Agency’s calculation

of the total exposure contained a

significant error. The Agency grossly

overestimated the exposure from the use

of chlorothalonil on mushrooms by

using an anticipated residue of 2.54

ppm which constitutes an illegal

residue. The tolerance is 1.0 ppm. There

were also other overestimates of less

magnitude in the April 1996 EPA

document. ISK believes that the correct

exposure, based on the current

registered uses for chlorothalonil, is

0.0000642 mg/kg bwt/day for the

general population and 0.000105 mg/kg

bwt/day for infants and children 1 to 6

years of age.

ii. Drinking water. Chlorothalonil was

included for monitoring in the National

Survey of Pesticides in Drinking Water

Wells conducted by EPA. No

chlorothalonil residues were detected in

any of the 1,300 community water

systems and domestic wells (using

methodology for chlorothalonil having a

limit of detection (LOD) of 0.06 μg/l and

limit of quantitation of 0.12 μg/l). The

absence of chlorothalonil detections in

the National Survey of Pesticides in

Drinking Water Wells provides adequate

information to conclude that

chlorothalonil is not a contaminant in

drinking water wells and that the

population is not exposed to

chlorothalonil in these water sources.

These findings are consistent with the

known physical/chemical properties of

chlorothalonil including low water

solubility (0.9 ppm) and high affinity for

organic matter including soil. It has also

been demonstrated that chlorothalonil

does not leach into groundwater from

applications made to growing crops.

Aerobic aquatic metabolism studies

with chlorothalonil establish a half-life

in natural aquatic habitats of less than

10 hours, depending on environmental

conditions. Considering the short halflife of chlorothalonil in natural water/

sediment systems and that surface water

is filtered and treated prior to

consumption, chlorothalonil is not

likely to be present in drinking water

obtained from natural surface water

systems.

An exposure estimate, based on

surface water concentration recently

cited by EPA, would conclude that the

average concentration in surface water

would be less than 0.002 ppm.

Assuming that everyone in the United

States consumed untreated surface

water, the exposure to chlorothalonil of

the general population would be less

than 5.8 × 10-7 mg/kg bwt/day. This

would be a worse case scenario, which

would greatly overestimate exposure.

2. Non-dietary exposure. Potential

non-dietary exposures to chlorothalonil

may result from the following uses of

chlorothalonil. In each case, the

exposure would be from the dermal

route and only for an intermittent

duration. The two 21-day dermal

studies that have been conducted in the

rabbit and rat indicate that there is no

nephrotoxicity associated with the

dermal exposure to chlorothalonil at

dose levels up to 600 mg/kg/day.

Therefore, the exposures from the uses

of chlorothalonil listed below would not
Federal Register / Vol. 62, No. 30 / Thursday, February 13, 1997 / Notices 6783

be expected to add to the carcinogenic

risk associated with chlorothalonil.

i. Golf course uses. Chlorothalonil

products are commonly applied to golf

course trees and greens to control a

broad complex of turf diseases.

Application to golf course fairways is

much less common. Golf is not a game

played by infants or small children,

therefore no exposure to infants and

children would be anticipated.

ii. Residential owner uses.

Applications of chlorothalonil products

to home lawns are rare. Thus, there is

very little exposure to chlorothalonil

related to use on residential turf.

Applications to roses and other

ornamentals in home gardens is also a

minor use of chlorothalonil.

iii. Paint. Chlorothalonil is used in

paints and stains for control of mildew

and molds on exterior surfaces of

buildings. Chlorothalonil is also

occasionally used for interior paints, but

this use represents only a small

proportion of the chlorothalonil used in

paints. About 2% of the chlorothalonil

used in paint is used in interior paint;

however, only 0.2% or less of interior

paints in the United States contain

chlorothalonil. In paints chlorothalonil

is tightly bound within the paint

matrices; thus, effective control of

mildew may last for several years and

the potential for exposure is very

limited.

iv. Grouts. Chlorothalonil is used in

cement tile grouts and for control of

mildew and molds. Chlorothalonil is

bound within the grout matrices and

very little is available for exposure. This

is a minor use of chlorothalonil and

non-occupational dermal exposure of

humans to chlorothalonil from this

source is extremely low.

v. Wood treatment. Chlorothalonil is

not currently used for pressure-treating

wood. It is used for control of sapstain

as a surface treatment on rough-cut,

newly-sawn lumber to protect it from

molds and mildews while drying. Being

a surface residue, it is removed during

the finishing operations prior to sale of

the wood. Chlorothalonil does not occur

in structural wood used for residential

or occupational scenarios.

D. Cumulative Effects

ISK has considered the potential for

cumulative effects of chlorothalonil and

other substances that have a common

mechanism of toxicity. Chlorothalonil is

a halogenated benzonitrile which

readily undergoes displacement of the 2,

4 and 6 chlorines by glutathione and

other thiol containing amino acids and

proteins. In the rat, the thiol metabolites

are sufficiently absorbed to produce a

nephrotoxic effect. In dogs where this

absorption does not occur,

nephrotoxicity does not occur. ISK does

not have any information to indicate

that toxic effects observed in rats occur

through a mechanism which is common

to any other agricultural chemical.

