15700 Federal Register / Vol. 62, No. 63 / Wednesday, April 2, 1997 / Notices

vigor is reduced by the toxin introduced

by the feeding of pear psyllas which

ultimately reduces overall yield. The

Applicants state that the need for a

method of reducing the overwintering

adult population before they lay

appreciable numbers of eggs in the

spring is critical to pear psylla control.

The only effective pre-bloom materials

for some years were the synthetic

pyrethroids, permethrin and fenvalerate.

When widespread resistance to these

materials became evident in the psylla

population by 1987–88, the Applicants

state that cyfluthrin was used under

section 18 exemptions in 1988 – 1992,

and was found to be efficacious.

In 1993, this use of fenoxycarb was

first requested by Washington state, who

claimed that resistance to cyfluthrin was

being observed. However, the toxicology

data available at that time for

fenoxycarb did not support this use, and

cyfluthrin was again used under section

18 during the 1993 season. In the 1994,

1995 and 1996 seasons, both

Washington and Oregon requested

exemptions for this use. Adequate

toxicology data were available to

support the use under section 18, and

the exemptions were subsequently

granted. The Applicants claim that most

of the pear psylla populations are now

resistant to cyfluthrin, and are therefore

again requesting this use of fenoxycarb

for control of pear psylla in pears.

The Applicants wish to treat up to

18,900 acres of pear trees in Oregon, and

up to 26,000 acres in Washington. This

would translate to a possible total of

4,725 pounds of active ingredient [(a.i.)]

(18,900 lbs. product) in Oregon, and up

to 6,500 lbs. a.i. (26,000 lbs. product) in

Washington. Up to two applications

would be made per growing season, at

a maximum rate of 2 oz. a.i. (8 oz.

product) per acre, diluted in water to

make a minimum spray volume of 50–

400 gallons per acre. Application of

fenoxycarb would not be allowed by air

or through chemigation equipment.

Fenoxycarb would be used pre-bloom

and would not be allowed to be applied

during or after pear bloom, nor to open

blossoms of weeds or cover crops.

Negligible residues are expected

because this is a pre-bloom only use and

available residue chemistry data

indicate non-detectable residues will

occur.

The regulations governing section 18

require publication of a notice of receipt

in the Federal Register and solicitation

of public comment on an application for

a specific exemption proposing the first

food use of an active ingredient.

Normally, a notice of receipt shall give

the public 15 days in which to file

comments on the application. The

Administrator may shorten or eliminate

the comment period if she determines

that the time available for a decision on

the application requires it (40 CFR

§166.24). The comment period has been

eliminated for these specific exemption

requests because implementation of the

Food Quality Protection Act delayed

application processing, the use season

had started and available data indicate

that there is a reasonable certainty that

no harm will result from aggregate

exposure to the pesticide chemical

residue, including all anticipated

dietary exposure and all other exposures

for which there is reliable information.

A record has been established for this

notice under docket number [OPP–

181038] (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 Resource Branch, Field

Operations Division (7506C), Office of

Pesticide Programs, Environmental

Protection Agency, Crystal Mall #2,

1921 Jefferson Davis Highway,

Arlington, VA.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption.

The official record for this notice, as

well as the public version, as described

above will be kept in paper form.

Accordingly, EPA will transfer all

comments received electronically into

printed, paper form as they are received

and will place the paper copies in the

official record which will also include

all comments submitted directly in

writing. The official record is the paper

record maintained at the address in

ADDRESSES at the beginning of this

document. Accordingly, interested

persons may submit written views on

this subject to the Filed Operations

Division at the address above.

List of Subjects

Environmental protection, Pesticides

and pests, Emergency exemptions.

Dated: March 24, 1997.

Stephen L. Johnson,

Director, Registration Division, Office of

Pesticide Programs.

[FR Doc. 97–8399 Filed 4–1–97; 8:45 am]

BILLING CODE 6560–50–F

[PF–726; FRL–5594–9]

ISK Biosciences Corporation;

Pesticide Tolerance Petition Filing

AGENCY: Environmental Protection

Agency (EPA).

ACTION: Notice of filing.

SUMMARY: This notice announces the

initial filing of a pesticide petition

proposing the establishment of timelimited tolerances for residues of the

fungicide, chlorothalonil and its

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

trichloroisophthalonitrile in or on nonbell peppers. This notice includes a

summary of the petition that was

prepared by the petitioner, ISK

Biosciences Corporation.