Thus, consideration of common

mechanisms of toxicity is not

appropriate at this time.

Chlorothalonil should not be

confused with chlorinated hydrocarbon

pesticides which have significantly

different chemical and biological

properties.

E. Safety Determination

1. U.S. population. In EPA’s Dietary

Exposure Analysis, dated April 1, 1996,

for chlorothalonil and its metabolite in/

on almond nutmeats and almond hulls,

the Agency determined that the

oncogenic dietary risks associated with

potential exposure from anticipated

residue of 0.05 ppm from almonds is

minimal. The risk assessment

concluded that chlorothalonil does not

pose a significant chronic or acute

dietary risk for uses that are currently

published or for uses recommended by

EPA for registration. Unfortunately, the

Agency’s calculation of the total

exposure for existing published uses

contained a significant error. The

Agency grossly overestimated the

exposure from the use of chlorothalonil

on mushrooms by using an anticipated

residue of 2.54 ppm which constitutes

an illegal residue. The tolerance is 1.0

ppm.

The Agency has used a linearized

model to estimate the carcinogenic risk

associated with chlorothalonil, whereas

ISK believes that a threshold based

model is appropriate. If the linearized

multistage model is used with the

corrected exposure estimates for food

presented earlier, the carcinogenic risk

would be estimated at 4.9 × 107 for the

general population and 8.0 × 107 for

infants and children. Using the

overestimated exposure estimates of

EPA, with a threshold based model and

using the conservative RfD of 0.018 mg/

kg bwt/day, the margin of safety for the

general population would exceed 10,000

and the margin of safety for infants and

children would exceed 7,000. Using

corrected exposure estimates would

obviously yield larger margins of

exposure. Using a conservative RfD of

0.018 mg/kg/day, as the Agency has

done in recent Dietary Risk Evaluation

System (DRES) analyses, and

incorporating corrections needed in

exposure values for mushrooms and

several other lesser corrections, ISK

calculated the overall dietary exposure

to anticipated residues of

chlorothalonil, from all registered uses

and pending uses of chlorothalonil, to

be 0.36% of the RfD for the general U.S.

population and 0.59% of the RfD for

children ages 1 to 6 years old, which is

the group with the highest exposure.

Because the worse case assumption

for human exposure from drinking

water indicates that exposure would be

only 1% of the dietary exposure, the

risk assessment is not significantly

altered by considering the exposure

from drinking water.

2. Infants and children. There is a

complete data base for chlorothalonil

which includes pre- and post-natal

developmental toxicity data as well as

mechanistic data related to the rodent

specific nephrotoxicity observed in

subchronic and chronic studies. The

toxicological effects of chlorothalonil in

rodents are well understood.

Chlorothalonil has a low level of

toxicity in dogs.

In a 2-generation reproduction study

in rats, all reproductive parameters

investigated showed no treatmentrelated effects except pup weight gain.

Specifically, the weights of pups

exposed to chlorothalonil were

comparable to controls at parturition

through day four of lactation. It was

only after day four of lactation, when

the pups begin to consume the test diet,

that body weight gain lags behind

controls. This only occurred at the

highest dose tested, which is 3,000 ppm.

The dose of chlorothalonil the pups

would receive would be far in excess of

the estimated adult dose of 150 mg/kg

bwt/day (3,000 ppm -20). The doses for

the pups could have easily exceeded

500 mg/kg bwt/day. Dose levels of 375

mg/kg bwt and above have been shown

to significantly affect body weight in the

rat. Therefore, the reduction of body

weight gain observed in the

reproduction study is considered to be

comparable to the effects that have been

observed in older rats. The NOEL for

this effect was 1,500 ppm.

In developmental toxicity studies

conducted in the rat and the rabbit,

chlorothalonil did not cause any

developmental effects even at dose

levels that produced significant

maternal toxicity. In the rabbit a dose

level of 20 mg/kg bwt caused maternal

toxicity, but there were no

developmental effects and in the rat, a

dose level of 400 mg/kg bwt caused

maternal toxicity without

developmental toxicity.

The extensive data base that is

available for chlorothalonil is devoid of

any indication that chlorothalonil

would represent any unusual or

disproportionate hazard to infants or

children. Therefore, there is no need to

impose an additional 10x safety factor
6784 Federal Register / Vol. 62, No. 30 / Thursday, February 13, 1997 / Notices

for infants or children. The standard

uncertainty factor of 100x should be

used for all segments of the human

population when calculating risks

associated with chlorothalonil.

F. International Tolerances

A maximum residue level has not

been set for chlorothalonil on almonds

by the Codex Alimentarius Commission.