DATES: Comments, identified by the

docket control number [PF-726], must

be received on or before, May 2, 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 be 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 5.1

file format or ASCII file format. All

comments and data in electronic form

must be identified by docket control

number [PF-726]. Electronic comments

on this notice may be filed online at

many Federal Depository Libraries.

Additional information on electronic

submissions can be found in Unit II. of

this document.

Information submitted as a 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
Federal Register / Vol. 62, No. 63 / Wednesday, April 2, 1997 / Notices 15701

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

(7505W), Office of Pesticide Programs,

Environmental Protection Agency, 401

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

Office location, telephone number, and

e-mail address: Rm. 229, CM #2, 1921

Jefferson Davis Highway, Arlington, VA,

(703) 305–6226; e-mail:

gilesparker.cynthia@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: EPA has

received a pesticide petition (PP

6F4676) from ISK Biosciences

Corporation, 5966 Heisley Road, P.O.

Box 8000, Mentor, Ohio 44061-8000

proposing pursuant to section 408(d) of

the Federal Food, Drug, and Cosmetic

Act, 21 U.S.C. section 346a(d), to amend

40 CFR 180.275 by establishing a timelimited tolerance for a period of 2 years

for residues of the fungicide

chlorothalonil and its metabolite, 4-

hydroxy-2,5,6-trichloroisophthalonitrile

in or on the raw agricultural commodity

non-bell peppers at 5.0 parts per million

(ppm). ISK Biosciences Corporation has

committed to providing additional

residue data during this 2–year period

from trials conducted in Mexico in

support of a permanent tolerance. 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); 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, ISK

Biosciences Corporation 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

Biosciences Corporation. EPA is in the

process of evaluating the petition. As

required by section 408(d)(3), EPA is

including the summary as a part of this

notice of filing. EPA has made minor

edits to the summary for the purpose of

clarity.

I. ISK Biosciences’ 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

non-bell peppers occurs as a surface

residue. 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 nonbell peppers support a tolerance of 5.0

ppm for combined residues of

chlorothalonil and its metabolite, 4-

hydroxy-2,5,6-trichloroisophthalonitrile

in or on the raw agricultural

commodity.

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 milligrams/kilograms (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. The

overall conclusion is 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

transformation assays. All were negative

with the following two exceptions:

Chlorothalonil was positive in an in

vitro chromosomal aberration assay in

CHO cells without metabolic activation

but was negative with metabolic

activation.

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 Bacillus

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, 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/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 two-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 subchronic

toxicity study (90 days) 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 no effect

level for renal histopathology was 10
15702 Federal Register / Vol. 62, No. 63 / Wednesday, April 2, 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.

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 no observed

adverse effect level (NOAEL) 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, 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, it can be concluded 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 NOAEL 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 no effect level 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 level

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, EPA’s 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 Biosciences

Corporation has provided a significant

amount of mechanistic data indicating

that the tumors result from a threshold

mechanism. A potency factor, Q1*, of

0.00766 (mg/kg/day)-1 has been used by

the Agency when conducting

mathematical modeling to estimate

carcinogenic risk to man. ISK

Biosciences Corporation 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.1

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 thiol 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 no effect

level for chlorothalonil in the rat is 1.8

mg/kg bwt based on the nephrotoxicity

observed in the chronic rat study. The

no effect level in the dog was 15 mg/kg

bwt in the 90–day study and 150 mg/kg

bwt based on the one-year study. No

effect levels for maternal toxicity from

developmental studies are 10 mg/kg bwt

in rabbits and 100 mg/kg bwt in the rat.

The no effect level 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 bromodeoxyuridine

(BRDU) 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 is 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 no effect

level would produce a RfD 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

Heath Organization’s International

Program for Chemical Safety, these
Federal Register / Vol. 62, No. 63 / Wednesday, April 2, 1997 / Notices 15703

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, based on the

most recent 90-day study in the dog.

Therefore, under the most

conservative scenario (using the

toxicological data in the rat), the RfD

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 in 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. ISK

Biosciences Corporation has conducted

a dietary exposure analysis for

chlorothalonil and its metabolite, 4-

hydroxy-2,5,6-trichloroisophthalonitrile

(SDS-3701) in or on non-bell peppers

utilizing EPA’s Dietary Risk Evaluation

System (DRES) based on the 1977-78

Food Consumption Survey. The results

demonstrate that the dietary exposure

from anticipated residues of 0.5 ppm

contributed from non-bell peppers is

0.00000218 mg/kg bwt/day for the U.S.

population or 0.0121% of the RfD.

The Agency had calculated that the

exposure of the general population from

existing published tolerances for

chlorothalonil is 0.000134 mg/kg bwt/

day or 0.744 percent of the RfD.

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 mg/l

and limit of quantitation of 0.12 mg/l).

The absence of chlorothalonil detections

in the National Survey 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 ppb. Assuming

that everyone in the U.S. consumed

untreated surface water, the exposure to

chlorothalonil of the general population

would be less than 5.8 x 10-7 mg/kg bwt/

day. This would be a worst 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 be expected to add to the

carcinogenic risk associated with

chlorothalonil.

i. Golf course uses. Chlorothalonil

products are commonly applied to golf

course tees 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, also 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 Biosciences 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

Biosciences 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. ISK Biosciences

Corporation has conducted a risk

assessment for chlorothalonil in or on

non-bell peppers using the 1977-78

Food Consumption Survey and a

potency factor, Q1*, of 0.00766 (mg/kg/

day)-1 and has determined that

oncogenic dietary risks associated with
15704 Federal Register / Vol. 62, No. 63 / Wednesday, April 2, 1997 / Notices

potential exposure using an anticipated

residue of 0.5 ppm, would 1.7 x 10-8.

The Agency has used a linearized

model to estimate the carcinogenic risk

associated with chlorothalonil, whereas

ISK Biosciences believes that a

threshold based model is appropriate.

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 DRES

analyses, and incorporating corrections

needed in exposure values for

mushrooms and several other lesser

corrections, ISK Biosciences

Corporation 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.

Because the worst case assumption for

human exposure from drinking water

indicate 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 two-generation reproduction

study in rats, all reproductive

parameters investigated showed no

treatment-related effects except pup

weight gain. Specifically, the weights of

pups exposed to chlorothalonil were

comparable to controls at parturition

through day 4 of lactation. It was only

after day 4 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;

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 divided

by 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

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

There is currently no maximum

residue level set for chlorothalonil on

non-bell peppers by the Codex

Alimentarius Commission.

II. Public Record

A record has been established for this

notice under docket control number

[PF–726] (including comments and data

submitted electronically as described

below). A public version of the 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 Resources Branch,

Field Operations Division (7506C),

Office of Pesticide Programs,

Environmental Protection Agency,

Crystal Mall #2, 1921 Jefferson Davis

Highway, Arlington, VA.

Electronic comments can be sent

directly to EPA at:

opp-docket@epamail.epa.gov

Electronic comments must be

submitted as an ASCII file avoiding the

use of special characters and any form

of encryption.

The official record for this

rulemaking, as well as the public

version, as described above will be kept

in paper form. Accordingly, EPA will

transfer all comments received

electronically into printed, paper form

as they are received and will place the

paper copies in the official rulemaking

record which will also include all

comments submitted directly in writing.

The official rulemaking record is the

paper record maintained at the address

in ADDRESSES at the beginning of this

document.

List of Subjects

Environmental protection,

Administrative practice and procedure,

Agricultural commodities, Pesticides

and pests, Reporting and recordkeeping

requirements.

Dated: March 24, 1997.

Stephen L. Johnson,

Director, Registration Division, Office of

Pesticide Programs.

[FR Doc. 97–8388 Filed 4–1–97; 8:45 am]

BILLING CODE 6560–50–F

FEDERAL COMMUNICATIONS

COMMISSION

Notice of Public Information

Collections Being Reviewed by the

Federal Communications Commission

March 25, 1997.

SUMMARY: The Federal Communications

Commissions, 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

following information collection, as

required by the Paperwork Reduction

Act of 1995, Public Law 104–13. An

agency may not conduct or sponsor a

collection of information unless it

displays a currently valid control

number. No person shall be subject to

any penalty for failing to comply with

a collection of information subject to the

Paperwork Reduction Act (PRA) that

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Comments are requested concerning (a)

whether the proposed collection of

information is necessary for the proper

performance of the functions of the

Commission, including whether the

information shall have practical utility;

(b) the accuracy of the Commission’s

burden estimate; (c) ways to enhance

the quality, utility, and clarify of the

information collected; and (d) ways to

minimize the burden of the collection of

information on the respondents,

including the use of automated

collection techniques or other forms of

information technology.

DATES: Persons wishing to comment on

this information collection should

submit comments June 2, 1997.

ADDRESSES: Direct all comments to

Dorothy Conway, Federal

Communications Commissions, Room