II. Public Record

EPA invites interested persons to

submit comments on this notice of

filing. Comments must bear a notation

indicating the docket number [PF-708].

A record has been established for this

notice of filing under docket number

[PF-708] including comments and data

submitted electronically as described

below. A public version of this record,

including printed paper versions of

electronic comments, which does not

include any information claimed as CBI,

is available for inspection from 8:30

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

excluding legal holidays. The public

record is located in Room 1132 of the

Public Response and Program Resources

Branch, Field Operations Division

(7506C), Office of Pesticide Programs,

Environmental Protection Agency,

Crystal Mall #2, 1921 Jefferson Davis

Highway, Arlington, VA.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as ASCII file avoiding the use

of special characters and any form of

encryption.

The official record for this notice of

filing, as well as the public version, as

described above will be kept in paper

form. Accordingly, EPA will transfer all

comments received electronically into

printed paper form as they are received

and will place the paper copies in the

official record which will also include

all comments submitted directly in

writing. The official record is the paper

record maintained at the address in

‘‘ADDRESSES’’ at the beginning of this

document.

List of Subjects

Environmental protection,

Administrative practice and procedure,

Agricultural commodities, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: February 7, 1997.

Donald R. Stubb,

Acting Director, Registration Division, Office

of Pesticide Programs.

[FR Doc. 97–3646 Filed 2–12–97; 8:45 am]

BILLING CODE 6560–50–F

[OPP–50825; FRL–5587–6]

Receipt of an Application for an

Experimental Use Permit of a PlantPesticide

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice.

SUMMARY: On November 15, 1996, EPA

received an application from Rogers

Seed Company for an experimental use

permit (EUP) for the plant-pesticide

Bacillus thuringiensis CryIA(b) deltaendotoxin and the genetic material

(plasmid vector pZ01502) necessary for

its production in corn. The Agency has

determined that this application may be

of regional and national significance.

Therefore in accordance with 40 CFR

172.11(a), the Agency is soliciting

public comments on this application.

DATES: Written comments must be

received by March 17, 1997.

ADDRESSES: Written comments, in

triplicate, should bear the docket

control number OPP–50825 and be

submitted to: Public Response and

Program Resources Branch, Field

Operations Division (7506C), Office of

Pesticide Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC 20460. In person bring

comments to: Rm. 1128, Crystal Mall #2,

1921 Jefferson Davis Highway, Crystal

City, VA.

Comments and data may also be

submitted electronically by sending

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

comments must be submitted as an

ASCII file avoiding the use of special

characters and any form of encryption.

Comments and data will also be

accepted on disks in WordPerfect in 5.1

file format or ASCII file format. All

comments and data in electronic form

must be identified by the docket control

number ‘‘OPP–50825.’’ No Confidential

Business Information (CBI) should be

submitted through e-mail. Electronic

comments on this document may be

filed online at many Federal Depository

Libraries.

Information submitted as a comment

concerning this document may be

claimed confidential 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.

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 Virginia

address given above from 8:30 a.m. to 4

p.m., Monday through Friday, excluding

legal holidays.

FOR FURTHER INFORMATION CONTACT: By

mail: Mike Mendelsohn, Regulatory

Action Leader, Biopesticides and

Pollution Prevention Division, Office of

Pesticide Programs, Environmental

Protection Agency, 401 M St., SW.,

Washington, DC 20460. Office location,

telephone number, and e-mail

address:5th Floor, Westfield Building

North Tower, 2800 Crystal Drive,

Arlington, VA, (703) 308–8715, e-mail:

mendelsohn.mike.@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: On

November 15, 1996, EPA received an

EUP application from Rogers Seed

Company, 600 N. Armstrong Pl., Boise,

Idaho 83704. The EUP application is

assigned EPA File Symbol 65268-EUPR. Rogers Seed has applied to test sweet

corn on a total of 7,730 acres in

California, Florida, Georgia, Idaho,

Iowa, Illinois, Kentucky, Maryland,

Minnesota, Washington, and Wisconsin.

Upon review of the Rogers Seed

application, any comments received in

response to this notice and any other

relevant information, the U.S. EPA will

set conditions under which the

experiments will be conducted. Any

issuance of an EUP amendment

approval will be announced in the

Federal Register.

Dated: January 30, 1997.

Janet L. Andersen,

Director, Biopesticides and Pollution

Prevention Division, Office of Pesticide

Programs.

[FR Doc. 97–3519 Filed 2–12–97; 8:45 am]

BILLING CODE 6560–50–F

FEDERAL COMMUNICATIONS

COMMISSION

Notice of Public Information

Collections Submitted to OMB for

Review and Approval

February 7, 1997.

SUMMARY: The Federal Communications

Commission, as part of its continuing

effort to reduce paperwork burden

invites the general public and other

Federal agencies to take this

opportunity to comment on the